CarolRivers-combined

Dr. Carol Rivers' 

PREPARING FOR THE WRITTEN BOARD EXAM 

IN EMERGENCY MEDICINE 

Eighth Edition 

Volume I 

Ohio 

ACEP 

American College of Emergency Physicians 

Advocacy 

-Education I Leadership

Published by: 

Ohio Chapter, American College of Emergency Physicians (Ohio ACEP) 

35 7 0 Snouffer Road 

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ISBN 978-0-9917470-0-7 

Date of original release: January 7 992 

Most recent update: January 20 7 7 

Copyright ©20 7 7 Ohio Chapter, American College of Emergency Physicians. All 

rights reserved. No part of this publication may be reproduced or transmitted in 

any form, electronic or mechanical, including photocopying, recording, storage 

in any information retrieval system, or otherwise, without the prior written 

permission of the publisher. 

DISCLAIMER 

Ohio Chapte,~ American College of Emergency Physicians publishes information 

believed to be in agreement with the accepted standards of practice at the date 

of publication. Due to the continual state of change in diagnostic procedures, 

treatment, and drug therapy, Ohio ACEP and the writers and editors are not 

responsible for any errors or omissions. In the practice of medicine, the reader 

should confirm the use of any information with other sources.

The object of education is not learning, but discipline 

and enlightenment of the mind. 

Woodrow Wilson

Dr. Carol Rivers' Preparing for the Written Board Exam in 

Emergency Medicine, Eighth Edition 

EDITORS 

SENIOR ASSOCIATE EDITOR 

Ann M. Dietrich, MD, FAAP, FACEP 

Associate Professor of Primary Care (Lead), Ohio University Heritage College of Osteopathic Medicine; Pediatric 

Associate Medical Director, MedFlight of Ohio, Columbus, Ohio 

SECTION EDITORS 

Thomas Green, DO, MMM, MPH, CPE, FACOEP, FACEP 

Associate Dean, Clinical Affairs; Chief Academic Officer (interim)-HEARTLand Network OPTI and Associate Professor 

Family Medicine, Des Moines University College of Osteopathic Medicine; Associate Professor Emergency Medicine/ 

Family Medicine, Midwestern University-Chicago College of Osteopathic Medicine; Attending Physician, Emergency 

Department, Central Iowa Healthcare, Marshalltown, Iowa 

Joseph P. Martinez, MD, FACEP, FAAEM 

Associate Professor of Emergency Medicine and Medicine, Assistant Dean for Student Affairs, and Assistant Dean for 

Clinical Medical Education and Residency Programs Liaison, University of Maryland School of Medicine, Baltimore, 

Maryland 

Amal Mattu, MD, FACEP 

Professor and Vice Chair of Education, Co-Director, Emergency Cardiology Fellowship, University of Maryland School 

of Medicine, Baltimore, Maryland 

Victor J. Scali, DO, FACOEP-D 

Director of EM, Residency Education, and Associate Professor, Department of Emergency Medicine, Rowan University 

School of Osteopathic Medicine, Stratford, New Jersey 

Howard A. Werman, MD, FACEP 

Professor of Clinical Emergency Medicine, The Ohio State University Wexner Medical Center; Medical Director, 

MedFlight, Columbus, Ohio 

Sandra L. Werner, MD, ROMS, FACEP 

Operations Director, Emergency Medicine, Associate Director, Emergency Medicine Residency Program, MetroHealth 

Medical Center; Associate Professor, School of Medicine, Case Western Reserve University School of Medicine, 

Cleveland, Ohio 

CONTRIBUTORS 

Michael Abraham, MD, MS 

Clinical Assistant Professor, Department of Emergency Medicine, University of Maryland School of Medicine, 

Baltimore, Maryland 

Nervous System Disorders 

Rudd J. Bare, MD, MMEL 

Chief of Emergency Medicine; Faculty, Emergency Medicine Residency Program, Western Reserve Hospital, Cuyahoga 

Falls, Ohio; Summa Health System EM Residency, Akron City Hospital, Akron, Ohio; Masters in Medical Education and 

Administration, University of New England Medical School, Portland, Maine; Assistant Professor of Emergency Medicine, 

NEOMED, Rootstown, Ohio; Professor of Emergency Medicine, Ohio University, Athens, Ohio 

Environmental Disorders 

iv

Michelle Blanda, MD, FACEP 

Professor and Chair Emeritus of Emergency Medicine, Northeast Ohio Medical University, Akron City Hospital, 

Summa Health System, Akron, Ohio 

Renal and Urologic Disorders 

Michael C. Bond, MD, FACEP, FAAEM 

Associate Professor, Residency Program Director, Department of Emergency Medicine, University of Maryland School 


Orthopedic Emergencies 

Laura J. Bontempo, MD, MEd, FAAEM 

Assistant Professor, Emergency Medicine, University of Maryland School of Medicine, Baltimore, Maryland 

Cutaneous Disorders 

Brian Browne, MD, FACEP 

Professor of Emergency Medicine, Chair, Department of Emergency Medicine, University of Maryland School of 

Medicine, Baltimore, Maryland 


Luca R. Delatore, MD 

Medical Director of the James Emergency Department, Assistant Professor, Department of Emergency Medicine, 

The Ohio State University Wexner Medical Center, Columbus, Ohio 

Oncologic Disorders 

Paul de Saint Victor, MD, FACEP, MHA, CPE 

Associate Director, Emergency Medicine Residency, Mercy St. Vincent Medical Center, Toledo, Ohio; President, 

Emergency Department Consultants 

Additional Tips for Good Performance, How to Take a Multiple-Choice Exam 

Sarah B. Dubbs, MD 

Clinical Assistant Professor, Assistant Residency Program Director, Department of Emergency Medicine, University 

of Maryland School of Medicine, Baltimore, Maryland 

Gynecologic and Obstetric Disorders 

Scott Felten, MD, FACEP 

US Acute Care Solutions Residency Director, Tulsa, Oklahoma 

Immune System Disorders 

William R. Fraser, DO, FACOEP-D 

Emergency Medicine Residency Director, Doctor's Hospital Ohio Health, Columbus, Ohio 

Abdominal and Gastrointestinal Disorders 

Hannah L. Hays, MD 

Assistant Professor, Department of Emergency Medicine and Pediatrics, The Ohio State University Wexner Medical 

Center and Nationwide Children's Hospital and Central Ohio Poison Center, Columbus, Ohio 

Toxicologic Disorders 

Colin G. Kaide, MD, FACEP, FAAEM 

Associate Professor of Emergency Medicine, Attending Physician of Emergency Medicine and Hyperbaric Medicine, 


Hematologic Disorders 

V

Jonathan Keary, MD, FACEP 

Staff Physician, Emergency Services Institute, Cleveland Clinic, Cleveland, Ohio 

Endocrine, Metabolic, and Nutritional Disorders 

Benjamin J. Lawner, DO, MS, EMT-P, FAAEM 

Assistant Professor, Department of Emergency Medicine, University of Maryland School of Medicine, Deputy EMS 

Medical Director, Baltimore City Fire Department, Baltimore, Maryland 

Emergency Medical Services 

Le N. Lu, MD, MS 

Clinical Assistant Professor, Director, Pediatric Emergency Medicine Education, Department of Emergency Medicine, 

University of Maryland School of Medicine; Director, Pediatric Emergency Department, Upper Chesapeake Medical 

Center, Baltimore, Maryland 

Pediatric Emergencies 

Patrick J. Maloney, MD 

Director, Pediatric Emergency Services, Mission Hospital and Mission Children's Hospital, Asheville, North Carolina 

Traumatic Disorders 

Laura Matrka, MD 

Assistant Professor, Otolaryngology-Head & Neck Surgery, The Ohio State University Wexner Medical Center, 

Columbus, Ohio 

Head, Ear, Eye, Nose, and Throat Disorders 

Stacy Mccallion, MD 

Summa Health System, Akron City Hospital, Akron, Ohio; Associate Professor of Emergency Medicine, NEOMED, 

Rootstown, Ohio; Professor of Emergency Medicine, Ohio University, Athens, Ohio 


Michael J. McCrea, MD, FACEP, FAAEM 

Assistant Residency Director, Simulation Education Director, Emergency Medicine Residency, Mercy St. Vincent 

Medical Center, Toledo, Ohio 

Cardiovascular Disorders 

Jillian L. McGrath, MD, FACEP 

Assistant Professor of Emergency Medicine, Department of Emergency Medicine, The Ohio State University Wexner 

Medical Center, Columbus, Ohio 


Colleen M. McQuown, MD, FACEP 

Director of Research Education, Department of Emergency Medicine, Summa Akron City Hospital; Associate Professor, 

Northeast Ohio Medical University, Rootstown, Ohio 

Other Components of the Practice of Emergency Medicine 

Siamak Moayedi, MD 

Assistant Professor, Department of Emergency Medicine, University of Maryland School of Medicine, Baltimore, Maryland 

Systemic Infectious Disorders 

Sreeja M. Natesan, MD 

Assistant Professor, Duke University Medical Center, Durham, North Carolina 

Thoracic and Respiratory Disorders 

vi

Sarah K. Sommerkamp, MD, RDMS 



Matthew Tabbut, MD, FACEP 

Attending Physician, Department of Emergency Medicine, MetroHealth Medical Center; Assistant Professor, Case 

Western University School of Medicine, Cleveland, Ohio 

Procedures and Skills Integral to the Practice of Emergency Medicine 

Laura R. Thompson, MD, MS, FACEP 

Assistant Professor, Department of Emergency Medicine, The Ohio State University Wexner Medical Center, 


Psychobehavioral Disorders 

Mercedes Torres, MD 




Melissa Tscheiner, MD, FACEP 

Adjunct Assistant Professor, University of North Carolina School of Medicine-Asheville; Department of Emergency 

Medicine, Mission Hospital, Asheville, North Carolina 

Musculoskeletal Disorders (Nontraumatic) 

Travis Ulmer, MD, FACEP 

Vice President, US Acute Care Solutions, Canton, Ohio; Clinical Assistant Professor of Emergency Medicine, 

Ohio University Heritage College of Osteopathic Medicine, Athens, Ohio 


PRODUCTION 

Laura L. Tiberi, MA, CAE 

Ohio ACEP Executive Director 

Holly J.F. Dorr, MBA, CAE 

Ohio ACEP Deputy Executive Director, Editorial and Production Coordinator 

Susan E. Aiello, ELS 

Medical Editor 

Sheryl Lazenby 

Designer 

vii

VIII

TABLE OF CONTENTS 

VOLUME I 

Foreword ........................................................................................................................................................................ x 

Introduction .................................................................................................................................................................. xi 

Recommended Study Plan ........................................................................................................................................... xiii 

Cardiovascular Disorders .............................................................................................................................................. 1 

Head, Ear, Eye, Nose, and Throat Disorders ................................................................................................................ 97 

Abdominal and Gastrointestinal Disorders ............................................................................................................... 169 

Thoracic and Respiratory Disorders .......................................................................................................................... 231 

Traumatic Disorders .................................................................................................................................................. 297 

Orthopedic Emergencies ........................................................................................................................................... 343 

Musculoskeletal Disorders (Nontraumatic) ............................................................................................................... 393 

Nervous System Disorders ........................................................................................................................................ 409 

Gynecologic and Obstetric Disorders ....................................................................................................................... 443 

VOLUME II 

Pediatric Emergencies ............................................................................................................................................... 489 

Toxicologic Disorders ................................................................................................................................................ 543 

Endocrine, Metabolic, and Nutritional Disorders ...................................................................................................... 591 

Environmental Disorders ........................................................................................................................................... 633 

Psychobehavioral Disorders ...................................................................................................................................... 673 

Hematologic Disorders ............................................................................................................................................. 711 

Oncologic Disorders ................................................................................................................................................. 743 

Systemic Infectious Disorders ................................................................................................................................... 759 

Immune System Disorders ........................................................................................................................................ 783 

Renal and Urologic Disorders ................................................................................................................................... 803 

Cutaneous Disorders ................................................................................................................................................. 829 

Emergency Medical Services ..................................................................................................................................... 869 

Procedures and Skills Integral to the Practice of Emergency Medicine ..................................................................... 883 

Other Components of the Practice of Emergency Medicine ...................................................................................... 941 

Mechanics of the Written Board Exam ....................................................................................................................... 975 

Additional Tips for Good Performance ....................................................................................................................... 979 

ix

FOREWORD 

FOREWORD 

Welcome to the eighth edition of Dr. Carol Rivers' Preparing for the Written Board Exam in Emergency Medicine. Initially 

created by Dr. Carol S. Rivers, a national leader in board review education, this book has long been the gold standard 

for comprehensive emergency medicine review and exam preparation. Dr. Rivers was residency trained in emergency 

medicine and extensively involved in the educational aspects of emergency medicine as a lecturer, a writer, a featured 

speaker, instructor, and tutor ... helping those who wanted and needed a firmer grasp of the practice of emergency 

medicine. In 1983, Dr. Rivers began to focus her teaching efforts on preparing physicians for the certifying examinations 

in emergency medicine. 

We celebrate her passion as a teacher, role model, and mentor. Since her early days as a leader and visionary in the 

specialty of emergency medicine, Dr. Rivers devoted her life to the advancement of emergency medicine and to the 

improvement of patient care, one physician at a time. Through her educational endeavors, providing publications and 

tutorials for emergency physicians and residents, she demonstrated outstanding service, leadership, and commitment to 

the specialty of emergency medicine. Ohio ACEP is proud to continue the tradition of the Rivers' board review with this 

current revision. 

This book was envisioned, written, and compiled to fill a need-the need for a teaching textbook (not another reference 

book) aimed directly at the written board examination (not the entire field of emergency medicine) and designed for the 

busy physician who has limited time to devote to study and whose study time comes in unequal segments. 

In its eighth edition, Dr. Carol Rivers' Preparing for the Written Board Exam continues the tradition as a premier teaching 

textbook for preparing for the Written Board exam in emergency medicine. Significant improvements have been made to 

this text to enhance the reader's experience and to cover the American Board of Emergency Medicine (ABEM) core content 

of the "Model of the Clinical Practice of Emergency Medicine" (The EM Model) and the "Table of Specificity" of the 

American Board of Osteopathic Board of Emergency Medicine. We are confident that your use of this two-volume review 

text will give you a foundation for exam preparation and for passing an emergency medicine written certification exam. 

X

INTRODUCTION 

INTRODUCTION 

This book has been written primarily for emergency physicians preparing for a written certification or recertification 

exam, and for residents preparing for in-service exams in emergency medicine. Its purpose is to provide a concise, 

focused review of material that usually appears on these exams. Information that may seem "basic" is included, because 

it is essential to your understanding of principles and concepts that are important parts of the exam. 

While this book has been used as a reference text, it is primarily a teaching text. The largest division of the book-the 

review of medical topics-is essentially a set of notes that contain the knowledge you must have to pass the exam. 

Treat them as notes-as your own notes. Read them with a pen, pencil, or highlighter in hand. Underline or highlight 

information you especially want to remember. Write notes of your own in the margins and other space provided. As 

you read, you will notice that some material is repeated-on purpose. A teaching text requires some redundancy for 

emphasis and coherence. 

The eighth edition is an expanded and updated revision of the prior editions. New topics have been added that are 

pertinent to both the board exam and the residency in-service exams. Outdated information has been removed, and 

controversial issues have been clarified wherever possible. To enhance clinical acuity for the resident in training, a few 

bedside diagnostic techniques, in addition to descriptions of selected procedures, are included. 

You will occasionally be referred to other materials to enhance your study. Depending on how much time you have to 

prepare for this exam (see "Recommended Study Plan"), you may find the following references helpful: 

1. Tintinalli, et al, Emergency Medicine: A Comprehensive Study Guide, Eighth ed. McGraw-Hill Company, Inc. 

(referred to in this text as Tintinalli's text). 

2. Marx, et al, Rosen's Emergency Medicine: Concepts and Clinical Practice, Eighth ed., 2 vols. Saunders (referred 

to in this text as Rosen's Text). 

3. The bookstore at Ohio ACEP (www.ohacep.org) 

4. Self-assessment testing products such as the Physician's Evaluation and Educational Review in Emergency 

Medicine (PEER) products available through ACEP. A variety of other self-assessment tools are also available 

online. 

These are supplemental resources. If asked to review a particular subject (eg, LeFort facial fractures), you should go to 

Tintinalli's and/ or Rosen's texts and read the appropriate section. Another text that has become popular with practicing 

emergency physicians is Hardwood-Nuss' Clinical Practice of Emergency Medicine (Lippincott Williams & Wilkins, 

Philadelphia). In general, it is easier to read than Tintinalli or Rosen and uses a numbered, itemized format similar to that 

found in this text. 

The self-assessment or mock exam products may be valuable in your preparation, because they reacquaint you with the 

process of answering multiple-choice questions and help you define areas of weakness that require further study. 

Several radiographic images are on the written exam. Whenever possible, those that merit review are noted. As you read 

through the medical topics included in this text, it is recommended that you have a pad of note paper and a pen handy. 

As you come to a paragraph in which a radiograph or CT review of a particular entity is recommended, jot it down. 

When you have completed your I ist, review common radiographs for each diagnosis. This is important for you to do 

because the radiographs, CT, and MRI prints on the written board exam are not usually taken from standard textbooks; 

they usually come from teaching files. A good text reference is The Radiology of Emergency Medicine by Harris and 

Harris. You can also view radiographs, CTs, and MRls online with Ohio ACEP's case pictorial review at www.ohacepelearning.org. 

ECGs and other pictorials are also presented on the exam. An ECG text that has been recommended is ECGs for the 

Emergency Physician by Mattu and Brady (Blackwell). Board preparation courses traditionally have hundreds of photos 

and ECGs that are ideal for many participants. Ohio ACEP's Web-based e-learning site features over 1,400 cases that 

include diagnostic photos, radiographs, ultrasounds, and other images integrated with key facts to reinforce key concepts 

of emergency medicine. Another excellent pictorial source is Atlas of Emergency Medicine by Knoop, Stack, and Storrow 

(McGrawHill). In addition to clinical presentations, each entity includes a differential diagnosis, emergency department 

treatment and disposition, and clinical pearls. 

A special feature of this text is clinical presentations of specific diagnoses as clinical scenarios in a storytelling format. 

This concept is based on the "simple chain technique," the object of which is to "chain" or link one item to the next in 

the order you wish to remember them. Basically, this chain is a story that involves all the items you want to remember in 

a particular sequence. You will be able to do this by using mental images and tying each item to the next. How does the 

chaining technique work? One item acts as a stimulus (or cue) for the next item. It's almost like seeing a slide show or a 

movie in your mind's eye, where you can automatically anticipate the next scene. You don't have to strain your mental 

faculty searching for it; it's right there. 

Chaining has been tested in scientific studies that have verified its effectiveness as a memory-enhancing tool for 

simple rote memory tasks. In this respect, imagery is probably the single most important aspect of memory training. In 

numerous studies, one group of students would be shown pictures of an array of items to remember, and the other group 

XI

INTRODUCTION 

would simply be given a list of words to remember. Both groups would be given the same test to determine what they 

remembered. The people who had been given images consistently scored higher than those who had been given lists. 

The important point here is that vivid images of items will improve your memory of those items. 

Why should the seemingly insignificant procedure of linking one item to another dramatically improve recall? The 

answer is found to be in the linking itself. Separate pieces of information become unified when connected to each other. 

In other words, when 20 pieces of information are presented separately, you have to remember 20 independent segments 

of information. But when we link the items together, as we do in chaining, the 20 items actually represent only one 

segment of data. 

Some areas of this text do contain memory recall facts (ie, lists), and they are unavoidable. However, these "lists" are 

easier to remember when they are mixed with imagery. Pure memorizing is a left brain function. Imagery is a right brain 

function. When combined, the reader remembers more detail. 

Before you begin reading this text, briefly scan each of the sections so that you can get an overview of the information 

presented. You might want to read the nonclinical/nonacademic sections first, because other activities are discussed 

there and you will want to allow time to schedule some or all of them in the time before the exam. You have enough 

information in this text to pass the exam, but other activities can help you as well. So pick and choose those that sound 

worthwhile, and then plan your time to include them in your final preparation. 

xii

RECOMMENDED STUDY PLAN 


Engage in regular and consistent study, because knowledge is acquired by studying over a reasonable period of time. 

What is learned in a hurry is seldom completely learned and soon forgotten. Do not "cram" for this exam. Cramming is 

an attempt to learn in a very short period of time what should have been learned through regular and consistent study 

over a period of weeks or months. Cramming seldom pays off in terms of effective learning. If you cram, it is likely that 

you will be more confused than prepared on the day of the exam. 

Conditions and Components 

Before you start reading this text, an organized approach will help maximize your time and effort. It is important 

to strategize and focus on the topics that generally have a greater degree of emphasis on the exams. The list below 

describes the relative weight given to different elements of the EM Model on the ABEM Examination. 



Signs, Symptoms, and Presentations 


Procedures and Skills 

Thoracic-Respiratory Disorders 





Obstetrics and Gynecology 




Other Components 

Renal and Urogenital Disorders 

Endocrine, Metabolic and Nutritional Disorders 




Total 

10% 

10% 

9% 

8% 

8% 

8% 

5% 

5% 

5% 

5% 

4% 

4% 

3% 

3% 

3% 

3% 

2% 

2% 

2% 

1% 

100% 

Pediatric: 8% minimum 

Geriatric: 6% minimum 

The next point you need to consider is how much time you have left before the exam. Check off the time frame that is 

most appropriate to your situation. 

Less than one month 

One to two months 

Two to three months 

Three months or more 

Now that you know which topics are covered most heavily on the written board exam and how much time you have left 

to study, a methodical approach is in order. There are four steps in this process: 

1. A self-assessment evaluation to determine strong and weak areas. 

2. A comparison of your self-assessment score with an analysis of your current level of preparedness for the exam. 

3. A study plan that includes the number of hours per day and the number of days per week you need to study. 

4. A method of reading and reviewing that promotes high retention and recal I of specific information. 

XIII


These four points will be described further in the paragraphs that follow. Using the time frame that you previously selected, 

choose the category that pertains to you and read the program outlined therein. That is your program, your study-approach 

method. Some of you will already have a plan in mind and may decide to incorporate parts of the information from within the 

different categories, and that's fine. But for those looking for direction, these categories have been written primarily for you. 

Category I: Less than 1 month 

1. Preceding each academic chapter is a series of multiple-choice questions. Go through the questions for every 

chapter in the academic section, recording your answers in the book or on a separate sheet of paper. When you're 

finished, use the answer key at the end of each series of questions and mark your incorrect answers. Use the 

pre-chapter multiple-choice question worksheet (on page xvi) to record and determine your percentage of correct 

answers for each section. 

2. Analyze your percentage score for the questions from each chapter to see where you are in the scheme of things: 

a. 85% or higher is a good score. Review the questions missed, and note the correct answers. 

b. 75%-85% is reasonably good, but further study is needed. For the questions you missed, review those 

particular subjects within the body of that chapter. 

c. Anything


Category Ill (2-3 months) 

1. With additional time to prepare, a self-assessment testing product such as PEER content review or an on line 

question assessment tool may be of value to your study plan. These products typically include multiple tests and an 

evaluation of your performance on the tests. The tests will give you a good sense of your priority areas. 

2. Plan your study schedule. If you have about 2 months, set aside about 3 hours a day, 5 days a week; it is 

recommended that you do not study more than 2 hours at one sitting, because your ability to retain information is 

likely to diminish after that time. If you have 3 months to study, 2 hours a day, 5 days a week should be sufficient. 

3. As you go through this text, use a marker to highlight key points, ie, information you didn't know previously or that 

seems important. Be sure to review the radiographs and other pictorials noted in the text, using the recommended 

sources. Divide your material into "easy reading" and "hard reading" categories. An example might be: 

Easy Reading 

Mechanics of the Written Board Exam 

"Light" academic chapters (eg, cutaneous, EMS, 

emergency department administration) 

Additional Tips for Good Performance 

Hard Reading 

Self-assessment test-taking and review 

The first nine academic chapters (especially 

Cardiovascular Disorders) 

Tintinalli's text reading 

Alternate your study time between the two categories. Do "hard reading" during one study session and "easy 

reading" the next. This will maximize your learning time as well as allow you to maintain your stamina. When you 

have finished, go back and reread this entire review book, looking especially for "pearls" (information that looks 

important) and other information that clarifies your understanding of a particular subject. Be sure to go through the 

questions preceding each academic chapter and record your scores on page xvi; it will help focus your attention as 

you read the academic material. If you have time, reread again but, this time only the material you have highlighted, 

and then stop. The material most likely to be tested already appears in bold type. 

4. In the final 7-10 days before the exam, go through the flashcards (an additional product available through Ohio 

ACEP) and practice clinical scenarios two or three times and stop studying the day before the exam. You're ready. 

Category IV (3 months or more) 

1. With additional time to prepare, a self-assessment testing product such as PEER content review or an on line 

question assessment tool may be of value to your study plan. These products typically include multiple tests and an 

evaluation of your performance on the tests. The tests will give you a good sense of your priority areas. 

2. Plan your study schedule. If you have 3-4 months before the exam, plan on studying about 2 hours a day, 5 days 

a week. If you have more than 4 months, 2 hours a day, 4 days a week is sufficient. You may also want to attend 

a written board course. (See the section titled "Additional Tips for Good Performance" for info on written board 

courses). 

3. As you go through this text, use a marker to highlight key points, ie, info you didn't know previously or that seems 

important. The material most likely to be tested already appears in bold type. Be sure to review radiographs and 

other pictorials noted in the text, using the recommended sources. Divide your material into "easy reading" and 

"hard reading" categories. An example might be as follows: 

Easy Reading 

Mechanics of the Written Board Exam 

"Light" academic chapters (eg, cutaneous, EMS, 

emergency department administration) 

Additional Tips for Good Performance 

Hard Reading 

Self-assessment test-taking and review 

The first nine academic chapters (especially 

Cardiovascular Disorders) 

Tintinalli's text reading 

Alternate your study time between the two categories. Do "hard reading" during one study session and "easy 

reading" the next. This will maximize your learning time as well as allow you to maintain your stamina. When you 

have finished, go back and reread the entire book, looking especially for "pearls" (info that looks important) and any 

information that clarifies your understanding of a particular subject. Be sure to go through the questions preceding 

each academic chapter and record your scores on the next page; it will help focus your attention as you read the 

academic material. If you have time, reread again but, this time, only material you have highlighted, and then stop. 

4. In the last 2 weeks before the exam, go through the flashcards (an additional product available through Ohio ACEP) 

and practice clinical scenarios until you know all the answers. Then stop studying. You are well prepared. 

xv


Regardless of in which "category" you place yourself, test-taking skills and strategies can play a significant role in your 

exam score. Be sure to read "How To Take a Multiple-Choice Exam" in the section titled "Mechanics of the Written 

Board Exam." Practice using the techniques described for answering questions for which you don't know the answers. 

Start first with the questions in this book. If you have time, do the same with the self-assessment testing products. Use 

other sources as well, such as the flashcards (an additional product available through Ohio ACEP) that supplement this 

text. Some written board preparation courses also offer practice questions. Under no circumstances is it recommended 

that you focus your attention on test-taking techniques at the expense of studying the academics of emergency medicine. 

If your knowledge base is lacking, no amount of test-taking skill is going to result in a passing score. In addition, these 

techniques don't work all the time. But if you're one of those candidates who scores 73%-74% on exam content, 

knowing how to use test-taking techniques can raise your score another percent or two- just enough to help you pass. 

Pre-chapter Multiple Choice Self-Assessment Questions Worksheet 

Chapter 

Cardiovascular Disorders 35 

Head, Ear, Eye, Nose, Throat Disorders 56 

Abdominal and Gastrointestinal Disorders 39 

Thoracic and Respiratory Disorders 27 

Traumatic Disorders 30 

Orthopedic Emergencies 35 

Musculoskeletal Disorders (Nontraumatic) 11 

Nervous System Disorders 16 

Gynecologic and Obstetric Disorders 19 

Pediatric Emergencies 41 

Toxicologic Disorders 21 

Endocrine, Metabolic, and Nutritional 29 

Disorders 

Environmental Disorders 34 

Psychobehavioral Disorders 15 

Hematologic Disorders 15 

Oncologic Disorders 11 

Systemic Infectious Disorders 14 

Immune System Disorders 14 

Renal and Urologic Disorders 11 

Cutaneous Disorders 17 

Emergency Medical Services 9 

Procedures and Skills 13 

Other Components 22 

Total 534 

Scoring 

• 85% or higher is a good score, Review any questions missed, and note the correct answers. 

# answered # of pre-chapter Percentage of Missed questions 

correctly questions correct answers to review 

• 75%-85% is reasonably good, but further study is needed. For the questions you missed, review those particular subjects within the body of 

that chapter. 

• Anything

CARDIOVASCULAR DISORDERS 


DYSRHYTHMIAS .......................................................................................................................................................... 9 

Basic Principles of Cardiac Conduction Disturbances ................................................................................................... 9 

Standard ECG and Rhythm Strips ............................................................................................................................ 9 

Normal Morphology ............................................................................................................................................... 9 

Causes of Abnormal Morphologies ......................................................................................................................... 9 

Specific Rhythm Assessments ...................................................................................................................................... 14 

Sinus Rhythm ....................................................................................................................................................... 14 

Premature Atrial Contractions ............................................................................................................................... 14 

Sinus Tachycardia ................................................................................................................................................. 14 

Sinus Bradycardia ................................................................................................................................................. 15 

Supraventricular Tachycardia ................................................................................................................................ 15 

Atrial Fibrillation .................................................................................................................................................. 15 

Atrial Flutter ......................................................................................................................................................... 15 

Multifocal Atrial Tachycardia ................................................................................................................................ 16 

Junctional Premature Contractions ....................................................................................................................... 16 

Premature Ventricular Contractions ...................................................................................................................... 16 

Ventricular Tachycardia ........................................................................................................................................ 17 

Ventricular Fibrillation .......................................................................................................................................... 18 

Pulseless Electrical Activity ................................................................................................................................... 18 

Bundle-Branch Blocks .......................................................................................................................................... 18 

Si noatrial Block .................................................................................................................................................... 1 9 

Sick Sinus Syndrome ............................................................................................................................................ 20 

Atrioventricular Blocks ......................................................................................................................................... 20 

Preexcitation Syndromes ...................................................................................................................................... 21 

Etiologies and Management of Dysrhythmias .............................................................................................................. 22 

Premature Atrial Contractions ............................................................................................................................... 22 

Sinus Tachycardia ................................................................................................................................................. 22 

Sinus Bradycardia ................................................................................................................................................. 22 

Supraventricular Tachycardia ................................................................................................................................ 23 

Atrial Fibrillation .................................................................................................................................................. 25 

Atrial Flutter ......................................................................................................................................................... 26 

Multifocal Atrial Tachycardia ................................................................................................................................ 26 

Junctional Premature Contractions ....................................................................................................................... 27 

Premature Ventricular Contractions ...................................................................................................................... 27 

Ventricular Tachycardia ........................................................................................................................................ 28 

Ventricular Fibrillation .......................................................................................................................................... 29 

Pulseless Electrical Activity ................................................................................................................................... 30 

Sick Sinus Syndrome ............................................................................................................................................ 30 

Atrioventricular Blocks ......................................................................................................................................... 30 

Wolff-Parkinson-White Syndrome ......................................................................................................................... 31 

Pacemakers ................................................................................................................................................................. 32 

Emergency Pacing Techniques .............................................................................................................................. 32 

Indications for Temporary Cardiac Pacing ............................................................................................................. 32 

Tips for Temporary Transvenous Pacemaker Placement ......................................................................................... 32 

r--· Pacemaker Failure ................................................................................................................................................ 33 

Automatic Implantable Cardioverter Defibrillators ..................................................................................................... 34 

ACUTE CORONARY SYNDROME .............................................................................................................................. 36 

Definition .................................................................................................................................................................... 36 

Clinical Presentations, Risk Factors, and Predictive Factors ........................................................................................ 36


Diagnosis .................................................................................................................................................................... 37 

Management ............................................................................................................................................................... 42 

Complications ............................................................................................................................................................. 47 

CONGESTIVE HEART FAILURE ................................................................................................................................... 49 

Etiology, Precipitating Factors, and Signs and Symptoms ............................................................................................ 49 

Diagnostic Evaluation ................................................................................................................................................. 50 

Management ............................................................................................................................................................... 50 

CARDIOMYOPATHIES AND SPECIFIC HEART MUSCLE DISEASES ............................................................................ 53 

Cardiomyopathies ....................................................................................................................................................... 53 

Definition ............................................................................................................................................................. 53 

Idiopathic Dilated (Congestive) Cardiomyopathy .................................................................................................. 53 

Restrictive Cardiomyopathy .................................................................................................................................. 54 

Hypertrophic Cardiomyopathy ............................................................................................................................. 54 

Specific Heart Muscle Diseases ................................................................................................................................... 56 

PERICARDIAL DISORDERS ......................................................................................................................................... 58 

Pericarditis .................................................................................................................................................................. 58 

Pericardia! Tamponade ................................................................................................................................................ 60 

MYOCARDITIS ............................................................................................................................................................ 62 

Etiology ....................................................................................................................................................................... 62 

Clinical Presentation ................................................................................................................................................... 62 


Management ............................................................................................................................................................... 63 

VALVULAR HEART DISEASE ....................................................................................................................................... 65 

Mitra! Valve Prolapse ("Click Murmur Syndrome") ..................................................................................................... 65 

Mitra! Stenosis ............................................................................................................................................................ 65 

Mitra! Regurgitation .................................................................................................................................................... 66 

Aortic Stenosis ............................................................................................................................................................ 68 

Aortic Regurgitation .................................................................................................................................................... 68 

Tricuspid Stenosis ........................................................................................................................................................ 70 

Tricuspid Regurgitation ............................................................................................................................................... 70 

Prosthetic Valves ......................................................................................................................................................... 71 

Conditions Necessitating Antibiotic Prophylaxis for Infective Endocarditis ................................................................ 73 

ENDOCARDITIS ......................................................................................................................................................... 74 

Definition .................................................................................................................................................................... 74 

Pathophysiology .......................................................................................................................................................... 7 4 



Diagnosis .................................................................................................................................................................... 76 

Management ............................................................................................................................................................... 7 6 

THORACIC AORTIC DISSECTIONS AND ABDOMINAL AORTIC ANEURYSMS ......................................................... 77 

Thoracic Aortic Dissections ........................................................................................................................................ 77 

Epidemiology ....................................................................................................................................................... 77 

Pathophysiology ................................................................................................................................................... 77 

Natural History ..................................................................................................................................................... 77 

Classification System ............................................................................................................................................ 77 

Clinical Presentation ............................................................................................................................................ 78 

Diagnostic Evaluation ........................................................................................................................................... 79 

Management ........................................................................................................................................................ 80 

Abdominal Aortic Aneurysms ...................................................................................................................................... 81 

Definition and Anatomic Location ........................................................................................................................ 81 

Pathogenesis ......................................................................................................................................................... 81 

Risk Factors .......................................................................................................................................................... 81 


Diagnosis and Management ................................................................................................................................. 82 

2


DEEP VENOUS THROMBOSIS .................................................................................................................................... 83 

Pathogenesis ................................................................................................................................................................ 83 


Acute Deep Venous Thrombosis ........................................................................................................................... 83 

Massive Deep Venous Thrombosis ........................................................................................................................ 83 

Risk Factors ................................................................................................................................................................. 83 

Predicting Pretest Probability for DVT: The Well's Clinical Criteria ............................................................................. 84 


Pharmacologic Therapy ............................................................................................................................................... 86 

Disposition-Admission Criteria ................................................................................................................................. 87 

HYPERTENSIVE EMERGENCIES AND URGENCIES ..................................................................................................... 88 

Hypertensive Emergencies .......................................................................................................................................... 88 

Definition ............................................................................................................................................................. 88 


Management ........................................................................................................................................................ 88 

Hypertensive Urgencies .............................................................................................................................................. 90 

Definition and Etiology ......................................................................................................................................... 90 

Management ........................................................................................................................................................ 90 

3

CARDIOVASCULAR DISORDERS: SELF-ASSESSMENT QUESTIONS 


1. ECG findings of tall T waves, wide QRS complexes, flattened P waves, and a prolonged PR interval are most 

consistent with the presence of: 

(a) 

Hypercalcemia 

(b) Hyperkalemia 

(c) Hypocalcemia 

(d) Hypokalemia 

2. The presence on ECG of sagging ST segments, short QT intervals, and flattened or inverted T waves is most 

accurately described as: 

(a) 

Digitalis effect 

(b) Digitalis toxicity 

(c) 

Hypercalcemia 

(d) Hypokalemia 

3. The treatment of ventricular tachycardia and supraventricular tachycardia is: 

(a) 

Lidocaine 

(b) Adenosine 

(c) Cardioversion 

(d) Dependent on the hemodynamic stability of the patient 

4. All of the following are indications for pacemaker therapy except: 

(a) Asymptomatic bifascicular or trifascicular block 

(b) Hemodynamically unstable bradycardia unresponsive to drug therapy 

(c) Mobitz II second-degree AV block in the presence of an acute Ml 

(d) Overdrive of tachydysrhythmias refractory to drug therapy or electrical cardioversion 

5. The most common cause of failure to pace is: 

(a) 

Battery depletion 

(b) Oversensing 

(c) Undersensing 

(d) Wire fracture 

6. ST segment elevation in leads V 1 

-V 6 

with reciprocal ST depression in leads II, Ill, and a VF is characteristic of: 

(a) Acute anterior wall Ml 

(b) Acute inferior wall Ml 

(c) Acute lateral wall Ml 

(d) Acute posterior wall Ml 

7. All of the following drugs may be given through an endotracheal tube except: 

(a) Atropine 

(b) Epinephrine 

(c) Naloxone 

(d) Sodium bicarbonate 

8. Appropriate early therapy for acute pulmonary edema may include al I of the following agents except: 

(a) 

Digitalis 

(b) Furosemide 

(c) Nitroglycerin 

(d) Oxygen 

9. What is the earliest radiographic finding of congestive heart failure? 

(a) 

Alveolar edema 

lb) Cardiomegaly 

(c) Interstitial edema 

(d) Pulmonary vascular redistribution to the upper lung fields 

4


10. What is the most effective medical therapy for the treatment of atypical chest pain associated with hypertrophic 

cardiomyopathy? 

(a) 

~-blockers 

(b) Digitalis 

(c) Morphine 

(d) Nitroglycerin 

11. The diagnostic procedure of choice for detecting a pericardia! effusion occurring in association with pericarditis is: 

(a) Chest radiograph 

(b) ECG 

(c) Echocardiography 

(d) Radionuclide scanning 

12. The differential diagnosis of neck vein distention associated with hypotension includes al I of the following except: 

(a) Acute mitral regurgitation 

(b) Infective endocarditis 

(c) Pericardia! tamponade 

(d) Tension pneumothorax 

13. Most pulmonary emboli originate from venous thrombi in the: 

(a) Calf 

(b) Heart 

(c) Lower extremities and pelvis 

(d) Upper extremities 

14. All of the fol lowing statements regarding the use of aortography in the evaluation of acute aortic dissections are 

true except: 

(a) It can miss dissection if the false lumen is thrombosed. 

(b) It has been the traditional diagnostic gold standard. 

(c) It is 1 00% accurate. 

(d) Unlike rapid-sequence CT scanning with contrast, aortography also assesses the aortic valves and branches. 

15. All of the following statements regarding DeBakey type Ill aortic dissections are accurate except: 

(a) 

Initial management of these dissections is medical. 

(b) They are equivalent to Stanford type B dissections. 

(c) They are the most common type of dissection. 

(d) Long-term management of these dissections is usually medical. 

16. Medical therapy for aortic dissections is aimed at controlling the forces that propagate the dissection. The first-line 

agent(s) used to accomplish this goal is/are: 

(a) 

~-blockers and nitroglycerin 

(b) ~-blockers and nitroprusside 

(c) Nitroprusside alone 

(d) Trimethaphan 

17. A 30-year-old woman presents with palpitations of sudden onset and a feeling of nervousness. The patient denies 

drug use of any type and has had no other episodes of palpitations or anxiety. The nurse hands you a rhythm strip 

demonstrating an irregular tachycardia at 250 beats per minute with QRS complexes that vary in width between 

narrow and wide. There is no evidence of torsades. The likely etiology of this rhythm is: 

(a) Anxiety 

(b) Cocaine use 

(c) Mitral valve prolapse 

(d) Wolff-Parkinson-White syndrome 

5


18. Atypical chest pain associated with mitral valve prolapse is treated with: 

(a) ~-blockers 

(b) Morphine 

(c) Nitroglycerin 

(d) Oxygen 

19. The treatment of choice for hypertension associated with eclampsia is: 

(a) 

Diuretics 

(b) Labetalol 

(c) Magnesium sulfate and hydralazine 

(d) Nitroprusside 

20. The primary difference between a hypertensive urgency and a hypertensive emergency is that in a hypertensive 

emergency: 

(a) It is usually treated with oral medications. 

(b) The diastolic blood pressure is 2:130 mmHg. 

(c) There is evidence of acute end-organ dysfunction or damage. 

(d) There is no history of hypertension. 

21. The ideal location of the catheter tip for temporary transvenous pacing is in the: 

(a) Apex of the right ventricle 

(b) lntraventricular septum 

(c) 

Right atrium 

(d) Superior vena cava 

22. Successful placement of a temporary transvenous pacemaker under ECG guidance is indicated by the observation 

of ____ on the cardiac monitor. 

(a) 

Small positive P waves and near-normal QRS complexes 

(b) Prominent inverted P waves and smaller negative QRS complexes 

(c) ST elevation 

(d) ST depression 

23. Placement of a pacemaker magnet over most permanent pacemakers results in: 

(a) 

Conversion from a demand to a fixed-rate mode 

(b) Conversion from a fixed-rate to a demand mode 

(c) 

Permanent disabling of the pacemaker 

(d) Temporary disabling of the pacemaker 

24. A 31-year-old man is brought in by ambulance for evaluation of a syncopal episode that occurred while he 

was playing a friendly game of competitive basketball. Examination reveals a rapid biphasic carotid pulse and 

a prominent systolic ejection murmur along the left sternal border and at the apex. You suspect hypertrophic 

cardiomyopathy and ask the patient to perform the Valsalva maneuver while you auscultate his heart. Assuming your 

diagnosis is correct, you would expect the intensity of the murmur to ____ with this maneuver. 

(a) 

Decrease 

(b) Disappear 

(c) 

Increase 

(d) Remain unchanged 

25. All of the following statements regarding hypertrophic cardiomyopathy are accurate except: 

(a) 

Amiodarone is the treatment of choice for the ventricular dysrhythmias that occur in patients with this disorder. 

(b) Digitalis and vasodilators are typically the most useful agents in the management of this disorder. 

(c) 

It is inherited in >50% of patients. 

(d) It is characterized by septa! hypertrophy without associated ventricular dilatation. 

6


26. Antibiotic prophylaxis for bacterial endocarditis is definitely recommended in high-risk patients for which of the 

following procedures? 

(a) Endotracheal intubation 

(b) Dental procedures associated with significant gingival bleeding 

(c) Placement of a Foley catheter 

(d) Suturing of a laceration 

27. Antibiotic prophylaxis for endocarditis is indicated for major dental procedures in patients with all of the following 

conditions except: 

(a) Congenital heart disease 

(b) History of bacterial endocarditis 

(c) Mitra! valve prolapse 

(d) Prosthetic heart valves 

28. All of the following statements regarding prosthetic heart valves are accurate except: 

(a) Endocarditis should be suspected in any patient with a prosthetic valve who presents with fever, especially if a 

new regurgitation heart murmur is heard. 

(b) Mechanical valves require lifelong systemic anticoagulation. 

(c) Patients with valve dysfunction secondary to thrombus formation usually present with acute onset of CHF, 

hypotension, and muting (or loss) of the prosthetic valve sound. 

(d) Tissue valves cause greater hemolysis and are more thrombogenic than mechanical valves. 

29. In patients with automatic implantable cardioverter defibrillators (AICDs) in place who require CPR: 

(a) CPR is performed in the usual manner. 

(b) The provider may perceive an AICD shock if the device has not been deactivated. 

(c) Perception of an AICD shock by a provider is neither dangerous nor uncomfortable. 

(d) Al I of the above are correct. 

30. Janeway lesions are most accurately described as: 

(a) Nontender, erythematous macular lesions on the fingers, palms, soles 

(b) Nontender erythematous nodules on the dorsal aspect of the fingertips 

(c) Retinal hemorrhages with central clearing 

(d) Tender, erythematous nodules on the volar aspect of the fingertips 

31. The most useful test for making the diagnosis of endocarditis is: 

(a) Blood culture 

(b) CBC 

(c) ECG 

(d) Erythrocyte sedimentation rate 

32. The organism responsible for most cases of right-sided endocarditis is: 

(a) Enterococcus spp 

(b) Streptococcus epidermidis 

(c) Streptococcus viridans 

(d) Staphylococcus aureus 

33. Which of the following statements regarding mitral stenosis is false? 

(a) Typical presenting symptoms include dyspnea on exertion and hemoptysis. 

(b) Common ECG findings are left atrial enlargement and atrial fibrillation. 

(c) Most cases are the result of rheumatic heart disease. 

(d) The most common complication is infective endocarditis. 

34. The type of CHF that occurs in association with beriberi is most accurately characterized as: 

(a) 

High-output left ventricular failure 

(b) High-output right ventricular failure 

(c) Low-output left ventricular failure 

(d) Low-output right ventricular failure 

7


35. When compared with the ST elevation that occurs in association with acute Ml, the ST elevation that occurs in 

association with acute pericarditis is: 

(a) 

Concave upward in configuration 

(b) More diffuse 

(c) Associated with concurrent PR depression 

(d) All of the above 

ANSWERS 

1. b 8. a 15. C 22. C 29. d 

2. a 9. d 16. b 23. a 30. a 

3. d 10. a 17. d 24. C 31. a 

4. a 11. C 18. a 25. b 32. d 

5. b 12. b 19. C 26. b 33. d 

6. a 13. C 20. C 27. C 34. a 

7. d 14. c 21. a 28. d 35. d 

Use the pre-chapter multiple choice question worksheet (page xvi) to record and determine the percentage of correct 

answers for this chapter. 

8


DYSRHYTHMIAS 

I. BASIC PRINCIPLES OF CARDIAC CONDUCTION DISTURBANCES 

A. Standard ECG and rhythm strips 

1. Recordings are obtained at a paper speed of 25 mm/sec. 

2. The vertical axis measures distance; the smallest divisions are 1 mm long x1 mm. 

3. The horizontal axis measures time; each small division is 0.04 sec/mm. 

B. Normal morphology 

Courtesy of Dr. Michael McCrea 

1. P wave= atrial depolarization 

a. Upright in leads I, 11, 111, aVL, and aVF; inverted in lead aVR 

b. Measures



(2) Conduction delays: PR, QRS, and QT intervals may all be prolonged. QT interval is prolonged 

primarily because of selective prolongation of the ST segment. 

(3) Dysrhythmias: sinus bradycardia and atrial fibrillation with a slow ventricular response are the most 

commonly encountered in this setting; the risk of developing dysrhythmias increases as the core 

temperature falls below 86°F (30°C); at core temperatures below 77°F (25°C), spontaneous ventricular 

fibrillation and asystole may occur. (These patients must be handled gently, because dysrhythmias are 

easily introduced). 

b. Management of hypothermia-induced dysrhythmias 

(1) Most usually require only supportive therapy, because the dysrhythmias resolve spontaneously with 

rewarming. 

(2) Cardiac arrest 

(a) 

In profoundly hypothermic patients who appear to be in cardiac arrest, palpating pulses may be 

extremely difficult. 

(b) If unsure, began CPR without delay. 

(3) Ventricular fibrillation 

(a) Often refractory to defibrillation attempts until the patient is rewarmed 

(b) Defibrillation should be attempted with up to three shocks but, if unsuccessful, CPR and rapid 

rewarming measures should be instituted. Further attempts at defibrillation should be withheld 

until the patient's temperature rises above 86°F (30°C). 

(c) As the myocardium rewarms, ventricular fibrillation may convert spontaneously or resolve in 

response to defibrillation. 

(d) Magnesium sulfate produces spontaneous conversion in these patients. 

(4) The role of ACLS medications, including vasopressors, in severe hypothermic patients in cardiac arrest 

is of uncertain value, and standard algorithms may be used. 

(5) If narcotic abuse is suspected, naloxone should be considered, because it may act on central opiate 

receptors to decrease the severity of hypothermia seen in overdoses. 

(6) In general, a patient is not considered "all dead" until "warm and dead, 11 with warm being 95°F (35°C). 

2. Hypokalemia 

a. Progressively more prominent U wave (best seen in VJ 

b. Flattening ofT wave (earlier) followed by inversion (later) 

c. Depression of ST segment 

d. Prominent P wave 

e. Prolongation of the PR and QT (U) interval 

f. Ventricular tachycardia/torsades 

g. In the presence of hypokalemia, susceptibility to digitalis toxicity and its associated dysrhythmias is increased. 

3. Hyperkalemia 


a. Tall hyperacute T wave (earliest ECG finding) 

b. Prolonged PR interval 

10


c. Flattened or absent P wave 

d. Wide QRS complex that eventually blends with the T wave to assume a "sine wave" appearance 

e. Heart blocks 

f. QT interval normal or shortened 

Table 1: Effects on ECC with Increasing Potassium Concentration 

Potassium 

Concentration (mEq/L) 

5.5-6.5 

6.5-8.0 

>8.0 

ECG Changes 

Large amplitude T waves, peaked, tented symmetric 

PR interval prolongation 

P wave flattening/disappearance 

QRS widening 

Conduction block with escape beats 

Sine wave appearance 

Ventricular fibrillation 

Asystole 

4. Hypocalcemia 

a. Prolonged QT interval because of prolongation of the ST segment 

b. Terminal T wave inversion (less consistent finding) 

c. Ventricular dysrhythmias (including torsades de pointes) 

5. Hypercalcemia 

a. Depressed ST segments, widened T waves, and shortened ST segments and QT intervals. 

b. Bradyarrhythmias may occur, with bundle-branch patterns that may progress to second-degree block or 

complete heart block. 

6. Hypomagnesemia 

a. Prolonged PR and QT intervals 

b. Widened QRS complex 

c. ST segment abnormalities 

d. Flattened or inverted T waves (especially in the precordial leads) 

e. Ventricular dysrhythmias (premature ventricular contractions, ventricular tachycardia, torsades de pointes, 

ventricular fibri I lation) 

f. Hypomagnesemia usually occurs in association with other electrolyte abnormalities (particularly 

hypokalemia), and many of the ECG findings are similar to those seen with hypokalemia and hypocalcemia 

(pictured above). 

g. In the presence of hypomagnesemia, susceptibility to digitalis toxicity and its associated dysrhythmias is 

increased. 

7. Digitalis effects 

a. Sagging ST segment with its concavity directed upward (resembles a hockey stick) 

b. Short QT interval 

c. Flattened or inverted T wave 

d. Modestly prolonged PR interval 

e. These effects are especially prominent in the lateral leads and occur in most patients who are adequately 

digitalized; they are not an indication of digitalis toxicity. 

11


8. Digitalis toxicity 

a. Pathophysiology: digitalis produces toxicity by 

(1) Poisoning the Na+-K+-ATPase pump - increased intracellular entry of Na+ and Ca++ and egress of K+ - 

increased excitability - ectopy and tachydysrhythmias 

(2) Increasing vagal tone and automaticity - decreased conduction in the AV node - bradydysrhythmias 

and AV blocks 

b. Factors that increase sensitivity to digitalis and predispose to toxicity 

(1) Electrolyte abnormalities (hyperkalemia or hypokalemia, hypomagnesemia, hypercalcemia) 

(2) Hypoxia 

(3) Metabolic alkalosis 

(4) Increasing age 

(5) Presence of underlying cardiac disease (ischemia, CHF, congenital heart disease) 

(6) Presence of chronic underlying systemic illness (COPD, renal failure, hypothyroidism) 

(7) Drug interactions (quinidine, calcium channel blockers, erythromycin, amiodarone, captopril, and 

ibuprofen) 

c. ECG findings 

(1) Premature ventricular contractions (most common arrhythmia), often bigeminal and multiform: the 

most common digitalis-induced rhythm disturbance 

(2) Junctional tachycardia (common) 

(3) Sinus bradycardia 

(4) Sinus tachycardia 

(5) Sinoatrial and AV nodal blocks 

(6) Sinus arrest 

(7) Torsades de pointes 

(8) Ventricular tachycardia 

(9) Ventricular fibrillation 

(10) Atrial tachycardias with AV block are very specific but not pathognomonic for digitalis toxicity 

(11) Nonparoxysmal junctional tachycardia 

(12) Atrial fibrillation with a slow ventricular response, ie, AV dissociation 

(13) Bidirectional ventricular tachycardia (highly suggestive of digitalis toxicity but rare) 

d. Clinical symptoms 

(1) Flu-like syndrome with profound malaise, anorexia, nausea, vomiting, and diarrhea 

(2) Visual disturbances (blurred vision, halos around objects, and yellow or green color aberrations) 

(3) Mental status changes, including confusion, drowsiness, and psychosis 

e. Acute digitalis toxicity is usually seen in young and otherwise healthy patients as a result of either 

accidental or intentional overdose; it is commonly associated with hyperkalemia, high digoxin levels, 

bradydysrhythmias, and AV blocks. Toxicity in these patients is most closely correlated with the degree 

of hyperkalemia (not the serum digoxin level). Chronic digitalis toxicity generally occurs in older cardiac 

patients with reduced renal function who are taking diuretics. These patients are usually normo- or 

hypokalemic, have digoxin levels that are minimally increased or normal, and most commonly have a 

ventricular dysrhythmia. 

f. Classic clinical scenario 

(1) Acute intoxication: A 3-year-old is brought in by his parents for evaluation after accidental ingestion 

of grandpa's "heart pills." Based on information obtained from the parents, the child has ingested 10.7 

mg of digoxin sometime within the past 2 hours and has vomited twice. The cardiac monitor shows 

a junctional rhythm with sinus block and type I second-degree AV block; laboratory studies reveal a 

potassium level of 6.2 mEq/L, along with a markedly increased digoxin level of 61. The child is on no 

medications and is otherwise healthy. 

(2) Chronic intoxication: A 65-year-old woman with a past medical history of coronary artery disease, 

CHF, and renal insufficiency is brought in by ambulance for evaluation. Her medications include 

furosemide, digitalis, sublingual nitroglycerin, and baby aspirin. According to family members, she 

has become progressively more confused and weak over the past few days and has not been eating 

well. The ECG shows a regular wide complex tachycardia with alternating QRS polarity (bidirectional 

ventricular tachycardia) and laboratory studies reveal a digoxin level of 3.5 and a potassium 

concentration of 3.0 mEq/L. 

12


g. Management 

(1) IV line, oxygen, pulse oximeter, cardiac monitor 

(2) Gastric lavage is contraindicated because of risk of vagal stimulation causing bradycardia or asystole. 

(3) Administer multiple doses of activated charcoal to all patients with potentially toxic ingestions; 

activated charcoal prevents systemic absorption and, when multiple doses are given, enhances 

elimination by interrupting the prominent enterohepatic circulation of digitalis. 

(4) Seek and treat factors that may contribute to digitalis toxicity. 

(a) Hypokalemia (correct cautiously in the presence of AV blocks; correction can actually exacerbate 

AV conduction defects) 

(b) Hyperkalemia is best treated with Fab fragments (digoxin-specific antibody fragments); do not 

administer calcium; it can potentiate cardiotoxicity. 

(c) Hypomagnesemia 

(d) Hypoxia 

(e) 

Dehydration 

(5) Control tachydysrhythmias 

(a) 

Phenytoin and lidocaine are the drugs of choice for tachydysrhythmias. 

(b) Magnesium sulfate may also be useful in suppressing ventricular irritability. 

(c) Avoid cardioversion (digoxin decreases the fibrillatory threshold); restrict its use to situations of 

last resort and use the lowest possible energy level. 

(d) Avoid use of bretylium, Class IA antidysrhythmics (eg, procainamide, isoproterenol) and 

propranolol; these agents can exacerbate dysrhythmias and AV conduction disturbances. 

(6) Manage symptomatic bradycardia or AV block with atropine. If atropine is unsuccessful, cardiac 

pacing (external or transvenous) may be used while waiting for Fab fragments to take effect. External 

pacing is preferred, because transvenous pacemaker insertion may induce tachydysrhythmias in these 

patients. 

(7) Fab fragments 

(a) Should be administered to patients with: 

i. Ventricular dysrhythmias (ventricular fibrillation, ventricular tachycardia) 

ii. Symptomatic bradycardias unresponsive to atropine 

iii. Hyperkalemia (K+ >5.0 mEq/L) secondary to digitalis intoxication 

iv. Coingestions of cardiotoxic drugs (~-blockers, cyclic antidepressants) 

v. Large, potentially lethal digitalis intoxications 

vi. Ingestions of plants known to contain cardiac glycosides (oleander, lily of the valley) with 

severe dysrhythmias 

(b) Fab fragments bind free digoxin in the vascular and interstitial spaces and form an inert compound 

that is eliminated by the kidneys. Treatment rapidly corrects conduction defects, ventricular 

dysrhythmias, and hyperkalemia. 

(c) Dosage 

i. If the serum digoxin level or total amount of digoxin ingested is known, the formulas found 

in the package insert can be used to calculate the number of vials of Fab fragments to be 

administered. 

11. If the amount of digoxin ingested is unknown, the initial dose of Fab fragments should be 

5-10 vials (titrated incrementally). 

(d) After administration of Fab fragments, conventional assays for determining digoxin levels (which 

measure both bound and unbound digoxin) are unreliable for at least a week. 

13


Table 2: ECG Findings in Various Conditions 

Condition ST PR QRS QT Pwave Twave Special Features 

Hypothermia Long Wide Long "J" wave, Osborne 

Hypokalemia Depressed Long Long Flat Progressively more 

prominent "U" wave 

Hyperkalemia Long Wide Flat Peaked May be associated 

with digitalis toxicity 

Hypocalcemia Long Inverted 

Hypercalcemia 

Short 

Hypomagnesem i a Abnormal Long Long Flat tSusceptibility to 

digitalis toxicity 

Digitalis effects Scooped Short Flat 

Digitalis toxicity 

Premature ventricular 

contractions most 

common 

II. SPECIFIC RHYTHM ASSESSMENTS 

A. Sinus rhythm 

Courtesy of Or. Michael McCrea 

1. Sinus rhythm is 60-100 beats per minute. 

2. The rhythm is regular with 1 :1 relationship of the P to QRS. 

3. P waves are upright in leads 1 1 

11 1 

and a VF. (Lead II is the typical lead for a rhythm strip.) 

4. There are no extra beats. 

B. Premature atrial contractions: extra beats that originate outside the sinus node from ectopic atrial 

pacemakers; appear interspersed throughout an underlying rhythm (usually sinus) 

1. These ectopic P waves are different in configuration from normal P waves and may or may not be conducted 

through the AV node. They usually have a normal PR interval (0.12-0.20 seconds) 

2. They are generally followed by a noncompensatory pause; the SA node is reset, and the returning sinus beat 

occurs ahead of schedule. 

C. Sinus tachycardia: exactly like a sinus rhythm except that the rate is> 100 (and usually


D. Sinus bradycardia: exactly like a sinus rhythm except that the rate is 45) beats per minute 

I 


E. Supraventricular tachycardia 

Courtesy of Dr. Daniel Schwerin 

1. P waves are abnormal and may not be visible (often hidden in the preceding T wave), or they may immediately 

follow the QRS complex, in which case they are often inverted ("retrograde P waves"); atrial rate is 120-200 

beats per minute. 

2. Rhythm is regular. 

3. QRS complexes are usually narrow but may be wide because of aberrant conduction through a bypass tract or 

preexisting bundle-branch block; ventricular rate is 120-220 beats per minute. 

F. Atrial fibrillation: an irregularly irregular rhythm due to uncoordinated atrial activation and random 

occurrence of ventricular depolarization. The atria are not pumping, but they do discharge electrical 

impulses to the ventricles; however, no single impulse depolarizes the atria completely, so only an 

occasional impulse gets through to the AV node. It is the most common sustained dysrhythmia; it occurs in 

2% of the general population and in 5% of people >60 years old. 


1. P waves are absent but small irregular deflections in the baseline ("f" or "fibrillation waves") may be seen. 

They are most easily detected in the inferior leads (11, 111, and a VF) and in V 1 

-V 3 

• The atrial rate is 400-700 beats 

per minute. 

2. Because P waves are not visible, there is no PR interval. 

3. QRS complexes are normal in configuration, unless there is aberrant conduction. 

4. The rhythm is irregularly irregular. 

5. Ventricular response rate is variable but is generally 160-180 beats per minute in untreated patients; a rate 

>200 beats per minute with a wide QRS complex suggests Wolff-Parkinson-White syndrome with conduction 

through the accessory pathway; a regular, slow ventricular rate may be digitalis toxicity. 

G. Atrial flutter: a very rapid atrial rhythm but, because of AV nodal delay, ventricular responses are slower. 

Therefore, atrial flutter always occurs with some sort of AV block (not all impulses are conducted); the 

resulting block is either a fixed ratio (2:1, 3:1, 4:1, etc) or variable AV block. 

Fixed AV block 3:1 atrial flutter 


15


Variable AV block atrial flutter 


1. P waves have a characteristic sawtooth pattern and are called "F" or "flutter waves." They are usually best seen 

in the inferior leads and leads V 1 

and V 2 

• The atrial rate is 250-350 beats per minute. 

2. The PR interval (when present) is always normal, but not every P wave is followed by a QRS complex. 

3. QRS complexes are normal in configuration. 

4. The ventricular rate is often 150 + 20 beats per minute but depends on the degree of block present and may be 

variable. Suspect atrial flutter with a 2:1 block in patients who present with a fixed regular ventricular rate of 

150 beats per minute. 

H. Multifocal atrial tachycardia: an irregular rhythm sometimes mistaken for atrial fibrillation; originates from 

multiple different atrial sites and is characterized by P waves of varying shape 


1. There must be at least three distinct types of P waves in one lead; atrial rate is 100-180 beats per minute. 

2. The rhythm is irregularly irregular. 

3. The PP, PR, and RR intervals vary. 

4. Nonconducted (blocked) P waves are frequently present, particularly when the atrial rate is rapid. Classically 

seen with COPD and theophylline toxicity. 

5. Management is directed at treatment of the underlying condition. Cardioversion is ineffective. The rhythm itself 

should not cause hemodynamic instability. 

I. Junctional premature contractions: impulses that originate from an ectopic focus within the AV node or the 

bundle of His above the bifurcation. They may be isolated, multiple, or multifocal. 


1. The ectopic P wave has a different shape and deflection (usually inverted in leads II, Ill, and a VF), and it may 

occur before, during, or after the QRS complex. 

2. When the P wave precedes the QRS, the PR interval is shorter than normal (often


1. Characteristics 

a. Occur earlier than the next expected normal QRS 

b. Wider than a normal QRS (usually 2'.0.12 second) 

c. The QRS morphology is generally bizarre. 

d. A preceding P wave is absent; however, retrograde conduction of a premature ventricular contraction can 

occasionally result in an inverted P wave after the QRS complex. 

e. The deflection of the ST segment and T wave is opposite that of the QRS. 

f. May occur in regular pattern, eg, bigeminy (as above) 

g. Generally followed by a compensatory pause; the sinoatrial node is not reset, and the next P wave occurs 

at its usual time. 

K. Ventricular tachycardia: three or more consecutive premature ventricular contractions occurring at a regular 

rate> 120 beats per minute 


1. P waves are usually absent; when present, they are either retrogradely conducted or have no relationship to the 

QRS (AV dissociation). 

2. QRS complexes are wide (2'.0.12 second) and may be bizarre. 

3. Fusion beats may be present; these are intermediate in appearance between a bizarre QRS complex and a 

normal QRS. When present, the diagnosis of ventricular tachycardia is certain. 

4. Capture beats are rarely seen but, when present, confirm the diagnosis of ventricular tachycardia. Capture beats 

are the result of an atrial impulse penetrating the AV node from above to stimulate ("capture") the ventricles. 

Because ventricular conduction occurs over the normal pathways, the resulting QRS of the captured beat looks 

normal (narrow) in appearance. 

5. Deflection of the ST segment and T wave is generally opposite that of the QRS complex. 

6. Rate is> 120 (usually 150-200) beats per minute. 

7. Rhythm is generally regular, although beat-to-beat variation may occur at the onset of tachycardia. 

8. QRS axis is generally constant. 

9. Ventricular tachycardia is classified as "monomorphic" (QRS complexes look the same) or "polymorphic" 

(QRS complexes have varying morphology). Current therapeutic modalities are based on this classification (see 

Etiologies and Management of Dysrhythmias, pages 22-32). 

10. Differentiation of supraventricular tachycardia with aberrancy from ventricular tachycardia 

a. Most published criteria that can be used to diagnose ventricular tachycardia are fairly reliable; however, 

there are no reliable criteria to exclude ventricular tachycardia. Because the misdiagnosis of ventricular 

tachycardia can be deadly, if there is any doubt about the diagnosis whatsoever, always assume that a wide 

complex tachycardia is ventricular tachycardia and treat as such! 

b. Fusion and capture beats indicate AV dissociation and are practically diagnostic of ventricular tachycardia. 

c. P waves preceding QRS complexes favor aberrancy. 

d. QRS concordance (all the QRS complexes from V 1 

to V 6 

are either positive or negative) strongly favors 

ventricular tachycardia. A fully compensatory pause is more likely to occur with ventricular tachycardia. 

e. Response to vagal maneuvers (Valsalva maneuver, carotid sinus massage) may occur with aberrant 

supraventricular tachycardia, whereas ventricular tachycardia is unaffected. (Carotid sinus massage is 

contraindicated in older patients with a history of carotid disease/stroke or the presence of a carotid bruit.) 

f. Marked left axis deviation (>30°) suggests ventricular tachycardia; any QRS axis deviation >40° in either 

direction (or an upright QRS in aVR) favors ventricular tachycardia. 

g. QRS duration >0.14 second favors ventricular tachycardia. 

h. QRS morphology in lead V 1 

: an RS, R or qR with left "rabbit ear" taller than the right suggests ventricular 

tachycardia, whereas an RSR' pattern is more likely supraventricular tachycardia with aberrancy; negative 

QRS morphology in this lead with a wide R wave (>0.03 second), RS interval >0.07 second, and a slurred 

or notched S wave favors ventricular tachycardia. 

1. QRS morphology in lead V 6 

: R/S ratio


j. A bundle-branch pattern that varies suggests supraventricular tachycardia with aberrancy. 

k. A history of prior heart disease (Ml, CHF, coronary artery bypass graft) strongly favors ventricular 

tachycardia (likelihood 85%), as does a prior history of ventricular tachycardia. 

I. Age 2:'.50 years old favors ventricular tachycardia, whereas age :S35 years old favors an aberrant 

supraventricular tachycardia. 

11. Torsades de pointes ("twisting of the points") is a type of polymorphic ventricular tachycardia in which the QRS 

axis swings from a positive to a negative direction in a single lead creating a "sine-wave" appearance. It originates 

from a single focus and is usually precipitated by diseases or drugs that prolong the QT interval, such as Class 

IA antidysrhythmics (procainamide, quinidine), Class IC antidysrhythmics (propafenone, fecainide), tricyclic 

antidepressants, droperidol, and the phenothiazines. The combined use of certain drugs such as terfenadine plus 

ketoconazole or erythromycin also prolong the QT interval and may therefore precipitate torsades. Other causes 

include hypomagnesemia and hypokalemia. The rate is typically 200-240 beats per minute. 


L. Ventricular fibrillation 


1. Most commonly recognized as a fine or coarse zigzag pattern without discernible P waves, QRS complexes, or 

T waves representing the presence of unorganized ventricular electrical activity 

2. By definition, there is no organized perfusion and therefore absence of a pulse. 

3. Sometimes the rhythm may look like ventricular tachycardia. The point is moot if the patient has no pulse and 

is unresponsive, because the treatment is the same, unsynchronized defibrillation. 

M. Pulseless electrical activity (PEA) 

1. Refers to a heterogeneous group of rhythms characterized by the presence of some type of electrical activity 

other than ventricular tachycardia or ventricular fibrillation in the absence of a perceptible pulse 

2. Includes electromechanical dissociation, pseudoelectromechanical dissociation, idioventricular rhythms, 

ventricular escape rhythms, bradyasystolic rhythms, and postdefibrillation idioventricular rhythms 

3. These dysrhythmias often occur in association with specific clinical conditions that if promptly identified and treated 

may result in a return of spontaneous circulation. Remember the "H's and T's," looking for reversible causes. 

a. Hypovolemia 

b. Hydrogen ion, ie, acidosis 

C. Hypothermia 

d. Hypo/hyperkalemia 

e. Hypoxia 

f. Toxins 

g. Tamponade, cardiac 

h. Tension pneumothorax 

i. Thrombosis, coronary 

j. Thrombosis, pulmonary 

N. Bundle-branch blocks (BBBs) 

1. Abnormal conduction abnormalities (not rhythm disturbances) in which the ventricles depolarize in 

sequence (rather than simultaneously), thus producing a wide QRS complex (0.09-0.11 - incomplete BBB; 

2:'.0.12 second - complete BBB) and an ST segment with a slope opposite that of the terminal half of the 

QRS complex 

18


2. Right BBB is a unifascicular block in which ventricular activation is by way of the left bundle branch; the 

impulse travels down the left bundle, thus activating the septum from the left side (as it normally does in 

the absence of right BBB). This is followed by activation of the free wall of the left ventricle and, finally, the 

free wall of the right ventricle. Because of the two changes in direction, there is a tendency toward triphasic 

complexes in right BBB. 


a. Wide QRS complex (::,:0.12 second) 

b. Triphasic QRS complex (rSR' variant) in lead VJ 

c. Wide S waves in leads I, V 5 

, andV 6 

d. Normal septa! Q waves in leads I and V 6 

because the initial activation of the ventricle occurs in the normal 

manner 

e. T wave has a deflection opposite that of the terminal half of the QRS complex. 

f. Associated axis is variable; a normal axis, left axis deviation, or even right axis deviation may be present. 

3. Left BBB is a bifascicular block in which the left ventricle is activated by way of the right bundle branch; the 

impulse travels down the right bundle, activating the septum and the free wall of the right ventricle, and then 

continues on in the same direction to activate the free wall of the left ventricle. Because the dominant forces 

are traveling in the same direction, there is a tendency toward monophasic QRS complexes. 


a. Wide QRS complex (::,:0.12 sec) 

b. Negative wave (QS or rS) in lead VJ 

c. Large, wide R waves in leads I, aVL, V 5 

, and V 6 

d. Absence of normal septa! Q waves in leads I and V 6 

e. T wave has a deflection opposite that of the terminal half of the QRS complex. 

f. Associated left-axis deviation is most common and implies the presence of additional myocardial disease. 

0. Sinoatrial block 

1. Occurs when there is abnormal conduction between the sinus node and atrial muscle; recognized by the 

unexpected absence of a P wave and its associated QRS complex. Like AV block, sinoatrial block is also 

divided into first-, second-, and third-degree varieties. 

2. First-degree sinoatrial block 

a. Impulse is delayed in its conduction from the sinoatrial node to the atria. 

b. Cannot be diagnosed from a surface 12-lead ECG 

3. Second-degree sinoatrial block 

a. Some of the sinus node discharges are blocked. 

b. Recognized on an ECG as the absence of an expected P wave and its associated QRS complex 

4. Third-degree sinoatrial block (sinus arrest) 


19


a. All of the sinus node discharges are blocked. 

b. On ECG, it may appear as a long sinus pause/arrest or a junctional/ventricular escape rhythm. 

P. Sick sinus syndrome 

1. An abnormality of cardiac impulse formation as well as intra-atrial and AV nodal conduction 

2. Manifests as a wide variety of, or combinations of, bradyarrhythmias and tachyarrhythmias 

3. Most common in the elderly 

4. Presenting symptoms may include dizziness, palpitations, dyspnea, fatigue, lethargy, or syncope. 

Documentation of a bradyarrhythmia or tachyarrhythmia in association with these symptoms is the cornerstone 

of diagnosis. 

Q. Atrioventricular blocks 

1. Occur when the conduction between the atria and ventricles is abnormal; the conduction delay can occur in 

the atria, the AV node, or the proximal His-Purkinje system. 

2. First-degree AV block: normal AV conduction is slightly prolonged. 

Note PR 390 msec. 


a. P waves and QRS complexes are normal. 

b. There is a 1 :1 relationship between the P and QRS. 

c. PR interval is prolonged (>0.20 second) 

d. The block is most often at the level of the AV node. 

3. Second-degree AV block: some atrial impulses are not conducted. 

a. Mobitz Type I (Wenckebach) 

(1) P waves and QRS complexes are normal, but there are P waves without QRS complexes 

(nonconducted P waves). 

(2) PR interval progressively lengthens and the RR interval progressively shortens until a beat is dropped. 

This cycle repeats itself, producing a pattern referred to as "group beating." 

(3) The longest cycles (those of the dropped beats) are less than twice the length of the shortest cycles 

(those of the impulses following the dropped beats). 

(4) The block is almost always within the AV node. 

b. Mobitz Type II 


(1) P waves are normal. 

(2) QRS complexes are often (but not always) wide because of the common occurrence of a coexisting 

bundle-branch block. 

(3) PR intervals (when they occur) are always the same duration. 

(4) There are dropped beats. 

(5) The block is below the level of the AV node, generally in the His-Purkinje system. 

20


4. Third-degree AV block: no atrial impulses are conducted; the atria and ventricles beat independently of 

one another. 


a. P waves appear normal. 

b. May occur at the level of the AV node, the bundle of His, or the bundle branches 

c. QRS complexes may be narrow or wide, depending on the location of the block: if the block is located 

above the His bundle, the QRS complexes will be narrow and reflect a junctional escape rhythm, whereas 

if the block is located at or below the bundle of His, the QRS complexes will be wide and reflect a 

ventricular escape rhythm. 

d. There is no relationship between P waves and QRS complexes. 

(1) There is an independent and regular atrial rate (constant PP interval) and a slower independent and 

constant ventricular rate (constant RR interval). 

(2) The P waves are not related (not conducted) to the QRS complexes but rather "march through them" as 

if they were not there. 

(3) The PR intervals are variable. 

R. Preexcitation syndromes 

1. Result from abnormal connections (accessory pathways) between the atria and ventricles. Impulses traveling 

down these pathways bypass all or part of the normal conduction system. This results in the ventricles being 

activated by atrial impulses sooner than would normally be anticipated (preexcitation) and is reflected 

by changes in the surface ECG. The ECG changes seen are determined by the exact pathway the impulse 

travels. Wolff-Parkinson-White syndrome and Lown-Ganong-Levine syndrome are the two major variants of 

preexcitation. Their characteristic ECG findings are listed below. Patients with preexcitation syndromes are 

prone to tachydysrhythmias (especially paroxysmal supraventricular tachycardia and atrial fibrillation) with very 

rapid ventricular rates (up to 300 beats per minute). 

2. Wolff-Parkinson-White: the accessory pathway (bundle of Kent) connects the atria directly to the ventricles, 

completely bypassing the AV node and the infranodal conduction system. 


a. Short PR interval (


Ill. ETIOLOGIES AND MANAGEMENT OF DYSRHYTHMIAS 

A. Premature atrial contractions 

1. There are multiple causes (drugs or underlying disease), but they may also occur as a normal variant. 

2. Clinical significance 

a. Can precipitate supraventricular tachycardia, atrial fibrillation, and atrial flutter 

b. Most frequent cause of a pause on the ECG 

3. In general, no treatment is indicated. If, however, the premature atrial contractions are frequent or 

symptomatic, treatment should be directed toward correcting the underlying cause. 

B. Sinus tachycardia 

1. There are multiple causes; common ones include: 

a. Anxiety (diagnosis of exclusion) 

b. Stimulant or sympathomimetic drugs (eg, cocaine) 

c. Fever 

d. Hypovolemia 

e. Hyperthyroidism 

f. Pulmonary embolism 

g. Anemia 

h. Hypoxia 

1. Pain 

2. Management in most instances should be directed at finding and correcting the underlying cause. 

3. In the setting of cocaine or stimulant toxicity, administration of a benzodiazepine is first-line treatment. 

C. Sinus bradycardia 

1. Common causes 

a. Acute inferior wall Ml 

b. Vasovagal events (eg, vomiting) 

c. Drug effect (eg, ~-blockers, calcium channel blockers) 

d. Sick sinus syndrome 

e. Hypothermia 

f. Hypothyroidism 

g. A normal variant, especially in those individuals who exercise aerobically on a regular basis 

2. Management 

a. Indicated for patients who demonstrate signs of hypoperfusion due to the bradycardia: those with shock, 

hypotension, ischemic chest pain, decreased mentation, or acute CHF 

b. Intervention sequence 

(1) Atropine 0.5 mg every 5 minutes as needed until a response is noted or a total of 0.03-0.04 mg/kg 

has been administered (3 mg for most adults). 

(a) Should be used cautiously in patients with an acute Ml, because it may worsen ischemia or 

precipitate ventricular tachycardia or ventricular fibrillation 

(b) Should also be used with caution in patients with Mobitz Type 11 second-degree AV block and 

new third-degree AV block with wide complexes - t atrial rate - t AV block - 1 ventricular 

rate and t blood pressure 

(c) Atropine is ineffective in patients with heart transplants because of lack of vagal innervation to 

the transplanted heart. Proceed directly to transcutaneous pacing and/or catecholamine infusion. 

(d) Can be parasympathomimetic in doses


(3) Dopamine 5-20 mcg/kg/min or epinephrine 2-10 mcg/min 

(a) Should be used when bradycardia is unresponsive to atropine and a transcutaneous pacer is not 

readily available 

(b) Most useful when associated hypotension is present 

(4) Transvenous pacing may be required if symptomatic bradycardia persists despite vasopressors and/or 

transcutaneous pacing. 

D. Supraventricular tachycardia (SVT) 

1. A generic term that refers to all tachydysrhythmias arising above the bifurcation of the bundle of His, including 

sinus tachycardia, atrial fibrillation, atrial flutter, multifocal atrial tachycardia, paroxysmal supraventricular 

tachycardia, and nonparoxysmal junctional tachycardia. It arises from reentry or an ectopic pacemaker in 

the atria. Most clinicians, however, use the term SVT to refer specifically to AV nodal reentry tachycardia 

(AVNRT) and other undetermined supraventricular rhythms. In the discussion that follows, SVT refers to AVNRT. 

Management is discussed separately for other specific forms of SVT (such as atrial fibrillation). 

2. Causes 

a. Preexcitation syndromes (Wolff-Parkinson-White and Lown-Ganong-Levine) 

b. Mitra! disease (prolapse, stenosis) 

c. Digitalis toxicity 

d. Drugs (eg, alcohol, tobacco, caffeine) 

e. Acute Ml and pericarditis 

f. Hyperthyroidism 

g. Rheumatic heart disease 

3. Management is determined primarily by the patient's hemodynamic stability and secondarily by the width of 

the QRS complex. 

a. Hemodynamically compromised patients (those with hypotension, ischemic chest pain, a decrease in 

mental status, or acute CHF) with a narrow complex SVT should be sedated (if possible) and treated with 

synchronized cardioversion. Start with 50 joules. 

b. Vagal maneuvers and pharmacologic therapy may be used in the hemodynamically stable patient with 

narrow complex SVT. 

(1) Vagal maneuvers (such as carotid sinus massage [should not be done if digitalis toxicity has not been 

excluded] or Valsalva maneuver) increase vagal tone and may be effective in either terminating the 

dysrhythmia or slowing the ventricular rate enough to uncover the actual underlying rhythm. These 

maneuvers should be attempted before starting pharmacologic therapy and may also be used to 

supplement it. The vagal maneuver of choice, ie, the most effective, is the Valsalva maneuver. 

(2) Adenosine, because of its safety profile, is the drug of choice for the hemodynamically stable patient 

with narrow complex SVT. It is an ultra-short-acting AV nodal blocker that is very effective in 

converting SVT. Its major advantages over verapamil are its short half-life (


(4) ~-blockers such as esmolol, metoprolol, or propranolol are also effective in the treatment of narrow 

complex SVT. Esmolol has the advantage of being cardioselective as well as having a very short halflife. 

Propranolol is the drug of choice for SVT secondary to thyrotoxicosis, because it partially blocks 

the conversion ofT 4 

and T 3 

• Avoid these drugs in patients with COPD, asthma, or CHF; in those who 

have received IV calcium channel blockers; and in those with atrial fibrillation with Wolff-Parkinson 

White, sick sinus syndrome, and advanced AV block. 

(5) Digoxin is vagotonic. Compared with the other agents listed above, its effects are mild and 

have a much slower onset (may take 2-4 hours or more to work). Digoxin should be avoided if 

cardioversion is being considered. 

(6) Magnesium sulfate, phenytoin, and lidocaine are the drugs of choice for ectopic SVT caused by 

digitalis toxicity. Management should also include correction of hyper/hypokalemia (if present) and 

discontinuation of digitalis. In the presence of hemodynamic instability (or potentially lethal digitalis 

intoxication), administration of Fab fragments should be considered. 

(7) Other antidysrhythmic agents (eg, procainamide, amiodarone, sotalol) may also be effective. 

(8) Patients who do not respond to drug therapy may be treated with synchronized cardioversion (as 

described above) or overdrive cardiac pacing. 

c. Drug dosages and administration 

(1) Adenosine 6 mg rapid IV push in a proximal vein followed by a 20-ml bolus of normal saline; if there 

is no response after 1-2 minutes, double the dose to 12 mg. 

(2) Verapamil 2.5-5 mg IV over 2-3 minutes; a second dose of 5-10 mg may be given in 15-30 minutes 

if necessary. 

(3) Diltiazem 0.25 mg/kg IV over 2 minutes, followed in 15 minutes by a second bolus of 0.35 mg/kg if 

the first bolus was tolerated but ineffective. Smaller dosages should be considered in elderly patients. 

(4) Esmolol 300-500 mcg/kg bolus over 1 minute followed by an infusion of 50 mcg/kg/min; the loading 

dose may need to be repeated and the infusion rate increased by 50 mcg/kg/min every 5 minutes as 

needed to a maximum of 200 mcg/kg/min. 

(5) Metoprolol 5 mg IV over 2 minutes; may be repeated twice every 5 minutes for total of three doses. 

(6) Propranolol 1 mg IV over 1 minute; this dose may be repeated every 5 minutes up to a total dosage 

of 0.1-0.5 mg/kg. 

(7) Digoxin 0.5 mg IV push initially, with repeated doses of 0.25 mg every 30-60 minutes as needed; 

total dosage should not exceed 0.02 mg/kg. 

(8) Magnesium sulfate 1-2 g slow IV push over 1-2 minutes followed by an infusion of 1-2 g/hr 

(9) Phenytoin 18 mg/kg IV bolus infusion; dissolve dosage in normal saline and administer at a rate of 50 

mg/min or less. 

(10) Lidocaine 1-1.5 mg/kg bolus infusion, repeat dosages 0.5-0.75 mg/kg every 5-10 minutes, to 

maximum bolus dose of 3 mg/kg. This can be followed by maintenance infusion of 1-4 mg/min. 

d. Patients with wide complex tachycardia should be presumed to have ventricular tachycardia. 

(1) If unstable _,. synchronized cardioversion 

(2) If stable -,. procainamide or amiodarone 

(a) Both convert SVT or ventricular tachycardia. 

(b) Both should be avoided in patients with tricyclic antidepressant overdose or in the setting of 

toxicity from other sodium-channel blockers. 

(c) Adenosine may initially slow either rhythm, but dysrhythmia may recur (short therapeutic effect 

of the drug). 

(d) If drug therapy fails _,. synchronized cardioversion 

24


E. Atrial fibrillation (most common SVT) 

1. Identify the type of atrial fibrillation the patient has by determining the probable duration of the dysrhythmia. 

First-detected episode 

of atrial fibri I lation 

versus 

Recurrent at1·i a I 

fibri I lation* 

I 

I 

I 

I 

I 

Paroxysmal 

I 

I 

Persistent 

I 

I 

I 

Permanent 

1 year 

Terminated 

spontaneously 

Sustained or terminated 

therapeutically 

Cardioversion failed 

or not attempted 

*lschemic stroke risk for recurrent atrial fibrillation is 5% per year 

or 2-7 times the risk for patients without atrial fibrillation. 

2. Search for reversible causes and treat any underlying medical condition; then determine the risk of 

subsequent stroke. Conditions with high risk of cardiogenic thromboembolism: 

a. Cardiac surgery 

b. Acute Ml 

c. Hyperthyroidism 

d. Myocarditis 

e. Acute pulmonary disease 

3. Plan the treatment using the following criteria: 

a. Cardiovascular stability 

b. Duration of the dysrhythmia 

c. Underlying cause/condition 

d. Presence/absence of an accessory pathway 

4. There are fundamentally two ways to manage atrial fibrillation: restore and maintain sinus rhythm, or allow 

atrial fibrillation to continue and ensure that the ventricular rate is controlled. 

a. Unstable patients _,. immediate electrical synchronized cardioversion 

b. Stable patients with significant symptoms _,. pharmacologic therapy 

(1) Control the ventricular rate first (choose one) 

(a) Calcium channel blocker (eg, verapamil, diltiazem) 

(b) ~-blocker (eg, esmolol, atenolol, metoprolol) 

(c) Digoxin 

(d) Amiodarone 

(e) The presence of Wolff-Parkinson-White syndrome is a special circumstance requiring changes in 

treatment protocols (see pages 31-32). 

(2) Cardiovert the dysrhythmia based on the duration of atrial fibrillation. 

(a)


(b) >48 hours duration (higher risk of systemic embolization) 

1. Avoid immediate cardioversion if possible. 

ii. If early cardioversion (within 24 hours) is anticipated, consider starting heparin and 

consulting cardiology for transesophageal echocardiography to exclude an atrial thrombus. 

iii. If delayed cardioversion is the best option, anticoagulation for 3 weeks is indicated before 

cardioversion. 

5. Discussion of selected treatment options 

a. Hemodynamically compromised patients should be sedated (if possible) and treated with synchronized 

cardioversion; start with 120 joules. In patients who have digitalis toxicity or are hypokalemic, 

cardioversion is potentially hazardous; use only as a last resort and start with lower joules. If the patient 

has hypertrophic cardiomyopathy (or has been in atrial fibrillation >48 hours), immediate systemic 

heparinization is also indicated. 

b. Hemodynamically stable patients with atrial fibrillation of acute (2 days duration should, when stable, receive anticoagulation before 

pharmacologic or electric cardioversion is attempted to decrease the risk of arterial embolization of an 

intra-atrial thrombus. 

F. Atrial flutter 

1. Causes are essentially the same as for atrial fibrillation, but it is most often associated with postcardiac surgery 

and peri-infarction periods. 

2. Usually a transitional rhythm between sinus rhythm and atrial fibrillation 

3. Management is determined by the patient's cardiovascular stability, duration of the dysrhythmia and whether or 

not the patient has an accessory pathway. 

a. Hemodynamically unstable patients should be sedated (if time permits) and treated with synchronized 

cardioversion; start with 50 joules. 

b. Hemodynamically stable patients should be managed with Vagal maneuvers and pharmacologic therapy. 

(1) Vagal maneuvers or adenosine may be of diagnostic value; by inducing a transient AV nodal blockade, 

they may reveal the characteristic flutter waves of this rhythm and confirm the diagnosis. 

(2) Once the diagnosis is confirmed, rate control should be accomplished with a calcium channel blocker 

(eg, diltiazem, verapamil) or a ~-blocker (eg, esmolol, metoprolol). Digoxin may also be used but is 

considered a second-line drug. Magnesium may be used in combination with one of the above agents 

as adjunctive therapy. 

(3) Once the ventricular response rate is controlled, pharmacologic conversion to sinus rhythm can be 

achieved with procainamide or quinidine. 

G. Multifocal atrial tachycardia 

1. Causes 

a. Decompensated COPD (most common) 

b. CHF 

c. Sepsis 

d. Theophylline toxicity 

e. Asthma 

26


2. Management 

a. Primarily aimed at correcting the underlying disease process 

(1) Correct hypoxia with supplemental oxygen (and bronchodilator therapy) in a patient with COPD, and 

(2) Evaluate for theophylline toxicity. 

b. If the above measures are unsuccessful and the patient is symptomatic, other modalities that may be used: 

(1) Calcium channel blockers (eg, diltiazem, verapamil) are usually effective in slowing the ventricular 

rate and decreasing atrial ectopy, and may produce conversion to a sinus rhythm in some patients. 

(2) Magnesium sulfate decreases atrial ectopy. 

(3) ~-blockers are generally not recommended, because they may worsen the underlying pulmonary 

disease process. 

c. Digoxin and cardioversion are usually ineffective. 

H. Junctional premature contractions 

1. Primary causes 

a. Digitalis toxicity 

b. Coronary artery disease 

C. CHF 

d. Acute Mis (especially inferior wall Mis) 

2. Treat the underlying cause; if junctional premature contractions precipitate more lethal dysrhythmias, consider 

using IV procainamide. 

I. Premature ventricular contractions (PVCs) 

1. Causes 

a. Hypokalemia 

b. Hypomagnesemia 

c. Hypoxia 

d. Ml 

e. Drugs 

(1) Alcohol, tobacco, caffeine 

(2) Cocaine 

(3) Digitalis or quinidine toxicity (PVCs are most common dysrhythmia with digitalis toxicity) 

(4) Methylxanthines (commonly used by patients with asthma or COPD) 

f. Hyperthyroidism 

g. CHF 

h. Cardiomyopathy 

1. Mechanical: PVCs are not uncommon when a catheter is placed in the right ventricle. 

j. Myocardial contusion 

2. Management is dictated by the underlying cause and is not indicated in all cases. 

a. Patients who are asymptomatic and have PVCs of unknown cause should not be treated (particularly when 

the PVCs are an incidental finding); PVCs in this setting may represent a normal variant. Isolated PVCs 

occur in as many as 50% of young healthy patients and increase in frequency with age. 

b. When an underlying cause is identified (hypokalemia, hypomagnesemia, hypoxia, etc), therapy should be 

directed toward correcting the underlying problem (rather than suppressing PVCs). This is usually sufficient. 

c. Mechanical causes, if present, should also be corrected. 

(1) A central line catheter that is located in the right ventricle may induce PVCs; withdraw the catheter, or 

advance it out of the ventricle. 

(2) To reduce the likelihood of inducing PVCs during Swan-Ganz placement, inflate the balloon to cover 

the catheter tip while advancing into the right ventricle; then deflate the balloon to avoid floating into 

the ventricular outflow tract. 

(3) If these measures fail to ameliorate the PVCs and the patient is symptomatic, lidocaine may be 

administered. 

d. "Escape" PVCs (those associated with bradycardia) should be treated with atropine (not lidocaine), because 

administration of lidocaine under these circumstances may suppress the existing functioning rhythm. 

e. Management of PVCs occurring in association with an acute Ml or ischemia is more controversial. Optimal 

treatment of the underlying ischemia/infarction with oxygen, nitroglycerin, aspirin, and percutaneous 

27


coronary intervention is clearly the first priority. If these measures fail, most authors currently recommend a 

conservative course of watchful waiting. 

f. In general, the identification of PVCs should prompt a search for and treatment of the underlying cause, 

rather than simply pharmacologic suppression of the PVCs. Empiric use of magnesium is sometimes 

recommended. If short bursts of frequent PVCs are occurring, consider empiric administration of a-blockers 

(to decrease adrenergic stimulation that often causes ventricular dysrhythmias). 

g. Pharmacologic agents 

(1) Lidocaine has historically been used as a first-line agent, though it is rarely used empirically now. If the 

decision is made to use lidocaine, administer a bolus of 1-1.5 mg/kg followed by a 2-4 mg/min drip. 

Repeat boluses of 0.5-0.75 mg/kg may be given every 5-10 minutes as needed to a maximum total 

dosage of 3 mg/kg. 

(2) Procainamide may be tried if lidocaine is ineffective or contraindicated. It is administered at an 

infusion rate of 20-50 mg/min until PVCs are suppressed, the QRS widens by 50% of its original 

width, hypotension develops, or a total dose of 17 mg/kg has been administered. This should be 

followed by a maintenance drip of 1-4 mg/min. 

(3) Magnesium sulfate is often effective in decreasing the frequency of PVCs. The dose is 1-2 g slow IV 

push over 1-2 minutes followed by an infusion of 1-2 g/hr. 

J. Ventricular tachycardia 

1. The causes are basically the same as those for PVCs. The most common causes are ischemic heart disease and 

acute Ml. 

2. Management depends on the status of the patient and QRS morphology. 

a. If there is no pulse for either monomorphic or polymorphic ventricular tachycardia, treat like ventricular 

fibrillation: begin CPR and defibrillate as soon as a defibrillator is available. Start with 200 joules. 

b. If the patient has a pulse but is hemodynamically unstable (hypotensive, decreased mental status, 

ischemic chest pain, acute CHF), synchronized cardioversion is indicated. Sedate first if time allows. Start 

with 100 joules, and increase energy if unsuccessful. 

c. If the patient is clinically stable (awake, pain free, and has good blood pressure), pharmacologic therapy 

is appropriate. Patients who do not convert with these agents should be sedated and cardioverted. If the 

patient is stable, the following are recommended: 

(1) Monomorphic ventricular tachycardia: procainamide, amiodarone, or sotalol 

(a) Procainamide 20-50 mg/min until rhythm is suppressed, QRS widens by more than 50%, 

hypotension develops, or maximal bolus dose of 17 mg/kg is reached. 

(b) Amiodarone 150 mg IV bolus over 10 minutes, followed by maintenance infusion of 1 mg/min 

for 6 hours. 

(c) Sotalol 100 mg (1.5 mg/kg) over 5 minutes; avoid if prolonged QT. 

(2) Polymorphic ventricular tachycardia 

(a) If the baseline QT interval is normal, all of the above agents are considered reasonable. 

(b) If the QT interval is prolonged, it should be assumed that the dysrhythmia is torsades de pointes 

(atypical ventricular tachycardia). Class 1 A and 1 C antidysrhythmic agents are contraindicated; 

they prolong ventricular repolarization, which can worsen torsades. 

1. The therapy of choice is magnesium sulfate 1-2 g IV over 1-2 minutes followed by an 

infusion of 1-2 g/hr; it is nondysrhythmogenic and rapidly effective. 

ii. Overdrive electrical pacing (transcutaneous or transvenous) is also effective by increasing 

the heart rate, thereby shortening ventricular repolarization. 

iii. Sustained torsades or unstable patients should be treated with direct cardioversion, ie, not 

synchronized; start with 200 joules, and begin a magnesium infusion after cardioversion. 

(3) Note: If a patient with polymorphic ventricular tachycardia or torsades is unstable but has a pulse, 

cardioversion is indicated. Because of concerns in delay of cardioversion due to trouble with 

synchronization, even in a patient with a pulse, use direct cardioversion, ie, unsynchronized and 

defibrillation doses starting at 200 joules. Once cardioversion is achieved, antidysrhythmic therapy 

with, amiodarone or procainamide should be given. If the patient had torsades, magnesium should 

be used instead, as noted above. 

d. For patients who have been cardioverted back to sinus rhythm or who are experiencing intermittent 

ventricular tachydysrhythmias, the use of B-blockers should also be considered. B-blockers decrease the 

adrenergic tone that contributes to ventricular tachydysrhythmias. 

28


3. It is a common misconception that all patients with ventricular tachycardia will appear clinically unstable; 

stable patients with a wide complex tachycardia are frequently assumed to have SVT with aberrancy rather 

than ventricular tachycardia. This is an inaccurate assumption. 

a. Ventricular tachycardia cannot be differentiated from SVT with aberrancy based on clinical symptoms 

and vital signs. 

b. Unstable patients with either rhythm should be cardioverted; it is effective in both cases. 

c. An ECG should be obtained in all stable patients. 

(1) Examine for evidence that favors one dysrhythmia over the other and treat accordingly. 

(2) If unable to decide, always assume it is ventricular tachycardia and treat as above based on QRS 

morphology and cardiac function. 

d. Adenosine will convert some forms of ventricular tachycardia to a sinus rhythm; therefore, use of 

adenosine as a diagnostic measure to distinguish ventricular tachycardia from SVT with aberrancy is not 

recommended. 

K. Ventricular fibrillation (and pulseless ventricular tachycardia) 

1. Causes 

a. By far the most common cause is acute coronary ischemia or infarction. 

b. Other possible causes include electrolyte abnormalities (eg, severe hypokalemia or hypomagnesemia), 

overdoses of sympathomimetics, electrical shock, and intracranial events. 

2. Management 

a. Initial therapy is immediate defibrillation. Time is of the essence. Chest compressions should be 

performed while preparing for defibrillation. Begin shocks at maximum joules (360 joules if using a 

monophasic defibrillator, 200 joules if using a biphasic defibrillator). Escalating dosages of shocks 

and stacked shocks are no longer indicated. After the defibrillation, immediately begin compressions 

at 100-120 times per minute for 2 minutes without checking for pulse or checking monitor. For 

persistent ventricular fibrillation/pulseless ventricular tachycardia, continue to follow the pattern 

of defibrillation - compressions for 2 minutes - check pulse and monitor. A key point is to minimize 

interruptions in compressions. 

b. If defibrillation is unsuccessful, follow the "CABs" as summarized in the ACLS 2015 Guidelines. 

(1) Circulation - high quality chest compressions with minimal interruptions for pulse checks, advanced 

airway insertion, or other procedures 

(2) Airway -;,. ensure open airway, place an advanced airway if unable to adequately bag-valve-mask; 

30 chest compressions to 2 breaths for adults regardless of one or two rescuers. Performance of 

endotracheal intubation or bag-valve-mask ventilation should not interrupt chest compressions. 

(3) Breathing - if an advanced airway is placed, confirm endotracheal tube placement, secure the tube, 

and confirm oxygenation and ventilation using monitored end-tidal CO 2 

capnography. 

c. Although no reduction in mortality has been shown with use of any IV medications in cardiac arrest, 

epinephrine is still recommended every 3-5 minutes as needed in doses of 1 mg for patients who remain 

pulseless. At this point, an active search for one of the reversible causes listed above should be sought 

and, if found, treated. Vasopressin is no longer recommended to replace either the first or second dose of 

epinephrine. 

d. If ventricular fibrillation or pulseless ventricular tachycardia persists despite defibrillation, epinephrine, 

chest compressions, and treatment of any obvious reversible cause (eg, hyperkalemia), an antidysrhythmic 

agent can be administered. 

e. No antidysrhythmics have been demonstrated to improve survival. Lidocaine was removed from the 

2010 ACLS pulseless arrest algorithm only to be relisted in 2015 as a second-line agent for refractory 

ventricular fibrillation/pulseless ventricular tachycardia. Lidocaine may be given as first line if 

amiodarone is not available. Exception: If the patient is being treated for torsades de pointes, magnesium 

is the drug of choice. 

f. Dosages 

(1) Amiodarone 300 mg IV bolus; may repeat once at 150 mg IV push followed by a 1 mg/min infusion 

for 6 hours, then 0.5 mg/min for 18 hours as needed 

(2) Lidocaine 1-1.5 mg/kg IV bolus 

(3) Magnesium sulfate 1-2 g IV push for torsades de pointes, known or suspected hypomagnesemia, or 

severe refractory ventricular fibrillation 

29


L. Pulseless electrical activity 

1. Causes 

Table 3: The Five H's and the Five T's 

!:!.ypovolemia (most common) 

!:!.ypoxemia 

!:!.ydrogen ion (acidosis) 

!:!.yper- and hypokalemia 

!:!.ypothermia 

Iablets (drug overdose) 

Iamponade (cardiac) 

Iension pneumothorax 

Ihrombosis, coronary (acute coronary syndrome) 

Ihrombosis, pulmonary embolism 

2. Management 

a. Begin resuscitation: perform CPR, intubate, start an IV line. 

b. Search for and treat the underlying cause when possible, focusing on the "H's and T's" as above. The 

approach should be guided by the clinical findings, medical history, and circumstances that preceded the 

development of the rhythm. Appropriate measures include: 

(1) Ventilate with 100% oxygen to treat hypoxia. 

(2) Listen for breath sounds in both lung fields, and assess the ease of manual ventilation to exclude 

tension pneumothorax. 

(3) Administer a fluid bolus to correct hypovolemia. 

(4) Assess the ECG for evidence of an acute Ml and hyperkalemia. 

(5) Check core body temperature to exclude hypothermia. 

(6) Look for distended neck veins as signs of tension pneumothorax and cardiac tamponade. 

(7) Perform bedside ultrasound if available to exclude pericardia! effusion causing cardiac tamponade and 

pneumothorax. 

(8) Obtain brief history from EMS or the patient's family or friends regarding the possibility of drug overdose. 

c. Administer epinephrine 1 mg every 3-5 minutes. Atropine was removed from the 2010 ACLS pulseless 

electrical activity algorithm because of absence of proven reduction in mortality. 

M. Sick sinus syndrome 

1. Causes 

a. lschemia 

b. Cardiomyopathy 

c. Myocarditis 

d. Trauma 

e. Atherosclerosis 

f. Aging 

2. Management depends on the hemodynamic stability of the patient. If symptoms of hypoperfusion are present, 

rate stimulation with atropine, a pacemaker (for bradydysrhythmias), or rate control with a calcium channel 

blocker, ~-blocker, or digoxin (for tachydysrhythmias) can be cautiously attempted (excessive tachycardia or 

bradycardia may result). Hemodynamically stable patients should be referred to a cardiologist for demand 

pacemaker insertion and antidysrhythmic therapy. 

N. Atrioventricular blocks 

1. Causes of impaired conduction 

a. Acute Ml (inferior wall or anterior wall) 

b. Drugs: digitalis, lidocaine, phenytoin, procainamide, quinidine, ~-blockers, calcium channel blockers, 

magnesium infusion (iatrogenic) 

c. Inflammation: myocarditis, endocarditis 

d. Hyperkalemia 

e 

Hypermagnesemia 

f. Hypothermia 

g. Congenital conduction defects 

30


2. Management 

a. First-degree AV block is often a normal variant. Other causes include increased vagal tone, digitalis 

toxicity, and myocarditis; specific therapy is not required. 

b. Second-degree AV block 

(1) Mobitz Type I (Wenckebach) 

(a) Usually transient 

(b) Often seen in the setting of an acute inferior wall Ml but can also be caused by digitalis toxicity, 

increased vagal tone, and myocarditis 

(c) Unless the patient is symptomatic, specific therapy is generally not required. 

(d) Symptomatic patients should be treated with atropine; if this fails, transcutaneous pacing is 

indicated. 

(2) Mobitz Type II 

(a) A more severe form of block; implies an organic lesion in the infranodal conduction system and 

is often permanent 

(b) Usually occurs in association with an acute anteroseptal Ml and can abruptly progress to 

complete block 

(c) These patients require pacing; transcutaneous pacing may be used as a bridging device, while 

preparations are made for insertion of a transvenous pacemaker. Atropine should be avoided (it 

can accelerate the atrial rate and produce a relative increase in the AV block - t ventricular 

response rate and t blood pressure). 

c. Third-degree (complete) AV block 

(1) Nodal (narrow complex) third-degree AV block occurs in association with an acute inferior wall Ml 

or drug toxicity and is usually transient. It should be treated like second-degree Mobitz Type I AV 

block with atropine or transcutaneous pacing. 

(2) lnfranodal (wide complex) third-degree AV block often occurs in association with an acute anterior 

wall Ml and implies significant structural damage to the infranodal conduction system. It almost 

always requires the insertion of a transvenous pacemaker. Transcutaneous pacing or catecholamines 

(dopamine or epinephrine infusions) may be used as a bridging device while awaiting pacemaker 

insertion. Atropine should be used cautiously (if at all) in this setting and is probably best avoided. 

0. Wolff-Parkinson-White (WPW) syndrome 

1. Recognition 

a. PR interval 200 beats per minute in an adult is very suspicious of an accessory pathway 

syndrome. 

e. Patients with WPW frequently do not have all of the classic features described above 011 their surface ECG, 

particularly if they are in sinus rhythm at the time of evaluation and conduction is occurring through the AV 

node in the normal fashion (concealed tract). 

2. The primary significance of WPW syndrome is that it predisposes to development of tachydysrhythmias 

(particularly atrial fibrillation). 

a. Patients with WPW have two parallel conducting pathways with different refractory periods, the AV node 

and an accessory pathway called the bundle of Kent. This predisposes them to the development of circusmovement 

tachycardias, in which an impulse is conducted anterograde to the ventricles by one pathway 

and retrograde back up to the atria by the other. 

b. When conduction is occurring anterograde down the AV node and retrograde back up the accessory 

pathway, ie, orthodromic tachycardia, the QRS complex appears normal. However, when the impulse is 

being conducted anterograde through the accessory pathway and retrograde through the AV node, the QRS 

complex is wide and cal led antidromic tachycardia. 

c. In the presence of antidromic conduction, the normal restraining effect of the AV node on conduction is 

lost, and rapid ventricular response rates (>200 beats per minute) can occur. This is particularly dangerous 

in atrial fibrillation, in which ventricular response rates can exceed 300 beats per minute and degeneration 

into refractory ventricular fibrillation can occur. 

3. Management of supraventricular tachydysrhythmias in patients with WPW is determined by the patient's 

cardiovascular stability, specific presenting dysrhythmia, the width of the QRS complex, and (with atrial 

fibrillation) how long the patient has been in it. 

31


a. WPW with a narrow complex SVT (orthodromic tachycardia; most common presentation) is treated in 

the same manner as other re-entrant SVTs. 

(1) Treat hemodynamically unstable patients with synchronized cardioversion. Start with 50 joules, and 

pretreat with a sedating agent. 

(2) In hemodynamically stable patients, vagal maneuvers and drugs that slow conduction through the 

AV node (adenosine, calcium channel blockers or ~-blockers, procainamide, or amiodarone) should 

be used. Adenosine is the most effective agent given its rapid onset and strong AV nodal-blocking 

effects. IV procainamide is also effective but is slower in onset. 

b. WPW with a wide complex SVT (antidromic tachycardia) 

(1) If the patient is hemodynamically compromised, treat with cardioversion. 

(2) In stable patients, IV procainamide or amiodarone can be used effectively. Because the rhythm will 

look just like ventricular tachycardia (regular wide complex tachycardia), lidocaine may be chosen as 

first-line treatment, and it is unlikely to have any effect on the rhythm or hemodynamic status. 

(3) AV nodal-blocking agents (especially calcium channel blockers and ~-blockers, but also digitalis and 

adenosine) are contraindicated and should be avoided. 

c. WPW with atrial fibrillation or flutter (regardless of QRS duration) 

(1) Atrial fibrillation with WPW is characterized by an extremely rapid (rates typically 150-300 beats 

per minute), irregularly irregular tachycardia with QRS complexes that randomly vary in width 

and amplitudes, distinguishing this rhythm from ventricular tachycardia and from atrial fibrillation 

with bundle branch block. Atrial flutter with WPW is characterized by extremely rapid ventricular 

rates (often >250 beats per minute) with wide or narrow QRS complexes. The rapidity of the rate 

distinguishes this rhythm from typical ventricular tachycardia and from typical atrial flutter. 

(2) In hemodynamically compromised patients, cardioversion is the treatment of choice. 

(3) In hemodynamically stable patients, IV procainamide is the drug of choice, because it suppresses 

conduction through the accessory pathway. 

(4) All AV nodal-blocking agents should be avoided, because they can accelerate conduction through 

the accessory pathway and increase heart rate. These agents include adenosine, calcium channel 

blockers, ~-blockers, digoxin, and amiodarone. Note that amiodarone has both ~-blocking and 

calcium channel-blocking effects, and therefore must be avoided. 

IV. PACEMAKERS 

A. Emergency pacing techniques 

1. Emergency cardiac pacing can be accomplished via transcutaneous, transesophageal, or transvenous electrodes. 

2. Transcutaneous pacing is the technique of choice in the emergency care setting, particularly in the presence 

of an acute Ml in patients who have received (or may receive) thrombolytic therapy. It is the most easily and 

rapidly applied technique as well as the least invasive. 

B. Indications for temporary cardiac pacing 

1. Emergent 

a. Hemodynamically unstable bradycardia 

b. Bradycardia associated with malignant escape rhythm that does not respond to pharmacologic therapy 

c. Overdrive pacing of a refractory tachydysrhythmia 

d. The pacing of asystole is no longer recommended. 

2. Prophylactic (standby kit at bedside) 

a. Stable bradycardias (asymptomatic or those that responded to initial drug therapy) 

b. The presence of one of the following in the setting of an acute Ml 

(1) Symptomatic sinus node dysfunction 

(2) Mobitz Type II second-degree AV block 

(3) Complete heart block 

(4) Newly acquired or age-indeterminate left bundle-branch block, right bundle-branch block, alternating 

bundle-branch block, or bifascicular block 

C. Tips for temporary transvenous pacemaker placement 

1. The ideal location of the catheter tip is lodged in the trabeculae of the apex of the right ventricle. 

32


2. The right internal jugular is the preferred access site, because it provides the most direct route to the right ventricle. 

3. Although more time consuming and not always possible, insertion using fluoroscopic or ECG guidance is 

preferred to blind placement (which is less reliable in achieving proper catheter positioning). 

4. When ECG guidance is used, the V lead is connected to the distal lead of the pacing catheter with a standard 

connector or alligator clip. Then, while monitoring the V lead, the pacing catheter is advanced and the size of 

the P wave and QRS complex is observed to determine location of the catheter tip; the size of these wave forms 

will increase when the corresponding heart chambers are entered. The development of ST elevation ("current of 

injury") indicates successful placement of the catheter tip. 

5. Pacing results in an abnormal QRS morphology. When the catheter tip is properly placed in the right ventricle, 

this ventricle is stimulated first, while stimulation of the left ventricle is delayed. This produces a left bundlebranch 

block pattern on the surface ECG. 

6. After pacemaker placement, chest radiographs (AP and lateral) should be obtained to confirm appropriate 

placement and exclude a procedural pneumothorax. 

D. Pacemaker failure 

1. Tools for evaluating pacemaker malfunction 

a. ECG to confirm that appropriate sensing and capture are occurring and to indirectly assess the position of 

the pacing catheter by evaluating QRS morphology 

b. Chest radiograph (PA and lateral) to evaluate lead position, exclude cardiac perforation, and look for lead 

fracture (not always visible) 

c. Pacemaker magnet: application of the magnet over the pacemaker turns off the sensing function (via the 

Reed switch) and temporarily converts the pacemaker from the demand (synchronous) mode to the fixedrate 

(asynchronous) mode_,. continuous asynchronous pacing at a specified rate (the magnet rate), which is 

usually around 70. This allows assessment of whether the pacing function is intact and whether the pacing 

stimulus can capture the myocardium. This maneuver is especially helpful in cases in which the baseline 

ECG does not reveal any pacemaker spikes. Moreover, it also al lows assessment of the battery status; a 

decrease in the magnet rate suggests battery depletion. 

2. Signs of pacemaker failure 

a. Slowing of the pacing rate is due to battery depletion. Replacement is urgent if the rate is 10% below the 

set point. 

b. A rapidly paced rhythm resembling ventricular tachycardia ("runaway pacemaker") is usually due to battery 

depletion or circuitry malfunction. 

3. Specific problems 

a. Failure to pace is detected clinically by the absence of pacemaker spikes in a patient whose intrinsic 

cardiac rhythm is slower than the programmed pacemaker rate. Causes include: 

(1) Wire fracture is accompanied by acute onset of symptoms that may be sustained or intermittent. It 

usually occurs at one of three sites: close to the pulse generator, where the lead enters the vein, or 

within the heart where the lead makes a sharp bend. The chest radiograph will demonstrate lead 

placement and may also reveal wire fracture. 

(2) Battery depletion is rare if the patient is being monitored often enough. 

(3) Oversensing (sensing electrical events not associated with atrial or ventricular depolarizations) 

suppresses impulse generation in pacemakers in the inhibit mode. It is more common in patients with 

unipolar leads and the most common cause of failure to pace. 

b. Failure to sense or capture is detected clinically by the presence of pacemaker spikes occurring at the 

wrong time (failure to sense) or the presence of pacemaker spikes without associated QRS complexes 

(failure to capture). Causes include: 

(1) Lead malposition 

(a) Lead displacement usually occurs in the first month after implantation. 

(b) Cardiac perforation usually occurs within 4 days of insertion. 

(2) Wire or insulation fracture 

(3) Battery depletion 

(4) Increased myocardial threshold due to 

(a) Fibrosis or inflammation at the electrode tip 

(b) Lead displacement 

(c) Metabolic and physiologic causes 

i. Metabolic acidosis 

ii. Hypoxia 

33


iii. Hyperkalemia 

iv. Antidysrhythmic drugs (particularly ones that prolong the QRS) 

v. lschemia 

vi. Ml 

(5) Undersensing (ie, voltage of the patient's intrinsic QRS complex is too low for the pacemaker to sense) 

is more common with bipolar pacemakers. Sensitivity may be increased by converting to a unipolar 

pacemaker. 

(6) Oversensing (in pacemakers in the triggered mode): pacemaker spikes appear when none is expected 

because the pacemaker senses and reacts to events other than true cardiac events. 

c. Pacemaker-mediated tachycardia 

(1) Occurs only in patients with dual-chamber pacemakers that are programmed for synchronous 

atrioventricular pacing 

(2) Requires the presence of ventriculoatrial conduction; is a form of reentrant tachycardia 

(3) Can be precipitated by a premature atrial contraction or a premature ventricular contraction 

(4) Management 

(a) May be terminated by using a pacemaker magnet to briefly turn off the sensing function 

(b) Definitive therapy requires reprogramming of the atrial refractory period by a pacemaker specialist. 

d. Runaway pacemaker 

(1) May be triggered by battery depletion 

(2) Rarely occurs today because most newer pacemakers have built-in safety circuits. 

(3) Heart rate is frequently >200 beats per minute. 


(a) Placement of a pacemaker magnet over the pacemaker may convert the pacemaker to the magnet 

rate and break the tachycardia. 

(b) If this is unsuccessful, and the patient is hemodynamically unstable, the pacemaker must be 

disconnected. To do this, exteriorize the pacer and cut the electrode wires. These wires may be 

reconnected to a temporary pacer if the patient's underlying rhythm is unstable. 

V. AUTOMATIC IMPLANTABLE CARDIOVERTER DEFIBRILLATORS 

{AICDs) 

A. Indications 

1. Placed in patients at high risk of fatal dysrhythmias (ventricular tachycardia, ventricular fibrillation) and sudden 

cardiac death 

2. Included in this high-risk group are patients who survived an episode of sudden cardiac death and those with a 

prior Ml or Brugada syndrome; in these patients, AICDs decrease the risk of sudden cardiac death remarkably 

from 30%-45% per year to


(4) Potassium, magnesium, and calcium levels (hypomagnesemia is a common cause of dysrhythmias in 

AICD patients) 

(5) Telemetry interrogation of the AICD 

(6) Consultation with the patient's cardiologist 

c. Inactivation: placement of a magnet over the AICD generator will inactivate it and thereby prevent further 

shocks (see below) 

3. Performance of CPR and defibrillation with an AICD in place 

a. CPR is performed in the usual manner; while the provider may perceive an AICD shock, it is neither 

uncomfortable nor dangerous. 

b. External transthoracic defibrillation may also be performed in the standard manner. The paddles should not 

be placed close to the AICD generator; paddle placement is otherwise unchanged. After successful external 

cardioversion/defibri llation, the AICD should be tested to confirm that sensing and therapy parameters have 

not been altered. 

4. AICD inactivation: AICDs are generally inactivated by the presence of a magnet; however, some device-todevice 

variability exists. 

a. With second-generation AICDs, the placement of a donut-shaped magnet over the upper right quadrant 

of the pulse generator for 30 seconds will inactivate the antitachycardic pacing and shock therapy 

components of the AICD. Reapplication of the magnet for 30 seconds reactivates it. 

b. With the newer third-generation AICDs, placement of the magnet over the pulse generator inactivates 

antitachycardic pacing therapy and shocks for as long as the magnet remains in place over the AICD. 

Removal of the magnet reactivates the device. 

5. Infection: Patients who present with erythema, induration, or drainage at the generator site require 

hospitalization for IV antibiotics. Early infections are usually caused by Staphylococcus spp. 

35


ACUTE CORONARY SYNDROME 

I. DEFINITION 

A. A continuum or progression of coronary artery disease from myocardial ischemia to infarction to necrosis 

B. Stable angina - unstable angina - acute Ml 

II. CLINICAL PRESENTATIONS, RISK FACTORS, AND PREDICTIVE 

FACTORS 

A. Classic presentations of acute coronary syndrome 

1. Stable angina 

a. Transient, episodic chest discomfort that is predictable and reproducible, ie, familiar symptoms occur from 

a characteristic stimulus that improve with rest or sublingual nitroglycerin within a few minutes 

b. These patients are usually sent home or observed briefly in the emergency department. 

2. Unstableangina 

a. Angina that is new in onset, occurs at rest, or is similar but somewhat "different" than previous episodes, 

and is severely limiting or lasts longer than a few minutes. Other signs are an increased frequency of attacks 

or resistance to prescribed medications that previously relieved the symptoms (eg, nitroglycerin, aspirin). 

b. These patients are admitted for observation or coronary care. 

3. Acute Ml 

a. Classically, chest discomfort of> 15 minutes duration associated with dyspnea, diaphoresis, light-headedness, 

palpitations, nausea, and/or vomiting. Pain radiation to the inner aspect of one or both arms, shoulders, neck, 

or jaw is not uncommon and increases the probability that the pain/pressure is ischemic in origin. 

b. Classified as non-ST-segment elevation myocardial infarction (NSTEMI) or ST-segment elevation myocardial 

infarction (STEM!) 

c. These patients are admitted to a cardiac care unit after appropriate treatment, including reperfusion therapy 

if needed. 

B. Atypical presentations (more common in the elderly, diabetic patients, and women) 

1. Chest pain or discomfort (not substernal chest pain/pressure) with or without any of the classic associated 

symptoms; a history of angina is often absent. 

2. Epigastric discomfort/indigestion or nausea and vomiting (may be the only complaint in women or those with 

an inferior wall Ml) 

3. Shortness of breath 

4. Syncope or confusion 

5. Fatigue, dizziness, or generalized weakness 

6. Women with prodromal symptoms (unusual fatigue, sleep disturbances, shortness of breath) for a month or more 

7. No chest or abdominal pain or discomfort; associated symptoms may or may not be present; patient frequently 

has vague complaints ("silent" Ml). 

a. Approximately 12.5% of all Mis 

b. The fol lowing patients should be suspect: 

(1) The elderly 

(2) Diabetic patients 

(3) Those with spinal cord injuries or disease 

(4) Alcoholic patients 

(5) Hypertensive patients or those with hypotensive insults 

(6) Postoperative patients receiving analgesics and postcoronary artery bypass graft patients; these patients 

generally have a worse prognosis than those with a classic presentation. 

36


C. Risk factors 

1. Major 

a. Cigarette smoking 

b. Hypertension 

c. Diabetes mellitus 

d. Hypercholesterolemia 

e. Family history of coronary artery disease before age 55 in a first-degree relative 

f. Previous history of coronary artery disease, peripheral vascular disease, hypercoagulability, or carotid 

arteriosclerosis 

2. Other 

a. Male sex 

b. Advanced age 

c. Methamphetamine use 

d. Cocaine use (especially within an hour of presentation or when combined with ingestion of ethanol-- 

cocaethylene, a longer-acting and more toxic metabolite of cocaine) 

e. Obesity 

f. Postmenopausal state 

g. Inflammatory disorders (eg, lupus) 

h. HIV disease 

i. Chronic kidney disease 

D. Predictive factors of an evolving acute Ml (greater clinical significance than risk factors) 

1. Prior history of ischemic heart disease 

2. Chest pain/discomfort that is worse than usual angina 

3. Pain that is similar to that of a prior acute Ml, lasts longer than an hour, or radiates to the left shoulder/arm 

Ill. DIAGNOSIS 

A. History 

1. A thorough history is the most important tool for identifying patients with cardiac ischemia and is adequate by 

itself to initiate hospital admission. 

2. Patients with a suspicious history and normal initial ECG and cardiac enzymes should be admitted to the 

hospital or chest pain evaluation/observation unit with a diagnosis of "exclude Ml"; typically,


with ECG evidence of left ventricular hypertrophy (most common) and left bundle-branch block; 

however, a new left bundle-branch block in this setting may indicate acute coronary syndrome. An 

isolated ST-segment elevation may also occur with a ventricular aneurysm. 

(2) Q waves without associated ST and T wave changes may be due to an old (not new) Ml in the 

presence of left bundle-branch block; however, Q waves in leads I, aVL, V 5 

, and V 6 

suggest acute Ml. 

(3) Isolated T-wave inversion (no Q waves or ST changes) indicates ischemia (not acute infarction). 

c. Reciprocal changes: ST segment depression (horizontal or downsloping) that occurs in leads opposite to 

those with ST-segment elevation. The presence of these changes increases the positive predictive value of 

the ECG diagnosis of STEMI to >90% and denotes a patient at higher risk of later complications. 

d. ECG localization of the site of infarction 

(1) Acute anterior wall Ml (left anterior descending): ST-segment elevation in leads I, aVL, and V 1 

-V 4 

(segment depression in leads II, Ill, and a VF) represents a greater risk of development of conduction 

abnormalities (AV blocks, bundle-branch blocks, fascicular, and infranodal blocks) and left 

ventricular dysfunction (CHF) 


(2) Acute lateral wall Ml (left anterior descending or left circumflex artery): ST segment elevation in 

leads I, aVL, and V 5 

-V 6 

with reciprocal ST-segment depression in leads V 1 

, II, Ill, and a VF represents a 

risk of development of left ventricular dysfunction. 


38


(3) Acute inferior wall Ml (right coronary artery): ST-segment elevation in leads II, Ill, and a VF with 

reciprocal ST depression in I, aVL, and V 1 

-V 4 

represents a greater incidence of increased vagal tonemediated 

dysrhythmias such as sinus bradycardia and varying degrees of AV block. 


(4) Right ventricular wall Ml (RCA): ST-segment elevation in leads V 3 

R and V 4 

R represents a greater 

risk of developing hypotension and cardiogenic shock. Most right ventricular wall Mis occur in 

association with an inferior wall Ml; ST elevation will be mild. 


39


(5) Acute posterior wall Ml (circumflex artery or posterior descending artery off right coronary artery): 

Because none of the "routine" ECG leads face the posterior surface of the heart, the presence is 

usually inferred from the finding of reciprocal changes in the anterior leads, particularly V 1 

and V 2 

; 

ST-segment depression in association with abnormally tall R waves in these leads is the main ECG 

feature of this diagnosis. When a posterior wall Ml is suspected, obtain "additional" posterior leads 

(V 71 

V 8 

, and V 9 

, placed on the patient's left mid-back area below the tip of the scapula); the presence 

of ST-segment elevation in these leads confirms the diagnosis. 


e. Additional lead ECGs 

(1) Allow more accurate characterization of acute inferior wall Mis by improving identification of 

associated right ventricular and posterior wall involvement 

(2) Incorporate additional leads to better visualize the right ventricle (V 4 R) and posterior wall of the left 

ventricle (V 7 

, V 8 

, and V 9 

), areas that are poorly defined on standard 12-lead ECGs. 

(3) These ECGs should be obtained in patients being admitted for suspected acute ischemia who have: 

(a) ST-segment depression or suspicious isoelectric ST segments in leads V 1 

-V 3 

(posterior infarct) 

(b) T-segment elevation in leads II, Ill, and a VF (inferior wall infarct) ----,, screen for right ventricular 

infarction as well (V 4 R). 

(c) Isolated ST-segment elevation in V 1 

or ST segment elevation in leads V 1 

and V 2 

(right ventricular 

infarct) 

(d) Borderline ST-segment elevation in leads II, Ill, and a VF or in leads V 5 

and V 6 

(inferior wall infarct) 

(e) Symptoms consistent with right ventricular ischemia (eg, epigastric pain, significant hypotension 

after administration of nitroglycerin) 

(4) Clinical significance 

(a) Patients with an acute posteroinferior wall Ml or right ventricular infarction usually have largersized 

Mis, lower ejection fractions, and higher morbidity/mortality rates. 

(b) Associated hypotension in patients with right ventricular infarction will likely respond to IV 

fluids; morphine, nitrates, and diuretics may further compound the situation. 

(5) Use of additional lead ECGs should be restricted to the patient population described above, ie, those 

patients with suspected posterior to right ventricular infarction. Obtaining additional lead ECGs in 

all emergency department patients with chest pain does not appear to have therapeutic or diagnostic 

benefits, and results in an unacceptable increase in false-positive diagnoses. 

2. The initial ECG is also useful in the following situations: 

a. Screening for nonischemic (but potentially serious) causes of chest pain, such as pericarditis and 

pulmonary embolism. 

b. Stratifying the risk of an adverse outcome in association with in-hospital disposition 

(1) Patients at high risk of complications and death should be admitted to a cardiac care unit or ICU. 

Included in this group are patients with any of the following ECG findings: 

40


(a) lschemic ST or T-wave changes in contiguous leads 

(b) Pathologic Q waves (>0.04 seconds long or 25% of R-wave height) 

(c) Left ventricular hypertrophy 

(d) Left bundle-branch block (new or age uncertain) 

(e) Right bundle-branch block and ST changes 

(f) 

Paced rhythm 

(2) Patients at low risk of complications can safely be admitted to a step-down unit. Included in this 

group are patients whose initial ECG is either normal or have nonspecific ST-T wave changes. 

c. Establishing the criteria that determine which therapeutic interventions will be used (~-blockers, 

thrombolytic therapy, etc) 

3. Serial ECGs 

a. Indicated in patients with nondiagnostic ECGs in whom there is concern of possible ongoing ischemia 

b. Capture ischemic ECG changes, demonstrate ECG stability, and detect silent ischemia; ST segment trend 

monitoring may improve detection. 

c. Patients with normal or nonspecific initial ECGs and subsequent confirmed acute Mis within 72 hours 

still have a high rate of mortality and life-threatening complications. 

D. Serum markers of acute Ml 

1. Myoglobin starts increasing within 2-3 hours of infarction and peaks within 4-24 hours. It is more sensitive 

than the total creatine kinase (CK) and CK-MB but is not specific for cardiac muscle and, therefore, has a high 

false~positive rate. Therefore, it cannot reliably identify or exclude a Ml at any time junction; it is best used in 

conjunction with other markers. 

2. CK starts increasing within 4-6 hours of infarction, peaks within 12-24 hours, and returns to baseline in ~48 

hours. However, it is not specific for an acute Ml; in addition to heart muscle, it is also found in skeletal muscle 

and brain tissue, so increases can be due to disorders of any of these organ systems. 

3. CK-MB starts increasing within 4-6 hours of infarction, peaks within 20 hours, and is more specific than CK 

(but still not nearly 100% specific for Ml). The newer monoclonal assays that directly measure CK-MB mass 

(and subforms) have essentially replaced the old electrophoretic assays, because they are more sensitive and 

faster to run. 

4. Troponin (TN) T and I: appear in the serum within 3-4 hours of infarction, peak in 12-24 hours, and remain 

increased for 1-2 weeks. The newest-generation TN assays detect TN release within 1-2 hours of infarction. 

Troponin I is the most specific cardiac marker available (>90%). Troponin Tis not as specific as Troponin I 

(but far more than CK-MB) and is valuable in predicting cardiovascular complications in unstable angina and 

acute Ml. 

5. Appropriate use of serum markers 

a. The decision to admit or discharge a patient should be based primarily on the patient's history and clinical 

presentation, not on the presence or absence of increased cardiac markers. 

(1) Detection of these markers requires that sufficient myocardial eel I damage has occurred and that 

enough time has passed for these markers to be released into the serum. 

(2) Initial determination of these markers has a low sensitivity for detecting ischemia and cannot be used 

to reliably diagnose or exclude the presence of acute coronary syndrome. 

(3) No single determination of one serum biomarker of myonecrosis reliably identifies or excludes acute 

Ml in


Table 4: Cardiac Serum Markers 

Serum Marker Increases (hr) Peaks (hr) Remains High (days) 

Myoglobin 2-3 4-24


c. Administer in the emergency department only as a substitute for aspirin in patients with true aspirin allergy. 

d. STEMI: loading dose of one of these agents should be given as early as possible or at the time of 

percutaneous coronary intervention (PCI). Delaying administration until the coronary anatomy is defined 

at catheterization prevents possible delay in coronary artery bypass graft (CABG) if needed because of 

prolonged antiplatelet effects of these agents. 

e. Unstable angina/NSTEMI: administer a loading dose of one of these as early as possible if there is planned 

early intervention, or begin maintenance dose at time of admission if delayed or no intervention is 

planned. 

f. Prasugrel is contraindicated in patients with any prior history of transient ischemic attack or stroke 

because of increased risk of intracranial hemorrhage. Prasugrel should not be administered in the 

emergency department for unstable angina/NSTEMI; its use should be deferred to the time of PCI. 

3. Glycoprotein lib/Illa receptor antagonists 

a. Available agents include abciximab, eptifibatide, and tirofiban. 

b. Mechanism of action: in the presence of platelet activation, the glycoprotein lib/Illa receptor inhibitors 

block the final common pathway for platelet aggregation. 

c. For both STEMI and unstable angina/NSTEMI, lib/Illa inhibitors may be used as adjunctive therapy 

and started either before or at the time of catheterization for PCI but do not have to be started in the 

emergency department. 

d. lib/Illa inhibitors are not indicated for patients who are being medically managed (ie, in patients who are 

not undergoing catheterization). 

C. Anticoagulant (antithrombotic) therapy 

1. Unfractionated heparin (UFH) 

a. Indicated for all patients presenting with acute coronary syndrome: STEMI, NSTEMI, and high-risk 

unstable angina 

b. Acts as an indirect thrombin inhibitor by accelerating the action of antithrombin Ill (a thrombin 

inhibitor) and activated factors IX, X, and XI. Its antithrombotic activity complements the antiplatelet 

activity of aspirin to prevent progression of ischemia to acute Ml; when used together, heparin and 

aspirin are more effective than either used alone. 

c. Beneficial effects 

(1) In the acute Ml setting, it decreases the incidence of deep-vein thrombosis, reinfarction, 

nonhemorrhagic stroke, and the formation (as well as embolization) of left ventricular thrombus. 

(2) When administered to patients receiving thrombolytic agents, it prevents/decreases the incidence of 

reocclusion. 

(3) In patients with unstable angina, it may be useful in decreasing the rate of subsequent transmural 

infarction. 

(4) It may be preferred by cardiologists who are taking patients to the catheterization laboratory, 

because it can be turned off. 

d. Recommended as the anticoagulant of choice by the AHA for STEMI patients undergoing PCI. Lowmolecular-weight 

heparin (LMWH) is no longer recommended for STEMI in the 2013 AHA STEMI update. 

e. Dosage: bolus of 50-70 units/kg (maximum 5,000 units) followed by an initial infusion of 12 units/kg/hr 

(maximum 1,000 units/hr) adjusted to maintain a partial thromboplastin time 1.5-2 times control 

(50-70 seconds) 

2. LMWHs may be considered acceptable alternative to UFH in patients


c. Bivalirudin may also be selected as initial anticoagulant for unstable angina/NSTEMI patients. However, 

in those patients, who then require PCI or CABC, bivalirudin should be stopped and the patient switched 

to UFH. 

4. Direct factor Xa inhibitor 

a. Selectively binds to antithrombin Ill, which potentiates factor Xa activation and thus inhibits thrombin 

formation 

b. Fondaparinux is preferred to LMWH in patients with renal dysfunction. 

c. Fondaparinux must be combined with UFH to avoid catheter-related thrombosis in patients undergoing PCI. 

D. Nitroglycerin 

1. Decreases ischemic pain (and consequently catecholamine release); no proven reduction in mortality but 

recommended nevertheless if no contraindications 

2. Pathophysiology 

a. Dilates collateral coronary vessels and increases collateral blood flow to ischemic myocardium 

b. Has antiplatelet effects and reduces infarct size and mortality 

c. Decreases myocardial oxygen demand by decreasing preload, left ventricular end-diastolic volume, and 

afterload (which makes it the drug of choice if coexisting left ventricular failure) 

d. May also reduce myocardial susceptibility to ventricular dysrhythmias during ischemia and reperfusion 

3. Should be administered to patients with ischemic chest pain whose systolic blood pressure is >90 mmHg. Start 

with sublingual nitroglycerin 0.4 mg every 3-5 minutes as needed for pain. Follow with an infusion of 10-20 

mcg/min and increase by 5-10 mcg/min every 5-10 minutes until pain is controlled or systolic blood pressure 

is decreased by 10%. 

4. Adverse reactions 

E. ~-Blockers 

a. Hypotension usually responds to a fluid bolus and leg elevation; it is particularly common when 

nitroglycerin is given to patients with inferior wall Mis with associated right ventricular infarction as well as 

to those with hypovolemia or bradycardia; caution should be exercised when administering nitroglycerin to 

these patients. 

b. Reflex tachycardia may be moderated by the concomitant use of ~-blockers. 

c. Administration of nitroglycerin to patients taking sildenafil citrate or other longer-acting medications 

for erectile dysfunction is contraindicated. In these patients, nitroglycerin can precipitate a sudden and 

profound decrease in blood pressure, which leads to decreased coronary perfusion and progression of 

myocardial ischemia to infarction with all of its potential consequences. Nitroglycerin should be avoided 

for 12-24 hours after using medications for erectile dysfunction. 

1. The routine use of early IV ~-blockers for patients presenting with acute coronary syndrome is associated 

with a mild increased risk of cardiogenic shock without a significant decrease in mortality. Consequently, 

IV ~-blockers are indicated only in patients with acute coronary syndrome who also demonstrate 

tachydysrhythmias (eg, rapid atrial fibrillation) or who have intractable hypertension despite nitrates. 

2. ~-blockers should be started orally within the first 24 hours of admission in patients who have none of the 

following: 

a. Signs of heart failure 

b. Evidence of low-output state 

c. Risk factors for cardiogenic shock 

(1) Age >70 years old 

(2) Systolic blood pressure 110 beats per minute or heart rate 240 milliseconds 

(2) Second- or third-degree AV block 

(3) Active asthma or reactive airway disease 

(4) Cocaine toxicity 

(5) Acute right ventricular infarction 

3. Unless contraindications exist, administer the following: 

a. Metoprolol 50-100 mg orally or 

b. Atenolol 50 mg orally or 

44


c. Labetalol 10-20 mg IV if blood pressure control is needed; may repeat dose or double the dose as needed 

in 20-30 minutes or 

d. Esmolol 500 mcg/kg IV (over 1 minute) followed by an infusion of 50 mcg/kg/min titrated to a maximum 

dosage of 200 mcg/kg/min if rate control of a tachydysrhythmia is needed 


F. Morphine 

a. Decrease myocardial oxygen demand by decreasing heart rate and myocardial contractility 

b. Increase coronary blood flow by increasing time of diastole and decreasing myocardial wall tension 

c. Markedly decrease rate of myocardial rupture (particularly in the elderly) 

d. Decrease incidence of ventricular fibrillation and cardiac rupture 

e. Decrease platelet aggregation 

1. Should be administered only if chest pain persists despite adequate management with antiplatelet, 

anticoagulant, and anti-ischemic agents 

2. Pathophysiology: decreases pain and anxiety--,. decreases circulating catecholamines--,. decreases tendency 

toward dysrhythmias and myocardial oxygen demand 

3. Administer 2-4 mg every 5-10 minutes as needed for pain. 

4. Adverse effects 

a. Hypotension and bradycardia: respond to fluid bolus and atropine 

b. Do not administer to patients with a heart rate


d. Agent availability and administration protocols vary from hospital to hospital. 

e. American Heart Association/ American College of Cardiology criteria for thrombolysis 

(1) Class I (treatment benefit has been established): ST elevation >0.1 mV in two or more contiguous 

leads with ischemic symptoms of 110 mm Hg) 

(2) Traumatic or prolonged (>10 minutes) CPR 

(3) Noncompressible vascular punctures 

(4) Major surgery or internal bleeding within 3-4 weeks 

(5) Any other CNS disease (structural or functional, eg, dementia) not noted above 

(6) Pregnancy 

(7) Active peptic ulcer 

(8) Current use of anticoagulants (the higher the INR, the greater the risk of bleeding) 

(9) Prior exposure/allergic reaction to streptokinase or anistreplase (if using these agents) 

h. Complications 

(1) Systemic bleeding: incidence 2%-10%; usually occurs in the setting of invasive procedures. 

(2) Cerebral hemorrhage: incidence


d. Creatinine >2.5 mg/dL 

e. Renal artery stenosis 

J. Glucose-insulin-potassium (GIK) therapy 

1. The results of a large, controlled, multinational study published in 2005 refuted smaller, earlier studies claiming 

a reduced mortality rate with GIK therapy. Therefore, GIK therapy is not recommended in the management of 

acute Ml. 

V. COMPLICATIONS 

A. Myocardial ischemia produces altered electrical depolarization and contractility, which are the major 

complications of an acute Ml (ie, dysrhythmias and left ventricular failure). 

B. Dysrhythmias 

1. The prehospital phase is the period associated with the highest incidence of lethal dysrhythmias; the 

occurrence of primary ventricular fibrillation (no evidence of CHF or hypotension) is greatest in the first hour of 

infarction. 


2. Treatment is indicated if the dysrhythmia 

a. Exacerbates myocardial ischemia or 

b. Could potentially deteriorate into cardiac arrest 

c. Treat specific dysrhythmias per current ACLS protocols. 

3. Lidocaine is no longer recommended as a prophylactic antidysrhythmic for acute Ml or ischemia; its use in this 

setting has been associated with an increased mortality rate. 

4. For premature ventricular contractions occurring in the presence of acute Ml, the initial treatment priority 

should be to optimally manage the underlying ischemia/infarction with oxygen, aspirin, nitroglycerin, 

and reperfusion therapy (ie, thrombolytics or PCI). Any electrolyte abnormalities should also be corrected. 

Previously, empiric treatment with ~-blockers was recommended to prevent premature ventricular contractions. 

However, new evidence refutes this practice, and there is possibly added harm by increasing risk of 

cardiogenic shock in patients with acute Ml. 

C. Left ventricular failure (CHF, pulmonary edema, cardiogenic shock) 

1. Acute Ml - impaired contractility of the left ventricle 

a. Impairment 2:25% of the left ventricle - (HF/pulmonary edema 

b. Impairment 2:40% of the left ventricle - cardiogenic shock 

2. Pathogenesis: pump failure= CHF; over time, this leads to increased pulmonary vascular congestion - 

pulmonary edema. Cardiogenic shock can occur with either acute, severe pump failure or acute, severe 

pulmonary edema (each of which further impairs left ventricular function). 

3. For management, see CHF/pulmonary edema, pages 50-52. 

D. Conduction disturbances 

1. AV blocks 

a. First-degree AV block and Mobitz Type I second-degree AV block 

(1) Generally due to increased vagal tone 

(2) Rarely progress to complete AV block 

(3) Usually associated with an inferior Ml (think Mobitz Type I and Inferior) 

(4) Generally responds to drug therapy (atropine) 

b. Mobitz Type II second-degree AV block 

(1) Generally due to destruction of infranodal conduction tissue 

(2) Sudden progression to complete AV block may occur 

(3) Usually associated with an anterior Ml 

(4) Prophylactic pacemaker therapy is indicated 

47


2. Bundle-branch blocks 

a. In general, bundle-branch blocks (old or new) associated with an acute Ml identify patients who are more 

likely to develop CHF, AV block, and ventricular fibrillation. 

b. In patients with an acute anterior wall Ml and a new right bundle-branch block, there is a high risk of 

developing complete AV block and/or cardiogenic shock. 

E. Other less common complications of acute Ml 

1. Free left ventricular wall rupture 

2. Ventricular septa! rupture 

3. Papillary muscle dysfunction/rupture 

4. Acute mitral regurgitation 

5. Left ventricular aneurysm 

6. Thromboembolism 

7. Acute pericarditis 

8. Most of these complications are delayed in onset, occurring 1 or more days after infarction. 

48


CONGESTIVE HEART FAILURE 

I. ETIOLOGY, PRECIPITATING FACTORS, AND SIGNS 

AND SYMPTOMS 

A. Left ventricular failure 

1. lschemic heart disease (most common cause) 

2. Idiopathic dilated cardiomyopathy 

3. Hypertension 

4. Valvular disease (aortic or mitral) 

5. High-output states (anemia, thyrotoxicosis, AV fistula, beriberi, Paget disease) 

6. Congenital heart disease 

7. Coarctation of the aorta 

B. Right ventricular failure 

1. Left ventricular failure (most common cause) 

2. Pulmonary arterial hypertension (and right ventricular failure= cor pulmonale) 

3. Valvular disease (tricuspid or pulmonic) 

4. Restrictive or infiltrative cardiomyopathies 

5. Myocarditis and some forms of congenital heart disease 

6. Right ventricular infarction 

7. Pulmonary embolism 

8. Chronic pulmonary disease 

C. Precipitating factors 

1. Myocardial ischemia or infarction 

2. Noncompliance with medications 

3. Tachydysrhythmias (eg, atrial fibrillation) and severe bradydysrhythmias 

4. Dietary indiscretion (sodium overload) 

5. Administration of drugs that impair cardiac function (fl-blockers or calcium channel blockers) or result in 

sodium retention (glucocorticoids, NSAIDs, nasal decongestants, vasodilators) 

6. Increased hemodynamic demand due to infection, trauma, physical overexertion, environmental stress, or 

pregnancy 

7. Hypoxia (due to pulmonary embolism or pneumonia) 

8. Cardiac disease progression (coronary insufficiency and CHF are the most common precipitating causes of 

acute cardiogenic pulmonary edema) 

9. Severe hypertension 

10. COPD (the leading cause of chronic cor pulmonale) 

11. Acute myocarditis or endocarditis 

12. Acute valvular dysfunction 

D. Signs and symptoms 

1 . Shortness of breath (most common symptom) 

2. Paroxysmal nocturnal dyspnea/orthopnea 

3. Nocturnal angina 

4. Moist rales and/or wheezing ("cardiac asthma") 

5. Cough 

6. Fatigue and/or weakness 

7. Pleural effusion (usually right-sided) 

8. Tachypnea and tachycardia 

9. S 3 

gallop (due to reduced left ventricular compliance) 

10. S 4 

gallop (not heard in patients with atrial fibrillation) 

11. Hepatojugular reflux--;. jugular venous distention (right ventricular failure) 

49


12. Pulsus alternans (alternating strong and weak arterial pulse waveform) 

13. Ascites (right ventricular failure) 

14. Hepatic enlargement/tenderness (right ventricular failure) 

15. Pale, clammy skin or diaphoresis 

16. Neck vein distention (right ventricular failure) 

17. Anxiety 

18. Nocturia 

19. Dependent edema (right ventricular failure) 

II. DIAGNOSTIC EVALUATION 

A. Radiographs 

The cardiac silhouette is generally enlarged (although it may be normal size) in all three stages, associated pleural 

effusions (usually right-sided) are common, and chest radiograph findings may be delayed up to 12 hours relative to 

symptom onset. 

1. Stage 1: pulmonary vascular redistribution to upper lung fields ("cephalization") 

a. Chest radiograph - fullness or prominence of the pulmonary vessels in the apices 

b. Predominant symptom (if any are present) is dyspnea. 

2. Stage II: interstitial edema 

a. Chest radiograph - pulmonary vessels enlarged with blurred shadows, Kerley B lines (1-cm horizontal 

markings at the periphery of lung fields) are also present. 

b. Predominant symptom is dry cough. 

3. Stage Ill: alveolar edema (frank pulmonary edema) 

a. Chest radiograph - bilateral confluent perihilar infiltrates creating a "butterfly" pattern 

b. Predominant symptom is a wet cough with production of a frothy, pink sputum. 

B. Laboratory studies 

1. Brain-type natriuretic peptide (BNP) is used as a serum marker for acute CHF. 

2. Pathogenesis: cardiac hypertrophy/wall stress and volume overload - release of endogenous BNP by atrial and 

ventricular myocytes - smooth muscle relaxation and vasodilation, diuresis and natriuresis 

3. Acute CHF can lead to high serum levels of BNP, which are especially significant in the absence of pulmonary 

disease and advancing age (when moderate increases can occur). 

4. A serum BNP level 60 mmHg 

despite receiving 100% oxygen, displays a progressive increase in pC0 21 

or demonstrates increasing 

50


acidosis. Do not wait for arterial blood gases if patient's clinical condition is deteriorating. Positive 

end-expiratory pressure (PEEP) can then be applied via the endotracheal tube. 

(5) Because positive-pressure ventilation (either NIPPV or endotracheal ventilation) increases 

intrathroacic pressure, there is a resultant decrease in preload, which can decrease cardiac output 

and blood pressure. Therefore, monitor blood pressure carefully. 

c. Initial medications 

(1) Nitroglycerin 

(a) At low doses, nitroglycerin is primarily a venodilator and rapidly acts to decrease preload. Its 

effects on arterial dilation are less profound and are usually associated with much higher doses. 

Nitroglycerin also acts to increase coronary blood flow by promoting dilation of large epicardial 

vessels and is, therefore, the vasodilator of choice in the presence of ischemia or an acute Ml. 

(b) Administer sublingual nitroglycerin 0.8-1.2 mg every 5-10 minutes (use higher doses if 

blood pressure is moderately to severely increased) as a loading dose, then start high-dose 

nitroglycerin IV drip. 

(c) Nitroglycerin IV at 10-20 mcg/min; titrate the drip upward in increments of 5-10 mcg/min 

every 5 minutes until the desired effect is attained or blood pressure decreases to 100 mm Hg (no signs/symptoms of shock) 

(1) Nitroprusside 

(a) A potent mixed venous and arteriolar dilator; reduces both preload and afterload, thereby 

decreasing pulmonary congestion and reducing cardiac output 

(b) Usually reserved for patients with a systolic blood pressure > 100 mm Hg who do not respond to 

adequate dosages of the standard preload reducers (nitroglycerin, furosemide) or for patients 

with low output who require controlled afterload reduction 

(c) Dosage: 0.1-5 mcg/kg/min IV; invasive hemodynamic monitoring is strongly recommended. 

b. Systolic blood pressure 70-100 mm Hg 

(1) No signs/symptoms of shock -> dobutamine 

(a) A direct-acting inotropic agent that is effective in increasing cardiac output and decreasing 

pulmonary capillary wedge pressure 

(b) Dosage: 2-20 mcg/kg/min IV (patients on ~-blockers may need the higher dosage) 

(c) Hemodynamic monitoring is advisable, because dobutamine may worsen hypotension. 

(d) If dobutamine successfully improves cardiac output and blood pressure, a nitroglycerin infusion 

can be carefully added for preload reduction, as the patient's blood pressure tolerates. 

(e) Dobutamine has some vasodilatory effect as well, so some patients will have a reduction in 

blood pressure. If this occurs, the addition of a vasopressor may be needed. 

(2) Signs/symptoms of shock present -> dopamine (or norepinephrine, below) 

(a) Indirect inotropic support as an effective pressor agent; the preferred agent when persistent 

oliguria or shock is present (systolic blood pressure


(c) The vasopressor effect of dopamine increases afterload, but it can actually worsen pulmonary 

congestion. To counter this adverse effect, the concurrent use of vasodilatory medications 

(nitroglycerin or nitroprusside) is recommended, as tolerated by the patient's blood pressure. 

(d) Dopamine may also be used in combination with dobutamine; dopamine maintains blood 

pressure, while dobutamine prevents further increase in pulmonary congestion. 

c. Systolic blood pressure


CARDIOMYOPATHIES AND SPECIFIC HEART 

MUSCLE DISEASES 

I. CARDIOMYOPATHIES 

A. Definition 

1. Diseases of the heart muscle of unknown etiology that produce both structural and functional damage to the 

myocardium 

2. Classified as dilated (most common), restrictive, or hypertrophic based on differences in pathophysiology and 

clinical presentation (however, there is some overlap). 

B. Idiopathic dilated (congestive) cardiomyopathy 

1. Characterized by dilatation of all four chambers (ventricles> atria), increased myocardial mass (hypertrophy), 

and systolic pump failure. There is a high association of idiopathic dilated cardiomyopathy with viral 

myocarditis; unexplained heart failure is commonly the only manifestation. 

2. Clinical presentation 

a. History 

(1) Signs and symptoms of left- and right-ventricular CHF (dyspnea on exertion and fatigue, which are the 

two most common complaints), paroxysmal nocturnal dyspnea, orthopnea, palpitations, dependent 

edema, ascites) and/or 

(2) Manifestations of systemic or peripheral embolization (acute neurologic deficit, flank pain and 

hematuria, pulseless cyanotic extremity) 

b. Physical findings 

(1) Bibasilar rales 

(2) Peripheral edema, jugular venous distention, and hepatomegaly (when associated with a pulsatile liver, 

tricuspid regurgitation is also present) 

(3) Abnormal heart sounds 

3. Diagnostic evaluation 

a. ECG 

(a) 5 3 

and 5 4 

gallop (most common auscultatory findings) 

(b) High-pitched systolic ejection murmur of mitral regurgitation (best heard at apex) 

(c) Holosystolic ejection murmur of tricuspid regurgitation (best heard at lower left sternal border) 

(d) Tachycardia (often with a narrow pulse pressure) when CHF is present 

(1) Left ventricular or biventricular hypertrophy 

(2) Left atrial or biatrial enlargement 

(3) Poor R-wave progression 

(4) A new bundle-branch block (may occur before any signs of chamber dilation or pump dysfunction) 

(5) AV block (usually first- or second-degree) 

(6) Atrial fibrillation (most common dysrhythmia) 

b. Chest radiograph 

(1) Cardiomegaly with enlargement of all four chambers 

(2) Pulmonary venous congestion 

c. Echocardiography 

(1) Enlargement of ventricles and atria 

(2) Increased systolic and diastolic volumes 

(3) Decreased ejection fraction (


b. Anticoagulants should be administered to patients with: 

(1) lntracardiac thrombi 

(2) Evidence of pulmonary or systemic thromboembolism 

(3) Chronic atrial fibrillation 

C. Restrictive cardiomyopathy 

1. Characterized by diastolic restriction of ventricular filling; the end-diastolic ventricular volume is low, the enddiastolic 

ventricular pressure is high, and cardiac output is decreased-a hemodynamic picture that mimics 

that of constrictive pericarditis. 


a. History 

(1) Similar to that of patients with dilated cardiomyopathy 

(2) Signs and symptoms of systemic and pulmonary venous congestion; however, evidence of right-sided 

CHF often predominates. 

(3) Exercise intolerance is a common complaint. 

b. Physical examination (similar to that of idiopathic dilated cardiomyopathy) 

(1) Bibasilar rales 

(2) Peripheral edema, jugular venous distention, hepatomegaly 


(a) 

S 3 

and S 4 

gallop (common) 

(b) Systolic ejection murmur of mitral or tricuspid regurgitation 

(c) Tachycardia 

(4) The apex impulse is usually easily palpable and mitral regurgitation is more common (in contrast to 

constrictive pericarditis). Other signs that are not present in constrictive pericarditis are a gallop rhythm 

and a positive Kussmaul sign (jugular venous distention on inspiration). 


a. ECG 

(1) Chamber enlargement (atria> ventricles) 

(2) Nonspecific ST-T-wave changes 

(3) Low voltage 

(4) Dysrhythmias (especially atrial fibrillation) are common. 


(1) May be normal initially (a small heart suggests constrictive pericarditis) 

(2) Cardiomegaly with pulmonary venous congestion is seen with disease progression. 

c. Echocardiography 

(1) Thickened walls 

(2) Normal or slightly enlarged ventricular cavity and moderate to markedly dilated atria 

(3) Normal or slightly decreased systolic function 

(4) Mitral and tricuspid regurgitation 

d. If differentiation from constrictive pericarditis is still uncertain after echocardiography, then CT, MRI, or 

combined Doppler and two-dimensional echocardiography may be required to make the diagnosis - 

thickened pericardium in constrictive pericarditis. Biopsy is the gold standard to exclude constrictive 

pericarditis if all else fails. 

4. Management 

a. Aimed at alleviating symptoms and usually includes a regimen of diuretics and digitalis 

b. In the absence of left ventricular enlargement, administration of digitalis may be without beneficial effect. 

c. Vasodilators reduce afterload but produce hypotension and have not been found to be beneficial. 

D. Hypertrophic cardiomyopathy 

1. Characterized by left ventricular hypertrophy without associated ventricular dilatation. The hypertrophy is 

generally asymmetric, involving the septum to a greater extent than the free wall; on histologic examination, 

the myocardial fibers have a marked and extensive disorganized whorled pattern (particularly in the septum). 

Other common features include ventricular cavities that are reduced in size, atrial dilatation, mitral valve 

thickening, impaired diastolic relaxation, and restricted left ventricular filling. 

54


2. In >50% of cases, this disorder is inherited via an autosomal dominant transmission pattern with variable 

penetration. The remaining cases appear to be sporadic. 


a. History 

(1) Dyspnea on exertion (most common initial complaint) 

(2) Atypical chest pain (poor response to nitroglycerin is common); chest pain that is relieved by assuming 

the recumbent position is pathognomonic of hypertrophic cardiomyopathy but rarely encountered. 

(3) Palpitations 

(a) Ventricular and atrial dysrhythmias are common. 

(b) Tachydysrhythmias (particularly atrial fibrillation) are poorly tolerated and may require emergent 

intervention. 

(4) Syncope and presyncope 

(a) Usually related to exertion 

(b) Due to dysrhythmias or a sudden decrease in cardiac output 

(5) Sudden death (usually due to dysrhythmias that occur with exercise, especially ventricular tachycardia) 

(6) Symptom severity correlates with the degree of hypertrophy which, in turn, correlates with the patient's 

age, ie, the older the patient, the more severe the symptoms. 

b. Physical examination 

(1) A prominent "a wave" may be noted on inspection of the neck veins, ie, a pulse wave that reflects the 

powerful systolic pressure of the hypertrophied left ventricle; this should not be confused with jugular 

venous distention, because jugular venous pressure is not usually increased. 

(2) Rapid biphasic carotid pulse (pulsus biferiens) 



(a) 5 4 

gallop: prominent systolic ejection murmur along the lower left sternal border and at the apex 

with radiation to the axil la 

(b) This murmur is the result of left ventricular outflow obstruction and mitral regurgitation; it is 

increased with maneuvers or therapies that decrease left ventricular end-diastolic volume: the 

Valsalva maneuver, sudden standing, exercise, amyl nitrate inhalation, and administration of 

isoproterenol. Remember to perform one of these maneuvers when evaluating young patients 

presenting with exertional syncope or chest pain. 

a. ECG: almost always abnormal 

(1) Left ventricular hypertrophy and left atrial enlargement 

(2) Changes in the anterior, lateral, or inferior leads 

(a) "Septal Q waves" >0.3 mV (represent septal depolarization) 

(b) "Dagger-like" deep, narrow (


hypertrophic cardiomyopathy patients have restricted left ventricular filling and, therefore, depend on atrial 

contraction to maintain efficient flow; when atrial fibrillation occurs, cardiac output drops suddenly. 

b. ~-blockers (eg, propranolol) 

(1) Improve most symptoms of this disease (dyspnea, chest pain, dizziness, syncope) and so are the 

mainstay of therapy 

(2) Decrease myocardial oxygen consumption by decreasing exertion-related outflow obstruction 

c. Calcium channel blockers (eg, verapamil, nifedipine) 

(1) May be useful in select patients who do not respond to ~-blockers 

(2) Decrease outflow obstruction, myocardial oxygen consumption, and incidence of angina; increase 

exercise capacity 

(3) Avoid in patients with conduction blocks or increased pulmonary venous pressures (CHF). 

d. Amiodarone 

(1) The treatment of choice for ventricular dysrhythmias; also indicated for patients who do not respond to 

~-blockers and calcium channel blockers. 

(2) Controls most atrial and ventricular dysrhythmias and appears to prevent sudden cardiac death (the 

most common cause of death in these patients) 

e. Diuretics are useful in the setting of pulmonary and venous congestion but must be used with caution to 

avoid hypotension. 

f. Agents that either increase myocardial contractility (digitalis, ~-adrenergic agents) and/or reduce ventricular 

volume (eg, nitrates, other vasodilators) should be avoided, because they can increase outflow obstruction. 

g. Surgical management (most common procedure is septa! myomectomy) 

(1) Reserved for very symptomatic patients with large systolic gradients (>50 mm Hg) who do not respond 

to drug therapy 

(2) Effectively relieves left ventricular outflow obstruction in 95% of patients but has a mortality rate of 

3%-8% 

h. Antibiotic prophylaxis is no longer indicated for dental or routine emergency department procedures. 

i. Avoiding competitive athletics is advised, because sudden death can follow vigorous exertion. 

II. SPECIFIC HEART MUSCLE DISEASES 

A. Definition 

1. Disorders of the heart muscle associated with a single known cause or systemic disease 

2. These diseases were previously referred to as secondary cardiomyopathies, but this terminology is no longer used. 

B. Categories 

1. Toxins 

a. Most commonly associated with dilated cardiomyopathy 

(1) Ethanol 

(2) Cobalt, cocaine 

(3) Lithium 

(4) Doxorubicin (adriamycin) 

(5) Daunorubicin 

(6) Emetine 

b. Others 

(1) Heavy metals 

(2) Amphetamines 

2. Nutritional deficiencies 

a. Thiamine (B 1 

) deficiency (beriberi) 

b. Vitamin C deficiency (scurvy) 

c. Vitamin B 6 

deficiency (pellagra) 

d. Selenium deficiency (Keshan disease) 

e. Kwashiorkor 

56


3. Metabolic 

a. Most commonly associated with restrictive cardiomyopathy 

(1) Hemochromatosis 

(2) Glycogen storage disease Type II 

b. Others 

(1) Hypothyroidism (myxedema) 

(2) Hyperthyroidism (thyrotoxicosis) 

(3) Uremia 

(4) Pheochromocytoma 

(5) Hypophosphatemia 

4. Infiltrative (most commonly associated with restrictive cardiomyopathy) 

a. Amyloidosis (most common cause in the Western hemisphere) 

b. Sarcoidosis 

c. Endomyocardial fibrosis (most common cause worldwide) 

5. Collagen vascular diseases 

6. Neuromuscular 

a. Muscular dystrophies 

b. Friedreich ataxia 

c. Myasthenia gravis 

7. Myocarditis 

a. Viral 

b. Bacterial 

c. Parasitic (Chagas' disease due to Trypanosoma cruzi) 

d. HIV-associated 

8. Peripartum (associated with dilated cardiomyopathy) 

9. lschemia 

10. Radiation 

57


PERICARDIAL DISORDERS 

I. PERICARDITIS 

A. Etiology 

1. Idiopathic (along with viral, most common causes) 

2. Infectious agents 

a. Viral (along with idiopathic, most common causes) 

b. 

(1) Coxsackie viruses A and B 

(2) Echovirus 

(3) Adenovirus 

(4) HIV 

(5) Epstein-Barr virus 

(6) Influenza 

(7) Hepatitis B 

Bacterial (uncommon cause) 

(1) Staphylococcus 

(2) Pneumococcus 

(3) Streptococcus 

(4) Meningococcus 

(5) Mycobacterium sp 

(6) Rickettsia sp 

(7) Borrelia burgdorferi 

(8) Mycoplasma 

c. Fungal 

(1) Histoplasmosis 

(2) Blastomycosis 

(3) Coccidiomycosis 

3. Malignancies 

a. Metastatic 

(1) Breast 

(2) Lung 

(3) Melanoma 

(4) Leukemia 

(5) Lymphoma 

b. Primary pericardia! tumors (mesotheliomas): rare cause 

4. Systemic illnesses 

a. Systemic lupus erythematosus 

b. Acute rheumatic fever 

C. Rheumatoid arthritis 

d. Scleroderma 

e. Polyarteritis nodosa 

f. Sarcoidosis 

g. Myxedema 

h. Amyloidosis 

5. Medications 

a. Anticoagulants 

b. Procainamide 

c. Hydralazine 

d. lsoniazid 

58


6. Radiation 

7. Cardiac injury 

B. Diagnosis 

a. Acute Ml 

b. Dressler syndrome (late post-Ml pericarditis) 


2. ECG 

a. History 

(1) Sharp precordial or retrosternal chest pain exacerbated by inspiration, swallowing, or movement 

of the upper torso (pain is increased in the supine position but relieved by sitting up and leaning 

forward); radiation to the trapezius muscle ridge (especially the left) is common and is a distinctive 

characteristic. 

(2) Dyspnea 

(3) Low-grade, intermittent fever 

b. Physical examination: pericardia! friction rub is pathognomonic. 

(1) May be positional and intermittent 

(2) Best appreciated when the patient is sitting and leaning forward or is in the hands-and-knees position 

(3) Scratchy in character; best heard with the diaphragm of the stethoscope positioned along the lower left 

sternal border or cardiac apex 

(4) Classically triphasic (with presystolic, systolic, and diastolic components) but may be biphasic or 

monophasic 

a. Normal sinus rhythm or sinus tachycardia; dysrhythmias are uncommon. 

b. Initial ST and PR segment changes 

(1) Diffuse, nonanatomic ST-segment elevation with upward concavity is seen acutely in multiple leads 

except aVR and V,. ST-segment elevation due to acute Ml may also be concave upward but can 

also be flat or convex in configuration and has a nondiffuse, anatomic distribution (eg, inferior or 

anterior wall pattern); ST elevation in Ill > II - think Ml 

(2) ST-segment depression in leads aVR and V, is common but nonspecific; however, ST-segment 

depression in any of the other leads strongly suggests Ml and not pericarditis. 

(3) PR-segment depression in multiple leads is common with viral pericarditis, most prominent in lead II, 

and often the earliest ECG manifestation. 


c. ST and PR segment changes then normalize 

d. Diffuse T-wave inversion a late sign 

e. Finally after several weeks, all ECG segments and waves should have returned to baseline. 

3. Chest radiograph: usually normal but, in the presence of a large pericardia! effusion (>200 ml), may reveal an 

enlarged cardiac si I houette 

4. Echocardiography: the most sensitive and most specific procedure for detecting the presence and size 

of an associated pericardia! effusion; considered the diagnostic method of choice. Two-dimensional 

echocardiography can detect as little as 15 ml of fluid and has the advantage of being able to provide 

information about cardiac function. Transesophageal echocardiography and chest CT are superior to 

transthoracic echocardiography for demonstration of pericardia! thickening (seen in constrictive pericarditis). 

5. CT scan 

a. Can define the presence and extent of pericardia! effusion but, unlike echocardiography, cannot assess 

cardiac function and may miss hemopericardium because of similar densities of blood and myocardium 

b. Usually reserved for times when echocardiography is unavailable or yields equivocal results 

59


6. Laboratory studies 

a. CBC: increased WBC count with a left shift is common. 

b. Erythrocyte sedimentation rate: usually increased 

c. BUN/creatinine: useful in excluding uremia 

d. Cardiac enzymes: often minimally increased 

e. Other specific tests (blood cultures, viral titers, thyroid function tests, etc): should be obtained as 

appropriate, depending on suspected underlying etiology 

C. Management 

1. Because they tend to follow a benign, self-limited course, patients with viral or idiopathic pericarditis may 

be treated as outpatients if reliable follow-up can be assured. All others, particularly those with severe 

intractable pain or an underlying precipitant that requires specific treatment (Ml, uremia, bacterial infection, 

etc) should be hospitalized. 

2. Pain relief 

a. Anti-inflammatory agents generally provide symptomatic relief within 24 hours of initiation. Use one of 

the following: 

(1) Aspirin 650 mg orally every 6 hours 

(2) Ibuprofen 600-800 mg orally every 6-8 hours 

(3) lndomethacin 25-75 mg orally every 6-8 hours 

(4) Colchicine decreases the duration of symptoms and recurrences when administered during the first 

episode. The recommended dosage is 2 mg/day for 1-2 days, followed by a maintenance dosage of 1 

mg/day (0.5 mg twice per day). The major adverse effect is diarrhea; if this develops, a lower dosage 

should be used. Additionally, reduced dosages should be used in patients >70 years old, and care 

should be exercised in the presence of renal insufficiency or if the patient is taking other drugs that 

are metabolized through the cytochrome P450 system. 

(5) A randomized trial in 2013 showed significant benefit of the combination of colchicine with 

standard NSAID therapy with reduction in duration of symptoms, decreased recurrence of 

pericarditis, and decreased need for hospitalization. 

(6) Prednisone (60 mg/day orally) should not be administered in the acute setting for patients with acute 

pericarditis. Steroids have been found to be an independent risk factor for recurrences. 

b. Opiate medications may be used when immediate pain relief is needed. 

3. Treat the underlying disorder. 

a. Antimicrobial agents for patients with underlying infections 

b. Dialysis for uremic patients 

c. Cessation of the causative agent for medication-induced pericarditis 

4. Pericardiocentesis for tamponade 

II. PERICARDIAL TAMPONADE 

A. Classic clinical presentation 

1. Beck triad (late findings occurring just before cardiac arrest) 

a. Hypotension 

b. Jugular venous distention 

c. Distant or "muffled" heart tones (quiet heart) 

2. Narrow pulse pressure 

3. Dyspnea 

4. Tachycardia (earliest sign) 

5. Pulsus paradoxus > 10 mmHg 

6. Kussmaul sign: a rise in central venous pressure (by observation of jugular venous pulsation) with 

spontaneous inspiration 

B. Diagnostic evaluation 

1. ECG 

a. Low QRS voltage: a nonspecific finding of pericardia( effusion 

60


b. Total electrical alternans: a beat-to-beat alternating pattern primarily affecting the QRS complex that 

occurs from shifting pericardia! fluid and heart position-highly suggestive of the presence of large 

pericardia! effusions, but this finding is poorly sensitive 

2. Chest radiograph: in patients with chronic effusions, may reveal an enlarged "water bottle"-shaped cardiac 

silhouette without associated pulmonary redistribution; this is not the case in acute traumatic tamponade, in 

which the cardiac silhouette is typically normal. 

3. Echocardiography 

a. The gold standard for diagnosing pericardia! effusion; it can quickly and accurately confirm the presence 

of tamponade. 

b. If rapidly available and the patient's condition allows, it should be performed whenever pericardia! 

tamponade is suspected. 

c. Findings consistent with tamponade 

(1) A large pericardia! effusion, visualized as an echo-free space behind the left ventricle and in front of 

the right ventricle 

(2) Diastolic collapse of the right ventricle and the right atrium 

(3) Swinging motion of the heart in the effusion (producing electrical alternans) 

4. Differential diagnosis in patients with neck vein distention and hypotension 

a. Acute pericardia! tamponade 

b. Tension pneumothorax 

c. Massive pulmonary embolism 

d. Acute left ventricular Ml with cardiogenic shock 

e. Acute right ventricular Ml 

f. Superior vena cava syndrome 

g. Acute valvular dysfunction with regurgitation 

5. Clinical picture of a patient who needs immediate pericardiocentesis 

a. Air-hunger and drowsiness or confusion 

b. Thready pulse and pulsus paradoxus that is >50% of the pulse pressure 

c. t jugular venous distention and t systolic blood pressure 

C. Management 

1. Perform stabilizing/temporizing measures while arranging for pericardiocentesis. 

a. Establish two large-bore IV lines, provide supplemental oxygen (5-10 L/min), and place cardiac monitor. 

b. Provide aggressive volume resuscitation with crystalloid solution or blood. 

c. Administer dobutamine or dopamine as needed for inotropic support. 

d. Obtain immediate cardiology and cardiothoracic surgery consult, depending on availability. Urgent 

pericardiocentesis can usually be performed in the catheterization laboratory by cardiology, but if the 

cardiothoracic surgeon is unable to perform the procedure or it is unsuccessful, he or she will likely need 

to perform pericardiotomy in the operating room. 

2. Definitive therapy is pericardiocentesis. Although pericardiocentesis can be performed blindly or by using 

ECG guidance, ultrasound guidance is safer and is the technique of choice if it can be performed in a timely 

manner. 

61


MYOCARDITIS 

I. ETIOLOGY 

A. Viruses: most common cause of myocarditis 

1. Coxsackie A and B (historically most common viral cause) 

2. Adenovirus (increase in incidence in the 1990s) 

3. Parvovirus 819 (increase in incidence in 2000s) 

4. Epstein-Barr 

5. Hepatitis Band C 

6. Human herpesvirus-6 

7. Echovirus 

8. Poliovirus 

9. HIV 

10. Cytomegalovirus 

11. Influenza and parainfluenza 

B. Bacteria 

1 . f3-hemolytic streptococci (rheumatic fever) 

2. Corynebacterium diphtheriae 

3. Neisseria meningitidis 

4. Borrelia burgdorferi (Lyme disease) 

5. Mycoplasma pneumoniae 

C. Parasites 

1. Chagas' disease 

2. Toxoplasmosis 

3. Trichinosis 

D. Systemic diseases 

1 . Kawasaki syndrome 

2. Systemic lupus erythematosus 

3. Sarcoidosis 

4. Giant-cell myocarditis 

E. Drug hypersensitivity 

1. Sulfonamides 

2. Penicillins 

3. Methyldopa 

F. Toxins 

1. Cocaine 

2. Inhalants (eg, toluene) 

II. CLINICAL PRESENTATION 

A. Determined by degree of cardiac involvement; ranges from nonspecific symptoms of fatigue and dyspnea 

to florid CHF, significant dysrhythmias, and sudden cardiac death. 

B. History of a preceding or concurrent viral illness is common. 

C. Often presents in association with acute pericarditis 

D. Signs and symptoms 

1. Fever and retrosternal or precordial chest pain (frequent complaints) 

2. Fatigue, palpitations, dizziness, and/or syncope 

62


3. Signs and symptoms of CHF (dyspnea, rales, peripheral edema, jugular venous distention) 

4. Sinus tachycardia disproportionate to the degree of fever(> 101 °F [38.5°C]) present and probably secondary to 

associated heart failure 

5. Cardiac dysrhythmias or conduction disturbances 

6. Abnormal heart sounds 

a. Pericardia! friction rub (when associated pericarditis is present) 

b. Soft S 1 

c. S 3 

or S 4 

gallop 

d. Murmurs of mitral or tricuspid regurgitation 

E. Suspect giant-cell myocarditis in patients with ventricular tachycardia, heart block, and progressively 

worsening clinical course despite therapy; high risk of death and often require cardiac transplant 

Ill. DIAGNOSTIC EVALUATION 

A. ECG 

1. Nonspecific ST-T wave changes (may be localized or diffuse) 

2. Dysrhythmias ranging from sinus tachycardia (most common) to atrial or ventricular dysrhythmias 

3. Conduction disturbances (AV block, bundle-branch block) 

4. Low QRS voltage 

5. Pseudoinfarction patterns, nonspecific ST-T wave changes 

B. Chest radiograph 

1. Generally normal 

2. Cardiomegaly, pulmonary venous hypertension, and/or pulmonary edema may be present. 

C. Echocardiography 

1. Demonstrates dilated chambers with either diffuse hypokinesis or focal wall motion abnormalities 

2. Most useful to exclude other causes of heart failure 

D. Laboratory studies 

1. CBC reveals mild to moderate leukocytosis. 

2. Erythrocyte sedimentation rate is increased. 

3. Cardiac enzymes 

a. Characteristically rise and fall slowly over a period of days (unlike the rapid rise seen in acute Ml) 

b. Troponin I levels are more sensitive and specific than creatine kinase-MB levels. 

E. Endomyocardial biopsy 

1. Can provide definitive diagnosis but suffers from poor sensitivity and specificity 

2. Most indicated for evaluation of suspected giant-cell myocarditis or in cases of fulminant myocarditis 

IV. MANAGEMENT 

A. Primarily supportive 

1. Admit to ICU. 

2. Bed rest; avoid strenuous activity. 

B. Pharmacotherapy 

1. Administer antibiotics if an underlying bacterial cause is present. 

2. lmmunosuppressive agents (steroids, cyclosporin) and NSAIDs are contraindicated in early myocarditis. 

3. High-dose IV gamma globulin beneficial in preliminary studies in children with Kawasaki syndrome. 

4. Antiviral agents (eg, interferon) are currently under investigation. 

5. Manage CHF with the usual drug protocols; however: 

a. Digoxin should be used with caution, because the inflamed myocardium is very sensitive to it. 

b. ACE inhibitors (eg, captopril) are particularly beneficial in that they decrease cellular necrosis and 

inflammation. 

63


6. Manage dysrhythmias with the standard antidysrhythmic agents and electrical therapies. 

a. Amiodarone recommended for ventricular dysrhythmias. 

b. Patients may require automatic implantable cardioverter defibrillator for persistent ventricular dysrhythmias. 

c. Temporary or permanent implanted pacemaker may be needed for persistent heart block. 

64


VALVULAR HEART DISEASE 

I. MITRALVALVE PROLAPSE ("CLICK MURMUR SYNDROME") 

A. Epidemiology and etiology 

1. Most common valvular heart disease; present in 5 %-10% of the population, with young women most 

frequently affected (female-to-male ratio of 2:1 ). 

2. It can occur as an autosomal dominant congenital disorder or as part of a connective tissue disorder (Ehlers 

Danlos syndrome, Marfan syndrome) in association with skeletal abnormalities (such as severe scoliosis, 

"straight" back, pectus excavatum), or it may occur sporadically. 

B. Clinical presentations 

1. Typical patients 

a. Young woman with palpitations 

b. Young female athlete passed out during a training or practice session. She is anxious and complains 

of chest pain and palpitations. A tachydysrhythmia and orthostatic hypotension are found on physical 

examination. 

c. Older man with a syncopal episode at home 

2. Physical examination findings 

a. The murmur is a high-pitched, late systolic regurgitant murmur heard best at the apex using the 

diaphragm of the stethoscope. One or more mid- or late-systolic clicks may also be heard. 

b. Maneuvers or therapies that decrease left ventricular volume (Valsalva maneuver, sudden standing, 

inhalation of amyl nitrate, isoproterenol infusion) - earlier and greater prolapse - movement of the 

click closer to S 1 

and an increase in the duration of the murmur 

c. Maneuvers or therapies that increase left ventricular volume (passive leg raising, maximal isometric 

handgrip, squatting, phenylephrine infusion) - delay of prolapse until late in systole - movement of the 

click and murmur away from S 1 

and a decrease in the duration of the murmur 

C. Diagnostic evaluation 

1. ECG: although most often normal, findings may include flattened or inverted T waves in the inferior leads 

(II, Ill, and a VF) and prolongation of the QT interval. 

2. Chest radiograph: unless significant mitral regurgitation is present, the lungs and cardiac silhouette are 

usually normal. 

3. Echocardiography: confirms the diagnosis; two-dimensional echocardiography is more sensitive than M-mode. 

D. Complications: although most patients are asymptomatic and without complications, patients may 

present with any of the following: 

1. Atypical (nonexertional, sharp) chest pain: thought to be due to localized ischemia from tension on the 

papillary muscles or to coronary artery spasm 

2. Palpitations, light-headedness, or syncope: due to dysrhythmias (premature atrial contractions, premature 

ventricular contractions, paroxysmal supraventricular tachycardia, ventricular tachycardia) 

3. Sudden death (rare): due to ventricular tachycardia or ventricular fibrillation 

4. Transient ischemic attacks or strokes: believed to result from embolization of leaflet thrombi 

5. CHF: due to severe mitral valve regurgitation associated with mitral valve prolapse 

E. Treatment: reserved for symptomatic patients 

1. !3-blockers for patients with chest pain and dysrhythmias 

2. Antiplatelet (eg, ASA) or anticoagulant therapy for patients with a history of systemic embolization (transient 

ischemic attack or stroke) 

II. MITRAL STENOSIS 

A. Etiology 

1. Rheumatic heart disease is responsible for 2:90% of cases of isolated mitral stenosis. 

2. Congenital malformations 

65


3. Calcification of the mitral annulus and leaflets 

4. Left atrial myxoma 

B. Clinical presentation 

1. History 

a. Exertional dyspnea (most common symptom) 

b. Hemoptysis (second most common symptom) 

c. Orthopnea and paroxysmal nocturnal dyspnea 

d. Palpitations (premature atrial contractions, paroxysmal atrial fibrillation) 

e. Fatigue 

f. Systemic emboli 


a. Mitral fades (malar rash) 

b. Palpable diastolic thrill at the apex 

c. loud S 1 

with early diastolic opening snap followed by a low-pitched, rumbling diastolic murmur heard 

best at the apex 


1. ECG 

a. left atrial enlargement (P mitrale) 

b. Atrial fibrillation 

c. Right ventricular hypertrophy (if marked pulmonary hypertension is present) 

2. Chest radiograph 

a. Straightening of the left heart border due to left atrial enlargement 

b. Calcification of the mitral annulus and leaflets 

c. Findings of pulmonary congestion 

d. Right ventricular lift (or hypertrophy) if pulmonary hypertension is present 

D. Complications 

1. Atrial fibrillation (most common) 

2. Embolic events, especially with atrial fibrillation 

3. Frequent respiratory infections 

4. Infective endocarditis (rare) 

5. Massive pulmonary hemorrhage from rupture of pulmonary bronchial venous connections 

E. Management 

1. Rate control with IV diltiazem or digoxin for atrial fibrillation with rapid ventricular response 

2. Blood transfusion and, possibly, surgery for massive hemoptysis 

3. Diuretics for pulmonary congestion 

4. Anticoagulation for patients with systemic embolization and atrial fibrillation 

Ill. MITRAL REGURGITATION 

A. Can be acute or chronic; these two disease entities differ significantly in terms of their causation, 

disease course, presentation, and management. 

B. Acute mitral regurgitation is the result of rupture of chordae tendineae, papillary muscle, or valve 

leaflet and is abrupt in onset. 

1. Etiology 

a. Acute Ml 

b. Infectious endocarditis 

c. Trauma 


a. Symptoms are those of fulminant CHF/pulmonary edema (eg, dyspnea) and those of the disease process 

that precipitated the event (eg, chest pain in the acute Ml patient) 

66


b. Physical examination findings 

(1) Tachycardia, tachypnea, and rales 

(2) Hypotension 

(3) Jugular venous distention with a prominent cannon "a" wave 

(4) Palpable thrill at apex 

(5) Soft s 1 

(6) Loud apical systolic murmur (radiating to the axilla) that can be holosystolic, late systolic, or 

crescendo-decrescendo 

(7) S 3 

and S 4 

(a common finding) 


a. ECG 

(1) Absence of left atrial enlargement and left ventricular hypertrophy 



(1) Normal cardiac silhouette 

(2) Severe pulmonary edema 

4. Management 

a. Airway and hemodynamic support (may include intra-aortic balloon pump to augment cardiac output) 

b. Supplemental oxygen 

c. Afterload reduction 

d. Emergent consult with a cardiothoracic surgeon 

e. Treatment of underlying cause (eg, antibiotics for infectious endocarditis) 

C. Chronic mitral regurgitation evolves slowly and frequently coexists with mitral stenosis. 

1. Etiology 

a. Rheumatic heart disease is most common cause. 

b. Mitral valve prolapse 

c. Connective tissue disorders (eg, Marfan syndrome) 


a. History 

(1) Exertional fatigue or dyspnea 

(2) Orthopnea and paroxysmal nocturnal dyspnea 

(3) Systemic emboli 


(1) Left parasternal heave and thrill 

(2) High-pitched holosystolic murmur that radiates to the axilla 

(3) Soft S 1 

that is often obscured by the murmur 

(4) Wide-split S 2 

(5) S 3 

and S 4 

are common with severe regurgitation. 


a. ECG 

(1) Left atrial enlargement 

(2) Left ventricular hypertrophy with strain 

(3) Atrial fibrillation (75% of patients) 


(1) Left atrial enlargement 

(2) Left ventricular enlargement 

(3) Pulmonary congestion 

4. Management 

a. Rate control of atrial fibrillation with diltiazem or digoxin 

b. Diuretics for symptoms of pulmonary congestion 

c. Anticoagulation if atrial fibrillation is present 

67


IV. AORTIC STENOSIS 

A. Etiology 

1. Congenital bicuspid aortic valve is the most common cause in patients 65 years old. 

3. Rheumatic heart disease with associated mitral valve disease is also common. 


1. Symptoms appear late in the disease process; patients remain relatively asymptomatic until the valve opening 

decreases to


(2) Apprehension 

(3) Other signs of heart failure (eg, paroxysmal nocturnal dyspnea, orthopnea) 

(4) Chest pain 


(1) Tachypnea, tachycardia, and inspiratory rales 

(2) Normal or low systolic and diastolic pressures 

(3) Normal pulse pressure (difference of 30-40 mmHg between systolic and diastolic blood pressures) 

(4) Signs of decreased cardiac output (cool, pale extremities, peripheral cyanosis, hypotension, 

diaphoresis, confusion) 

(5) Short diastolic murmur of aortic regurgitation best heard at the left sternal border with the 

diaphragm of the stethoscope 

(6) Diminished or absent S 1 

(7) Loud S 3 

(8) Midsystolic flow murmur 


a. ECG 


(2) Nonspecific ST-T wave changes 

(3) Left ventricular strain 


(1) Normal cardiac silhouette 

(2) Signs of increased pulmonary venous pressure and pulmonary edema 

4. Management 

a. Determine and treat the underlying cause (eg, administer IV antibiotics to patients with bacterial 

endocarditis). 

b. Treat CHF with supplemental oxygen, diuretics, digitalis, and vasodilators (eg, nitroglycerin, 

nitroprusside). 

c. Obtain immediate cardiothoracic surgery consult for emergent valve replacement. 

C. Chronic aortic regurgitation 

1. Etiology 

a. Rheumatic heart disease 

b. Congenital (bicuspid) valve 

c. Prior infective endocarditis 

d. Diseases that dilate the aortic wall (eg, Marfan syndrome, ankylosing spondylitis) 


a. History 

(1) Exertional fatigue and dyspnea 

(2) Orthopnea, paroxysmal nocturnal dyspnea 

(3) Palpitations 

(4) Angina 

(5) Pulmonary edema 


(1) Wide pulse pressure 

(2) Displaced, hyperdynamic point of maximal impulse 

(3) Soft S 1 

(4) High-pitched, decrescendo diastolic blowing murmur best heard along the left sternal border (sine 

qua non of aortic regurgitation) 

(5) Rapid and forceful carotid upstroke with dramatic collapse (Corrigan or water-hammer pulse) 

(6) Head bobbing with each heartbeat (deMusset sign) 

(7) Prominent nail pulsations (Quincke pulse) 

(8) Singsong murmur over the femoral artery (Duroziez murmur) 

(9) A presystolic or mid-diastolic murmur (Austin-Flint murmur) may be present with severe aortic 

regurgitation. 

69



a. ECG 

(1) Left ventricular hypertrophy 

(2) Conduction abnormalities such as left bundle-branch block 


(1) Cardiomegaly 

(2) Aortic root dilatation 

(3) Pulmonary vascular congestion 

4. Management: treat CHF with supplemental oxygen, diuretics, vasodilators, and digitalis. 

VI. TRICUSPID STENOSIS 

A. Etiology 

1. Rheumatic heart disease 

2. Endocarditis secondary to IV drug abuse 


1. History: patients complain of fatigue and symptoms due to increased systemic venous pressure (eg, edema). 

2. Physical examination 

a. Diastolic murmur best heard along the left sternal border and accentuated with inspiration 

b. Peripheral edema 

c. Hepatosplenomegaly 

d. Ascites 

e. Jugular venous distention and giant jugular cannon "a" waves 

3. Tricuspid stenosis rarely exists in isolation. Coexisting mitral and aortic valve disease is common and, when 

present, typically dominates and determines the clinical course. 


1. ECG 

a. Tall, pointed P waves if sinus rhythm is present 

b. Atrial fibrillation 

2. Chest radiograph: enlarged right atrium 

D. Management 

1. Rate control with IV diltiazem for atrial fibrillation with rapid ventricular response 

2. Anticoagulation for chronic atrial fibrillation 

3. Treatment of underlying cause (eg, IV antibiotics for infectious endocarditis) 

VII. TRICUSPID REGURGITATION 

A. Etiology 

1. Right ventricular dilatation secondary to pulmonary hypertension 

2. Rheumatic heart disease 

3. Infective endocarditis 

4. Trauma 


1. History 

a. Fatigue and dyspnea on exertion 

b. Peripheral edema 

c. Throbbing in the neck and abdomen 

d. Anorexia 

70



a. Palpable left ventricular heave 

b. Prominent systolic pulsations of the jugular veins known as "v" waves or "CV" waves 

c. Holosystolic murmur best heard at the xiphoid area adjacent to the left sternal border 


1. ECG 

a. Right atrial enlargement 

b. Right ventricular enlargement 

c. Atrial fibri I lation (80% of patients) 


a. Right atrial enlargement 

b. Right ventricular enlargement 

c. Normal pulmonary vasculature 

D. Management: patients in atrial fibrillation require rate control with IV diltiazem and long-term 

anticoagulation. 

VIII. PROSTHETIC VALVES 

A. Types and characteristics: there are two types of prosthetic valves (mechanical and bioprosthetic), each 

with its own particular characteristics. 

1. Mechanical (nontissue) valves 

a. Manmade materials 

b. Life span >20 years 

c. Typically make a loud metallic closure sound and softer opening click and, when located in the aortic 

position, an associated systolic ejection murmur is normally present. 

d. Require life-long systemic anticoagulation 

e. Cause greater hemolysis and are more thrombogenic than tissue prostheses 

f. Common designs include the tilting disc variety (eg, Bjork-Shiley, Medtronic-Hall), the caged ball variety 

(eg, Starr-Edwards), and the bi leaflet variety (eg, St. Jude). 

2. Bioprosthetic (tissue) valves 

a. Made with human, porcine, or bovine tissue cups 

b. Life span 8-10 years 

c. Make opening and closing sounds that are similar to (but louder than) those of native valves 

d. Except for the initial postoperative period and patients in atrial fibrillation, anticoagulation is optional; ASA 

is sufficient in most patients. 

e. Cause less hemolysis and are less thrombogenic than mechanical valves 

B. Complications and their clinical presentations 

1. Thromboembolic events 

a. Most serious complication of prosthetic valves; occur more frequently with mechanical valves than with 

bioprosthetic ones 

b. Patients with valve dysfunction secondary to thrombus formation typically present with acute onset of 

CHF, hypotension, and muting or loss of the prosthetic valve sounds. Signs and symptoms in patients with 

embolic events depend on the location of the emboli and may include paralysis, aphasia, abdominal pain, 

chest pain, or a cold extremity. 

2. Primary valve failure 

a. Significant cause of morbidity and mortality 

b. May result in regurgitant blood flow, acute valvular occlusion, embolization of a prosthetic fragment, or 

severe hemolysis 

c. The Bjork-Shiley 60° and 70° convexoconcave valves were taken off the market, because they were 

associated with a high incidence of strut fracture with resultant embolization of the disc. Patients with this 

complication present with sudden onset of CHF, hypotension, loss of the metallic valve sound, and a new 

regurgitant murmur. Although these valves are no longer manufactured, many patients still have them. 

71


3. Paravalvular leak 

a. A portion of the prosthetic valve becomes unseated from the valve annulus. 

b. If immediately after surgery, it is usually due to suture disruption, whereas delayed leaks are generally due 

to endocarditis. 

c. More common with mechanical valves 

d. Patients typically present with sudden onset of pulmonary edema or severe hemolytic anemia. Physical 

examination reveals a regurgitant murmur. 

4. Endocarditis 

a. The causative organism varies with the length of time the valve has been present;


IX. CONDITIONS NECESSITATING ANTIBIOTIC PROPHYLAXIS 

FOR INFECTIVE ENDOCARDITIS 

A. Patients at high risk of infection 

1. Prosthetic cardiac valves or prosthetic material used for cardiac valve replacement 

2. A history of infective bacterial endocarditis 

3. Congenital heart disease (CHD), unrepaired cyanotic CHD, underlying palliative shunts and conduits 

4. Completely repaired CHD with prosthetic material or device, whether placed by a surgery or by catheter 

intervention, during the first 3 postoperative months 

5. Repaired CHD with residual defects at the site or adjacent to the site of a prosthetic patch or prosthetic device 

6. Valve regurgitation caused by a shunt abnormal valve in a cardiac transplant patient 

B. Emergency department procedures that merit prophylaxis 

1. Antibiotic prophylaxis is recommended for emergency department patients at high risk (as above) undergoing 

dental procedures that manipulate the gingiva or periapical region of the tooth or that perforate the oral 

mucosa. 

2. Antibiotic prophylaxis is not recommended for the vast majority of emergency department procedures such as 

laceration repair, intubation, line placement, or Foley catheterization. 

3. No specific recommendations are made for or against prophylaxis for emergency department procedures 

that involve infected skin (eg, cutaneous abscess drainage) or musculoskeletal tissue, but it is reasonable to 

administer antibiotics to only high-risk patients. 

73


ENDOCARDITIS 

I. DEFINITION 

A. A localized infection of the endocardium, the hallmark of which is vegetation 

B. Can involve the valve leaflets, the walls of the heart cavities, or the tissue surrounding prosthetic heart valves 

II. PATHOPHYSIOLOGY 

A. Injury to the endothelium results in formation of a platelet-fibrin complex that is subsequently colonized by 

microorganisms during periods of transient bacteremia. 

B. Although endocarditis does occur in patients with normal valves, patients with congenital/acquired valvular 

disease and prosthetic valves are most commonly affected. 


1 . Prosthetic valve(s) 

2. Congenital valvular heart disease (eg, mitral valve prolapse) 

3. Acquired valvular heart disease (eg, rheumatic heart disease) 

4. IV drug abuse 

5. Calcific valve degeneration 

6. Indwelling venous catheters, vascular shunts 

7. Hemodialysis 

8. Peritoneal dialysis 

9. Cardiac surgery 

10. HIV infection 

11. History of endocarditis 

12. Extensive burn injury 

D. Causative organisms 

1. Although endocarditis is most commonly caused by bacteria, it may also be caused by fungi, rickettsiae, and 

viruses. 

2. The causative organism varies with the type of valve involved (native versus prosthetic) and in the presence of 

IV drug abuse or immunocompromise. 

3. Common bacterial pathogens 

a. Native valves 

(1) Non-viridans streptococci (most common) 

(2) Staphylococcus aureus 

(3) Streptococcus viridans 

(4) Enterococci 

b. Prosthetic valves 

(1) Coagulase-negative Staphylococcus (early, 60 days after surgery) 

(3) S viridans 

(4) Enterococci 

c. IV drug abusers, immunocompromised patients 

(1) S aureus 

(2) Streptococci 

(3) Gram-negative bacilli 

74


E. Left- versus right-sided disease 

1. Left-sided endocarditis....,. systemic vascular involvement 

a. Most common in patients with acquired valvular disease and congenital heart disease (and is more 

common than right-sided disease) 

b. Depending on the virulence of the infecting organism, it can present as an acute or subacute illness. 

c. The mitral valve is most commonly affected. 

d. 5 viridans and 5 aureus are the most frequent pathogens. 

2. Right-sided endocarditis....,. pulmonary vascular involvement 

a. Primarily a disease of IV drug abusers 

b. Usually has an acute presentation 

c. Most commonly involves tricuspid valve 

d. Caused by 5 aureus in -75% of cases 

Ill. CLINICAL PRESENTATION 

A. History 

1. Protean and nonspecific; may include intermittent fever, chills, sweating, malaise, fatigue, weight loss, chest 

pain, cough, and neurologic complaints/focal deficits 

2. Most common presentation in children is malaise and weight loss. 

B. Physical findings 

1. Fever (most common finding) 

2. Heart murmur 

3. CHF 

4. Signs of metastatic infection (eg, meningitis, pneumonia) 

5. Ophthalmologic signs 

a. Conjunctiva! hemorrhages 

b. Roth spots (retinal hemorrhages with central clearing) 

6. Cutaneous signs 

a. Splinter hemorrhages 

b. Osler nodes (tender erythematous nodules found on the volar surface of the fingertips) 

c. Janeway lesions (nontender erythematous macular lesions appearing on the fingers, palms, and soles) 

d. Petechiae 

7. Neurologic findings 

a. Focal motor deficits 

b. Altered level of consciousness 

IV. DIAGNOSTIC EVALUATION 

A. Laboratory studies 

1. CBC reveals leukocytosis with a left shift and a mild normocytic anemia. 

2. Erythrocyte sedimentation rate, C-reactive protein, and serum rheumatoid factor are increased. 

3. Urinalysis reveals microscopic hematuria in >50% of patients. 

B. Chest radiograph 

1. Often unremarkable 

2. May reveal septic emboli in patients with right-sided endocarditis 

C. ECG 

1. Usually normal 

2. May demonstrate conductive deficits in the presence of extensive myocardial damage 

75


D. Blood cultures 

1. The most useful test for making the diagnosis; positive in >90% of patients with bacterial endocarditis. 

2. Three blood cultures from three different sites should be obtained, and each should be evaluated for aerobic, 

anaerobic, and fungal pathogens. 

E. Echocardiography 

1. Useful if positive for vegetations, but a negative examination does not exclude the diagnosis. 

2. Transesophageal echocardiography 

a. More sensitive in revealing vegetations than transthoracic echocardiography, especially in patients with 

prosthetic valves. 

b. Recommended as the initial study for low-risk patients 

c. Recommended as the initial study for high-risk patients and as the follow-up study for low-risk patients with 

a negative or technically inadequate transthoracic echocardiography 

V. DIAGNOSIS 

A. A presumptive diagnosis of endocarditis should be made in the patient presenting with risk factors and 

clinical findings (eg, a patient with a prosthetic valve or a recent history of IV drug use and fever). 

B. Positive blood cultures and evidence of valvular injury or vegetations usually confirm the diagnosis; if any 

doubt, a tissue biopsy is the gold standard. 

VI. MANAGEMENT 

A. Antibiotic therapy 

1. Ideally, empiric antibiotic therapy should be started after appropriate blood cultures have been obtained. 

However, in hemodynamically unstable patients, antibiotic therapy should be started immediately and not 

delayed while waiting for culture results. 

2. The initial antibiotic regimen selected should reflect the susceptibilities of the suspected organism, the 

acuteness of the presentation, and local resistance patterns. 

3. Acceptable empiric antibiotic regimens 

a. In patients with native valves and a subacute presentation: 

(1) Penicillin G (or ampicillin) IV plus nafcillin (or oxacillin) IV plus gentamicin IM or IV or 

(2) Vancomycin IV plus gentamicin IM or IV in penicillin-allergic patients 

b. In patients with a prosthetic valve: 

(1) Vancomycin IV plus gentamicin IV plus rifampin orally 

(2) Early consult with a cardiothoracic surgeon should be obtained in all patients with a prosthetic valve. 

c. Vancomycin-resistant enterococcal infections occur, especially in IV drug abusers, patients with prosthetic 

valves, and those recently hospitalized or taking antimicrobial agents. Current suggested therapy for these 

patients: quinupristin/dalfopristin combination plus doxycyline and rifampin. 

B. Although ambulatory treatment is possible in certain select cardiovascularly stable patients, patients with 

endocarditis should generally be admitted to the hospital for treatment, particularly those with prosthetic 

valves or a history of IV drug abuse. 

76


THORACIC AORTIC DISSECTIONS AND 

ABDOMINAL AORTIC ANEURYSMS 

I. THORACIC AORTIC DISSECTIONS 

A. Epidemiology 

1. Thoracic aortic dissections are 2-3 times more common than abdominal aortic aneurysm (AAA) ruptures. 

2. Men are affected more commonly than women (ratio 3:1). 

3. Most patients are 50-70 years old. 

4. Risk factors (> 1 increases overall risk) 

a. A history of systemic hypertension: this is the most common predisposing factor, and it is present in 

70%-90% of patients. 

b. Connective tissue disorders 

(1) Ehlers-Danlos syndrome 

(2) Marfan syndrome (patients may present when


2. DeBakey classification 

a. Type I: ascending aorta and part of distal aorta (most common type) 

b. Type II: ascending aorta only 

c. Type Ill: descending aorta only 

(1) Subtype IIIA (extension limited to above the diaphragm) 

(2) Subtype 111B (continuation below the diaphragm) 

3. Stanford classification 

a. Type A: ascending aorta (DeBakey type I and type II) 

b. Type B: limited to the descending aorta (DeBakey type Ill) 

E. Clinical presentation 

1. Pain is the most common presenting symptom. 

a. The pain is excruciating, starts abruptly, is maximal from its onset and migrates as the dissection 

propagates. It generally (but not always) has a tearing or ripping quality and is most commonly located in 

the chest, upper back, or abdomen. 

b. The location of pain provides a clue to the location of the dissection. 

(1) Ascending (proximal) dissections typically present with anterior chest pain (± radiation into the neck, 

jaw, or arms). 

(2) Arch dissections cause pain in the neck and jaw. 

(3) lnterscapular back pain (± radiation into the abdomen or lumbar area) is typical of descending (distal) 

dissections. 

2. Based on the location of the dissection, patients may also present with: 

a. Acute stroke, visual changes 

b. Acute paraplegia, spinal cord deficits 

c. A cool, pulseless extremity 

d. CHF and pulmonary edema 

e. Abdominal pain (mesenteric ischemia), nausea and vomiting 

f. Flank pain, hematuria, or oliguria (impaired renal blood flow) 

g. Syncope 

h. Acute Ml (if dissection involves a coronary artery or ostia) 

i. Aortic regurgitation 

3. A significant number of patients present with only ischemic or neurologic complications of a "silent" (painless) 

aortic dissection (most frequently encountered in Type A dissection that has extended to involve the descending 

aorta [similar to a Debakey Type I dissection]). This is important, because inadvertent administration of a 

thrombolytic agent to a patient who seems to be having a "stroke" or an "Ml" would be disastrous. 

78


4. Blood pressure findings 

a. Normal or decreased - ascending aorta 

b. Increased - descending aorta 

c. A difference in extremity blood pressure of 20 mm Hg 

5. Shock-like appearance (cool, clammy skin) despite increased blood pressure 

6. Focal neurologic deficits 

7. Unequal or absent pulses (hallmark of aortic dissection) between extremities 

8. Diastolic murmur of aortic insufficiency (with Types I, II, and A) 

9. Signs of cardiac tamponade (with Types I, II, and A) 

F. Diagnostic evaluation 

1. Initial studies 

a. Chest radiograph 

(1) Should be taken immediately 

(2) Patient should be in upright position. 

(3) Usually abnormal but findings are nonspecific; a normal chest radiograph does not exclude the 

diagnosis. 

(4) Suggestive findings 

b. ECG 

(a) Mediastinal widening >8 cm (most common finding) 

(b) A change in the configuration or size of the thoracic aorta when compared with older 

radiographs; loss of space between the aorta and pulmonary artery 

(c) "Eggshell" or "calcium" sign - extension of the aortic shadow by >5 mm beyond its calcified 

aortic wall (when present, is pathognomonic for dissection) 

(d) A blurred aortic knob or one with a localized hump 

(e) 

(f) 

A "double density" appearance of the aorta, which suggests the presence of true and false 

channels; the false lumen is less radiopaque than the true lumen. 

On the right side of the radiograph 

i. Deviation of the trachea/nasogastric tube 

ii. Shift and elevation of the right mainstem bronchus 

iii. Deviation of the right paraspinous line 

(g) On the left side of the film 

i. A pleura-apical cap 

ii. Depressed left mainstem bronchus 

iii. Pleural effusion 

(1) Abnormal in most patients with aortic dissection 

(2) Changes consistent with acute ischemia have been reported in up to 40% of cases (the most common 

misdiagnosis in these patients). STEM\ ECG patterns may occur in up to 8% of cases and usually 

involve the inferior leads, because they involve the right coronary artery. A dissection-induced Ml 

should be excluded (with transesophageal echocardiography or CT) in patients who are candidates 

for thrombolytic therapy and have clinical findings that suggest the possibility of thoracic aortic 

dissections. 

(3) Varying degrees of AV block can be produced by propagation of the dissection into the ventricular 

septum. 

(4) Left ventricular hypertrophy (due to long-standing hypertension) is a frequent finding. 

2. Definitive studies: one (or more) of the following tests may be used to confirm the diagnosis. Each has certain 

advantages and disadvantages (and their 24-hour availability is variable). The diagnostic approach chosen will 

vary from institution to institution and patient to patient depending on the technology available, the speed 

of obtaining each diagnostic test, the experience of the radiologist in interpreting each test, the preference of 

the surgeon, the probability of the diagnosis, and comorbid disease of the patient. When the probability of 

dissection is high, the most readily available study should be the initial study of choice. 

a. Transesophageal echocardiography (with color-coded Doppler imaging) 

(1) Most expedient technique for confirming the diagnosis of aortic dissection; the diagnostic study of 

choice in many hospitals 

(2) Sensitivity and specificity nearly 100% 

79


(3) All the information required for decision-making regarding emergency surgical intervention can be 

obtained with this study; in addition to identifying the dissection, it detects the intimal tear site, flow in 

the proximal coronary arteries, aortic regurgitation, and pericardia/ effusion; it also differentiates true 

from false lumens. 

(4) Advantages: only minimally invasive, requires only 10-15 minutes to complete, does not necessitate 

exposure to IV contrast, and can be performed at the bedside in the emergency department while the 

patient is being treated and appropriately monitored. 

(5) Disadvantages: contraindicated in patients with esophageal disease (eg, strictures, varices), and the 

necessary equipment/expertise are not readily available in all hospitals. 

b. Aortography 

c. MRI 

(1) The traditional diagnostic gold standard but now largely replaced by CT aortography 

(2) Sensitivity and specificity ~90% 

(3) In addition to confirming the diagnosis, it defines the intimal tear site, the extent of the dissection, and 

assesses the aortic valves and branches. 

(4) Disadvantages: invasive, time-consuming, requires special personnel, cannot be performed in the 

emergency department, necessitates exposure to IV contrast, is not 100% accurate (can miss dissection 

if the false lumen is thrombosed) 

(5) Best reserved for situations in which transesophageal echocardiography is not available or is 

nondiagnostic 

(1) Sensitivity and specificity 1 00% 

(2) Delineates the desired anatomy: type and extent of dissection, site of the intimal tear, presence of aortic 

insufficiency, and differential flow velocities in the true and false channels and in aortic branch vessels 

(3) Advantages: noninvasive, does not require IV contrast material or ionizing radiation 

(4) Disadvantages: time-consuming (requires >60 minutes to perform), cannot be performed in the 

emergency department or on patients with metallic implants, allows only limited access to the patient 

during the examination, some patients cannot tolerate the scanner, most units cannot accommodate 

monitoring or advanced life support equipment 

d. CT aortography 

G. Management 

(1) CT aortography has almost 100% specificity and sensitivity and is now accepted as a diagnostic gold 

standard. 

(2) Can confirm the diagnosis, define the extent of the dissection, and distinguish between Type A and 

Type B dissections but cannot identify aortic insufficiency or extension to the aortic branches 

(3) Advantages: less invasive and provides greater contrast resolution than aortography, may reveal other 

abnormalities in cases in which dissection is excluded 

(4) Disadvantages: time-consuming, cannot be performed in the emergency department, exposes the 

patient to IV contrast, and may miss a dissection flap (if it is moving rapidly) 

(5) good choice for emergency departments without access to transesophageal echocardiography because 

of its high sensitivity 

1. All patients require 10-15 units of blood on stand-by and immediate consult with a thoracic surgeon. 

2. Initial management for all types of dissections is medical and involves controlling the forces that propagate 

the dissection: pulse rate, systolic blood pressure, and rate of elevation of the aortic pulse pressure (dP/dT). If 

suspicion of dissection is high, begin treatment immediately; do not delay to await confirmatory study results. 

a. IV ~-blockers (eg, propranolol, metoprolol, atenolol, or esmolol) are administered first and titrated to a 

heart rate of 60-80 beats per minute. 

b. Nitroprusside is then started and titrated to a systolic blood pressure of 100-110 mmHg. 

3. Hypotensive patients should be managed with small boluses of a crystalloid solution or blood. 

4. Pain should be treated with IV narcotics. 

5. Long-term management 

a. Dissections involving the ascending aorta (Types A, I, and II) are treated surgically. 

b. Dissections involving only the descending aorta (Types B and Ill) are treated medically unless 

complications are present. 

80


II. ABDOMINAL AORTIC ANEURYSMS (AAA) 

A. Definition and anatomic location 

1. Aortic aneurysms are true aneurysms (they involve al I three layers of the arterial wal I). 

2. The vast majority (97%) are infrarenal in location. 

B. Pathogenesis 

1. Although AAAs often occur in patients with atherosclerotic disease, atherosclerosis is no longer believed to be 

the primary etiologic factor in the development of these aneurysms. 

2. They are currently theorized to be due to a combination of genetic, structural, and metabolic factors including: 

a. Genetic predisposition 

b. Increased levels of elastase and collagenase 

c. Failure or loss of blood vessel elastin 

d. Copper deficiency 

e. Infection (mycotic aneurysms) 

f. Inflammatory disorders 

g. Local mechanical forces 


1. Advanced age (75% of AAAs are in patients >60 years old) 

2. Male sex (particularly white males) 

3. Family history of an AAA in a first-degree (blood) relative 

4. Smoking history 

5. Hypertensive history 

6. History of coronary artery disease or peripheral vascular disease 

7. Increased serum cholesterol levels 

D. Clinical presentation 

1. Frequently a middle-aged or older man (and a heavy smoker) who had a syncopal episode at home with 

transient improvement 

2. Sudden onset of severe abdominal, back, or flank pain with or without an associated syncopal episode (due 

to sudden hemorrhage) is the classic presentation: retroperitoneal bleeding with hematoma formation (usually 

on the left) occurs in most patients and accounts for the variety of clinical presentations that are possible and 

confusing. 

a. Flank pain (usually on the left side) may radiate to the groin and be accompanied by microscopic 

hematuria, thus simulating a kidney stone (the most common misdiagnosis). 

b. Low back pain may be dull and radiate into the legs, thus mimicking musculoskeletal back pain. 

c. Abdominal pain that is localized to the left lower quadrant and accompanied by guaiac-positive feces are 

common in patients with diverticulitis, but it is also seen in a ruptured AAA (and may be associated with a 

nonpulsatile mass). 

d. A scrotal hematoma can be interpreted as a "mass" in the scrotum and thus simulate an incarcerated hernia. 

e. Ecchymoses can result from significant bleeding and may be seen on the abdominal wall, flank, scrotum, 

penis, inguinal region, perineum, or perianal area. 

f. Femoral neuropathy (pain in the hip and thigh, quadricep muscle weakness, diminished sensation over 

the anteromedial thigh and a weakened patellar reflex) may be from femoral nerve compression due to a 

hematoma. 

3. Physical examination findings are variable. 

a. A pulsatile (and occasionally tender) mass is palpable in the epigastric area in 77% of patients with a 

ruptured AAA; unruptured aneurysms are smaller in size and less frequently detected; in the presence of 

obesity or abdominal distention, a pulsatile mass may not be felt. 

b. A tender (pulsatile) mass is highly suggestive of a rapidly expanding or recently ruptured AAA; most intact 

aneurysms are not tender. 

c. Bruits may be heard over the abdominal aorta or femoral arteries. 

d. Signs of distal extremity ischemia (not always present): unequal or unsynchronized distal pulses and cool, 

pale skin. 

81


E. Diagnosis and management 

1. Presence of a symptomatic AAA is usually suggested by the clinical presentation and physical examination. 

This information alone is sufficient evidence in many patients to take them immediately to the operating 

room (particularly the hemodynamically unstable ones). 

2. Once this diagnosis is suspected, the following measures should be undertaken immediately: 

a. Two large-bore IV lines (normal saline or lactated Ringer's), cardiac monitor, pulse oximeter, 

supplemental oxygen 

b. Draw blood for preoperative laboratory studies, and type and cross for at least 10 units of blood. 

c. Order an ECG. 

d. Obtain immediate surgical consult (preferably with a vascular surgeon). 

3. Further evaluation is determined by the hemodynamic stability of the patient. 

a. Hemodynamically unstable patients with a suspected AAA require prompt surgical repair. Fluid and blood 

resuscitation should be initiated in the emergency department, and the patient should be transferred 

to the operating room for definitive treatment as soon as the surgeon is available. Any delay for further 

diagnostic testing increases the risk of death from exsanguination. 

b. Hemodynamically stable patients in whom this diagnosis is suspected may undergo further diagnostic 

testing (under close medical supervision) before surgical intervention. The various imaging modalities 

available are described below. Of these, ultrasonography or CT is the most appropriate studies in this 

setting. 

(1) Plain abdominal radiographs (AP and lateral films): although most patients with an AAA (75%) have 

suspicious findings on plain radiographic evaluation (aneurysmal calcification, soft-tissue mass, loss 

of renal shadow, renal displacement, and/or change in the posterior peritoneal flank stripe) except 

for aneurysmal calcification, none of these findings is specific for AAA and their absence does not 

reliably exclude the presence of an AAA. Furthermore, plain radiographs are not very accurate in 

determining the extent of the aneurysm, rupture, or associated vascular pathology. 

(2) Ultrasonography has a sensitivity of nearly 100% in detecting an AAA and has the advantage of 

being quick, readily available, noninvasive, and portable. It cannot, however, accurately detect 

aneurysmal leaking and complications such as visceral or renal artery involvement. Moreover, the 

study may be limited in the presence of obesity or intestinal gas. Thus, ultrasound is most useful in 

determining whether or not an aneurysm is present, which may be more than enough information in 

the appropriate setting. 

(3) CT with contrast also has a sensitivity of ~ 100% in detecting an AAA but is more accurate than 

ultrasound in detecting aneurysmal rupture and visceral artery involvement; it is not limited by 

obesity or intestinal gas. Visualization of the retroperitoneal structures and diagnosis of other 

pathology are also superior with this modality. Disadvantages include exposure to IV contrast 

material and longer study time. 

(4) MRI: excellent at imaging the aorta and is superior to CT in assessing branch vessel involvement. 

However, it is of limited use in this setting because it is time consuming, has limited availability, 

cannot be performed in the emergency department or in the patient with metallic implants, and 

allows only limited access to the patient during the study. This modality is usually reserved for 

evaluation of asymptomatic patients. 

(5) Angiography: although useful in determining the anatomy of the aorta and demonstrating occlusive 

lesions, angiography is not entirely reliable in detecting the presence (high false negative rate) or 

diameter of an AAA. Furthermore, it is time consuming, invasive, requires specialized personnel, and 

necessitates exposure to IV contrast. For these reasons, angiography is the least desirable study for 

emergent diagnostic evaluation of these patients. 

82


DEEP VENOUS THROMBOSIS (DVT) 

I. PATHOGENESIS 

DVTs have their origin from Virchow's triad of venostasis, hypercoagulability, and vessel wall injury/abnormality. 

II. CLINICAL PRESENTATION 

A. Acute DVT 

1. The physical manifestations of DVT are determined by the degree of thrombosis present (partial versus totally 

occluding), its location, and the extent of collaterals at the level of the occlusion. Physical findings may be 

minimal or absent and cannot be relied on by themselves to make or exclude the diagnosis. 

2. Common signs and symptoms 

a. Unilateral pain, swelling, edema (most reliable sign), and tenderness 

b. Presence of a palpable cord (most often detected in the popliteal fossa), superficial venous dilatation, 

discoloration, and Homans sign (the least reliable finding) 

3. Unilateral swelling is the most specific physical finding (especially if the measured difference is >3 cm). 

4. Tenderness, erythema, or induration in the groin and popliteal fossa (where the femoral and popliteal veins are 

quite superficially located) are also highly suggestive of acute thrombosis of the underlying vessel. 

B. Massive DVT: an ischemic form of venous occlusion due to massive iliofemoral thrombosis that also involves 

most of the venous collateral system 

1. Phlegmasia cerulea dolens (painful blue inflammation) 

a. Occurs in 40 years old 

4. MI/CHF/stroke 

5. Obesity 

6. Estrogen therapy 

7. Polycythemia vera 

8. Pregnancy or postpartum state 

9. Immobility or prolonged bed rest 

83


10. Recent trauma (including burns) or surgery 

11. Inherited abnormalities of coagulation (deficiency of antithrombin Ill, protein C, or protein S) or fibrinolysis 

12. Catheter placement (central venous, Swan-Ganz) and IV drug abuse 

13. Thrombocytosis 

14. Immune (eg, AIDS) and autoimmune (eg, systemic lupus erythematosus) 

IV. PREDICTING PRETEST PROBABILITY FOR DVT: 

THE WELL'S CLINICAL CRITERIA 

Table 5: Wei l's Clinical Prediction Rule for DVT 

Active cancer (palliative, within 6 months or ongoing treatment) 

Paralysis, paresis, or recent immobilization 

Recently bedridden (>3 days) or major surgery (within 4 weeks) 

Localized tenderness along deep venous system 

Entire leg swollen 

Calf swelling >3 cm when compared with opposite leg (10 cm below tibial tuberosity) 

Pitting edema (greater in suspected leg) 

Collateral superficial veins (nonvaricose) 

Alternative diagnosis as likely as (or greater than) DVT 

-2 

Total score interpretation 

c:".3 = high pretest probability (>65% risk) 

1-2 = moderate pretest probabi I ity (1 7% risk) 

:SO= low pretest probability (


2. Contrast venography 

3. MRI 

a. Formally the accepted standard against which all other diagnostic tests are measured 

(1) Largely been replaced by duplex ultrasonography 

(2) Now used primarily in patients with uncertain ultrasound results 

b. Advantages 

(1) Sensitivity and specificity of nearly 1 00 % 

(2) Outlines the entire venous system 

c. Disadvantages 

(1) Invasive, painful, expensive, limited in availability, and associated with risk of contrast-related 

allergic reactions and postvenography phlebitis/DVT 

(2) One-quarter of patients with suspected DVT have contraindications to venography (renal failure, dye 

allergy, pregnancy) or nondiagnostic studies. 

a. Detects calf, thigh, pelvic, renal, and pulmonary thrombi; can also diagnose other anatomic causes of leg 

pain and swelling 

b. Advantages 

(1) Noninvasive 

(2) No ionizing radiation or IV contrast 

(3) 97% sensitive and 95% specific for DVT 


(1) Expensive, not readily available, and requires significant patient cooperation 

(2) Should not replace ultrasound as the primary screening tool 

d. Most useful during the second and third trimesters of pregnancy when ultrasound is less accurate 

4. o-dimer assay 

a. o-dimer 

B. Diagnosis 

(1) Fibrin degradation product, which is increased in patients with DVT and pulmonary embolism 

(2) Increased in many conditions (poor specificity) such as acute Ml, stroke, trauma, and pregnancy 

b. There are a number of rapid o-dimer assays, including qualitative whole blood agglutination tests 

(SimpliRED) and quantitative turbidimetric or ELISA tests, in which levels >500 mg/Lare abnormal. 

c. Like duplex ultrasonography and impedance plethysmography, it is more sensitive for proximal clots 

(93%) than for distal ones (70%). 

1. DVT should be suspected from the patient's signs, symptoms, and history of risk factors. However, a clinical 

diagnosis of DVT is insensitive and inaccurate; therefore, the diagnosis must be confirmed (with one of the 

diagnostic tests described above) before treatment. 

2. The current recommended diagnostic algorithm is to use a combination of a clinical scoring system (eg, 

Well's Criteria [see Table 5]) to determine pretest probability in conjunction with a o-dimer assay and/or 

venous ultrasound. 

3. For patients at low risk of DVT 

a. A negative o-dimer excludes DVT. 

b. A positive o-dimer warrants venous ultrasound. If this is negative, DVT is excluded. If positive, proceed 

with anticoagulation. 

4. For patients at moderate or high risk of DVT 

a. Initially order venous ultrasound. If positive, anticoagulate. 

b. However, a negative ultrasound in a predicted moderate- or high-risk patient does not exclude DVT. It is 

recommended to then order a o-dimer to further risk stratify these higher-risk patients. 

(1) If the o-dimer is negative, a DVT is excluded, and no further testing is required. 

(2) If the o-dimer is positive, the patient requires a repeat ultrasound in 2-7 days. 

5. The treatment of isolated calf DVT remains controversial, even though ~25% of these thrombi propagate 

proximally and may subsequently embolize. If an isolated calf DVT is detected, the risk and benefit of 

anticoagulation should be weighed against patient's pre-test probability. 

a. For moderate- and high-risk patients, anticoagulation should be started unless contraindications exist. 

b. For low-risk patients, repeat ultrasound is required with either no treatment or simply starting aspirin 

therapy. 

85


VI. PHARMACOLOGICTHERAPY 

A. Goals 

1. Prevent pulmonary embolism 

2. Reduce morbidity associated with the acute event 

3. Prevent (or minimize) postphlebitic syndrome 

B. Anticoagulation 

1. In 2016, the American College of Chest Physicians released their most current guidelines on "Antithrombotic 

Therapy for VTE Disease." 

a. Multiple new oral anticoagulants have been released in recent years, collectively called "NOAC" (nonvitamin 

Koral anticoagulants). 

(1) Dabigatran 

(2) Rivaroxaban 

(3) Apixaban 

(4) Edoxaban 

b. Advantages 

(1) Oral dosing as opposed to injections 

(2) No need for blood level monitoring 


(1) Lack of reversibility (some new agents are reported to be coming to market soon for specific NOACs) 

(2) Lack of real-time monitoring for therapeutic effect with recurrent presentations suggestive of venous 

thromboembolism (VTE) 

d. Recommendations 

(1) For patients with VTE and no cancer, a NOAC is recommended over vitamin K antagonist (VKA) 

therapy, and VKA therapy is recommended over low-molecular-weight heparin (LMWH). 

(2) For patients with VTE and cancer, LMWH is recommended overVKA or NOAC therapy. 

2. IV heparin (unfractionated) or LMWH are still viable treatment options forVTE. However, LMWH and 

unfractionated heparin are contraindicated in patients with a history of heparin-induced thrombocytopenia; 

these patients should receive alternative agents. Four LMWHs are approved for therapy, but enoxaparin is most 

commonly prescribed. 

a. Enoxaparin 

(1) 1 mg/kg SC every 12 hours (inpatient or outpatient) 

(2) 1.5 mg/kg/day SC (inpatient only) 

3. Patients with antithrombin Ill deficiency require pretreatment with antithrombin Ill concentrate or fresh frozen 

plasma to replenish this factor before heparinization. 

4. Warfarin 5 mg/day should generally be started on day one of treatment; anticoagulation parameters should be 

checked on day three. 

5. Outpatient treatment may be considered for carefully selected patients, especially with development of 

NOACs, which do not require therapeutic blood level monitoring. 

a. No serious concomitant disease requiring hospitalization 

b. Communication and transportation is adequate 

c. If patient is placed on warfarin, INR blood level checked in 2-3 days 

C. Thrombolytic therapy 

1. Compared with heparin therapy, thrombolytic therapy resolves symptoms more rapidly, preserves valve 

integrity, and may decrease the incidence of postphlebitic syndrome. However, indications for thrombolytics in 

patients with DVT are unclear. 

2. Usually reserved for patients


D. Inferior vena caval interruption with a Greenfield filter 

1. Primary indication 

a. Proximal DVT (above the level of the knee) in a patient with a contraindication to anticoagulation or 

thrombolytic therapy 

b. Those who require urgent surgery that precludes anticoagulation or those in whom treatment has not been 

effective 

2. Other indications 

a. Recurrent DVT despite adequate anticoagulation 

b. Presence of a large free-floating caval thrombus 

c. Chronic recurring embolization in a patient with pulmonary hypertension 

3. Patients with malignancies seem to benefit most from this procedure. 

VII. DISPOSITION-ADMISSION CRITERIA 

A. Extensive ileofemoral DVT with circulatory compromise 

B. Increased risk of bleeding requiring close monitoring of therapy 

C. Limited cardiorespiratory reserve 

D. Risk of poor compliance with home therapy or inadequate assistive support 

E. Contraindications to LMWH heparin necessitating IV heparin therapy 

87


HYPERTENSIVE EMERGENCIES AND URGENCIES 

I. HYPERTENSIVE EMERGENCIES 

A. Definition 

1. Patients with severely increased diastolic blood pressure (> 140 mm Hg) and evidence of acute end-organ 

dysfunction or damage 

2. The presence of end-organ damage (not the absolute blood pressure) determines a patient with a hypertensive 

emergency. 

3. The heart, brain, and kidneys are the organs most often affected. 


1. Malignant hypertension 

2. Hypertensive encephalopathy 

3. Hypertension with acute intracranial events (hemorrhagic stroke, thrombotic stroke, subarachnoid hemorrhage) 

4. Aortic dissection 

5. Acute pulmonary edema 

6. Acute myocardial ischemia or injury 

7. Eclampsia 

8 Acute hypertensive renal insufficiency 

9. Catecholamine-induced hypertensive crisis: an acute increase in circulating catecholamines that produces an 

increased blood pressure with headache, palpitations, sweating, and tachycardia. Causes include: 

a. Pheochromocytoma (adrenal tumor) 

b. Concomitant use of monoamine oxidase inhibitors and sympathomimetic agents. Commonly implicated 

sympathomimetics include: 

(1) Tyramine (Chianti wine, aged cheese, beer, pickled herring, chicken liver) 

(2) Ephedrine and phenylpropanolamine (found in OTC cold and cough preparations and appetite 

suppressants) 

c. Acute cocaine intoxication 

d. Acute clonidine withdrawal (particularly when withdrawn simultaneously with a 13-blocking agent) 

C. Management 

1. The goal of therapy is to halt and reverse the progression of endorgan dysfunction while maintaining organ 

perfusion and avoiding complications. To do this, the blood pressure must be lowered rapidly and in a 

controlled manner. The exact extent of blood pressure reduction is determined by the clinical situation; 

however, a reasonable target is to reduce the blood pressure by 20%-30% of pretreatment levels over the first 

hour of therapy. 

2. Medications are usually given by the IV route, which provides a faster onset of action and is more easily titrated. 

3. The antihypertensive agent of choice varies with the specific hypertensive emergency. 

a. Malignant hypertension and hypertensive encephalopathy: Historically, nitroprusside was the drug of 

choice. However, IV labetalol is now used most commonly, particularly when intra-arterial pressure 

monitoring is not available. Nicardipine IV is also effective. 

b. Hypertension with an ischemic stroke: treatment of hypertension in the immediate poststroke period can 

be detrimental in these patients and should not be initiated in most instances; acute reduction in blood 

pressure can reduce perfusion to the surrounding watershed areas and may thereby extend the infarction. 

Therefore, blood pressure reduction should be considered only in patients with extremely high blood 

pressures (>220/120 mmHg). Short-acting agents with few CNS effects (such as IV nitroprusside or IV 

labetalol) are the drugs of choice. 

c. Hypertension with hemorrhagic stroke: although somewhat more controversial, most authors agree that 

mild to moderate hypertension is generally well-tolerated in these patients, but that severe hypertension 

(blood pressu1·e > 220/120 mm Hg) may promote further hemorrhage and should be judiciously controlled 

with a titratable agent such as IV labetalol (other acceptable agents: esmolol, enalapril, nicardipine). 

d. Hypertension with subarachnoid hemorrhage: nimodipine or nicardipine (calcium channel blockers) is the 

initial therapeutic agent of choice. In addition to its antihypertensive effect, nimodipine also decreases the 

cerebral vasospasm that occurs after subarachnoid hemorrhage. The goal of treatment is to reduce the mean 

88


arterial pressure to prehemorrhagic levels. Blood pressure reduction is associated with a decrease in the 

risk of rebleeding in these patients. 

e. Aortic dissection: nitroprusside in combination with an IV B-blocker (propranolol or esmolol) is the therapy 

of choice; the B-blocking agent should be administered first to prevent the reflex tachycardia that can occur 

in association with nitroprusside. IV labetalol as a single drug therapy is the alternative agent of choice. 

f. Acute myocardial ischemia or injury: IV nitroglycerin is the primary agent of choice because of its 

beneficial effects on coronary perfusion. IV B-blockers can be considered, although they typically affect 

the heart rate more than blood pressure, so their effect is frequently inadequate. In addition, their use in 

acute Ml is still controversial. If blood pressure remains increased despite aggressive use of nitroglycerin, 

nitroprusside is the alternative of choice; however, it can increase myocardial ischemia via the coronary 

steal syndrome, so it is prudent to run nitroglycerin concurrently. 

g. Acute pulmonary edema: if standard measures for pulmonary edema (eg, noninvasive positive pressure 

ventilation, high-dose IV nitroglycerin, IV furosemide) fail to adequately decrease blood pressure, specific 

antihypertensive therapy should be initiated. IV nitroglycerin is the drug of choice. If blood pressure 

remains increased despite aggressive use of nitroglycerin, nitroprusside is the alternative agent. 

h. Eclampsia: IV magnesium sulfate in combination with IV hydralazine are first-line agents. IV labetalol is 

also safe and effective. Nitroprusside may be used in postpartum eclampsia but, because of the risk of fetal 

cyanide poisoning, is relatively contraindicated antepartum; it should be reserved for those patients who do 

not respond to the above-mentioned treatment regimens. 

1. Acute hypertensive renal insufficiency: nitroprusside is the drug of choice, but patients must be carefully 

monitored for thiocyanate toxicity (which is more common in this setting). Nifedipine or labetalol are good 

alternatives. 

j. Catecholamine-induced hypertensive crisis due to: 

(1) Pheochromocytoma or monoamine oxidase inhibitor interaction: phentolamine followed by an IV 

B-blocker are first-line agents; nitroprusside followed by an IV B-blocker is also effective. 

(2) Acute clonidine withdrawal: restart clonidine; phentolamine followed by an IV B-blocker can be 

effective. 

(3) Acute cocaine intoxication: sedation with a benzodiazepine such as diazepam is usually very 

effective. If hypertension persists despite adequate sedation, administer phentolamine (followed by an 

IV B-blocker if severe tachycardia is present). Nitroglycerin can be used if the patient is experiencing 

cardiac ischemia. 

4. Medications to avoid in hypertensive emergencies 

a. Malignant hypertension/hypertensive encephalopathy 

(1) ACE inhibitors 

(2) Clonidine 

(3) Pure B-blockers 

b. Acute myocardial ischemia or injury/aortic dissection 

(1) Diazoxide 

(2) Hydralazine 

(3) Minoxidil 

c. Acute pulmonary edema 

(1) Diazoxide 

(2) Hydralazine 

(3) Minoxidil 

d. Eclampsia 

(1) Diuretics (furosemide, bumetanide, hydrochlorothiazide) 

(2) ACE inhibitors 

(3) Nitroprusside: relatively contraindicated antepartum because of possible cyanide toxicity 

e. Acute hypertensive renal insufficiency 

(1) Diazoxide 

(2) Pure B-blockers as single agents 

f. Catecholamine-induced hypertensive crisis 

(1) Minoxidil 

(2) Pure B-blockers as single agents 

89


II. HYPERTENSIVE URGENCIES 

A. Definition and etiology 

1. A diastolic blood pressure ?:115 mmHg without evidence of end-organ dysfunction or damage 

2. These patients are asymptomatic and usually present to the emergency department for an unrelated problem. 

3. Most common in patients with chronic hypertension who are noncompliant with their medications 

B. Management 

1. Goal of therapy is to lower the blood pressure gradually over a period of 24-48 hours with oral medications. 

Catastrophic consequences may occur with IV administration. 

2. Commonly used agents 

a. Nifedipine 

b. Labetalol 

c. Clonidine 

d. ACE inhibitors 

90

CARDIOVASCULAR DISORDERS: PRACTICE CLINICAL SCENARIOS 


Answers immediately follow the practice clinical scenarios. 

Scenario A 

Presentation: A middle-aged man who has diabetes and hypertension presents with substernal, left-sided 

chest pain and a crushing/heavy pressure sensation, radiating to the left jaw and down the left arm. He 

appears diaphoretic and in obvious distress. 


What is the diagnosis? 

Scenario B 

Presentation: A patient with acute decompensated heart failure presents with respiratory distress and gives 

a history that includes increasing lower extremity edema, orthopnea, paroxysmal nocturnal dyspnea, and a 

nonproductive cough. 

Physical examination: The patient is in respiratory distress with hypoxia. Physical examination findings 

include jugular venous distention, rales on lung auscultation, and symmetrical, pitting lower extremity 

edema. 


Scenario C 

Presentation: An elderly patient with a history of uncontrolled hypertension presents with sudden onset of 

severe ripping, tearing chest pain radiating to the mid back between the scapulae. Since onset, the pain in 

the back has migrated caudally. 


91


Scenario D 

Presentation: A 45-year-old woman with end-stage renal disease presents to the emergency department 

from her dialysis center after a syncopal episode. She has missed the previous three weeks of dialysis. 

On examination, she is hypotensive, minimally responsive, and in severe respiratory distress. She is 

tachycardic and has barely audible heart sounds with marked jugular venous distension. 


Scenario E 

Presentation: A 22-year-old man with a history of Wolff-Parkinson-White (WPW) syndrome presents after 

a syncopal episode at work. On arrival at the emergency department, he is awake but has a blood pressure 

of 100/50 mm Hg and is feeling lightheaded. His ECG shows an irregularly irregular wide-complex 

tachycardia with QRS complexes that vary in width. 


Scenario F 

Presentation: A 66-year-old man presents with palpitations. He has been feeling weak and tired today and 

had chest pain earlier but that has resolved. On arrival, he appears well and nontoxic. After the patient has 

been placed on the monitor, the nurse calls outs and shows you this rhythm strip: 



ScenarioG 

Presentation: A 74-year-old woman is transferred from her extended-care facility for a "psych work-up." 

She is confused, hallucinating, and states all the nurses are "angels" because "everyone has a halo." Her 

past medical history is significant for atrial fibrillation and CHF, and she is currently being treated for 

a UTI. On examination, she has an irregularly irregular bradycardic pulse. After initial management is 

started, the nurse tells you the patient has a potassium level of 6.9 mEq/L. 


Scenario H 

Presentation: A 73-year-old man presents from church after a syncopal episode with severe left-sided back 

pain. He states he has a history of kidney stones. His blood pressure is 86/43 mmHg with a heart rate of 

127 beats per minute. On examination, he has significant left-sided abdominal tenderness with ecchymosis 

along his left flank. 


92


ANSWERS TO PRACTICE CLINICAL SCENARIOS 

Scenario A 

Diagnosis: STEMI 

Diagnostic evaluation: The ECG shows ST-segment elevation in contiguous leads in an anatomic 

distribution (anterior). 

Management: After IV access has been established, the patient should be placed on a monitor, provided 

low-flow supplemental oxygen for any dyspnea or hypoxia, and given aspirin 325 mg (chewed) unless he 

has a true aspirin allergy. Nitroglycerin can be administered as needed for chest pain. Coronary reperfusion 

is the definitive treatment and wi 11 be guided by avai labi I ity of PCI. If the patient presents to a hospital 

with PCI capabilities, the cardiac catheterization team should be activated immediately and the patient 

prepared for emergent PCI with a first medical contact-to-device time of 90 minutes. If the patient had 

presented to a hospital that does not have PCI capabilities, the goal for "door-in, door-out" at the initial 

hospital is 30 minutes, with a first medical contact-to-device time of 120 minutes, allowing for transport 

time to the PCI hospital. The patient should also be given a heparin bolus followed by infusion. 

Scenario B 

Diagnosis: decompensated congestive heart failure 

Diagnostic evaluation: Possible triggers for acute decompensation include medication noncompliance, 

dietary indiscretion (excess sodium intake), dysrhythmias, or acute coronary syndrome. Chest radiograph 

may show cardiomegaly depending on the cause of the heart failure. Chest radiograph will also show 

pulmonary venous congestion. An ECG should be obtained to evaluate for concurrent dysrhythmia or 

acute coronary syndrome. Laboratory studies should include renal function testing, cardiac biomarkers, 

and a brain natriuretic peptide. 

Management: The patient should be started on Bi PAP with supplemental oxygen if needed for hypoxia. 

ACE inhibitors and high-dose nitroglycerin should be given to lower afterload and preload, respectively. 

After this, if the patient is volume overloaded and has normal renal function, furosemide should be given 

for diuresis. 

Scenario C 

Diagnosis: thoracic aortic dissection 

Diagnostic evaluation: Depending on the location of the dissection, there may be differences in the 

upper extremity blood pressures or a pulse difference between the right arm and left arm (Debakey 1/ 

II or Stanford A). A dissection below the origin of the left subclavian artery (Debakey Ill or Stanford B) 

would not necessarily have a difference in upper extremity pulses or blood pressures but would likely 

have a difference when comparing upper and lower extremities. An ECG should be done to exclude 

acute coronary syndrome as a cause of the chest pain or to evaluate for concomitant STEMI, because a 

proximal dissection could involve the aortic root and coronary arteries. An initial chest radiograph should 

be obtained, because there are classic findings of aortic dissection on chest radiograph, most notably 

a widened mediastinum. However, the lack of classic radiographic findings does not exclude aortic 

dissection, especially in a patient with a classic presentation and risk factors as above. In stable patients, 

CTA of the chest or an echocardiogram (preferably transesphogeal) could be ordered depending on 

availability. Unstable patients should not have any additional imaging in the emergency department and 

should proceed to the operating room. 

Management: Rapid control of heart rate and blood pressure is the primary treatment concern while 

arranging for definitive surgical care, especially in unstable patients. A ~-blocker should be given to 

decrease the heart rate, and a vasodilator such as nitroprusside should then be given for rapid control of 

blood pressure. The patient should be typed and crossmatched for 10 units of blood while preparing for the 

operating room. 

93


Scenario D 

Diagnosis: pericardia! tamponacle 

Diagnostic evaluation: This patient exhibits the classic findings of Beck's triad for pericardia! tamponacle: 

hypotension, clistenclecl neck veins, and distant heart sounds. She is a noncompliant dialysis patient and 

has developed a large pericardia! effusion that needs to be drained emergently. Bedside ultrasound should 

be performed to confirm the diagnosis. An ECG may show electrical alternans. 

Management: After placing the patient on the monitor and placing two large-bore IV lines, the patient 

should be given crystalloicl fluids (2 L bolus) to treat hypotension and help increase preloacl to combat 

tamponacle collapse of the ventricles. Emergent pericarcliocentesis should be performed, ideally with 

ultrasound guidance, although ECG monitoring with an ECG lead clipped to the needle may be performed 

as well. 

Scenario E 

Diagnosis: atrial fibrillation with WPW 

Diagnostic evaluation: WPW can present with a variety of tachyclysrhythmias with important distinctions 

in management. The rhythm described, an irregularly irregular wide complex rhythm, is the most 

concerning and serious of the WPW presentations. The irregular nature suggests this is not simple AV 

reentry tachycardia but rather atrial fibrillation. 

Management: In a patient with known WPW, the fact that the QRS is wide means that the anterogracle 

direction is clown the accessory pathway and then conducted retrograde back through the AV node. 

Therefore, any AV nodal blocking agent, eg, aclenosine, ~-blockers, calcium channel blockers, or cligoxin, 

are contraindicated in management of this patient. This would also extend to amioclarone, because it has 

AV nodal blocking properties as well. Treating this patient with any AV nodal blocking agent could result in 

fatal deterioration to ventricular fibrillation, which may be refractory to therapy. Therefore, the treatment of 

choice for this patient is procainamicle. Should the patient become unstable, he would require immediate 

carclioversion, as with any unstable tachycarclic patient. However, because the rhythm is a wide complex 

irregular tachycardia, per the ACLS guidelines, treatment would be with an unsynchronized carclioversion 

at clefibrillation closes, ie, 200 joules. 

Scenario F 

Diagnosis: ventricular tachycardia 

Diagnostic evaluation: The rhythm strip shows a regular wide complex tachycardia, which is concerning 

for ventricular tachycardia in a 66-year-olcl man who had chest pain before presentation. A 12-leacl ECG 

should be obtained to confirm the diagnosis of ventricular tachycardia. Although multiple clinical decision 

tools exist to assist in the differentiation of ventricular tachycardia versus SVT with aberrant conduction, if 

there is any doubt, the patient should be treated as if in ventricular tachycardia. 

Management: Because this a wide complex tachycardia and the patient is currently stable, ACLS guidelines 

state that the patient should be treated with either amioclarone 150 mg over 10 minutes or procainamicle 

25-50 mg/min infusion. An external defibrillator should be applied to the patient in case any clinical 

deterioration occurs. Should the patient become unstable or his chest pain recur, he should immediately 

be treated with synchronized carclioversion, with a recommended starting close of 100 joules and 

increasing closes as needed. 

94


ScenarioG 

Diagnosis: digitalis toxicity 

Diagnostic evaluation: The patient is exhibiting classic signs of chronic digitalis toxicity induced by a 

change in renal function due to the UTI for which she is being treated. The ECG shows atrial fibrillation 

with slow ventricular response and ST segment downsloping. The classic ST changes of digoxin indicate 

only that the patient is on digoxin, not that the patient has digitalis toxicity. Checking the potassium level is 

of utmost importance, because an increased level is itself an indication for digoxin-specific antibody. 

Management: Because the patient is bradycardic, initial treatment with atropine should be attempted 

and an external pacemaker should be at the bedside. If the bradycardia is not responsive to atropine or 

the patient becomes symptomatic, external transcutaneous pacing is indicated. However, this patient 

meets multiple criteria for digoxin-specific antibodies: bradycardia and hyperkalemia. Hyperkalemia 

may be treated with insulin, glucose, and bicarbonate, but classic teaching is to avoid administration 

of calcium. Similarly, classic teaching is to avoid transvenous pacing because of concern of inducing a 

tachydysrhythmia while floating the pacemaker wire. 

Scenario H 

Diagnosis: ruptured abdominal aortic aneurysm (AAA) 

Management: This patient has a classic presentation for a ruptured AAA, including the foil of a possible 

kidney stone. The combination of syncope, hypotension with a pulsatile abdominal mass, and ecchymosis 

on the flank alone are indication to call emergently for vascular surgery. No additional testing is necessary, 

although a bedside ultrasound to confirm the AAA may be completed, a CT at this point would be 

inappropriate given the instability of the patient. Fluid resuscitation should be started until crossmatched 

blood is available while the operating room is prepared. 

95

96 

NOTES

HEAD, EAR, EYE, NOSE, AND THROAT DISORDERS 


OTOLOGIC EMERGENCIES ...................................................................................................................................... 107 

Anatomy ................................................................................................................................................................... 1 07 

Sensory Supply to the Ear ................................................................................................................................... 1 07 

Auditory Transmission ........................................................................................................................................ 107 

Infections .................................................................................................................................................................. 107 

Acute Otitis Externa (Swimmer's Ear) .................................................................................................................. 1 07 

Malignant (Necrotizing) Otitis Externa ................................................................................................................ 107 

Posttraumatic Perichondritis ............................................................................................................................... 108 

Acute Otitis Media ............................................................................................................................................. 1 08 

Bullous Myringitis .............................................................................................................................................. 109 

Mastoiditis ................................................................................................................................................................ 1 09 

Sudden Hearing Loss ................................................................................................................................................. 110 

Vertigo ...................................................................................................................................................................... 111 

Trauma ...................................................................................................................................................................... 112 

EYE EMERGENCIES ................................................................................................................................................... 113 

Conjunctivitis ............................................................................................................................................................ 113 

Viral Conjunctivitis ............................................................................................................................................. 113 

Bacterial Conjunctivitis ...................................................................................................................................... 113 

Chlamydia! (inclusion) Conjunctivitis ................................................................................................................. 114 

Vernal Conjunctivitis .......................................................................................................................................... 115 

Inflammatory Disorders of the Eyelids and Cornea ................................................................................................... 115 

Anterior Blepharitis ............................................................................................................................................ 115 

Hordeolum (Stye) ............................................................................................................................................... 116 

Chalazion ........................................................................................................................................................... 116 

Dacryocystitis ..................................................................................................................................................... 116 

Corneal Ulcers ................................................................................................................................................... 117 

Herpes Simplex Keratitis ..................................................................................................................................... 117 

Herpes Zoster Ophthalmicus .............................................................................................................................. 118 

Ultraviolet Keratitis ............................................................................................................................................. 119 

Periorbital and Orbital Cellulitis ............................................................................................................................... 119 

Acute Eye Pain ........................................................................................................................................................... 121 

Acute lritis .......................................................................................................................................................... 121 

Acute Angle Closure Glaucoma .......................................................................................................................... 122 

Acute Visual Loss ....................................................................................................................................................... 123 

Central Retinal Artery Occlusion ........................................................................................................................ 123 

Central Retinal Vein Occlusion ........................................................................................................................... 124 

Optic Neuritis .................................................................................................................................................... 124 

Eclipse Burn ....................................................................................................................................................... 125 

Retinal Detachment. ........................................................................................................................................... 126 

Vitreous Hemorrhage ......................................................................................................................................... 126 

Functional Blindness .......................................................................................................................................... 127 

Temporal (Giant Cell) Arteritis ............................................................................................................................ 127 

Nonacute Visual Loss ................................................................................................................................................ 127 

Primary Open Angle Glaucoma .......................................................................................................................... 127 

Cytomegalovirus Retinitis ................................................................................................................................... 128 

97


Trauma ...................................................................................................................................................................... 128 

Chemical Burns .................................................................................................................................................. 128 

Lid Lacerations ................................................................................................................................................... 129 

Corneal Injuries .................................................................................................................................................. 129 

Ruptured Globe .................................................................................................................................................. 130 

Hyphema ........................................................................................................................................................... 131 

Lens Subluxation and Dislocation ...................................................................................................................... 131 

Blowout Fractures of the Orbit... ......................................................................................................................... 132 

Retrobulbar Hematoma ...................................................................................................................................... 132 

lntraocular Foreign Body .................................................................................................................................... 132 

Traumatic lritis/lridocyclitis ................................................................................................................................. 133 

Traumatic Miosis and Mydriasis ......................................................................................................................... 133 

Anisocoria ................................................................................................................................................................. 133 

Ophthalmic Medications ........................................................................................................................................... 134 

Packaging ........................................................................................................................................................... 134 

Topical Anesthetics ............................................................................................................................................. 134 

Mydriatics and Cycloplegics ............................................................................................................................... 135 

Miotics ............................................................................................................................................................... 135 

Topical Antibiotics .............................................................................................................................................. 135 

Antivirals ............................................................................................................................................................ 136 

Topical Steroids .................................................................................................................................................. 13 6 

Hyperosmotic Agents ......................................................................................................................................... 136 

Carbonic Anhydrase Inhibitors ........................................................................................................................... 136 

Topical Adrenergic Agents .................................................................................................................................. 136 

Tonometry ................................................................................................................................................................. 137 

NASAL TRAUMA ....................................................................................................................................................... 138 

Nasal Fractures ......................................................................................................................................................... 138 

Major Complications ................................................................................................................................................. 138 

Septal Hematoma ............................................................................................................................................... 138 

CSF Rhinorrhea .................................................................................................................................................. 138 

Hemorrhage ....................................................................................................................................................... 139 

NASAL FOREIGN BODIES ........................................................................................................................................ 140 

Clinical Presentation ................................................................................................................................................. 140 

Diagnosis and Treatment ........................................................................................................................................... 140 

EPISTAXIS ................................................................................................................................................................. 141 

Vascular Supply to the Nose ..................................................................................................................................... 141 

Etiology ..................................................................................................................................................................... 141 


Treatment .................................................................................................................................................................. 142 

Complications ........................................................................................................................................................... 142 

FACIAL INFECTIONS ................................................................................................................................................ 143 

Sinusitis ..................................................................................................................................................................... 143 

Parotitis ..................................................................................................................................................................... 144 

FACIAL FRACTURES .................................................................................................................................................. 146 

Mandibular Injuries ................................................................................................................................................... 146 

Hal !marks of Mandibular Dysfunction ................................................................................................................ 146 

Mandibular Fractures .......................................................................................................................................... 146 

Mandibular Dislocation ...................................................................................................................................... 146 

Temporomandibular Joint Dysfunction ............................................................................................................... 147 

Midfacial Fractures ................................................................................................................................................... 147 

Midfacial Area .................................................................................................................................................... 147 

Isolated Zygomatic Arch Fractures ...................................................................................................................... 147 

Zygomatic-Maxillary Complex ("Tripod") Fractures ............................................................................................ 148 

Orbital Floor Fractures ........................................................................................................................................ 148 

Multiple Facial Fractures ..................................................................................................................................... 148 

98


ACUTE AIRWAY OBSTRUCTION .............................................................................................................................. 150 


Differential Diagnosis ............................................................................................................................................... 150 

ORAL AND PHARYNGEAL INFECTIONS ................................................................................................................. 154 

Oral Infections .......................................................................................................................................................... 154 

Masticator Space Abscess ................................................................................................................................... 154 

Ludwig Angina ................................................................................................................................................... 154 

Pharyngeal Space Infections ..................................................................................................................................... 155 

Parapharyngeal Abscess ...................................................................................................................................... 155 

Peritonsil lar Abscess ........................................................................................................................................... 155 

Retropharygeal Abscess ...................................................................................................................................... 156 

Prevertebral Infection ......................................................................................................................................... 156 

PHARYNGITIS .......................................................................................................................................................... 158 

Trauma ...................................................................................................................................................................... 158 

Irritant Inhalant ........................................................................................................................................................ 158 

Viruses ...................................................................................................................................................................... 158 

Infectious Mononucleosis ................................................................................................................................... 158 

Herpes Simplex Pharyngitis ................................................................................................................................ 158 

Bacteria ..................................................................................................................................................................... 159 

Group A j3-Hemolytic Streptococci ..................................................................................................................... 159 

Group C and G Streptococci .............................................................................................................................. 159 

Diphtheria .......................................................................................................................................................... 160 

Gonorrhea .......................................................................................................................................................... 1 60 

Fungi ......................................................................................................................................................................... 160 

DENTAL EMERGENCIES ............................................................................................................................................ 161 

Neuroanatomy of the Face ........................................................................................................................................ 161 

Facial and Oral Anesthesia ........................................................................................................................................ 162 

Anatomy of a Tooth ................................................................................................................................................... 162 

Dental Emergencies .................................................................................................................................................. 163 

Trauma ............................................................................................................................................................... 163 

Hemorrhage ....................................................................................................................................................... 1 63 

Orofacial Pain .................................................................................................................................................... 164 

Systemic Diseases with Oral Manifestations ....................................................................................................... 165 

Infections .................................................................................................................................................... 165 

Automimmune/lnflammatory States ............................................................................................................. 165 

Toxic/Metabolic States ................................................................................................................................. 165 

Granulomatous Diseases ............................................................................................................................. 165 

Benign Tumors and Tumor-Like Lesions ....................................................................................................... 165 

Blood Dyscrasias ......................................................................................................................................... 165 

HIV/AIDS .................................................................................................................................................... 165 

99

HEAD, EAR, EYE, NOSE, AND THROAT DISORDERS: SELF-ASSESSMENT QUESTIONS 

HEAD, EAR, EYE, NOSE, AND THROAT DISORDERS: 

SELF-ASSESSMENT QUESTIONS 

1. All of the following are true of peripheral vertigo except: 

(a) Onset is gradual. 

(b) Nystagmus may be horizontal or horizontorotary in direction. 

(c) It may be associated with nausea, vomiting, hearing loss, and tinnitus. 

(d) Episodes generally self-limited. 

2. The most reliable sign of acute otitis media is: 

(a) A tympanic membrane that is erythematous 

(b) The presence of fever 

(c) Loss of mobility of the tympanic membrane on pneumatic otoscopy 

(d) The presence of a scarred and retracted tympanic membrane 

3. Which of the following statements regarding malignant otitis externa is true? 

(a) It is a common complication of otitis externa that afflicts otherwise healthy patients. 

(b) It is treated on an outpatient basis with oral antibiotics. 

(c) It is caused by Pseudomonas. 

(d) Patients with this disease process are generally afebrile and experience little pain. 

4. Which of the following is least characteristic of croup? 

(a) Barking cough 

(b) High fever 

(c) Preceding upper respiratory infection 

(d) Insidious onset 

5. All of the following are true of temporal arteritis except: 

(a) It is associated with a markedly increased sedimentation rate. 

(b) It may present as sudden, painless, unilateral loss of vision. 

(c) It is treated with steroids. 

(d) It is a nonsegmental vasculitis. 

6. Appropriate antibiotic therapy of pharyngitis caused by group A ~-hemolytic streptococci can limit or prevent all of 

the following complications except: 

(a) Rheumatic fever 

(b) Glomerulonephritis 

(c) Pharyngeal space infections 

(d) Spread of the infection to others 

7. 

____ is/are the most common cause(s) of pharyngitis. 

(a) Group A ~-hemolytic streptococcus 

(b) Mycoplasma 

(c) Viruses 

(d) Gonorrhea 

8. Which statement is true regarding group A ~-hemolytic streptococcus pharyngitis? 

(a) Accurate diagnosis can be made on the basis of clinical findings alone. 

(b) It commonly affects children


10. Al I of the following statements regarding Ellis II fractures are true except: 

(a) They involve both the enamel and dentin. 

(b) They are associated with hot and cold sensitivity. 

(c) Bleeding from the tooth is characteristic. 

(d) Dental follow-up within 24 hours is recommended. 

11. Which of the following descriptive statements is most consistent with alveolar osteitis? 

(a) It occurs within 24 hours of extraction and responds to oral analgesics. 

(b) It is seen several days after extraction, after an initial pain-free time interval, and is not relieved by oral analgesics. 

(c) It is associated with dental caries and treated by tooth extraction. 

(d) It is a periodontal lesion in which bacteria invade non-necrotic tissue. 

12. Which is true regarding treatment of avulsed teeth? 

(a) The tooth should be wiped clean before replanting. 

(b) Primary teeth should be replaced immediately. 

(c) Handling the tooth by the root is preferred. 

(d) Hank's solution and milk are better transport solutions than tap water. 

13. The most common arterial source of posterior epistaxis is: 

(a) 

Sphenopalatine artery 

(b) Anterior ethmoidal artery 

(c) Posterior ethmoidal artery 

(d) Kiesselbach plexus 

14. All the following statements regarding posterior epistaxis are accurate except: 

(a) It is less common than anterior epistaxis. 

(b) It most commonly occurs in children and young adults. 

(c) Placement of a posterior pack can result in hypoxia and hypercarbia. 

(d) Patients treated with a posterior pack should be admitted. 

15. The treatment of choice for simple group A ~-hemolytic streptococcus is: 

(a) Penicillin 

(b) Erythromycin 

(c) Cephalosporins 

(d) TMP-SMX 

16. The following statements regarding glomerulonephritis are accurate except: 

(a) 

It is a suppurative complication of group A ~-hemolytic streptococcus infection. 

(b) It can result from either pharyngeal or cutaneous infection with group A ~-hemolytic streptococci. 

(c) 

Patients usually present after a latent period of 1 .5-3 weeks. 

(d) The most useful laboratory test for making the diagnosis is the urinalysis. 

17. The following statements regarding rheumatic fever are accurate except: 

(a) The Jones Criteria (revised) are used to establish the diagnosis. 

(b) Evidence of a preceding group A ~-hemolytic streptococcus infection plus the presence of one major and one 

minor criteria make the diagnosis highly probable. 

(c) Patients usually present with severe migratory joint pain. 

(d) Morbidity is most closely related to the development of carditis and valvular damage. 

18. Bacterial tracheitis is most commonly caused by ___ _ 

(a) 

Haemophi/us influenzae 

(b) Streptococcus pneumoniae 

(c) Staphylococcus aureus 

(d) Group A ~-hemolytic streptococci 

101


19. A mother brings in her 3-year-old child for evaluation. She states that he was playing on the floor while she was 

preparing dinner and he suddenly started coughing. As you evaluate the child, you note that he is playful and in no 

acute distress. Which of the following statements is most accurate? 

(a) You should reassure the mother and send the child home; further evaluation is unnecessary, because foreign 

body aspiration is unlikely in this scenario. 

(b) You should obtain further history and perform PA and lateral chest radiographs; normal findings on these 

radiographs exclude the possibility of foreign body aspiration. 

(c) You should obtain further history and perform PA, lateral, and (possibly) bilateral decubitus chest radiographs; 

if these radiographs are negative (and your suspicion for foreign body aspiration remains high), bronchoscopy 

should be arranged. 

(d) You should immediately arrange for diagnostic bronchoscopy in every child with this presentation. 

20. Which of the following is not true regarding peritonsillar abscesses? 

(a) It most commonly occurs as a complication of suppurative tonsillitis. 

(b) Needle aspiration followed by incision and drainage provides sufficient initial drainage for most abscesses. 

(c) 

It is most common in infants. 

(d) The causative organism(s) is usually polymicrobial. 

21. A child presents with complaint of decreased hearing after being slapped on the ear by his brother. Examination 

reveals a small perforation of the tympanic membrane and a conductive hearing loss but is otherwise entirely 

normal. The child is acting normally, appears to be comfortable, and has normal vital signs. The most appropriate 

treatment is: 

(a) 

Emergent ENT referral for possible surgical repair. 

(b) A prescription for an oral antibiotic and referral for follow-up with ENT in 24 hours 

(c) A prescription for a topical antibiotic and referral for follow-up with ENT in 1 week. 

(d) Recommend the ear be kept dry, and refer to ENT on a nonurgent basis. 

22. Which of the following statements regarding the diagnosis of sinusitis is most accurate? 

(a) 

It requires diagnostic imaging in most instances. 

(b) Normal findings on plain radiographs (Water, Caldwell, submental-vertex, and lateral views) excludes the 

diagnosis. 

(c) 

Plain films are the most useful in diagnosing sphenoid and ethmoid sinusitis. 

(d) The "gold standard" for diagnosing sinus disease and its complications is CT of the sinuses. 

23. Which of the following statements regarding hairy leukoplakia is false? 

(a) It is a white plaque-like lesion with hairy projections. 

(b) It is usually asymptomatic. 

(c) 

It is easily removed with a tongue blade. 

(d) It is one of the most common virally induced, oral diseases of HIV-infected individuals, with a prevalance as 

high as 25%-50%. 

24. The initial study of choice for confirming the presence of a retropharyngeal abscess is a soft-tissue lateral radiograph 

of the neck. To avoid obtaining a false-positive result, this film must be taken: 

(a) 

During expiration with the neck in slight extension 

(b) During expiration with the neck in slight flexion 

(c) 

During inspiration with the neck in slight extension 

(d) During inspiration with the neck in slight flexion 

25. Croup (laryngotracheobronchitis) is most commonly caused by: 

(a) 

Respiratory syncytial virus 

(b) Parainfluenza virus 

(c) Adenovirus 

(d) Influenza virus 

102


26. A 3-year-old is brought in for evaluation of sore throat, fever, and refusal to eat. The child's voice is muffled. 

Examination reveals a unilateral bulging of the posterior pharyngeal wall, tender anterior cervical adenopathy, and 

temperature of 102°F (39°C). The most likely diagnosis is: 

(a) Retropharyngeal abscess 

(b) Peritonsillar abscess 

(c) Ludwig angina 

(d) Masticator space abscess 

27. An infant who was delivered at home and received no perinatal care is brought in 12 days after birth for evaluation 

of a purulent eye discharge and cough. Examination reveals diffuse conjunctiva! injection and normal pupillary 

reactivity. The most likely etiologic agent is: 

(a) Staphylococcus aureus 

(b) Adenovirus 

(c) Chlamydia trachomatis 

(d) Neisseria gonorrhoeae 

28. A sexually active 20-year-old man presents with redness and irritation of his right eye with an associated discharge. 

Findings include diffuse conjunctiva! injection and a copious purulent ocular discharge. Visual acuity and pupillary 

reactivity are normal. The most likely etiologic agent is: 

(a) 

Neisseria gonorrhoeae 

(b) Herpes simplex 


(d) Vernal conjunctivitis 

29. The most appropriate therapy for a patient with conjunctivitis and corneal ulceration due to Neisseria gonorrhoeae is: 

(a) Discharge to home with topical erythromycin or tetracycline ophthalmic ointment 

(b) Discharge to home with tobramycin ophthalmic ointment or drops 

(c) Hospital admission with administration of IM or IV ceftriaxone 

(d) Hospital admission with administration of IV ceftriaxone, topical erythromycin, oral erythromycin (in children) 

or doxycycline (in adults), and saline irrigation 

30. Which of the following entities is most characteristically associated with painless decrease (or loss) of vision? 

(a) Central retinal artery occlusion 

(b) Acute iritis 

(c) Acute narrow angle closure glaucoma 

(d) Optic neuritis 

31. Which of the following is associated with pain and loss of central vision only? 

(a) Primary open angle closure glaucoma 

(b) Acute iritis 

(c) Acute anterior uveitis 

(d) Optic neuritis 

32. A patient presents with eye pain, slight blurring of vision and severe photophobia. Examination reveals a red eye 

with a ciliary flush, a constricted pupil, and a clear cornea. Slit lamp examination reveals flare and cells in the 

anterior chamber. The most likely diagnosis is: 

(a) 

Acute angle closure glaucoma 

(b) Retrobulbar neuritis 

(c) Acute iritis 

(d) Primary open angle closure glaucoma 

33. Which of the following is most appropriate in the treatment of acute traumatic iritis? 

(a) 

Oral steroid therapy 

(b) Topical steroids (in consultation with an ophthalmologist) 

(c) Antibiotic ointment or drops 

(d) Epsilon aminocaproic acid 

103


34. The mechanism of action by which timolol and acetazolamide work in treatment of acute narrow angle glaucoma is: 

(a) 

They pull the iris back from its anterior position, thereby opening the angle and allowing escape of aqueous humor. 

(b) They decrease the secretion of aqueous humor by the ciliary body. 

(c) They cause pupillary block by dilating the iris and allowing the egress of aqueous humor. 

(d) None of the above 

35. A 77-year-old woman presents with a headache and loss of vision in her left eye. Visual acuity is measured as bare 

light perception in this eye. The cornea is clear, pupillary reactivity is normal, and the sedimentation rate is 60. The 

most appropriate therapy for this patient is: 

(a) Topical pilocarpine solution 

(b) A topical steroid agent 

(c) Ophthalmology referral for follow-up in 3-4 days 

(d) High-dose corticosteroids, preferably IV 

36. Which of the following is a common sign of a blowout fracture of the orbit with entrapment? 

(a) Ptosis 

(b) Exophthalmos 

(c) Afferent pupil defect 

(d) Pain and diplopia on upward gaze 

37. A patient presents with a laceration to his upper eyelid. On evaluation, you note a deep horizontal laceration 

toward the middle of the upper lid and associated ptosis. The globe itself does not appear to be injured. The most 

likely associated injury is damage to the: 

(a) 

Lacrimal canaliculi 

(b) Orbital septum 

(c) Levator muscle/tendon 

(d) Canthal tendon 

38. The finding most consistent with a ruptured globe: 

(a) Teardrop or irregularly shaped pupil 

(b) Increased intraocular pressure 

(c) Exophthalmos 

(d) Diminished intraocular pressure 

39. The shortest-acting cycloplegic agent is: 

(a) 

Cyclopentolate 

(b) Tropicamide 

(c) 

Homatropine 

(d) Atropine 

40. The topical antibiotic agent associated with the development of skin sensitivity in 10%-15% of patients is: 

(a) 

Sulfacetamide 

(b) Chloramphenicol 

(c) Erythromycin 

(d) Neomycin 

41. Topical ophthalmic drops have color-coded caps to facilitate the identification of the various types of agents. The 

color cap associated with miotic agents is: 

(a) 

Green 

(b) Red 

(c) Yellow 

(d) White 

42. The presence of a Marcus-Gunn pupil on examination is most indicative of: 

(a) Acute iritis 

(b) Optic neuritis 

(c) Vitreous hemorrhage 

(d) Functional blindness 

104


43. A 70-year-old woman presents with obvious signs and symptoms of acute angle closure glaucoma. Her past medical 

history is significant for poorly controlled CHF. Which of the following would be inappropriate? 

(a) 

Pilocarpine 2% solution 

(b) Glycerol 50% solution 

(c) Timolol 0.5% solution 

(d) Acetazolamide 

44. Which of the following statements regarding periorbital cellulitis is most accurate? 

(a) Children > 10 years old are rarely affected. 

(b) Patients present with erythema, warmth, and swelling of one or both eyelids. 

(c) Patients complain of pain with ocular movement, and ophthalmoplegia may be present. 

(d) Fever is uncommon. 

45. Which of the following statements regarding use of a tonometer is most accurate? 

(a) 

Its use is contraindicated in the presence of a ruptured globe. 

(b) lntraocular pressure is always high in acute iritis. 

(c) Use of an air-puff tonometer requires direct eye contact. 

(d) The Schiotz tonometer gives a direct reading in millimeters of mercury. 

46. Which of the following conditions does not classically produce a decrease in visual acuity? 

(a) Traumatic lens dislocation 

(b) Retrobulbar hematoma 

(c) Periorbital cellulitis 

(d) Retrobulbar neuritis 

47. A 25-year-old patient presents with a foreign body sensation in his left eye, photophobia, and tearing. Evaluation reveals 

a visual acuity of 20/30, diffusely reddened eye, decreased corneal sensation, and a dendritic lesion on fluorescein 

staining. Which of the following could produce rapid worsening of his condition and should not be prescribed? 

(a) A topical antibiotic 

(b) A topical steroid 

(c) A topical antiviral agent (in consultation with an ophthalmologist) 

(d) A mydriatic agent 

48. A patient who uses extended-wear soft contact lenses presents with complaints of photophobia, eye pain, blurred 

vision, and a purulent discharge. Examination reveals a corneal ulcer. The causative agent in this setting is most likely: 

(a) Neisseria gonorrhoeae 

(b) Klebsiella 


(d) Pseudomonas 

49. Immediate ophthalmology consult, hospital admission and treatment is mandatory for which of the following conditions? 

(a) Orbital (postseptal) cellulitis 

(b) Herpes zoster ophthalmitis 

(c) Corneal ulcers 

(d) Acute iritis 

50. Regarding chemical burns of the eye, which of the following statements is most accurate? 

(a) Alkali burns are usually worse than acid burns. 

(b) Alkali burns produce a coagulation necrosis. 

(c) A neutralizing agent should be used to irrigate the eye. 

(d) Irrigation can be discontinued after 30 minutes, once the pH of the conjunctiva! fornix is neutral at 8.5. 

51. The most appropriate management sequence for an acid or alkali burn of the eye is: 

(a) 

Detailed eye examination, assessment of visual acuity, copious irrigation, pH assessment 

(b) Evaluation of visual acuity, pH assessment, copious irrigation, detailed eye examination 

(c) pH assessment, copious irrigation, evaluation of visual acuity, detailed eye examination 

(d) Copious irrigation, pH assessment, evaluation of visual acuity, detailed eye examination 

105


52. A 42-year-old man presents with painful swelling below the inner aspect of his right eye of 1 day duration. 

Examination reveals localized erythematous swelling and tearing. His visual acuity is 20/20, the remainder of his 

eye examination is unremarkable, and he otherwise appears well. The most appropriate treatment is: 

(a) 

Immediate incision and drainage 

(b) Admission for parenteral antibiotics 

(c) A topical antibiotic ointment 

(d) A broad-spectrum oral antibiotic and warm compresses 

53. A patient with AIDS and a CD4 count


OTOLOGIC EMERGENCIES 

I. ANATOMY 

A. Sensory supply to the ear 

1. Tympanic membrane: auriculotemporal (V3), cranial nerves IX and X 

2. Auricle: auriculotemporal (V3), cranial nerves XII and X, lesser occipital, greater auricular 

3. External auditory canal: auricolutemporal (V3), cranial nerves VII, IX, and X 

B. Auditory transmission 

Sound waves enter ear canal_,. tympanic membrane_,. ossicles _,. perilymph _,. endolymph _,. organ of Corti _,. 

spiral ganglion_,. cochlear nulei _,. temporal lobes 

II. INFECTIONS 

A. Acute otitis externa (swimmer's ear) 

1 . Pseudomonas aeruginosa and Staphylococcus aureus are responsible for most cases of otitis externa. Other 

pathogens include Proteus, Streptococcus, and fungi (usually Aspergillus). 

2. A major predisposing factor is exposure to a warm, moist environment, so most cases occur in the summer 

months and in patients exposed to tropical environments; foreign body trauma and water exposure are 

obvious risk factors. 


a. Itching: may be intense with severe fungal infections 

b. Pain: may be intense, constant, and aggravated by pulling on the ear or pressing on the tragus 

c. Sense of fullness in the ear 

d. Purulent discharge 

e. External auditory canal is often edematous and erythematous with significant debris. 

f. If the tympanic membrane can be visualized, it is sometimes red, thick, and covered with flat vesicles or 

areas of desquamating epithelium. 

4. Differential diagnosis 

a. Malignant otitis externa 

b. Suppurative otitis media with tympanic membrane perforation 

c. Contact dermatitis (eg, neomycin) 

d. Eczema 

e. Psoriasis 

f. Temporal bone/external auditory canal malignancy 

5. Management 

a. Cleanse the ear canal of debris using suction, irrigation, or gentle curettage; this is the most important 

part of therapy. 

b. Use topical agent 

(1) Mild infections: otic hydrocortisone/acetic acid (rarely used) 

(2) Moderate infections: otic quinolones with steroids (eg, otic ciprofloxacin/dexamethasone) 

(3) Avoid otic aminoglycosides because of ototoxicity. 

(4) If significant edema is present, a wick should be inserted in the external canal, moistened with the 

desired medication, and left in place for 24-48 hours. Patient must return for removal. 

c. Advise the patient to avoid getting water in the ear for 2-3 weeks. 

d. Cellulitis is often present in severe cases; a systemic antibiotic (eg, dicloxacillin or amoxacillin/ 

clavulanate) is required. 

B. Malignant (necrotizing) otitis externa 

1. Complication of otitis externa that is associated with a high mortality rate 

2. Epidemiology 

107


a. Occurs primarily in adults with diabetes 

b. Also seen in debilitated and immunocompromised patients 

3. Etiology: a Pseudomonas osteomyelitis of the underlying bone of the external canal 


a. Distinguishing features include fever, excruciating pain, presence of friable granulation tissue in the 

external auditory canal, and edema and erythema of the pinna and periauricular tissues. 

b. Cranial nerve palsies and trismus may also be seen. 

5. Diagnostic evaluation: CT is the most appropriate emergency department imaging study to evaluate for 

osteomyelitis and determine the extent of disease. 

6. Management 

a. Immediate otolaryngology consult 

b. Hospitalization for IV antibiotics (fluoroquinolones or antipseudomonal cephalosporins) and possible 

surgical debridement 

C. Posttraumatic perichondritis 

1. An infection of the auricular cartilage, usually due to a complication of auricular trauma 

a. Auricular hematoma ("cauliflower ear") is the most common cause. 

b. Also caused by ear piercing, or after ear surgery 


a. Ear pain, swelling, and fever are typical. 

b. Examination reveals erythema and warmth/swelling of the outer ear (usually excluding the lobule). 

3. Management 

a. Consult with an otolaryngologist 

b. Administration of parenteral antibiotics effective against Pseudomonas, Proteus, and Staphylococcus 

D. Acute otitis media 


a. Children 6 months to 6 years old are most often affected; incidence peaks at 6-18 months of age. 

b. More common in the winter and spring months; frequently occurs in association with a viral upper 

respiratory infection 


a. Eustachian tube dysfunction plays a central role in pathogenesis. 

b. Eustachian tube dysfunction - negative middle ear pressure and retention of secretions - colonization 

(usually bacterial, although antibiotics are not always necessary) 

3. Etiology - the most common bacterial pathogens: 

a. Streptococcus pneumoniae (most common in all age groups), Haemophilus influenzae, Moraxella 

catarrhalis, Streptococcus pyogenes (less common) 

b. Staphylococcus aureus, Group B streptococcus, and gram-negative enteric bacilli may be seen as 

pathogens in the neonatal period. 


a. Represents a continuum of an illness that begins as an asymptomatic otitis media with effusion to acute 

otitis media with effusion plus signs and symptoms of an infection 

b. History varies from irritability, poor feeding, and ear-pulling in infants, to otalgia and hearing loss in older 

children. Upper respiratory symptoms are often present. 

c. Physical examination 

(1) Cerumen often obscures visualization and prevents initial diagnosis; if present, it must be removed. 

(2) The tympanic membrane is usually red or cloudy and may be full or bulging (bony landmarks are 

difficult to discern). Otorrhea may be present if spontaneous perforation has occurred. However, 

the most reliable sign of acute otitis media is decreased mobility of the tympanic membrane on 

insufflation. 

(3) Fever is present in only one-third of patients. 

5. Management 

a. "Wait and see prescription" for treatment of acute otitis media in children >2 years old, unilateral 

involvement, and no otorrhea is becoming the standard of care. Parents are asked not to fill the 

antibiotic prescription for 72 hours and only if the child is no better or worsening. This approach has 

resulted in reduced antibiotic use in children. 

108


b. First-line antibiotics 

(1) Amoxicillin 80-90 mg/kg/day; despite increasing resistance, it is still considered initial agent of choice. 

(2) Azithromycin, clarithromycin, and clindamycin are alternative agents for penicillin-allergic patients; 

they do not cover H influenzae. Cefdinir 14 mg/kg/day if penicillin allergy is not an immediate type 

1 hypersensitivity. 

c. Second-line agents are usually reserved for treatment failures or for patients having received antibiotics 

within the previous 30 days. A broad-spectrum antibiotic that provides coverage of ~-lactamaseproducing 

species should be selected; choose one of the following: 

(1) Amoxicillin-clavulanate if recent antibiotic exposure or suspicion of H influenzae as a cause 

(coexistent purulent conjunctivitis is a sign of H influenzae as cause) 

(2) Ceftriaxone (with possible repeat dosing depending on response) 

d. Patients should be advised to return in 48-72 hours if signs and symptoms do not improve and 

immediately if temperature increases, irritability worsens, or lethargy develops. 

e. The possibility of systemic infection should be considered in infants with acute otitis media (especially 

those


D. Diagnostic evaluation 

1. CT scan of the temporal bone confirms diagnosis and identifies presence of complications. 

2. MRI may be considered, especially if intracranial complications are suspected. 

E. Management 

1. Analgesia 

2. Parenteral antibiotics: vancomycin (initial choice until cultures available); also consider Pseudomonas coverage 

for recurrent infection 

3. Immediate ENT consult regarding the possible need for surgical debridement, which may be necessary because 

of poor bone penetration of antibiotics 

4. Hospitalization 

IV. SUDDEN HEARING LOSS 

A. Pathophysiology 

1. Acute hearing loss may be associated with lesions of the external, middle, or inner ear. 

2. Lesions of the external auditory canal, tympanic membrane, middle ear, and ossicles result in conductive 

hearing loss, whereas lesions of the cochlea, the auditory nerve, and brainstem auditory pathways result in 

sensorineural hearing loss. 

3. Sudden sensorineural hearing loss may also occur in the absence of any detectable lesions, presumably from 

microvascular insult or occult autoimmune process. 

B. Etiology 

1. Conductive loss 

a. Otitis externa 

b. Impacted cerumen or foreign body 

c. Tympanic membrane perforation 

d. Sclerosis of the tympanic membrane or ossicles 

e. Middle ear effusion (otitis media, barotitis media) 

2. Sensorineural loss 

a. Unilateral 

(1) Viral neuritis of the cochlear branch of cranial nerve VI I 

(2) Acoustic neuroma 

(3) Meniere disease 

(4) Temporal bone fracture 

(5) Autoimmune hearing loss 

(6) Sudden sensorineural hearing loss: idiopathic hearing loss that develops suddenly or over 72 hours 

b. Bilateral 

(1) Ototoxic drug exposure 

(a) Antibiotics (aminoglycosides, erythromycin, vancomycin, antimalarials) 

(b) NSAIDs, ASA 

(c) Loop diuretics (furosemide, ethacrynic acid) 

(d) Chemotherapy 

(2) Exposure to loud noise 

(3) Autoimmune hearing loss 

C. Clinical presentation 

1. Physical examination should include a thorough HEENT examination, including the cranial nerves; these 

patients may have associated deficits of adjacent cranial nerves, particularly V (corneal reflex) and VI I as well 

as tinnitus, vertigo, and dysequilibrium. 

2. Otoscopic examination may help distinguish patients with conductive hearing loss (due to cerumen impaction, 

tympanic membrane perforation, or the presence of middle ear fluid) from those with sensorineural hearing loss. 

3. The Rinne and Weber tests are also useful in distinguishing conductive from sensorineural hearing loss. 

110


a. Rinne test: compares air conduction (AC) versus bone conduction (BC) and is performed by placing the 

base of a vibrating 512-Hz tuning fork against the mastoid process. It must be pushed against the mastoid 

with some force. When the patient can no longer hear the vibration, the tuning fork tips are placed 

adjacent to the external auditory canal of the ear. In patients with normal hearing, the vibrations of the 

tuning fork will still be heard (AC>BC). 

(1) If there is unilateral conductive loss, vibrations will not be heard (BC>AC). 

(2) If there is a unilateral sensorineural loss, test will be normal (AC>BC). 

b. Weber test: performed by placing the base of the vibrating tuning fork against the middle of the forehead, 

again with some force, and asking the patient in which ear the sound is loudest. Normally, it is equal in 

both ears. 

(1) If a unilateral conductive hearing loss is present, vibrations will be heard better in the ear with 

conductive loss. 

(2) If a unilateral sensorineural hearing loss is present, vibration will be heard better in the normal ear. 

c. If bilateral sensorineural hearing loss is present, both the Rinne and Weber tests will be normal despite a 

bilateral decrease in hearing acuity. 


1. CT of the temporal bone should be obtained if fracture is suspected. 

2. MRI with attention to auditory canals should be considered if a tumor is suspected based on the history and 

examination. 

E. Management 

1. Early steroids can save hearing in patients with idiopathic sudden sensorineural hearing loss. Consult with 

ENT and initiate steroids as early as possible. 

2. Cerumen and foreign body impactions should be removed, and infections (otitis media or externa) treated. 

3. Patients with tumors require appropriate ENT or neurosurgical consult. 

4. If an ototoxic drug is the presumed cause of hearing loss, it should be discontinued. 

V. VERTIGO 

A. Definition 

1. A sensation of movement of oneself or the environment 

2. Most commonly described as a feeling of spinning or of being pulled to one side 

B. Epidemiology 

1. Vertigo is either peripheral or central in origin. 

2. Peripheral vertigo accounts for 85 %-90% of cases and is considered less serious prognostically than central 

vertigo, which accounts for 10%-15 % of cases. 

3. Peripheral vertigo arises from diseases of the vestibular apparatus or cranial nerve VIII and is usually self-limited. 

4. Central vertigo originates from diseases of the CNS (brainstem or cerebellum). 

C. Peripheral vertigo 

1. Abrupt onset 

2. Severe intensity 

3. Brief/intermittent duration 

4. Worsening with change in position 

5. Associated symptoms may include nausea and vomiting, diaphoresis, tinnitus, and hearing loss 

6. Nystagmus that is: 

a. Fatigable 

b. Suppressed by visual fixation 

c. Unidirectional: horizontal or horizontorotary (never vertical) 

d. No associated neurologic abnormalities 

D. Central vertigo 

1. Insidious onset 

2. Mild intensity 

3. Prolonged/continuous duration 

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4. Little or no effect with change in position 

5. Associated symptoms may include headache, diplopia, dysarthria, dysphagia, ataxia, facial numbness, and 

hemiparesis. 

6. Nystagmus that is: 

a. Nonfatigable 

b. Not suppressed by visual fixation 

c. Multidirectional (changes direction with changes in position): horizontal, rotary, or vertical 

7. Not usually associated with hearing loss 

VI. TRAUMA 

A. Lacerations of the auricle 

1. Must be repaired carefully to avoid cosmetic defects 

2. Primary goal is to reapproximate the cartilage (with absorbable sutures) and then cover the cartilage with skin. 

B. Hematomas of the auricle 

1. Should be drained and dressed with a compressive dressing that maintains normal ear contours; this will 

prevent formation of "cauliflower ear." 

2. Patients should be started on oral antibiotics with cartilage penetration (eg, quinolones) and reassessed in 24 

hours for reaccumulation of blood, which (if present) will require repeat drainage and dressing replacement. 

C. Frostbite of the auricle 

1. Should be treated by rapid rewarming 

2. Use warm water (40°-42°C) irrigation. 

D. Foreign body in the ear-requires urgent referral to an ENT specialist if: 

1. It cannot be safely removed without damage to the tympanic membrane. 

2. It is expanding organic material (eg, bean). 

3. There is any chance it is a battery. 

E. Perforation of the tympanic membrane 

1. Pathophysiology: a penetrating object, loud noise, infection, lightning strike, or rapid changes in pressure, eg, 

scuba diving accidents 


a. Otoscopic examination usually reveals the tear. Immobility of the tympanic membrane on bulb insufflation 

or autoi nsufflation confirms it. 

b. Acute perforations have irregular borders, sometimes with blood. 

c. Chronic perforations have smooth margins without blood. 

d. Patients with associated symptoms of complete hearing loss, nausea, vomiting, vertigo, or facial palsy 

need immediate ENT referral. These symptoms suggest the presence of concurrent injury to the ossicles, 

labyrinth, or temporal bone. 

3. Management 

a. Most perforations generally heal spontaneously (especially traumatic tears), and follow-up with ENT can be 

on a less-urgent basis. In either case, the ear should be kept dry. 

b. If coexisting otitis media or externa is present, a topical otic antibiotic suspension should be prescribed. 

F. Severe blunt injury to the ear 

1. May be associated with fracture of the temporal bone 

2. May cause hearing loss or facial nerve injury 

3. Evaluation typically involves temporal bone CT 

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EYE EMERGENCIES 

I. CONJUNCTIVITIS 

A. Viral conjunctivitis ("pink eye") 

1. Viruses, particularly adenoviruses, are the most frequent cause of conjunctivitis. 

2. The infection is often unilateral initially but usually spreads quickly (via autoinoculation) to involve both eyes. 

3. Up to 50% of patients have constitutional symptoms or a viral prodromal illness consistent with a viral 

syndrome (fever, rhinorrhea, myalgias, and preauricular adenopathy). 


a. Patients classically present with redness, itching, and tearing (watery discharge). 

b. Typical examination findings include diffuse conjunctiva! injection, a follicular response on the palpebral 

(lid) conjunctiva, a thin watery discharge, and preauricular adenopathy. (Herpes simplex keratitis and 

chlamydia! conjunctivitis can also be associated with follicular conjunctivitis and preauricular adenopathy.) 

c. Unless an associated keratitis is present, the cornea is clear; visual acuity and pupillary reactivity are normal. 

Courtesy of David Effron, MD, FACEP 

5. Infection with adenovirus types 8 and 19 (and others) 

a. Epidemic keratoconjunctivitis (a highly contagious eye infection) 

b. Clinical presentation: itchy irritated eyes - tender preauricular nodes (a few days later) - painful keratitis 

with severe photophobia and decreased visual acuity (1 week later) 

c. Diagnostic evaluation: fluorescein staining of the cornea reveals multiple tiny pinpoint dots. 

6. Management 

a. Antibiotic therapy: because the symptoms and clinical appearance of viral conjunctivitis are usually 

inadequate to distinguish it from bacterial conjunctivitis, most patients are treated with a topical antibiotic. 

b. Meticulous hygiene (frequent hand washing, separate hand linens), especially with epidemic 

keratoconjunctivitis, because patients may be contagious for 2 weeks. 

c. Cool compresses and artificial tears 

d. Consider a topical vasoconstrictor-antihistamine combination for relief of symptoms. 

e. Obtain prompt ophthalmologic consult for patients with evidence of keratitis. 

f. Steroids should be strictly avoided. 

B. Bacterial conjunctivitis 


a. Patients usually present with redness, a gritty sensation (like a foreign body), and discharge. 

b. The discharge is mucopurulent and often results in the eyelids being matted together on awakening. 

c. A Gram stain and culture should be obtained in all cases of neonatal conjunctivitis or whenever Neisseria 

gonorrhoeae conjunctivitis is suspected (see below), or with severe or worsening symptoms despite treatment. 

d. Examination findings include diffuse conjunctiva! injection, mucopurulent discharge, and a clear cornea 

that does not stain with fluorescein dye; visual acuity and pupillary responses are normal. 

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e. Complications of any bacterial conjunctivitis can include corneal involvement such as keratitis, corneal 

ulcer formation, or even corneal perforation. 

f. Contact lens use must be discontinued until infection resolves. Topical quinolones are first-line antibiotics 

in contact lens wearers because of the risk of Pseudomonas infection. 

Courtesy of David Effron, MO, FACEP 

2. Types of bacterial conjunctivitis important for this examination 

a. Staphylococcus aureus, Streptococcus pneumonia, and Haemophilus influenzae conjunctivitis 

(1) Onset is acute. 

(2) The discharge is typically mucopurulent in nature. 

(3) White ulcers may be seen at the limbus ("marginal ulcers") as a result of an allergic reaction to the 

staphylococcal toxin. 

(4) There is no central corneal staining with fluorescein dye and cobalt blue light. 


(a) Topical antibiotics: quinolones, aminoglycosides, or trimethoprim-polymyxin for 5-7 days 

(b) Good hygiene (frequent hand washing, separate hand linens) 

(c) Discontinuation of contact lens wear (Contact lens-related conjunctivitis should be treated with 

an aminoglycoside or quinolone to cover Pseudomonas.) 

(d) Ophthalmologic follow-up in 2-3 days to exclude subsequent corneal involvement 

b. N gonorrhoeae conjunctivitis (an ocular emergency) 

(1) An extremely aggressive form of conjunctivitis that can ulcerate and perforate an intact cornea within 

hours or days 

(2) Most commonly seen in newborns (ophthalmia neonatorum), typically in the first 3 days of life; also 

seen occasionally in sexually active adults 

(3) Incubation period is 2-5 days; onset is hyperacute. 

(4) Discharge is characteristically hyperpurulent and an important diagnostic clue. 

(5) Diagnostic evaluation: culture (obtained with calcium alginate swab of lower conjunctiva and plated 

on sheep blood agar is more sensitive than Gram stain, and should be obtained in all neonatal cases 

and when N gonorrhoeae conjunctivitis is suspected) 


(a) 

Parenteral antibiotic coverage for gonorrhea: IM or IV ceftriaxone 

(b) Oral and topical antibiotic coverage for possible concomitant Chlamydia 

i. Oral erythromycin (newborns and children), oral doxycycline or azithromycin (adults) 

ii. Topical erythromycin 

(c) Frequent ocular irrigation with a saline solution 

(d) Immediate ophthalmology consult and hospital admission 

(e) 

Evaluation and treatment of sexual partners 

C. Chlamydia! (inclusion) conjunctivitis 

1. Leading cause of preventable blindness worldwide 

2. Caused by an obligate intracellular parasite that produces a chronic conjunctivitis with scarring of the cornea 

and underside of the lids (Arlt lines) 

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3. Occurs in newborns (ophthalmia neonatorum), in whom an associated chlamydia! pneumonia may also occur; 

also seen in sexually active adults 

4. Clinical presentation: signs of infection occur 5-14 days after inoculation/birth (compared with only 2-5 days 

with gonorrhea). 

5. Diagnostic evaluation: Gram stain may not be helpful (lack of organisms), but an immunofluorescent antibody 

screen should be positive. 

6. Management 

a. Systemic and topical antibiotic therapy (nearly half of infants will have concomitant chlamydia! nasopharyngitis) 

(1) Oral erythromycin (children and newborns); oral doxycycline or azithromycin (adults), and 

(2) Topical erythromycin 

b. Evaluation and treatment of sexual partners 

D. Vernal conjunctivitis 

1. One of several types of allergic conjunctivitis 

2. Most commonly affects male children; a family history of atopy is common. 

3. A recurrent seasonal inflammation; occurs in the warmer months of the year 

4. Characterized by intense itching, burning photophobia, chemosis (edema of the bulbar conjunctiva), bilateral 

lid edema, cobblestone papillae under the upper lid, and a stringy mucoid discharge 

5. Management 

a. A topical antihistamine preparation (eg, levocabastine) or a topical decongestant/antihistamine 

combination (eg, naphazoline/pheniramine) 

b. A topical mast cell stabilizer (eg, lodoxamide tromethamine or cromolyn sodium) 

c. Cool compresses 

d. If bacterial coinfection is suspected or the cause of the conjunctivitis is unclear, a topical antibiotic agent 

should also be prescribed. 

6. A potential complication is a "shield ulcer" produced from the irritated papillae and discharge; if the ulcer 

becomes infected or scarred, loss of vision may occur. 

II. INFLAMMATORY DISORDERS OF THE EYELIDS AND CORNEA 

A. Anterior blepharitis 

1. A chronic and frequently bilateral inflammation of the I id margins due to a staphylococcal infection and/or 

seborrheic dermatitis; itching and lid margin irritation are common symptoms. 

2. Examination reveals crusty, scaly lid margins that may be erythematous and slightly swollen. 

Courtesy of David Effron, MO, FACE? 

3. Management 

a. Warm compresses and gentle scrubbing of the eyelids and lashes with baby shampoo (to remove debris), 

followed by application of a topical antibiotic ointment (erythromycin or bacitracin) to the eyelid margins 

daily for 4-6 weeks; warm compresses and artificial tears are also helpful. 

b. If seborrheic dermatitis of the scalp and eyebrows is present, it should be treated with selenium sulfide 

shampoo. 

c. Cases resistant to these measures can be treated with oral tetracycline or doxycycline for 2-3 weeks. 

11 5


B. Hordeolum (stye) 

1. An acute infection (usually staphylococcal) of the eyelid margin, involving either the meibomian sebaceous 

glands, Zeis sebaceous glands, or Moll apocrine sweat glands 

2. Clinical presentation: pain, erythema, focal swelling with a tender nodule or pustule on the eyelid margin 

3. Treatment: although styes often point and drain spontaneously, topical antibiotic ointments (bacitracin or 

erythromycin) and hot compresses hasten the process. 

C. Chalazion 

1. A subacute or chronic granulomatous inflammation of a meibomian sebaceous gland in the eyelid 

2. Clinical presentation: a nontender bump in the mid portion of the eyelid (as opposed to the lid margin in 

hordeolum stye) 


3. Treatment 

a. Initial treatment is with a topical antibiotic ointment (bacitracin or erythromycin) and hot compresses. 

b. Persistent or chronic recurrent chalazions often respond to the addition of doxycycline for 2-3 weeks. 

c. Chalazions that persist for several weeks (or months) despite these measures may eventually require 

surgical incision and curettage by an ophthalmologist. 

D. Dacryocystitis 

1. An acute inflammation of the lacrimal sac due to infection or obstruction of the nasolacrimal duct 

2. Most often seen in infants and in adults >40 years old 

3. Etiology: most common causative organism is Staphylococcus aureus, followed by Streptococcus epidermidis, 

Streptococcus spp, and Haemophilus influenzae. 

4. Clinical presentation (be able to identify on pictorial) 

a. Patients present with epiphora (overflow of tears onto the face) and an acute, unilateral, painful, red 

swelling below the medial canthus (location of the lacrimal sac). 

b. Digital pressure applied over this area may result in expression of purulent material from the puncta. 


5. Management 

a. Broad-spectrum oral antibiotics (eg, amoxicillin-clavulanate), topical ophthalmic antibiotics, warm compresses, 

gentle massage of the lacrimal sac (to empty stagnant tear accumulation), and ophthalmologic referral 

b. Signs of systemic illness may require admission. 

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E. Corneal ulcers (a true ocular emergency) 


a. Patients present with pain, foreign body sensation, photophobia, and tearing. 

b. Examination reveals conjunctiva! hyperemia, lid edema, and a localized whitish corneal infiltrate that has 

a staining epithelial defect; may also be associated with a hypopyon (accumulation of WBCs in the anterior 

chamber). 

c. Signs of iritis (eg, miosis, cells, and flare in the anterior chamber on slit-lamp examination) may also be 

present. 

2. Etiology 


a. Often seen in patients who use soft contact lenses 

b. The most common pathogen is Pseudomonas; Staphylococcus and Streptococcus are also common. 

c. Ulceration may lead to corneal melting and perforation. (Pseudomonas is particularly virulent, able to 

destroy the cornea in :::::24 hours). 

3. Management 

a. Immediate ophthalmology consult for culture and treatment 

b. Hospital admission is rarely needed, unless the patient is a neonate or there is extensive corneal involvement. 

c. Topical broad-spectrum antibiotics (quinolones such as ciprofloxacin, gatifloxacin, moxifloxacin, or 

ofloxacin every 30-60 minutes) or topical fortified antibiotics (cefazolin plus gentamycin) 

d. A topical cycloplegic (cyclopentolate) for associated iritis and ciliary spasm to control pain 

e. Discontinuation of contact lens use; no patch 

F. Herpes simplex keratitis 

1. May be the result of primary or recurrent infection with the herpes simplex virus (usually type I). 

2. Skin and mucocutaneous lesions are more common in primary infections, whereas corneal involvement 

(keratitis) is more common in recurrent infections. 


a. Patients present with ocular pain, a foreign body sensation, photophobia, and tearing. 

b. Visual acuity may be reduced. 

c. Examination reveals a diffusely reddened eye, decreased corneal sensation, and preauricular adenopathy. 


a. Slit lamp evaluation of the unstained cornea may reveal localized corneal haziness. 

b. Fluorescein staining usually demonstrates the classic dendritic (branching) pattern over the cornea in wellestablished, 

recurrent infections; however, in primary infections and early on in recurrent infections, only a 

superficial punctate keratitis may be seen. 

117


Courtesy of Dr. Thomas Steinemann 

Herpes simplex virus keratitis ghost dendrite 

5. Management 

a. Prompt ophthalmology consult regarding specific treatment recommendations and follow-up is mandatory; 

these infections are aggressive and may lead to corneal destruction resulting in permanent disability. 

b. A topical antiviral agent (eg, trifluridine or vidarabine) or oral antiviral agent (eg, acyclovir, valacyclovir, 

or famciclovir) 

c. A topical cycloplegic (eg, cyclopentolate or homatropine) for pain relief from ciliary muscle spasm if an 

associated iritis is present 

d. Although topical steroids are occasionally prescribed by ophthalmologists for patients with refractory or 

advanced stromal keratitis, they can promote rapid progression of the corneal epithelial infection and are 

contraindicated in all other forms of herpetic keratoconjunctivitis; they should not be prescribed by the 

emergency physician. 

G. Herpes zoster ophthalmicus 

1. Results from reactivation of latent varicella zoster virus in the trigeminal ganglion 


a. Patients present with pain, paresthesias, tearing, and a unilateral vesicular eruption in the dermatome 

supplied by the ophthalmic branch (V1) of the trigeminal nerve (cranial nerve V). 

b. Ocular involvement can range from conjunctivitis to iritis, keratitis, corneal anesthesia, or ocular muscle 

palsies; lesions on the tip of the nose (Hutchinson sign) signal nasociliary nerve involvement and a very 

high likelihood of ocular lesions. 


3. Management 

a. Immediate ophthalmology consult 

b. Oral acyclovir, valacyclovir, or famciclovir 

c. A topical broad-spectrum antibiotic to prevent secondary infection 

d. A topical cycloplegic agent and a topical steroid (in consultation with an ophthalmologist) if iritis is present 

e. Oral analgesics as needed 

118


H. Ultraviolet keratitis 

1. Prolonged ultraviolet radiation exposure can cause damage to the corneal epithelium. 

2. Typical sources of ultraviolet radiation 

a. Arc welding (welders' keratitis/flash) 

b. Reflected sunlight, especially at high altitude (snow blindness) 

c. Artificial sunlight (tanning booths, sun lamps) 


a. Symptoms develop 6-8 hours after exposure and include severe pain, photophobia, a foreign body 

sensation, tearing, and blepharospasm. 

b. There is decreased visual acuity, conjunctiva! injection, and a diffuse punctate keratopathy (multiple 

pinpoint fluorescein-stained dots on the corneal surface seen with cobalt blue light). 


Severe ultraviolet keratitis 

4. Management 

a. A topical cycloplegic agent (eg, cyclopentolate or homatropine) for pain control 

b. A topical broad-spectrum antibiotic ointment 

c. Oral analgesic 

d. Topical anesthetics are contraindicated in all cases of keratitis, because they can inhibit corneal healing 

and lead to corneal ulceration. 

e. Follow-up with ophthalmology in 24 hours 

Ill. PERIORBITAL AND ORBITAL CELLULITIS 

A. Periorbital (preseptal) cellulitis 

1. An infection confined to superficial tissues that are anterior to the orbital septum (the fascia I layer that acts as a 

partition separating the eyelids from the orbit) 

2. More common and generally less serious than orbital cellulitis 

3. Children (particularly those




a. Laboratory studies 

(1) Blood cultures 

(2) CT of the orbits (thin cuts with coronal reconstruction) if orbital cellulitis cannot be definitively 

excluded by clinical evaluation 

b. Soft-tissue aspirates for Gram stain and culture are no longer recommended because of risk of septum 

perforation with subsequent risk of deeper infection. 

7. Management 

a. A broad-spectrum antibiotic that covers streptococci and staphylococci; older children and adults with 

early/mild periorbital cellulitis can be treated on an outpatient basis with an oral antibiotic (eg, amoxicillinclavulanate) 

and follow-up in 24 hours. 

b. Adults with more advanced infections and children 20 mm Hg with vision loss, surgical treatment might be necessary in 

addition to medications to decrease intraocular pressure. 

7. Management 

a. Hospital admission 

b. Broad-spectrum IV antibiotic covering S aureus, S pneumoniae, H influenzae, and methicillin-resistant 5 aureus 

120


c. Ocular antihypertensives (eg, acetazolamide, timolol) if intraocular pressure >20 mmHg 

d. Immediate ophthalmology/ENT consults 

e. Canthotomy and cantholysis if strong evidence of orbital compartment syndrome 

8. Complications 

a. Visual loss 

b. Cavernous sinus thrombosis 

c. CNS involvement 

d. Osteomyelitis 

IV. ACUTE EYE PAIN (ASSOCIATED DECREASE IN VISUAL ACUITY) 

A. Acute iritis (acute anterior uveitis) 

1. Classic clinical scenario 

a. The patient presents with a painful red eye, severe photophobia, and blurring of vision. He or she often 

has a prior history of iritis or similar undiagnosed pain. Generally, only one eye is affected, and symptoms 

develop over time. 

b. Physical examination reveals a constricted and sometimes irregular pupil, a ciliary flush 

(diffuse reddening of the sclera at the limbus), and a decrease in visual acuity. 


c. The intraocular pressure is variable; it is often decreased (due to paralysis of ciliary body function) 

but may be normal or increased (due to inadequate aqueous drainage). Slit-lamp examination is 

diagnostic and reveals flare (protein) and cells (leukocytes) in the anterior chamber. Keratitic 

precipitates (an accumulation of WBCs on the endothelial surface of the cornea) may also be seen. 


lritis with keratitic precipitates 

121



a. Presence of consensual photophobia (the photophobia produced by iritis is both direct and consensual) 

b. Presence of pain unrelieved by diagnostic application of a topical anesthetic agent; unlike the superficial 

pain associated with a corneal abrasion that is readily relieved by the diagnostic application of a topical 

anesthetic agent, the deep-seated ache of iritis is not. 

3. Etiology 

a. Trauma (occurs 1-4 days after trauma) 

b. Seronegative arthritides (idiopathic ankylosing spondylitis, Reiter syndrome, etc) 

c. Inflammatory bowel disease 

d. Chronic granulomatous conditions (tuberculosis, sarcoidosis, etc) 

e. Local infection/ulcers 

f. Sexually transmitted diseases (syphilis, gonorrhea) 

g. Corneal abrasions and foreign bodies 

h. Idiopathic 

4. Treatment 

a. A long-acting topical cycloplegic (eg, cyclopentolate or homatropine) to provide comfort (by eliminating 

ciliary spasm) and prevent formation of posterior synechiae (adhesions between the iris and lens) 

b. A topical steroid such as prednisolone acetate 1 % to relieve inflammation; consult with an 

ophthalmologist first, and arrange follow-up in 24 hours. 

5. Complications: if the pupil is not dilated, iritis may result in formation of posterior synechiae; these adhesions 

produce permanent pupillary disfigurement and can lead to secondary glaucoma. 

B. Acute angle closure glaucoma (an ocular emergency) 


a. Occurs in patients with shallow (narrow) anterior chamber angles. Narrowing of this angle (either 

congenital or as a result of aging) results in closer contact between the iris and lens, producing resistance 

to flow of aqueous humor from the posterior to the anterior chamber (a relative pupillary block). When 

the angle closes completely, flow of the aqueous humor is prevented and the intraocular pressure 

increases abruptly. 

b. This condition is precipitated by stress or pupillary dilation by medications (parasympatholytics, 

sympathomimetics or anticholinergics), inadvertent administration of a topical cycloplegic in a patient 

with a shallow anterior chamber, or more commonly by moving from daylight to a darkened room. 

c. This is predominantly a condition of the elderly, is more common in farsighted (hyperopic) individuals 

and in women, and typically occurs abruptly in patients with no previous history of glaucoma. 


a. History: nausea/vomiting, pain (either localized to the eye/eyebrow or generalized as headache pain), 

blurred vision, halos around lights (due to corneal edema), and (occasionally) abdominal pain 

b. Physical examination 

(1) Decreased visual acuity 

(2) A shallow anterior chamber (causing a broad eclipse sign using an oblique flashlight) 

(3) A red, congested-looking eye with a fixed, mid-dilated, nonreactive pupil, a hazy cornea and ciliary 

(perilimbal) injection 

(4) Rock-hard consistency of the globe on gentle palpation 

(5) lntraocular pressure >40 mmHg (normal range 0-20 mmHg) 


122


3. Management 

a. Have the patient lie completely supine (gravity may allow the lens to pull away from the iris). 

b. Pharmacologic therapy consists of the sequential administration of several different agents (which act by 

various means) to decrease the intraocular pressure. 

(1) Topical ~-blockers (eg, timolol), topical a-agonists (eg, apraclonidine), and oral or IV carbonic 

anhydrase inhibitors (acetazolamide) decrease the secretion of aqueous humor by the ciliary body. 

(2) Topical steroids (eg, prednisolone 1 %) reduce inflammation. 

(3) Hyperosmotic agents (eg, mannitol) decrease the volume of fluid in the eye and rapidly lower 

intraocular pressure (check hourly). Note that osmotic diuretics have the greatest potential for 

serious adverse effects, especially in the setting of cardiovascular or renal disease. 

(4) Topical miotics (eg, pilocarpine) pull the iris back from its anterior position, thereby reopening the 

angle and allowing egress of aqueous humor; they do not usually have an effect until the intraocular 

pressure is 90 minutes 

usually results in permanent visual loss. 

123


b. Goal is to restore retinal artery blood flow by dislodging the clot, dilating the artery, and lowering 

intraocular pressure. 

c. Management 

(1) Intermittent digital massage of globe (5 seconds on, 5 seconds off) for 5-15 minutes 

(2) Acetazolamide 500 mg IV and a topical ~-blocker (timolol 0.5%) to reduce intraocular pressure 

(3) Hyperbaric oxygen therapy may be beneficial if readily available. 

(4) Immediate ophthalmology consult for paracentesis of the anterior chamber 

(5) Evaluate (and treat) for associated disease processes. 

B. Central retinal vein occlusion 


a. The patient complains of a sudden, painless, monocular decrease in vision. The visual loss is usually noted 

on awakening and is due to thrombosis of the central retinal vein. 

b. The pupil reacts sluggishly to light, and the funduscopic examination reveals retinal hemorrhages and 

tortuous retinal veins ("blood and thunder fundus"). Edema of the disc may also be present. The degree of 

visual loss is variable but is typically less severe than that which occurs in association with central retinal 

artery occlusion. 


2. Risk factors 

a. Hypertension 

b. Diabetes mellitus 

C. Arteriosclerosis 

d. Chronic glaucoma 

e. Vasculitis 

3. Management 

a. No immediate treatment is effective. 

b. Ophthalmology follow-up is required for confirmation of the diagnosis and ongoing monitoring for 

development of complications. 

c. Identify and treat contributing factors. 

d. Aspirin is often recommended but not proved to be beneficial. 


a. Neovascularization of the retina and/or iris 

b. Neovascular glaucoma 

C. Optic neuritis 

1. An inflammatory process and focal demyelination of the optic nerve; typically monocular in adults and 

binocular in children; more common in women than men 

2. Characterized by reduction of central vision with preservation of peripheral vision; visual loss ranges from 

mild to severe (finger counting to light perception). 

3. Most cases of optic neuritis are retrobulbar and do not have changes in the optic disc. 

4. Classic clinical scenario: The patient is usually 15-45 years old and presents with a rapidly progressive (hours 

to days) reduction or blurring of vision in association with ocular pain that is worsened by eye movement. 


124


a. The presence of a Marcus-Gunn pupil (afferent pupillary defect), red vision desaturation (the color red is 

perceived as less intense in the affected eye), and a central visual field defect confirms optic pathology. 

b. The disc may be normal (retrobulbar optic neuritis) or swollen and hyperemic (papillitis). 

c. Remainder of the eye examination is normal. 


6. A clear association with multiple sclerosis exists; approximately one-third of these patients go on to develop 

multiple sclerosis in the ensuing years. MRI of the orbit and brain is both sensitive and specific for optic 

nerve inflammation and may also show demyelination in the brain. 

7. Management 

a. Emergent ophthalmology consult 

b. Admission for IV steroids (eg, methylprednisolone) for 3 days, followed by oral steroids for 11 days. Use 

of oral steroids initially is controversial and may increase the risk of recurrence of optic neuritis. 

D. Eclipse burn (solar retinopathy) 

1. Caused by prolonged or accidental viewing of the sun, which leads to permanent central retinal (macular) 

loss of vision. 

2. Visual acuity is decreased, and funduscopic examination demonstrates discrete retinal disruption in the 

macular area. 


Solar maculopathy 

Courtesy of Dr. Rishi P Singh 

Solar retinopathy 

3. No treatment is effective; the patient should be referred to an ophthalmologist. 

125


E. Retinal detachment (an ocular emergency} 

1. Involves a separation of the inner neuronal retina from the outer retinal pigment epithelial layer, usually as 

the result of a tear in the retina from vitreous traction. 

2. Painless and usually seen in patients with one or more risk factors 

a. Severe myopia 

b. Older age 

c. Trauma 

d. Previous cataract surgery 

e. An inherited connective tissue disorder (eg, Marfan syndrome) 

f. Diabetes mellitus 

g. A family history of retinal detachment 


a. Early symptoms are flashing lights (as the retina begins to tear) and the presence of "spider webs" or 

"coal dust" across the visual field (small vitreous hemorrhages). As the retina detaches, the patient 

experiences a sensation of a curtain that is gradually lowering or raising in front of the affected eye. 

Visual acuity may or may not be affected, depending on the size or involvement of the macula. 

b. Examination with a direct ophthalmoscope may reveal an undulating, dull gray, detached, or even "out 

of focus" retina. Direct funduscopy is not sensitive enough to exclude retinal detachment and should 

be suspected based on clinical symptoms. The tear itself often originates in the retinal periphery and 

can be seen with the indirect ophthalmoscope. Bedside ultrasound (linear probe) may be useful in the 



4. As long as the macula remains attached, the probability of preserving central retinal vision is very good. 

5. Management 

a. Immediate ophthalmology consult for evaluation and retinal attachment surgery is indicated. 

b. The patient should avoid vigorous activity and preferably remain at bed rest until evaluated by the 

ophthalmologist. 

~ VltraoushemoIThage 

1. A common cause of sudden, painless, unilateral loss of vision 


a. Greatest risk factor is proliferative diabetic retinopathy 

b. Posterior vitreous detachment and retinal vessel occlusion occur most commonly in older patients. 

c. Other risks include sickle cell disease, trauma, tumors, arterial microaneurysms, branch vein occlusion, 

and macular degeneration. 


a. If hemorrhage is preceded by retinal detachment, the patient may experience flashes of light (photopsias). 

Otherwise, unilateral painless vision loss occurs (often described as haze, shadows, cobwebs, or smoke). 

b. On examination, the red reflex is diminished or absent (may have appearance of a red haze or a black 

reflex), and the fundal view is hazy. Visual acuity may or may not be affected. An afferent pupillary defect 

suggests a retinal detachment in addition to hemorrhage. 

126



4. Management 


b. Bedrest with elevation of the head of the bed 

c. Some patients may benefit from surgery (photocoagulation, cryotherapy, vitrectomy). 

G. Functional blindness 


a. Unilateral or bilateral blindness in the presence of normal pupillary reactions, a normal funduscopic 

examination, and lack of an afferent pupillary defect is very suggestive of a functional problem (hysteria/ 

conversion disorder or malingering). 

b. An intact visual pathway can be confirmed with use of an optokinetic drum or strip, which will elicit 

optokinetic nystagmus. 

c. Despite the serious nature of their complaint, hysterical patients are often remarkably calm. Malingerers, 

on the other hand, are usually overly emotional and less cooperative. 

2. Management: ophthalmologic and psychiatric referrals 

H. Temporal (giant cell) arteritis 

1. A vasculitis of medium and large arteries that can cause optic nerve infarction and permanent visual loss 

(see also page 123); it is notorious for involving the optic nerve within hours or weeks. For unknown reasons, 

incidence appears to be rising. 


a. Patients usually present with a unilateral headache. Sudden monocular loss of vision may also be a 

presenting symptom. Eye pain is not typical. Preceding symptoms may include jaw pain (claudication), 

weight loss, and malaise. Up to 50% of these patients have polymyalgia rheumatica (a syndrome of 

aching, pain, and stiffness in the proximal muscles, especially neck and shoulders); some patients may 

have associated neurologic symptoms that simulate a transient ischemic attack or stroke. 

b. Patients are more commonly women, and most patients are ::0:50 years old. 

c. Examination can reveal scalp tenderness, temporal arteries that are tender and tortuous (and sometimes 

pulseless), visual loss, and an afferent pupillary defect. Funduscopic examination may be normal or show 

dilated retinal veins. 

d. Diagnosis is suggested by an increased sedimentation rate (>50 mm/hr). Sedimentation rate increases 

with age; a simple rule of thumb for estimating the upper range of "normal" for patients >50 years old is 

age/2 for men and (age + 10)/2 for women. 

e. Diagnosis is confirmed by temporal artery biopsy (although treatment should not be delayed awaiting 

biopsy). 

3. Management 


b. Administration of high-dose steroids (eg, 60 mg oral prednisone) 

VI. NONACUTE VISUAL LOSS 

A. Primary open angle glaucoma 

1. Most common type of glaucoma and a major cause of slowly progressive blindness in the United States 

2. A painless condition of chronically increased intraocular pressure that ultimately damages the optic nerve; 

frequently bilateral with strong familial tendency 

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a. Normal appearing cornea and pupil 

b. Increased intraocular pressure (>21 mmHg) 

c. Increased optic nerve cup/disc ratio (>0.4) 

d. Arcuate scotomas 

e. Gradual loss of peripheral vision with sparing of central vision 

4. Management 

a. Unlike acute angle closure glaucoma, open angle glaucoma is a chronic, painless, nonemergent condition 

that does not generally present to the emergency department. 

b. Patients should be referred to an ophthalmologist for evaluation and treatment. 

c. Treatment: topical agents that decrease intraocular pressure by reducing the production of aqueous 

humor (carbonic anhydrase inhibitors, ~-blockers, and a 2 

-agonists) and/or increasing aqueous outflow 

(prostaglandin agonists, sympathomimetics) 

B. Cytomegalovirus (CMV) retinitis 

1. A necrotizing retinitis that, if untreated, results in progressive visual loss 

2. Occurs in immunocompromised patients, most notably those with advanced AIDS 


a. Although patients can be asymptomatic early on, they typically present with scintillating scotomas, visual 

distortions, and visual loss. 

b. Funduscopic examination reveals fluffy white retinal lesions that are usually perivascular in location and 

associated with hemorrhage (the characteristic "pizza pie" or "cheese and ketchup" fundus). 

c. Ophthalmic screening is recommended if the CD4 count is


b. Irrigation should be followed by: 

(1) A complete eye examination (including visual acuity and measurement of intraocular pressure, 

which requires treatment if increased) 

(2) Instillation of a topical cycloplegic (eg, cyclopentolate or homatropine) and an antibiotic ointment 

(eg, bacitracin, erythromycin) 

(3) Use of a nonpreserved lubricant may prevent symblepharon (adhesion of lid to conjunctiva). 

(4) Administration of oral analgesics as needed 

(5) Ophthalmology referral for follow-up in 24 hours 

(6) Severe burns, particularly those due to alkalis, require immediate ophthalmology consult, discussion 

of additional treatment measures (eg, topical steroids), and hospital admission. 

B. Lid lacerations 

1. Once injury to the underlying globe has been excluded, superficial lacerations can be repaired with 6-0 or 

7-0 nonabsorbable suture. 

2. Lacerations in the following anatomically high-risk areas require referral for repair: 

a. Lacrimal canaliculi (lacerations of the lid margin that lie medial to the lacrimal puncta) 

b. Levator muscle/tendon (deep horizontal lacerations of the upper lid): the presence of ptosis is suggestive. 

c. Canthal tendons (penetrating wounds that transect the lateral or medial canthi) 

d. Orbital septum (deep horizontal lacerations of the upper lid): protrusion of fat into the laceration 

confirms septal perforation. 

e. Lid margins and lid lacerations with extensive tissue loss 

C. Corneal injuries 

1. Corneal abrasions 

a. Clinical presentation 

(1) Patients complain of pain, foreign body sensation, tearing, and photophobia. 

(2) Conjunctiva! injection is frequently present; visual acuity may be decreased if the abrasion is large or 

centrally located. 

b. Diagnostic evaluation 

(1) Instillation of a topical anesthetic agent provides temporary pain relief and permits a better 

examination. (Although topical anesthetic agents are useful diagnostically, they should never be 

prescribed for pain on an outpatient basis; corneal toxicity and retardation of epithelial regrowth 

occur with repetitive use.) 

(2) Always evert the lids to look for entrapped conjunctiva! foreign bodies; multiple fine linear abrasions 

of the corneal surface ("ice rink sign") are highly suggestive of a foreign body trapped under the 

upper lid. 

(3) Examination using a cobalt blue light source (slit lamp or Wood's light) with fluorescein staining 

reveals the abraded area, which appears bright green. 

c. Management 

(1) A cycloplegic agent (eg, cyclopentolate or homatropine) to relieve ciliary spasm and reduce pain 

(2) A topical antibiotic to prevent secondary infection; use an agent with gram-negative coverage 

(a topical quinolone [eg, ciprofloxacin, ofloxacin] or a topical aminoglycoside [eg, tobramycin, 

gentamicinl) for abrasions associated with soft contact lens use. 

(3) Contact lens users should be instructed to refrain from contact lens use until symptoms resolve. 

(4) Eye patching 

(a) Does not appear to facilitate healing (or provide comfort) and can have detrimental effects, 

especially if the injury was caused by vegetable matter or the patient wears contact lenses. 

(b) Should clearly be avoided in corneal abrasions due to prolonged contact lens use. These 

abrasions are associated with an increased incidence of gram-negative bacterial infections 

(particularly Pseudomonas) and ulceration. The warm, dark, and relatively hypoxic environment 

created by patching may further predispose these abrasions to infection. 

(5) Oral analgesics are seldom needed if the eye is adequately treated with a cycloplegic agent (eg, 

cyclopentolate or homoatropine; however, if the patient cannot be redosed with a cycloplegic, then 

oral analgesia will become necessary. 

(6) Ophthalmology referral for reevaluation in 24-36 hours 

129


2. Corneal foreign bodies and rust rings 

a. Clinical presentation: corneal foreign bodies containing iron produce a rust ring that is irritating and can 

be difficult to remove. 

b. Management (Note that rust ring removal is never a true eye emergency and can be deferred to a 

specialist if the physician does not have access to the correct equipment or is not familiar with its use.) 

(1) Apply a topical anesthetic agent, and then remove the rust ring with a commercial burr drill or a 

sterile 25-gauge needle under slit-lamp magnification. 

(2) The burr drill is preferred, because the removal can be accomplished more quickly and easily with 

this instrument. 

(3) Once the foreign body or rust ring has been removed, apply a topical broad-spectrum antibiotic 

(eg, erythromycin, polymixin-trimethoprim, tobramycin, ciprofloxacin, ofloxacin) and a cycloplegic 

agent (eg, cyclopentolate or homatropine); refer to an ophthalmologist for reevaluation in 24-48 

hours. 

(4) If the rust ring cannot be easily removed, treat as above and refer to an ophthalmologist for removal 

the next day. 

3. Corneoscleral lacerations and perforations 

a. Because of Bell phenomenon (eyeball rolling upward and outward in response to eye closure), they are 

commonly located in the inferior aspect of the globe. 

b. Clinical presentation 

(1) Teardrop or irregularly shaped pupil 

(2) Flattening of the anterior chamber 

(3) Small fragments of black (iris) pigment at the wound edges (uveal prolapse) 

c. Diagnostic evaluation 

(1) Examination with the cobalt blue light source of the slit-lamp with fluorescein staining will mark the 

area of suspected aqueous leak. 

(2) The efflux of aqueous humor will cause the fluorescein to flow from the laceration in a "riverlike" 

pattern (positive Seidel test), which is diagnostic if present. 

d. CT of the orbits with thin sections (cuts of 1-2 mm) and coronal reconstruction may confirm the 

presence of a foreign body. Bedside ocular ultrasound is contraindicated if globe rupture is suspected. 

e. Management 

(1) Do not put any pressure on the globe (not even an intraocular check with a tonopen or Schiotz 

tonometer). 

(2) Apply a rigid metal eye shield (not a patch) to protect the eye from any inward pressure. 

(3) Keep patient nothing per os (because many will need repair in the operating room). 

(4) Provide tetanus prophylaxis as needed. 

(5) Administer 

(a) Prophylactic IV broad-spectrum antibiotics (to cover Staphylococcus and Streptococcus) to 

prevent endophthalmitis 

(b) Prophylactic antiemetics 

(c) Analgesics as needed 

(d) Update tetanus immunization 

(6) Obtain immediate ophthalmology consult. 

D. Ruptured globe 


a. Teardrop or irregularly shaped pupil 

b. Hemorrhagic chemosis 

c. Decrease in visual acuity 

d. Distorted anterior chamber 

e. Uveal prolapse 

f. Vitreous hemorrhage 

g. Positive Seidel test 

2. Management: same as that for corneoscleral lacerations and punctures (see above) 

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E. Hyphema 

1. Blunt ocular injury may cause bleeding into the anterior chamber (hyphema). The bleeding originates from 

the blood vessels of the ciliary body or iris. 


a. Although some patients with small hyphemas are asymptomatic, most complain of blurred vision, dull eye 

pain, and photophobia. 

b. Hyphemas are graded according to the percentage of blood in the anterior chamber. 

Grade 0: microscopic 

Grade 1: layered blood 30 

mmHg in a normal patient or >24 mmHg in a sickle cell patient. Avoid carbonic anhydrase inhibitors in 

sickle cell patients; they can cause RBCs to sickle in the anterior chamber, which clogs the trabecular 

meshwork and further increases intraocular pressure. 

g. Immediate ophthalmology consult 

h. Administration of other medications (mydriatics, cycloplegics, steroids, and antifibrinolytics) and the 

need for hospitalization should be decided in consultation with the ophthalmologist. 

(1) A cycloplegic/mydriatic agent is often used to dilate the pupil and avoid "pupillary play" (pupil size 

fluctuations due to changing ambient lighting) so as not to stretch the leaking blood vessel. 

(2) Steroids and antifibrinolytics may prevent rebleeding. Surgical evacuation may be necessary with 

large (grade IV) hyphemas. 


a. Rebleeding-usually occurs 2-5 days after the initial bleed (when clots begin to lyse) and is the most 

common complication; it can cause an abrupt and sight-threatening rise in intraocular pressure. 

b. Blood staining of the corneal epithelium 

c. Secondary glaucoma: intraocular hypertension is seen more commonly in sickling hemoglobinopathies 

(sickle cell disease, thalassemia) and should be treated initially with topical ~-blockers, avoiding carbonic 

anhydrase inhibitors. 

d. Anterior and posterior synechia formation 

F. Lens subluxation and dislocation 

1. Usually caused by blunt trauma to the globe but can occur spontaneously or with trivial trauma in patients 

with Marfan syndrome, homocystinuria, tertiary syphilis, and rheumatoid arthritis 

2. Lens subluxation produces visual distortion and monocular diplopia, which persists despite covering the 

other eye (as opposed to binocular diplopia, which can be corrected by covering either eye). 

3. Lens dislocation causes severe blurring of vision. 

4. The lens may dislocate either anteriorly into the anterior chamber or posteriorly into the vitreous cavity. 

a. Anterior dislocations can produce acute angle closure glaucoma by mechanically blocking the egress of 

aqueous humor. 

b. Posterior dislocations produce iridodonesis (a quivering of the iris after rapid eye movement). 

5. With subluxations, the edge of the lens will be seen on slit-lamp examination when the pupil is dilated. 

131


6. Management 

a. Obtain immediate ophthalmology consult. 

b. Anterior dislocations require immediate repositioning or removal of the lens. 

c. Posterior dislocations are handled more conservatively, often only with refractive correction. 

G. Blowout fractures of the orbit 

1. Etiology 

a. Blunt trauma to the eye transmits hydraulic forces throughout the globe. The floor and medial wall of the 

orbit are most susceptible to blowout fractures. 

b. Orbital floor fractures (see below) can entrap the inferior rectus and inferior oblique muscles as well as 

fat; contusion or laceration of the infraorbital nerve may also occur. Fractures of the medial wall of the 

orbit (less common; see also page 148) can entrap the medial rectus muscle. 

2. Clinical presentation of orbital floor fractures 

a. Enophthalmos (posterior displacement of the eyeball causing slight ptosis) 

b. lnfraorbital nerve distribution anesthesia 

c. Subcutaneous orbital emphysema (suggests a medial wall fracture with ethmoid sinus disruption) 

d. Be sure to perform a careful eye examination in these patients, because up to one in four will have 

concomitant injuries to the globe. 

e. Pain and diplopia on upward gaze occur secondary to limitation of upward gaze, which indicates 

muscular entrapment and is a true emergency. 

3. Diagnostic evaluation: CT scanning is the standard of care. 

4. Management 

a. Exclude entrapment. 

b. Although symptoms of fracture without entrapment usually resolve with conservative management, 

ophthalmology consult is still indicated to exclude associated injuries to the globe. 

c. Broad-spectrum prophylactic antibiotics and decongestants should be considered for those patients 

with sinus fractures, especially with evidence or suspicion of sinusitis. Patients with subcutaneous 

emphysema should be given nasal precautions (eg, no nose blowing, sneeze with mouth open, no Valsalva 

maneuvers). 

H. Retrobulbar hematoma (an ocular emergency) 

1. Etiology: extreme blunt or deep penetrating trauma to the eye produces orbital hemorrhage with 

accumulation of blood behind the globe. 


a. Exophthalmos (forward displacement of the eyeball)-may be severe 

b. Decreased visual acuity 

c. Eye pain 

d. Limited mobility of the globe 

e. Increased intraocular pressure 

f. Afferent pupillary defect (or Marcus-Gunn pupil) 

3. Diagnostic evaluation: CT of the orbit will demonstrate the hematoma. 

4. Management 

a. Immediate ophthalmology consult for emergent decompression via a lateral canthotomy, cantholysis, and 

anterior chamber paracentesis. 

b. lntraocular hypertension can be treated with topical ~-blocker as well as IV carbonic anhydrase inhibitor 

and mannitol. 

I. lntraocular foreign body 

1. Clinical presentation and history 

a. Work that involves pounding metal on metal or using a grinding wheel 

b. Physical examination clue is an irregular pupil that is usually peaked toward the site of penetration. 

c. Onset of symptoms may be delayed (c':24 hours) 

(1) Reduced visual acuity 

(2) Dull, unlocalized ocular pain 

132



a. Radiographic confirmation and localization of the penetrating foreign body is indicated, because these 

foreign bodies may need to be surgically removed. 

b. Plain radiographs of the orbit may demonstrate the foreign body. 

c. CT of the orbits (1-2 mm cuts with coronal reconstructions) are very helpful in the precise localization of 

intraocular foreign bodies (or associated air). 

d. MRI also provides accurate localization but is not as readily available and is contraindicated if potentially 

any metallic objects (could dislodge them). 

e. Although bedside ocular ultrasound may also identify intraocular foreign bodies, it is contraindicated if 

globe rupture is suspected. 

3. Management 

a. Perform a Seidel test to see if an aqueous leak from the site of penetration is present. Do not attempt to 

check intraocular pressure if penetration of the globe is suspected. 

b. Place a metal shield over the eye, administer a broad-spectrum antibiotic IV, and provide tetanus 

prophylaxis as needed. 

c. Obtain an immediate ophthalmology consult for the decision to remove (or not) an intraocular foreign 

body, which is based on the composition/reactivity of the object as well as on its location in the eye. 

(1) Wood, vegetable matter, and metals (eg, iron, copper, and steel) typically incite an intense 

inflammatory reaction when left in the eye. BBs and pellets are also poorly tolerated, because they 

are composed of iron as well as lead. Emergent surgical extraction is indicated. 

(2) Inert foreign bodies (eg, glass, lead, plaster, rubber, silver, stone) that are minimally symptomatic 

may be treated with a nonoperative approach. However, many inert foreign bodies can cause toxicity 

by virtue of a coating or chemical additive, which may influence management decisions. 

J. Traumatic iritis/iridocyclitis 


a. The patient has blunt ocular trauma. Onset of symptoms (aching pain, photophobia, and reduced visual 

acuity) usually begin 1-4 days after injury. The pupil is constricted, and a deep ciliary flush is usually 

present. 

b. Slit-lamp examination reveals cells and flare in the anterior chamber. 

2. Management 

a. A cycloplegic agent (eg, cyclopentolate or homatropine) 

b. A topical steroid (only in consult with an ophthalmologist) 

c. Ophthalmology referral 

K. Traumatic miosis and mydriasis 

1. Blunt ocular trauma can produce 

a. Bruising and irritation of the iris sphincter___,. constriction and spasm of the pupil (miosis), while 

b. Tears in the iris sphincter muscle fibers ___,. loss of constriction ability ___,. dilation (mydriasis) 

2. These defects may resolve spontaneously over days to weeks or, in the case of actual iris sphincter muscle 

fiber damage, may become permanent. 

3. Management 

a. No acute treatment is indicated, unless hyphema is present. 

b. Referral to an ophthalmologist for follow-up 

VIII. ANISOCORIA 

A. Clinical presentation 

1. Normal finding: simple physiologic anisocoria (unequal pupil size; usually :Sl mm difference) is seen in up to 

20% of the population. 

2. lntracranial third nerve palsy secondary to an expanding supratentorial mass/bleed or a posterior 

communicating artery aneurysm (absence of an isolated third nerve palsy does not exclude an aneurysm); look 

for ptosis, diplopia from extraocular muscle dysfunction with "down and out" position of involved eye. 

3. Prior eye surgery 

4. Traumatic miosis or mydriasis 

133


5. Uniocular drug exposure: pilocarpine 1 % will constrict a pupil that has been dilated from a third nerve palsy 

but not from anticholinergic agent exposure. 

6. Adie tonic pupil: benign condition primarily affecting women 20-40 years old who often present with blurred 

vision 

a. Blurred near vision but normal vision at distance 

b. Diminished deep tendon reflexes 

c. Sector palsies of iris on slit-lamp examination 

d. Slow constriction with accommodation 

e. Strong constriction to cholinergic drop (pilocarpine 0.1%) 

7. Horner syndrome: due to loss of sympathetic innervation 

a. Look for ptosis, miosis, and anhidrosis 

b. "Dilatation lag" is classic, in which the involved pupil takes as much as 15 seconds to dilate, with 

anisocoria greatest at 5 seconds of darkness. 

c. Causes include stroke, neck mass or cancer, carotid dissection, brachia! plexus trauma, and others. 


1. Compare pupil sizes in bright light and under dark conditions. 

a. With simple physiologic anisocoria, the pupil size discrepancy is the same in all levels of illumination. 

Furthermore, the pupils in these patients are round and respond normally to light and accommodation; 

associated findings (eg, ptosis) are absent. 

b. Anisocoria that is more pronounced in the dark suggests that the smaller pupil is abnormal (eg, Horner 

syndrome). 

c. Anisocoria that is greater in bright light suggests the larger pupil is abnormal (eg, third nerve palsy, Adie 

tonic pupil, or pharmacologic blockade). 

2. Inquire about prior eye surgery/trauma. 

3. Consider the setting and associated signs and symptoms. 

a. Head trauma and altered level of consciousness - exclude an expanding supratentorial mass/hemorrhage 

b. Headache and third nerve palsy - exclude a posterior communicating artery aneurysm 

c. Miosis, ptosis, and anhydrosis - exclude Horner syndrome 

4. Ask about the use of medications. 

a. Topical parasympatholytics (eg, atropine) or sympathomimetics (eg, phenylephrine, cocaine) 

b. Nebulized anticholinergics (causing ocular exposure) 

c. Scopolamine patches (with inadvertent ocular contact via the hands) 

IX. OPHTHALMIC MEDICATIONS 

A. Packaging 

Table 6: Cap/Bottle Colors ofTopical Ophthalmic Medications 

Medication 

Anesthetics 

Mydriatics and cycloplegics 

Miotics 

Antibiotics 

Steroids 

Cap/Bottle Color 

White or clear 

Red 

Green 

Tan 

Pink 

B. Topical anesthetics 

1. Used to facilitate examination of patients with painful ocular conditions and to allow performance of ocular 

procedures (foreign body removal, irrigation, tonometry) 

2. Deprive the cornea of its normal protective reflexes; in repeated doses will retard healing of the cornea 

3. Should never be dispensed as pain medications for outpatient use 

134


4. Types (no cross reaction between esters and amides) 

a. Esters 

(1) Proparacaine 0.5% 

(a) Rapid onset 

(b) Duration of action ~ 15 minutes 

(2) Tetracaine 0.5% 

(a) More irritating than proparacaine 

(b) Delayed onset 

(c) Duration of action ~30 minutes 

(3) Fluorocaine: a premixed combination of proparacaine and fluoroscein dye that has thimerosal as a 

preservative (which may cause a local allergic conjunctivitis in susceptible patients) 

(4) Benoxinate 0.4% 

(a) Onset 1-2 minutes 

(b) Duration of action 15 minutes 

b. Amides: dibucaine 0.1 % 

C. Mydriatics and cycloplegics 

1. Mydriatics 

a. Topical sympathomimetic agents that paralyze the iris sphincter only, thereby producing pupillary dilation 

(mydriasis) without affecting accommodation 

b. Used diagnostically to facilitate evaluation of internal ocular structures 

c. Example: phenylephrine 2.5%: onset 15-60 minutes, duration of action 3-4 hours 

2. Cycloplegics 

D. Miotics 

a. Topical parasympatholytic agents that paralyze both the iris sphincter (mydriasis) and the ciliary muscle 

(cycloplegia) 

b. Used therapeutically in the treatment of iritis and deep corneal abrasions to relieve pain by eliminating 

ciliary spasm 

c. Use of cyclopentolate or tropicamide is preferred in the presence of acute inflammation, because their 

effective duration of action is shorter than that of other agents, which allows repetitive dosing to keep the 

patient comfortable. 

(1) Cyclopentolate: onset 30-60 minutes, duration :S24 hours 

(2) Tropicamide: onset 15-20 minutes, duration 4-6 hours 

d. Homatropine is useful (short term) for subacute inflammation (iritis) caused by trauma or abrasion: onset 

30-40 minutes, duration 2-3 days 

e. Atropine is more effective for chronic inflammation seen after surgery and in severe uveitis; because of the 

long duration of action (1-2 weeks), its use in the emergency department is limited. 

f. These agents are contraindicated in patients with a history of glaucoma, evidence of increased intraocular 

pressure, presence of a shallow anterior chamber, or suspicion of a ruptured globe. 

1. Pilocarpine (2%): used for treatment of acute angle closure glaucoma 

2. Mechanism of action: constricts the pupil, pulling the iris back from its anterior position, which opens the angle 

and allows egress of the aqueous humor 

E. Topical antibiotics 

1. Solution (drops) are rapidly absorbed and require frequent instillation. In contrast, ointments have a longer 

duration of action and require less frequent administration but transiently blur vision when applied. 

2. Types/examples 

a. Erythromycin: broad-spectrum, primarily bacterostatic 

b. Sulfacetamide: broad-spectrum, bacterostatic 

c. Bacitracin: broad-spectrum, primarily bacterostatic 

d. Aminoglycosides (gentamicin, tobramycin): gram-negative coverage, including Pseudomonas; bactericidal. 

Avoid neomycin-containing antibiotics because of the risk of hypersensitivity reaction in 4% of the 

population. 

e. Polymyxin B/trimethoprim: broad spectrum, especially gram-positive organisms such as Staphylococcus 

and methicillin-resistant 5 aureus; bacteriostatic 

135


F. Antivirals 

f. Quinolones (ciprofloxacin, norfloxacin, ofloxacin, gatifloxacin, moxifloxacin): broad spectrum, including 

Pseudomonas; bactericidal. Drug of choice for monotherapy in treatment of corneal ulcers; poor 

streptococci coverage; expensive 

1. Interfere with viral DNA synthesis 

2. Topical antivirals (vidarabine, trifluridine) 

a. Used in treatment of herpes simplex keratitis 

b. Shorten treatment time and improve rate of healing 

c. Obtain ophthalmologic consult before prescribing. 

3. Systemic antivirals: used in consultation with ophthalmology and internal medicine in the treatment of herpes 

simplex keratitis, herpes zoster ophthalmicus, and cytomegalovirus retinitis 

a. Acyclovir (oral and IV) is useful for both herpes simplex keratitis and herpes zoster ophthalmicus. 

b. Valcyclovir (oral) is useful for both herpes simplex keratitis and herpes zoster ophthalmicus; requires less 

frequent dosing than acyclovir. 

c. Famciclovir (oral) is used to treat herpes zoster ophthalmicus; requires less frequent dosing than acyclovir. 

d. Valganciclovir (oral), gangliclovir (IV), or foscarnet (IV) is used in the treatment of cytomegalovirus retinitis. 

G. Topical steroids 

1. Used in treatment of iritis to reduce inflammation 

2. In general, they should not be prescribed in the emergency department; if they are prescribed, this should 

be done only in consult with an ophthalmologist, and prompt (within 24 hours) ophthalmology follow-up is 

indicated. 

3. A primary contraindication to steroid drops is early herpes simplex keratoconjunctivitis. 

4. Examples: prednisolone acetate, fluorometholone, dexamethasone 

H. Hyperosmotic agents 

1. Used in treatment of acute angle closure glaucoma 

2. Decrease intraocular pressure by decreasing the volume of fluid in the eye 

3. Examples 

a. IV mannitol (20% solution): works rapidly, very effective in the emergency department 

b. Oral glycerol (50% solution): avoid in diabetic patients because glycerol is metabolized to glucose and can 

produce hyperglycemia and ketosis; may cause nausea 

c. Oral isosorbide (45% solution): may cause nausea 

I. Carbonic anhydrase inhibitors 


2. Act to reduce intraocular pressure by decreasing the secretion of aqueous humor by the ciliary body 

3. These agents are sulfa compounds; sickle cell patients who present with hyphema are at risk of red cell sickling 

in the anterior chamber, further compromising aqueous outflow and increasing intraocular pressure. 

4. Examples: acetazolamide (IV or oral), methazolamide (oral), dorzolamide hydrochloride (topical) 

J. Topical adrenergic agents: ~-blockers or a 2 

-agonists 


2. Reduce intraocular pressure by decreasing secretion of aqueous humor by the ciliary body 

3. Preferred for initial management of acute angle closure glaucoma, because they do not produce the adverse 

effects associated with miotics 

4. Most commonly used ~-agonist is timolol (a nonselective ~-blocker), but betaxolol is cardioselective and, 

therefore, preferred by some clinicians; both are packaged in bottles with yellow or blue caps. 

5. Most commonly used a 2 

-agonists are apraclonidine and brimonidine; they are usually packaged in bottles with 

white caps. 

6. All topical adrenergic agents can cause serious systemic adverse effects (especially cardiopulmonary). Topical 

~-blockers can result in heart failure, heart block, and asthma, whereas a 2 

-agonists can cause orthostatic 

hypotension and syncope. 

136


X. TONOMETRY 

A. Measurement of intraocular pressure (IOP) using a calibrated device called a tonometer 

B. Indicated whenever the diagnosis of glaucoma or intraocular hypertension (eg, retrobulbar hemorrhage) is 

considered. IOP may be low in cases of iritis. 

C. Devices 

1. Schiotz impression tonometer: a handheld instrument that is available in most emergency departments and 

easy to use; a conversion table is required to translate the reading to mmHg. 

2. TonoPen: a handheld device that gives a digital readout of the IOP and uses disposable covers 

3. Goldman applanation tonometer: an instrument that is used in conjunction with a slit lamp 

4. Air-puff tonometer: an instrument that has the advantage of not requiring direct eye contact 

D. Contraindications include the presence or suspicion of a penetrating ocular injury (absolute) or an eye 

infection (relative). 

137


NASAL TRAUMA 

In evaluating nasal trauma, it is important to elicit any history of previous nasal deformity or surgery. 

I. NASAL FRACTURES 

A. Uncomplicated nasal fracture 

1. Can be determined on clinical grounds alone 

2. Clinical presentation: suggestive findings include the presence of nasal bridge tenderness, swelling, 

ecchymosis, deformity, or crepitance. Anterior rhinoscopy may reveal septal deviation. 

3. Diagnostic evaluation: radiographs add little or nothing to initial or subsequent management and need not be 

obtained in most isolated cases. 

4. Management 

a. If patients present early (usually within 2 hours) and the swelling does not preclude an accurate assessment 

of nasal contour, early reduction is frequently possible. 

b. If swelling does not allow an accurate assessment, reduction can be deferred. 

c. All patients with suspected or confirmed nasal fractures should be referred to ENT for reevaluation within 

2-5 days. Delaying longer may allow fractures to begin healing in their displaced position (especially in 

children), making intervention more difficult. 

B. Complex fractures 

1. Nasoethmoid fractures and nasal fractures associated with other facial fractures (eg, orbital floor fractures, 

tripod fractures of the zygomatic bone) 

2. Diagnostic evaluation requires CT scanning to assess the extent of injury present and establish a treatment plan. 

3. Management 

a. Nasoethmoid fractures are particularly complex and difficult injuries. 

b. These fractures are usually produced by a blow to the bridge of the nose and require CT scanning; possibly 

admission; and neurosurgical, ENT, and/or ophthalmology consults. 

C. Prophylactic antibiotic therapy (antistaphylococcal) 

1. Warranted in patients discharged with nasal packing and may be warranted for nasal fractures associated with 

a laceration of the nasal mucosa or skin (potential bacterial contamination) 

2. Nasal saline irrigation helps remove blood and cleanse the mucosa; cold compresses will help reduce swelling. 

II. MAJOR COMPLICATIONS 

A. Septal hematoma 

1. Clinical presentation: patients with nasal trauma should always be carefully evaluated to exclude the presence 

of a septa[ hematoma (a bluish purple, grapelike swelling of the nasal septum). 

2. Management 

a. These subperichondrial hematomas should be vertically incised and drained. 

b. After this, the anterior nasal cavity is packed to prevent blood from reaccumulating. 

c. The patient is then placed on an anti staphylococcal antibiotic and referred to ENT for follow-up in 24-48 

hours. 

3. Complications: if not drained, these hematomas can result in formation of a septa! abscess or avascular 

necrosis of the nasal septum with subsequent development of septa! perforation and a permanent "saddlenose" 

deformity. 

B. CSF rhinorrhea 

1. Due to fracture of the cribriform plate of the ethmoid bone 


a. May not develop for days to weeks 

b. Should be suspected whenever a patient develops a clear nasal discharge after facial trauma and may be 

associated with hyposmia (or anosmia) and headache 

138


c. Usually unilateral and may be increased by having the patient lean forward or by compressing the 

jugular vein. 


a. The diagnosis is most reliably confirmed by high resolution CT. 

b. Fluid can be collected and send for beta-2 transferrin to confirm CSF. 

4. Management 

C. Hemorrhage 

a. If CSF rhinorrhea is suspected: 

(1) Place the patient in the upright position. 

(2) Collect fluid if possible. 

(3) Obtain immediate neurosurgical and/or ENT consults (depending on local practice environment). 

(4) Avoid nasal packing. 

(5) Advise patient on nasal precautions (eg, no nose blowing, sneeze with mouth open, no Valsalva 

maneuvers). 

b. Administration of prophylactic antibiotics (penicillin, cephalosporins) remains controversial and should 

be determined by the neurosurgical and/or ENT consultant. 

1. Bleeding may be profuse but is usually of short duration. 

2. If bleeding does not subside spontaneously, and CSF rhinorrhea is not suspected, nasal packing may be 

required; if so, be sure to prescribe an antistaphylococcal antibiotic. 

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NASAL FOREIGN BODIES 

I. CLINICAL PRESENTATION 

A. History 

1. Most common in children 2-3 years old 

2. History is often lacking 

B. Physical examination 

1. Unilateral foul-smelling nasal discharge, persistent unilateral epistaxis, or a foul body odor 

2. Application of a vasoconstrictor (eg, 1 % phenylephrine or oxymetazoline) and a topical anesthetic (eg, 4% 

lidocaine) facilitates examination (as well as subsequent treatment) by providing patient comfort and improving 

the visual field. 

II. DIAGNOSIS AND TREATMENT 

A. Inspecting the nares with a nasal speculum in combination with a head lamp usually confirms the diagnosis. The 

first step is always to confirm that there is no chance the foreign body is a battery. 

B. Removal techniques 

1. Many nasal foreign bodies can be removed in the emergency department by using one of the techniques 

described below. 

2. Method selected depends on the age and cooperativeness of the child as well as the characteristics of the 

foreign body. 

3. Patient restraint is frequently necessary. 

4. Options 

a. Positive-pressure techniques have the advantage of being simple and noninvasive and probably should 

be tried first. Have the child forcefully blow his or her nose while occluding the uninvolved nostril. This 

method works best in older, cooperative children and may require several attempts. 

b. A suction catheter with a flange may also be used to remove the foreign body. 

c. Forceps (alligator, bayonet), right angle probes, wire loops, or a small Fogarty catheter are acceptable 

alternatives, but particular care must be exercised to avoid injuring the mucosa or pushing the object 

posteriorly with these instruments. 

5. After the foreign body has been removed, the nasal cavity should be inspected for the presence of additional 

foreign objects, infection, and trauma. 

6. If the foreign body cannot be safely removed, the patient should be referred to an otolaryngologist. 

a. Follow-up on an outpatient basis in 24 hours is appropriate for most of these patients, although surgical 

removal is occasionally required. Patients should be sent home nothing by mouth (NPO) when possible. 

b. However, immediate ENT consult (and possible admission) are required for patients with a lodged 

battery, an unknown object (cannot exclude a battery), associated facial cellulitis, or associated systemic 

symptoms. The long-term damage created by even brief contact with a battery cannot be overemphasized. 

140


EPISTAXIS 

I. VASCULAR SUPPLY TO THE NOSE 

A. Upper half of the nose: anterior and posterior ethmoidal arteries (internal carotid__,. ophthalmic arteryethmoidal 

arteries) 

B. Lower half of the nose: sphenopalatine and greater palatine arteries (both are distal branches of the 

external carotid) 

C. Most common sources of nosebleeds 

1. Anterior nosebleeds_,, anteroinferior nasal septum (Little area): Kiesselbach plexus 

2. Posterior nosebleeds, venous _,, posteromedial turbinate: Woodruff plexus 

3. Posterior nosebleeds, arterial _,, sphenopalatine artery 

II. ETIOLOGY 

A. Anterior bleeds (90% of all nosebleeds): more common in children (have a high level of suspicion for blood 

dyscrasias [eg, hemophilia, leukemia]) and young adults 

1. "Winter syndrome": dry air and upper respiratory infection 

2. Trauma: look for septa I hematoma 

3. Foreign body: especially children 

4. Nose picking: "epistaxis digitorum" 

5. Allergies 

6. Nasal irritants (eg, cocaine, nasal sprays) 

7. Pregnancy: epistaxis due to increased blood volume and venous engorgement 

8. Rapid changes in atmospheric pressure 

9. Infection: rhinitis, sinusitis 

10. Osler-Weber-Rendu syndrome (hereditary hemorrhagic telengectasia) 

11. Nasal malignancy 

B. Posterior bleeds (10% of all nosebleeds): more common in the elderly 

1. Coagulopathy: pharmaceutical anticoagulants, blood dyscrasias, or liver disease 

2. Neoplasm 

3. Hypertension 

4. Nasal malignancy 

Ill. CLINICAL PRESENTATION 

A. History 

1. Onset (spontaneous or precipitated), duration, severity 

2. Isolated event or recurrent problem 

3. Home management 

4. Environment (eg, dry, dusty) 

5. Medications and illicit drug use 

6. Underlying medical problems (eg, blood dyscrasias, hepatic or renal failure, hematologic cancers) 

7. Presence of unilateral obstruction or neurologic deficit suggests possibility of mass 

8. Easy bruising and bleeding at other sites 

9. Recent chemotherapy or prior history of neoplasm 

10. Hypertension is controversial; most literature suggests no association, especially with anterior bleeds. 

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1. Vital signs (note any orthostatic change) 

2. Eva I uate the blood and clots 

3. Identify location of bleeding site 

4. Signs of underlying bleeding disorder (ecchymoses, purpura, petechiae, spider angiomata) 

5. Nasal mass 

IV. TREATMENT 

A. General preparation 

1. Assemble the necessary supplies and equipment at bedside; appropriately gown both the patient and yourself. 

2. Then, with the patient seated and his or her head in the sniffing position, evacuate accumulated blood and 

clots from the nose, apply a topical anesthetic (eg, 4% lidocaine) and vasoconstrictor (eg, 1 % phenylephrine 

or oxymetazoline), then use a nasal clamp or have the patient firmly pinch his or her nose for 10 continuous 

minutes. 

B. Anterior sites 

1. Chemical cautery (silver nitrate sticks) 

2. A small piece of a hemostatic material on the bleeding site if the bleeding is mild 

3. Anterior nasal packing if tamponade is needed to control the bleeding; packs are left in place for 1-3 days. 

Prescribe antistaphylcoccal antibiotics if packing placed. 

4. Follow-up with ENT or primary care physician in 2-3 days. 

C. Posterior sites 

1. Posterior packing is indicated; use a gauze pack, intranasal balloon device, or Foley catheter. 

2. Admit patients with posterior bleeds. 

3. Closely monitor airway status, especially if history of obstructive sleep apnea. 

D. Drug treatment 

1. Because packing impairs sinus drainage, all patients who require anterior or posterior packing should be 

started on an antibiotic (eg, amoxicillin-clavulanate or a first-generation cephalosporin) as prophylaxis against 

sinusitis, otitis media, and toxic shock syndrome. 

2. Analgesic agents and decongestants are also appropriate. 

3. Aspirin and NSAIDs should be avoided. 

V. COMPLICATIONS 

A. May be due to the bleeding itself or as a consequence of the packs used to tamponade the bleeding 

B. Severe bleeding seen more commonly with posterior bleeds; transfusion may be needed if signs of 

cardiovascular compromise. 

C. Sinusitis and otitis media: due to obstruction of the sinus ostia and the eustachian tubes by nasal packing 

D. Toxic shock syndrome: due to the rapid growth of toxin-producing staphylococcal organisms precipitated 

by nasal packing 

E. Pressure necrosis of the columella or nasal ala: from improper padding 

F. Fatal airway obstruction: precipitated by accidental dislodgment of a posterior pack into the airway 

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FACIAL INFECTIONS 

I. SINUSITIS 

A. Definition: an infection of the paranasal sinuses (ethmoid, maxillary, frontal, or sphenoid). Maxillary sinusitis 

is the most common. Infection of the sphenoid and frontal sinuses is least common. 

1. Acute sinusitis: infection 3 months duration 

B. Pathophysiology 

1. Results from occlusion of the sinus ostia 

2. Usually precipitated by a viral upper respiratory infection or allergic rhinitis 

3. Ostial obstruction - ideal culture medium in occluded sinus -a- secondary bacterial infection (increased 

likelihood after 10-14 days of symptoms) 

C. Etiology 

1. Acute sinusitis: viral etiology in 98%-99.5% 

2. Antibiotics are rarely indicated in immunocompetent adults with symptoms for 50%) or polymicrobial 


1. Two cardinal symptoms: purulent rhinorrhea and nasal obstruction; other symptoms below are also suggestive. 

2. Headache or facial pain/pressure in a distribution defined by the sinuses involved 

3. Swollen erythematous nasal mucosa 

4. Purulent yellow-green nasal discharge 

5. Low-grade fever 

E. Diagnostic evaluation 

1. In most instances, the diagnosis of acute sinusitis can be made based on the history. 

2. Use a topical decongestant (eg, 1 % phenylephrine or oxymetazoline) to better visualize purulent secretions on 

rhinoscopy. 

3. If the diagnosis is uncertain (or complications are suspected), imaging studies may be indicated. 

4. CT of the sinuses is the most sensitive technique: the "gold standard" for diagnosing sinus disease and its 

comp/ ications. 

5. Plain films are no longer used in diagnosis of sinus disease. 

F. Management 

1. Topical decongestants (eg, oxymetazoline or phenylephrine) for a maximum of 3-5 days to avoid rebound 

effect 

2. Oral decongestants (eg, pseudoephedrine) for 2-4 weeks 

3. Avoid antihistamines while acutely ill. 

4. Reserve antibiotic therapy for patients with moderate to severe sinusitis with symptoms persisting over 10 

days and specific findings of acute sinusitis (nasal congestion and purulent nasal discharge). Amoxicillin and 

TMP-SMX are favored by many as first-line agents. However, in regions with a high percentage of ~-lactamaseproducing 

bacteria, a broad-spectrum agent should be selected: amoxicillin-clavulanate or a second- or 

third-generation cephalosporin (eg, cefuroxime axetil, cefprozil, cefaclor, cefpodoxime, proxetil, loracarbef). 

Antibiotics should be continued for 10-14 days. 

5. Adjunctive therapy 

a. Analgesics 

b. Mucolytics (eg, guaifenesin) and decongestants (pseudoephedrine preferred over phenylephrine) 

c. Saline irrigations 

d. Home humidifiers 

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G. Complications 

1. Ethmoid sinusitis can lead to periorbital/orbital cellulitis and abscess formation (especially in children). 

2. Frontal sinusitis may extend anteriorly and posteriorly. 

a. If it extends to the anterior table of the frontal bone, it may produce osteomyelitis of the surrounding bone 

("Pott's puffy tumor"). These patients present with a doughy-feeling, tender mass above their eye. 

b. If it extends to the posterior table of the frontal bone, it may cause osteomyelitis, which can lead to: 

(1) Meningitis 

(2) Epidural abscess 

(3) Subdural empyema 

(4) Brain abscess 

3. Sphenoid or ethmoid sinusitis can extend intracranially via the vascular or lymphatic channels of these sinuses, 

thus producing cavernous sinus thrombosis. 


a. Proptosis 

b. Eyelid edema 

c. Dilatation of the episcleral veins 

d. Palsies of cranial nerves Ill-VI 

e. Venous engorgement of the fundus 

f. Decreased mental status 

g. High fever 

h. Headache 

5. Patients demonstrating these complications require admission, parenteral antibiotics, and appropriate consults. 

II. PAROTITIS 

A. An infection of the parotid gland that can be bacterial (usually Staphylococcus aureus) or viral (eg, 

paramyxovirus) 

B. Suppurative parotitis 

1. Most common in older, debilitated, or postoperative patients with decreased salivary flow due to drugs, 

dehydration, or irradiation 

2. Etiology: 5 aureus (most common) but often polymicrobial 


a. Tender parotid swelling (often unilateral) 

b. Trismus 

c. Purulent discharge from the opening of Stensen (parotid) duct (opens into the mouth adjacent to the 

maxillary second molar) 

d. Fever 

4. Management 

a. An antistaphylococcal antibiotic (eg, clarithromycin has good salivary penetration); consider Klebsiella, 

Pseudomonas, and anaerobic coverage if ill or diabetic. 

b. Hydration 

c. Local heat 

d. Massage 

e. Sialogogues (eg, sour candy, lemon juice) 

C. Paramyxovirus ("mumps") 


a. Most common in winter and spring in children 5-15 years old 

b. Rare because of childhood immunizations 


a. Incubation period of 12-25 days 

144


b. Characteristic clinical findings 

(1) Tender parotid swelling at the angle of the jaw (frequently bilateral) 

(2) Low-grade fever, headache, malaise 

(3) Clear saliva from Stensen (parotid) duct 

c. Occasionally, the infection may involve: 

(1) Gonads (epididymitis, orchitis) 

(2) Meninges (meningoencephalitis) 

(3) Pancreas (pancreatitis) 

3. Management 

a. Hydration 

b. Analgesics 

c. Antipyretics 

d. Sialogogues (eg, lemon drops) to encourage salivary flow 

4. Infected individuals are contagious up to 6 days before to 9 days after the onset of parotid swelling. 

145


FACIAL FRACTURES 

In facial injuries, consider the possibility of concomitant cervical spine injury. 

I. MANDIBULAR INJURIES 

A. Hallmarks of mandibular dysfunction: limited opening or deviation on opening of the mouth, malocclusion, 

pain, and trismus 

B. Mandibular fractures 

1. Second most commonly fractured facial bone (nose is the first) 

2. Because of its ringlike structure, the mandible fractures in two or more places in most cases (so don't stop 

looking after finding the first fracture). 

3. The most common sites of fracture are the condyle, the body, and the angle. 


a. Most important question to ask is whether the patient feels that his or her teeth are not coming together as 

they used to when biting down; this indicates malocclusion. 

b Teeth that are angulated and sometimes avulsed ---'> alveolar fractures 

c. Lateral crossbite - unilateral condylar fractures 

d. Displacement of the lower incisors, interruption of arch continuity - symphysis fractures 

e. Ecchymosis or hematoma of the floor of the mouth---'> highly suspicious for a mandibular fracture 

f. Anesthesia of the lower lip - injury of the inferior alveolar or mental nerve secondary to a mandibular 

fracture 


a. A dental panoramic view of the maxilla and mandible is the best study for diagnosing mandibular fractures. 

b. If a dental panoramic view cannot be done, a maxillofacial CT should be obtained. 

6. Management 

a. Mandibular fractures require consult with an ENT or a plastic or oral surgeon for reduction and fixation. 

The time course involved (immediate or delayed) is determined by the specific injury, the presence of 

airway compromise, and associated injuries. 

(1) Patients with open fractures require antibiotics, and fractures should be reduced within 24 hours. Any 

fracture in the tooth-bearing region should be considered "open" because the periodontal ligament 

communicates with the oral cavity. Penicillin is the drug of choice. Clindamycin is an alternative for 

penicillin-allergic patients. 

(2) Patients with closed fractures that are nondisplaced may be discharged to home if there is no question 

of airway compromise. All subcondylar fractures and fractures in edentulous patients are considered 

"closed" unless accompanied by a laceration. 

b. Tetanus prophylaxis should be updated as needed. 

7. Disposition 

a. If discharged, the patient should be placed on a liquid diet and given adequate analgesia; close follow-up 

is required. 

b. Admission is required for patients with: 

(1) Airway compromise (early intubation is critical) 

(2) Excessive bleeding 

(3) Severely displaced fractures (impair swallowing) 

(4) Grossly infected fractures 

(5) Comorbid disease/disability (uncontrolled diabetes, elderly) 

C. Mandibular dislocation 

1. Can result from trauma, yawning, or laughing 

2. The jaw is locked open (mandibular condyle is locked anterior to the articular eminence), and the patient has 

difficulty talking or swallowing. 

3. Bilateral dislocation presents with an anterior open bite; if the dislocation is unilateral, the jaw is displaced 

toward the unaffected side. 

146



a. Identify on radiograph. 

b. Radiographic evaluation to exclude fracture should be obtained before manipulation if the dislocation is 

related to trauma. 


5. Management 

a. The treatment is manual reduction with downward pressure applied to the posterior teeth to dislodge the 

condyle; the chin is then pressed posteriorly, so that the condyle returns to the fossa. 

b. Procedural sedation may be required if significant muscle spasm is present. 

c. After reduction, the patient should be placed on a soft diet, advised to avoid opening the mouth widely, 

and referred to an oral surgeon for follow-up. A muscle relaxant and an NSAID should also be prescribed. 

D. Temporomandibular joint (TMJ) dysfunction 


a. Patients typically complain of dull, aching unilateral pain in the region of the TMJ that worsens as the day 

progresses. Referred ear pain is also common. 

b. On examination, there is pain on palpation of the TMJ that worsens with mouth opening and engagement 

of the muscles of mastication (masseter and internal pterygoid muscles). Palpable spasm of these muscles 

and a limited ability to open the mouth widely may also be present. 

2. Management 

a. NSAIDs, a muscle relaxant, and referral to a dentist (with a specialty in TMJ disorders) for a bite splint 

b. Warm moist heat to the area, limited jaw movement, and a soft diet are also helpful. 

II. MIDFACIAL FRACTURES 

A. The midfacial area includes the maxillary teeth up to the lateral ca nth us of the eye. 

B. Isolated zygomatic arch fractures 

1. Clinical presentation: if depressed, the cheek may be flattened, and opening of the mouth may be painful or limited. 

2. Diagnostic evaluation: these fractures are best visualized with a maxillofacial CT scan. 

3. Management 

a. Treatment is generally delayed until facial swelling has resolved but should be done within 10 days. 

b. Surgical reduction is indicated for compromised mandibular excursion and unacceptable cosmesis. 

147


C. Zygomatic-maxillary complex ("tripod") fractures 

1. Generally result from a blow to the cheek and involve fractures at three sites: the zygomatic arch, 

zygomaticofrontal suture, and infraorbital rim. Fracture of the lateral wall of the maxillary sinus and orbital 

floor is also invariably present. A fourth fracture site at the connection with the sphenoid bone can be present. 


a. A palpable step-off deformity of the inferior orbital rim 

b. Anesthesia of the cheek, upper teeth, lip, and gum from infraorbital nerve injury 

c. Periorbital swelling and ecchymosis 

d. Flattening of the cheek (if presents before significant swelling occurs) 

e. Diplopia and possible enophthalmos 

3. Diagnostic evaluation: maxillofacial CT scanning is replacing plain radiographs in the evaluation of all facial 

fractures. 

4. Management 

a. Control bleeding and arrange appropriate consult with facial trauma. 

b. Prescribe adequate analgesia. 

c. In the absence of eye involvement, patients with these fractures can often be discharged to home with 

follow-up in 5-7 days. 

d. Open reduction is required for open/displaced fractures. 

D. Orbital floor fractures 

1. May occur as isolated injuries resulting from blunt ocular trauma ("blowout" fracture) or as a component 

of a zygomatic-maxillary complex fracture. Orbital fat, bone, and extraocular muscles may protrude into 

the maxillary sinus and become entrapped. (See also blowout fractures on page 132 and in the chapter on 

Traumatic Disorders on pages 315-31 6.) 

2. Clinical presentation: enophthalmos, upward gaze palsy with diplopia, hypoesthesia of the infraorbital nerve 

3. Diagnostic evaluation: CT scan 

4. Management 

a. All of these patients should be referred to ophthalmology for fol low-up. 

b. Prophylactic antibiotics should be considered for patients with evidence of sinus involvement 

(subcutaneous emphysema, blood in the maxillary sinus). 

c. Nasal precautions 

d. Persistent enophthalmos, visual changes, and muscle entrapment are indications for urgent surgical repair. 

E. Categories and characterization of multiple facial fractures 

1. Result from massive, direct facial trauma (eg, high-speed deceleration injuries) and may result in airway 

compromise 

2. Classification 

a. LeFort I (palate-facial dysjunction) is a horizontal fracture of the maxilla at the level of the nasal floor. 


b. LeFort II (pyramidal dysjunction) includes fractures through the maxilla, nasal bones, and infraorbital rim. 

c. LeFort Ill (craniofacial dysjunction) involves fractures through the zygomaticofrontal suture or zygoma and 

the frontal bone above the nose. 

148



3. Clinical presentation: massive soft-tissue swelling, midfacial mobility, malocclusion, and CSF rhinorrhea 

4. Diagnostic evaluation: maxillofacial CT is generally needed to delineate the extent and number of fractures as 

well as the presence of associated injuries. 

5. Management 

a. Airway management, cervical spine assessment (including associated neurologic deficits), and evaluation of 

the globe; vascular injury (carotid) may be associated. 

b. Administration of prophylactic antibiotics if the sinuses are involved 

c. Consult facial trauma specialist. 

d. Surgical reduction if weight-bearing buttresses involved 

149


ACUTE AIRWAY OBSTRUCTION 

I. CLINICAL PRESENTATION 

A. Labored respirations (tachypnea, chest retractions, nasal flaring) 

B. Stridor: a high-pitched crowing sound caused by airflow through a partially obstructed upper airway 

(larynx or trachea). Although it is most commonly heard during inspiration, it may be biphasic or 

expiratory when the obstruction is more distal (trachea). 

1. lnspiratory (supraglottic or glottic): indicates obstruction above or at the larynx, eg, epiglottitis 

2. Biphasic (subglottic): indicates obstruction below the larynx, eg, croup 

3. Expiratory: indicates lower tracheal obstruction 

C. Hoarseness 

D. Dysphagia 

E. Coughing 

F. Cyanosis 

G. Degree of airflow in the upper airway depends on the diameter of the airway in any given situation: 

t airway diameter - t resistance to airflow (by a factor of ~4). 

H. Oxygen saturation is not typically a useful measure in situations of suspected airway obstruction 

(which presents an issue of ventilation rather than of oxygenation). 

II. DIFFERENTIAL DIAGNOSIS 

A. The following conditions should be included in the differential diagnosis. Foreign body aspiration 

and infections are covered in more detail below. 

1. Foreign body aspiration 

2. Infections (croup, epiglottitis, bacterial tracheitis, retropharyngeal abscess) 

3. Angioedema (hypersensitivity to irritants, allergens, ACE inhibitors) 

4. Trauma (including burns, hematomas) 

5. Vascular anomalies 

6. Neoplasms 

B. Foreign body aspiration 

1. Most common in children 1-4 years old; boys are more commonly affected. 

2. Although any type of object may be aspirated, peanuts are the most common offending agent and one of the 

most inflammatory. 

3. The narrowest part of the upper airway is where most airway foreign bodies become lodged. 

a. In children__,. cricoid cartilage 

b. In adults__,. vocal cords 


a. The presenting signs vary with the location of the foreign body and the degree of obstruction produced. 

(1) Aphonia __,. complete upper airway obstruction at the level of the glottis or below 

(2) Stridor __,. incomplete upper airway obstruction 

(3) Wheezing __,. incomplete lower airway obstruction 

(4) Coughing__,. incomplete obstruction at the supraglottic, glottic, or distal airways; cough is a 

presenting symptom in at least 80% of patients. 

b. Consider a diagnosis of foreign body aspiration in a previously well child of the appropriate age who has 

a history of any of the following: 

(1) A choking episode 

(2) An acute bout of paroxysmal coughing 

(3) Sudden onset of wheezing without an associated upper respiratory infection or past history of wheezing 

(4) Persistent or recurrent pneumonia 

150



a. The initial approach to the child who has aspirated a foreign body (eg, a penny) is often accomplished 

with plain radiographs; diagnostic laryngoscopy or bronchoscopy is sometimes required, especially when 

the object is small and radiolucent. 

b. Battery ingestion should be excluded first and foremost and, if suspected, requires emergent referral to 

ENT. Further assistance in identification of batteries is provided by the National Battery Ingestion Hotline 

(202-625-3333) and www.poison.org/battery/guideline; the "double rim" can be useful, but its absence 

does not exclude the presence of a battery. 

c. PA and lateral chest radiographs can be used to distinguish a radiopaque foreign body in the esophagus 

from one in the trachea. In the esophagus, a flat foreign body (like a coin) lies in the frontal/coronal 

plane and appears round in the PA view. A tracheal foreign body is generally oriented in the sagittal plane 

(aligning with the vocal cords) and appears round in the lateral view. 

d. The PA and lateral chest radiographs may also show indirect signs of the presence of an airway foreign 

body; complete bronchial obstruction produces resorption atelectasis distal to the site of obstruction, 

and pulmonary infiltrates may be seen in the presence of an inflammatory reaction to a foreign body 

(particularly vegetable matter). 

e. The presence of a radiolucent foreign body that is partially obstructing a mainstem bronchus can 

be demonstrated on an expiratory radiograph or bilateral decubitus chest radiographs (in the young 

uncooperative child). These views accentuate the "ball-valve" effect of a partially obstructing foreign 

body, thereby producing hyperinflation of the obstructed lung (due to air trapping) and a shift of the 

mediastinum away from this side. Review radiographs (expiratory and bilateral decubitus chest films) that 

demonstrate air trapping. 

6. Management 

a. Very close airway monitoring while operating room prepared 

b. Foreign body removal in the operating room (under anesthesia) by laryngoscopy or rigid bronchoscopy 

C. Infections 

Croup and epiglottitis are the most important. You should know these "cold" for the exam. Look up the 

radiographs so that you can identify these conditions on soft-tissue radiographs. 

1 . Croup (laryngotracheobronchitis) 

a. Epidemiology 

(1) Age group: usually 6 months to 3 years old, with a male predominance 

(2) Organism: virus (most commonly parainfluenza virus) 

(3) Season: fall and winter (particularly October through December) when the causative viruses are 

most prevalent 

(4) Site of inflammation/obstruction: glottic and subglottic area 


(1) Prodrome: preceding viral upper respiratory infection of 2-3 days duration with a gradually 

increasing cough 

(2) Onset and progression: insidious (over days) 

(3) General appearance: nontoxic 

(4) Barking cough (worse at night) 

(5) Hoarse voice 

(6) Respiratory distress (tachypnea, dyspnea, retractions, and stridor) 

(7) Nasal discharge 

(8) No or low-grade fever 


(1) In children who present with the classic clinical picture and the characteristic barking, seal-like 

cough, the diagnosis can be made on clinical grounds alone. 

(2) When the presentation is less typical, radiographs can exclude other causes of airway compromise 

(eg, epiglottitis, foreign body aspiration, retropharyngeal abscess). These radiographs should be taken 

in the emergency department as portable studies. 

(3) Characteristic radiograph findings 

(a) PA chest radiographs - subglottic narrowing of the tracheal air column ("steeple sign") 

(b) Soft-tissue lateral of the neck - distended hypopharynx, normal epiglottis, and normal 

retropharyngeal space 

151


d. Management 

(1) Cool mist (use is not evidence-based) 

(2) Oxygen as needed 

(3) Hydration (oral or IV) 

(4) Steroids (dexamethasone 0.15-0.6 mg/kg orally or 0.6 mg/kg IM as a one-time dose) are beneficial 

for outpatient management. 

(5) Racemic epinephrine aerosol (0.5 ml of a 2.25% solution diluted in 3 ml of saline) should be 

administered to patients with resting stridor or respiratory distress that is not relieved by the above 

measures. Although evidence to support the phenomenon of "rebound" is lacking, children sick 

enough to receive racemic epinephrine should be observed in the emergency department for 3-4 

hours after therapy to assure that they do not return to their pretreatment stridorous state once the 

effect of racemic epinephrine wears off. 

(6) Admission criteria 

(a) Persistent stridor at rest 

(b) Inability to tolerate fluids 

(c) Unreliable social situation 

(d) Incomplete response to racemic epinephrine 

(e) Multiple doses of racemic epinephrine 

(f) Severe croup at presentation (even if responsive to therapeutic measures), particularly in 

children


(2) In less severe cases, diagnosis may be confirmed with a lateral soft-tissue radiograph of the neck that 

demonstrates the classic finding of an enlarged "thumbprint-like" epiglottis. The radiographs should 

be portable; if this is not feasible, someone skilled in airway management must accompany the 

patient to the radiography suite with airway equipment. 

(3) In cooperative patients with mild to moderate symptoms and a negative lateral neck radiograph (only 

40% sensitivity and 75% specificity for epiglottitis), careful direct visualization of the epiglottis may 

be performed to resolve the problem of false-negative results on lateral neck radiographs in patients 

with early epiglottitis. It is unlikely that this procedure will trigger acute airway obstruction in these 

patients. If direct inspection of the airway is not feasible, CT may be of value but should be done 

only in patients without airway distress. 

d. Management 

(1) Avoid agitation of the patient; allow him or her to assume a position of comfort and remain in the 

company of family. 

(2) Provide supplemental humidified oxygen. 

(3) Set up airway equipment at bedside. 

(4) Obtain immediate ENT and anesthesia consults. 

(5) After airway stabilization by consultants, order appropriate laboratory studies, start an IV line and 

fluid therapy, and begin antibiotics. Acceptable antibiotics include a second- or third-generation 

cephalosporin (cefuroxime, cefotaxime, ceftriaxone) or ampicillin-sulbactam. 

(6) Admit to ICU. 

(7) If H influenzae type B is isolated, household contacts require prophylaxis with rifampin, particularly 

if there is an unvaccinated child :S:4 years old in the contact group. 

3. Bacterial tracheitis (membranous laryngotracheobronchitis): a life-threatening, bacterial infection of the 

subglottic region that is characterized by copious tracheal secretions. It is often superimposed on a viral 

upper respiratory infection and has features of both croup and epiglottitis, as well as inflammation. 


(1) Age group: 3 months to 1 0 years old 

(2) Organism: most commonly Staphylococcus aureus; others include: 

(a) H influenzae 

(b) Streptococcus pyogenes 

(c) Moraxella catarrhalis 

(3) Nonseasonal 


(1) Prodrome: preceding viral upper respiratory infection or croup symptoms of several days duration 

(2) Onset and progress: hours to days; once bacterial superinfection occurs, progression is rapid (over hours). 

(3) General toxic appearance 

(4) Barking cough (present in 50% of cases) 

(5) Respiratory distress (stridor and retractions) 

(6) High fever 


(1) Suspect this diagnosis when a child with symptoms of viral croup becomes acutely more toxic, 

develops a high fever, and has progressive respiratory distress that is unresponsive to usual croup 

management. 

(2) Direct laryngotracheobronchoscopy (performed by ENT) reveals pseudomembranes and purulent 

secretions and confirms the diagnosis. Removal of this debris via suctioning helps prevent airway 

obstruction. 

d. Management 

(1) Provide supplemental humidified oxygen. 

(2) Obtain immediate ENT and anesthesia consults. 

(3) After airway suctioning and stabilization by consultants, obtain appropriate laboratory studies 

(including Gram stain and culture of tracheal secretions), hydrate with IV fluids, and administer 

antibiotics effective against S aureus. Acceptable choices include IV nafcillin, methicillin, or oxacillin 

plus ceftriaxone or another third-generation cephalosporin. 

(4) Admit to ICU. 

153


ORAL AND PHARYNGEAL INFECTIONS 

Infections can occur throughout the mouth and throat, and can range from minor localized infections to deep and 

spreading infections that may lead to airway compromise and other complications. The deep neck spaces, including the 

peritonsillar space, masticator space, parotid space, submandibular space, parapharyngeal space, retropharyngeal space, 

mediastinum, etc, essentially all communicate with one another, and infection in one space always has the potential to 

spread to the others. The prevertebral space is the only deep neck space that does not communicate as directly with the 

others; its microbiology is therefore different and typically related to adjacent spine infection or instrumentation. 

I. ORAL INFECTIONS 

A. Masticator space abscess 

1. The masticator space is the area bounded by muscles of mastication (the masseter and internal pterygoid 

muscles). 

2. Infection is secondary, resulting from extension of an anterior space infection (buccal, sublingual, or 

submandibular spaces) or from an infection around the third molar. 

3. Etiology: streptococci and anaerobes 

4. Clinical presentation: lateral facial swelling with pain, fever, and trismus 

5. Management 

a. IV antibiotics (penicillin or clindamycin are the drugs of choice) 

b. Emergent ENT or oral maxillofacial surgery consult 

c. Admission 

B. Ludwig angina 

1. A progressive cellulitis of the floor of the mouth; the submandibular and sublingual spaces are involved 

bilaterally, producing induration and massive swelling that can result in airway obstruction (33% of cases). 

2. Common precipitants include an abscess of (or trauma to) the posterior mandibular molars (second and third 

molars), the roots of which communicate directly with the submandibular space. Sometimes, infection of the 

anterior teeth leads to sublingual space infection that spreads to the submandibular space, rather than vice 

versa. 

3. Etiology: combination of anaerobic (Bacteroides spp) and aerobic (streptococci, staphylococci) oral flora 

4. Clinical presentation: dysphagia, odynophagia, dysphonia, trismus, drooling, neck and sublingual pain, 

massive swelling/induration of the floor of the mouth and anterior neck that is brawny in character, fever, 

and an elevated tongue 

5. Management 

a. If possible, allow the patient to maintain a sitting position; supine positioning can result in sudden airway 

obstruction. 

b. Set up airway management equipment, including tracheostomy tray, at bedside; the most frequent cause 

of death in these patients is asphyxiation. 

c. Obtain immediate anesthesia and ENT or oral maxillofacial surgery consults. 

d. Administer parenteral antibiotics (penicillin and metronidazole, cefoxitin, clindamycin, ampicillinsulbactam, 

or ticarcillin/clavulanate). 

e. Admit to ICU. 


a. Airway compromise 

b. Extension of infection into the deeper layers of the neck or into the thoracic cavity (mediastinitis, 

mediastinal abscess) 

154


II. PHARYNGEAL SPACE INFECTIONS 

Review soft-tissue imaging of the neck with a radiologist. Ask him or her to teach you the normal size limits of 

the following spaces: parapharyngeal, peritonsillar, retropharyngeal, and prevertebral. Then look at imaging that 

demonstrates infection or abscess formation in these spaces. 

A. Parapharyngeal abscess 

1. Occurs in the space lateral to the pharynx and medial to the masticator space; this space extends from the base 

of the skull to the hyoid bone. 

2. Common precipitants of abscesses in this region are dental, pharyngeal, and tonsillar infections. 

3. Etiology: Streptococcus viridans is the most commonly isolated organism from any deep neck space infection, 

but a combination of anaerobes and aerobes is common, and the specific organisms isolated may reflect the 

original site of infection. 

4. Clinical presentation: neck pain, sore throat, dysphagia, odynophagia, unilateral swelling of the neck and 

angle of the mandible, restricted movement of the neck, torticollis, pharyngitis, bulging of the pharyngeal wall, 

drooling, cervical adenopathy, and fever 

5. Management 

a. Emergency airway equipment set up at bedside 

b. Parenteral antibiotics (same as for Ludwig angina) 

c. Consider steroids in nonimmunocompromised hosts 

d. Emergent ENT consult 

e. Hospital admission 

6. Complications: airway obstruction, spread of infection into the surrounding spaces, cranial nerve neuropathies 

(IX-XII), carotid artery erosion, and septic thrombosis of the internal jugular vein 

B. Peritonsillar abscess 

1. Occurs between the tonsillar capsule and the superior constrictor muscle; it is usually the complication of 

untreated or partially treated suppurative tonsillitis and is most frequently seen in teenagers and young adults. 

2. Etiology 

a. Usually a polymicrobial infection caused by a mixture of aerobes and anaerobes. 

b. Group A 13-hemolytic streptococci is the predominant species. Other Streptococcus spp, Haemophilus 

influenzae type B, Staphylococcus, Bacteroides, and Fusobacterium spp are less frequent pathogens. 


a. Sore throat (?.2 days and localized to one side) 

b. Dysphagia and odynophagia-.. drooling 

c. Muffled ("hot potato") voice 

d. Inferior and medial displacement of the involved tonsil 

e. Soft palate fluctuance 

f. Deviation of the uvula to the opposite side 

g. lpsilateral ear pain 

h. Trismus 

1. Fever 

j. Tender cervical adenopathy 

k. Foul breath odor 

4. Diagnostic evaluation: if you are unable to visualize the abscess, ultrasound can help identify it. CT can also be 

used but is rarely necessary. 

5. Management 

a. Incision and drainage 

(1) Abscess evacuation by needle aspiration or by incision and drainage. Needle aspiration may be 

performed by the emergency physician if trained in the technique; incision and drainage is usually 

performed by the ENT consultant. 

(2) Gram stain and culture of aspirated fluid should be ordered. 

b. IV hydration 

c. Parenteral antibiotics (penicillin, ampicillin-sulbactam, clindamycin, cefoxitin, or erythromycin) 

d. Dexamethasone 

155



a. After abscess evacuation, many patients have significant relief of their symptoms and may be discharged 

to home on oral antibiotics (amoxicillin-clavulanate, clindamycin, or a secondgeneration cephalosporin). 

ENT follow-up should be available in event of relapse. Tonsillectomy is not indicated for history of a single 

episode of peritonsillar abscess. 

b. If the abscess cannot be drained or the patient remains symptomatic, appears toxic, or cannot tolerate 

fluids, he or she should be admitted to ENT and continued on IV antibiotics. 

C. Retropharyngeal abscess 

1. Occurs in the space posterior to the constrictor muscles of the pharynx. Specifically, it is between two layers of 

the deep cervical fascia: the alar fascia (a layer of the prevertebral fascia) posteriorly and the buccopharyngeal 

fascia (a portion of the pretracheal fascia) anteriorly. The danger space is immediately posterior to the 

retropharyngeal space and is the means by which these infections can spread to the mediastinum if they 

penetrate the alar fascia. It most commonly affects children 6 months to 3 years old. 

2. Etiology: Staphylococcus aureus, group A ~-hemolytic streptococci, and anaerobes are the most common 

pathogens. 


a. Sore throat 

b. Dysphagia __.. refusal to eat and drooling 

c. Labored respirations and (sometimes) stridor 

d. Muffled voice 

e. Fever 

f. Unilateral bulging of the posterior pharyngeal wall 

g. Swelling of the anterolateral neck with limited cervical mobility 

h. Tender anterior cervical adenopathy 

1. Systemic toxicity 

j. A preference for the supine position with the head and neck held in extension 

k. The presence of chest pain suggests that mediastinal extension has occurred. 


a. A soft-tissue lateral radiograph of the neck is the initial study of choice. Supportive findings include 

widening of the retropharyngeal space with anterior displacement of the larynx and the presence of air or 

an air-fluid level in this space. 

(1) The normal width of the retropharyngeal space is less than half the width of the adjacent vertebral body. 

(2) The radiograph must be taken during inspiration with neck in slight extension: the expiratory phase 

of respiration and neck flexion __.. buckling and redundancy of the retropharyngeal tissues - falsepositive 

result. 

b. The presence of chest pain should raise suspicion of mediastinal extension, and plain chest radiographs or 

a chest CT should be obtained. 

5. Management 

a. Airway stabilization equipment at bedside 

b. IV hydration 

c. Parenteral antibiotics 

(1) A penicillinase-resistant penicillin and metronidazole or 

(2) Clindamycin or 

(3) Cefoxitin or 

(4) Ampicillin/sulbactam 

d. Emergent ENT consult for incision and drainage 

e. Hospital admission 

6. Complications: airway obstruction, aspiration, invasion of contiguous structures (mediastinum, vessels), and sepsis 

D. Prevertebral infection 

1. Occurs in the space posterior to the prevertebral fascia and anterior to the cervical spine; this space extends 

al I the way to the coccyx. In the absence of CT or MRI, it can be hard to differentiate from retropharyngeal 

infection except by patient age and any relevant medical history; retropharyngeal space infection is more 

common in an otherwise healthy child. 

156


2. Usually results from surgical instrumentation, hematologic seeding, or cervical osteomyelitis, eg, 

Staphylococcus or tuberculosis; different microbiology than retropharyngeal or other deep neck space 

infections, and no odontogenic causes. 

3. Clinical presentation: may include bulging of the pharynx (usually bilateral) and tenderness of the cervical 

spine on palpation 


a. Lateral neck radiographs revealing retropharyngeal swelling or osteomyelitis of the cervical spine are 

suggestive. 

b. CT, MRI, or a cervical myelogram are needed to confirm the diagnosis. 

5. Management 

a. ICU admission 

b. Parenteral antibiotics 

c. Neurosurgical consult 

157


PHARYNGITIS 

Pharyngitis is an inflammation or infection of the mucous membranes of the oropharynx. Both noninfectious (trauma, 

irritant gas) and infectious (viral, bacterial, fungal) agents may be responsible. Patient complaints include dysphagia, sore 

throat, fever, and cervical adenopathy. Airway compromise is a potential complication. In the emergency department, the 

evaluation of pharyngitis is primarily aimed at the diagnosis of group A 0-hemolytic streptococci; appropriate treatment 

of this infection limits its spread, decreases the incidence of suppurative complications, prevents rheumatic fever, and 

hastens clinical recovery. Pharyngeal injuries, foreign bodies, and burns may present as pharyngitis. 

I. TRAUMA 

II. IRRITANT INHALANT 

A. Many gases and vapors irritate the throat (chlorine, steam, smoke). 

B. Assess respiratory effort and oxygenation; supplemental oxygen or intubation may be needed. 

Ill. VIRUSES 

Viruses are the most frequent cause of acute pharyngitis. Adenovirus, Epstein-Barr virus, influenza virus, parainfluenza 

virus, enteroviruses, and herpes simplex virus are commonly implicated. Cough, coryza, conjunctivitis, hoarseness, 

diarrhea, and stomatitis are more suggestive of viral etiology. These infections are usually self-limited and require only 

symptomatic treatment. 

A. Infectious mononucleosis 

1. Caused by the Epstein-Barr virus (human herpes virus 4); most commonly affects patients 10-25 years old 


a. Patients classically present with sore throat, fever, malaise, and fatigue. Abdominal pain and/or left shoulder 

pain (Kehr sign), particularly if associated with dizziness, nausea, and left upper quadrant tenderness, 

suggests splenic rupture (a serious complication). 

b. Examination reveals an exudative pharyngitis and tender cervical adenopathy. Posterior cervical 

adenopathy is characteristic and helps distinguish infectious mononucleosis from other causes of 

pharyngitis. Hepatosplenomegaly is also common; splenic rupture may occur with minor trauma. 


a. Peripheral blood smear reveals a lymphocytosis (>50%) and an increase in the proportion of atypical 

lymphocytes (> 1 0%). 

b. A monospot test (heterophile antibody) confirms the diagnosis if positive but takes 2-7 days. False-negatives 

may also be seen, particularly in children


IV. BACTERIA 

A. Group A (3-hemolytic streptococci (GABHS) 


a. Often seen in late winter 

b. Usually in patients


C. Diphtheria 

1. This rare but serious cause of pharyngitis typically occurs secondary to noncompliance with diphtheriapertussis-tetanus 

(DPT) immunizations. Spread is primarily by contact with respiratory secretions, and the 

period of incubation is~ 1 week. 

2. Morbidity is due to both infectious and toxic reactions. 

a. Infectious invasion causes enough tissue necrosis to produce a pseudomembrane in the posterior pharynx 

that can progressively enlarge and lead to airway obstruction. 

b. Corynebacterium diphtheriae elaborates a powerful exotoxin that can cause widespread organ damage. 

(1) Myocarditis/AV block/endocarditis 

(2) Nephritis 

(3) Hepatitis 

(4) Neuritis with both bulbar and peripheral paralysis 

(a) The most commonly observed paralysis involves the intrinsic and extrinsic muscles of the eyes, 

leading to ptosis and strabismus. 

(b) Involvement of the palate produces a change in voice quality and difficulty speaking. (The 

muscles of the palate are usually the first to become paralyzed). 

(c) 


Limb paralysis and loss of deep tendon reflexes may also occur. 

a. The patient has an acute onset of sore throat, fever, and general malaise, and appears toxic and is 

tachycardic. His or her voice is hoarse, muffled, or even absent. 

b. Physical examination reveals an exudative pharyngitis with a white to gray, closely adherent 

pseudomembrane, marked cervical adenopathy ("bul I neck"), and fetid breath ("dirty mouse" smel I). 

A serosanguineous nasal discharge may also be present. 


a. Gram stain of pharyngeal swab specimen reveals gram-positive rods with clubbing. 

b. Culture on Loeffler or tellurite media is positive. 

c. CBC may show thrombocytopenia. 

5. Management 

D. Gonorrhea 

a. ABC stabilization 

b. Definitive treatment is aimed at both the bacteria and the exotoxin and should be started as soon as the 

diagnosis is suspected. Do not wait for a positive culture report. 

(1) Parenteral penicillin (or erythromycin in penicillin-allergic patients) and 

(2) Diphtheria antitoxin 

c. All patients should be hospitalized with respiratory isolation. 

d. Recommendations for close contacts 

(1) Asymptomatic, immunized contacts should be given a tetanus-diphtheria booster if >5 years have 

elapsed since their last dose. 

(2) Asymptomatic, partially immunized or unimmunized contacts must receive one dose of IM penicillin (7-10 

days of oral erythromycin may be used in the penicillin-allergic patient) and begin the immunization series. 

1. Should be considered in adolescents and adults who engage in orogenital sex. 

2. When it occurs in young children, sexual abuse should be suspected. 

3. Treatment is with ceftriaxone (ciprofloxacin resistance is increasingly common). A regimen that is effective against 

Chlamydia (eg, azithromycin, doxycycline) should also be prescribed because of the possibility of co-infection. 

V. FUNGI 

A. Fungi, such as Candida, Cryptococcus, and Histop/asma, can produce pharyngitis in immunocompromised 

patients. 

B. Candida a/bicans overgrowth 

1. Most common in immunocompromised patients (eg, HIV, chemotherapy, diabetes, chronic steroid use), 

patients with history of recent antibiotic and steroid courses, and neonates. 

2. Clinical presentation: physical examination reveals white, removable plaques on an erythematous base. 

3. Treatment: nystatin swish and swallow, or systemic fluconazole 

160


DENTAL EMERGENCIES 

I. NEUROANATOMY OF THE FACE 

Sensory innervation of the face and mouth is via the three branches of the trigeminal nerve (cranial nerve V): ophthalmic 

branch, maxillary branch, and the mandibular branch. The detailed anatomy of these branches is somewhat complex, 

especially that of the maxillary branch. The schematics that follow have been simplified to facilitate the learning process. 

A. Ophthalmic branch of the trigeminal nerve 

Ophthalmic branch of the trigeminal nerve 

Supraorbital nerve* 

Nasociliary nerve 

Forehead and vertex 

of the scalp 

Cornea and dorsal nose 

*Involved in nerve blocks 

B. Maxillary branch of the trigeminal nerve 

Maxillary branch of the trigeminal nerve 

Nasopalatine and greater 

(anterior) palatine nerves 

Hard palate and 

adjacent gingiva 

I 

I 

Anterior 

I / '------,---~ 

V 

Maxi I lary central, 

lateral, and 

cuspid teeth 

Superior alveolar nerves 

Middle 

First and second 

bicuspid teeth (and 

part of first molar) 

*Posterior 

Maxillary molar 

teeth (except 

a part of the 

first molar) 

lnfraorbital nerve* 

Midface, maxillary incisors and premolar teeth, 

upper lip, lower eyelid, side of the nose, and part 

of the first molar 


161


C. Mandibular branch of the trigeminal nerve 

Mandibular branch of the trigeminal nerve 

Buccal nerve Lingual nerve Inferior alveolar nerve* 

Buccal mucous 

membrane and 

mucoperiosteum of the 

posterior 

mandibular teeth 

Anterior 2/3 of the 

tongue 

Mental nerve* 

Chin and 

lower lip 

Mandibular 

teeth, lower lip, 

and chin 


It. FACIAL AND ORAL ANESTHESIA 

A. lntraoral local anesthesia can be achieved with an anesthetic agent (eg, lidocaine or bupivacaine). Unless 

contraindicated, a vasoconstrictor such as epinephrine (1:100,000) is generally combined with the 

anesthetic agent to prolong its duration of action. 

B. Nerve blocks 

1. Supraorbital nerve block - anesthesia to ipsilateral forehead and scalp 

2. lnfraorbital nerve block - anesthesia to the ipsilateral area between the lower eyelid and upper lip, including 

the maxillary incisors, premolars, and a portion of the first molar 

3. Posterior superior alveolar nerve block - anesthesia to ipsilateral maxillary molars (except a portion of the first 

molar) 

4. Inferior alveolar nerve block - anesthesia to ipsilateral mandibular teeth, lower lip, and chin 

5. Mental nerve block - anesthesia to ipsilateral lower lip and chin; bilateral mental nerve blocks are required for 

midline lip lacerations due to cross-innervation. 

C. Supraperiosteal infiltrations provide anesthesia to individual teeth. 

D. Complications 

1. Vascular injection and spasm 

2. Mechanical nerve injury 

3. Needle misplacement resulting in incomplete anesthesia or inadvertent anesthesia of other facial structures 

4. Infections in peripharyngeal spaces (especially with inferior alveolar nerve block) 

Ill. ANATOMY OF A TOOTH 

A. Structural anatomy 

1. Two main portions: crown and root 

2. Enamel covers the dentin which, in turn, covers the pulp (the neurovascular supply of the tooth). 

3. Embedded in the alveolar bone and held in place by cementum and a periodontal ligament. 

B. Sensory innervation 

1. Maxillary teeth: via the anterior, middle, and posterior superior alveolar nerves 

2. Mandibular teeth: via the inferior alveolar nerve 

162


IV. DENTAL EMERGENCIES 

A. Trauma 

1. Management of tooth fractures is determined by the extent of the fracture and the patient's age. 

a. Ellis I 

(1) Only the enamel is fractured; no pain or sensitivity to hot and/or cold. 

(2) Treatment is elective (dentist). 

b. Ellis II 

(1) Enamel is fractured and dentin is exposed; hot and/or cold sensitivity often present. 


c. Ellis Ill 

(a) Apply a dressing of calcium hydroxide paste over the exposed dentin, and cover it with aluminum 

foil or dental dry foil. 

(b) All patients should see a dentist for follow-up within 24 hours and be advised to avoid 

temperature extremes in food and drink. 

(1) Enamel is fractured, and both dentin and pulp are exposed; a pink tinge or drop of blood on the 

fracture site is characteristic (indicates pulpal exposure). Severe pain is common but may be absent if 

the neurovascular supply of the tooth has been disrupted. 

(2) This is a true dental emergency, and immediate dental referral is indicated. If a dentist or endodontist 

is not immediately available, place a piece of moist cotton over the exposed pulp, and cover with a 

piece of aluminum foil or dental dry foil. Provide tetanus immunization as needed. 

2. Alveolar fractures 

a. May be evident (exposed bone) or diagnosed per radiograph (dental panoramic view) 

b. May be associated with dental fractures/avulsions/subluxations 

c. Management 

(1) Immediate dental/oral surgery evaluation for reduction and fixation; wire stabilization is accomplished 

via the dentition. 

(2) Prophylactic antibiotics (penicillin or clindamycin) and tetanus immunization (if indicated) 

3. Avulsed tooth 

a. Permanent tooth 

(1) Holding the tooth by its crown, rinse it gently with saline and immediately replace it in the socket. Do 

not "brush" the tooth clean, because this will remove the periodontal ligament. 

(2) Viability of the tooth decreases with length of time out of the socket(~ 1 % for every 1 minute out). 

(3) Immediate dental referral for stabilization is indicated. 

(4) Prophylactic antibiotics (penicillin or clindamycin) should be prescribed, and tetanus immunization 

provided (if indicated). 

(5) If a tooth cannot be immediately reimplanted, the best storage and transplant medium is Hank's 

solution. Viability of the periodontal ligament can be maintained for 4~6 hours or more in this 

solution. Milk is a good second choice, as is the inner cheek of the mouth of a reliable patient (caution 

to avoid aspirating the tooth). 

b. Deciduous/primary tooth (children 6 months to 5 years old) should not be replaced, because alveolar 

ankylosis may result. These patients should be referred to a pedodontist because spacemaintaining 

procedures and/or appliances are sometimes required. 

4. Intra-oral lacerations 

a. Close with absorbable sutures. 

b. Recheck in 24-48 hours. 

c. Although controversial, antibiotic coverage (penicillin or clindamycin) is recommended by many, 

particularly if the wound is extensive or involves significant amounts of crushed tissue. 

B. Hemorrhage may be due to one of the following: 

1. Trauma 

2. Recent dental manipulation (cleaning, extraction, etc) 

3. Gingivitis 

4. Blood dyscrasias or coagulopathies 

163


C. Orofacial pain 

1. Dental pain 

a. Tooth eruption in adults 

(1) Usually involves the third molars ("wisdom teeth") 

(2) If the gingivae are inflamed (pericoronitis), instruct the patient to irrigate the area with warm saline or 

hydrogen peroxide. 

(3) If fluctuance and pus are present (pericoronal abscess), make a superficial incision and drain, and 

place the patient on an antibiotic (penicillin VK or clindamycin). 

(4) Refer these patients to an oral surgeon for definitive treatment (extraction). 

b. Dental caries 

(1) Oral analgesia and dental referral are usually all that is needed. 

(2) Suspect an associated periapical abscess if the patient complains of sharp, severe pain on tooth 

percussion, especially if the tooth is sensitive to hot or cold. A fluctuant swelling requires incision and 

drainage, an antibiotic, and warm saline rinses every 2 hours. The patient should be seen by a dentist 

within 24 hours. 

c. Postextraction pain 

(1) Periostitis 

(a) 

Pain within 24 hours of extraction 

(b) Responds well to oral analgesics 

(2) Alveolar osteitis ("dry socket") 

(a) Due to loss of clot plus localized osteomyelitis 

(b) Clinical presentation: history of a pain-free interval of 2-4 days after extraction followed by 

sudden onset of excruciating pain unrelieved by analgesics, and a foul breath odor. 

(c) Management 

i. Anesthetic nerve block 

ii. Irrigation of the socket 

iii. Packing with iodoform gauze saturated with a medicated dental paste, eugenol, or 

camphorated phenol provides almost immediate relief. 

iv. Dental follow-up in 12-24 hours 

d. Acute necrotizing ulcerative gingivostomatitis ("trench mouth") 

(1) Only periodontal lesion in which bacteria actually invade non necrotic tissue 

(2) Caused by Fusobacterium and spirochetes 

(3) Clinical presentation 

(a) The patient complains of pain, a metallic taste, and foul breath, which is frequently accompanied 

by fever, malaise, and regional lymphadenopathy. 

(b) Gingivae are swollen and fiery red; the interdental papillae (tissue between the teeth) are swollen, 

ulcerated (or "punched out"), and covered with a grayish pseudomembrane. 


(a) Warm saline irrigation and hexadine rinse 

(b) Antibiotic (penicillin or clindamycin) for patients with fever and lymphadenopathy provides 

dramatic relief within 24 hours. 

(c) Systemic analgesics and topical anesthetic agents can provide the patient sufficient relief to use 

warm saline rinses, as well as eat and drink. 

(d) Dental follow-up is required; a potential complication is the destruction of underlying alveolar bone. 

2. Other causes of facial pain 

a. Sinusitis (see page 143) 

b. Trigeminal neuralgia ("tic douloureux") 

c. Herpes zoster (see page 118) 

d. lschemic heart disease (see page 36) 

e. TMJ disease (see page 147) 

f. Temporal arteritis (see page 438) 

g. Cluster headache 

164



D. Systemic diseases with oral manifestations 

1. Infections 

a. Herpes 

b. Coxsackie virus (hand-foot-mouth disease) 

c. Gonococcus 

d. Syphilis 

e. Measles 

2. Autoimmune/inflammatory states 

a. Systemic lupus erythematosus: large intraoral ulcerations with necrotic borders 

b. Reiter syndrome (urethritis, arthritis, conjunctivitis, oral ulcers) 

c. Sjogren syndrome 

(1) Autoimmune disease characterized by diminished secretion of the lacrimal and salivary glands 

(2) Symptoms include gritty sensation of the eyes, dry mouth (xerostomia), and diminished sense of taste. 

d. Behcet disease, lesions of inflammatory bowel disease, aphthous ulcers 

3. Toxic/metabolic states 

a. Heavy metal poisoning 

(1) Gingival "lead line" in lead poisoning 

(2) Argyria: a blue to bronze discoloration of the oral mucosa in silver poisoning 

b. Gingival hyperplasia 

(1) Diabetes mellitus 

(2) Phenytoin: not related to toxicity; may be secondary to alteration of calcium metabolism 

(3) Nifedipine: not related to toxicity; may be secondary to alteration of calcium metabolism 

4. Granulomatous diseases 

a. Tuberculosis: granulomatous ulcerations of the oral cavity 

b. Wegener granulomatosis: gingival hyperplasia with petechiae 

5. Benign tumors and tumor-like lesions 

a. Pyogenic granuloma 

(1) A proliferation of capillary-rich connective tissue that develops mostly on the lips and gingiva and 

commonly occurs secondary to trauma 

(2) Particularly common during pregnancy ("pregnancy tumor") 

b. Epidermoid cyst 

6. Blood dyscrasias 

a. Acute leukemia: a marked hyperplastic gingivitis (almost covers the teeth) that has a bluish red 

discoloration 

b. Thrombocytopenic purpura 

7. HIV/AIDS 

(1) Petechiae of the oral mucosa 

(2) Spontaneous gingival bleeding 

a. Oropharyngeal candidiasis 

(1) Painless curd-like plaques on an erythematous base that are easily removed with a tongue blade 

(2) Frequently one of the earliest manifestations of AIDS 

b. Hairy leukoplakia 

(1) Asymptomatic white patches with hair-like projections; most commonly located on the lateral aspect 

of the tongue; cannot be removed with a tongue blade 

(2) Believed to be associated with Epstein-Barr virus 

(3) 80% of patients presenting with these lesions go on to develop AIDS within the ensuing 3 years. 

c. Oral Kaposi sarcoma 

(1) Flat bluish red lesions with irregular borders; most commonly found on the hard palate but can be 

located anywhere in the mouth 

(2) Most common AIDS-related malignancy 

165

HEAD, EAR, EYE, NOSE, AND THROAT DISORDERS: PRACTICE CLINICAL SCENARIOS 

HEAD, EAR, EYE, NOSE, AND THROAT DISORDERS: 

PRACTICE CLINICAL SCENARIOS 


Scenario A 

Presentation: An elderly patient with diabetes complains of constant and severe otalgia that is out of 

proportion to the examination, purulent otorrhea, and redness (inflammatory changes) of both the external 

auditory canal and periauricular soft tissue. 


Scenario B 

Presentation: An elderly patient reports nearly a week of prodromal influenza-like illness with dermatomal 

pain, followed by a unilateral rash of the forehead, upper eyelid, and nose. 


Scenario C 

Presentation: A 55-year-old patient with significant myopia (near sightedness) and a history of cataract 

removal complains of flashing lights with floaters and vision loss. He also reports a shadow that varies from 

light grey to completely black spreads across his visual field like a curtain being closed. 


166

HEAD, EAR, EYE, NOSE, AND THROAT DISORDERS: PRACTICE CLINICAL SCENARIOS 


Scenario A 

Diagnosis: malignant otitis externa 

Diagnostic evaluation: Laboratory studies include a CBC (leukocytes may be normal or mildly increased), 

a serum chemistry panel (to look for glucose intolerance) and erythrocyte sedimentation rate (invariably 

increased), and cultures of the otorrhea (Pseudomonas is causative organism in 95% of cases). MRI and 

CT are helpful in evaluating the extent of soft-tissue involvement, abscess formation, and intracranial 

extension. However, they are not reliable for detection of early osteomyelitis. 

Management: Management consists of pain control, systemic and ototopic antibiotics that cover 

Pseudomonas (eg, fluoroquinolones), and consult with ENT. Mild to moderate cases may be treated on 

outpatient basis. More severe cases typically require admission. 

Scenario B 

Diagnosis: herpes zoster ophthalmicus 

Diagnostic evaluation: V1 rash may present at any stage of progression from erythematous macules to 

vesicles to pustules that crust over within 1 week. Hutchinson sign (herpes zoster lesion at the tip, side, or 

root of the nose) is prognostic of ocular involvement. Corneal epithelial lesions are best seen with a slitlamp 

and fluorescein staining. Herpes zoster ophthalmicus is typically a clinical diagnosis, and laboratory 

studies are often not necessary. If unclear, a Tzanck smear and Wright stain may be obtained. Nearly 100% 

of the U.S. population have been infected with varicella-zoster virus by the age of 60. 

Management: Management consists of pain control and antiviral treatment (eg, acyclovir, valacyclovir) for 

7-10 days. Oral corticosteroids may be considered. Consult with ophthalmology. 

Scenario C 

Diagnosis: retinal detachment 

Diagnostic evaluation: Laboratory studies are often not necessary unless part of a preoperative plan. Plain 

radiographs, CT, and MRI are also not necessary unless traumatic injury indicates. Ocular ultrasound (of 

the closed eye) may be diagnostic with experienced operators. 

Management: Avoid any pressure on the globe and limit activity. Consult with ophthalmology. 

167

168 

NOTES

ABDOMINAL AND GASTROINTESTINAL DISORDERS 


Upper Gastrointestinal Bleeding ............................................................................................................................... 176 

Evaluation .......................................................................................................................................................... 1 76 

Blatchford Score ................................................................................................................................................. 1 77 

Specific Treatment of Ruptured Varices ............................................................................................................... 1 77 

Treatment of Bleeding Due to Peptic Ulceration ................................................................................................. 177 

Esophageal Disorders ................................................................................................................................................ 1 78 

Functional Anatomy ........................................................................................................................................... 1 78 

Dysphagia .......................................................................................................................................................... 1 78 

Esophageal Trauma ............................................................................................................................................. 180 

Esophageal Foreign Body Ingestion ..................................................................................................................... 181 

Peptic Ulcer Disease ................................................................................................................................................. 183 

Pathophysiology ................................................................................................................................................. 1 83 

Predisposing Factors ........................................................................................................................................... 183 

Clinical Presentation .......................................................................................................................................... 183 

Diagnostic Evaluation ......................................................................................................................................... 183 

Management of Uncomplicated Peptic Ulcer Disease ........................................................................................ 184 

Comp I ications .................................................................................................................................................... 1 85 

Perforated Viscus ....................................................................................................................................................... 185 

Gallbladder Perforation ...................................................................................................................................... 185 

Small-Bowel Perforation ..................................................................................................................................... 186 

Large-Bowel Perforation ..................................................................................................................................... 186 

Management of a Known or Suspected Perforated Viscus ................................................................................... 186 

Acute Abdomen ........................................................................................................................................................ 187 

Appendicitis ....................................................................................................................................................... 187 

Bowel Obstruction ............................................................................................................................................. 1 89 

Volvulus ............................................................................................................................................................. 191 

Mesenteric Vascular lschemia/lnfarction ............................................................................................................. 191 

Hernias .............................................................................................................................................................. 193 

Ileitis and Colitis ................................................................................................................................................. 194 

Irritable Bowel Syndrome ................................................................................................................................... 197 

Colonic Diverticular Disease .............................................................................................................................. 198 

Anorectal Disorders .................................................................................................................................................. 199 

Hemorrhoids ...................................................................................................................................................... 1 99 

Anal Fissure ........................................................................................................................................................ 200 

Peri rectal (Anorectal) Abscesses .......................................................................................................................... 200 

Miscellaneous Anorectal Disorders ..................................................................................................................... 201 

Fistula-in-Ano ............................................................................................................................................. 201 

Rectal Prolapse ........................................................................................................................................... 201 

Pi lonodal Sinus ........................................................................................................................................... 202 

Anorectal Tumors ........................................................................................................................................ 202 

Rectal Foreign Bodies .................................................................................................................................. 202 

Diarrhea and Food Poisoning .................................................................................................................................... 203 

General Information ........................................................................................................................................... 203 

Viral Diarrheal Diseases ..................................................................................................................................... 203 

Bacterial Diarrheal Diseases ............................................................................................................................... 203 

Parasitic Gastrointestinal Infections ..................................................................................................................... 212 

Diarrhea in the Al DS Patient ............................................................................................................................... 21 5 

Biliary Tract Disorders ............................................................................................................................................... 216 

General Information ........................................................................................................................................... 216 

169


Cholelithiasis ...................................................................................................................................................... 216 

Cholecystitis ....................................................................................................................................................... 21 6 

Variations and Comp I ications of Cholecystitis .................................................................................................... 21 7 



Management ...................................................................................................................................................... 21 8 

Hepatitis ................................................................................................................................................................... 218 

Viral Hepatitis .................................................................................................................................................... 218 

Toxic Hepatitis ................................................................................................................................................... 221 

Alcoholic Liver Disease ............................................................................................................................................. 222 

Syndromes ......................................................................................................................................................... 222 

Comp I ications .................................................................................................................................................... 223 

Pancreatitis ............................................................................................................................................................... 224 

Etiology .............................................................................................................................................................. 224 



Management ...................................................................................................................................................... 225 

Poor Prognostic Signs ......................................................................................................................................... 225 

Comp I ications .................................................................................................................................................... 22 6 

170

ABDOMINAL AND GASTROINTESTINAL DISORDERS: SELF-ASSESSMENT QUESTIONS 

ABDOMINAL AND GASTROINTESTINAL DISORDERS: 


1. The most common cause of oropharyngeal (transfer) dysphagia is: 

(a) 

Obstructive lesions 

(b) Spasm 

(c) 

Neuromuscular disorders and inflammatory lesions 

(d) Carcinoma 

2. All of the following statements regarding Boerhaave syndrome are accurate except: 

(a) 

It is usually the result of sudden, violent, repeated vomiting. 

(b) It is a partial-thickness tear of the esophageal wall. 

(c) Associated physical findings with this entity include subcutaneous emphysema and the presence of a 

mediastinal crunch (Hamman sound). 

(d) Radiographic findings may include a left pneumothorax, a left pleural effusion, mediastinal emphysema, and a 

widened mediastinum. 

3. The most common area for an esophageal foreign body to lodge in an adult is the: 

(a) Aortic arch (T4) 

(b) Cricopharyngeal muscle (C6) 

(c) Lower esophageal sphincter/diaphragmatic hiatus (Tl 0-Tl 1) 

(d) Tracheal bifurcation (T6) 

4. Which of the following is 0the most appropriate therapy for a button battery lodged in the esophagus? 

(a) Observation 

(b) Removal with a Foley catheter 

(cl IV glucagon 

(d) Immediate removal via endoscopy 

5. What is the most likely diagnosis in patients with abdominal pain that awakens them at night and is relieved by food 

intake and ingestion of antacids? 

(a) 

Duodenal ulcer 

(b) Myocardial ischemia 

(c) Gastric ulcer 

(d) Perforated peptic ulcer 

6. Factors that have definitely been demonstrated to predispose to peptic ulcer disease include all of the following except: 

(a) Alcohol ingestion 

(b) Cigarette smoking 

(c) Type O blood 

(d) Use of NSAIDs or aspirin 

7. Which of the following statements regarding sucralfate is accurate? 

(a) It neutralizes gastric acid. 

(b) It works most effectively at a gastric pH of 4.5. 

(c) It inhibits secretion of mucus. 

(d) It inhibits pepsin, adsorbs bile acids, and increases mucosa! prostaglandin production. 

8. The most common cause of small-bowel obstruction is: 

(a) 

Neoplasms 

(b) Hernias 

(c) Adhesions 

(d) Gallstones 

171


9. All of the following statements regarding volvulus are accurate except: 

(a) Although cecal volvulus can occur at any age, it most commonly affects patients in their twenties and thirties. 

(b) Volvulus is an example of a closed-loop obstruction. 

(c) Sigmoid volvulus occurs in patients with a history of chronic, severe constipation; it primarily affects older, 

bedridden patients with significant comorbid disease and psychiatric patients of any age. 

(d) Cecal volvulus is more common than sigmoid volvulus. 

10. The following statements regarding ulcerative colitis are accurate except: 

(a) 

Inflammation involves all layers of bowel as well as the mesenteric lymph nodes. 

(b) There is a much higher incidence of colon cancer in patients with ulcerative colitis than in the general 

population. 

(c) 

It is characterized clinically by bloody feces associated with crampy abdominal pain. 

(d) Complications include intestinal hemorrhage and toxic megacolon. 

11. Unlike small-bowel obstruction due to other causes, an important therapeutic modality in the treatment of smallbowel 

obstruction due to Crohn disease is: 

(a) 

Administration of antibiotics 

(b) Nasogastric suction 

(c) Administration of steroids 

(d) IV hydration and correction of electrolyte imbalance 

12. All of the following statements regarding pseudomembranous colitis are accurate except: 

(a) 

It is due to ingestion of broad-spectrum antibiotics (such as the cephalosporins or ampicillin) that alter the 

gut flora. 

(b) Although they may be delayed, symptoms usually begin within 7-10 days after antibiotic treatment is started. 

(c) 

Diagnosis is confirmed by identifying the C!ostridium difficile toxin in the feces. 

(d) Vancomycin is the treatment of choice for patients with mild to moderate disease. 

13. A patient presents with the complaint of slight hematochezia and intense rectal pain with bowel movements that 

linger for several hours and then resolve. The most likely diagnosis is: 

(a) Internal hemorrhoids 

(b) Anal fissure 

(c) Thrombosed external hemorrhoid 

(d) Perirectal abscess 

14. A patient presents to the emergency department complaining of frothy, foul-smelling diarrhea and abdominal pain. 

He says he feels bloated and has a lot of gas. Nine days ago he returned from a hiking trip in Colorado, where he 

had been drinking water from streams. The most likely cause of his diarrhea is: 

(a) 

Ciardia lamblia 

(b) Vibrio parahaemolyticus 

(c) Aeromonas hydrophila 

(d) Vibrio cholerae 

15. Except for __ , the primary mechanism by which the following bacteria induce illness is by excretion of a toxin. 


(b) Bacillus cereus 

(c) C!ostridium difficile 

(d) Yersinia enterocolitica 

16. An adolescent presents with fever, crampy abdominal pain, and watery diarrhea. Physical examination reveals 

exquisite tenderness in the right lower quadrant, and a wet mount of the feces reveals WBCs. The most likely 

organism responsible for this presentation is: 

(a) 

Yersinia enterocolitica 

(b) Shigella 

(c) C/ostridium perfringens 

(d) Vibrio parahaemolyticus 

172


17. The organism most often responsible for traveler's diarrhea is: 

(a) Salmonella 

(b) Invasive£ coli 

(c) Ciardia lamblia 

(d) Enterotoxigenic £ coli 

18. Staining of the feces for leukocytes is helpful in uncovering the probable cause of an acute episode of diarrhea as 

well as determining appropriate therapy, particularly when this information is combined with a detailed history. 

Leukocytes are typically present with infections induced by all of the following organisms except: 

(a) Clostridium difficile 

(b) Viruses 

(c) Invasive £ coli 

(d) Salmonella 

19. All of the following statements regarding scombroid fish poisoning are accurate except: 

(a) It is most commonly associated with ingestion of dark-fleshed or red-muscled fish. 

(b) It results from ingestion of toxins with histamine-like properties that form in improperly preserved or 

refrigerated fish. 

(c) Epinephrine IM should be administered. 

(d) Symptoms include facial flushing, conjunctiva! hyperemia, palpitations, nausea, vomiting, and diarrhea. 

20. The most common cause of post-transfusion hepatitis is: 

(a) Hepatitis A 

(b) Hepatitis B 

(c) Hepatitis C 

(d) Hepatitis D 

21. During the "window period" between the disappearance of HB 5 

Ag and the appearance of anti-HB 5 

, the only marker 

of hepatitis B infection that may be present in the serum is: 

(a) HBeAg 

(b) Anti-HB 0 

(c) Anti-HBc 

(d) HBCAg 

22. The presence of anti-HBs in the serum indicates: 

(a) Ongoing viral replication and high infectivity 

(b) Immunity 

(c) The carrier state 

(d) Low infectivity 

23. The presence of marked eosinophilia is typical in patients infected with: 

(a) 

Necator americanus 

(b) Enterobius vermicularis 

(c) Ciardia lamblia 


24. A SO-year-old man with a history of chronic alcoholism presents with hematemesis. The bleeding followed an 

episode of violent and repeated vomiting. It was moderate in quantity and associated with pain on swallowing but 

has resolved on its own. The diagnostic study of choice for evaluating this patient is: 

(a) A chest radiograph 

(b) A barium esophagogram 

(c) A CT of the chest 

(d) Endoscopy 

173


25. An 8-year-old child presents with a foreign body sensation in his throat and relates that he "accidentally swallowed" 

a quarter a couple of hours before presentation. The PA view of the chest reveals the flat surface of the coin. Where 

is the coin located? 

(a) In the esophagus 

(b) In the trachea 

(c) Unable to tell from the information given 

26. All of the following types of viral hepatitis may be associated with development of a chronic infectious state except: 

(a) 

Hepatitis B 

(b) Hepatitis C 

(c) Hepatitis delta 

(d) Hepatitis E 

27. All of the following statements regarding Helicobacter pylori are accurate except: 

(a) It is a gram-negative, spiral-shaped organism that colonizes only gastric mucosa. 

(b) It has been associated with the development of peptic ulcer disease (particularly duodenal ulcers). 

(c) In patients with peptic ulcer disease who are infected with this organism, eradication of the infection effectively 

eliminates the ulcer diathesis. 

(d) Single-agent therapy with either bismuth or amoxicillin is very effective in eliminating this organism. 

28. A 38-year-old woman presents with epigastric pain of several hours duration. She states that it started shortly after 

eating a meal of fried shrimp and onion rings. She recalls that she has had similar pain in the past, but states that 

it has never lasted this long. She is moderately obese and has a history of hypercholesterolemia for which she is 

taking gemfibrozil. Her past medical history is otherwise noncontributory, and there is no prior history of abdominal 

surgery. Examination reveals epigastric and right upper quadrant tenderness. She is afebrile, and her rectal 

examination is negative. The most useful initial test for evaluating this patient is: 

(a) A CT scan of the abdomen 

(b) Biliary scintiscanning (HIDA, DISIDA) 

(c) Abdominal ultrasonography 

(d) Plain radiographs of the abdomen 

29. The most accurate study for confirming diagnosis of acute cholecystitis is: 

(a) A CT scan of the abdomen 

(b) Biliary scintigraphy (HIDA, DISIDA) 

(c) Abdominal ultrasonography 

(d) Plain radiographs of the abdomen 

30. All of the following statements regarding anal canal tumors are accurate except: 

(a) They are defined as tumors that occur proximal to the dentate line. 

(b) Presenting symptoms may include rectal bleeding, decrease in fecal caliber, constipation, and weight loss. 

(c) They represent 80% of al I a no rectal tumors. 

(d) They are slow to metastasize and have a low-grade malignant potential. 

31. Most acute episodes of diarrhea are caused by: 

(a) Viruses 

(b) Enterotoxin-producing bacteria 

(c) Invasive bacteria 

(d) Parasites 

32. Which of the following statements regarding diarrhea in patients with AIDS is false? 

(a) Cytomegalovirus and Cryptosporidium are the two most common causes of diarrhea in these patients. 

(b) Multiple organisms are responsible in up to 25% of cases. 

(c) It is not a self-limited disease in these patients. 

(d) Empiric antibiotics should be administered immediately. 

174


33. Which of the fol lowing statements regarding chest pain due to esophageal spasm is least accurate? 

(a) It is frequently triggered by emotional upset. 

(b) It can be precipitated by drinking extremely hot or cold liquids. 

(c) It can produce a dull discomfort, localized pressure, or a sensation of severe squeezing pressure across the 

middle of the chest. 

(d) Pain associated with esophageal spasm can be distinguished from that which occurs in association with 

myocardial ischemia by evaluating its response to nitroglycerin; pain of esophageal spasm is not relieved 

by nitroglycerin. 

34. The finding of __ on plain abdominal radiographs is strongly suggestive of mesenteric infarction. 

(a) 

lieus 

(b) Pneumatosis intestinalis 

(c) Gasless abdomen 

(d) Sentinel loop 

35. Evaluation of an elderly patient who presents with severe abdominal pain reveals a diagnosis of nonocclusive 

mesenteric ischemia. In the absence of peritonitis/necrotic bowel, definitive therapy for this patient consists of: 

(a) Systemic heparinization 

(b) Urokinase infusion 

(c) Intra-arterial papaveri ne infusion 

(d) Exploratory laparotomy 

36. In a patient with acute pancreatitis, which of the following laboratory reports is most likely to be associated with the 

highest mortality rate according to the Ranson criteria? 

(a) Amylase 800 units/L, AST 300 units/L, WBC count 3,000/mm 3 

(b) Lipase 1100 units/L, AST 350 units/L, WBC count 17,000/mm 3 

(c) LOH 300 units/L, ALT 200 units/L, glucose 50 mg/dL 

(d) LOH 400 units/L, glucose 400 mg/dL, WBC count 18,000/mm 3 

37. Hepatitis D is caused by: 

(a) An RNA virus 

(b) A defective RNA virus 

(c) A DNA virus 

(d) A defective DNA virus 

38. Which of the following laboratory findings is not consistent with a diagnosis of alcoholic hepatitis? 

(a) AST> ALT 

(b) AST and ALT levels in the thousands 

(c) Prolonged prothrombin time 

(d) Increased bilirubin and alkaline phosphatase levels 

39. The toxic metabolite responsible for producing hepatic necrosis in patients who overdose on acetaminophen is: 

(a) APAP-mercapturate and cysteine 

(b) APAP-sulfate 

(c) APAP-glucuronide 

(d) N-acetyl-p-benzoquinone imine (NAPQI) 

ANSWERS 

1 . C 8. C 15. d 22. b 29. b 36. d 

2. b 9. d 16. a 23. a 30. d 37. b 

3. C 10. a 17. d 24. d 31. a 38. b 

4. d 11 . C 18. b 25. a 32. d 39. d 

5. a 12. d 19. C 26. d 33. d 

6. a 13. b 20. C 27. d 34. b 

7. d 14. a 21. C 28. C 35. C 



175


I. UPPER GASTROINTESTINAL BLEEDING 

A. Evaluation 

1. Evaluation of the patient with a presumed upper GI bleed must start with an assessment of hemodynamic 

stability. 

a. Unstable patients require immediate resuscitation and stabilization. 

(1) Two large-bore (at least 18-gauge) IV lines for crystalloid infusion (2 L bolus); continue fluids until 

vital signs have stabilized or 40 ml/kg have been given (adults). 

(2) Cardiac monitoring. 

(3) Oxygen administration as needed. 

(4) Blood should be sent immediately for hemoglobin and hematocrit, platelet count, prothrombin time/ 

INR, and type and crossmatch. 

(5) Immediate transfusion of type-specific or crossmatched blood (4 units minimum) if available (type 0 

if type-specific blood unavailable). 

(6) May need reversal of coagulation abnormalities; the following regimen is a Class 1 C recommendation: 

(a) Hold anticoagulation therapy 

(b) Vitamin K 10 mg (may be given IV slowly) 

(c) Fresh frozen plasma or 

(d) Prothrombin complex concentrate or 

(e) Activated recombinant factor VII 

(7) Novel anticoagulants may require specific reversal agents such as idarucizumab for reversal of 

dabigatran. Reversal agents for other novel anticoagulants are in development. 

b. Patients who remain unstable require immediate consult with a gastroenterologist for immediate 

endoscopy. 

c. Nasogastric lavage does not decrease mortality or transfusion requirements. Clear aspirate may miss up 

to 15 % of clinically relevant lesions. 

d. Administration of proton-pump inhibitors for acute undifferentiated upper GI bleed does not improve 

mortality. It may decrease incidence of rebleeding (controversial) and does decrease need for surgery. 

e. Somatostatin analog (octreotide) initiation does not decrease mortality in upper GI bleed from 

esophageal varices. However, administration combined with endoscopy increases initial hemostasis and 

decreases rebleeding. 

f. Restrictive transfusion strategy (transfuse only if hemoglobin 30 (LR +7.5) 

(4) Hematocrit 100 beats/min 

(3) Nasogastric lavage showing bright red blood 

(4) Hemoglobin 90 mg/dl, or WBC >12,000/mm 3 

176


B. Blatchford Score 

1. Accurately predicts the need for urgent or emergent intervention in a patient with acute upper GI bleeding 

(may still require validation in U.S. hospitals) 

2. Does not require nasogastric lavage 

3. Based on hemoglobin, BUN, systolic blood pressure, pulse, melena, syncope, and history of hepatic disease 

or cardiac failure 

4. Specific scores 

a. Patients with upper GI bleed and a score of O have an LR of 0.02 of needing urgent intervention. 

b. Those with a score of :S:2 have an LR of 0.08 of needing urgent intervention. 

C. Specific treatment of ruptured varices 

1. Immediate therapy: octreotide or vasopressin infusion 

a. Octreotide is considered more effective than vasopressin and has fewer adverse effects. 

b. Vasopressin has no proven mortality benefit but may be of use in the exsanguinating patient. 

2. Placement of a balloon tamponade device may be used as a temporary measure while awaiting endoscopy. 

3. Endoscopic band ligation or sclerotherapy 

4. If endoscopic intervention is unsuccessful, perform angiography with embolization of the gastric vein. 

5. Transjugular intrahepatic portosystemic shunt placement for refractory bleeding helps prevent rebleeding. 

6. Surgical therapy is rarely used but may be only option in continuously bleeding patient. 

7. In patients with cirrhosis and upper GI bleed, prophylactic antibiotic use decreases all-cause mortality, 

rebleeding, death from bacterial infection, and length of hospital stay. 

D. Treatment of bleeding due to peptic ulceration 

1. Peptic ulceration is the most common cause of upper GI bleeding, even in patients with history of varices. 

2. Duodenal ulcers (most common): 29% of upper GI bleeds 

3. Gastric ulcers: 16% of upper GI bleeds 

4. Combined, gastric and duodenal ulcers cause 45%-50% of all upper GI bleeding. 

5. Management 

a. Volume replacement with normal saline or lactated Ringer's via two large-bore IV lines 

b. Oxygen as needed 

c. Foley catheter placement to monitor volume resuscitation 

d. Lavage 

(1) Can be used to monitor blood loss and prepare patients for endoscopy but is not helpful in stopping 

the bleeding or preventing its recurrence. 

(2) To prevent complications, only room-temperature solutions (normal saline or water) should be used; 

pneumoperitoneum must first be excluded. 

(3) Many gastroenterologists do not consider performance of gastric lavage necessary to establish the 

diagnosis or monitor bleeding. 

e. Erythromycin 250 mg IV push over 20 minutes provides satisfactory conditions for endoscopy without 

the need for nasogastric lavage. 

f. IV proton-pump inhibitor therapy should be given to any patient with active upper GI bleeding. 

(1) No proven benefit on mortality, but recent evidence suggests decreased rate of rebleeding and 

decreased need for surgical intervention. 

(2) IV formulations of pantoprazole and esomeprazole are available. 

6. Consult with a gastroenterologist and a general surgeon is prudent in any patient with significant upper GI 

bleeding (see above). 

7. If the patient does not respond to the above measures and bleeding persists, early or emergent endoscopic 

evaluation may be needed for both localization of the bleeding site and treatment. Although arteriography is 

also useful in locating the bleeding site (if the rate of bleeding is :0:0.5 ml/min), it has largely been supplanted 

by endoscopy, which is usually more accurate; it is currently reserved for situations in which endoscopy is 

unavailable or nondiagnostic. 

8. Surgical intervention is indicated for patients who do not respond to medical therapy and endoscopic 

hemostasis. 

9. Older patients are more likely to bleed, re-bleed, require surgery to control bleeding, and require blood 

products. 

177


II. ESOPHAGEAL DISORDERS 

A. Functional anatomy 

1. The esophagus originates in the hypopharynx at the level of the cricoid cartilage (C6) and terminates in the 

cardia of the stomach (T11 ). It is -25 cm (1 O") long and is divided into three segments (helpful in locating 

foreign bodies and abnormalities of contiguous structures on radiograph). 

a. Upper (cervical) = 4-5 cm 

b. Middle (thoracic) = 15-20 cm 

c. Lower (abdominal)= 2-3 cm 

2. Layers of the esophagus 

a. Inner mucosa: Esophagitis involves both the inner mucosa and submucosa; if severe and prolonged, 

esophagitis may result in scarring and stricture formation. Treatment is dilatation. If the cause is eliminated, 

recurrent stricture is not a problem. 

b. Submucosa: Because there is no serosa, perforation of the submucosa extends into surrounding mediastinal 

structures and leads to a diffuse, malignant, often rapidly progressive and fatal mediastinitis. 

c. Muscle layers: If the two muscle layers are split by bougienage or by repeated dilatation, they scar, which 

leads to stricture formation. Treatment is dilatation, but strictures recur. 

3. Cricopharyngeal muscle (upper esophageal sphincter) is located at the level of C6. 

4. Muscle composition of the esophagus 

a. Upper third is striated muscle. 

b. Middle third is smooth and striated muscle. 

c. Distal third (and remaining GI tract) is smooth muscle. 

5. Neuromuscular anatomy 

B. Dysphagia 

a. Extrinsic nervous system 

(1) Spinal accessory nerve innervates the cervical esophagus. 

(2) Vagus nerve innervates the remainder of the esophagus. Stimulation of this parasympathetic nerve 

during esophageal intubation and endoscopy causes bradycardia. 

(3) Sympathetic fibers from the cervical and thoracic ganglia also innervate the esophagus. Stimulation 

causes dysphagia and referred pain to the chest and epigastrium. 

b. Intrinsic nerve supply (Auerbach and Meissner plexuses, which are contained between the muscle layers 

of the esophageal wall) is altered in motor disorders (achalasia, diffuse spasm) and destroyed by corrosives 

and some collagen vascular disorders (scleroderma, those associated with Raynaud syndrome). 

1. Dysphagia is defined as "difficulty swallowing"; it signifies the presence of organic pathology of the 

esophagus in nearly all cases. Odynophagia means "pain on swallowing"; it often indicates the presence of an 

inflammatory or infectious lesion. 

2. Oropharyngeal (transfer) dysphagia (difficulty swallowing) 

a. Symptoms occur within the first 2 seconds of swallowing (cough, choking, drooling, repeated swallowing 

attempts) 

b. Neuromuscular disorders account for most cases. (Difficulty swallowing liquids [particularly cold liquids] 

suggests a neuromuscular disorder.) 

(1) Neuromuscular causes (80% of cases) 

(a) Stroke (most common cause) 

(b) Polymyositis and dermatomyositis 

(c) Scleroderma (>50% complain of dysphagia) 

(d) Myasthenia gravis (reversible with edrophonium) 

(e) Multiple sclerosis, amyotrophic lateral sclerosis, Parkinson disease 

(f) 

Lead poisoning 

(2) Inflammatory/infectious causes 

(a) 

Pharyngitis (Streptococcus, Candida, herpes) 

(b) Oropharyngeal abscess 

(3) Infectious/neuromuscular causes 

(a) Poliomyelitis 

(b) Diphtheria 

178


(c) Botulism 

(d) Rabies 

(e) Tetanus 

c. Cancer of the tongue, pharynx, or larynx may also cause oropharyngeal dysphagia. 

3. Upper esophageal dysphagia 

a. Difficulty swallowing occurs within the first 2-4 seconds and is caused by obstructive lesions in most cases. 

(1) Intrinsic causes of luminal narrowing are esophageal webs (which are associated with iron deficiency 

anemia, Plummer-Vinson syndrome), and carcinoma. 

(2) Extrinsic compression can be produced by numerous conditions, eg, thyroid enlargement, Zenker 

diverticulum, left atrial enlargement, aortic aneurysm. 

b. Dysphagia due to obstructive lesions is typically progressive (starts with solid foods and eventually 

progresses to liquids). 

4. Lower esophageal dysphagia (difficulty swallowing) 

a. Symptoms occur 4-10 seconds after the bolus is swallowed and are usually worse with solids. 

b. Clinical presentation: patients complain of a substernal "sticking" sensation and are usually able to 

accurately pinpoint the location. 

c. Lower esophageal dysphagia is usually due to luminal narrowing. This narrowing can be either constant 

(eg, strictures, carcinoma) or intermittent (eg, spasm). 

(1) Carcinoma is the most common cause of lower esophageal dysphagia. Difficulty swallowing solids 

occurs initially and progresses to difficulty swallowing semisolids and finally liquids. 

(2) Achalasia is characterized by marked increase in the resting pressure of the lower esophageal 

sphincter and absent peristalsis in the body of the esophagus. Dysphagia is the most common 

presenting complaint. 

(a) Patients are usually 20-40 years old. 

(b) A diagnostic clue is that dysphagia occurs with both solids and liquids. 

(c) The patient may regurgitate undigested material; no acidic taste. 

(3) Esophageal strictures result from esophageal reflux. There is a history of heartburn before the onset 

of dysphagia, which is worse with solid foods and is constant; reflux-induced spasm without stricture 

produces intermittent dysphagia. 

(4) "Steakhouse syndrome" is characterized by intense discomfort that develops shortly after swallowing 

a large piece of meat. It can occur in patients with a normal esophagus but is more commonly 

associated with one of the fol lowing if the problem has occurred repeatedly: 

(a) Carcinoma 

(b) Stricture 

(c) Schatzki ring (a fibrous, diaphragm-like stricture near the gastroesophageal junction); is actually 

an esophageal web 

d. Lower esophageal dysphagia and chest pain: gastroesophageal reflux disease or ischemic heart disease? 

Chest pain arising from the esophagus may mimic chest pain due to myocardial ischemia because of 

similar segmental innervation of the heart and esophagus; both may present with ST segment abnormalities 

on ECG. The history is by far the most useful information in differentiating these two entities. 

(1) A substernal burning sensation (heartburn/pyrosis) is a common complaint in patients with esophageal 

reflux. However, a dull discomfort, localized pressure, or severe squeezing pain across the middle of 

the chest may be seen when reflux is associated with esophageal spasm. 

(2) Exacerbation of symptoms with stooping, lying, or leaning forward suggests reflux. Postural 

exacerbation of pain is uncommon with ischemic heart disease. 

(3) Water brash (a hypersalivation response) is commonly associated with reflux. 

(4) Radiation of pain into the abdomen occurs more often in patients with reflux than in those with 

coronary artery disease. Radiation into both arms is rarely seen in reflux. 

(5) A feeling of fullness after meals and relief of chest pain with antacids are key points in the history. This 

history is rarely present in patients with ischemic heart disease. 

(6) Diffuse esophageal spasm without reflux may appear clinically similar to myocardial ischemia. 

Differentiating features include the following: 

(a) Emotional upset frequently triggers spasm. 

(b) Chest pain from esophageal spasm occurs spontaneously and most often at rest. 

(c) Diffuse spasm may be precipitated by swallowing liquids of extreme temperatures (hot or cold). 

179


(d) Esophageal spasm and myocardial ischemia are both relieved by nitroglycerin. Although the latter 

generally responds more quickly, response to nitroglycerin is not useful in distinguishing these clinical 

entities. 

(e) 

If a barium swallow is done, "corkscrew" appearance. 

5. Esophagi tis (inflammation of the esophagus) 


(1) Chest pain, dysphagia, odynophagia, or those of reflux 

(2) Chest pain is typically constant, acute in onset, and unresponsive to treatment with antacids. 

b. Etiology 

(1) Most common cause is gastroesophageal reflux disease (GERO) 

(2) Infections: typically present with severe odynophagia; may have dysphagia to solids and liquids 

(a) 

Fungal (Candida albicans) 

(b) Viral (herpes simplex, varicella zoster, cytomegalovirus) 

(c) Bacterial (mycobacterium) 

(d) lmmunosuppressed patients are more likely to have herpes simplex virus or cytomegalovirus as 

etiology because of prophylactic treatment of fungal infections. 

(3) Radiation 

(4) Corrosive agents (alkalis, acids) 

(5) Pill esophagitis: antibiotics (especially doxycycline and tetracycline), bisphosphonates, antiinflammatory 

agents, potassium chloride, and iron sulfate 

c. Management 

(1) Fluconazole is the drug of choice for esophageal candidiasis. 

(2) lmmunocompromised patients should be assumed to have herpes simplex and should receive acyclovir. 

C. Esophageal trauma 

1. Etiology 

a. Swallowing (foreign body, caustic agent) 

b. Instrumental (surgery, bougienage, rigid endoscopy, intubation, etc); iatrogenic perforation is the most 

common cause of esophageal perforation. 

c. Chest trauma (open, closed) 

d. Sudden, violent, and usually repeated increase in the intra abdominal pressure against a weakened 

esophageal wall; most common cause is violent and repeated vomiting/retching. 

(1) Mallory-Weiss syndrome 

(a) A partial thickness tear (mucosal lesion) of the distal esophagus or gastric cardia associated with 

dysphagia, odynophagia, and upper GI bleeding. 

(b) Clinical presentation: the prominent symptom is bleeding, which is usually mild to moderate and 

usually resolves spontaneously. 

( c) Predisposing factors 

i. Alcoholism 

ii. Hiatal hernia 

iii. Gastritis/esophagitis 

(d) Diagnostic study of choice is endoscopy. 

(2) Boerhaave syndrome 

(a) 

Specifically refers to spontaneous esophageal rupture, usually due to retching 

(b) A full-thickness tear (perforation) typically of the left posterolateral aspect of the distal esophagus 

(an intrinsically weak area) 

(c) Clinical presentation 

1. The prominent symptom is severe, lancinating chest pain. 

ii. Physical findings include subcutaneous emphysema, mediastinal "crunch" (Hamman sound), 

a left pneumothorax and/or pleural effusion, and possibly epigastric tenderness. 

(d) Diagnostic evaluation 

1. Chest radiograph: characteristic findings include a left pneumothorax, a left pleural effusion, 

mediastinal emphysema, and a widened mediastinum. 

ii. An esophagram using water-soluble oral contrast confirms the diagnosis. 

180


(e) Management 

(f) 

• Water-soluble contrast causes less inflammatory response (mediastinitis) than barium but 

has a lower sensitivity. If an initial water-soluble contrast esophagram is negative, it should 

be followed by a barium study if suspicion persists. 

• Option following water-contrast or barium swallow if nondiagnostic is CT scan in the 

noncritical patient whose diagnosis is unclear. 

i. Fluid resuscitation 

ii. Broad-spectrum IV antibiotics 

iii. Boerhaave syndrome is a surgical emergency; do not delay surgical consult for CT or other 

advanced imaging. 

This lesion produces the most malignant type of mediastinitis (acid burn and bacterial infection). 

Morbidity and mortality, due to shock and septicemia, occur very rapidly (


(3) Button batteries in the esophagus require immediate endoscopic removal. 

(4) Radiopaque esophageal foreign bodies will show on chest radiographs. 

(5) Some fish bones are radiolucent and not visible on plain radiographs. This is also true of plastic objects 

and toothpicks. 

(6) Radiographic evaluation of asymptomatic patients with suspected or known ingestions should also 

be considered, because many patients are asymptomatic; up to one-third of children with esophageal 

foreign bodies are asymptomatic. Newer recommendations include use of CT scan to demonstrate 

foreign bodies not visualized on plain radiographs. 

(7) If the esophageal foreign body is not detected by neck and chest radiographs, an esophagram or 

endoscopy should be performed. 

(a) 

Endoscopy: the diagnostic modality of choice (if readily available), because it can be used to both 

visualize and remove the foreign body. 

(b) Esophagram: if a perforation is suspected, a watersoluble contrast agent should be selected. 

If aspiration is a concern, barium should be used. If both perforation and aspiration are 

considerations, a nonionic contrast media should be used. Before the procedure, a nasogastric 

tube should be inserted above the obstruction to prevent aspiration of unswallowed liquids that 

collect there. 

(c) Barium should not be used if subsequent endoscopy is anticipated because it may limit or obscure 

visualization of the esophageal foreign body by the endoscopist. 

4. Although objects do occasionally lodge or become impacted in the esophagus (particularly those with sharp 

edges), most will pass as a matter of course. Low-risk objects (blunt, small, nonmagnetic, or button battery) can 

be watched in the esophagus for up to 24 hours. Once an object has passed the gastroesophageal junction, the 

probability of eventual passage is >90%. The foreign body usually arrives at the rectum in 3-5 days. As long as 

the patient is asymptomatic, management in these cases is expectant. 

5. Management 

a. Because most esophageal foreign bodies are in the cervical esophagus, removal is usually accomplished 

with a laryngoscope and Magill forceps or with an endoscope. 

b. Food impactions 

(1) A distal esophageal food impaction can occasionally be dislodged with IV glucagon (frequently causes 

nausea and vomiting), sublingual nitroglycerin, or nifedipine. IV glucagon relaxes smooth muscle and 

decreases lower esophageal sphincter pressure. After a test dose to exclude hypersensitivity, administer 

1 mg IV; an additional 2 mg may be given if there is no relief in 20 minutes. Nitroglycerin and 

nifedipine are rarely used because of the high incidence of adverse effects and limited efficacy. 

(2) Gas-forming agents (eg, effervescent granule packets, carbonated beverages) may also be used to 

dislodge an esophageal food impaction. They work by producing CO 2 

, which increases intraluminal 

pressure and pushes the food bolus into the stomach. These agents should be avoided in patients with 

chest pain (possible perforation) and in those with symptoms >24 hours duration. 

c. The practice of removing an impacted, smooth foreign body (such as a coin) with a Foley or Fogarty 

catheter requires a cooperative patient, fluoroscopic guidance, and an object that has been present for 


h. Sharp or pointed objects, as well as objects >5 cm long and >2 cm wide, must be removed endoscopically. 

They should be removed before they pass the pylorus, because 15%-35% will cause perforation, usually in 

the region of the ileocecal valve. 

i. After an esophageal foreign body has been removed, esophageal function should be thoroughly evaluated 

(including motility studies) to ensure that there is no underlying pathology that led to the obstruction. This 

is particularly true of adults with meat impactions; underlying pathology of the esophagus is present up to 

97% of the time. 

Ill. PEPTIC ULCER DISEASE 


1. Peptic ulcers are mucosa! defects that extend beyond the muscularis mucosae. They are most commonly 

located along the lesser curvature of the stomach or in the first portion of the duodenum. 

a. Gastric ulcers are thought to be due to damage to the gastric mucosa I barrier itself, which allows diffusion 

of hydrogen ions from the lumen to the gastric mucosa and results in ulceration. 

b. Duodenal ulcers are usually associated with hypersecretion of gastric acid (by an enlarged parietal cell 

mass) and with markedly increased gastric emptying that overwhelms the capacity of the duodenum to 

neutralize gastric acid, and results in damage to the duodenal mucosa/ barrier. Helicobacter pylori causes 

~90°/c, of al I duodenal ulcers. 

2. Uncommon sites of peptic ulceration 

a. Distal esophagus 

b. Ectopic gastric mucosa with a Meckel diverticulum 

c. Margins of surgical anastomoses ("marginal ulcers") 

3. A stress ulcer is not the same as a peptic ulcer, ie, the mucosa! lesion of a stress ulcer does not extend through 

the muscularis mucosae. Stress ulcers are most commonly found in the body and fundus of the stomach and 

are a common cause of gastric bleeding (hemorrhagic gastritis). 

B. Predisposing factors 

1. Peptic ulcer disease is considered to have two main causes: H pylori infection and NSAID usage 

2. Zollinger-Ellison syndrome or other gastrin-secreting tumors cause 1 % 

3. Cigarette smoking 

4. Bile salts 

5. Emotional stress 

6. Prolonged use of corticosteroids (combination of NSAIDs and corticosteroids increases risk of peptic ulcer 

disease 15 times) 

7. Caffeinated beverages (coffee, soda, tea) 


1. The pain associated with gastric and duodenal (peptic) ulcers is visceral in nature and, therefore, is vague (not 

well defined). It is generally felt in the midline and is typically described as gnawing, aching, or burning. 

2. Gastric pain is generally perceived at the midline or to the left of the epigastrium. 

3. Duodenal bulb pain is usually perceived to the right of the midepigastrium. With posterior penetration, the 

pain may radiate straight through to the back. 

4. The patient presents with epigastric pain that may be easily confused with the substernal chest pain of 

myocardial ischemia. A significant diagnostic clue is the character of the pain: a patient with peptic ulcer 

disease will describe the pain as a burning sensation; the Ml patient generally will not. This descriptor, 

however, cannot reliably exclude cardiac causes of pain. 


1. Definitive diagnosis is generally not made in the emergency department. 

2. Peptic ulcers may be diagnosed with an upper GI or endoscopy. Endoscopic evaluation with biopsy is key to 

differentiating malignant from benign gastric ulcers and should be suspected in patients >50 years old as well 

as in those with markers of malignancy. 

3. Infection with H pylori can be diagnosed noninvasively via serology or the urea breath test, or by tests that 

require endoscopy (rapid urea/Cl O test, histology). An lgG H pylori serum test is also available. 

183


E. Management of uncomplicated peptic ulcer disease is generally on an outpatient basis and may be started 

in the emergency department. 

1. Advise patients to avoid substances that exacerbate gastric and duodenal ulcers (smoking, alcohol, NSAIDs, etc). 

A bland diet with frequent feedings has not been demonstrated to be effective and is probably unnecessary. 

2. Provide pain relief and facilitate ulcer healing with one of the following agents: 

a. Antacids 

(1) Provide pain relief and accelerate healing by neutralizing gastric acid 

(2) Dose: 30 ml at bedtime and at 1 and 3 hours after meals 

(3) Their major drawback is how frequently they must be taken, which decreases compliance. They may 

also cause constipation (aluminum salts) or diarrhea (magnesium salts). In addition, antacids decrease 

the absorption of certain drugs (warfarin, digoxin, several anticonvulsants, and some antibiotics). 

b. Histamine (H 2 

)-antagonists 

(1) Promote healing by inhibiting gastric acid secretion 

(2) The major advantage of these drugs is their convenient dosing (once or twice daily). 

c. Proton-pump inhibitors 

(1) Promote healing by blocking the secretion of gastric acid 

(2) Inhibit the H+/K+ ATPase enzyme system (the "proton pump") of parietal cells, thereby preventing the 

release of hydrogen ions into the gastric lumen 

(3) Indicated for the short-term treatment of duodenal and gastric ulcers, and usually reserved for those in 

whom H 2 

-blockers have not been effective 

(4) Agents 

(a) 

d. Misoprostol 

Omeprazole 

(b) Lansoprazole 

(c) Pantoprazole (available in IV form; has been shown to i bleeding from peptic ulcers) 

(d) Esomeprazole and rabeprazole are newer agents. 

(1) A synthetic prostaglandin E 1 

analogue that acts in a way similar to that of the naturally occurring 

prostaglandins secreted by the gastric mucosa in response to injury. 

(2) Indicated only for the prevention of NSAID-induced gastric ulcers in high-risk patients (the elderly, 

those with concomitant debilitating disease or a history of ulcers) 

(3) Can cause spontaneous abortion and is, therefore, contraindicated in pregnant women and in women 

of childbearing age who are not using reliable contraceptive measures 

e. Sucralfate: drug of choice for erosive esophagitis secondary to large "stuck" pills (eg, doxycycline, docusate) 

(1) Works locally at the ulcer site, where it binds to the base of the ulcer, thereby protecting it from the 

adverse effect of gastric acid; also adsorbs bile acids, inhibits pepsin activity, and increases mucosa! 

prostaglandin production 

(2) Dosage is 1 g orally qid on an empty stomach. It works best in an acid environment (pH


F. Complications 

1. The most common complications are bleeding (20% of ulcer patients), perforation (7%), and gastric outlet 

obstruction. 

2. Elderly patients are at greatest risk of hemorrhage. 

3. Ulceration into an artery can lead to life-threatening hemorrhage. 

4. Perforation 

a. Exposure of the peritoneal cavity to gastric or duodenal contents produces a chemical peritonitis that, in 

the absence of prompt and adequate treatment, rapidly progresses to bacterial peritonitis. 


(1) History of ulcer-like pain in weeks before presentation helpful in making diagnosis. 

(2) Sudden onset of abdominal pain with guarding and rebound is characteristic of anterior perforations; 

back pain is characteristic of posterior perforation of a duodenal ulcer. 

(3) Pain may radiate to shoulder and or chest. 

(4) Posterior, perforated duodenal ulcer may appear similar to pancreatitis (but the serum lipase will be 

normal or slightly increased initially if the perforation is adjacent to the pancreas), or the perforation 

may actually cause pancreatitis. 


(1) Absence of free air on radiographs does not exclude the diagnosis. 

(a) Anterior perforations: only 60%-70% demonstrate free air. 

(b) Posterior perforations: no free air will be evident because the posterior duodenum is located 

retroperitoneal ly. 

(2) Diagnosis may require CT scan of abdomen or endoscopy. 

d. Management 

(1) IV fluids (normal saline or lactated Ringer's) and electrolyte replacement 

(2) Nasogastric tube drainage 

(3) Broad-spectrum IV antibiotics 

(4) Immediate surgical consult 

5. Gastric outlet obstruction 

a. When an ulcer heals, it can form a scar that blocks the pyloric outlet. The resulting obstruction can result in 

gastric dilation, vomiting, dehydration, and a hypokalemic, hypochloremic metabolic alkalosis. 


(1) Upper abdominal pain and vomiting (most common) 

(2) Early satiety 

(3) Recent weight loss 

(4) A succussion splash (a splashing sound elicited by gently rocking the abdomen) 

c. Diagnostic evaluation: an upright abdominal radiograph typically reveals a prominently dilated stomach 

shadow with a large air-fluid level. 

d. Management 

(1) Constant nasogastric suctioning 

(2) Fluid replacement and correction of electrolyte abnormalities 

(3) Admission for further evaluation and definitive management 

(4) Anticholinergic agents are contraindicated, because they may aggravate gastric distention by 

decreasing gastric motility. 

IV. PERFORATED VISCUS 

A. Gallbladder perforation (rare) 

1. Gallstone obstruction of the cystic or common bile duct - gallbladder distention - vascular compromise - 

gangrene - perforation 

a. More commonly, gallstones erode through the gallbladder wall, cystic duct, or common duct and produce 

fistulas between the gallbladder and another portion of the GI tract, rather than perforate directly into the 

peritoneal cavity. 

185


b. Gallstone ileus occurs when a large gallstone enters the small intestine through such a fistula. It usually 

lodges in the terminal ileum, producing a small-bowel obstruction. May see pneumobilia on abdominal 

radiograph. 

c. Gangrene of the gallbladder (with subsequent perforation) can occur in the absence of stone formation 

(acalculous cholecystitis), especially in diabetic patients. 

2. Patients at increased risk 

a. Older patients 

b. Those with diabetes 

c. Those with atherosclerotic cardiovascular disease 

d. Those with a history of gallstones and repeated cholecystitis 

e. Those with a hemolytic disorder (sickle cell disease) 

3. Classic clinical scenario: An older man with a fever appears ill and has a tender right upper quadrant mass on 

physical examination. A careful history reveals one or more risk factors. In addition, a nonalcoholic may give 

a past history of jaundice or pancreatitis, which should suggest common duct stones. Laboratory studies reveal 

leukocytosis, possibly an increased bilirubin, and slightly increased serum amylase. On abdominal radiograph, 

a stone may be seen free in the abdomen. Subhepatic or subphrenic abscesses can form after a gallbladder 

perforation and cause restricted movement of the right leaf of the diaphragm. 

B. Small-bowel perforation 

1. Etiology of jejunal rupture 

a. Drugs (enteric-coated potassium tablets) 

b. Infection (eg, typhoid, tuberculosis) 

c. Tumor 

d. Strangulated hernia 

e. Regional enteritis (Crohn disease) 

2. A jejuna I perforation causes a chemical peritonitis that is more severe than that caused by an ilea! perforation 

because the pH of the jejuna! contents is higher (pH 8), and there is also a greater number of enzymes 

present in this part of the bowel. lleal perforations are associated with considerable bacterial contamination; 

these small-bowel perforations can rapidly wall off (particularly in patients with Crohn disease), so that early 

evaluation may reveal only localized findings. 

3. Mortality varies directly with the extent of peritoneal soiling and time delay to diagnosis and treatment. 

C. Large-bowel perforation 

1. Etiology 

a. Carcinoma 

b. Diverticulitis 

C. Colitis 

d. Foreign body 

e. Diagnostic instrumentation 


a. The signs and symptoms of large-bowel perforations are largely due to sepsis and, therefore, are usually 

slower in onset than those produced by small-bowel perforations. 

b. The patient appears septic and has a feculent breath odor. The abdomen is distended, and the patient has 

been unable to pass feces. When a nasogastric tube is inserted and hooked to suction, fecal material is seen 

in the aspirate. Radiograph often demonstrates free air and small-bowel obstruction. 

D. Management of a known or suspected perforated viscus 

1. IV fluid replacement with normal saline or lactated Ringer's; large volumes (up to 12 Lover 24 hours) may be 

required because of third spacing. 

2. Bladder catheterization (to monitor urine output/volume status) 

3. Nothing by mouth; nasogastric tube drainage 

4. Broad-spectrum IV antibiotics 

5. Immediate surgical consult (delay in surgical intervention significantly increases mortality) 

186


V. ACUTE ABDOMEN 

A. Appendicitis 

1. The most common indication for emergency surgery; appendicitis is also the most common surgical 

emergency seen in pregnancy, and the most common cause of emergency abdominal surgery in children. 

2. Although all age groups are affected, the highest incidence is in patients 10-30 years old (particularly males). 


a. Obstruction of the appendiceal lumen (the primary inciting event) - increased intraluminal pressure and 

distention - vascular compromise of the appendiceal wall and bacterial invasion 

b. Etiologies of appendiceal obstruction include: 

(1) Fecalith (most common) 

(2) Enlarged lymphoid follicles 

(3) lnspissated barium 

(4) Worms 

(5) Granulomatous disease 

(6) Tumors 

(7) Adhesions 

(8) Dietary matter (seeds) 

4. Clinical presentation (listed in order of decreasing frequency) 

a. History 

(1) Abdominal pain (with migration to right lower quadrant increases likelihood) 

(2) Anorexia 

(3) Nausea and vomiting 

(4) Fever and chills (minimal statistical association between temperature >99°F [37.2°C] and 

appendicitis) 

(5) Diarrhea (can be a particularly prominent symptom in very young children and patients with pelvic 

appendices; often results in misdiagnosis as acute gastroenteritis) 

b. Physical evaluation 

(1) Abdominal tenderness 

(2) Percussion or rebound tenderness 

(3) Rectal tenderness (examination not useful to diagnose or exclude) 

(4) Cervical motion tenderness (28%-34%) 

(5) Psoas sign (right lower quadrant pain on passive extension of right hip) 

(6) Obturator sign (right lower quadrant pain on passive internal rotation of the flexed right hip) 

(7) Rovsing sign (right lower quadrant pain on palpation of the left lower quadrant) 

(8) Right lower quadrant pain on rectal examination (retrocecal appendicitis) 

c. Visceral pain is the first symptom to develop; it is dull and vague in character. In nonpregnant patients, 

pain usually begins in the periumbilical area and then, over time, moves to the right lower quadrant. 

Where the pain eventually migrates is determined by the actual location of the appendix; radiation of 

pain to the flank is suspicious of a retrocecal appendicitis. (Remember that kidney stone pain usually 

comes on suddenly; retrocecal appendiceal pain usually has a gradual onset). In pregnant patients, the 

appendix moves laterally and superiorly as the uterus enlarges, so be suspicious of flank or right upper 

quadrant pain. If the appendix is located near the uterus, ovary, or tubes, there will be pain on cervical 

motion. (Patients with pelvic inflammatory disease are generally seen later in the course of their illness, 

have fewer GI symptoms, and have a more increased sedimentation rate). Anorexia, nausea, and vomiting 

usually begin after the onset of pain. A sudden decrease in pain followed by a dramatic increase suggests 

perforation. 

d. Unfortunately, one-third to one-half of patients do not present "classically" (migratory abdominal pain 

and the typical associated signs and symptoms); the pain can be anywhere. 

e. Be particularly suspicious in very young and very old patients; their symptoms are frequently vague, and 

clinical presentation is less classic. Delayed diagnosis with resulting perforation and increased morbidity 

and mortality is common in these age groups. 

187



a. May provide additional information even when the history and physical examination are classic; they can 

also be helpful in less typical cases when the diagnosis remains in doubt. 

b. Routine studies 

(1) Pregnancy test: should be done in all women of childbearing age to exclude ectopic pregnancy 

(2) CBC: a WBC count > 10,000/mm 3 is statistically associated with appendicitis but has such poor 

sensitivity and specificity that it is of almost no clinical utility. 

(3) Urinalysis: pyuria and hematuria may be seen if the inflamed appendix lies in close proximity to the 

ureter; a few WBCs and RBCs in the urine are characteristic. 

(4) Plain abdominal radiographs (an option to be considered only if CT is unavailable): a calcified 

fecalith in the right lower quadrant is very suggestive of appendicitis but is present in only 2%-22% 

of cases. 

c. Additional studies may be indicated when the diagnosis remains uncertain and should be chosen in 

consultation with the evaluating surgeon. Availability and usefulness of these studies may be institutiondependent. 

(1) Abdominal CT is generally considered the radiographic procedure of choice for diagnosing acute 

appendicitis in men and nonpregnant women. Data suggest that abdominal CT is >97% sensitive 

and 98%-100% specific for acute appendicitis. (In addition, abdominal CT may unmask other cases 

of abdominal pain.) Abdominal CT is often performed with IV contrast and oral or rectal contrast; 

presence of periappendiceal fat stranding is the most specific radiographic finding for appendicitis. 

Unenhanced (noncontrast) CT is also highly sensitive and specific. 

(2) ACEP Level B recommendation for CT scan with or without IV, oral, and or rectal contrast states that 

addition of IV contrast may increase sensitivity of CT for diagnosis of appendicitis. 

(3) Diagnostic laparoscopy has high sensitivity and specificity. It is clearly indicated in equivocal cases 

of surgical abdominal pain, and its use as a diagnostic tool is increasing because laparoscopic 

appendectomies are now performed more frequently than open surgical appendectomies. 

(4) Graded compression ultrasonography has a sensitivity of ~40% and a specificity of -90%, and it 

may be especially valuable for evaluating children and pregnant patients. It is noninvasive, without 

radiation exposure, safe in pregnancy, rapid, inexpensive, and rarely requires sedation in children. 

Visualization of a noncompressible, immobile appendix >6 mm in diameter is very suggestive of 

the diagnosis. Furthermore, an alternative definitive diagnosis can be established in up to 50% 

of patients when appendicitis is absent. The disadvantages of ultrasound are that it is not always 

available, it is operator-dependent, and it has a very poor sensitivity in the presence of perforation. 

(5) Lifetime risk of all cancers from one CT abdomen is calculated at 0.14% in neonates and 0.06% 

in adults. 

(6) In children, use ultrasound to confirm suspected acute appendicitis but not definitely exclude the 

diagnosis. Recommendation to follow ultrasound with CT of abdomen and pelvis if diagnosis is still 

highly suspected. (ACEP Clinical Policy: Critical Issues in the Evaluation and Management of Patients 

with Suspected Appendicitis) 

(7) MRI appears to be a useful modality in pregnant women (to avoid ionizing radiation) in whom 

ultrasound is inconclusive. 


a. Mesenteric adenitis 

b. Yersinia gastroenteritis 

c. Pelvic inflammatory disease 

d. Ectopic pregnancy 

e. Ovarian cyst 

f. Pyelonephritis 

g. Crohn disease 

h. Diverticulitis 

7. Management 

a. Nothing by mouth 

b. Establish an IV line 

c. Obtain early surgical consult. (Delay in laparoscopy or surgical intervention -- gangrene -- perforation 

-- increased morbidity and mortality, particularly in the very young and very old.) 

188


d. If a decision to operate is reached, administer prophylactic parenteral antibiotics; they decrease the 

incidence of postoperative wound infection and, in patients who have perforated, they decrease the 

incidence of postoperative abscess formation. Acceptable regimens: 

(1) Piperacillin/tazobactam 

(2) Cefoxitin 

(3) Cefotetan 

(4) Ampicillin, gentamicin, and metronidazole/clindamycin 

e. Judicious amounts of parenteral narcotic may be administered for pain relief and to facilitate diagnostic 

evaluation. (ACEP Clinical Policy: Critical issues for the initial evaluation and management of patients 

presenting with a chief complaint of nontraumatic acute abdominal pain.) 

f. Recent literature confirms that delaying appendectomy in stable patients is a safe alternative to 

immediate surgery. Antibiotic therapy as noted above should be initiated. 

g. Several studies have suggested that nonsurgical management of acute, uncomplicated appendicitis is 

acceptable. 

B. Bowel obstruction 

1. Etiology 

(1) Nonoperative treatment for acute appendicitis (the NOTA study) showed good outcomes with a 2-year 

recurrence rate of about 14%. Amoxicillin/clavulanic acid was the antibiotic used in this study. 

(2) This method of treatment is now considered acceptable in many centers. It is not well studied in 

children and elderly patients and should not be used in patients when there is any suspicion of 

complicated appendicitis. 

a. Small-bowel obstruction 

(1) Adhesions (most common) 

(2) Hernia (second most common) 

(3) Neoplasms (lymphoma, adenocarcinoma) 

(4) lntussusception (common in children


c. Peristalsis is initially increased early in the course of bowel obstructions (hyperactive bowel sounds). 

Passage of feces and flatus often continues in the first few hours after an obstruction occurs. With persistent 

complete obstruction, the bowel loses its ability to contract rigorously, bowel sounds become infrequent, 

and the passage of feces/flatus stops. 

d. Strangulation occurs most often in the small bowel and is due to vascular compromise that leads to 

infarction. In the large bowel, strangulation can occur with a volvulus, because it is a closed loop 

obstruction and vascular supply is quickly compromised. 


a. Pain 

(1) Crampy, intermittent, and poorly localized pain is typical. 

(2) A change in the quality of the pain (greater intensity, more constant) may indicate that a complication 

has developed. 

b. Vomiting 

(1) The more proximal the obstruction, the sooner it begins. 

(2) If it is bilious, the obstruction is distal to the pylorus. 

(3) Feculent emesis is associated with distal ilea! and large-bowel obstruction and, if long-standing, may 

be due to infarcted bowel. 

c. Abdominal distention: the more distal the obstruction, the more pronounced the distention. 

d. Tympany may be present on percussion. 

e. Abdominal tenderness 

(1) Mi Id, diffuse tenderness is typical. 

(2) A tender mass may be palpated with a closed-loop obstruction. 

(3) Severe localized tenderness or rebound tenderness suggests the possibility of gangrenous or perforated 

bowel. 


a. Radiographs of the abdomen should include supine and upright films and are the first choice for imaging. 

b. Sm al I-bowel obstruction 

(1) Abdominal radiographs are diagnostic in 30%-70% (specificity ~50%). 

(2) Small-bowel diameter >3 cm 

(3) Air fluid levels 

(4) Stepladder appearance of dilated loops 

(5) "String of pearls" appearance is a late finding. 

(6) Cause of obstruction rarely identified on plain radiographs. 

c. CT of the abdomen and pelvis 

(1) The American College of Radiology considers CT an appropriate first choice for imaging; emergency 

medicine sources usually suggest abdominal radiographs. 

(2) Oral contrast not usually required, because fluid in bowel acts as contrast. 

(3) IV contrast helps diagnose strangulation. 

(4) Transition zone often identified. 

(5) Sensitivity 94%; specificity for small-bowel obstruction is 95% for high-grade obstructions but only 

50% for low-grade obstructions. 

d. Gas patterns in small- and large-bowel obstructions 

(1) Colon gas is distinguished from gas in the small bowel by its peripheral location and the presence of 

haustrations that do not involve the entire transverse diameter of the bowel. 

(2) Small-bowel gas is more central in location, and one can see valvulae conniventes that involve the 

entire transverse diameter of the small bowel. They are spaced closer together than the haustrations of 

the large bowel. 

e. Large-bowel obstruction 

5. Management 

(1) Abdominal radiographs unreliable in diagnosis (may be only 84% sensitive and 72% specific) 

(2) Dilation of colon >5 cm with> 10 cm at cecum 

(3) CT of abdomen and pelvis is considered modality of choice. 

a. Sm al I-bowel obstruction 

(1) IV fluid resuscitation 

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C. Volvulus 

(2) Correction of electrolyte abnormalities 

(3) Nasogastric tube decompression is mainstay of conservative therapy; no benefit for long intestinal tubes. 

(4) Broad-spectrum antibiotic coverage may be of benefit. 

(5) Early surgical consult: patients with pneumoperitoneum, peritonitis, and sepsis require immediate 

surgical intervention. 

b. Large-bowel obstruction 

(1) Volume resuscitation and correction of electrolyte abnormalities. 

(2) Patients with perforated bowel, sepsis, etc, require immediate surgery. 

(3) Colonic dilatation> 12 cm or of prolonged duration may require immediate intervention. 

(4) Nasogastric decompression if vomiting present. 

1. Volvulus is a closed-loop obstruction that results from the twisting of a mobile segment of bowel on its 

mesocolon; it is responsible for approximately 10%-13% of colonic obstructions in the United States. 

2. Sigmoid volvulus is more common (60%) than cecal volvulus (40%). 

3. Epidemiology and pathophysiology 

a. Sigmoid volvulus occurs almost entirely in two patient populations: elderly, bedridden patients with 

debilitating comorbid diseases and patients of any age with profound neurologic or psychiatric illness. 

These patients invariably have a history of chronic severe constipation that leads to an elongated 

(redundant) sigmoid colon. 

b. Cecal volvulus results from incomplete embryologic fixation of the cecum, ascending colon, and terminal 

ileum to the posterior abdominal wall. Although it is seen in patients of all ages, it is most common in 

patients in their twenties and thirties. 

4. Clinical presentation of sigmoid and cecal volvulus 

a. Sudden onset of crampy lower abdominal pain 

b. Nausea, vomiting, obstipation 

c. Diffuse abdominal tenderness 

d. Progressive abdominal distention 

e. Tympany 

f. Gangrenous bowel in 20% of patients with cecal volvulus 


a. Radiographic findings: a markedly dilated single loop of colon 

b. Sigmoid volvulus: bent "inner tube" appearance with dilated bowel segment doubled back; the proximal 

large bowel is dilated. 

c. Cecal volvulus: the loop is usually seen in the mid or upper abdomen toward the left but may be anywhere; 

single dilated segment of cecum with a kidney or "coffee bean" shape. The distal large bowel is collapsed, 

and the small bowel is dilated. 

6. Management 

a. Initial measures are the same as those for bowel obstruction (IV hydration, nasogastric tube decompression, 

and broad-spectrum antibiotics). 

b. Sigmoid volvulus 

(1) Surgical consult and nonoperative reduction using a rectal tube via the sigmoidoscope or barium 

enema. Because recurrence is common (90%), this is usually followed by an elective resection if the 

patient's underlying medical condition can tolerate it. 

(2) If nonoperative management fails or strangulation is suspected, immediate operative reduction is 

required. 

c. Cecal volvulus: early and immediate surgical reduction, because this is a closed-loop obstruction. 

D. Mesenteric vascular ischemia/infarction 

1. Most commonly affects patients who are >50 years old and have a history of cardiovascular disease 

2. Mortality rate is 50% overall (but rises to ::,:70% once infarction has occurred) and reflects the difficulty in 

making an early diagnosis as well as the presence of significant underlying disease. 

3. Etiology 

a. Most common cause is arterial embolus (50% of cases). Another 25% are caused by arterial thrombosis. 

b. Nonocclusive mesenteric ischemia accounts for 20% of cases. Common pathway is mesenteric 

vasoconstriction due to low flow states with decreased cardiac output. Associated conditions are CHF, 

191


cardiogenic shock, septic shock, etc, and medications that cause splanchnic vasconstriction such as 

digoxin, vasopressors. It is common in hospitalized patients. 

c. Mesenteric venous thrombosis is responsible for 5%-15% of cases and most commonly occurs in association 

with a hypercoagulable state (eg, polycythemia vera, antithrombin Ill deficiency). Affected patients are 

usually younger in age, and up to 60% of them have a history of peripheral deep-venous thrombosis. 

4. Predisposing factors for 

a. Acute mesenteric arterial embolism 

(1) Dysrhythmias (particularly atrial fibrillation) 

(2) Atherosclerotic heart disease 

(3) Valvular heart disease 

(4) Recent Ml with mural thrombosis 

b. Venous thrombosis 

(1) History of prior thromboembolic events 

(2) Hypercoagulable states 

c. Nonocclusive ischemia 

(1) Use of diuretics or vasoconstrictive medications or digitalis 


(3) CHF 

(4) Dialysis 


a. The patient is typically middle-aged or elderly and presents with severe abdominal pain, fever, and 

tachycardia; sudden onset suggests arterial occlusion, while insidious onset suggests venous thrombosis or 

nonocclusive ischemia. 

b. A history of similar, spontaneously resolving pain episodes after meals ("intestinal ischemia 11 ) is not uncommon. 

c. Early on, the pain is poorly localized and out of proportion to findings on physical examination. Diarrhea 

is common, and the feces frequently test positive for guaiac. Grossly bloody feces may also be seen. Other 

commonly associated symptoms are anorexia, nausea, and vomiting. Abdominal distention and peritoneal 

signs are late findings and signal the presence of bowel infarction. 


a. Helical CT angiography is the primary diagnostic modality for patients with a high clinical index of 

suspicion. Catheter angiography is used for equivocal cases. 

b. CBC reveals hemoconcentration (increased hematocrit) and leukocytosis (WBC count is often > 15,000/mm 3 ). 

c. Serum amylase is usually moderately increased (lipase is normal). 

d. Serum phosphate may be increased. 

e. Serum lactate is nearly 100% sensitive when bowel infarction is present but lacks specificity and is not 

often increased without infarction. 

f. Blood gases, arterial or venous, often reveal a metabolic acidosis, particularly late in the disease course. 

Presence of metabolic acidosis that cannot otherwise be explained should prompt investigation for 

mesenteric ischemia in appropriate patients. 

g. Plain abdominal and upright chest radiographs are usually the first radiographic studies to be obtained, 

although they are often normal (especially early on). Findings may include: 

(1) lieus 

(2) Small-bowel obstruction 

(3) Gasless abdomen 

(4) Irregular thickening of the bowel wall ( 11 thumbprinting 11 -although rarely seen, strongly suggests 

intestinal infarction) 

(5) Gas in the bowel wall (pneumatosis intestinal is) or portal venous system (although rarely seen, strongly 

suggests intestinal infarction) 

h. Abdominal ultrasound and MRI are not useful in the initial evaluation. 

i. Abdominal CT angiography 

(1) Most commonly ordered test in the emergency department for evaluation of suspected mesenteric 

ischemia 

(2) Sensitivity reported to be as high as 96% with a specificity of 94% 

(3) Test of choice for suspected mesenteric venous thrombosis 

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7. Management 

E. Hernias 

a. Initial stabilization measures 

(1) IV of normal saline or lactated Ringer's to correct volume deficit 

(2) Supplemental oxygen 

(3) Nasogastric tube to decompress stomach and bowel 

(4) Initial laboratory studies, type and cross, cultures, and radiographs 

(5) Broad-spectrum IV antibiotics 

(6) Heparin or low-molecular-weight heparin may be given, particularly for mesenteric venous thrombosis. 

(7) Thrombolytics are an option in consultation with an appropriate specialist such as a vascular surgeon 

or interventional radiologist. 

(8) Correction of precipitating or predisposing causes of ischemia (eg, CHF, dysrhythmias) 


(a) Vascular surgery for possible revascularization 

(b) lnterventional radiology for angioplasty or intra-arterial thrombolytic administration 

(10) If pressors are required, positive inotropes are preferred. Avoid a-agonists. 

(11) If angiography is performed, papaverine may be infused to dilate mesenteric arteries. 

b. Specific treatment measures depend on the underlying cause of the ischemia and if peritoneal signs or 

necrotic bowel are present. 

1. Definitions 

(1) Nonocclusive mesenteric ischemia: unless peritonitis or necrotic bowel is present, treatment is 

nonoperative; papaverine alone is considered definitive therapy in these patients. 

(2) Mesenteric venous thrombosis: immediate anticoagulation with heparin is the initial treatment of 

choice and, in the absence of peritonitis and necrotic bowel, may be the only treatment given. 

(3) Acute mesenteric arterial occlusion (embolic and thrombotic): initial treatment may be papaverine, 

while plans are made for revascularization. Papaverine should be continued postoperatively to treat 

vasospasm of the smaller branches of the superior mesenteric artery. 

(4) Immediate surgery is indicated for: 

(a) Patients with peritonitis 

(b) Resection of necrotic bowel 

a. Hernia: the protrusion of a structure from its normal position into another through an opening that is either 

congenital or acquired 

b. External hernia: protrudes to the outside (eg, umbilical) 

c. Internal hernia: protrudes within the body (eg, diaphragmatic) 

d. lncisional hernia: protrudes through a previous incision 

e. Reducible hernia: protruding contents can be pushed back in 

f. Irreducible (incarcerated) hernia 

(1) Protruding contents cannot be moved back into place 

(2) Seen most often when large contents herniate through a small defect 

g. Strangulated hernia: vascular compromise of herniated contents 

h. "Sports hernia": refers to groin pain related to participation in athletics but is not an anatomic hernia. 


a. Men are 8 times more likely than women to develop a hernia, and 20 times more likely to require surgical 

repair. 

b. Lifetime risk of developing a groin hernia is 25% in men. 

c. Women present at an older age than men. 

d. 96% of groin hernias are inguinal; 4% are femoral. 

3. Types 

a. Inguinal hernia 

(1) Direct 

(a) Protrudes directly through the floor of Hesselbach triangle 

(b) Results from relaxation/weakening of the abdominal musculature 

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(c) Increased frequency with age 

(d) Rarely incarcerates 

(2) Indirect 

(a) Protrudes through the internal inguinal ring lateral to the inferior epigastric vessels 

(b) Represents a congenital defect (incomplete closure of processus vaginal is) 

(c) Most common hernia occurring in both sexes 

(d) Most common in younger patients 

(e) Frequently incarcerate, especially in infancy 

b. Femoral hernia 

(1) Protrudes below the inguinal ligament and the femoral vessels in the femoral canal 

(2) More common in women 

(3) Frequently incarcerates (40% present as acute incarceration) 

c. Umbilical hernia 

(1) Usually presents as a lump 

(2) Common in newborns 

(3) Most close spontaneously by the age of 2-3 years 

d. Obturator hernia 

(1) Protrudes through the obturator foramen into the medial thigh 

(2) Most occur in older women 

(3) Patients present with pain and decreased sensation along the medial aspect of the thigh to the knee. 


a. Inguinal: ultrasonography is considered the best initial modality in patients with high clinical suspicion but 

negative findings on examination. 

b. Femoral: ultrasonography may help differentiate inguinal from femoral hernias, but CT scan may be required. 

F. Ileitis and colitis 

1. Crohn disease (terminal ileitis, granulomatous ileocolitis, regional enteritis) 

a. Pathology 

(1) A chronic inflammatory disease that involves all layers of the bowel as well as the mesenteric lymph nodes 

(2) Any segment of the GI tract from the mouth to the anus may be affected. 

(3) The disease is discontinuous with normal areas of bowel ("skip areas") between one or more involved 

areas; the ileum is involved in most cases. 

(4) The thickened bowel wall leads to narrowing of the lumen, which frequently results in obstruction. 

(5) Longitudinal deep ulcerations are characteristic; with progression of the disease, a "cobblestone" 

appearance of the mucosa results from crisscrossing of these ulcers with intervening normal mucosa. 

(6) Noncaseating granulomas are present in 2:50% of specimens and are helpful (but not necessary) in 

making the diagnosis. 

(7) Perianal complications occur in 90% of cases and may be the initial presenting symptom in many 

patients. 

b. Epidemiology 

(1) Onset of disease common in teens and early twenties but can occur at any age 

(2) Four to eight times more common in the Jewish population 

(3) Genetic predisposition 

(4) Etiology remains undetermined. 

c. Clinical presentation 

(1) Abdominal pain and diarrhea (inflammation of ileum and/or colon) 

(a) 

Past history of recurrent abdominal pain, diarrhea, and fever for several years 

(b) Nocturnal diarrhea may be a diagnostic clue. 

(c) Weight loss is common. 

(2) Right lower quadrant pain and tenderness (acute inflammation of the terminal ileum only) 

(a) 

Looks like appendicitis ("pseudoappendicitis"): anorexia, diarrhea, vomiting, fever, leukocytosis 

(b) Diagnostic clue: occult blood and fecal leukocytes favor regional enteritis 

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(3) Extraintestinal manifestations are seen in one-quarter to one-third of cases and may be the presenting 

and/or dominant manifestation of the disease process. 

(a) Arthritic (peripheral arthritis, ankylosing spondylitis) 

(b) Vascular (vasculitis, arteritis, thromboembolic disease) 

(c) Hepatobiliary (gallstones, pericholangitis, chronic active hepatitis) 

(d) Dermatologic (erythema nodosum, pyoderma gangrenosum) 

(e) Ophthalmic (uveitis, episcleritis, iritis, conjunctivitis) 

(f) 

d. Comp! ications 

Renal calculi occur with increased frequency due to increased intestinal absorption of oxalic acid. 

(1) Perianal (abscess, fissure, fistula, rectovaginal fistula, rectal prolapse) 

(2) Intestinal (obstruction, abscess, fistula, stricture, perforation, hemorrhage) 

(3) Toxic megacolon is an infrequent complication of Crohn disease and is associated with massive GI 

bleeding in >50% of cases. 

(4) Malignancies of both the small and large bowel are three times more common in patients with Crohn 

disease than in the general population. 

e. Diagnostic evaluation 

(1) Previously undiagnosed patients require radiologic, colonoscopic, and histologic confirmation to 

establish the local and systemic extent of the disease, 

(2) Stable patients with mild disease may be evaluated as an outpatient with close follow-up. 

f. Management 

(1) Make a diligent effort to exclude associated small-bowel obstruction, because early institution of 

nasogastric suction, IV fluids, and steroids may reduce inflammatory edema, restore bowel patency, 

and avoid the need for emergency surgery. 

(2) Fluid and electrolyte replacement (especially those patients with a history of anorexia, vomiting, and 

diarrhea) 

(3) Indications for admission 

(a) Dehydration or metabolic/electrolyte disturbances 

(b) Severe exacerbation of the primary illness 

(c) Acute complications (eg, obstruction, hemorrhage, peritonitis) 

(4) Outpatient therapy for mild cases 

(a) 

Bed rest, analgesics, antidiarrheal agent 

(b) Milk products should be avoided; they frequently aggravate diarrhea in these patients, in whom 

the incidence of lactose intolerance is high. 

(c) Steroids: beginning therapy with (or changing the dosage of) should be done in conjunction 

with the patient's primary physician, because these agents have many adverse effects and are 

ineffective as maintenance therapy. 

(d) Mesalamine, a 5'-ASA derivative is preferred over sulfasalazine, because it has fewer adverse 

effects. 

(e) Antibiotics 

(f) 

2. Ulcerative colitis 

i. May be of use in Crohn disease 

ii. Ciprofloxacin or metronidazole show some benefit. 

Azathioprine and its metabolite 6-mercaptopurine (immunosuppressive agents) are useful: 

i. As steroid-sparing agents (allow patients to decrease their dose of prednisone) 

ii. In patients with refractory disease and contraindications to surgery 

iii. In patients with enterocutaneous or enteroenteric fistulas 

(g) Anti-TNF therapies (infliximab, adalimumab, certolizumab pegol) may be helpful in severe cases. 

These agents are rarely initiated in the emergency department, but clinicians should be aware of 

immunocompromise in patients taking them. 

a. Definition and pathology 

(1) Ulcerative colitis is a chronic inflammatory and ulcerative disease of the colon and rectum, most often 

characterized clinically by bbgloody diarrhea and crampy abdominal pain. 

(2) Inflammation is generally limited to the mucosa and submucosa; the muscular layer and serosa are 

usually spared. 

195


(3) Unlike the "skip lesions" of Crohn disease, mucosal involvement in ulcerative colitis is continuous and 

uniform; it always begins in the rectum and can remain limited to this area or spread proximally to 

involve the upper segments of the colon. 

(4) Chronic inflammation leads to the formation of crypt abscesses, epithelial necrosis, and mucosal 

ulceration. 

b. Epidemiology closely approximates that of Crohn disease. 


(1) Occurs intermittently with complete remission between attacks 

(2) Mild disease in 60% of cases 

(a) 6 bowel movements/day 

(b) Fever, tachycardia, weight loss, anemia 

(c) Extraintestinal manifestations (essentially the same as those seen with Crohn disease) 

d. Complications 

(1) Hemorrhage 

(a) Most common 

(b) However, massive hemorrhage is infrequent (occurs in only 2%-3% of patients). 

(2) Toxic megacolon (occurs more commonly with ulcerative colitis than with Crohn disease) 

(a) Clinical picture: The patient appears severely ill and has abnormal vital signs (hypotension, 

tachycardia, and fever). The abdomen is distended, tender, and tympanitic. Laboratory studies 

reveal leukocytosis with anemia, electrolyte imbalance, and hypoalbuminemia. Plain radiograph 

of the abdomen reveals dilatation of the colon with a colonic diameter >6 cm. 

(b) Management 

i. Nasogastric suction, IV fluids, and broad-spectrum antibiotics 

ii. IV steroids (hydrocortisone or methylprednisolone) 

iii. Frequent abdominal examinations and radiographs with surgery (colectomy) if no 

improvement in 24-48 hours 

(3) Perforation (occurs more often during first episodes of colitis) 

(4) Obstruction (due to stricture) 

(5) Perianal fistulas and abscesses (occur less commonly with ulcerative colitis than with Crohn disease) 

(6) Carcinoma of the colon (incidence is 15 times greater in patients with ulcerative colitis than in the 

general population and correlates with the duration and extent of disease) 


(1) The most sensitive method for establishing the diagnosis of ulcerative colitis and determining the 

extent of disease is a sigmoidoscopy. 

(2) Diagnosis of toxic megacolon is usually obvious on plain radiographs. 

f. Management 

(1) Mild to moderate disease 

(a) 5'-ASA derivative such as mesalamine or olsalazine 

i. Mainstay of therapy 

ii. Therapeutic properties are because of its 5-aminosalicylic acid (5' -ASA) component. 

(b) Corticosteroids may also be needed, either as supplemental therapy or as alternative therapy when 

mesalamine is ineffective. 

(c) 5'-ASA and corticosteroid enemas are useful for patients with ulcerative proctitis and left-sided 

colitis. 

(d) Supportive therapy (supplemental iron and a lactose-free diet); antidiarrheal agents should be 

avoided because they are usually ineffective and can precipitate toxic megacolon. 

(e) Azathioprine, cyclosporine, and 6-mercaptopurine are used in patients who do not respond to 

steroid therapy. 

(2) Severe ulcerative colitis (inpatient therapy) 

(a) 

IV fluids and correction of electrolyte abnormalities 

196


(b) Nasogastric tube 

(c) IV steroids, cyclosporine, or infliximab 

(d) Broad-spectrum antibiotics active against coliforms and anaerobes (ampicillin, clindamycin, or 

metron idazole) 

(e) Surgical consult if toxic megacolon suspected 

3. Pseudomembranous enterocol itis 

a. Definition: an inflammatory bowel disorder characterized by the formation of yellowish exudative 

pseudomembranous-like plaques that overlie and replace necrotic intestinal mucosa, particularly in the 

area of the rectosigmoid 

b. Etiology and epidemiology 

(1) Ingestion of broad-spectrum antibiotics alters the gut flora - proliferation of Clostridium difficile, 

a cytopathic toxin-producing bacterium (emerging strain NAP-1 /027 has high association with 

fluoroquinolone usage) 

(2) Any antibiotic can cause pseudomembranous colitis, but fluoroquinolones, clindamycin, 

cephalosporins, and penicillins are the most common. 

(3) Nosocomial transmission among hospitalized patients via hands of healthcare workers (contaminated 

with C difficile toxin) who are caring for these patients also occurs, even in the absence of 

antimicrobial therapy. 

(4) Traditionally considered a disease of frail, elderly, hospitalized patients, it is now recognized in those 

who have not been exposed to hospital environment or antibiotics. The CDC warns of transmission by 

close contact with infected persons in nontraditional patients (such as the young and otherwise healthy 

individuals); suggests person-to-person spread. 


(1) The patient presents with crampy abdominal pain, fever, and watery diarrhea (which may be bloody). 

(2) Symptoms generally begin 7-10 days after antibiotics are started but may occasionally be delayed 

several weeks after antibiotics have been discontinued. 

d. Diagnostic evaluation 

(1) The presence of C difficile toxin in the feces confirms the diagnosis. 

(2) If this assay is not readily available, colonoscopy or sigmoidoscopy can be used to establish a tentative 

diagnosis. 

e. Management 

(1) Discontinue antibiotics and institute supportive therapy with IV fluids and electrolyte replacement. 

(2) Oral metronidazole considered first choice for mild to moderate disease. 

(3) Oral vancomycin is first choice for severe infection and refractory infections. 

(4) Toxic megacolon a potential complication of C difficile infection. 

(5) Relapse occurs in about 25% of patients. In patients who have had one relapse, the rate increases to 

45% for a second relapse. 

(6) Fecal microbiota transplant is an accepted therapy for recurrent C difficile infection. 

G. Irritable bowel syndrome (IBS) 

1. Definition: a state of disturbed intestinal motility (without anatomic cause) that is functional in nature and 

diagnosed only after more serious causes are excluded 


a. Patients are usually 20-40 years old. 

b. Women are affected more often than men (ratio is 2:1 ). 

c. A familial predisposition is present. 

d. Psychiatric disease may coexist. Depression and anxiety disorder are common. 

e. Fibromyalgia is a frequent comorbid illness. 

f. It is exacerbated by stress. 

g. Patients with !BS have demonstrable disturbance of rhythmic electrical activity in the intestine. 


a. The patient is usually a young woman who presents with recurrent episodes of altered bowel function 

(diarrhea or constipation) with or without associated abdominal pain. 

b. The abdominal pain is described as crampy or achy in character and is confined to the lower abdomen. It 

generally occurs in association with constipation and is relieved by defecation or the passage of gas. 

197


c. Extracolonic symptoms (eg, bloating, belching, gastroesophageal reflux) are common. 

d. Presence of fever, abdominal mass, weight loss, and rectal bleeding are not associated with IBS and suggest 

a more serious diagnosis. 

e. Examination findings are most often nonspecific but may include vague lower abdominal tenderness and a 

palpable feces-filled sigmoid colon. 

f. Laboratory evaluation is unremarkable. 


a. IBS is a diagnosis of exclusion. 

b. Diagnosis is difficult to make in the emergency department. Patients are often discharged with diagnosis of 

"abdominal pain, etiology uncertain." If the diagnosis is suspected, patients should be referred to primary 

care provider for additional evaluation. 

c. The Rome Criteria were developed to standardize research protocols: diagnosis of JBS requires recurrent 

abdominal pain or discomfort for at least 3 days per month in the last 3 months associated with at least two 

of the following: 

(1) Improvement with defecation 

(2) Onset associated with change in frequency of defecation 

(3) Onset associated with change in form/appearance of feces 

5. Management 

a. Directed toward relief of symptoms 

(1) Constipation predominant: may benefit from high-fiber diet and bulk-forming agents 

(2) Diarrhea predominant: antidiarrheals, antispasmodics 

b. Drug therapy should be reserved for patients who do not respond to the above measures. It is usually 

initiated by the primary care provider and may include one or more of the following: 

(1) Antidiarrheal agents 

(2) Antispasmodic (anticholinergic) agents 

(3) Anxiolytics 

(4) Antidepressants 

(5) A number of drugs, including 5-hydroxytryptamine (5-HT) (serotonin) 3 receptor antagonists and 5-HT 

4 receptor agonists, have been removed from the market because of severe adverse effects. 

H. Colonic diverticular disease 

1. Diverticula are saclike herniations of colonic mucosa and submucosa through the muscularis; they may penetrate 

through areas of potential weakness in the bowel wall, such as where wall is penetrated by blood vessels. 

a. Associated with a diet low in fiber and high in refined carbohydrates; promotes less bulky stools, increased 

GI transit time, and increased intracolonic pressure. 

b. Although the location of diverticula may vary, most are confined to the sigmoid colon (left lower quadrant) 

in Western countries. 

2. The frequency of diverticular disease is directly correlated with age, especially if the diet is low in fiber and 

roughage. 

a. Frequency of diverticulosis increases with age: incidence is 10% in those


(5) Caution in elderly and immunocompromised, because abdominal examinations and systemic 

response may be unreliable. 

(6) Patients are likely stable for outpatient therapy. 

4. Complicated diverticulitis 

a. Process has advanced such that microperforation, abscess, or phlegmon has occurred. Fistula formation 

may occur, and 2% have free perforation. 

b. Physical examination is likely to show peritoneal signs with signs of systemic toxicity. 

c. Leukocytosis and sepsis may also occur. 

d. Abdominal CT is required to determine extent of pathology and identify complicating factors such as 

fistula, perforation, abscess. 


(1) CT of the abdomen is recommended as initial radiologic examination. 

(a) Helps establish the diagnosis when it is unclear 

(b) Helps establish extent of disease and complications 

(c) Excludes other etiologies 

(d) No risk of perforation 

(2) Colonoscopy is usually avoided when acute because of risk of perforation. 

(3) Barium enema is not done in acute stage. 

5. Management 

a. Uncomplicated diverticulitis: may be treated on outpatient basis 

(1) High-fiber diet prevents recurrence for 5 years in 70% of patients. 

(2) Antibiotics to cover anaerobes and gram-negative organisms. 

(a) TMP-SMX + metronidazole or 

(b) Ciprofloxacin + metronidazole or 

(c) Amoxicillin/clavulanate for 10 days 

(3) Analgesics 

b. Complicated diverticulitis 

(1) IV fluids and broad-spectrum antibiotics to provide both aerobic and anaerobic bacterial coverage 

(a) Ciprofloxacin + metronidazole 

(b) Ticarcillin/clavulanate 

(c) Ampicillin/sulbactam 

(d) lmipenem for more severe cases 

(2) Nothing by mouth; bowel rest 

(3) Nasogastric suction if ileus or intestinal obstruction is present 

(4) Surgery required in only 10% of patients with acute disease 

(a) Small abscesses may be treated with antibiotics only; abscesses >4 cm may require percutaneous 

drainage. 

(b) Surgical consult for all with peritoneal signs or free air 


VI. ANORECTAL DISORDERS 

A. Hemorrhoids 

1. Definition 

a. Dilated venules of the hemorrhoidal plexuses 

b. Associated with chronic constipation, straining, increased intra-abdominal pressure, pregnancy, increased 

portal pressure, and a low-fiber diet 

2. Types 

a. External hemorrhoids arise from below the dentate line (which separates the rectum from the anus) and are 

covered with well-innervated squamous epithelium. They are visible on external inspection. 

b. Internal hemorrhoids originate from above the dentate line and are covered by relatively insensitive rectal 

mucosa. Although not normally palpable on examination, they can be visualized with anoscopy at the 2, 

5, and 9 o'clock positions and may visibly prolapse with the Valsalva maneuver. 

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a. Patients with external hemorrhoids most commonly present with painful thrombosis. Examination reveals a 

tender mass at the external anal orifice. 

b. Patients with internal hemorrhoids usually present with painless bright-red bleeding that occurs in 

association with defecation. (Hemorrhoids are the most common cause of rectal bleeding). The blood 

covers the feces or drips into the toilet bowl and is usually small in volume. 

4. Management 

B. Anal fissure 

a. Thrombosed external hemorrhoids 

(1) WASH regimen 

Warm water soaks 

Analgesics (mild oral analgesics) 

~tool softeners 

.!::!.igh-fiber diet 

(2) Topical steroids are of limited value and should be avoided. 

(3) Topical anesthetics may offer some relief, but their use is controversial. 

(4) If pain is severe and the thrombosis is acute (


2. Etiology: most anorectal abscesses result from obstruction of mucusproducing glands at the base of the anal 

crypts. Other causes include inflammatory bowel disease, cancer, radiation injury, trauma, tuberculosis, and 

lymphogranuloma venereum. The resulting infections are frequently polymicrobial and involve the colonic flora. 

3. Perianal abscesses are the most common. 

a. Located outside the anal verge 

b. Patient complains of painful perianal mass. 

c. Likely afebrile with normal WBC count 

d. May be incised in the emergency department 

4. lschiorectal abscess 

a. Form outside the sphincter muscles and below levator ani 

b. Patient likely complains of buttock pain. 

c. Fever and increased WBC count are likely. 

d. Almost all require drainage in the operating room, because appearance maybe misleading. 

5. lntersphincteric abscess 

a. Deep to anal sphincter and below levator ani 

b. Patient complaint of constant rectal pressure and increased pain with defecation and sitting. 

c. Rectal examination shows painful mass occasionally with purulent drainage. 

d. Inguinal adenopathy common 

e. Require drainage in the operating room 

6. Supralevator abscess 

a. Perianal and buttock pain, often associated with fever 

b. External evidence of infection is lacking. Rectal examination may show tender mass. 

c. Surgical drainage in operating room required. 

7. Management: anorectal abscesses require early and extensive drainage. 

a. Simple perianal abscesses may be drained in the emergency department under local anesthesia. 

b. All other perirectal abscesses need to be drained in the operating room. 

c. Routine use of antibiotics is not warranted; they should be reserved for immunocompromised patients, 

patients with diabetes or valvular heart disease, and patients with associated cellulitis. 

8. Complication: fistula formation is a common sequela. 

D. Miscellaneous anorectal disorders 

1. Fistula-in-ano 

a. An abnormal tract between the anal canal and skin that is lined with granulation tissue 

b. Most commonly occurs as a complication of a perianal or ischiorectal abscess; may also be associated with 

ulcerative colitis, Crohn disease, tuberculosis, radiation, and cancer of the anus or rectum 

c. If the tract remains open, there is a persistent, purulent, blood-stained discharge; if the tract becomes 

blocked (most common), an abscess may be the only physical finding. 

d. Treatment is surgical excision. 

2. Rectal prolapse (procidentia) 

a. Types 

(1) Mucosa! prolapse (seen primarily in young children and in association with internal hemorrhoids) 

(2) Prolapse involving all layers of the rectum 

(3) lntussusception of the upper rectum into the lower rectum with the apex protruding through the anus 

b. Complete rectal prolapse occurs in the very young and the very old (particularly older women). 

c. Rectal prolapse in children should prompt consideration of cystic fibrosis. 

d. Clinical presentation: patients typically complain of a painless anal mass noticed after straining, coughing, 

or defecation. 

e. Management 

(1) Reduction can be accomplished in almost all patients, although recurrence (particularly in older 

patients) is likely. 

(2) In the presence of vascular compromise, emergency reduction is mandatory. 

(3) After reduction of the prolapse, patients should be placed on fecal softeners and referred for further 

evaluation (to uncover any underlying pathology) and potential surgical correction (commonly 

required in the elderly). 

201


3. Pilonidal sinus (abscess) 

a. Occurs in the midline (at the superior edge of the buttock crease) and is more common in men than women 

b. The sinus is formed when an ingrowing hair penetrates the skin and induces a foreign body granuloma 

reaction. 

c. A single opening at the base of the spine with hair protruding is the most common physical finding. 

d. When the sinus becomes plugged and cannot drain---,, abscess 

e. Management 

(1) Surgical incision longitudinal and lateral to the sacral midline with drainage of purulent material 

(2) Refer for definitive surgical care. 

(3) Antibiotics are indicated if there is an associated cellulitis or the patient is immunocompromised. 

4. Anorectal tumors 

a. Classification: based on their virulence, these tumors have been arranged into two groups with distinct 

anatomic locations. 

(1) Anal canal neoplasms (found proximal to the dentate line) 

(a) Represent 80% of anorectal tumors 

(b) Have a high-grade malignant potential and metastasize early; prognosis is poor. 

(c) Tumors occurring in this region 

i. Adenocarcinoma (common) 

ii. Mucoepidermoid carcinoma 

iii. Malignant melanoma 

1v. Kaposi sarcoma 

v. Squamous cell carcinoma 

vi. Basaloid carcinoma 

vii. Vil lous adenoma 

(2) Anal margin neoplasms (found distal to the dentate line) 

(a) Represent 20% of anorectal tumors 

(b) Have a low-grade malignant potential, slow to metastasize, good prognosis 

(c) Tumors occurring in this region include: 

i. Basal cell carcinoma 

ii. Squamous cell carcinoma 

iii. Bowen disease 

iv. Extramammary Paget disease 

v. Giant solitary trichoepithelioma 

b. Clinical presentation: pruritus, rectal bleeding, pain, weight loss, anorexia, constipation, decrease in fecal 

caliber, tenesmus, and obstruction 

c. Management: prompt surgical referral 

5. Rectal foreign bodies 

a. Diagnostic evaluation 

(1) Abdominal radiographs should be obtained to ascertain the location, size, shape, and number of 

objects present as well as to exclude the presence of free air. 

(2) Multiple views may be needed. 

b. Management 

(1) If there is clinical or radiographic evidence of free air, the patient should be prepared for surgery and 

an immediate surgical consult obtained. 

(2) After removal of the foreign body, the patient should be observed for 12 hours, and radiograph studies 

and sigmoidoscopy performed. 

c. Complications 

(1) Perforation is the most frequent; it results from the foreign body itself or attempts to remove it. 

(2) Mucosa! tears can also occur. 

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VII. DIARRHEA AND FOOD POISONING 

A. General information 

1. The vast majority of patients in the emergency department suspected of having "gastroenteritis" have a benign, 

self-limited disease. Evaluation should distinguish between acute or chronic diarrhea as well as the presence of 

invasive or noninvasive organisms. 

2. Acute gastroenteritis is defined as symptoms being present for 2 weeks) suggests an alternative cause such as intestinal parasites or 

other disorders. 

4. Invasive gastroenteritis is associated with fever, abdominal pain, blood in the feces, and tenesmus. Presence of 

these symptoms suggests a bacterial cause, and testing for specific organisms may be warranted. 

5. Noninvasive disease is suggested by the absence of the above symptoms. The feces are not bloody in most 

cases. Suggests a viral cause or pre-formed toxin, and testing is rarely warranted. 

6. If tested, the presence of fecal blood and leukocytes helps distinguish invasive from noninvasive. 

B. Viral diarrheal diseases (most acute episodes of diarrhea) 

1. Although many viruses can cause gastroenteritis, two groups have become most common over the last 10 

years: reovirus-like agents such as rotavirus and the noroviruses, which include norovirus. 

a. Rotavirus infection 

(1) Outbreaks are usually sporadic, usually in winter months. 

(2) Primarily in children 6-24 months old 

(3) Incubation period of 1-3 days 


(a) Onset usually abrupt with vomiting, low-grade fever, and watery diarrhea. Vomiting usually lasts 

1-1 .5 days and resolves spontaneously. Diarrhea may last 4-7 days. 

(b) Abdominal cramping is common. 

(5) Diagnostic evaluation: diagnosis is confirmed by detection of antigens in the feces by latex 

agglutination, PCR, or ELISA. However, testing is not usually required. 

(6) Not uncommonly, children become dehydrated and require IV hydration and hospitalization. The 

disease is an uncommon cause of mortality in the United States. 

(7) A vaccine, introduced in 2006, is given to babies at 2, 4, and 6 months of age. 

b. Norovirus 

(1) Up to 80% of diarrheal illness in industrialized countries 

(2) Most common cause of epidemic, nonbacterial gastroenteritis in the world 

(3) Can be transmitted person to person by fecal-oral route 

(4) Water and food-borne outbreaks common; up to 50% of food-borne outbreaks caused by norovirus 

(a) Stored water on cruise ships a common source 

(b) Shellfish, food handlers; raw oysters implicated 

(5) In January 2013, the CDC reported a new strain, Gll.4 Sydney, which appears to cause more severe 

disease and results in more hospitalizations and deaths. 


(a) After an incubation period of 1-2 days, patients typically have an abrupt onset of nausea, 

nonbloody watery diarrhea, abdominal cramps, and low-grade fever. Vomiting may be severe, 

nonbloody, nonbilious. 

(b) There is no upper or lower respiratory tract involvement. 

(c) Symptoms last for 1-2 days. 

(7) Diagnosis is usually clinical, although blood and fecal tests are available. 

(8) Management: disease is self-limited and requires only supportive, symptomatic care. 

C. Bacterial diarrheal diseases (20% of acute diarrheal cases) 


a. Invasive bacteria act primarily on the large bowel and produce diarrhea by damaging cell membranes and 

eliciting an inflammatory response - blood and mucus in the feces 

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(1) Campylobacter 

(2) Salmonella 

(3) Shigella 

(4) Vibrio parahaemolyticus 

(5) Vibrio vulnificus 

(6) Yersinia enterocolitica 

(7) Enteroinvasive E coli 

(8) Enterohemorrhagic E coli serotype 0157:H7 

(9) Clostridium difficile 

b. Enterohemorrhagic E coli serotype 0157:H7 and C difficile are actually toxin-producing bacteria that 

induce diarrhea by elaborating a cytopathic toxin that destroys the intestinal wall. They are grouped with 

the invasive bacteria, because the clinical syndrome they produce most closely resembles that produced by 

these organisms. 

c. Enterotoxin-producing bacteria release a toxin that acts primarily in the small intestine and produces 

diarrhea by altering water and electrolyte transport in epithelial cells - profuse watery diarrhea 


(2) Bacillus cereus 

(3) Ciguatera fish poisoning 

(4) Scombroid fish poisoning 

(5) Enterotoxigenic E coli 

(6) Clostridium perfringens 

(7) Aeromonas hydrophila 

(8) Vibrio cholerae 

2. Fecal leukocytes (a wet mount or methylene blue stain of the feces) 

a. May be used as a screen for those patients who may benefit from antibiotic therapy 

(1) Invasive bacterial pathogens producing fever, systemic illness, or bloody feces: Salmonella, Shigella, 

Campylobacter, and f coli 0157:H7 

(2) Pseudomembranous enterocolitis 

(3) Amebiasis 

(4) Inflammatory bowel disease (Crohn disease and ulcerative colitis) 

Table 7: Fecal Leukocytes in Diarrheal Syndromes 

Fecal Leukocytes Present 

Campylobacter 

Salmonella 

Shigella 

Vibrio parahaemolyticus 

Vibrio vulnificus 

Yersinia 

Amebiasis 

Enteroinvasive E coli 

Enterohemorrhagic E coli 

Clostridium difficile 

Ulcerative colitis 

Crohn disease 

Fecal Leukocytes Absent 

Rotavirus 

Norovirus 

Enteric type adenovirus 

Staphylococcus aureus 

Bacillus cereus 

Ciguatera fish poisoning 

Scombroid fish poisoning 

Enterotoxigenic E coli 

Clostridium perfringens 

Aeromonas hydrophila 

Vibrio cholerae 

Giardia lamblia 

204


b. Although treatment based on the presence or absence of fecal leukocytes is not 1 00% accurate, it is a good 

place to start, and is one of the few test results for diarrheal illnesses that is immediately available. Presence 

of fecal leukocytes (>5 WBCs per high-power field) has an LR of 4.5 for the presence of an invasive 

pathogen. 

3. Traveler's diarrhea 

a. Definition: syndrome acquired by travelers who eat food or water that is fecally contaminated 

b. Risk factors 

(1) Travel to developing tropical regions (Mexico, Latin America, southern Asia, Africa) where sanitation 

is poor 

(2) Ingestion of food prepared by street vendors 

(3) Ingestion of certain unsafe (often contaminated) items such as tap water, ice cubes, unpasteurized 

dairy products, raw vegetables, unpeeled fruit, and raw or undercooked seafood or meat 

c. Most cases (70%-75%) are caused by bacteria, of which enterotoxigenic E coli is the most commonly 

involved pathogen; it is responsible for up to 50% of cases worldwide. 

d. Clinical presentation: symptoms often begin abruptly and consist of watery diarrhea and abdominal 

cramps; other associated symptoms may be present and vary with the particular etiologic agent involved. 

e. Antibiotic prophylaxis 

(1) Not recommended for healthy individuals because of the associated risks (eg, emergence of resistant 

organisms, allergic reactions, photosensitivity reactions, etc) 

(2) Bismuth subsalicylate 2 tablets 4 times a day and strict adherence to preventive methods (avoiding the 

above) recommended by the CDC. 

(3) Initiation of treatment at the onset of symptoms is preferred. 

f. Management 

(1) Oral rehydration with electrolyte replacement such as found in sports drinks, caffeine-free soft drinks, 

or diluted fruit juice effectively maintains fluid and electrolyte balance in most patients. 

(2) Antibiotics 

(a) The CDC recommends a fluoroquinolone such as ciprofloxacin or norfloxacin for 3-5 days. 

(b) Rifaximin also approved for treatment at onset of symptoms. 

(c) TMP-SMX no longer recommend because of resistance. 

(3) Anti motility agents such as loperamide provide rapid symptomatic relief but should not be continued 

for >2 days and should not be used in patients who have fevers or bloody diarrheas, because these 

may increase severity and prolong symptoms. 

(4) Bismuth subsalicylate is an anti secretory agent that is also effective in reducing the number of bowel 

movements and the duration of illness. It works by decreasing the outpouring of fluids by the mucosa 

of the smal I intestine. 

4. Specific bacterial infections 

a. f coli: several strains have been shown to be diarrheagenic, two of which are discussed below. These 

strains differ in terms of their virulence, epidemiology, and clinical characteristics. 

(1) Enterotoxigenic f coli 

(a) Most common cause of traveler's diarrhea worldwide 

(b) Acquired by ingesting fecally contaminated food and water 

(c) Causes diarrhea by producing both heat-labile and heat-stable toxins 

(d) Clinical presentation 

i. Incubation period 1-4 days 

ii. Symptoms usually begin suddenly and consist of watery diarrhea associated with abdominal 

cramping. 


i. Most cases resolve in 2-3 days with supportive measures alone. 

ii. The use of antibiotics and antimotility agents (see traveler's diarrhea, above) can shorten the 

duration of this syndrome. 

(2) Shiga toxin-producing f coli (STEC), also known as enterohemorrhagic f coli 

(a) Serotype 0157:H7 is most common isolate in the United States. 

(b) Transmission occurs by ingesting small amounts of human or animal feces. Person-to-person 

spread is also possible. Exposure to cattle can also transmit disease. 

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(c) Outbreaks commonly occur due to improperly cooked ground beef, fruits, or vegetables. Highrisk 

foods are raw milk, soft cheeses made from unpasteurized milk, unpasteurized apple cider, 

and nondisinfected water. 

(d) Outbreaks are associated with ingestion of contaminated, undercooked ground beef, seed 

sprouts, or unpasteurized milk; however, person-to-person spread also occurs. 

(e) Most common in children, the elderly, and post-gastrectomy patients. 

(f) This organism produces Shiga toxins that are cytotoxic to the intestinal vascular endothelium. 

(g) Clinical presentation 

1. Incubation period 3-4 days on average 

ii. Patient presents with diarrhea, crampy abdominal pain, and vomiting. The cramps can be 

severe enough to masquerade as an acute abdomen. The diarrhea is watery early on but 

eventually becomes bloody. Fever is absent or low grade. WBCs are present on the wet 

mount but are few in number. 

(h) Diagnostic evaluation: fecal testing for Shiga toxin along with cultures for f coli O157:H7 

(i) 

(j) 

Management 

i. Antibiotic therapy is contraindicated; antibiotics have not been shown to decrease the 

duration of symptoms, and they may increase the risk of hemolytic uremia syndrome. 

ii. Antidiarrheal agents may also increase the risk of hemolytic uremia syndrome. 

iii. Most cases resolve in 7-10 days with supportive measures. 

Complications 

i. Hemolytic uremic syndrome 

• Occurs in about 8% of children, of which 5%-10% of cases are fatal 

• Occurs in nearly 40% of elderly patients who acquire STEC in a nursing-home outbreak; 

up to 80% fatality rate 

11. Thrombotic thrombocytopenic purpura develops in ~2% of patients, usually 

immunocompromised. 

b. Shigella (a common cause of bacterial diarrhea) 

(1) Shigellosis (bacillary dysentery) occurs worldwide but is especially common in countries where 

adequate sanitary facilities are lacking. 

(2) The CDC estimates an annual incidence in the United States of 4 cases per 100,000 persons. 

(3) Common in "contained" populations, eg, nursing homes, prisons, schools, day care facilities; 

outbreaks have been reported in water parks, swimming pools, etc. 

(4) Shige!la sonnei causes ~75% of cases in the United States; Shige!!a flexneri causes most of the rest. 


(a) 

Incubation period is 24-48 hours after exposure to even a very small inoculum. 

(b) Mild, watery diarrhea with scant systemic symptoms may be seen in most early disease. 

Dysentery can then ensue with fevers, crampy abdominal pain, grossly bloody diarrhea, vomiting, 

headaches, and myalgia. Profound dehydration may develop, especially in infants and the elderly. 

(c) Convulsions may occur in young children, usually those 800 is suggestive of 

shigellosis. 

(b) A wet mount of the feces with methylene blue demonstrates numerous fecal leukocytes. 

(c) 


Fecal cultures are positive in most cases, particularly if obtained within the first few days of illness. 

(a) Fluid resuscitation or maintenance of hydration is of paramount importance. 

(b) Antibiotics decrease the duration of illness and excretion of Shigella organisms in the feces. They 

are recommended in patients with dysentery, in the very young and very old, and in institutional 

outbreaks. Management should continue for 3 days in immunocompetent patients and for 10 days 

in immunocompromised. 

i. Quinolones (ciprofloxacin, norfloxacin, ofloxacin) are the drugs of first choice, but they are 

contraindicated in pregnancy and in children


ii. Ceftriaxone may be useful. 

iii. Ampicillin and TMP-SMX are not effective and are no longer considered viable treatment 

options unless fecal culture indicates effectiveness. 

(c) Antimotility drugs should be avoided, because they can prolong duration of disease. 

(8) Complications 

(a) Dehydration secondary to profuse diarrhea 

(b) Arthralgias 

(c) Reiter syndrome (nongonococcal urethritis, polyarthritis, conjunctivitis) 

(d) Hemolytic uremic syndrome 

(e) Febrile seizures (common in children


(b) Septicemia or typhoid fever (enteric fever): ceftriaxone is the agent of choice; alternatives 

include ciprofloxacin, chloramphenicol, and ampicillin. 

(c) Antidiarrheal agents are contraindicated, because they prolong the illness and increase the 

incidence of bacteremia and the carrier state. 

d. Campylobacter enteritis 

(1) Campylobacter infection is the most common cause of bacterial diarrhea. 

(2) It is transmitted by ingestion of fecally contaminated water or food (particularly poultry) or by direct 

contact with feces of infected animals or people; it produces disease by directly invading the colonic 

epithelium. 


(a) 

Incidence of infection is greater in young children. 

(b) Incubation period is 2-5 days. 

(c) Onset of disease is usually rapid and consists of fever and crampy, abdominal pain. Malaise, 

myalgia, and headache are common. Abdominal pain may be severe enough to mimic an acute 

abdomen. 

(d) Diarrhea usually begins 1-2 days after the fever and pain. It is frequently loose and bile colored, 

subsequently turning watery and bloody. Gross blood is seen in 60% of cases. 

(4) Diagnostic evaluation 

(a) Wet mount shows blood and fecal leukocytes. 

(b) Fecal culture confirms the diagnosis. 


(a) Antimotility agents should be avoided. 

(b) Patients with mild disease do not require treatment other than supportive care. Empiric 

antibiotics are not recommended. 

(c) Patients who are still symptomatic when culture results are returned may be treated with 

erythromycin or azithromycin. Ciprofloxacin in no longer recommended because of widespread 

resistance. 


(a) Reiter syndrome 

(b) Hemolytic uremic syndrome 

(c) Guillain-Barre syndrome (a late sequela) 

e. Yersinia enterocolitis 

(1) Infection results from ingestion of contaminated food or drink and is most common in childhood. 


(a) 

Patient presents with fever and diarrhea 2-6 days after exposure that is accompanied by severe, 

cramping abdominal pain that may last up to 2 weeks. 

(b) Dysentery (bloody diarrhea) may be present in up to 25% of patients. 

(c) On physical examination, the abdomen is tender and, if the organism has caused mesenteric 

adenitis or terminal ileitis (which it sometimes does), you may think the patient has appendicitis. 

(d) Recent exposure to domestic, farm, or wild animals can be a significant diagnostic clue. 

(e) 

Postinfectious manifestations (erythema nodosum, polyarthritis) sometimes occur, particularly in 

adults. 


(a) Wet mount of the feces shows fecal leukocytes and occasionally RBCs. 

(b) Fecal culture (special techniques are required) confirms the diagnosis. 


(a) Mild to moderate infections: supportive therapy; however, Yersinia takes a long time to isolate 

and identify. 

(b) If antibiotics are started pending results, TMP-SMX is the antibiotic of choice. Quinolones are 

also effective. 

(c) Antimotility drugs should be avoided. 

f. Clostridium perfringens 

(1) A common cause of food poisoning; relatively large outbreaks are typical. 

208


(2) Food poisoning occurs when food contaminated with the live organism containing type A heatresistant 

spores are ingested. Typically, the food (meat or poultry, gravies, steam-table meats) was 

prepared earlier and allowed to cool. C perfringens multiplies and is then ingested. In the gut, the 

organism produces an enterotoxin _,. diarrhea and abdominal cramps 


(a) 

Incubation period is generally 1-5 hours. 

(b) Diarrhea and abdominal cramps common. Vomiting is not as common. 

(c) Fever, headache, and chills are uncommon. 

(d) No WBCs are seen on a wet mount of the feces. 


(a) This is a self-limited disease, with symptoms resolving in 10-12 hours. 

(b) Only supportive treatment is indicated. 

g. Staphylococcus aureus (the most common cause of food poisoning) 

(1) Illness results from ingestion of a heat-stable enterotoxin. 

(a) Cooking at a temperature> 140°F (60°C) will kill bacteria but not destroy the toxin. 

(b) Most protein-rich foods (eg, ham, eggs, mayonnaise, potato salad) support growth of staphylococci. 

(c) Contaminated food has no abnormal odor or taste. 

(2) Large outbreaks are common; the attack rate is >75%. 


(a) Incubation period is 1-6 hours, followed by abrupt onset of abdominal cramping and violent 

vomiting. Diarrhea may or may not occur. 

(b) Usual scenario: patient went to a barbecue or buffet about 6 hours before arrival where he or 

she had eaten some potato salad or sliced ham that had been sitting at room temperature for 

several hours. 

(4) Treatment is supportive; resolves in 6-1 0 hours. 

h. Bacillus cereus 

(1) Two clinical syndromes 

(a) An emetic syndrome caused by a heat-stable enterotoxin 

1. Begins 1-6 hours after ingestion of contaminated food. Fried rice is a common source; beef, 

poultry and milk have been implicated. 

ii. Symptoms are indistinguishable from those of staphylococcal poisoning. Abrupt onset of 

vomiting and crampy abdominal pain. Up to 25% have diarrhea. 

iii. Treatment is supportive; resolves in :::10 hours. 

(b) A diarrheal syndrome caused by a heat-labile enterotoxin 

1. Begins 6-24 hours after ingestion of contaminated meal (usually meat or vegetables) 

ii. Syndrome is similar in presentation to that of Clostridium poisoning. Symptoms include 

diarrhea and abdominal cramps. Vomiting is present in 20%. 

(2) Diagnosis can be confirmed by isolation of> 10 5 colonies of B cereus from the food source. However, 

because of the extremely short nature of the disease, this is rarely done. 

(3) Treatment is supportive; resolves in 10-24 hours. 

1. Aeromonas hydrophila 

(1) More common in summer. Usually acquired by drinking untreated water from a well or spring, or 

eating seafood or vegetables. 

(2) Most commonly affects children and immunocompromised patients 


(a) Watery diarrhea, crampy abdominal pain, vomiting (25%), fever (50%) 

(b) History of drinking from wells or fresh springs increases likelihood. 


(a) Confirmed by fecal culture; however, routine culture does not test for Aeromonas, so it must be 

specifically requested. 

(b) Fecal leukocytes and occult blood are usually absent. However, some patients present with 

symptoms suggesting colitis and have fecal leukocytes and blood; this may mimic Crohn disease. 

209



(a) 

Supportive measures will suffice in most patients, because disease is usually self-limited. 

(b) Antibiotic therapy with one of the following agents: 

i. TMP-SMX has shown good activity. 

ii. Fluoroquinolones are also effective. 

(c) Without antimicrobial therapy, the diarrhea generally persists for c::2 weeks. 

(d) Lactobacillus decreases duration of diarrhea in children. 

j. Vibrio cholerae 

(1) Transmitted by ingestion of contaminated water or seafood (especially raw oysters), which produces an 

enterotoxin-mediated diarrheal illness (cholera). 

(2) Large epidemics related to ingestion fecally contaminated water supplies. 


(a) Copious amounts of watery diarrhea ("rice water" feces) is the hal I mark of clinical cholera and 

can lead to significant fluid and electrolyte imbalances. 

(b) Severe dehydration (loss of isotonic fluid from bowel) 

(c) Hyperchloremic acidosis (loss of bicarbonate in the feces) 

(d) Hypokalemia (loss of potassium in the feces) 

(e) 

(f) 

Dehydration and hypoglycemia most common lethal complications of cholera in children. 

After an incubation period of 2 days, the patient presents with copious watery diarrhea and 

abdominal distention. Vomiting may also be present. 


(a) Diagnosis is confirmed by fecal culture. 

(b) Crystal VC® rapid diagnostic test can be used for rapid identification of two serotypes in epidemic 

situations to establish diagnosis. 


(a) 

Fluids (oral or IV) should be the focus of therapy. 

(b) Antibiotic therapy in those with moderate to severe dehydration. Doxycycline is drug of choice in 

adults; azithromycin is first choice in children and pregnant women. 

(c) Zinc is recommended for all patients to decrease duration and quantity of diarrhea. 

k. Vibrio parahaemolyticus 

(1) Leading cause of seafood-associated gastroenteritis in the United States 

(2) Invasive bacterial infection; other Vibrio species produce an enterotoxin to cause disease. 

(3) Acquired by ingestion of raw or improperly prepared seafood (especially oysters, clams, shrimp, and 

crabs); exposure to brackish or salty water is potential cause as wel I. 

(4) In temperate climates, this infection is usually confined to the summer months. 


(a) Symptoms begin after an average incubation period of 12 hours and range from mild 

gastroenteritis to explosive diarrhea with vomiting, cramps, and dysentery. 

(b) Fever may also be present. 

(c) Can also cause wound infection if open wound exposed to seawater 


(a) Wet mount of the feces reveals numerous WBCs. 

(b) Fecal culture requires special growth media, so laboratory must be notified. 


(a) 

Symptomatic therapy is generally all that is needed, because the illness is self-limited and resolves 

in 2-3 days. 

(b) Tetracycline or a quinolone may be given for severe infections (dysentery), but their efficacy 

remains unclear; they neither shorten the clinical course nor decrease the duration of shedding of 

the organism. 

I. Scombroid fish poisoning 

(1) The most commonly implicated fish is mahi mahi (blue dolphin or dolphin fish), but it is also 

common with ingestion of tuna, mackerel, and other dark-fleshed or red-muscled fish. 

(2) Most cases are in Hawaii and Florida, although it can be seen anywhere "fresh fish" is flown in. 

210


(3) Poisoning results from ingestion of heat-stable toxins with histamine-like properties produced by 

bacterial action on dark-meat fish; high levels of histamine correlate with the manifestations of the 

illness. Formation of the toxin is related to improper preservation and refrigeration of the fish. (This 

is not an allergic reaction.) 


(a) Patient presents with signs and symptoms of histamine intoxication 20-30 minutes after 

ingestion of the fish: 

i. Facial flushing (resembles a sunburn and can extend over entire upper body) 

ii. Throbbing headache 

iii. Abdominal cramps 

iv. Nausea, vomiting, and diarrhea 

v. Palpitations 

vi. Bronchospasm or hypotension (with severe toxicity) 

(b) Historical clue: at time of ingestion, the patient noticed a sharp, metallic, bitter, or peppery 

taste to the fish. 


(a) Diagnosis is based on clinical grounds with symptoms beginning shortly after ingestion of the fish. 

(b) If necessary, histamine levels can be checked on the suspect fish. 


(a) Depending on severity of symptoms, H 1 

- and H 2 

-blockers should be administered IV or orally. 

(b) Activated charcoal may be administered if a large amount of fish was ingested. 

(c) Additional therapy may be required. 

i. Antiemetics (for nausea and vomiting) 

ii. Albuterol and steroids (for bronchospasm) 

iii. Epinephrine (for anaphylactoid reaction) 

m. Ciguatera fish poisoning 

(1) Most common cause of nonbacterial fish-associated food poisoning in the United States 

(2) Results from ingestion of ciguatoxin, a tasteless, odorless, heat-stable neurotoxin that accumulates 

in the flesh of certain carnivorous tropical and semitropical coral-reef fish when a particular 

dinoflagellate is present in their food chain during the late spring and summer months. The most 

commonly affected species are grouper, snapper, barracuda, king fish, and jack. Because the toxin 

accumulates in the flesh of these fish, the bigger and older the fish, the more likely that it carries 

the toxin. 


(a) Ciguatoxin affects the sodium channels, so effects are most pronounced in nervous, cardiac, 

and GI tissues. 

(b) Incubation period is usually 2-6 hours but ranges from 15 minutes to 24 hours. 

(c) GI symptoms last 1-2 days and include abdominal pain, nausea, vomiting, and diarrhea. 

(d) Neurologic symptoms occur within hours up to 3 days and include painful paresthesias, 

circumoral and throat paresthesias, weakness, and coma. Paralysis of respiratory muscles has 

been reported. Pruritus is a common complaint. Neurosensory symptoms may persist for months 

and are exacerbated by ingestion of alcohol. 

(e) Pathognomonic "hot-cold reversal" likely represents intense dysesthesia experienced with cold 

stimuli rather than true reversal of temperature perception. 

(f) Cardiovascular symptoms occur least frequently but may include symptomatic bradycardia. 


(a) Supportive measures (IV fluids, antiemetics, analgesics) 

(b) H 1 

- and H 2 

-blockers may help with pruritus. Amitriptyline may be useful for pruritus and 

dysesthesia. 

(c) IV mannitol is no longer considered an effective therapy and is not recommended. 

(d) Absolute abstinence from alcohol, seafood, and nuts until all symptoms have resolved; 

continued abstinence is recommended for 3-6 months after exposure. 

5. Summary recommendations for gastroenteritis 

a. Antibiotics should be limited to patients who are significantly ill or toxic in appearance that are believed 

(based on clinical grounds) to have an invasive or infectious diarrhea. 

211


b. Early administration of antibiotics to these patients decreases the intensity and duration of symptoms, 

prevents systemic and suppurative sequelae, and reduces spread of infection. 

c. Unless contraindications exist (eg, pregnancy, children 7 days should be tested for parasites. 

1 . Entamoeba histolytica 

a. Protozoa with cystic and trophozoite phases 

b. Transmission usually occurs through ingestion of cysts (the infective phase) in water or food contaminated 

with feces. Cysts are stable in the environment and passed via fecal-oral transmission. Infection occurs as 

the cysts change into a trophozoite phase in the terminal ileum or colon. This is the invasive form, which 

causes symptoms. 

c. Trophozoites can invade the mucosa I barrier of the colon and produce bloody diarrhea and colitis, which 

may resemble inflammatory bowel disease. It is estimated that only 10%-20% of those exposed develop 

disease symptoms. 

d. Risk factors 

(1) People who have traveled to tropical areas with poor sanitation; St. Petersburg, Russia, has had an 

ongoing outbreak. 

(2) Immigrants from tropical areas with poor sanitation 

(3) People who live in institutions with poor sanitation 

(4) Native Americans living on reservations 

(5) Men who have sex with other men 

e. Clinical presentation 

(1) Chronic amoebic colitis is the usual manifestation. 

(a) Gradual onset with intermittent diarrhea 

(b) Foul-smelling feces with bloody mucus 

(c) Mild abdominal cramping and flatulence 

(2) Acute amoebic dysentery 

(a) 2-4 weeks after exposure, although can be longer 

(b) Sudden onset of severe abdominal cramping 

(c) Profuse bloody diarrhea 

(3) Amoebic abscess 

(a) 

Liver (most common) 

(b) Fever, right upper quadrant pain and tenderness, weight loss 

(c) Usually diagnosed by ultrasound or CT 

f. Diagnostic evaluation 

(1) Fecal studies 

(a) Trophozoites from single fecal specimen only 33% sensitive; examination of three samples within 

1 0 days is 90% sensitive. 

(b) Fecal leukocytes may be present in small numbers. 

(c) Fecal examination in patients with extraintestinal amebiasis is rarely helpful, because organisms 

are found in


2. Giardiasis 

a. Causative organism is Ciardia lamblia (also known as Ciardia intestinalis); most frequently diagnosed 

parasitic disease in the United States and travelers with chronic diarrhea. 

b. Transmitted by cysts via the fecal-oral route. 

(1) Found in soi I, food, and water that have been contaminated with feces containing the parasite. 

(2) The parasite is protected by an outer coat that allows it to survive outside the body for long periods of 

time. This also makes it resistant to disinfection by chlorine. 

(3) Most common method of transmission is by drinking contaminated water, ponds, streams etc; often 

called "backpackers diarrhea." 

(4) Beavers play a role in the spread of this disease by contaminating streams with cysts. 

(5) Venereal transmission among homosexuals (by direct fecal-oral contamination) is also common. 

c. Symptoms, if they occur, are produced by trophozoites and begin after an incubation period of 1-3 weeks; 

most patients, however, are asymptomatic. 

d. Risk factors 

(1) Backpackers, others who drink unsafe water 

(2) Playing in contaminated water, swallowing water 

(3) lmmunocompromised patients (lgA deficiency) 

(4) People who live in institutions 

(5) Children attending daycare centers 

(6) Travelers returning from underdeveloped countries (especially Russia) or a backpacking trip to Colorado 

(7) Patients with decreased gastric acidity from any cause 

e. Classic clinical scenario: The patient has recently returned from a back-packing trip in Colorado (or 

from travel to Russia) and presents with abdominal pain and feeling bloated and gaseous. Most common 

symptoms are explosive diarrhea, flatulence, colicky pain, and greasy, floating, foul-smelling feces. 

f. Diagnostic evaluation 

(1) Presence of trophozoites or cysts in the feces; several samples over separate days may be required. 

(2) Fecal immunoassays are available that are more sensitive and specific. The CDC recommends using 

these tests to screen high-risk patients (eg, daycare), but ova and parasite examination of the feces is 

the primary means of diagnosis. 

(3) Duodenal aspiration may need to be performed in asymptomatic patients and those with chronic 

symptoms. 

(4) Eosinophilia is absent. 

g. Management 

(1) Asymptomatic patients who shed the organism should be treated only to prevent spread to high-risk 

household contacts. 

(2) All asymptomatic patients should be treated. 

(a) Metronidazole (drug of choice) 

(b) Furazolidone (less effective than metronidazole but is available as a suspension and, for this 

reason, is often preferred in children) 

(c) Tinidazole (a congener of metronidazole or albendazole) 

h. Patients with recurrent or refractory giardiasis should be tested for immunoglobulin A deficiency. 

3. Cryptosporidium 

a. Intestinal protozoan coccidial parasite; causes disease with clinical features similar to those of /sospora. 

b. Most common cause of chronic diarrhea in patients with AIDS 

c. Transmitted by cysts from human or animal sources via the fecal-oral route; highly infectious and highly 

resistant to disinfection 

d. Symptoms, if they occur, are produced by trophozoites after an incubation period of 1-2 weeks; some 

patients are asymptomatic. 

e. Risk factors 

(1) lmmunocompromised patients (especially those with AIDS) 

(2) Homosexual men 

(3) Swallowing or drinking untreated water 

(4) Children attending daycare centers 

213


f. Clinical presentation 

(1) Profuse watery diarrhea, abdominal cramping, anorexia, nausea, and flatulence 

(2) In immunocompetent patients, these symptoms may persist for 1-3 weeks and result in significant 

dehydration, but they are generally self-limited. 

(3) In immunocompromised patients, malabsorption and significant weight loss occurs as well; symptoms 

may persist for months to years, producing significant discomfort and morbidity. 

g. Diagnostic evaluation 

(1) Fecal studies for oocysts using an acid-fast stain or enzyme immunoassay testing for Cryptosporidium 

(> 95% sensitive); must specify to the laboratory that the sample is to be tested for Cryptosporidium 

(2) Fecal blood and leukocytes are usually absent. 


h. Management 

(1) lmmunocompetent patients 

(a) 

Rehydration and symptomatic therapy 

(b) Nitazoxanide may hasten recovery. 

(2) Immunodeficient patients are resistant to treatment. 

(a) When possible, therapy should be directed toward correcting the underlying immunodeficiency. 

(b) Nitazoxanide or paromomycin plus azithromycin may decrease symptoms in these patients, but is 

not curative. 

(c) In AIDS patients, initiation of highly active antiretroviral therapy (HAART) is probably the best 

treatment, because it directly increases host immunity by suppressing HIV replication. 

4. Cystoisospora (formerly lsospora bell,) 

a. Coccidian parasite 

b. Transmitted by cysts via the fecal-oral route 

c. Usually an opportunistic infection, it is seen most commonly in patients with AIDS (especially in 

developing countries); most common in tropical and subtropical regions. 

d. Clinical presentation 

(1) Symptoms, when present, begin after an incubation period of 1-2 weeks and last for 2-6 weeks; 

some immunocompetent patients are asymptomatic, whereas immunocompromised patients tend to 

have a severe protracted course. 

(2) The typical patient is a 30-year-old Haitian male with a history of AIDS who presents with profuse 

watery diarrhea, abdominal cramps, nausea and vomiting. He also complains of weight loss and has 

signs of malabsorption. Fecal examination reveals oocysts. 


(1) Diagnosis is usually made by identifying oocysts in the feces, performing acid-fast staining of a fecal 

specimen, or identifying intracellular forms on biopsy of the small bowel. 

(2) Leukocytosis with moderate eosinophilia occurs in 50% and is an important clue to diagnosis. 

f. Management 

5. Cyc!ospora 

(1) TMP-SMX is the drug of choice; prolonged therapy is required in AIDS patients. 

(2) Pyrimethamine, nitrofurantoin, or furazolidone may be used in patients allergic to sulfa. 

a. Coccidial parasite found in tropical and subtropical regions. 

b. Affects both immunocompetent and immunocompromised individuals 

c. North American outbreaks have been traced to foods grown in tropical environments. 

d. Disease occurs after eating or drinking contaminated food or water. Person-to-person transmission is unlikely. 

e. After about 1 week, explosive watery diarrhea occurs with associated cramping, bloating, and nausea. 

Severe diarrhea lasts 2-3 days then becomes intermittent. Fatigue and weight loss are constant features. 

f. Disease is self-limited in healthy patients but may last 6-8 weeks, and up to a year in immunocompromised 

patients. 

g. Diagnosis is made by examination of feces for the oocysts; can be easily confused with Cryptosporidium. 

h. Management 

(1) TMP-SMX is the drug of choice. 

(2) Ciprofloxacin may be useful in allergic patients. 

214


6. Necator americanus (hookworm) 

a. Infection occurs when the hookworm larvae penetrate through intact skin on contact with fecescontaminated 

soil. 

b. Mainly acquired by walking barefoot on contaminated soil. 

c. After penetrating the skin, the larvae enter the bloodstream, ascend the trachea, descend to the esophagus 

to differentiate into adult worms, and migrate to the upper intestine where they attach to the mucosa! wall 

and feed on host blood. 


(1) Intermittent diarrhea, epigastric discomfort, weakness, low-grade fever, cough, rash, and weight loss 

(2) Anemia and protein deficiency most serious effects 


(1) Identify ova in the feces. 

(2) The presence of hypochromic, microcytic anemia and marked eosinophilia further support the diagnosis. 

f. Management 

(1) Mebendazole, albendazole, or pyrantel pamoate 

(2) An iron supplement 

7. Enterobius vermicularis (pinworm) 

a. Transmission is via ingestion of E vermicu/aris eggs. 

b. Once ingested, eggs develop into adult worms in the large bowel; then the gravid females migrate to the 

anus at night to deposit their eggs. 

c. Outbreaks often occur in schools, daycare centers, and other institutional settings. 


(1) Patients most commonly complain of pruritus ani, particularly at night. 

(2) Secondary skin changes and bacterial infection may also be present. 

(3) Other associated problems may include insomnia, enuresis, urinary tract infections, and vaginitis. 


(1) Identify either adult worms migrating in the perinea! area or eggs on a cellophane tape swab of the anus. 


f. Management 

(1) A single dose of mebendazole or pyrantel pamoate that is repeated again after 2 weeks 

(2) All family members should be treated. 

E. Diarrhea in the AIDS patient 

1. Patients who are HIV-positive are more susceptible to the typical enteric organisms and to many opportunistic 

organisms as well. In addition, it is believed that HIV itself may produce an enteropathy. 

a. Cytomegalovirus and Cryptosporidium are the two most common causes of diarrhea in these patients. 

Mycobacterium avium is another important cause. 

b. Multiple organisms are responsible in some patients (up to 25%). 

c. HIV-positive patients on the HAART regimen living in developed countries are more likely to have diarrhea 

related to their medications (most commonly protease inhibitors) than to an infectious cause. When 

diarrhea is the sole complaint of a patient on the HAART regimen, an infectious cause is found in


VIII. BILIARY TRACT DISORDERS 

A. General information 

1. Bile is produced in the canaliculi of biliary tract. While fasting, 50% of bile is stored in the gallbladder and 

50% flows into the duodenum. 

2. Food in the stomach results in release of cholecystokinin-pancreozymin and vagal impulses, which induce 

gallbladder contraction. 

3. Symptoms related to biliary disease are a frequent reason for emergency department visits. 

B. Cholelithiasis 

1. Gallstones 

a. 20% of women and 8% of men have gallstones. 

b. The vast majority of gal I stones are cholesterol stones. 

c. Risk factors for cholesterol stones 

(1) Female 

(2) Obesity 

(3) Increased parity 

(4) Advancing age 

(5) Rapid weight loss 

(6) Cystic fibrosis 

(7) Medications: oral contraceptives 

(8) Family tendency: very high rate in Pima Indians 

d. Pigmented stones 

(1) Black: associated with hemolysis such as sickle cell disease 

(2) Brown: associated with infection (bacterial as well as with Ascaris, Clonorchis) 

2. Clinical features: biliary colic 

a. Pain usually not colicky in nature (despite the name). 

b. Steady constant right upper quadrant pain (may be felt over epigastrium as well) 

c. Associated with nausea and vomiting 

d. May radiate to scapula or shoulder 


a. ALT and AST to assess for hepatitis 

b. Bilirubin and alkaline phosphatase to assess for duct obstruction 

c. Lipase to determine if pancreatitis present 

d. Ultrasound is the test of choice. 

4. Management 

a. Correction of fluid and electrolyte abnormalities if vomiting present 

b. Relief of nausea and vomiting 

c. Pain control 

(1) Anticholinergics to decrease spasm: glycopyrrolate 

(2) NSAIDs: ketorolac IV frequently useful 

(3) Opiates as needed 

d. Definitive treatment is cholecystectomy. 

C. Cholecystitis 

1. Acute cholecystitis represents acute inflammation of the gallbladder. 

2. Most cases result from acute obstruction of the cystic duct; 95% of patients will have gallstones identified. 

Duct obstruction may also be related to tumor, lymphadenopathy, fibrosis, parasitic disease. 

3. Risk factors are identical to those of cholelithiasis. 


a. Patients usually present with right upper quadrant pain that may be colicky but often becomes constant. 

b. Fever may be present. 

c. Nausea and vomiting are common. 

216



a. Ultrasonography showing stones, thickened gallbladder wall, and pericholecystic fluid is virtually 

diagnostic. 

b. Absence of stones has a very high negative predictive value. 

D. Variations and complications of cholecystitis 

1. Acalculous cholecystitis (5 % of cases) 

a. Occurs in postpartum/postoperative patients and those with burns or other major trauma, vascular 

disease, diabetes, sepsis, and CHF 

b. More common in the elderly 

c. Gangrene and perforation are relatively frequent in contrast to calculous cholecystitis. 

2. Calculous cholecystitis is the most frequent cause of acute pancreatitis: a gallstone passes into the common 

bile duct and may occlude the pancreatic duct at the sphincter of Oddi. 

3. Ascending cholangitis 

a. Occurs when stones passing through the common bile duct cause a purulent infection within the bile 

ducts that extends into the liver; may occur in the absence of stones with sclerosing cholangitis 


(1) Fever and chills, abdominal pain, and jaundice (Charcot triad) 

(2) In severe cases, mental confusion and shock may also be present (Reynold pentad). 

c. This is a surgical emergency with a high mortality rate requires emergent decompression through open 

surgery, percutaneous drainage, or endoscopic retrograde cholangiopancreatography. 

4. Emphysematous cholecystitis (rare) 

a. Infection with gas-forming bacteria (f coli, C/ostridium perfringens, Klebsiella, and/or anaerobic 

streptococci) 

5. Empyema of the gallbladder (an advanced stage of cholecystitis) 

a. Bacterial invasion of the gallbladder wall 

b. Leads to gross suppuration 

6. Gallstone ileus (uncommon) 

a. Mechanism: a large gallstone erodes into the duodenum, lodges in the terminal ileum, and produces 

intestinal obstruction. 

b. Most commonly seen in elderly women (causes 25% or all small-bowel obstructions in this group) with 

multiple underlying medical problems and a history of gallstones. 

c. Diagnostic evaluation: radiographic findings show pneumobilia (air in the biliary tree), evidence of 

mechanical small-bowel obstruction, and a stone in the GI tract. 

E. Clinical presentation 

1. History 

a. Family history of gallbladder disease (common) 

b. Fatty food intolerance (common) 

c. Nausea (common) 

d. Bile-stained vomitus (variable because vomiting may not be present) 

e. Abdominal pain: most common presenting complaint, often precipitated by ingestion of a fatty or heavy 

meal. Initially, the pain is visceral in nature and felt in the midline. With prolonged obstruction of the cystic 

duct, somatic fibers become involved and the pain localizes to the right upper quadrant. 

(1) Distention of the gallbladder (due to obstruction of the cystic duct by a gallstone)--,, epigastric pain 

(2) Prolonged obstruction of the cystic duct--,, increased pressure within the gallbladder--,, chemical 

and/or bacterial inflammation of the gallbladder wall --,, right upper quadrant pain (which may radiate 

to the interscapular area, right scapula, or shoulder) 


a. Tachycardia and fever 

b. Tenderness in the right upper quadrant or epigastrium 

c. Murphy's sign: t pain and transient arrest of inspiration when direct pressure is applied to the right upper 

quadrant while the patient is taking a deep breath 

217



1. Laboratory abnormalities 

a. Mild leukocytosis with a left shift 

b. Bilirubin and alkaline phosphatase (may be normal) 

(1) Mildly increased__,, cholecystitis alone 

(2) Greatly increased__,, common duct stone 

c. Significantly increased serum amylase or lipase__,, pancreatitis due to a common duct stone 

2. Radiographic abnormalities 

a. Plain films of the abdomen are usually negative or demonstrate nonspecific findings. Positive findings, 

when present, include: 

(1) Radiopaque gal I stones (1 0%-1 5%) 

(2) Sentinel loop in the right upper quadrant 

(3) Air or an air-fluid level in the gallbladder__,, emphysematous cholecystitis 

(4) Air in the biliary tree__,, biliary enteric fistula 

b. U ltrasonography 

(1) Most useful initial test for imaging the gallbladder in the emergency setting 

(2) It is rapid, noninvasive, and can identify the following: 

(a) Thickness of the gallbladder wall (2:5 mm is diagnostic of cholecystitis) 

(b) Gallstones 

(c) Common duct stones 

(d) Dilated common duct 

(e) 

(f) 

Pericholecystic fluid 

Other sources of right upper quadrant pain (pathology of the liver, pancreas, and kidneys) 

c. Nuclear scintigraphy (HIDA scan) 

(1) Most accurate test for establishing diagnosis of cholecystitis 

(2) Indicated if no stones are seen on ultrasound or there was equivocal thickness of the gallbladder wall 

(3) If the isotope does not pass into the gallbladder within 1 hour of ingestion, the cystic duct is presumed 

to be obstructed. 

d. CT scanning rarely offers any advantage over ultrasound, except that it may visualize common duct 

stones better. 

G. Management 

1. Patients with acute cholecystitis (fever, leukocytosis, significant abdominal tenderness, and vomiting) and/or its 

comp I ications (pancreatitis, ascending cholangitis, jaundice) should be admitted. 

2. Initial therapy should consist of: 

a. IV fluids 

b. Antiemetics and nasogastric tube suction (if persistent vomiting is present) 

c. Surgical consult 

d. Pain relief 

e. Broad-spectrum IV antibiotics 

(1) Current recommendation is monotherapy with piperacillin/tazobactam, ampicillin/sulbactam, or 

meropenem. lmipenem/cilastin may be used in life-threatening cases. 

(2) Triple antibiotic therapy (ampicillin, an aminoglycoside, and clindamycin or metronidazole) is 

indicated in the presence of sepsis. 

3. Definitive therapy is cholecystectomy at the earliest convenient time (usually within 72 hours). 

IX. HEPATITIS 

A. Viral hepatitis 

1. Sequence of events: hepatic enzymes begin to increase before the prodromal phase __,, prodromal symptoms 

(usually constitutional) for 1-2 weeks__,, icteric phase (when present) may be preceded by pruritus and 

dark urine followed by jaundice and possibly right upper quadrant pain with hepatomegaly or splenomegaly 

__,, recovery phase (symptoms resolve and hepatic enzymes normalize). In most cases, there is complete 

recovery in 3-4 months. (Note that most patients do not develop jaundice.) 

218


2. Hepatitis A 

a. Caused by hepatitis A virus (HAV), an RNA virus spread by the fecal-oral route directly via personto-person 

contact or indirectly through ingestion of contaminated water or food (particularly raw or 

undercooked shellfish) 

b. Illness is generally mild with a 15-50 day incubation period. 

c. Fecal shedding of the virus is maximal late in the incubation period and early in the prodromal phase. 

d. There is no carrier state, and it does not cause chronic liver disease. 

e. Serologic marker is anti-HAV. 

(1) Anti-HAV lgM indicates acute infection. Levels rise at same time as first increase in ALT. 

(2) Anti-HAV lgG indicates past infection or vaccination rather than acute infection. 

3. Hepatitis B 

a. Caused by hepatitis B virus (HBV), a DNA virus spread primarily by the percutaneous route but may also 

be transmitted by intimate contact via blood, semen, or saliva 

b. Illness is usually more severe and protracted than that produced by hepatitis A and has an incubation 

period of 45-160 days (mean 120 days); fulminant hepatic failure develops in 1 % of cases (rapidly rising 

bilirubin levels, coagulopathy, and encephalopathy), and 80% of comatose patients die. 

c. Chronic hepatitis or a chronic carrier state develops in 90% of infected neonates and in 10% of infected 

adults. These chronic carriers are all at increased risk of developing hepatocellular cancer; those with 

circulating virus continue to be a source of possible transmission. 

d. Serologic markers in hepatitis B infection 

(1) Hepatitis B surface antigen (HB,Ag) represents the outer protein coat of the virus. In most cases 

(>90%), it is detectable in the serum before hepatic enzymes increase and clinical symptoms appear; 

it lasts -6 months. Its presence implies active hepatitis or the carrier state but not necessarily 

infectivity. 

(2) Antibody to HB,Ag (anti-HB,) appears in the serum 2-6 months after HB,Ag disappears; it is a sign 

of previous infection or vaccination and indicates immunity. Chronic carriers usually have persistent 

HB,Ag in their serum and, therefore, do not develop anti-HB,. 

(3) Hepatitis B core antigen (HBcAg) (the core of the virus) is present only in hepatocytes, not in serum. 

Its presence, in conjunction with a negative anti-HB, is suggestive of early infection. 

(4) Antibody to HBcAg (anti-HBc) is present in the serum -2 weeks after HB,Ag appears. It may be the 

only marker of recent infection during the "window period" between the disappearance of HB,Ag 

and the appearance of anti-HB,. The presence of lgM anti-HBc in high titer indicates acute infection 

and high infectivity, whereas the presence of lgG anti-HBc, in association with anti-HB,, implies 

remote infection. 

(5) Hepatitis B epsilon antigen (HBeAg) is found in serum containing Hb,Ag. Its presence indicates 

ongoing viral replication and high infectivity. The antigen disappears in those patients who recover 

from hepatitis B but persists in those who develop chronic hepatitis. 

(6) Antibody to HBeAg (anti-HBe) appears during the acute phase of hepatitis Band implies that the 

patient is not likely to be infective. Anti-HBe persists several months after HBeAg disappears. 

(7) Sound confusing? Well, it is, especially because the presence of active infection does not necessarily 

correlate with infectivity, or how likely the patient is to transmit the disease. 

Table 8: One Method of Evaluating Serologic Results 

No infectivity 

+ anti-HB, 

Low infectivity 

+ anti-HB 0 

lnfectivity 

+ HBSAg 

High infectivity 

+ HBeAg 

(8) Only two serologic markers (HB,Ag and lgM anti-HBJ are actually needed to establish the diagnosis 

of infection with hepatitis B and determine its chronicity; HB,Ag confirms that infection is present, 

while IgM anti-HBc implies that it is acute. 

e. The CDC believes that successful hepatitis B vaccination (ie, that which is documented by anti-hepatitis B 

surface antibodies ?::10 IU at any time during a patient's life) confers lifetime protection. Therefore, do not 

test the source of (or recipient of) a blood exposure (eg, needle stick) if the patient has been successfully 

immunized. Otherwise, perform routine testing (including antihepatitis B surface antibodies). 

219


4. Hepatitis C 

a. Caused by hepatitis C virus (HCV) and transmitted percutaneously, with infrequent sexual transmission 

(less than HBV) 

b. Most common cause of viral hepatitis in the United States 

(1) Prior to 1992, most cases occurred in association with the transfusion of blood/blood products; thus, 

hepatitis C was referred to as "post-transfusion hepatitis." Since the introduction of a marker in 1992 

to screen blood for hepatitis C (anti-HCV), the number of transfusion-related cases of hepatitis Chas 

been declining. 

(2) Currently, IV and intranasal drug (using shared straws) abuse accounts for a growing number of new 

infections with hepatitis C. 

c. Incubation period is 15-160 days (mean = 50 days); the illness is similar to (but milder than) that caused 

by hepatitis B. 

d. Chronic hepatitis develops in 70% of these patients, 20% of whom go on to develop cirrhosis. The 

delayed development of hepatocellular cancer in these cirrhotic patients is not uncommon. 

e. Anti-HCV is the serologic marker for hepatitis C; it is detectable in the serum 1-6 months after the onset 

of symptoms; anti-HCV test is 97% specific but does not distinguish acute from chronic infection. 

f. Health care workers who sustain needle-stick injury from HCV-positive patients should be tested 

immediately and retested every 2 months for 6 months. 

g. Postexposure prophylaxis is not available. 

h. Curative therapy is now available. 

5. Hepatitis E 

a. Caused by hepatitis E virus, an RNA virus; incubation period is 15-60 days. 

b. Resembles hepatitis A in its mode of transmission and the clinical course but is associated with a higher 

incidence of fulminant liver failure and mortality, particularly in pregnant patients. 

c. Chronic infection does not occur. 

d. A serologic marker has not yet been identified. 

6. Hepatitis delta virus (HDV) 

a. A "defective" RNA-containing virus that can only occur in patients who are currently infected with HBV. 

Infection may occur concomitantly with an acute HBV infection (co-infection) or as a superinfection in 

patients with chronic hepatitis B. 

b. Patients with acute co-infection have a better prognosis than those with superinfection; the illness is 

generally self-limited. 

c. Superinfection is associated with a high mortality rate (relative to acute HBV infection) and frequent 

development of chronic HDV hepatitis with subsequent cirrhosis. 

d. The serologic marker is anti-HDV. 


a. Serum aminotransferases are increased; AST is 10-100 times normal and ALT is usually higher than AST. 

b. Bilirubin (total and direct) is increased. 

c. Prothrombin time is usually normal; prolongation points to a more complicated course and a poorer 

prognosis. 

8. Prevention and prophylaxis 

a. Immune globulin, formerly known as gamma globulin or serum immune globulin, is 80%-90% effective 

in preventing infection with HAV if administered within 14 days of exposure. 

b. Postexposure prophylaxis with immunoglobulin is required for close personal contacts (home, daycare, 

etc). Exposed school, hospital, workplace contacts do not require prophylaxis. 

c. Hepatitis A vaccine should be recommended for those traveling to endemic areas. The CDC recommends 

the vaccine be administered at least 2 weeks before travel to endemic areas. Immunity develops by 20 

days after administration. Travelers who cannot receive the vaccine should receive immune globulin 

before travel for passive immunity that will last 3 months. 

d. Hepatitis B immune globulin (HBIG) and hepatitis B vaccine have both been demonstrated to prevent 

hepatitis B; HBIG confers passive immunity, while the vaccine confers active immunity. For maximal 

effectiveness, HBIG must be administered within 7 days of exposure; the sooner the better. High-risk 

exposure (percutaneous/mucosal from a known HB,AG+ individual) in patients who have completed the 

HBV vaccine series who are known to be HB,AB+ do not require HBIG. If unknown response, can test for 

presence of surface antibody. If negative, should receive HBIG. Nonresponders to the vaccine should be 

treated as unimmunized and receive HBIG. 

220


e. No vaccine is available for hepatitis C. Postexposure prophylaxis with immune globulin is not 

recommended, and results with interferon are inconclusive. 

(1) For potential exposures, the CDC recommends determining the serologic status of the source case; 

however, the average incidence of anti-HCV seroconversion after unintentional needle stick or other 

sharp exposure from an HCV-positive source is only 1.8% (range 0-7%) 

(2) The exposed worker should have baseline hepatitis C antibody tests and liver function tests (including 

AST and ALT), which should be repeated in 6 months. 

f. There is no specific vaccine for hepatitis delta. The best preventive measure is vaccination for hepatitis B, 

because infection with hepatitis delta cannot occur in the absence of infection with hepatitis B. 

g. A hepatitis E vaccine has been very promising in trials but is not yet commercially available. 

9. Indications for admission 

a. Refractory vomiting 

b. Fluid or electrolyte imbalance 

c. Prolonged prothrombin time (>3-5 seconds compared with control) 

d. Bilirubin >20-30 mg/dl 

e. Hypoglycemia 

f. lmmunosuppression 

g. Severe underlying disease 

h. Early signs of encephalopathy (eg, agitation, altered mental status) 

i. Age >45-50 years old 

B. Toxic hepatitis 

1. Hepatotoxins that can produce morphologic changes in the liver and resemble those of acute viral hepatitis 

a. Halothane 

(1) Produces toxicity via a toxic metabolite and a hypersensitivity reaction 

(2) Most cases (75%) occur in patients who have been exposed to halothane in the past. 

(3) More common in adults (particularly women) and obese individuals. 

(4) Postoperative fever, rash, and eosinophilia may be present. 

(5) Onset is abrupt; usually occurs a couple of days after exposure. 

(6) Mortality rate is 20%-40% in severe icteric cases. 

b. Methyldopa 

(1) Produces injury via a toxic metabolite and a hypersensitivity reaction. 

(2) Mild transient increase of transaminase levels is seen in ~5% of patients treated with this drug, and 


3. Hepatotoxins that can produce massive hepatic necrosis 

a. Acetaminophen (APAP) 

I 

t 

APAP 

A PAP-sulfate 

(not hepatotoxic) 

~ 

t 

NAPQI 

(hepatotoxic metabolite) 

Cytochrome oxidase 

system 

I 

t 

APAP-glucoronide 


Glutathione 

t 

APAP-mercapturate and cysteine 


Mechanism of Toxicity of Acetaminophen 

i dose of APAP - saturation of the sulfate and glucuronide pathways and depletion of glutathione ➔ buildup of toxic 

metabolite (NAPQI) 

b. Carbon tetrachloride 

c. Yellow phosphorus 

d. Mushrooms (eg, Amanita phalloides) 

X. ALCOHOLIC LIVER DISEASE 

A. Syndromes 

1. Hepatic steatosis (fatty liver) 

a. Consumption of even moderate amounts of alcohol can lead to deposition of fat within hepatocytes. 

b. Clinical presentation: nontender hepatomegaly associated with mild increase in serum transaminase 

c. Resolves in 4-6 weeks with abstinence from alcohol 

2. Alcoholic hepatitis 


(1) Ranges from a mild illness to acute liver failure, depending on the degree of hepatocellular necrosis 

and intrahepatic inflammation 

(2) Presence of encephalopathy is the strongest predictor of short-term mortality. Other scoring systems 

are based on presence of jaundice and coagulopathy. Maddrey discriminant function score 2:32 is 

prognostic of severe disease, and these patients may benefit from glucocorticoid therapy. 

(3) Patients classically present with generalized weakness, anorexia, nausea, abdominal discomfort, and 

weight loss. 

(4) Urine may be dark in color. 

(5) Examination usually reveals a low-grade temperature, jaundice, and a tender, enlarged liver. 


(1) CBC shows macrocytic anemia, leukocytosis, and thrombocytopenia. 

(2) Bilirubin and alkaline phosphatase levels are increased. 

(3) AST and ALT levels are 2-10 times normal, with the AST level higher than the ALT level. 

(4) INR > 1.5 portends a complicated course. 

3. Alcoholic (Laennec) cirrhosis 

a. An irreversible disease that produces permanent histologic changes in the liver (hepatocytic nodules 

and fibrous tissue) that disrupt normal hepatic blood flow and result in portosystemic shunting with 

concomitant portal hypertension 

222



(1) Patients typically present with chronic fatigue and anorexia; however, some remain relatively 

asymptomatic until they develop a complication (eg, hepatic encephalopathy, GI bleed). 

(2) Classic clinical findings include jaundice, spider angiomata, palmar erythema, gynecomastia, muscle 

wasting, Dupuytren contracture, ascites, and pedal edema. 


(1) CBC: anemia, leukopenia, thrombocytopenia 

(2) AST and ALT levels minimally increased 

(3) Prolonged prothrombin time (useful predictor of severity of liver disease), INR > 1.5 

(4) Increased bilirubin (useful predictor of severity of liver disease) and alkaline phosphatase levels 

(5) Hypoalbuminemia 

(6) Hyponatremia 

(7) Hypokalemia 

B. Complications 

1. Bleeding esophageal varices 

a. 25%-40% of patients with cirrhosis bleed from varices, and each episode of hemorrhage carries a 30% 

mortality risk. 

b. Clinical presentation: hemorrhagic shock with massive hematemesis 

c. Diagnostic evaluation: emergency endoscopy should be performed as soon as possible to confirm the 

diagnosis, exclude other sources of bleeding, and provide therapy. (See also Esophageal Disorders, pages 

178-183.) 

2. Portosystemic encephalopathy 

a. Due to accumulation of toxic substances in the blood 

b. Develops in patients with cirrhosis with extensive portosystemic shunting when the diseased liver is no 

longer able to perform its metabolic function of detoxifying wastes adequately 

c. Precipitating factors 

(1) Azotemia (GI bleeding, high-protein diet) 

(2) Injudicious use of medications (sedatives, analgesics, and tranquilizers) 

(3) Hypokalemic metabolic alkalosis 

(4) Infection 

(5) Hypoxemia 

(6) Hypoglycemia 

(7) Dehydration 


(1) Altered level of consciousness, fetor hepaticus, and asterixis ("liver flap"-best demonstrated with the 

dorsiflexed wrist), along with other signs and symptoms of chronic liver disease 

(2) Serum ammonia level is usually increased, although levels correlate poorly with mental status. 

e. Management 

(1) General supportive measures 

(2) Correction/elimination of precipitating factors 

(3) Administration of lactulose and/or neomycin (to eliminate ammonia) 

(4) Protein-restricted diet 

3. Hepatorenal syndrome 

a. Syndrome of acquired renal failure of unknown cause that occurs in decompensated cirrhotic patients 

b. Pathogenesis: vasoconstriction and shunting of blood away from renal cortex---,. ! glomerular filtration 

rate ---,. ! renal output_,. azotemia 

c. Prognosis is dismal, with a mortality rate of nearly 100%. 

4. Spontaneous bacterial peritonitis 

a. Occurs in up to 33% of patients with liver disease and ascites 


(1) Patients with liver disease who present with fever, abdominal tenderness, worsening ascites, and 

decreasing hepatic function. 

(2) Many have no symptoms; consider paracentesis for any patient with ascites ill enough to require 

hospital admission. 

223



(1) Evaluation of ascitic fluid (obtained via paracentesis) confirms the diagnosis. 

(2) A granulocyte count >500/mm 3 is very suggestive, with an absolute PMN count >250 cells/mm 3 

diagnostic. 

(3) A positive culture is diagnostic. 

d. E coli and Streptococcus spp are the most common bacterial isolates. 

e. Treatment is with IV antibiotics (eg, a third-generation cephalosporin). 

f. Mortality rate ranges from 30% to 100%. 

XI. PANCREATITIS 

A. Etiology 

1. Acute pancreatitis is most often due to ethanol ingestion or biliary tract disease (gallstones). Other 

causes include abdominal trauma, surgery, endoscopic retrograde cholangiopancreatography, drugs 

(thiazides, furosemide, azathioprine, tetracycline, sulfonamides), penetrating peptic ulcer, hyperlipidemia, 

hypercalcemia, infections (mumps, viral hepatitis, infectious mononucleosis, Mycoplasma), and pregnancy. 

2. Chronic pancreatitis is the result of repeated episodes of acute pancreatitis and is usually due to chronic 

alcoholism of long duration (75 % of cases in United States). Other causes include severe protein-calorie 

malnutrition, hyperthyroidism, and pancreas divisum. 


1. Patients classically present after ingestion of a fatty meal or after binge drinking and complain of epigastric 

pain, nausea, and vomiting. 

2. The epigastric pain is constant in nature with radiation directly into the back, and it is often eased when the 

patient leans forward. 

3. Examination may reveal epigastric tenderness with guarding, tachycardia (due to fever, hypovolemia, and 

pain), tachypnea (due to pulmonary involvement), a low-grade fever, and hypoactive bowel sounds. However, 

because of the retroperitoneal location of the pancreas, rebound is generally absent. 

4. Grey Turner sign (bluish discoloration of the flanks) and Cullen sign (bluish discoloration around the 

umbilicus) indicate the presence of retroperitoneal hemorrhage and point to the diagnosis of hemorrhagic 

pancreatitis; unfortunately, these signs are not usually present. They are also not specific for pancreatitis. 


1. Serum amylase and lipase levels are typically increased in acute pancreatitis; however, the degree of increase 

does not correlate with the severity of disease. 

2. Very high levels are usually seen when biliary tract disease (gallstones) is the underlying cause. 

3. However, pancreatic enzymes are not usually increased in patients with chronic pancreatitis, because their 

pancreas is "burned out." 

4. Serum amylase 

a. Increases shortly after the onset of symptoms and returns to baseline levels within 1-4 days 

b. An increase 1.5 times the upper limit of normal typically indicates acute pancreatitis. 

5. Serum lipase 

a. Found primarily in the pancreas (unlike serum amylase, which is released by several organs) 

b. As sensitive as serum amylase but has the advantage of being more specific; specificity is almost 100%. 

c. Assays are readily available, reliable, and inexpensive. 

6. Other laboratory studies 

a. Glucose to exclude hyperglycemia 

b. Calcium to exclude hypocalcemia (most common laboratory abnormality) 

c. WBC count: leukocytosis is common 

d. Hematocrit O hematocrit is suggestive of hemorrhagic pancreatitis) 

e. BUN and creatinine usually increased due to hypovolemia. 

f. AST and lactate dehydrogenase: significant increase suggests severe disease. 

224


7. Plain radiographs are most helpful in excluding other diagnoses. Radiographic findings associated with 

pancreatitis include: 

a. Abdominal films 

(1) Scattered calcifications in the area of the pancreas are suggestive of chronic pancreatitis. 

(2) Evidence of ileus and air-trapping in the small bowel adjacent to the pancreas - sentinel loop 

(suggests acute pancreatitis) 

(3) Distended colon and collapse of the distal colon -,, colon-cutoff sign 


(1) Left pleural effusion or elevated left hemidiaphragm 

(2) Findings consistent with ARDS may be seen in patients with severe disease. 

c. Ultrasound 

(1) Should be performed early if gallstone pancreatitis suspected 

(2) May miss common duct stones or dilatation of duct 

(3) Endoscopic ultrasound may be required. 

d. CT scan: used to identify other causes of abdominal pain, establish severity of disease, and exclude 

complications such as pancreatic necrosis, hemorrhage, vascular abnormalities, and pseudocyst or 

abscess 

e. MRI cholangiopancreatography: noninvasive and may help establish cause 

D. Management: primarily supportive 

1. Hydration 

a. Fluid resuscitation with normal saline as required. Most patients are dehydrated because of vomiting and 

fluid sequestration. 

b. Close monitoring of vital signs, urine output 

c. Electrolyte replacement as necessary 

2. Pain control 

a. Morphine, hydromorphone are appropriate (despite potential to induce spasm of sphincter of Oddi, no 

adverse outcome in people has been demonstrated). 

b. Meperidine is the traditional choice but has no proven advantage. 

3. Control of vomiting 

a. IV antiemetics as required 

b. Nasogastric suctioning only for patients with intractable vomiting or ileus 

c. No evidence to support fasting in mild to moderate pancreatitis 

4. Nutritional support 

a. Enteral feeding if tolerated 

b. If enteral feeding not tolerated, consider parenteral feeding. 

5. Monitoring for complications of acute pancreatitis 

E. Poor prognostic signs (Ranson criteria) 

1. On admission 

a. Age >55 years old 

b. Leukocytosis (WBC count > 16,000/mm 3 ) 

c. Hyperglycemia >200 mg/dL 

d. AST > 250 U/L 

e. Lactate dehydrogenase >350 IU/L 

2. 48 hours later 

a. Calcium 5 mg/dL 

e. Base deficit >4 mEq/L 

f. Sequestration >4 L of fluid 

3. Mortality correlates directly with the number of poor prognostic signs present; the greater the number, the 

greater the mortality. 

225



1. Pleural effusions (usually left-sided) 

2. ARDS is due to deactivation of surfactant (most common cause of death due to acute pancreatitis) 

3. Pancreatic phlegmon - pseudocyst 

4. Pancreatic abscess - sepsis 

5. Hemorrhage (intrapancreatic or intraperitoneal) - shock 

6. Pancreatic ascites 

7. Third spacing of fluids - hypovolemia - acute tubular necrosis 

8. Disseminated intravascular coagulation 

226

ABDOMINAL AND GASTROINTESTINAL DISORDERS: PRACTICE CLINICAL SCENARIOS 

ABDOMINAL AND GASTROINTESTINAL DISORDERS: PRACTICE 

CLINICAL SCENARIOS 


Scenario A 

Presentation: A patient presents complaining of vomiting blood (may or may not be actively vomiting 

at time of presentation) and has dried blood on the lips. Heart rate is 175 beats per minute, and blood 

pressure is 60/30 mmHg. 


Scenario B 

Presentation: A patient presents with a history of ingesting a foreign body and complains of a sensation of 

something stuck in the throat. Symptoms include vomiting, gagging, choking, and dysphagia. 


Scenario C 

Presentation: A patient has had a gradual onset of periumbilical discomfort that subsequently localized to 

the right lower quadrant. Other symptoms include anorexia, nausea, and vomiting. The pain started before 

the vomiting. 

Physical examination: Findings reveal right lower quadrant tenderness to palpation with positive McBurney 

and Rovsing signs. 


Scenario D 

Presentation: An elderly patient with new onset atrial fibrillation (controlled or uncontrolled) presents with 

sudden onset of abdominal pain. The patient is not anticoagulated. 

Physical examination: Abdominal examination findings are generally nonspecific despite significant pain. 


Scenario E 

Presentation: A patient with known colonic diverticuli presents complaining of lower quadrant abdominal 

pain (left sided). The pain is crampy, vague, and poorly localized. 

Physical examination: The physical examination is relatively benign. Pain localizes on palpation to the left 

lower quadrant or suprapubic region. 


227



Scenario A 

Diagnosis: upper GI bleeding 

Management: Initial efforts are directed at determining hemodynamic stability and need for immediate 

resuscitation. 

Unstable patients require two large-bore IV lines with fluid boluses of normal saline. Administer blood 

product transfusion as necessary. If patient is anticoagulated, may need immediate reversal as appropriate. 

Immediate endoscopy may be needed for control of esophageal or ulcer bleeding. Administer IV protonpump 

inhibitor. Regardless of history, ulcer bleeding is more common than variceal bleeding, but if 

variceal bleeding is suspected, administer octreotide. 

For stable patients, determine the source of bleeding. If actively vomiting, the source is obvious. If not 

vomiting, presence of melena, or nasogastric aspiration with presence of blood or "coffee grounds," is highly 

predictive of upper GI source. However, absence of blood via nasogastric tube does not exclude upper GI 

source. Bright red blood or blood clots per rectum are more predictive of lower GI source. Determine need 

for immediate intervention or admission. Blatchford score helps predict need for intervention. 

Scenario B 

Diagnosis: esophageal foreign body 

Key facts: Most cases (80%) of ingested esophageal foreign bodies are in children. They may not be 

old enough to give history. The cricopharyngeus muscle (C6) is the most common site of obstruction in 

children


Scenario D 

Diagnosis: mesenteric ischemia, embolic occlusion of the superior mesenteric artery from a thrombus in 

the atria 

Diagnostic evaluation: Laboratory investigation is frequently not helpful early on. Serum lactate is 

usually increased but not until bowel infarction has occurred. Acidosis may be present late. Helical CT 

angiography of the abdomen is currently the test of choice, although some centers may still perform 

conventional angiography. 

Alternative presentation: Another typical presentation is an elderly patient with a history of coronary artery 

disease who presents with diffuse abdominal pain. The patient may report having had abdominal pain after 

eating on prior occasions. This is "intestinal ischemia" due to vascular disease. Examination early on shows 

few specific findings. Pain is out of proportion to findings. Feces may be positive for guaiac; there may be 

gross blood per rectum. 

Management: Fluid resuscitation as required. If pressors are needed, use positive inotropes rather than 

vasoconstrictors. If nonocclusive disease, may use interventional radiology or papaverine injection; if 

occlusive disease, revascularization is required. 

Scenario E 

Diagnosis: diverticular disease 

Key facts: Signs of systemic toxicity are absent unless diverticuli have perforated or abscess formation has 

begun. Peritoneal signs are unlikely unless the patient has complicated diverticular disease, which involves 

microperforation of the bowel wall with formation of phlegmon in the immediate area. Minority of these 

will have frank free air in abdomen. 

Alternative presentation: Another less likely presentation consists of massive lower GI hemorrhage that is 

painless. This is responsible for up to 40% of lower GI hemorrhage in elderly patients. 

Diagnostic evaluation: CBC, hematocrit, and blood type and screen should be done in patients with 

diverticular hemorrhage. WBC count is likely to be increased, particularly in complicated disease. 

If complicated diverticulitis is suspected, CT of the abdomen and pelvis should be done. (Neither 

colonoscopy nor barium enema are done in the acute setting.) Patients in whom diverticular disease 

is suspected but have no known history may also benefit from CT to establish the diagnosis as well as 

exclude other pathology. Patients with history of diverticulosis and mild symptoms may not require 

imaging in the emergency department. 

Management: Patients with uncomplicated diverticulitis can be treated on an outpatient basis with pain 

control and antibiotic therapy. Acceptable regimens include ciprofloxacin + metronidazole, TMP-SMX + 

metronidazole, or amoxicillin/clavulanate for 10 days. 

Patients with complicated diverticulitis need resuscitation as necessary, IV antibiotic therapy similar to 

the above or ticarcillin/clavulanate or ampicil lin/sulbactam. Percutaneous drainage of the abscess may be 

required. A surgical consult should be obtained for all with free air. 

229

230 

NOTES

THORACIC AND RESPIRATORY DISORDERS 


Pneumonia ................................................................................................................................................................ 236 

Bacterial Pneumonia .......................................................................................................................................... 236 

Atypical Pneumonia ........................................................................................................................................... 246 

Viral Pneumonia ................................................................................................................................................. 249 

Types of Pneumonia: Classic Clinical Scenario and Etiology ............................................................................... 251 

Tuberculosis .............................................................................................................................................................. 252 

Pleural Effusion ......................................................................................................................................................... 256 

Aspiration Pneumonia ............................................................................................................................................... 259 

Lung Abscess ............................................................................................................................................................. 261 

Empyema .................................................................................................................................................................. 263 

Hemoptysis ............................................................................................................................................................... 264 

Pneumothorax ........................................................................................................................................................... 266 

Asthma ...................................................................................................................................................................... 269 

Chronic Obstructive Pulmonary Disease (COPD) ..................................................................................................... 276 

Acute Respiratory Distress Syndrome (ARDS) ........................................................................................................... 280 

Pulmonary Embolism ................................................................................................................................................ 282 

Cyanosis .................................................................................................................................................................... 290 

231

THORACIC AND RESPIRATORY DISORDERS: SELF-ASSESSMENT QUESTIONS 

THORACIC AND RESPIRATORY DISORDERS: 


1. The most common cause of community-acquired bacterial pneumonia is: 

(a) Group A ~-hemolytic streptococci 

(b) Haemophilus influenzae 

(c) Streptococcus pneumoniae 

(d) Klebsiella pneumoniae 

2. A sputum Gram stain revealing encapsulated gram-positive lancet-shaped diplococci is most consistent with: 



(c) Mycoplasma pneumoniae 

(d) Streptococcus pneumoniae 

3. Although abscess formation is not common, it can be seen in association with each of the following causes of 

pneumonia except: 

(a) 

Klebsiella pneumoniae 

(b) Chlamydia pneumoniae 

(c) Pseudomonas aeruginosa 


4. A 55-year-old male smoker presents in August with signs of an atypical pneumonia, relative bradycardia, and 

diarrhea. He is on no medications. Laboratory results reveal increased liver enzymes. The most probable cause of 

the pneumonia is: 

(a) Mycoplasma pneumoniae 

(b) Francisella tularensis 

(c) 

Legionella pneumophila 

(d) Coxiella burnetii 

5. Al I of the fol lowing statements regarding Klebsiella pneumonia are true except: 

(a) Sputum Gram stain reveals encapsulated gram-positive organisms that are seen in pairs. 

(b) The sputum is thick and brown in color, resembling currant jelly. 

(c) 

Patients with alcoholism, diabetes, or COPD are most commonly affected. 

(d) Chest radiograph commonly reveals a necrotizing right upper lobe infiltrate. 

6. Which of the following statements regarding the TB skin test is most accurate? 

(a) 

It is positive in 100% of patients with TB meningitis. 

(b) A positive reaction indicates the presence of infection with Mycobacterium tuberculosis but not necessarily the 

presence of active disease. 

(c) It is always positive in patients infected with M tuberculosis. 

(d) Criteria for interpreting the test as positive are the same for all patients regardless of background/concurrent 

illnesses. 

7. lsoniazid therapy for TB is associated with the multiple complications listed below. Which one of these 

complications can be prevented or minimized by the simultaneous administration of pyridoxine? 

(a) 

Phenytoin toxicity 

(b) Hepatitis 

(c) 

Hypersensitivity reaction 

(d) Peripheral neuritis 

8. On which of the following views of the chest is a small pleural effusion most likely to be detected? 

(a) Supine 

(b) PA 

(c) Lateral decubitus 

(d) Lateral 

232


9. All of the following are appropriate in the acute treatment of aspiration pneumonia except: 

(a) Administration of steroids and prophylactic antibiotics 

(b) Administration of supplemental oxygen 

(c) Bronchoscopy to remove large particles 

(d) Use of continuous positive-airway pressure (CPAP) 

10. A patient has pleural effusion on chest radiograph. A diagnostic thoracentesis is performed. Which of the following 

is an indication for a thoracostomy tube placement? 

(a) No organisms on Gram stain 

(b) LOH two times the upper limit of serum LOH 

(c) Glucose >60 mg/dL 

(d) pH 12 mmHg 

16. All of the following statements regarding the use of ~-adrenergic agonists in the treatment of asthma are accurate 

except: 

(a) Their primary effect is on the large central airways. 

(b) They promote bronchodilation by increasing cyclic AMP. 

(c) Their onset of action is


1 8. Al I of the following statements regarding noncardiogenic pu Imo nary edema are true except: 

(a) The heart size is smal I or normal. 

(b) Pulmonary arterial wedge pressure is increased. 

(c) Chest radiograph shows bilateral pulmonary infiltrates. 

(d) Lung compliance is reduced. 

19. Pneumonia is most commonly acquired via ___ _ 

(a) Hematogenous spread from another site 

(b) Direct introduction of organisms into the pleura or lungs 

(c) Aspiration of oropharyngeal secretions 


20. All of the following statements regarding pneumococcal pneumonia are accurate except: 

(a) Patients usually give a history of a single shaking chill followed by the development of a cough productive of 

rust-colored sputum. 

(b) The WBC count is usually


27. A patient received a liver transplant 1 month ago and presents to the emergency department with complaints of 

fever, chills, cough, and shortness of breath. What pathogen is most likely causing his illness? 

(a) Pseudomonas 

(b) Staphylococcus aureus 

(c) Cytomegalovirus 

(d) Haemophi/us influenzae 

ANSWERS 

1. C 

2. d 

3. b 

7. 

8. 

9. 

4. c 10. d 

5. a 11. d 

d 

C 

a 

13. b 19. C 

14. C 20. b 

15. a 21. b 

16. a 22. a 

17. b 23. d 

6. b 12. b 18. b 24. a 

25. C 

26. C 

27. C 



235


I. PNEUMONIA 

A. Bacterial pneumonia (most common cause of a focal infiltrate) 


a. Accounts for up to 10% of hospital admissions in the United States 

(1) Typical versus atypical 

(a) Typical: fever, shaking chills, cough with yellow/green sputum, chest radiograph with lobar 

infiltrate; Gram stain will reveal organism. 

(b) Atypical: little cough or nonproductive cough, chest radiograph with interstitial pattern; organisms 

do not show up on Gram stain. 

b. Most pneumonias are the result of a single species of bacteria. 

(1) Streptococcus pneumoniae 

(2) Haemophilus influenzae 

(3) Klebsiella pneumoniae 


(5) Escherichia coli 

(6) Pseudomonas aeruginosa 

(7) Group A streptococci 

(8) Moraxella catarrhalis 

c. Mechanisms of infection 

(1) Aspiration of oropharyngeal secretions is the primary mechanism of acquisition. 

(a) 

50%-70% of normal healthy individuals aspirate in their sleep. 

(b) An abnormal swallowing mechanism (eg, from an altered mental status) or GI disease can lead to 

increased frequency of aspiration. 

(2) Other mechanisms 

(a) 

Hematogenous spread from another site 

(b) Colonization 

(c) 

d. Predisposing factors 

Direct introduction of organisms into the pleura or lungs, both of which are uncommon 

(1) Impaired cough and gag reflex 

(a) Altered mental status 

(b) Seizures 

(c) Syncope 

(d) Stroke 

(2) Impaired mucociliary transport 

(a) Smoking 

(b) Viral or mycoplasmal infection 

(c) COPD 

(3) Chronic underlying disease 

(a) Hepatic or renal failure 

(b) Diabetes mellitus 

(c) CHF 

(4) Impaired immunity 

(a) AIDS 

(b) Chemotherapy 

(c) Alcoholism 

(d) Cystic fibrosis 

(e) Malnutrition 

(f) 

(g) 

Sickle cell disease, splenectomy 

Congenital immune deficiencies 

(h) lmmunocompromised patients (elderly, transplant patients) 

236


(5) Underlying lung pathology 

(a) Bronchial obstruction (foreign body, tumor or cancer); if recurrent pneumonias, consider foreign 

body as etiology, especially in pediatric patients. 

(b) Pulmonary embolus, contusion 

(c) Atelectasis 

(d) COPD (bronchitis, emphysema) 

(6) Chest wall dysfunction 

(a) Neuropathies or myopathies 

(b) Postoperative pain 

(c) Chest trauma with rib fractures 

(7) Mechanical bypass of normal defense mechanisms 

(a) 

Endotracheal tube 

(b) Nasogastric tube 

(c) Chest tube 

(d) Bronchoscopy 

(e) Tracheostomy 

(8) Altered upper respiratory tract flora 

(a) Recent antibiotic therapy 

(b) Hospitalization 

e. Defense mechanisms 

(1) Cough and gag reflex prevents gross aspiration. 

(2) Tracheobronchial cilia remove particles >5 µm. 

(3) Alveolar macrophages remove particles 15,000/mm 3 ) should prompt 

consideration of pneumonia as a diagnosis. 

(2) In an elderly, debilitated patient, or immunocompromised patient (transplant or cancer patient, or 

patient on chronic steroids), the WBC count may be increased, normal, or decreased (even if there is 

an associated sepsis); the only clue may be a left shift. 

(3) A very high or very low WBC count is associated with increased mortality. 

b. Gram stain: sputum gram stain is rarely helpful. Diagnostic samples must have 25 

WBCs/high power field. Knowing the gram stain findings for the examination may help with identifying the 

etiology. 

Table 9: Gram-Stain Findings with Common Organisms 

Organism 

Streptococcus pneumoniae 

Staphylococcus aureus 

Influenza 

Klebsie//a sp 

Legionella sp 

Oral flora (aspiration) 

Atypicals, viral 

Gram-Stain Findings 

Gram-positive, lancet-shaped cocci in pairs, 

PMNs 

Gram-positive cocci in clusters, PMNs 

Gram-negative coccobacillus, PMNs 

Gram-negative rods, PMNs 

Few weakly gram-negative rods, many PMNs 

Mixed gram-positive and -negative cocci and 

rods, PMNs 

Few bacteria, many PMNs, or monocytes 

237


c. Chest radiographs 

(1) Types of findings: lobar vs atypical 

(a) 

Lobar pneumonia: consolidation 

i. White area on radiograph 

ii. Air bronchograms 

iii. Loss of hemidiaphragm, but no volume loss; no pulling up/down of fissures, no collapse of lung 

(b) Atypical pneumonia: interstitial infiltrates on chest radiographs 

(2) Certain patterns suggest, but do not prove, a specific organism 

(a) Streptococcus pneumoniae (most common cause of lobar pneumonia) 

i. Single lobar infiltrate 

ii. Small pleural effusion 

iii. Abscess formation 


(c) 

i. Patchy (frequently basilar) infiltrates 

ii. Occasional pleural effusion 

Klebsiella pneumoniae 

i. Upper lobe infiltrates 

ii. Abscess formation 


i. Patchy, multicentric infiltrates 

ii. Abscess formation (most common cause of abscess) 

iii. Empyema 

iv. Pneumothorax 

(e) £ coli: patchy, bilateral lower lobe infiltrates 

(f) Pseudomonas aeruginosa 

i. Patchy, mid or lower lobe infiltrates 

ii. Abscess formation 

(g) Group A streptococci 

i. Patchy, multilobar infiltrates (usually lower) 

ii. Large pleural effusion 

(2) When infiltrates (patchy or lobar) are identified, always scan the radiographs for other associated 

findings. 

(a) 

Pneumothorax 

(b) Pleural effusion 

(c) Abscess formation 

(3) Although CT scan may show pneumonia earlier, the radiation exposure makes it less desirable than a 

plain chest radiograph. 

(4) Leukopenic or dehydrated patients may have normal-appearing radiographs. 

(5) Other diagnoses (pathology) to consider when pneumonitis is present on a chest radiograph 

(a) Pulmonary infarction 

(b) Pulmonary edema 

(c) Metastatic cancer 

(d) Pleural thickening 

(e) 

(f) 

Parenchymal scarring 

Atelectasis 

(6) Cavitary lesion on chest radiograph 

(a) MRSA 

(b) Tuberculosis 

(c) Pseudomonas 

(d) Fungal superinfection 

(e) Cancer 

238


(7) Abscess formation 

(a) 5 aureus 

(b) Klebsiella 

(c) Pseudomonas 

d. Pulse oximetry/arterial blood gases: in patients with pneumonia, the lungs may be adequately perfused but 

gas exchange at the alveolus is poor, resulting in hypoxia (and VQ mismatch). 

e. Sputum analysis 

(1) Expectorated sputum has a limited role in diagnosing the microbiologic organism involved because of 

contamination with oropharyngeal flora. Sputum Gram-stain results are helpful in making therapeutic 

decisions in only about one-third of patients. 

(2) Fiberoptic bronchoscopy is the standard invasive procedure of choice for seriously ill or 

immunocompromised patients. 

(3) Smears for acid-fast bacilli should be done in patients at risk of tuberculosis (immigrants, patients with 

AIDS, IV drug abusers, and others who are immunocompromised). 

f. Blood cultures 

(1) A CMS core competency requirement to be ordered on all ICU patients for pneumonia 

(2) Should be obtained before antibiotic administration 

(3) To be ordered only for patients who are seriously ill, as well as for those with presumed bacteremia, 

comorbid disease, immunosuppression, or rigors 

(4) "Routine" cultures on patients with pneumonia are discouraged because of a low yield of clinically 

useful data. 

g. Pleural fluid aspiration, although not generally an emergency department procedure, is helpful in excluding 

empyema and, in the case of a large pleural effusion, drainage can also reduce respiratory embarrassment. 

With smaller effusions, determining the glucose and pH of the fluid is helpful in determining treatment. 

(1) pH >7.2 or glucose >60 mgldL - antibiotics 

(2) pH


3. Treatment 

I 

Treatment of 

community-acquired pneumonia 

I 

I 

I 

Outpatient therapy (oral) 

I 

I I I 

I 

I 

Inpatient therapy (IV) 

I 

I 

Comorbidity or risk 

I 

Not in ICU 

No history of factors for higher-risk I 

comorbid illness 1 

organisms 

I 

Use one: RTF 3 

Azithromycin 

Clarithromycin 

Doxycycl i ne 2 

I 

Use one: 

Levofloxacin 

Sparfloxacin 

Gatifloxacin 

Moxifloxacin 

Gemifloxacin 

Suspected 

aspiration with 

infection 

I 

Amoxacillinclavulanate 

or 

an RTF 3 alone 

I 

Recent 

antibiotic 

treatment for 

infection 

I 

Macrolide 

(advanced) + 

a E,-lactam or 

an RTF 3 alone 

ICU 

I 

1 Ca rdiopulmonary disease, diabetes, uremia, 

ma lignancy 

2 Fo r patients who cannot take a macrolide 

3 

RT F = respiratory tract fluoroquinolone 

(an tipneumococcal) 

If p atient cannot take an RTF, refer to text 

for alternative therapy. 

No risk of 

Pseudomonas 

A G,-lactam (cefotaxime 

or ceftriaxone) + 

azithromycin 

or 

an RTF 3 if allergic to a 

G,-lactam ± clindamycin 

At risk of 

Pseudomonas 

An antipseudomonal 

G,-lactam (cefepime, 

imipenem, meropenem, 

or piperacillin/tazobactam) + 

ciprofloxacin 

or 

I 

An antipseudomonal agent+ 

aminoglycoside + RTF 3 

or macrolide 

Aztreonam + levofloxacin or 

aztreonam + moxifloxacin or 

gatifloxacin (± aminoglycoside) 

Treatment of Community-Acquired Pneumonia 

a. For inpatients with one of the following conditions requiring general medical admission: 

(1) Suspected aspiration with infection-.,. amoxicillinclavulanate or clindamycin 

(2) Recent antibiotic therapy for another condition -.,. azithromycin or clarithromycin plus a ~-lactam or a 

respiratory fluoroquinolone alone (the regimen selected depends on the nature of the recent antibiotic 

therapy) 

b. For ICU patients in whom: 

(1) Pseudomonas infection is not an issue-.,. a ~-lactam and an advanced macrolide (azithromycin, 

clarithromycin) or a respiratory fluoroquinolone 

(2) Pseudomonas infection is not an issue, but the patient has a ~-lactam allergy-.,. a respiratory 

fluoroquinolone (with or without clindamycin) 

240


(3) Pseudomonas infection is an issue----'> 

(a) An antipseudomonal agent (piperacillin, imipenem, meropenem, cefepime, or piperacillintazobactam) 

and ciprofloxacin or 

(b) An antipseudomonal agent and an aminoglycoside and a respiratory fluoroquinolone or a 

macrolide 

(4) Pseudomonas infection is an issue but the patient has a ~-lactam allergy - 

4. Types of pneumonia 

(a) Aztreonam and levofloxacin or 

(b) Aztreonam and moxifloxacin or gatifloxacin (with or without an aminoglycoside) 

a. Pneumococcal pneumonia 

(1) Etiology 

(a) Caused by 5 pneumoniae, a gram-positive lancet-shaped, encapsulated diplococcus 

(b) At least 83 serotypes have been isolated. 

(2) Most common cause of community-acquired bacterial pneumonia and the number one cause of 

bacterial pneumonia in HIV-infected patients 

(a) Seen in 1 in 500 persons annually 

(b) Peak incidence in winter/early spring 

(c) Mortality rate is 90% 

are sensitive to ceftriaxone. 

(e) Classic patient: extremes of age and chronically ill, immunocompromised (eg, HIV, splenectomy, 

transplant) 

(3) Classic clinical scenario: The patient appears acutely ill and can usually report exactly when the illness 

began (abrupt onset). The presence of fever, tachypnea, and tachycardia is coupled with sharp pleuritic 

chest pain associated with marked splinting on the affected side. There may be a history of a single, 

acute shaking chill, followed by a cough productive of a rust-colored sputum. Flank or back pain, 

anorexia, and vomiting are additional symptoms. On physical examination, the skin may be cyanotic 

or jaundiced, auscultation reveals crackles in the involved region (isolated to a specific lobe of the 

lung), and there are signs of pulmonary consolidation (bronchial breath sounds, egophony, increased 

tactile and vocal fremitus). A pleural friction rub may be heard. 


(a) WBC count 12,000-25,000/mm 3 but may be higher 

(b) Chest radiograph 

i. Single lobar infiltrate (patchy in infants and the elderly) 

ii. Occasionally bulging fissures 

iii. Pleural effusion (25%) 

(c) Sputum 


i. Rust-colored sputum 

ii. Gram stain reveals a single predominant gram-positive organism in pairs or chains. 

iii. Sputum culture is positive in 50%, and blood cultures are positive in 30% of cases. 

(a) Despite the prevalence of increasingly resistant strains (up to 40%), penicillin is still the drug of 

choice. 

(b) A macrolide or doxycycline is preferred for uncomplicated infections in outpatients. 

(c) Fluoroquinolones are no longer recommended for empiric outpatient therapy in otherwise healthy 

patients; they are reserved for outpatients with comorbidities (COPD, diabetes, renal failure, CHF, 

or malignancies) and for those who have recently received antibiotics for another infection. 

(d) For those patients requiring IV therapy, one of the following protocols is recommended: 

i. Cefotaxime or ceftriaxone and a macrolide (regimen preferred by the CDC) or 

ii. Monotherapy with an extended-spectrum fluoroquinolone 

(e) Vaccinations indicated for: 

i. Alcoholics 

ii. Cigarette smokers 

241


iii. COPD patients 

iv. CHF patients 

v. Diabetic patients 

vi. lmmunocompromised patients (eg, HIV, cancer, transplant) 

vii. Asplenic (functional or anatomical) 

viii. Patients >65 years old 


(a) Sepsis 

(b) Meningitis 

(c) Endocarditis/pericarditis 

(d) CHF 

(e) Empyema (


(b) When patients require IV therapy, a second- or third-generation cephalosporin (cefuroxime, 

ceftriaxone) should be used. 


(a) Sepsis 

(b) Meningitis 

(c) Empyema 

(d) Arthritis 

c. Klebsiella pneumonia 

(1) Etiology 

(a) 

Caused by K pneumoniae, a short, plump, encapsulated gram-negative bacillus that is seen in pairs 

(b) On a poor-quality Gram stain, Klebsiella is easily confused with pneumococcus. 

(2) Epidemiology: most common in patients with 

(a) Alcoholism 

(b) Diabetes 

(c) COPD 

(d) Renal failure 

(e) Nursing-home patients 

(f) 

Recent use of antibiotics 

(3) Classic clinical scenario: sudden onset of cough followed by multiple shaking chills and shortness of 

breath. The patient (usually a middle-aged or older man, history of alcoholism) complains of pleuritictype 

chest pain and is cyanotic. Sputum is currant jelly or dark brown colored. Signs of pulmonary 

consolidation are present on physical examination. 


(a) Leukocytosis (75% of cases) 


i. Necrotizing right upper lobe infiltrate or abscess formation with an air-fluid level 

ii. Perihilar and patchy infiltrates are occasionally seen. 

iii. Bulging minor fissure (35 %) 

(c) Gross sputum examination 


i. Dark brown, tenacious, and occasionally blood-stained 

ii. Resembles currant jelly 

(a) Attentive airway management because the sputum is frequently so thick that clearance is difficult 

(b) IV cephalosporin (ceftriaxone, cefuroxime, or cefotaxime) plus an aminoglycoside (gentamicin, 

tobramycin, or amikacin) are the initial agents of choice. Alternative agents include aztreonam 

and imipenem. 


(a) Empyema within 24-48 hours (20%) 

(b) Sepsis 

(c) Pneumothorax 

d. Other gram-negative pneumonias (occur rarely) 

(1) Etiology 

(a) f coli 

(b) Pseudomonas 

(c) Enterobacter 

(d) Serratia 

(2) Clinical presentation: usually immunosuppressed and debilitated patients 

(3) Treatment: piperacillin/tazobactam 

e. Staphylococcal pneumonia 

(1) Etiology: large gram-positive cocci in pairs and clusters 

(2) Epidemiology 

(a) 1 % of all bacterial pneumonias 

243


(b) Peak incidence is during measles and flu epidemics. 

(c) Classic patient: IV drug abusers, nursing-home patients, debilitated patients, patients recovering 

from influenza infection, very young patients 

(3) Classic clinical scenario: The patient presents with fever, multiple chills, and pleuritic chest pain. A 

previous course of flu was followed by the insidious onset of a cough productive of purulent sputum. 

Coarse rhonchi and rales are heard on chest auscultation; signs of consolidation are rare. 


(a) WBC count usually> l 5,000/mm 3 


i. A patchy infiltrate that is initially multicentric or peripheral (because it results from 

hematogenous spread) ultimately progresses to necrotizing pneumonia, including lobar 

consolidation and abscess formation. 

ii. Empyema is common. 

iii. A pleural effusion may also occur. 

(c) Blood cultures are usually negative unless the pulmonary involvement is metastatic. 


(a) IV oxacillin or nafcillin are the antibiotics of choice. 

(b) IV vancomycin is the alternative agent; it is usually reserved for patients who are allergic to (or 

resistant to) penicillin. 

f. Group A streptococcal pneumonia (rare) 

(1) Etiology: gram-positive cocci in pairs or chains 

(2) Classic clinical scenario: sudden onset of fever, chills, and productive cough. The sputum is usually 

bloody and purulent; chest examination reveals fine rales without signs of consolidation. 

(3) Diagnostic evaluation: chest radiograph shows multi lobular bronchial infiltrates with a large pleural 

effusion. 

(4) Management: Because of the high mortality associated with this rapidly progressive pneumonitis, 

patients generally require admission for IV antibiotics 

(a) 

Aqueous penicillin is the drug of choice. 

(b) A cephalosporin (ceftriaxone) or erythromycin is an alternative agent. 

5. Patient assessment and risk stratification: The Pneumonia Severity Index (ACEP Clinical Policy: Management and 

Risk Stratification of Community-Acquired Pneumonia in Adults in the Emergency Department) 

a. There are five severity classes based on mortality rate. 

(1) Classes I, II, and Ill:


(5) Laboratory studies and radiographs 

(a) Arterial pH


Table 12: SMART-COP 

Community-Acquired Pneumonia Confirmed on Chest Radiograph 

Points 

Systolic blood pressure 125 beats per minute 

!:. Confusion (new onset) 

Q 

Oxygen low - age-adjusted cut-offs 

Age -S50 years, PaO 2 


(b) Earache (33%) 

(c) Anorexia, nausea, vomiting, and diarrhea in the first week (12%-14%) 

(2) Most patients have segmental rales and rhonchi on physical examination. Other findings include: 

(a) Conjunctivitis 

(b) Pharyngitis 

(c) Bullous myringitis (3%-10%) 

c. Comp I ications 

(1) Aseptic meningitis or encephalitis 

(2) Hemolytic anemia 

(3) Glomerulonephritis 

(4) Gui I lain-Barre syndrome 

(5) Cardiac abnormalities, eg, pericarditis, myocarditis, AV block, CHF 

(6) Splenomegaly 

(7) Erythema multiforme 


(1) WBC count is usually normal or moderately increased. 

(2) Does not show up on Gram stain 

(3) Chest radiograph 

(a) One or more segmental infiltrates, dense consolidation, or a generalized interstitial pattern may 

be present. 

(b) Segmental (or patchy) infiltrates are usually in the lower lobes and appear as streaks radiating from 

the hilum. 

(c) Interstitial pneumonia characterized by a reticulonodular pattern is often associated with 

deterioration of pulmonary function and can progress to respiratory failure. 

(d) Small pleural effusions are present in 20% of patients. 

(e) The hallmark of this disease is the disparity between the patient's clinically benign appearance 

and the extensive radiographic findings. 

(4) Cold agglutinin titers are increased in up to 60% of these patients and are supportive of the diagnosis 

but are neither sensitive nor specific. 

(5) A 4-fold increase in complement-fixing antibody titers is diagnostic; an initial titer >1:64 is very 

suggestive. 

e. Treatment 

(1) Erythromycin, clarithromycin, and azithromycin are the drugs of choice. 

(2) Fluoroquinolones and doxycycline are alternative agents. 

3. Chlamydia! pneumonia (6% of community-acquired pneumonia) 

a. Etiology: Chlamydia pneumoniae, an obligate intracellular, gram-negative organism 


(1) Common cause of atypical pneumonia in young adults 

(2) Spread is from person to person by droplet transmission. 

(3) Outbreaks generally occur as a cluster of cases in enclosed populations (eg, boarding schools, dorms, 

army barracks, prisons). 

c. Classic clinical scenario: The patient is usually a young adult who complains of a prolonged dry cough and 

low-grade fever that was preceded by a sore throat. Other complaints may include laryngitis/hoarseness 

(present in one-third of patients), mild headache, myalgias, and diarrhea. Examination reveals rales or 

rhonchi (and sometimes wheezing) on auscultation of the lungs and a nonexudative pharyngitis. 


(1) WBC count is usually normal. 

(2) Chest radiograph typically reveals a subsegmental pneumonitis. 

(3) Nasopharyngeal culture or serology confirms the diagnosis. 

e. Treatment 

(1) Tetracycline, doxycycline, and erythromycin are the agents of choice; a 3-week course of therapy is 

recommended. 

(2) Azithromycin or clarithromycin (and quinolones) are also effective. 

247


4. Psittacosis 

a. Etiology: Chlamydia psittaci 

(1) An obligate intracellular, gram-negative organism harbored in avian species 

(2) Transmitted by inhalation of infected dust or droplets 

b. Epidemiology: owners of pet birds (particularly parrots), pet-shop employees, poultry workers, and 

veterinarians most commonly affected 


(1) Hyperpyrexia (up to 105°F [40.6°C]) 

(2) Severe headache (often the major complaint) 

(3) Cough (occasionally associated with hemoptysis) 

(4) Hepatosplenomegaly 

(5) A flu-like syndrome consisting of malaise, myalgias, and an upper respiratory infection 

(6) Relative bradycardia 


(1) Leukopenia (25%) 

(2) Proteinuria 

(3) Abnormal liver profile (high enzymes) 

(4) Patchy perihilar or lower lung field infiltrates on chest radiograph 

(5) Increased complement fixation antibody titer 

e. Treatment 

(a) A 4-fold rise (1 :32) is diagnostic. 

(b) A 1 :16 titer is presumptive evidence. 

(c) False-positives are seen in patients with brucellosis and Q fever. 

(1) Doxycycline is the drug of choice; a 2-week course is recommended. 

(2) Azithromycin and clarithromycin are alternative agents. 

f. Complications 

(1) Multiple and severe without antibiotic therapy 

(2) Include hepatitis, myocarditis, endocarditis, meningitis, renal failure, disseminated intravascular 

coagulation 

5. Q fever pneumonia 

a. Etiology 

(1) Coxiella burnetii, an obligate intracellular bacterium 

(2) Highly infectious; can survive in dried soil or excrement up to 18 months and in tap water or milk for 

up to 42 months 


(1) People usually become infected by inhaling dust contaminated with excreta, placenta, or uterine 

excretions of infected sheep, goats, cattle, or parturient cats. 

(2) Slaughterhouse workers, dairy farmers, and those who work closely with animals (especially farm 

livestock) are most commonly affected. 

c. Classic clinical scenario: The patient is a farmer who presents ill and is diaphoretic and febrile. The usual 

history is sudden onset of shaking chills, high fever, myalgias, severe headache, and a nonproductive 

cough. Physical examination shows hepatomegaly. Chest findings are frequently minimal (fine rales) or 

absent. 


(1) Abnormal liver function studies (85%) 

(2) Proteinuria (62%) 

(3) Sterile pyuria (12%) 

(4) Rounded segmental densities in the lower lobes or lobar consolidation on chest radiograph 

(5) Serologic studies are the diagnostic test of choice. 

e. Treatment 

(1) Early antibiotic therapy helps promote a quick response and prevents relapse or chronic Q fever. 

(2) Tetracycline, doxycycline, or chloramphenicol 

(3) If patient is pregnant, consider TMP-SMX. 

248


f. Complications associated with a prolonged illness 

6. Tularemia 

(1) Relapse despite antibiotic therapy 

(2) Endocarditis 

(3) Hepatitis 

(4) Meningitis 

a. Etiology: Francisella tularensis, a gram-negative, nonmotile, pleomorphic coccobacillus bacterium that is 

harbored principally in hard ticks and wild rabbits 


(1) Transmission is usually via direct contact with tissues or body fluids of infected animals, exposure to 

an infected tick, or inhalation of contaminated dust or water aerosol. 

(2) Hunters, trappers, butchers, cooks, and campers are most commonly affected. 

c. Clinical forms 

(1) Ulceroglandular (most common): characterized by an indurated skin lesion at the site of inoculation 

and regional lymphadenopathy 

(2) Typhoidal: characterized by fever, chills, weight loss, and hepatosplenomegaly 

(3) Glandular 

(4) Oculoglandular 

(5) Oropharyngeal 

d. Tularemia pneumonia: usually acquired via inhalation of contaminated aerosol or from bacteremia but may 

also arise as a complication of either the ulceroglandular or typhoidal forms 

e. Classic clinical scenario of tularemia pneumonia: The patient is a rabbit hunter (often a male) presents with 

high fever (104°-106°F [40°-41 °C]), shaking chills, and cough (usually nonproductive). Other symptoms 

include chest pain, shortness of breath, and hemoptysis. Examination of the chest is often normal but may 

reveal rales, consolidation, or a pleural rub. Hepatosplenomegaly and a maculopapular rash may also be 

present. Chest radiograph usually reveals bilateral, patchy, poorly defined or ovoid infiltrates, as well as 

hilar lymphadenopathy and pleural effusion. 

f. Diagnostic evaluation: serologic studies (ELISA) confirm the diagnosis. 

(1) A 4-fold rise between acute and convalescent titers is diagnostic. 

(2) A single convalescent titer 2':1 :160 is very suggestive. 

g. Management 

(1) Streptomycin is the drug of choice. 

(2) Gentamicin and kanamycin are alternative agents. 

(3) Tetracycline and chloramphenicol are also effective but are associated with a high rate of relapse and 

should be reserved for patients who cannot tolerate any of the above agents. 

(4) A live, attenuated vaccine is available for high-risk laboratory personnel. 

h. Complications 

C. Viral pneumonia 

(1) Mortality rate is 5%-30% without antibiotic therapy and



(a) 

b. Parainfluenza 

Primarily supportive; if admission is required, specific therapy may be indicated. 

(b) Infants should receive a trial of ~-adrenergic therapy during the first 24 hours. 

(1) Second most common cause of pneumonia in children 

(2) Also causes croup and bronchitis 

c. Adenovi ruses 

(1) Target populations: children and military recruits 

(2) Clinical presentation: fever, cough, rhinitis, conjunctivitis, and pharyngitis 

(3) Diagnostic evaluation: chest radiographs show lower lobe infiltrates. 

d. Varicella zoster virus 

(1) Occurs primarily in adults; especially severe in pregnant patients 


(a) 

Illness begins with a rash that is followed within a week by fever and cough associated with 

tachypnea and dyspnea. 

(b) 20%-40% of patients also develop cyanosis, hemoptysis, and pleuritic chest pain. 


(a) Sputum analysis may reveal multi nucleated giant cells. 

(b) Chest radiograph usually reveals an interstitial pneumonia; however, micronodular and lobar 

patterns may also be seen. 


(a) This is a serious adult illness and requires admission. 

(b) Administration of IV acyclovir is indicated. 

e. Influenza viruses (most common cause of viral pneumonia in adults) 

(1) Occurs between November and April 


(a) 

Usual syndrome has an incubation period of 1-5 days followed 2 weeks later by fever, headache, 

and a nonproductive cough. 

(b) Patients may have an associated bacterial pneumonia. 

(c) Up to 40% of patients with a normal chest radiograph have rales, rhonchi, and wheezing on 

examination. 

(d) Pure influenza pneumonia (no associated bacterial infection) is much more deadly. The elderly, 

pregnant patients, and those with chronic health conditions (eg, heart disease, COPD, diabetes 

mel I itus) are at risk. 

i. Sudden weakness is followed by dyspnea, cyanosis, and ARDS. 

ii. Chest radiographs show bilateral interstitial infiltrates. 

(3) Diagnostic evaluation: rapid antigen detection assay is recommended for epidemiologic reasons. 


(a) 

Primarily supportive 

i. Begin antiviral therapy if onset of symptoms within 48 hours or at any time if a high-risk 

population. 

ii. Zanamivir or oseltamivir is effective for A and B strains. 

(b) Amantadine (or rimantadine) is helpful in the treatment and prophylaxis of patients with influenza A. 

f. Cytomegalovirus (CMV) 

(1) CMV pneumonia is a complication in transplant recipients and patients with advanced AIDS. 


(a) 

CMV can be either a true pathogen or a coexistent organism. 

(b) In transplant recipients, CMV is a true pathogen. It generally produces pneumonia within 1-3 

months after transplantation and is the most common cause of death in recipients of bone 

marrow transplants. 

(3) Classic clinical scenario: In AIDS patients, CMV is often found in association with other pathogens and 

may represent a coexistent organism rather than a true pathogen. Thus, a definitive diagnosis of CMV 

pneumonitis in these patients requires all of the following: 

250


(a) A compatible clinical picture (fever, hypoxia, and infiltrates on chest radiograph) 

(b) Positive cultures for CMV 

(c) Absence of other pathogenic organisms 

(4) Diagnostic evaluation: chest radiograph most often reveals bilateral interstitial (or reticulonodular) 

infiltrates that begin in the periphery of the lower lobes and spread centrally and superiorly. 


g. Hantavirus 

(a) IV ganciclovir or foscarnet 

(b) lmmunoglobulin is combined with the above regimen in.bone marrow recipients (who are 

particularly susceptible to CMV infection). 

(1) Infection results from inhalation of aerosols that contain material contaminated with rodent urine and feces. 

(2) Epidemiology: residents of the southwestern United States (New Mexico, Arizona, Colorado, Utah) are 

most commonly affected. 

(3) Clinical presentation: an initial prodrome of fever, myalgia, and malaise progresses over several days 

and evolves into a syndrome of severe respiratory distress and shock. 

(4) Diagnostic evaluation: chest radiograph reveals bilateral interstitial infiltrates (most prominent in 

dependent lobes). 

(5) Management: supportive care and IV ribavirin (experimental) 

D. Types of pneumonia: classic clinical scenario and etiology 

Table 13: Classic Clinical Scenario and Etiology of Pneumonia 

Classic Clinical Scenario 

Pneumonia plus hyponatremia, increased liver enzymes, watery diarrhea, 

nausea/vomiting, seizure, history of being at a convention 

Elderly, post influenza, nursing home, cocci in clusters, lung abscess formation 

Young, healthy male, 5-day prodrome (upper respiratory infection), respiratory 

failure (ARDS) 

Young, bullous myringitis, chest radiograph worse than clinical picture 

COPD, gram-negative pleomorphic rods 

Alcoholic, bulging fissures, currant jelly sputum 

Elderly, recent upper respiratory infection, winter months, sudden prostration 

Military recruits, fever, cough, rhinitis, conjunctivitis 

Rusty sputum, single shaking chill, pleuritic chest pain 

Staccato cough, prolonged dry cough in college student 

Transplant patient 1-3 months after transplant with cough, hypoxia 

IV drug abuser, fungal infection throat, CD4 

Hunter, trapper, butcher, cook, high fever 

Bird (parrot) owner, relative bradycardia 

Slaughterhouse worker, goat, sheep, parturient cats 

From southwest US with cough, fever, weight loss, diffuse pulmonary infiltrates 

Abrupt onset of fever, infiltrates, wide mediastinum 

Cause/Type 

Legionella 

Staphylococcus 

Hanta virus 

Mycoplasma 

Haemophilus influenzae 

Klebsiel/a 

Influenza pneumonia 

Adenovirus pneumonia 

Streptococcus pneumoniae 

Chlamydia 

CMV pneumonia 

Pneumocystis jiroveci 

pneumonia 

Tularemia pneumonia 

Psittacosis pneumonia 

Q fever pneumonia 

Coccidiomycosis 

Bacillus anthracis 

251


II. TUBERCULOSIS (TB) 


1. TB is the second most common infectious cause of death (HIV is most common); one-third of the world's 

population is infected with Mycobacterium tuberculosis. There are 9 million new cases per year, and 1.7 

million deaths per year (2009). 

2. TB is an AIDS-defining opportunistic infection and is the only opportunistic infection in AIDS patients that is 

transmitted by the respiratory route to both immunocompromised and immunocompetent hosts. 


1. The causative organism is Mycobacterium tuberculosis, a weakly gram-positive obligate aerobic rod with acidfast 

staining properties that multiplies very slowly (once every 12-24 hours). 

2. Transmission occurs via aerosolized droplets produced by coughing, sneezing, talking, or breathing. Infection 

develops when these contaminated droplets are inhaled and reach the alveoli. 

3. Once in the alveoli, tubercle bacilli are phagocytized (but not killed) by alveolar macrophages and proliferate 

within these cells to form a primary focus of infection (primary TB), usually in the lower lobes. Organisms may 

also spread from this initial site of infection through the lymphatics to regional lymph nodes and to distant 

organs via the bloodstream. This bacillemia is usually asymptomatic, but it produces metastatic foci throughout 

the body that may become active later in life. These foci are preferentially established in areas of high oxygen 

tension such as the apical and posterior segments of the upper lobes of the lung, the kidneys, bones, and brain. 

4. Most infected patients mount an effective immune response and have no further infectious sequelae. 

T lymphocytes reach sufficient numbers to control the infection 2-1 0 weeks (average 6-8 weeks) after 

exposure. The tuberculin skin test becomes positive at this time, indicating that cell-mediated immunity has 

developed. lmmunocompromised patients, however, may be unable to mount an adequate immune response. 

In these individuals, a rapidly progressive primary infection resulting in early death can evolve. 

5. After a period of dormancy, some infected patients go on to develop active disease. This generally occurs when 

the patient's immune response is altered in some manner. 

a. The lifetime risk of reactivation in the general population is 10% but is much greater in patients with 

impaired cellular immunity. 

b. Conditions associated with an increased rate of conversion to active disease 

(1) AIDS (rate of progression is 7%-10% per year) 

(2) lmmunosuppressive therapy, including steroids 

(3) Renal failure, hemodialysis 

(4) Diabetes mellitus 

(5) Malnutrition, alcoholism 

(6) Malignant disease, malignant lymphoma 

(7) Postgastrectomy and postintestinal bypass states 

(8) Transplant recipients 


1. Pulmonary TB (inactive, or dormant, foci) 

a. Asymptomatic in 90% of patients; can be identified only by development of a positive TB skin test and 

possibly a Ghan complex on chest radiograph 

b. A pneumonitis may also be seen (usually in the lower lobes). 

2. Reactivation TB (endogenous reactivation of dormant foci) 

a. Most common clinical form of TB and is seen most often in the elderly 

b. Symptoms include low-grade fever, night sweats, malaise, weight loss, and productive cough (most 

common symptom), pleuritic chest pain. 

c. Signs of chronic wasting are present in most patients. 

d. Sites of involvement include the apical and posterior segments of the upper lungs, kidneys, bones/joints, 

and brain. 

(1) Pulmonary involvement is present in >80% of patients. 

(2) Extrapulmonary involvement is present in 15% of the general population but is greater in patients 

with HIV. 

3. Pulmonary TB (active foci) 

a. Clinical onset 

252


(1) Insidious: patients (usually debilitated) present with a chronic cough (most common symptom) and 

constitutional symptoms of reactivation such as malaise, weight loss, night sweats, and fever. As the 

cough progresses over time, it becomes productive of mucopurulent sputum and is often associated 

with hemoptysis. Patients may also complain of a dull ache or tightness in the chest. 

(2) Abrupt: some patients present with acute onset of fever, chills, cough (most common symptom), and 

myalgias that mimic an episode of acute bronchitis or pneumonia. Unless TB is considered in the 

differential diagnosis and smears of sputum for acid-fast bacilli are obtained, these patients may be 

misdiagnosed as having bacterial pneumonia. 

b. Chest examination is often unremarkable but may reveal rales or consolidation in the presence of extensive 

pulmonary involvement. 

4. Extrapulmonary TB can result from primary infection or reactivation and may involve almost any organ in the 

body. It may also take a disseminated form (miliary TB). The signs and symptoms produced are determined by 

the structures that are affected. 

a. TB meningitis (most rapidly progressive form ofTB) 

(1) Results from seeding during the primary infection or from rupture of a subependymal lesion (Rich foci) 

into the subarachnoid space. 

(2) Clinical onsets 

(a) Insidious: patients often present with a nonspecific febrile illness of 1-6 weeks duration, followed 

by intermittent headache, confusion, personality changes, stiff neck, diplopia, photophobia, 

cranial nerve palsies, decreased level of consciousness, and seizures. 

(b) Fulminant: some patients, particularly children, may present acutely with fever and delirium in 

association with a severe headache and stiff neck. 

(3) Diagnostic testing 

b. Pleural TB 

(a) Positive TB skin test (75%) 

(b) Cerebrospinal fluid analysis (acid-fast stain not usually positive) 

1. t Pressure and protein 

ii . .J, Glucose 

iii. t WBC count of 100-1,000/mL (predominantly lymphocytes) 

(1) Results from rupture of a parenchymal focus into the pleural space 

(2) Associated pleural effusion is exudative in nature with laboratory evaluation revealing: 

(a) Increased protein 

(b) Low pH 

(c) Normal or low glucose 

(d) WBC count of 1,000-5,000/mL (mostly monocytes) 

(e) An acid-fast smear that is often negative 

(3) Pleural biopsy is helpful in making the diagnosis. 

c. Genitourinary TB 

(1) Patients usually present with urinary symptoms (dysuria, frequency) hematuria, or flank pain. 

Constitutional symptoms may also be present. 

(2) Urinalysis reveals: 

(a) Pyuria without bacteriuria 

(b) Low pH 

d. Miliary (disseminated) TB 

(1) A multisystemic process resulting from a progressive primary infection (immunocompromised patients) 

or from secondary bloodstream seeding during recrudescence of previously dormant foci 


(a) Symptoms are usually nonspecific and may include fever, anorexia, weight loss, and weakness. 

Depending on the sites of involvement, more specific symptoms (eg, dyspnea, cough, headache) 

may also be present. 

(b) Physical findings may include: 

i. Fever 

ii. Pulmonary findings 

iii. Hepatomegaly 

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5. TB and HIV 

iv. Lymphadenopathy 

v. Splenomegaly 

vi. Tubercles of the retina (circumscribed, spheroid, granulomatous lesions with three distinct 

zones, the only specific finding) 


(a) Anemia and WBC abnormalities (leukopenia, leukemoid reactions, agranulocytosis) 

(b) Hyponatremia 

(c) Negative TB skin test 25%-50% of the time (especially in the elderly and immunocompromised) 

(d) Chest radiograph typically reveals small nodular densities that are uniformly distributed 

throughout both lung fields. A pleural effusion may also be present. 

a. TB is an AIDS-defining illness and generally produces disease at an earlier stage of HIV infection than other 

opportunistic infections. 

b. The incidence ofTB in HIV-infected patients approaches 60% and currently represents the greatest health 

care risk to the general public from the HIV epidemic. 

c. Co-infection with TB and HIV results in: 

(1) A greater incidence of extrapulmonary disease 

(2) More atypical clinical findings 

(3) An increased incidence of tuberculin nonreactivity and negative acid-fast bacilli smears 

(4) A greater frequency of unusual and atypical chest radiographs 

(5) Decreased cavitary disease 

(6) More antibiotic resistance 

(7) Higher relapse and mortality rates 

(8) A larger number of adverse drug reactions and multidrugresistantTB (especially to rifampin and 

isoniazid) 


1. TB must be considered in the differential diagnosis of any patient who presents with respiratory complaints 

or extrapulmonary symptoms, particularly if the patient is a member of a high-risk group (patients with AIDS, 

immigrants, IV drug abusers, residents/employees of longterm care facilities). 

2. Tests used to establish the diagnosis include the TB skin test, chest radiograph, and microbiologic studies for 

acid-fast baci 11 i. 

3. TB skin test 

a. The standard test for detecting infection with M tuberculosis 

b. Involves intradermal administration of purified protein derivative and is read 48-72 hours after 

administration 

c. A positive reaction indicates the presence of infection but not necessarily the presence of active disease 

(must be confirmed by culture). 

d. Criteria for interpreting the test as true-positive vary with patient background and are noted in Table 14. 

Table 14: TB Skin Test Interpretation 

>5 mm 

>10 mm >15 mm 

Known or suspected HIV 

infection 

Close contact with a person with 

active TB 

lmmunocompromised 

Organ transplant 

Nodular or fibrotic changes on 

chest radiograph 

Residents of or employees in highrisk 

settings (eg, health care facilities, 

homeless shelters, and prisons) 

IV drug abusers 

Immigrants from an area with a high 

incidence of TB 

Certain high-risk minority groups 

(Hispanics, black Americans, Native 

Americans) 

Children


e. A negative test does not exclude the diagnosis, because some patients (particularly those who are 

immunocompromised) are anergic. 

f. A false-positive test may be due to infection with M avium or M kansasii (nontuberculous mycobacteria). 

Clues to this diagnosis include the following: 

(1) No history of risk factors for TB 

(2) A negative skin test (or a reaction smaller than a true-positive) 

(3) History of COPD 


a. Primary TB 

(1) Small parenchymal infiltrates located in any area of the lung and unilateral hilar adenopathy 

(2) These lesions may subsequently calcify to form a Ghan complex. 

(3) Inflammatory infiltrates of the lower lobes with associated hilar adenopathy are seen in patients with 

progressive primary infections and clinically evident disease. 

(4) Hilar adenopathy is the radiologic hallmark of primary TB. 

(5) Pleural effusions are seen in one-third of patients, typically in first 3-4 months after infection. 

b. Reactivation/pulmonary TB 

(1) Typically affects the apical-posterior segments of the upper lobe. Nodular densities are most often seen 

in the apical (Simon foci) or posterior segments of the upper lobe but may also be found in the upper 

segment of the lower lobe. 

(2) Associated cavitation may or may not be present. 

c. Miliary (disseminated) TB 

(1) May initially be normal but classically reveals small nodules (1-3 mm) scattered throughout both lung 

fields in a miliary pattern. 

(2) A pleural effusion (frequently unilateral) may also be present. 

d. HIV-infected patients 

(1) The chest radiograph is often atypical and may even be normal. 

(2) Upper lobe cavitary lesions are rare, while hilar or mediastinal adenopathy and lower lobe infiltrates 

are more common. 

(3) A diffuse interstitial pattern that is easily mistaken for Pneumocystis jerovici pneumonia may also be 

seen. 

5. Microbiologic studies 

a. Staining of sputum for acid-fast bacilli with Ziehl-Neelsen or fluorescent (fluorochrome) staining (which is 

more sensitive) 

(1) Provides a rapid presumptive diagnosis ofTB; number of bacilli seen correlates with the degree of 

i nfectivity. 

(2) Positive smears have a specificity of 98%. 

(3) Smear results should be confirmed by culture. 

b. Culture of sputum or tissue for acid-fast bacilli 

E. Management 

(1) More sensitive than staining and is the "gold standard" for confirming the diagnosis ofTB 

(2) Although traditional cultures take 3-6 weeks, new radiometric techniques can confirm the diagnosis 

in as few as 5 days; DNA probes, reverse transcription, and polymerase chain reaction tests allow 

for identification of TB in a matter of hours but, because of technical problems, have not received 

approval for routine clinical use. 

1. As soon as the diagnosis is suspected, the patient should wear a mask and be placed in an isolation room. 

2. Because of the emergence of multidrug-resistant strains ofTB, it is now recommended that initial therapy for TB 

include four drugs until susceptibility tests are available. 

3. The initial drug regimen of choice is isoniazid, rifampin, pyrazinamide, and streptomycin or ethambutol; in the 

absence of drug resistance, isoniazid and rifampin taken for 9 months is curative. (Preventive drug therapy also 

includes isoniazid [ie, for those with a positive intradermal skin test].) 

4. Adverse effects associated with these drugs: 

a. lsoniazid 

(1) Multiple neurologic entities, including peripheral neuritis; pyridoxine (vitamin 8 6 ) is administered 

concurrently to prevent isoniazid-induced neuropathy. 

255


(2) Hepatitis 

(3) Hypersensitivity reactions 

(4) Drug-induced interactions with ketoconazole and fluconazole 

(5) Intractable seizures if patient is not on pyridoxine in conjunction with isoniazid: must treat with highdose 

vitamin 8 6 

(6) Lupus 

b. Rifampin 

(1) Hepatitis 

(2) Thrombocytopenia 

(3) Drug interactions with coumadin, oral contraceptives, digitalis derivatives, methadone, dapsone, 

cyclosporin, corticosteroids, oral hypoglycemic agents, ketoconazole, and fluconazole-,, decreased 

blood levels and effectiveness 

(4) Orange-colored tears, saliva, and urine 

c. Pyrazinamide 

(1) Hyperuricemia 

(2) Hepatitis 

(3) Arthralgias 

(4) Rash 

d. Ethambutol 

(1) Optic neuritis 

(2) Rash 

e. Streptomycin 

(1) Vestibular nerve damage 

(2) Nephrotoxicity 

5. Before starting therapy with these agents, baseline studies should be obtained. 

a. Liver function tests, BUN/creatinine, and CBC with platelet count for all patients 

b. Visual acuity (and red-green color perception) for patients being treated with ethambutol 

c. Serum uric acid for patients being treated with pyrazinamide 

Ill. PLEURAL EFFUSION 

A. Definition 

1. An abnormally large collection of fluid within the pleural space, reflecting the presence of an underlying 

i ntrathoracic or extrathoracic disease process 

2. Types of effusions 

a. Transudates: excessive hydrostatic pressure (eg, CHF) or insufficient oncotic pressure (t serum protein)-,, 

low protein plasma infiltrates 

b. Exudates: lymphatic blockage due to malignancy or pleural capillary damage due to infectious disease-,, 

high protein plasma infiltrates 

3. Most common malignancies causing pleural effusion 

a. Bronchogenic lung carcinoma 

b. Breast cancer 

c. Lymphoma 

d. Leukemia 


1. The patient presents with chest pain that is pleuritic with associated symptoms of fever, cough, and shortness of 

breath. 

2. Physical examination findings can help to narrow differential. 

a. Splinting± a pleural friction rub-,, pleurisy 

b. Dullness to percussion+ t breath sounds+ t tactile fremitus-,, pleural fluid 

c. Bronchial breath sounds+ egophony-,, atelectasis 

d. Normal breath sounds+ distended neck veins+ left parasternal lift+ accentuated P 2 

on cardiac 

examination-,, massive pulmonary embolism 

256



1. Chest radiographs 

a. Small effusions are most easily detected on a lateral decubitus film with the affected side down; 

accumulations of 5-50 ml of fluid can be detected with this view. 

b. Small effusions can be missed entirely on supine films and are generally not apparent on PA and lateral 

films until 2:200 ml of fluid is present. 

c. Early signs of smal I effusion 

(1) PA view-.. faint obscuring of the costophrenic angle 

(2) Lateral view-.. blunting or loss of the costophrenic angle 

(3) Lateral decubitus view - fluid layers out 

d. Signs of a moderate effusion 

(1) Ground-glass appearance of lung fields 

(2) No air bronchograms 

e. Sign of a large effusion -.. opacification (partial or complete) 

f. Pleural fluid in a fissure-.. a "phantom" or "pseudotumor" 

2. Ultrasound 

3. 

a. Small effusions can be easily detected with point-of-care ultrasound. 

b. Anechoic space seen on ultrasound image 

(1) Complicated effusions may show septations and hypoechoic material. 

(2) Important to identify surrounding structures of diaphragm and atelectic lung tissue 

Thoracentesis: the definitive procedure 

a. 

b. 

Contraindications 

(1) Uncooperative patient 

(2) Coughing or hiccups 

(3) Local skin infection 

(4) Coagu Iopa th ies 

(5) Anticoagulant therapy 

Technique 

(1) Mark the site with ultrasound. 

(2) Anesthetize the area with lidocaine. 

(3) The posterior entry is the primary approach. Insert the needle immediately above the rib to avoid the 

neurovascular bundle. 

(4) Loculated effusions may require CT-guided needle aspiration. 

(5) Withdrawing fluid 

(a) Reexpansion pulmonary edema may occur if fluid is removed too rapidly. 

(b) Limit removal of fluid to ~2 L. 

(6) After the procedure, obtain a chest radiograph to exclude an iatrogenic pneumothorax. 


(1) CBC with differential 

(2) Serum protein, lactate dehydrogenase (LDH), amylase, and glucose (


f. Pleural fluid characteristics that indicate further drainage is required 

(1) Frank pus 

(2) Gram stain positive 

(3) pH


D. Critical facts 

1. Most common cause of pleural effusion in developed countries: CHF 

2. Most common cause of pleural effusion in developing countries: TB 

3. Most common cause of transudate: CHF 

4. Most common cause of exudate: infection 

5. Normal amount of pleural fluid: 0.1-0.2 ml/kg body weight 

6. Transudate pathophysiology: increased hydrostatic pressure or decreased oncotic pressure; very little protein 

7. Exudate pathophysiology: increased membrane permeability or defective lymphatic drainage; large amount of 

protein 

8. Massive effusions are more commonly due to malignancy, but CHF can do it, too. 

9. Effusions are best seen in lateral decubitus with the effusion side down. 

10. Pulmonary embolism is the most commonly overlooked condition in the evaluation of patients with pleural 

effusion. 

11. If the difference between serum albumin and pleural albumin is > 1.2 g/dL, the effusion is a transudate. 

12. If pH


5. Foreign-body aspiration 

a. The leading cause of accidental home death in children 90%) develop signs and symptoms within 1 hour of the event. 

5. Patients who have aspirated a foreign body (and have incomplete obstruction) present with choking, a 

spasmodic cough, and wheezing. Examination of the chest may reveal asymmetric chest wall movement, 

decreased breath sounds, wheezing, and hyperresonance to percussion on the involved side. 

6. Putrid discharge in sputum or pleural fluid is diagnostic of anaerobic infections. Anaerobic infections are 

typically indolent with absence of rigors. Predisposing conditions include IV drug abuse, alcoholism, 

concurrent periodontal disease, recent anesthesia, or dysphagia. 


1. Arterial blood gases 

a. The usual finding is hypoxia with respiratory alkalosis. 

b. Severe aspiration respiratory failure with a combined respiratory and metabolic acidosis 

2. Cultures 

a. Difficult to isolate from sputum cultures or bronchoscopy/bronchoalveolar lavage 


a. Radiographic findings are often delayed. 

(1) Atelectasis is the initial finding and may be seen as early as 1 hour after aspiration. 

(2) Infiltrates develop 6-12 hours later and most frequently involve the right lower lobe (if aspiration 

occurred in the upright position). 

b. Foreign body aspiration_,. an end-expiratory PA film demonstrates a hyperexpanded lung on the involved 

side (usually the right side, because the right mainstem bronchus has less of an acute angle than the left). 

E. Management 

1. Provide supplemental oxygen. 

a. High-flow oxygen by nasal cannula or face mask may be sufficient for some patients. 

b. Patients who are hypercarbic (or remain hypoxic) despite these measures should be intubated and 

mechanically ventilated. 

c. If the patient has an altered level of consciousness and a decreased gag reflex, immediate endotracheal 

intubation is needed. 

260


2. Consider noninvasive positive-pressure ventilation (NIPPV); if little or no improvement in respiratory distress or 

hypoxemia while on NIPPV after 30-60 minutes, intubation will likely be required. 

3. Bronchoscopy is useful in removing large particles and clearing the large airways in large-volume aspirations. 

Bronchial irrigation with saline solution, however, should be avoided; it has no beneficial effect and may be 

harmful. 

4. Antibiotics should be reserved for elderly and chronically ill patients, as well as for those who develop clinical 

evidence of infection (fever, purulent sputum, leukocytosis). Bacterial aspiration pneumonia occurs over a 

period of several days in >60% of cases of chemical aspiration. Antibiotic therapy is based on the origin of the 

infection. 

a. Aspiration pneumonitis: occurs immediately after aspiration event: supportive care (airway management, 

pulmonary toilet), no role for antibiotics because this is a chemical pneumonitis 

b. Community-acquired aspiration pneumonia - empiric treatment with a third- or fourth-generation 

cephalosporin or a fluoroquinolone (with antipneumococcal coverage) or a (3-lactam with a (3-lactamase 

inhibitor and a macrolide 

c. Nosocomial aspiration pneumonia - empiric treatment with piperacillin/clavulanate or a fluoroquinolone 

(with antipneumococcal coverage) and clindamycin (If an abscess is present, clindamycin has excellent 

penetration.) 

5. Supportive care measures 

a. Humidified oxygen 

b. Bronchodilators 

c. Chest physiotherapy 


1. Acute respiratory failure 

2. Severe sepsis 

3. Pneumonia, empyema, and lung abscess 

4. Pulmonary fibrosis (for chronic aspiration) 

G. Mortality rate 

1. Varies with the pH and contamination of the aspirate 

2. 40%-70% if the pH is


B. Etiology: most lung abscesses are polymicrobial and involve either strictly anaerobes or a mixture of 

anaerobic organisms. 

1 . Anaerobic 

a. Fusobacterium 

b. Bacteroides 

c. Streptococci (microaerophilic and anaerobic) 

2. Aerobic 

a. Staphylococcus aureus (often follows influenza in a flu epidemic) 

b. Streptococcus pneumoniae 

c. Alpha streptococci 

d. Pseudomonas 

e. Klebsiella pneumoniae 

f. E coli 

g. Proteus 

h. Nocardia (particularly in immunocompromised individuals on prolonged course of steroids) 

3. Other organisms 

a. Mycobacterium 

b. Histoplasma 

c. Coccidioides 

d. Lung flukes and Entamoeba histolytica 


1. Coincident with the development of cavitation (1-2 weeks after aspiration) 

2. History 

a. Systemic signs and symptoms: weakness, fever, weight loss, night sweats 

b. Pulmonary signs and symptoms: dyspnea, chest pain, and a cough productive of a fetid and bloody sputum 


a. Poor dentition, gingivitis, and foul-smelling breath 

b. Signs of localized consolidation or cavitation on auscultation 

c. Hemoptysis 


1. CBC: increased WBC count with a left shift and anemia 

2. Cavitation with an air-fluid level 

a. Chest radiograph or CT scan of the chest 

b. Most common sites are the posterior segment of the right upper lobe and superior segment of the left and 

right lower lobes. 

c. Findings that suggest empyema rather than abscess 

(1) An air-fluid level at the site of a previous pleural effusion 

(2) A cavity with an air-fluid level that tapers at the pleural border 

(3) An air-fluid level that crosses a fissure 

(4) An air-fluid level that extends to the lateral chest wall 

3. Sputum analysis: because of oropharyngeal contamination, only bronchoscopically obtained sputum, 

transtracheal, or transthoracic specimens are reliable for anaerobic culture and sensitivity. 

E. Management 

1. Antibiotic therapy 

a. Clindamycin is currently the antibiotic of choice for an uncomplicated lung abscess. It is given IV until the 

patient remains afebrile for 5 days and then is continued orally for 6-8 weeks. 

b. Alternative agents include penicillin (when penicillin resistance is not a problem), metronidazole (should 

not be used alone because there is a 50% failure rate when used alone), or cefoxitin. 

2. Indications for surgery 

a. Life-threatening hemoptysis 

b. Bronchopleural fistula 

262


c. Tumor or empyema 

d. A residual cavity 

F. Late complications 

1. Chronic lung abscess 

2. Empyema 

3. Bronchopleural fistula 

4. Brain abscess 

VI. EMPYEMA 


1. A collection of pus in the pleural space or fissures 

2. Mechanism of formation 

B. Etiology 

a. Hematogenous or lymphatic spread from pneumonia 

b. Infection from a chest tube, thoracentesis, or thoracotomy 

c. Esophageal perforation and mediastinitis 

d. Rupture of a mediastinal lymph node 

e. Aspiration pneumonia 

f. Direct extension from retropharyngeal or subdiaphragmatic abscesses or from vertebral osteomyelitis 

1. Mycobacterium tuberculosis 

2. Staphylococcus (MRSA) 

3. Streptococcus pneumoniae 

4. Pseudomonas 

5. Klebsiella 

6. Gram-negative organisms 

7. Anaerobes (difficult to isolate) 


1. Acute illness: fever and chills with pleuritic chest pain, cough, and shortness of breath 

2. Subacute illness (more common): weight loss and fatigue 

3. Physical examination: decreased breath sounds, egophony, dullness on percussion, and decreased excursion of 

the involved hemithorax 


1. Chest radiograph: abnormal pleural-based opacity that does not appear to flow freely on lateral decubitus view 

2. Thoracentesis: confirms the diagnosis 

E. Clinically useful classifications for empyema 

1. American Thoracic Society categorization of empyema by volume 

a. Minimal: 10 ml of fluid less than half of hemithorax 

c. Large: greater than half of hemithorax 

2. Fluid analysis categorization 

a. pH


G. Complications 

1. Empyema necessitans (dissection into the subcutaneous tissues or through the chest wall) 

2. Bronchopleural fistula 

3. Permanent loss of lung tissue 

VII. HEMOPTYSIS 

A. Definitions 

1 . Hemoptysis 

a. Coughing up blood originating from the pulmonary parenchyma or tracheobronchial tree 

b. Can range from blood streaking of sputum to gross blood with the absence of any accompanying sputum 

c. Most often not life threatening 

d. However, when massive, hemoptysis can produce airway obstruction as well as hemorrhagic shock and 

require urgent intervention. 

2. Massive hemoptysis 

a. A single expectoration >50 ml or 600 ml blood in 24 hours 

b. Necessitates transfusion to maintain stable hematocrit 

B. Etiology varies with age of patient 

1. Infection/inflammation: most common cause 

a. Bronchitis (especially chronic): most common cause 

b. Pneumonia (especially Klebsie//a, Staphylococcus, or influenza virus) 

c. Parasites (ascariasis, schistosomiasis) 

d. Endocarditis 

e. Bronchiectasis (most common causes of massive hemoptysis are bronchiectasis, tuberculosis, lung abscess, 

and neoplasm) 

f. Tuberculosis 

g. Lung abscess 

h. Aspergilloma 

2. Neoplasms (especially bronchogenic cancer) 

3. Cardiovascular disorders 

a. Mitra! stenosis 

b. CHF 

c. Pulmonary hypertension (primary) or embolism/infarction 

d. AV malformation/fistula 

e. Congenital heart disease 

f. Thoracic aortic aneurysm 

g. Pulmonary embolism 

4. Trauma 

5. Immunologic disorders 

a. Goodpasture syndrome 

b. Vasculitis 

6. Other 

a. Cystic fibrosis 

b. Blood dyscrasias 

c. Drugs (cocaine-induced pulmonary hemorrhage, ASA, tissue plasminogen activator, ethanol, etc) 

d. Coagulopathies 

7. Idiopathic (-5%-15% of cases) 

8. Iatrogenic 

a. Swan-Ganz catheter__,, rupture of pulmonary artery 

b. Chronic tracheostomy __,, tracheoinominate fistula 

264


C. Hemoptysis versus hematemesis 

1. Need to distinguish from hematemesis or blood swallowed from epistaxis via physical examinations 

2. "True" hemoptysis is: 

a. Initiated and accompanied by vigorous coughing 

b. Generally bright red and foamy and does not contain particles of food 

D. Clinical presentation: determined in large part by underlying cause 

1. Bacterial pneumonia 

2. CHF 

a. Sm al I amounts of blood in sputum, productive cough, and fever 

b. Examination may reveal rales or rhonchi and signs of consolidation. 

a. Small amounts of blood in sputum, shortness of breath 

b. Examination may reveal rales, an S3 gallop, jugular venous distention, hepatomegaly, ascites, or peripheral 

edema. 

3. Bronchogenic carcinoma 

a. Generally have chronic cough and weight loss 

b. Examination may reveal signs of consolidation and clubbing. 

4. Tuberculosis 

a. May be massive hemoptysis 

b. Patients are often cachectic and have a chronic cough. 

c. Examination may reveal post-tussive rales. 


1. The severity and suspected etiology of the hemoptysis determine the extent of the evaluation performed in the 

emergency department setting. 


a. Should be obtained in all patients and may reveal signs of underlying pulmonary or cardiovascular disease 

b. 50% are normal. 

3. CBC: establishes a baseline hematocrit 

4. Prothrombin time (INR)/partial thromboplastin time and platelet count: useful in patients who are on 

anticoagulants to exclude blood dyscrasias 

5. Arterial blood gases: indicated in patients with respiratory distress or massive hemoptysis 

6. Type and crossmatch: should be obtained in all patients with massive hemoptysis 

7. Sputum: should be sent for Gram and acid-fast stains, culture (for bacteria, fungi, and mycobacteria), and 

cytologic examination 

8. Bronchoscopy 

a. Useful initially because both diagnostic and therapeutic 

b. Should be obtained on an emergent basis in patients with massive hemoptysis 

9. Selective arteriography 

a. Can be used to localize and embolize the site of bleeding in patients with massive hemoptysis 

b. Particularly useful when the site is peripheral to the bronchoscope's field of view 

10. High-resolution chest CT: usually reserved for patients in whom the chest radiograph is normal. Useful in 

detecting bronchiectasis or aspergillomas. 

F. Management: determined by the volume of hemoptysis and underlying condition 

1. Minimal hemoptysis 

a. Treatment is aimed at correcting the underlying problem. 

b. For example, patients with pneumonia should receive antibiotics. 

c. Specific therapy for the hemoptysis itself is generally unnecessary. 

2. Massive hemoptysis 

a. Initial therapy is aimed at maintaining the airway, stabilizing the patient, and terminating the bleeding. 

b. Intubate the patient: mainstem intubation may be helpful if able to isolate nonbleeding hemithorax. 

c. Place the patient in Trendelenburg with the bleeding side down (to protect the uninvolved lung and 

maximize gas exchange). 

d. Suction as needed. 

265


e. Establish two large-bore IV lines and replace blood loss rapidly. 

f. Obtain immediate consult with pulmonologist and thoracic surgeon. 

g. Consider interventional radiology early for embolization. 

h. Perform bronchoscopy to identify source of bleeding. 

i. Once the patient is stabilized and bleeding has been controlled, further evaluation and treatment of the 

underlying pathology can be done. 

VIII. PNEUMOTHORAX 

A. Spontaneous pneumothorax 

1. A collection of air in the pleural space (in the absence of trauma) 

a. Divided into primary and secondary forms 

2. Primary (idiopathic) spontaneous pneumothorax 

a. Occurs in healthy individuals who lack evidence of underlying pulmonary pathology, usually without a 

precipitating event 

b. Results from rupture of a subpleural bleb (often apical) or a weak pleural segment__.. air leaking into the 

pleural space__.. pulmonary collapse 

c. Causative factors are not always present but may include: 

(1) Atmospheric pressure changes (eg, scuba diving, fighter pilots) 

(2) Performance of the Valsalva maneuver in association with abuse of marijuana/cocaine or injection into 

the central venous system (the "pocket shot") by IV drug users 

(3) Marfan syndrome 

(4) Cigarette smoking 

(5) Family history of pneumothorax 

(6) Vigorous exercise 

d. Incidence is greatest in young adults 20-40 years old. 

e. More common in males than females (male to female ratio is 5:1 ); tall, thin males who smoke are most 

commonly affected. 

f. Onset is usually during rest or sleep. 

g. Recurrence rate is 20%-50% over the following 2-5 years, although most recurrences are seen within the 

first year. 

3. Secondary spontaneous pneumothorax 

a. Occurs in individuals with underlying lung pathology that damages the alveolar/pleural barrier or causes 

an increase in intrabronchial pressures 

b. Associated medical conditions 

(1) Airway disease 

(a) COPD (most common cause) 

(b) Chronic bronchitis 

(c) Asthma 

(d) Cystic fibrosis 

(2) Infection 

(a) Pneumonia, particularly Pneumocystis jerovici pneumonia in AIDS patients, 5 aureus, Klebsie/la, 

Pseudomonas, 5 pneumoniae 

(b) Tuberculosis (rupture of the TB cavity into the pleural space) 

(3) Neoplasms 

(4) Interstitial lung disease 

(a) Collagen vascular disease 

(b) Pneumoconioses 

(c) Sarcoidosis 

(d) Idiopathic pulmonary fibrosis 

(5) Other 

(a) Toxic drugs, especially aerosolized pentamidine 

266


(b) Chemical and radiation pneumonitis 

(c) Smoking 

(d) Endometriosis ("catamenial" pneumothorax) 

(e) Trauma (penetrating injury via gunshot wound, stab wound to the chest) 

c. Individuals >40 years old are most commonly affected. 

4. Iatrogenic pneumothorax: occurs in association with performance of procedures such as: 

a. Subclavian vein catheterization and CPR (most common causes in emergency department) 

b. Endotracheal intubation (increased frequency with mainstem intubation) 

c. lntercostal nerve block 

d. Percutaneous lung biopsy 

e. Thoracentesis 

f. Bronchoscopy (with transbronchial biopsy) 

g. CT-guided thoracic procedures 

B. Classic clinical scenario 

1. The patient presents with sudden onset of pleuritic chest pain and dyspnea. Mild tachycardia and tachypnea 

may also be present. Your first thought might be pulmonary embolism, especially if the patient is a middle-aged 

woman with risk factors for thromboembolic disease. The chest pain is usually anterior but may radiate into the 

neck, back, or ipsilateral shoulder. An associated cough and subcutaneous emphysema of the neck and chest 

are occasionally present. 

2. On physical examination, the breath sounds will decipher the etiology. Classic physical findings on the 

affected side are decreased or absent breath sounds, decreased tactile fremitus, and hyperresonance to 

percussion on the affected side. However, these signs may be subtle or absent in patients with COPD or small 

pneumothoraces. 

3. On ECG, ST segment changes and T-wave inversion may be found, thus mimicking cardiac ischemia. 


1 . Chest radiographs 

a. Consider portable AP chest film. 

b. Best view to find a small pneumothorax: end-expiratory, upright position 

c. Findings on a standard PA chest film (taken in inspiration) 

(1) A fine line (the edge of the collapsed lung) running parallel to the chest wall but separated from it by 

a space 

(2) Absence of lung markings along the lung periphery in the space beyond this line 

d. If the standard chest radiograph does not reveal a suspected pneumothorax, a supine film may be helpful 

(especially in the hypotensive patient; upright films are not advised in these patients). 

(1) In this position, a pneumothorax will collect along the costophrenic sulcus creating a "deep 

sulcus sign" (rather than along the apex of the lung in an upright position), thus making a small 

pneumothorax more apparent. 

(2) Lateral decubitus positioning can reveal as little as 5 ml of pleural gas, which would accumulate in 

the nondependent lateral location. 

e. Radiologic findings that may be confused with pneumothorax 

(1) Skin folds 

(2) Tubing outlines 

(3) Clothing 

(4) Bullae or cysts 

2. Ultrasound for diagnosis (curvilinear probe) 

a. Loss of pleural sliding 

(1) Shallow probe depth 

(2) Decrease gain. 

(3) Minimize any image processing setting; look for artifacts. 

(4) Use zoom setting to view pleural line. 

(5) Identify "bat sign" of two ribs with pleural sliding between rib cross-section. 

b. Absence of B lines/lung rockets/lung comet tail artifact 

267


c. M-mode demonstrates stratosphere or barcode sign; seashore sign present with normal lung sliding (see 

Ultrasound, page 929) 

d. Lung point (site at which the visceral and parietal pleura separate) may be visible. 

3. If the diagnosis is unclear by conventional chest radiograph, chest CT is the best modality to determine 

presence, location, and amount of intrapleural air. 

D. Management 

1 . Observation and tube thoracostomy 

2. Approach selected is determined by the size of the pneumothorax, the degree of symptomatology, the presence 

of underlying pulmonary pathology, the rel iabi I ity of the patient, and whether the patient has had prior 

pneumothoraces. 

3. All patients should be placed on supplemental oxygen, because it hastens resolution of the pneumothorax. 

4. Observation (inpatient or outpatient) 

a. Acceptable if the pneumothorax is small (25% 

(4) Bilateral or tension pneumothorax 

(5) Trauma 

(6) Significant dyspnea 

(7) Detectable pleural fluid 

(8) Positive-pressure ventilation (require intubation) 

(9) Previous contralateral pneumothorax 

c. Chest tube management: presence of a persistent air leak should raise concern for a tracheobronchial 

injury, particularly in a trauma patient who presented with a penetrating chest wound. 

E. Tension pneumothorax 

1. A life-threatening complication 

2. Evolution: air enters the pleural space on inspiration but cannot escape on expiration (ball-valve effect) - 

progressive accumulation of air within the pleural cavity and total collapse of the affected lung - a shift of 

mediastinal structures to the opposite hemithorax - compression of the contralateral lung and impairment of 

venous return - decrease in cardiac output and development of signs of shock 

3. Classic clinical scenario: The patient is hypotensive, cyanotic, and in severe respiratory distress. Air hunger 

develops, and the respiratory rate increases. The patient becomes agitated and restless and displays decreasing 

mental activity. The trachea is deviated to the contra lateral side (even significant tracheal deviation may be 

difficult to detect clinically), and there is hyperresonance to percussion and absent breath sounds on the 

involved side. Jugular venous distention may be present. When the diagnosis is made, or even suspected, the 

positive intrapleural pressure must be released immediately; do not wait for radiograph confirmation. Insert 

a large-bore needle (14 gauge) anteriorly in the involved hemithorax through the second intercostal space 

midclavicular line. This allows time for a tube thoracostomy to be performed. 

268


IX. ASTHMA 

A. Definition and epidemiology 

1. A chronic lung disorder characterized by: 

a. Increased airway responsiveness (an exaggerated bronchoconstriction response) to a variety of stimuli 

b. Airway inflammation 

c. Reversible airway obstruction 

2. Can occur at any age but is more common in children and adolescents; 50% of patients develop asthma before 

age 1 0; approximately 80% of children with asthma develop symptoms before age 5. 

3. Prevalence is increasing; most common chronic disease of childhood 

4. Asthma-related morbidity and mortality rates have been climbing over the last 20 years, especially in children 


C. Pathophysiology 

I 

Triggers 

I 

I 

Non immunologic 

(viral repiratory infections, 

oxidant pollutants, chemicals) 

Immunologic 

(antigen) 

I 

I 

i 

Release of cytokines 

i 

Recruitment of inflammatory cells 

(eosinophils, neutrophils, lymphocytes, 

macrophages, mast cells) to the airway 

i 

Release of inflammatory mediators 

+ 

Bronchoconstriction/airway 

hyperresponsiveness 

+ 

Mucus hypersecretion 

+ 

Airway edema 

+ 

Increased airway resistance 

i 

Decrease in maximum expiratory flow rates 

(.j, PEFR, t FEV,) 

+ 

Air trapping 

i 

Increased airway pressure+ possible barotramua 

I 

I 

Asthma Triggers 

270



1. Symptoms usually awaken the patient at night. 

a. Cough 

(1) May be dry or productive of sputum 

(2) May be the only finding in patients with cough-variant asthma 

b. Dyspnea 

c. Wheezing 

d. Chest tightness 

2. Typical examination findings 

a. Tachypnea 

b. Tachycardia 

c. Wheezing: Although the most common manifestation of asthma, wheezing is not an accurate indicator of 

the severity of an attack; it may be absent in patients with severe obstruction. Also remember that not all 

that wheezes is asthma. 

d. Prolonged expiratory phase 

e. Hyperresonance to percussion 

3 Findings suggestive of severe airway obstruction 

a. Dyspnea so severe the patient is able to speak only a few words at a time, and air movement on 

auscultation of the lungs is poor. 

b. Use of accessory muscles (sternocleidomastoid, scalenus) reflects diaphragmatic fatigue. 

c. Heart rate > 120 beats per minute 

d. Respiratory rate >30 breaths per minute 

e. Pulsus paradoxus 2':12 mm Hg (defined as 2':12 mmHg drop in systolic blood pressure during inspiration) 

implies that the FEV 1 

is less than half the normal predicted FEV1 for that patient and reflects the degree of 

airway obstruction, air-trapping, and ventilatory effort. 

f. Silent chest indicates that airflow is dramatically reduced and is no longer adequate to promote wheezing. 

g. Diaphoresis 

h. Inability to recline on the stretcher 

i. Paradoxical respirations herald impending respiratory failure. 

j. Cyanosis is a late finding appearing just before respiratory arrest. 

k. Altered mental status (confusion, agitation, somnolence) may indicate hypercapnia and often reflects 

impending respiratory failure. 

E. Differential diagnosis 

1. Pulmonary embolus: most of these patients have one or more risk factors for deep venous thrombosis/ 

pulmonary embolism. Order spiral CT with contrast if suspected (V/Q scans may be indeterminant in patients 

with acute asthma); angiography is indicated if the CT is negative, but clinical suspicion is high. 

2. CHF (cardiac asthma): distinguishing features include older age, bibasilar rales, an S 3 

gallop, pink frothy 

sputum, and jugular venous distention; ~-natriuretic hormone assays may be useful in distinguishing CHF from 

asthma exacerbation. 

3. Upper airway obstruction (cancer, laryngeal edema, foreign body inhalation): remember that these patients 

usually have stridor (not wheezing); a patient with wheezing usually has lower airway obstruction. If in doubt, 

listen to tracheal breath sounds; any abnormality indicates upper airway obstruction. 

4. Carcinoid tumors are typically associated with postprandial flushing and GI upset. 

5. Chronic bronchitis or COPD with acute exacerbation: these patients are generally older, have a history of 

smoking (along with a chronic productive cough), and no true symptom-free intervals. 

6. Eosinophilic pneumonias and invasive worm infestations 

7. Endobronchial conditions (cancer, foreign body aspiration, bronchial stenosis): wheezing is unilateral 

8. Drugs (~-blockers, ACE inhibitors) 

9. Allergic or anaphylactic reactions: urticaria, angioedema, hypotension, and/or GI symptoms are clinical clues. 

10. Chemical irritants, insecticides, and anticholinergics: a clue is a history of exposure in an otherwise normal 

individual. 

11. Noncardiogenic pulmonary edema (ARDS) 

271



1. Pulmonary function tests (PEFR or FEV 1 

): Although recommended to gauge treatment efficacy and severity of 

the exacerbation, PEFR and FEV 1 

have not proved beneficial or predictive based on multiple studies. However, 

they are useful in documenting a trend and serve as a comparison to baseline. 

2. CBC 

a. Should be measured before and after each treatment with an adrenergic agent 

b. The PEFR is the easiest test to perform in the emergency department, because it is done at the bedside with 

a portable peak expiratory flow meter. 

c. These studies provide an objective measure of the degree of airflow obstruction present; they are useful 

in assessing the severity of an attack, the response to treatment, and the need for close follow-up or 

admission. 

d. Indicators of severe bronchospasm and probable hospital admission 

(1) PEFR



a. May reveal evidence of hyperinflation (increased AP diameter and/or flattening of the diaphragms), 

increased bronchial markings, and/or atelectasis but is generally nondiagnostic 

b. Is most useful in excluding the complications of asthma and conditions that mimic it 

c. Not obtained routinely but indicated in patients who: 

7. ECG 

(1) Are febrile 

(2) Have focal physical findings suggestive of pneumonia or barotrauma (pneumothorax, 

pneumomediastinum) 

(3) Do not respond to aggressive treatment 

(4) Present with their first episode of wheezing 

(5) Persistent localized wheezing 

(6) Chronic purulent sputum production 

(7) Significant hypoxemia 

(8) Presence of hemoptysis 

a. Unless ischemia is suspected, routine ECGs are generally not helpful diagnostically. 

b. A right ventricular strain pattern is seen in 30%-40% of patients. 

8. Theophylline level should be checked in patients taking this medication. 

G. Management 

1. Pharmacologic agents and their mechanism of action 

a. ~i-adrenergic agonists 

(1) First-line treatment is typically albuterol. 

(2) Promote bronchodilation by increasing cyclic AMP 

(3) May also modulate mediator release from mast cells and basophils as well as promote mucociliary 

clearance 

(4) Primary effect is on the small peripheral airways. 

(5) Onset of action is


(1) Inhaled agents: administer albuterol using a handheld nebulizer. 

(a) Albuterol 0.5% solution: the preferred agent because of its B 2 

-specificity and fewer adverse effects 

(b) Dosage: 2.5 mg in 2-3 ml normal saline every 20-30 minutes up to 3 doses, then hourly 

(c) Continuous nebulization at 15 mg/hr for 2 hours is safe and effective in adults with severe 

bronchospasm; it should be considered for those patients who present with a PEFR


(7) Patients who receive steroids in the emergency department and are subsequently discharged should 

be continued on oral steroids (methylprednisolone or prednisone 1 mg/kg/day) at home for a 

minimum of 3-5 days and a maximum of 14 days. Prolonged therapy with a gradually tapering dose is 

recommended for patients taking maintenance doses for> 10 days. 

(8) Aerosolized corticosteroids are potentially irritating (can stimulate cough or bronchospasm) and, 

therefore, should not be used during an acute attack. 

e. Other considerations 

(1) Evaluate for evidence of dehydration, and administer replacement fluids (orally or IV) as needed. 

(2) Do not administer sedatives, narcotics, or tranquilizers. 

(3) Avoid the use of IV isoproterenol; it is highly dysrhythmogenic and carries a risk of myocardial injury 

resulting from ischemia or infarction. 

(4) Magnesium sulfate should be administered in moderate to severe, nonresponding acute asthma. The 

dosage is 2-3 g over 10 minutes and should be given while continuing inhalation therapy. 

(5) Administration of helium should be considered for patients with severe asthma. It decreases the work 

of breathing and, therefore, allows time for medications that have already been administered to work 

(thereby avoiding the need for intubation, which is a problem in some asthmatic patients). 

(6) Check serum electrolytes in adult patients who require >3 doses of ~-agonists, because these drugs 

can cause hypokalemia, hypomagnesemia, and hypophosphatemia. 

(7) Reserve antibiotics for patients with evidence of infection (fever, infiltrate on chest radiograph, evidence 

of sinusitis); respiratory tract infections that trigger exacerbations of asthma are usually viral in etiology. 

f. Noninvasive positive-pressure ventilation 

(1) May be used in patients with respiratory failure (or impending failure) who are not responsive to 

therapy but who have normal mentation and facial anatomy 

(2) Bi level positive-airway pressure is the modality of choice for patients who are able to cooperate. 

(a) Start with an inspiratory pressure of 8 cm H 2 

O and an expiratory pressure of 3 cm H 2 

O. 

(b) Increase settings based on pulse oximetry and arterial blood gas results. 

(c) Patients who do not improve over 30-60 minutes require intubation. 

g. Intubation with assisted ventilation 

(1) Mechanical ventilation in these patients can produce excessively high airway pressures and is 

associated with considerable morbidity and mortality. 

(2) The initial goal of mechanical ventilation in these patients is not necessarily to restore the pCO 2 

to 

normal; the respiratory rate and tidal volume required to do this can produce excessive peak inflation 

pressures - alveolar gas trapping and overdistention - high risk of barotrauma 

(3) These patients should be intentionally hypoventilated (a technique referred to as "controlled 

mechanical hypoventilation" or "permissive hypercapnia"). This technique increases the amount of 

time available for expiration and thereby minimizes air trapping. Suggested initial ventilator settings 

are tidal volume 6-8 ml/kg, respiratory rate 8-10 breaths per minute, and an inspiratory flow rate of 

80-1 00 L/min. The moderate hypercapnia that may occur with these ventilator settings is wel I tolerated 

and less dangerous than persistently high airway pressures. 

(4) Volume-cycled ventilators with higher peak pressures and flow rates should be used initially to deliver 

an adequate tidal volume. Plateau pressure is most important in minimizing barotrauma. Aim for 

plateau pressure of


(c) Succinylcholine is the paralytic of choice. Pancuronium is useful when muscle paralysis is 

required to facilitate ventilation; it does not cause histamine release. 

(d) Benzodiazepines may be used when sedation is needed (it will minimize emergence of 

hallucinations if ketamine was used); opiates induce histamine release and should be avoided. 

(e) 

Heliox should be considered for mechanically ventilated asthmatic patients with significant respiratory 

acidosis and markedly increased airway pressures; it lowers airway resistance and decreases the work 

of breathing. A helium-oxygen mixture of 80:20 or 70:30 (preferred) should be used. 

(7) If an asthmatic patient who is intubated becomes hypotensive, hypoxic with high plateau pressures 

alarming on the ventilator, detach the patient from the ventilator and help with exhalation because 

the patient may have breath stacking and increased his or her intrathoracic pressure causing 

decreased preload and hypotension. When returning the patient to the ventilator, ensure an l:E ratio 

of 1 :3 to allow adequate time for exhalation. 

h. Asthma in pregnancy 

(1) Incidence of asthma can increase in pregnancy: one-third of patients with asthma get worse with 

pregnancy, one-third have no change, and one-third may get better. 

(2) Respiratory alkalosis (pC0 2 

of 30-35) is a normal finding in pregnancy. Do not be concerned about 

respiratory compromise unless the pC0 2 

is >35. 

(3) Management of asthma in pregnant patients is similar to that in nonpregnant patients. The goal of 

treatment is to ensure adequate oxygenation for both mother and fetus while avoiding (whenever 

possible) any drugs that may pose a risk to the fetus. 

(a) All patients should receive supplemental oxygen (maternal hypoxia - impaired fetal oxygenation 

-s- fetal complications). Place the pregnant patient on her left side to minimize compression of the 

inferior vena cava. 

(b) Inhaled ~-agonists are the first-line drugs of choice. If parenteral therapy is required, terbutaline 

is preferred over epinephrine; the use of SC epinephrine early in pregnancy is associated with an 

increased incidence of congenital malformations, and in late pregnancy with premature labor 

(and should be avoided). 

(c) Corticosteroids are safe in pregnancy and should be administered in all but the mildest 

exacerbations. 

(d) Anticholinergic agents and theophylline may also be used. The clearance of theophylline in the 

third trimester, however, is reduced; serum levels must be carefully monitored. 

(e) Asthma medications that are appropriate for administration during pregnancy are also safe for use 

during lactation. 

X. CHRONICOBSTRUCTIVE PULMONARY DISEASE (COPD) 

A. Definition and pathophysiology 

1. Often referred to as a single disease but is actually a triad of three distinct disease processes 

a. Chronic bronchitis: defined clinically as a productive cough for 3 months over 2 consecutive years, 

characterized by airway hypersecretion and inflammation that causes a chronic productive cough for an 

extended period of time 

b. Emphysema: defined anatomically and characterized by irreversible enlargement of the air spaces distal to 

the bronchioles 

c. Asthma: characterized by airway hyperreactivity and inflammation. In most COPD patients, these three 

entities coexist, but the contribution each makes to pulmonary dysfunction varies from individual to 

individual. However, some COPD patients present with predominately emphysema (pink puffers) or 

chronic bronchitis (blue bloaters). 

2. Evolution 

a. COPD begins in the early twenties and is detected only by pulmonary function testing. Early pathologic 

changes are completely silent. 

b. As the disease progresses, signs and symptoms appear with a full-blown clinical picture as early as in the 

thirties in some patients. 

c. Chronic bronchitis ensues with a typical history of chronic, recurrent production of excessive mucus. 

d. Repeated inflammation leads to increased resistance or decreased caliber of the small bronchi and 

bronchioles. As alveolar hypoventilation subsequently occurs, hypoxemia and hypercarbia result. 

276


Ventilation-perfusion mismatching occurs (thus promoting hypoxemia), while increased physiologic dead 

space ventilation leads to alveolar hypoventilation, hypercarbia, and further hypoxemia. 

e. In addition to obstruction of the peripheral airways, destruction and coalescence of the alveolar cell 

structure (particularly in dominantly emphysematous disease) results in reduction of the total "matched" 

alveolar-capillary surface area for diffusion of gases (oxygen cannot get in, CO 2 

cannot get out). 

f. Later on, chronic and progressive airflow obstruction can lead to right-sided cardiac strain that results in 

pulmonary hypertension (loud P2 on auscultation) and cor pulmonale. 

3. Fourth most common cause of death 

B. Risk factors 

1. Smoking (most important factor) 

2. Exposure to second-hand smoke 

3. Environmental pollution 

4. Industrial or occupational exposure 

5. a 1 

-antitrypsin deficiency 

6. Cystic fibrosis 

7. Recurrent pulmonary infections 

C. Etiology of acute decompensation 

1. Superimposed respiratory infection (acute bronchitis, pneumonia): the most common precipitating factor of 

acute COPD exacerbation. Influenza and pneumococcal vaccination recommended. 

2. Changes in ambient temperature, humidity, or air pollution levels 

3. Noxious environmental exposures 

4. Spontaneous pneumothorax 

5. Pulmonary embolus 

6. Noncompliance with (or underdosing of) medications 

7. Inappropriate treatment (~-blockers, sedatives) 

8. Acute CHF 

9. Continued cigarette smoking 

D. Clinical presentation in combined disease 

1. Dyspnea is the most common complaint, followed by cough (occasionally with hemoptysis), chest tightness, 

and fatigue. A history of morning headache may be due to a rising PaC0 2 

(hypercapnia). 

2. Physical findings 

a. Tachypnea 

b. Prolonged expiratory phase 

c. Increased AP chest diameter ("barrel chested") 

d. Decreased breath sounds 

e. Wheezing, rales, and rhonchi 

f. Lip-pursing, accessory muscle use, cyanosis, and diaphoresis 

g. Pulsus paradoxus 

h. Distant heart sounds, a loud P 2 

, and right-sided CHF 

E. Clinical presentation when emphysema or bronchitis predominates 

1. Emphysema ("pink puffer") 

a. Dyspneic 

b. Thin, anxious, alert appearance 

c. Increased AP chest diameter (overinflation) 

d. Tachypneic and hypotensive 

e. Uses accessory muscles to breathe 

f. Decreased breath sounds, faint end-expiratory rhonchi, and hyperresonance on percussion 

2. Chronic bronchitis (blue bloater) 

a. Productive "wet" cough 

b. Stocky build, polycythemic, and cyanotic 

c. Normal chest diameter 

d. Little air-hunger 

277


e. Subxiphoid or retrosternal heave _,. right ventricular hypertrophy 

f. Signs of CHF (jugular venous distention, S 3 

or S 4 

gallop, murmur of tricuspid insufficiency, scattered rales and 

rhonchi, edema) 



a. Most useful in excluding other disease processes or complications (pneumonia, pneumothorax, atelectasis, 

effusions, cancer, CHF): > 15% of acutely decompensated COPD patients have treatable findings. 

b. Signs of hyperinflation are common (60% of patients) 

(1) Increased AP diameter 

(2) Increased retrosternal airspace 

(3) Increased parenchymal I ucency 

(4) Low and flattened diaphragm 

(5) Long and narrow cardiac silhouette (unless chronic bronchitis predominates the clinical picture, in 

which case, an enlarged right ventricle is seen on the lateral film) 

c. Bullae may also be seen. 


a. Provide information regarding the seriousness and acuteness of airway compromise in the COPD patient 

b. PaO 2 

is generally low. 

(1) Hypoxemia is common in these patients and worsens as the disease progresses, as well as with acute 

exacerbations. 

(2) It is due to ventilation-perfusion mismatching and can usually be corrected by increasing the amount 

of oxygen being inspired. 

c. PaCO 2 

(1) Reflects the adequacy of ventilation 

(2) Normocarbia may be present early on, but hypercarbia develops with disease progression and may 

worsen with acute exacerbations. 

(3) A rapid rise in the PaCO 2 

decreases the pH, whereas with a more gradual rise, the kidneys are able to 

compensate by retaining bicarbonate, which normalizes the pH. Therefore: 

(a) An increased PaCO 2 , a normal pH, and an increased bicarbonate level suggest chronic CO 2 

retention. 

(b) An increased PaCO 2 

, a decreased pH, and an increased bicarbonate level point to acute 

respiratory failure superimposed on chronic respiratory insufficiency. 

3. Pulmonary function tests 

a. More useful in patients with asthmatic bronchitis than with COPD in evaluating the degree of airway 

obstruction present and in monitoring the response to treatment. 

b. Either the FEV 1 

(or the PEFR) may be used; both provide a measurable index of airway obstruction. 

c. Because bronchospasm is not the major component of lung dysfunction in COPD patients, the response to 

treatment is less than that of asthmatics. 

4. ECG 

d. Lung volume measurements in COPD patients reveal an increase in the amount of dead space and a 

decrease in the vital capacity; clinical signs develop when the vital capacity drops 50%. 

a. Detects ischemic disease or dysrhythmias associated with COPD (especially multifocal atrial tachycardia 

and atrial fibrillation, both of which are common and should be assumed to be secondary to CHF) and may 

also demonstrate evidence of COPD or cor pulmonale 

(1) P pulmonale (peaked P waves in II, Ill, and AVF) _,. very suggestive of COPD 

(2) Low voltage, right axis deviation and poor R wave progression _,. also very suggestive of COPD 

(3) Criteria for right ventricular hypertrophy_,. very suggestive of cor pulmonale 

b. Troponin elevation is relatively common in COPD patients with acute exacerbations and is not usually 

associated with a codiagnosis of acute coronary syndrome. 

G. Management 

1. Directed toward improving oxygenation and respiratory function 

2. Oxygen is the most important therapy. 

278


a. COPD patients who chronically retain CO 2 depend on their hypoxic respiratory drive to breathe. Raising 

the p0 2 

too quickly in these patients depresses the respiratory center and shuts off this drive. Concern over 

suppressing this drive must be balanced against the need to increase the p0 2 

to a satisfactory level. 

b. To minimize the risk, begin treatment using low concentrations of oxygen and a controlled delivery system 

such as a Venturi mask. Start with an Fi0 2 

of 24%-28%, and increase it as needed. The goal is to raise the 

p0 2 

to >60 and the saturation to >88%. 

c. Continuous pulse oximetry (supplemented with arterial blood gases when there is concern that the pC0 2 

is rising) should be used to monitor response to treatment and guide adjustments in the Fi0 2 

; continuous 

capnometry can also be useful. 

d. Assurance of adequate oxygenation should take precedence over concern about suppressing the hypoxic 

respiratory drive; if a high concentration of oxygen is needed, it should be administered. 

e. Long-term 0 2 

therapy for patients with PaO 2 


e. Dosage guidelines for IV aminophylline 

(1) Loading dosage: 5 mg/kg (ideal body weight) over 10-15 minutes 

(2) Maintenance dosage: based on ideal body weight and associated conditions 

(a) Adult smokers


c. Toxic inhalation (smoke, corrosives, paraquat, oxygen) 

d. Liquid aspiration (gastric contents, fresh- or saltwater) 

e. Pneumonia (bacterial or viral) 

f. Emboli (pulmonary, fat, air, amniotic fluid) 

g. Major trauma (burns, pulmonary contusion, multiple injuries) 

h. Transfusion-related acute lung injury 

1. Pancreatitis 

j. Acute neurologic crisis (head injury, subarachnoid hemorrhage, stroke, brain tumor) 

k. Cancer therapy (tumor lysis, radiation) 


Inflammatory 

response 

Fluid flux into 

the lung+ t lung 

compliance 

This process is frequently 

irreversible if the inciting 

event is not controlled. 

Microvascular 

membrane damage 

t permeability 

of the microvascular 

membrane 

Pathophysiology of ARDS 

1. The inflammatory response results from activation of enzyme systems (which is caused by the inciting event) 

and involves a variety of biochemical mediators that typify an inflammatory response. 

2. In many disorders associated with permeability pulmonary edema, the activation of enzyme cascades leads 

to microvascular membrane damage and increased permeability of the microvascular membrane. There are 

primarily two enzyme cascades that are activated: 

a. The complement system is triggered by: 

(1) Antigen-antibody complexes (the classic pathway) 

(2) Endotoxins 

(3) Exposure to cell surfaces by bacteria or fungi 

(4) Complex polysaccharides 

b. The coagulation pathways are activated when collagen in exposed basement membrane is exposed to 

plasma. This causes activation of Hageman factor (factor XII) which, in turn, activates components of the 

coagulation system, the fibrinolytic system, and the kinin generation system. 

3. In addition, metabolism of arachidonic acid through major biochemical pathways leads to the release of a 

variety of mediators (including a host of leukotrienes and prostaglandins) that contribute to further endothelial 

and alveolar injury. 

4. Neutropenic patients may also develop permeability pulmonary edema. Injury to the pulmonary endothelium 

results from one of the following: 

a. Direct effects of bacterial endotoxin and complement 

b. Oxygen toxicity 

c. Release of prostaglandins and leukotrienes from alveolar macrophages 

5. Once the microvascular membrane is damaged and its permeability is increased, it is no longer an effective 

barrier to protein flux. Any subsequent increase in hydrostatic pressure then accelerates fluid flux into the lung. 

6. The mechanical properties of the lung are also adversely affected: surfactant is reduced or inactivated___,. 

collapse of alveoli___,. stiff lung (which requires greater pressure to inflate it)___,. t lung compliance 

281



1. Diagnostic criteria 

a. Symptom onset is within 1 week of the clinical insult. 

b. Chest radiograph: diffuse bilateral interstitial and alveolar infiltrates with a normal-sized heart consistent 

with pulmonary edema (noncardiogenic pulmonary edema) 

c. Respiratory failure not fully attributed to heart failure or volume overload. 

d. Oxygen impairment as measured by Pa0/Fi0 2 

with PEEP setting >5. 

(1) Mild: PaO/Fi0 2 

>200 but 100 but


B. Clinical importance 

1. Significant morbidity and mortality are associated with pulmonary embolism in the United States, and 

progressive right ventricular failure is the most common cause of death in these patients (usually secondary to 

massive embolization). 

2. The diagnosis is missed antemortem in up to 70% of cases (>400 1 

000/year); one-third of these patients die, 

while the other two-thirds are at risk of recurrent pulmonary embolism and development of pulmonary 

hypertension. 

3. A significant percentage of patients with DVT develop pulmonary embolism, and many of these cases go 

unrecognized. The so-called 11 clinically silent 11 

calf vein thrombus can be deadly. In fact, clinically significant 

embolization from calf DVT is not uncommon. 


1. All known risk factors for pulmonary embolism (and DVT) have their basis in Virchow's triad of venostasis 1 

hypercoagulability, and vessel wall injury or abnormality. (Most common risk factors in patients with proven 

pulmonary embolism are indicated below with an asterisk.) 

a. Current DVT* (high risk of occult cancer) 

b. Obesity* 

c. Prior DVT or pulmonary embolism* 

d. Immobility (including travel) or prolonged bedrest* 

e. Recent trauma (including burns) or surgery (especially orthopedic)* 

f. Carcinoma* or chemotherapy 

g. Autoimmune (eg 1 

systemic lupus erythematosus) and immune (eg 1 

AIDS) disorders 

h. MI/CHF/COPD/stroke 

i. Estrogen therapy 

j. Hypercoagulable settings (use of oral contraceptives, pregnancy, postpartum period) 

k. Inherited abnormalities of coagulation or fibrinolysis 

I. Indwelling central venous catheter 

m. IV drug abuse 

n. Polycythemia vera 

2. Most patients (c:90%) with thromboembolic disease have at least one of these risk factors, although some 

(those with cancer, inherited abnormalities of coagulation) may not be apparent at the time of presentation. 

Furthermore, the risk represented by these factors is additive: the greater the number of risk factors present, 

the greater the risk of pulmonary embolism. Thus, knowledge of whether or not a patient has risk factors for 

pulmonary embolism can be used to increase or decrease clinical suspicion of the diagnosis. For example: A 

patient with at least one common risk factor or two or more other risk factors should be considered to have a 

moderate to high risk of having a pulmonary embolism. 


1. Presenting signs and symptoms of acute pulmonary embolism are determined by the extent of pulmonary 

vascular occlusion (massive versus submassive) and the patient's baseline cardiopulmonary status. 

2. History 

a. Dyspnea (the most common symptom by far) 

b. Pleuritic chest pain 

c. Apprehension 

d. Cough 

e. Hemoptysis 

f. Sweating 

g. Nonpleuritic chest pain 

h. Syncope (more common with massive than submassive emboli) 


a. Tachypnea 

b. Rales 

c. Accentuated S 2 

d. Tachycardia (heart rate > 100 beats per minute) 

e. Diaphoresis 

283


f. 5 3 

or 5 4 

gallop 

g. Clinically evident thrombophlebitis 

h. Decreased breath sounds 

i. Lower-extremity edema 

j. Cardiac murmur 

k. Cyanosis 

I. Hypotension (more common with massive emboli) 

4. Dyspnea, pleuritic chest pain, or tachypnea is present in 95% of patients; if all three of these findings are 

absent, pulmonary embolism is unlikely (especially if there are no risk factors). The "classic triad" of dyspnea, 

pleuritic chest pain, and hemoptysis is uncommon (seen in 100 beats per minute 

Immobilization (or surgery) within 4 weeks 

History of previous DVT or pulmonary embolism 

History of hemoptysis 

History of malignancy (treatment within 6 months or palliative) 

3.0 

3.0 

1.5 

1.5 

1.5 

1.0 

1.0 

Total score interpretation 

>6 = high pretest probability (66.7% risk) 

2-6 = moderate pretest probability (20.5% risk) 


(3) The A-a gradient is abnormally increased in 95% of patients with pulmonary embolism. 

(4) The finding of an increased A-a gradient increases the probability a pulmonary embolism is present, 

but a normal gradient does not exclude the diagnosis; therefore, it should not be used as a "screening" 

test for pulmonary embolism. 


4. ECG 

a. Useful in excluding other disease processes and also needed to interpret the ventilation/perfusion scan 

b. Abnormal in >80% of patients with pulmonary embolism, but the findings are neither sensitive nor specific 

c. Suspected disease processes in pulmonary embolism 

(1) Atelectasis or pulmonary parenchymal abnormalities (consolidation or patchy infiltrates) 

(2) Elevated hemidiaphragm 

(3) Pleural effusion 

(4) Hampton's hump: a triangular pleural-based density with a rounded apex that points toward the 

hilum 

(5) Westermark sign: dilatation of pulmonary vessels proximal to the embolus in association with 

regional oligemia distally 

d. Most common radiographic abnormalities are atelectasis, pulmonary parenchymal abnormalities, an 

elevated hemidiaphragm, and small unexplained pleural effusions. 

e. Hampton hump and Westermark sign are rare but, when present, are very suggestive of pulmonary 

embolism. 

f. The presence of a normal chest radiograph (present in


Therefore, V/Q scans are classified as normal or near-normal; indeterminate (most common reading); 

or low, intermediate, or high probability of pulmonary embolism based on the number and size ofV/Q 

mismatches present. 

d. The V/Q scan result should be interpreted in the context of clinical suspicion of pulmonary embolism, 

because it increases the predictive value of this test (especially if there is a level of clinical suspicion of 

pulmonary embolism before obtaining the V/Q scan results). 

e. In patients with low to moderate pretest probability, a normal V/Q scan excludes clinically significant 

pulmonary embolism 98% of the time. A normal perfusion scan also decreases the probability that an 

angiographically provable pulmonary embolism is present, at least to the point at which further evaluation 

is indicated only in the presence of high clinical suspicion. 

f. An indeterminate or nondiagnostic (low or intermediate probability) V/Q scan neither confirms nor 

excludes the diagnosis of pulmonary embolism and should not be taken as a diagnostic end point. 

g. A high probability scan in a patient with high pretest clinical probability for pulmonary embolism is 

considered confirmatory and should result in treatment; no further evaluation is required. 

h. Advantages 

(1) Relatively noninvasive 

(2) Can be performed in critically ill patients 

(3) Safer for pregnant patients (in whom, after duplex Doppler, it is considered the diagnostic test of 

choice; it is less invasive and has less fetal exposure than angiography) 

i. Disadvantages 

(1) Nondiagnostic most of the time 

(2) Less useful in patients with lung disease (or abnormal chest radiograph) 

(3) Takes time to perform 

(4) Requires isotope injection 

2. CT angiography (CTA) 

a. Most extensively studied new confirmatory test with a good overall test performance that is equal to or 

slightly better than that of the V/Q scan. However, a CTA scan read as negative for pulmonary embolism 

does not have as high a negative predictive value as a V IQ scan read as normal; therefore, a negative CTA 

in a patient with high probability for pulmonary embolism requires pulmonary angiography. 

b. In settings in which a V/Q scan reading is indeterminate (or likely to be so in patients with pulmonary 

pathology (eg, COPD, pneumonia, etc), a CTA with contrast is the procedure of choice. 

c. An intraluminal filling defect or vascular occlusion characterizes a positive result; the sensitivity and 

specificity of CTA are higher for pulmonary embolism in the central vessels than in the peripheral vessels 

(95% sensitivity for segmental or large pulmonary embolism, 75% sensitivity for subsegmental pulmonary 

embolism). Newer generation CTA (thin collimation spiral CT) may increase diagnostic accuracy. 

d. Advantages overV/Q scanning 

(1) Can be performed within minutes 

(2) Marked reduction of indeterminate readings; useful for its ability to identify a convincing diagnostic 

alternative to pulmonary embolism 

e. Disadvantages 

(1) Cost 

(2) Need for patient transport 

(3) Use of iodinated contrast material 

(4) Radiation exposure 

3. Pulmonary angiography 

a. Gold standard for diagnosing pulmonary embolism; although false-positive and false-negative results do 

occur occasionally, angiography offers the best available combination of sensitivity and specificity for 

diagnosing thromboembolic disease. 

(1) Current techniques are unable to detect obstruction in small, subsegmental arterial branches, so many 

small peripheral emboli may be missed. 

(2) Augmentation techniques (subselective injections, magnification, radiography, balloon occlusion 

angiography) are able to demonstrate emboli as small as 1 mm in diameter. 

(3) Standard angiography (without augmentation techniques) may completely miss emboli as large as 2.5 

mm in diameter. 

286


b. A positive study demonstrates an embolus obstructing a vessel (a dye "cut-off" sign) or an intraluminal 

filling defect (in more than one projection). 

c. Advantage: currently the most reliable test available for diagnosing pulmonary embolism 

d. Disadvantages 

(1) Invasive 

(2) Not universally available 

(3) Mortality of 0.1 %-0.5% and morbidity of 1 %-5% 

(4) Relatively contraindicated in patients with pulmonary hypertension 

e. Complications 

(1) More common in older patients with underlying cardiopulmonary disease 

(2) Include anaphylactoid reactions, dysrhythmias, cardiac arrest, endocardial injury, and perforation 

4. Color-flow duplex ultrasonography 

a. In patients with nondiagnostic V/Q scans, this is the next study of choice in excluding pulmonary 

embolism, because a lower-extremity DVT confirmed by duplex ultrasound is considered de facto evidence 

that pulmonary embolism also exists. 

b. Demonstration of a DVT in the setting of suspected pulmonary embolism is an indication to start 

appropriate therapy. 

c. Negative lower-extremity vascular studies cannot eliminate the possibility of pulmonary embolism and, 

therefore, do not change the clinical management. A single negative lower-extremity ultrasound duplex 

study should not be used to exclude pulmonary embolism in patients with moderate to high pretest 

probability and a nondiagnostic V/Q scan. (ACEP Clinical Policy). 

d. In pregnant patients, duplex Doppler is the initial diagnostic study of choice for the evaluation of 

pulmonary embolism, because it is the least invasive. In these patients, duplex Doppler is performed first; if 

positive, treatment is started, and if negative, then a V/Q or spiral CTA scan is performed. 

5. Echocardiography 

a. Should be considered for patients with shock of uncertain cause in whom the diagnosis of pulmonary 

embolism is suspected but who is not stable enough for other diagnostic tests 

b. Right ventricular dysfunction in the absence of an acute Ml or pericardia! tamponade supports the 

diagnosis of right ventricular failure secondary to pulmonary embolism. 

c. Bedside techniques 

(1) Transthoracic echocardiography rarely provides image resolution adequate enough to visualize the 

inferior vena cava or cardiac chambers, but it can detect right ventricular strain. 

(2) Transesophageal echocardiography has more consistent cardiac imaging, but it is invasive and requires 

specialty consult and equipment. 

6. Point-of-care ultrasound 

a. Useful in unstable patients when comprehensive echocardiography unavailable or delayed 

b. Pseudonormalization of chamber sizes (1 :1 ratio); loss of normal right ventricular to left ventricular ratio of 

0.6:1 .0 

c. McConnell sign: akinesia of mid free wall with normal movement of cardiac apex 

d. Right ventricular thrombus may be seen in 4% of patients with pulmonary embolism. 

G. Diagnostic approach 

1. The clinical presentation, history, risk factors, and physical examination findings lead to clinical suspicion. 

2. Diagnostic evaluation proceeds to include an ECG and chest radiograph, which may indicate another diagnosis 

or provide additional evidence in support of the diagnosis of pulmonary embolism. 

3. If these tests do not reveal another diagnosis (pneumothorax, Ml) that explains the patient's signs and 

symptoms, then the patient's pretest probability for pulmonary embolism should be determined and a screening 

test performed. 

4. Further management decisions should incorporate assessment of the patient's pretest probability of having a 

pulmonary embolism and the test results (screening and diagnostic). 

5. If CTA reveals pulmonary embolism, the patient should be treated. 

6. If CTA is negative and the study was technically adequate, another diagnosis should be considered. 

287


Clinical suspicion for 

pulmonary embolism 

t " t 

Low Intermediate High 

( 2% but 40%) 

i 

I 

No further testing for 


Consider alternative 

diagnosis 

D-dimer 

t 

I 

♦ 

Negative 

• 

Consider 

alternative diagnosis 

Positive 

I - 

t 

Allergy to IV dye*, increased 

creatinine, pregnant 

• 

I 

• 

Yes 

No 

+ + 

V/Q scan 

CT angiography 

I 

I 

♦ ♦ t 

• 

t 

Normal 

Low or 

intermediate 

High Positive Negative 

• • • • 

t 

Consider 

alternative 

diagnosis 

CT angiography 

or 

Treat 

presumptively 

and admit 

Consider 

Treat Treat alternative 

diagnosis 

*Premedication may be necessary in some clinical scenarios to obtain CT pulmonary embolism. 

Evaluation of Pulmonary Embolism 

288


H. Management 

1 . Objectives 

a. Short term: prevent thromboembolic propagation and additional embolic events and eliminate 

thromboemboli from the pulmonary vasculature 

b. Long term: prevent or minimize recurrence of pulmonary embolism, chronic venous insufficiency, and 

development of chronic pulmonary hypertension 

2. Basic supportive measures 

a. Assess and stabilize the ABCs: establish an IV of normal saline or lactated Ringer's, provide supplemental 

oxygen, place the patient on a cardiac monitor, and check a rhythm strip. 

b. If patients are hypotensive, any fluid resuscitation should be performed with extreme care. Volume loading 

can worsen right ventricular function and can actually worsen blood pressure. If blood pressure or clinical 

status worsens with fluids, immediately switch to vasopressors (eg, norepinephrine, dopamine) for blood 

pressure support. 

3. Anticoagulation with IV unfractionated heparin or low-molecular-weight heparin (LMWH) given SC 

a. The cornerstone of therapy for pulmonary embolism, heparinization should be started as soon as the 

diagnosis is strongly suspected (unless contraindications exist); do not wait for confirmatory test results. 

b. The decision to use unfractionated heparin or a LMWH is an arbitrary one, because both appear to be 

equally effective and safe for the initial treatment of submassive pulmonary embolism. The choice is often 

made by the admitting/consulting cardiologist. 

(1) Because pulmonary embolism is not (generally) treated on an outpatient basis, some cardiologists still 

prefer IV unfractionated heparin, because the anticoagulation effect can be monitored more accurately 

and the cost is less than that of an LMWH. 

(2) Others prefer using an LMWH given SC until the patient can be anticoagulated on warfarin. Again, 

better bioavailability, fewer blood draws for laboratory studies, and no need for a continuous infusion 

pump are reasons for this choice. 

c. Heparin prevents propagation of the clot and decreases the risk of further embolic events but does not 

dissolve clots that are already present. It works by binding to (and enhancing) the activity of antithrombin 

Ill, a naturally occurring substance that prevents thrombosis by inhibiting activated coagulation factors of 

the intrinsic and common pathways, particularly thrombin and Factor Xa. 

d. If unfractionated heparin is the agent selected, administer a bolus of 100 units/kg IV (7,000 units/70- 

kg patient) followed by a continuous infusion of 18 units/kg/hr. Check the partial thromboplastin time 

(PTT) in 6 hours, and adjust the infusion rate as needed to maintain it at 1.5-2.5 times the control value. 

This weight-adjusted heparin regimen minimizes the time needed to achieve a therapeutic PTT without 

increasing the likelihood of bleeding complications. 

e. Enoxaparin is the LMWH of choice and is rapidly becoming the therapeutic method preferred by many 

clinicians; the dosage is 1 mg/kg SC every 12 hours or 1 .5 mg/kg/day SC. 

f. Both unfractionated heparin and LMWHs are safe to use in pregnancy, because neither crosses the 

placenta. Do not give warfarin in pregnancy! 

g. Complications 

(1) Hemorrhage can be reversed by stopping the infusion and administering protamine sulfate (1 mg 

neutralizes 100 units of heparin but not enoxaparin or other LMWHs). 

(2) Thrombocytopenia requires discontinuation of all forms of heparin. It is immune-mediated and 

generally develops 7-1 0 days after therapy has started. 

h. LMWHs have a number of advantages over unfractionated heparin; when these agents become more 

widely used for treatment of pulmonary embolism and DVT, they are likely to replace current anticoagulant 

therapy with unfractionated heparin. 

4. Thrombolytic (fibrinolytic) therapy 

a. Current indications (ACEP Clinical Policy: Critical Issues in the Evaluation and Management of Adult 

Patients Presenting with Suspected Pulmonary Embolism) 

(1) Hemodynamic instability in patients with confirmed pulmonary embolism 

(2) Hemodynamic instability in patients with a high clinical index of suspicion (especially with right 

ventricular dysfunction on bedside echo) 

(3) Right ventricular dysfunction on echo in hemodynamically stable patients with confirmed pulmonary 

embolism 

b. Thrombolytic agents work by directly lysing clots. 

289


c. Before administering these agents, the diagnosis of pulmonary embolism should ideally be established with 

a high degree of certainty. However, if there is a high suspicion of pulmonary embolism in a patient who is 

hemodynamically compromised, thrombolytic therapy may be administered before diagnostic testing. 

d. Administration of these thrombolytic agents should be followed immediately by full-dose heparin 

anticoagulation (There is no increase in bleeding complications when heparin is administered concurrently 

with tissue plasminogen activator.) 

e. Advantages: in contrast to heparin, thrombolytic therapy prevents the postphlebitic syndrome, reduces the 

risk of recurrent pulmonary embolism/DVT, restores normal myocardial and valvular function, normalizes 

pulmonary vascular resistance and pulmonary arterial pressure, improves long-term exercise capacity, and 

normalizes pulmonary capillary volume and pulmonary gas diffusion. There is also some evidence that it 

does decrease mortality but this has not yet been clearly demonstrated. 

f. Contraindications: identical to those for acute Ml (see reperfusion therapy in Ml, pages 45-46) 

g. Complications 

(1) Thrombolytic therapy and anticoagulant therapy produce a similar incidence of systemic bleeding 

complications. However, the risk of hemorrhage increases directly with the duration of infusion of 

the thrombolytic agent: urokinase and streptokinase are usually infused over a 12-24 hour period, 

whereas the usual protocol for TPA is a 2-hour infusion. 

(2) If serious bleeding complications occur, the thrombolytic infusion should be discontinued, and 

aminocaproic acid should be administered along with transfusions of fresh frozen plasma and 

cryoprecipitate. 

h. Thrombolytic agents approved for treatment of pulmonary embolism include streptokinase and TPA; TPA is 

preferred because it significantly improves hemodynamic parameters in


2. Etiology of central cyanosis (decreased arterial oxygen saturation) 

a. Decreased atmospheric pressure (high altitude) 

b. Impaired pulmonary function 

(1) Alveolar hypoventilation 

(2) Disparities between pulmonary ventilation and perfusion 

(3) Impaired oxygen diffusion 

c. Anatomic shunts 

(1) Certain types of congenital heart disease 

(2) Pulmonary AV fistulas 

(3) Multiple small intrapulmonary shunts 

d. Hemoglobin with low affinity for oxygen 

e. Hemoglobin abnormalities (may be drug-induced) 

(1) Methemoglobinemia (acquired and hereditary) 

(2) Sulfhemoglobinemia (acquired) 

(3) Both may result from the use of phenacetin, acetanilid, aniline, and sulfonamides. 

3. Etiology of peripheral cyanosis (normally saturated arterial blood with increased oxygen extraction) 

a. Reduced cardiac output (eg, CHF) 

b. Cold exposure vasoconstriction (eg, frostbite, severe hypothermia) 

c. Redistribution of blood flow from extremities (eg, shock states) 

d. Arterial or venous obstruction (eg, peripheral vascular disease) 

e. Polycythemia 

291

THORACIC AND RESPIRATORY DISORDERS: PRACTICE CLINICAL SCENARIOS 

THORACIC AND RESPIRATORY DISORDERS: 


Answers immediately follow practice clinical scenarios. 

Scenario A 

Presentation: An elderly male patient presents in respiratory distress with an audible wheeze. He has a 

significant smoking history, appears malnourished, and has difficulty speaking in complete sentences. He 

complains of shortness of breath that has been present for several days. The patient has noted a change in 

the character of his sputum. He does not have a fever. 

Physical examination: The patient appears tachypneic, cyanotic, and is showing some use of accessory 

muscles of respiration. Lung examination reveals grossly diminished air movement throughout with 

expiratory wheezing. There is no peripheral edema. 


Scenario B 

Presentation: A patient presents with symptoms of urinary tract infection/pyelonephritis. He has not been 

feeling well, with intermittent flank pain and nausea, for 3 days. There is no history of CHF, liver disease, 

or malnutrition. 

Physical examination: Vital signs are temperature 102°F (39°C), blood pressure 110/64 mmHg, heart rate 

130 beats per minute, respiratory rate 22 breaths per minute, and SpO 2 

95%. The patient is ill appearing. 

Chest examination reveals scattered, bilateral rales. The abdomen is soft. There is mild left costoverterbral 

angle (flank) tenderness. There is no lower extremity edema. 


Scenario C 

Presentation: An adult patient presents with chest pain and shortness of breath that began after landing 

from an 8-hour plane flight. The chest pain is pleuritic in nature. 

Physical examination: The patient is no distress. Lung examination is clear. One leg appears swollen 

compared with the other. Vital signs show tachycardia and tachypnea. 


Scenario D 

Presentation: A patient presents with a gunshot wound to the left side of the chest. 

Physical examination: The heart rate is 125 beats per minute, blood pressure is 80/40 mm Hg, and the 

respiratory rate is 22 breaths per minute with 0 2 

saturations 85% on nonrebreather. The patient appears 

uncomfortable but is answering questions. Jugular venous distention is noted on neck examination. 

Cardiovascular examination reveals tachycardia, regular rhythm, and no murmurs. Pulmonary examination 

reveals decreased breath sounds on the left side. 

What is the diagnosis and next step in management? 

292


Scenario E 

Presentation: A patient presents with fever, pleuritic chest pain, and cough. 

Physical examination: The patient is ill appearing with a heart rate of 110 beats per minute, blood pressure 

of 110/72 mm Hg, and respiratory rate of 24 breaths per minute with 0 2 

saturations 90% on 1 L by nasal 

cannula. Pulmonary examination reveals decreased breath sounds on the right side with dullness on 

percussion. A chest radiograph shows loss of the costophrenic angle with a moderate pleural effusion. A 

sample obtained from thoracentesis has a pH of 7.05 with glucose of 55 mg/dL. 

What is the diagnosis and next step in management? 

Scenario F 

Presentation: A white woman with a history of asthma presents with shortness of breath. She complains of 

wheezing and cough. 

Physical examination: The patient appears in respiratory distress, speaking in 1 or 2 word sentences, with 

a respiratory rate of 26 breaths per minute and minimal air movement on pulmonary examination. You 

note intercostal retractions. The patient is intubated and given f:1-agonists through the ventilator. Less than 

an hour later, you are called into the room because the patient's heart rate is 130 beats per minute and her 

blood pressure is 82/55 mmHg. The ventilator shows decreased tidal volumes with high plateau pressures 

alarming. 

What is the next step in management? 

Scenario G 

Presentation: An immigrant from Asia presents with cough, fever, night sweats, and fatigue for 2-3 weeks. 

She is visiting family here in the United States. 

Physical examination: The patient appears cachetic. Temperature is 37.9°(, heart rate is 95 beats per 

minute, and respiratory rate is 20 breaths per minute with 0 2 

saturations of 95% on room air. Pulmonary 

examination reveals decreased breath sounds in the right upper lobe. A chest radiograph demonstrates a 

cavitary lesion in the upper lobe of the lung. 


Scenario H 

Presentation: A patient presents with acute onset of dyspnea. He states the symptoms started suddenly, 

and he denies any fever, chills, or chest pain although he does admit to a nonproductive cough. It is 5 days 

after he underwent surgery for a total hip replacement. 

Physical examination: The patient's blood pressure is 80/50 mm Hg, heart rate is 130 beats per minute, 

and respiratory rate is 28 breaths per minute with 0 2 

saturation on 15 L by nonrebreather of 88%. 

Cardiovascular examination demonstrates tachycardia, normal rhythm, and no murmurs. Pulmonary 

examination demonstrates diminished breath sounds in the bases with no crackles and no rhonchi. 

What is the next step in management? 

293



Scenario A 

Diagnosis: COPD exacerbation 

Management: Begin nebulized albuterol, steroid therapy, and antibiotic coverage for COPD exacerbation. 

Influenza testing is appropriate when in season. Chest radiograph will show evidence of hyperinflation 

and flattened diaphragms. Consider venous blood gas testing to evaluate for hypercarbia. Hypoxia will be 

manifest by increased oxygen requirement. Monitor the patient for improvement or decline in respiratory 

status. Noninvasive positive-pressure ventilation may be necessary to assist with work of breathing for 

severe exacerbations. Patients may be discharged if there is immediate clinical improvement in symptoms, 

and if they appear clinically well and can ambulate safely without evidence of tachypnea or hypoxia. 

Patients with persistent distress, continued wheezing, or who need frequent nebulized treatments, 

increased oxygen requirements, or Bi PAP should be admitted to an appropriate level of care. 

Scenario B 

Diagnosis: severe sepsis with evidence of acute lung injury 

Management: The patient has acute lung injury from severe sepsis due to pyelonephritis. Chest 

radiograph may be suspicious for volume overload with bilateral infiltrates; however, this is related to 

pulmonary capillary leak related to sepsis. The patient is in need of early antibiotic and fluid resuscitation. 

Noncardiogenic pulmonary edema should not prevent fluid resuscitation. Arterial blood gases can be 

helpful to determine the degree of acute lung injury. Increased oxygen requirement may require intubation. 

Intubated patients should be treated with lung protective ventilation of 6 ml/kg ideal body weight based 

on ARDSNet data. 

Scenario C 

Diagnosis: pulmonary embolism 

Management: There is high clinical suspicion of pulmonary embolism based on history. Empiric 

anticoagulation may be appropriate for clinically unstable patients. The diagnosis of pulmonary embolism 

is confirmed by CT study. Hypotensive patients or patients with right ventricular strain may benefit from 

thrombolysis. Point-of-care ultrasound in the emergency department or comprehensive echocardiography 

may be helpful. The decision for thrombolysis can be made in conjunction with appropriate consultants 

(pulmonary, cardiology, radiology, surgery, etc), depending on your institution's practice patterns. 

Scenario D 

Diagnosis: tension pneumothorax 

Management: This patient has symptoms and signs consistent with a tension pneumothorax and requires a 

needle decompression. 

A patient that presents in extremis (tachycardia, hypotension, jugular venous distention) with penetrating 

trauma to the left side of the chest is concerning for either a tension pneumothorax or pericardia! 

tamponade. Auscultation of breath sounds can differentiate between these two diagnoses. If breath sounds 

are absent or diminished on one side, the patient has a tension pneumothorax, and needle decompression 

with a 14-gauge needle in the second intercostal space on the affected side should be performed. If breath 

sounds are bilateral and symmetric, the patient has cardiac tamponade, and pericardiocentesis should be 

performed. 

294


Scenario E 

Diagnosis: empyema 

Management: A sample obtained from diagnostic thoracentesis with a pH of

296 

NOTES

TRAUMATIC DISORDERS 


General Information ................................................................................................................................................. 302 

General Approach to the Trauma Patient. .................................................................................................................. 303 

Hemorrhagic Shock .................................................................................................................................................. 307 

Common Injuries by Anatomic Location ................................................................................................................... 307 

Traumatic Brain Injury (Head Injury) ................................................................................................................... 307 

Overview .................................................................................................................................................... 307 

Specific Types of Head Injuries .................................................................................................................... 309 

Diffuse Brain Injuries ......................................................................................................................... 309 

Focal Brain Lesions ............................................................................................................................ 310 

Cerebral Edema ................................................................................................................................. 311 

Herniation Syndromes ....................................................................................................................... 312 

Skull Fractures ................................................................................................................................... 312 

Complications of Head Injuries ................................................................................................................... 313 

Management ............................................................................................................................................... 314 

Facial lnjuries ..................................................................................................................................................... 315 

Adult Spinal Trauma ........................................................................................................................................... 316 

Spinal Cord Injury ....................................................................................................................................... 316 

Vertebral Spine Trauma ............................................................................................................................... 320 

Pediatric Vertebral and Spinal Cord Injuries ........................................................................................................ 322 

Thoracic Trauma ................................................................................................................................................. 322 

Abdominal Injuries ............................................................................................................................................. 326 

Pelvic and Extremity Injuries ............................................................................................................................... 329 

Unique Situations ...................................................................................................................................................... 329 

Electrical Injury .................................................................................................................................................. 329 

Rhabdomyolysis ................................................................................................................................................. 331 

Thermal Burns .................................................................................................................................................... 331 

Trauma in Pregnancy .......................................................................................................................................... 332 

Penetrating Trauma ............................................................................................................................................. 334 

Blast Injuries ....................................................................................................................................................... 335 

Additional Pearls ................................................................................................................................................ 336 

297

TRAUMATIC DISORDERS: SELF-ASSESSMENT QUESTIONS 


1. The smallest amount of blood loss that consistently produces a decrease in the systolic blood pressure in adults is: 

(a) 

Loss 40% of blood volume 

2. When evaluating a child who has sustained blunt trauma as a result of a motor vehicle collision, which of the 

following signs would most likely be the earliest and most reliable indication of hemorrhagic shock? 

(a) 

Altered mental status 

(b) Hypotension 

(c) Tachypnea 

(d) Tachycardia 

(e) Hypoxemia 

3. The leading cause of death and disability in trauma victims is: 

(a) 

Head injury 

(b) Spinal cord injury 

(c) Abdominal injury 

(d) Thoracic injury 

4. Which of the following statements regarding cardiac tamponade is inaccurate? 

(a) It is most commonly caused by blunt chest trauma. 

(b) Clinical findings include hypotension, decreased pulse pressure, jugular venous distention, pulsus paradoxus, 

and muffled heart tones. 

(c) Initial therapy may be IV fluids and pericardiocentesis. 

(d) It can manifest as pulseless electrical activity. 

5. A patient with chest trauma is hypotensive on presentation and complains of shortness of breath. Examination 

reveals jugular venous distention, tracheal deviation, and decreased breath sounds associated with hyperresonance 

to percussion on one side of the chest. In addition to providing oxygen, starting IV lines, and placing the patient on 

a cardiac monitor, what is the most appropriate immediate intervention? 

(a) 

Pericardiocentesis 

(b) Tube thoracostomy 

(c) Intubation 

(d) Needle thoracostomy 

6. Of patients with the following acute traumatic injuries, which is most likely to survive at the scene of injury and 

present to the emergency department with signs of life? 

(a) Complete airway obstruction 

(b) Atlanta-axial dissociation 

(c) Liver laceration 

(d) Aortic rupture 

(e) 

Cardiac laceration 

7. The most common abdominal organ injured in blunt trauma is: 

(a) Spleen 

(b) Liver 

(c) 

Pancreas 

(d) Kidney 

8. Of the following potential therapies, which is the most useful in treatment of myoglobinuria/rhabdomyolysis? 

(a) Aggressive IV hydration 

(b) IV mannitol 

(c) Alkalinization of the urine 

(d) Loop diuretics 

298


9. All of the following chest radiograph findings are consistent with the diagnosis of traumatic rupture of the aorta 

except: 

(a) Widening of the superior mediastinum 

(b) Apical pleural cap 

(c) Deviation of the trachea to the right 

(d) Elevation of the left mainstem bronchus 

10. Which of the following techniques provides the best assessment of retroperitoneal organs (eg, pancreas, duodenum)? 

(a) 

Physical examination 

(b) Diagnostic peritoneal lavage 

(c) CT of the abdomen and pelvis 

(d) FAST examination 

11. Although all of the following techniques should be used when available, the most reliable method of confirming 

endotracheal tube position is by: 

(a) Listening over the upper lung fields for equal breath sounds 

(b) Checking the position of the tube on a postintubation chest radiograph 

(c) Noting the presence of condensation in the tube 

(d) Seeing the endotracheal tube pass through the vocal cords 

12. Which of the following patients with head injuries is least likely to have a clinically important traumatic brain injury 

(ie, an injury resulting in death, neurosurgical intervention, endotracheal intubation, or prolonged hospitalization)? 

(a) A 12-month-old who ran into the corner of a coffee table, fell to the ground, and cried immediately, but is now 

acting normally per his parents; the child has a large frontal hematoma but an otherwise normal examination. 

(b) A 10-year-old who fell 15 feet while climbing a tree and initially had brief loss of consciousness but was awake 

and alert when EMS arrived; en route to the emergency department, he vomited three times and on arrival he is 

poorly responsive to voice. 

(c) A 1-month-old who was brought in by her parents after reportedly rolling off the changing table (3-4 feet) and 

falling to the floor; the parents report that the child cried immediately and has not vomited. On examination, 

the child is crying and has signs of external trauma. 

(d) A 75-year-old nursing-home resident who tripped and fell while in the bathroom has a large posterior scalp 

laceration and hematoma; she is awake and alert, albeit slightly confused, and her neurologic exam is nonfocal. 

(e) A 35-year-old unrestrained driver who was involved in a single car roll-over motor vehicle collision at highway 

speeds, ejected from the vehicle, and found by EMS in the roadside ditch. He has a Glasgow Coma Score 

of 13, is confused, and has abrasions on his face, chest, and extremities. The remainder of the primary and 

secondary surveys is unremarkable. 

13. All of the following statements regarding epidural hematomas are accurate except: 

(a) Associated parietal or temporal skull fracture is common. 

(b) CT reveals a lens-like, biconvex lesion. 

(c) Signs and symptoms are due to the mass effect of an arterial bleed. 

(d) Pupillary findings are typically contralateral to the side of the lesion. 

14. All of the following statements regarding basilar skull fractures are accurate except: 

(a) Placement of a nasogastric tube and nasotracheal intubation are contraindicated in the presence of these 

fractures. 

(b) Standard CT scan of the head can reliably exclude basilar skull fractures in patients with clinical suspicion of 

such injury. 

(c) Clinical findings include CSF rhinorrhea or otorrhea, hemotympanum, raccoon's eyes, Battle sign, and the "ring 

sign" on filter paper. 

(d) Patients should have a neurosurgical consult and possibly be admitted for observation. 

15. Listed below are several cervical spine injuries and their mechanism of injury. Which is incorrectly matched? 

(a) Jefferson fracture: axial loading mechanism 

(b) Hangman fracture: flexion injury 

(c) Clay-shoveler's fracture: flexion injury or direct trauma 

(d) Unilateral facet dislocation: flexion-rotation injury 

299


16. The best view on plain cervical radiographs for visualizing a Jefferson fracture is: 

(a) 

Open-mouth odontoid 

(b) Cross-table lateral 

(c) AP 

(d) Oblique 

1 7. Al I of the following statements regarding pulmonary contusions are accurate except: 

(a) They usually result from blunt chest wall trauma. 

(b) Associated rib fractures may be present. 

(c) Chest radiograph findings are typically delayed 24-72 hours after injury. 

(d) Pneumonia is the most common and most significant complication. 

18. Cardiac contusions most commonly involve the: 

(a) 

Left ventricle 

(b) Right ventricle 

(c) Left atrium 

(d) Right atrium 

19. The earliest clinical finding in a patient with a compartment syndrome is: 

(a) Pain 

(b) Paralysis 

(c) Palpable tenseness and tenderness of the involved compartment 

(cl) Pulselessness 

20. The most common intracranial bleed associated with closed head trauma is: 

(a) 

Subarachnoid 

(b) Subdural 

(c) Epidural 

(cl) 

lntraparenchymal 

21. Epidural hematomas frequently occur in association with skull fractures that traverse the groove of the: 

(a) Middle meningeal artery 

(b) Middle cerebral artery 

(c) Anterior cerebral artery 

(d) Anterior meningeal artery 

22. An 80-year-old patient presents to the emergency department complaining of bilateral arm weakness after she fell to 

the ground with walking her dog on a leash. Examination findings reveal 3/5 strength in both arms and 4/5 strength 

in both legs. Her sensation is normal. The most likely mechanism to cause this specific injury pattern is ___ _ 

(a) 

Hyperflexion 

(b) Axial loading 

(c) Rotational forces 

(cl) 

(e) 

Penetrating injury 

Hyperextension 

23. Which of the following treatments used for increased intracranial pressure is most rapidly effective? 

(a) Mannitol 


(c) Ventilation to a PaCO 2 

of 30-35 mmHg 

(cl) Steroids 

300 

24. Which of the following characteristics of a thoracolumbar compression fracture is not associated with vertebral 

column instability? 

(a) 

Compression fractures at multiple levels 

(b) Loss of> 1 0% vertebral body height 

(c) Kyphosis >30% 

(d) Rotational component of fracture 

(e) Posterior vertebral wedging


25. Of the following modalities, which is least useful in identifying pneumothoraces? 

(a) Ultrasound 

(b) Upright, expiratory chest radiograph 

(c) CT of the chest 

(d) Supine, inspiratory chest radiograph 

(e) Physical examination 

26. Advantages of FAST exam include all of the following except: 

(a) High sensitivity for identifying intra-abdominal hemorrhage 

(b) High sensitivity for identifying intra-abdominal injuries 

(c) May be performed at the bedside 

(d) May be repeated if clinical condition deteriorates 

(e) 

Noninvasive 

27. All of the following findings are suggestive of a cord injury except: 

(a) Diaphragmatic breathing 

(b) Priapism 

(c) Flaccid areflexia 

(d) Hypertension and bradycardia 

28. The presence of which of the following is the most accurate parameter when evaluating diagnostic peritoneal lavage 

fluid for suspected intra-abdominal injury? 

(a) 

Bile 

(b) Red blood cells 

(c) White blood cells 

(d) Amylase 

(e) Lactate dehydrogenase 

29. Rh immunoglobulin administration would be indicated in all of the following Rh-negative patients except: 

(a) G3P2; 38 weeks gestation; tripped and fell onto abdomen this morning; denies pain, contractions, vaginal 

bleeding, or discharge 

(b) G6P5; 30 weeks gestation; victim of domestic violence (punched and kicked in face, abdomen, back); 

complains of painless vaginal spotting 

(c) Gl PO; 25 weeks gestation; restrained passenger in low-speed motor vehicle collision; no complaints 

(d) Gl PO; 25 weeks gestation; tripped and fell while trail running yesterday, landing on knees and then abdomen; 

complains of decreased fetal movement but not pain, cramping, bleeding, or discharge 

(e) All of the women should receive Rh immunoglobulin. 

30. Which of the following organs is least likely to be injured as a result of primary blast injury? 

(a) 

Eye 

(b) Ear 

(c) Lungs 

(d) Liver 

(e) Colon 

ANSWERS 

1. C 6. C 11. d 16. a 21. a 26. b 

2. d 7. a 12. a 17. C 22. e 27. d 

3. a 8. a 13. d 18. b 23. C 28. b 

4. a 9. d 14. b 19. a 24. b 29. e 

5. d 10. c 15. b 20. a 25. d 30. d 



301


I. GENERAL INFORMATION 

A. Trauma is the leading cause of death in people 1-44 years old worldwide. 

B. The primary role of the emergency physician is to assess, resuscitate, and stabilize the trauma patient 

on a priority basis; this includes both suspicion for and recognition of potentially serious injuries and 

complications. 

1. Trauma management is best provided by a multidisciplinary team, including emergency medicine, general 

(trauma) surgery, and various surgical subspecialities. 

2. Trauma victims have a significantly lower likelihood of morbidity and mortality when treated at a designated 

trauma center. 

C. Trauma-related mortality has a trimodal distribution, ie, three peak times for trauma deaths. 

1. Immediate death 

a. Occurs within seconds to minutes of injury 

b. Generally die at the scene 

c. Accounts for greatest number of trauma deaths 

d. Death is usually due to: 

2. Early death 

(1) Massive head injury 

(2) High cervical spine injury with high spinal cord disruption 

(3) Cardiac laceration 

(4) Aortic rupture 

(5) Laceration of other great vessels 

(6) Airway obstruction 

a. Occurs within minutes to a few hours of injury, the so-called "golden hour" 

b. Generally die within 4 hours of arrival at trauma center 

c. Death is generally secondary to: 

(1) Subdural and epidural hematomas 

(2) Ruptured spleen or lacerated liver 

(3) Multiple injuries associated with hypovolemic shock 

(4) Fracture of the pelvis or multiple long bones 

(5) Hemopneumothorax 

(6) Tension pneumothorax 

(7) Cardiac tamponade 

(8) Massive hemothorax 

(9) Aortic dissection/rupture 

(1 0) Airway compromise 

d. Application of advanced trauma life support (ATLS) guidelines regarding rapid ABC assessment and 

stabilization (definitive airway management, fluid resuscitation, and blood replacement) reduces the 

mortality and morbidity rate of these patients. 

3. Delayed death 

a. Occurs days to weeks after the initial injury 

b. Usually die in intensive care setting 

c. Death is usually due to: 

(1) Multisystem organ failure 

(2) Systemic inflammatory response syndrome 

d. With advances in trauma critical care management, relatively few trauma victims die beyond 24 hours after 

injury. Therefore, some experts suggest that distribution of trauma mortality is bimodal rather than trimodal. 

302


II. GENERAL APPROACH TO THE TRAUMA PATIENT 

A. ATLS guidelines provide a clear, organized, and rapid approach to the evaluation and management of 

trauma patients. 

B. Primary survey: assessment and management of the ABCs 

1. Airway and cervical spine assessment 

a. Airway management is the single most important prehospital/arrival priority. 

b. Immediately assess the airway for potential compromise (nonpatent or poorly protected airway). 

(1) Airway patency 

(a) 

If the patient can speak, the airway is patent. 

(b) If the respirations are noisy (stridulous, sonorous, gurgling, etc), partial obstruction is present. 

(2) Airway protection 

(a) Assume the airway is poorly protected if: 

i. Decreased level of consciousness (Glasgow Coma Score ::;8) 

ii. Secretions are pooling 

iii. Gag reflex is depressed or absent 

(b) The poorly protected airway is at risk of aspiration of gastric/oral secretions, blood, food, foreign 

bodies. 

c. Beware of the potential for associated cervical spine injuries. 

(1) Always maintain the cervical spine in neutral position with in line manual cervical immobilization or 

appropriate immobilization devices when evaluating and managing the airway. 

(2) Significant cervical spine injury should always be suspected in the patient with: 

(a) 

Blunt trauma 

(b) Multiple injuries 

(c) Altered level of consciousness 

(d) Evidence of blunt injury above the clavicle 

(e) 

Dive injuries 

d. Airway management in patients with possible cervical spine injury 

(1) Open the airway using the chin lift or jaw thrust maneuver. Do not use head tilt maneuver. 

(2) Remove dentures and foreign bodies if present. 

(3) Consider placement of an oropharyngeal (unconscious patient) or nasopharyngeal (conscious 

patient) airway. 

(4) Patients who do not have a patent airway or are not protecting their airway require definitive airway 

management (orotracheal intubation or a surgical airway). 

(5) Orotracheal laryngoscopy and intubation with in-line cervical spine immobilization is the procedure 

of choice (even in the presence of suspected cervical spine injury). 

(a) Front of the cervical immobilization device should be removed while maintaining in-line 

cervical spine immobilization to facilitate intubation. 

(b) Direct laryngoscopy may be more difficult in the trauma patient. 

(c) Video-assisted laryngoscopy has been shown to have a high success rate of intubation with less 

movement of the cervical spine. 

(d) Fiberoptic laryngoscopy is an option if the patient's condition permits and the physician is skilled 

in this technique. 

(e) An endotracheal tube introducer (gum elastic bougie) is a valuable tool in airway management 

in trauma patients. 

(6) Failed airway management 

(a) If orotracheal intubation is unsuccessful or relatively contraindicated (see below), surgical airway 

is indicated. 

(b) Surgical cricothyrotomy is surgical airway of choice for the emergency physician. (Some authors 

consider a surgical airway the procedure of choice for patients with severe midfacial injuries; 

however, most clinicians would make a single attempt at orotracheal intubation with in-line 

manual cervical immobilization before proceeding to a surgical airway.) 

303


(c) In children 0.85. 

d. Observe, palpate, and auscultate the thorax to quickly identify and manage life-threatening injuries that 

may compromise cardiopulmonary function. 

(1) Tension pneumothorax: perform needle thoracostomy, and follow immediately with thoracostomy 

tube placement. 

(2) Sucking chest wound: cover with a sterile occlusive dressing, taped down on three of its four sides. 

(3) Flail chest: intubation with positive-pressure ventilation indicated for large flail segments. 

e. Ventilator settings should reflect potential for hemodynamic compromise induced by positive-pressure 

ventilation in hypovolemic patients. 

(1) Positive-pressure ventilation may decrease venous return to the heart (preload) and worsen 

hypotension; low tidal volumes are appropriate (5 ml/kg at a rate of 20-30 breaths per minute). 

(2) Close monitoring of pulse and blood pressure and frequent arterial blood gases ultimately determine 

the optimal ventilator settings. 

3. Circulation and hemorrhage control 

a. Control obvious external bleeding. 

(1) Direct manual pressure followed by application of a pressure dressing is considered first-line 

management; elevation of affected extremity may help. 

(2) Application of a tourniquet may be necessary to control life-threatening hemorrhage from a severely 

injured extremity (eg, explosion injury). 

(3) Bleeding from posterior scalp lacerations is often overlooked initially. 

(4) Various topical hemorrhage control agents have been adapted from those used on modern battlefields 

and are now commercially available. 

b. Assess circulation for signs of shock. 

(1) Check central and peripheral pulses for quality, rate, and regularity. 

(2) Evaluate skin color, capillary refill time, and level of consciousness. 

(3) The FAST exam should be performed in the primary survey in unstable patients to assess for internal 

hemorrhage. 

c. Take measures to control internal sources of bleeding. 

304


(1) Unstable pelvic fractures may be temporarily stabilized with a pelvic binder device (either a 

commercially available product or a simple bedsheet) to decrease blood loss. 

(2) Reduce and temporarily splint obvious long bone fractures to reduce ongoing hemorrhage. 

(3) Unstable patients with massive hemoperitoneum should be transferred to the OR as quickly as 

possible. 

d. Place the patient on a cardiac monitor, and check a rhythm strip. 

e. Establish IV access. 

(1) Place two short, large-bore peripheral IV catheters (16-gauge or larger). Draw blood for laboratory 

studies at the same time. 

(2) If peripheral access is difficult or delayed, place an intraosseous catheter in the seriously injured, 

hemodynamically unstable patient. 

(3) Consider central IV access, but remember that short, large-bore peripheral catheters can infuse fluid 

faster than long central lines. 

f. Hemorrhagic shock resuscitation 

(1) Administer 1-2 L warmed lactated Ringer's or normal saline over 5 minutes (fluid bolus in children is 

20 ml/kg x 2 or 3 boluses). 

(2) If the patient remains in shock, packed RBCs should be administered. 

(3) For patients needing large volumes of packed RBC transfusions, consideration should be given to 

administering other blood products (fresh frozen plasma, platelets) as well. There is no standard 

approach to massive transfusions; protocols vary by institution. Increased survival has been 

demonstrated with use of a 1 :1 :1 ratio of RBCs:platets:fresh frozen plasma. 

g. Cardiac tamponade 

(1) Classic signs are muffled heart sounds, jugular venous distention, and hypotension (Beck's triad). 

(2) Bedside echocardiography (FAST) is highly sensitive for diagnosing pericardia! effusion. 

(3) Perform pericardiocentesis. 

h. Indications for emergency thoracotomy in the emergency department: no consensus guidelines 

(1) Penetrating thoracic trauma 

(a) 

Hemodynamically unstable on arrival to the emergency department despite adequate fluid 

resuscitation; ideally, the patient loses pulses in front of resuscitation team. 

(b) Pulseless for


306 

c. Patients with severe head injury plus an altered level of consciousness (or a GCS ::08) usually require 

intubation for airway protection. The presence of nonpurposeful motor responses (4 or fewer) also suggests 

the need for a definitive airway. 

5. Exposure/environmental control: completely undress the patient to facilitate a thorough examination, but 

remember to cover with warmed blankets to prevent iatrogenic hypothermia. 

C. Initial diagnostic testing and continued management 

1. Laboratory studies, type and cross, CBC with platelets, prothrombin time (INR)/partial thromboplastin time, 

BUN/creatinine, electrolytes, glucose, amylase, lipase, ethanol, toxicology screen, ~-human chorionic 

gonadotropin (pregnancy test), urinalysis, arterial or venous blood gases, lactate, etc, as appropriate. Selective 

laboratory testing is appropriate. 

2. Bedside radiographs: cross-table lateral cervical spine, AP chest, and AP pelvis; may be ordered in major 

trauma, especially when there are signs of hemodynamic instability. 

3. FAST examination (if not performed in the primary survey): indicated in all trauma patients with signs of 

abdominal, pelvic, or thoracic injury; femur fracture; or hemodynamic instability. 

4. Cardiopulmonary monitoring: continuous ECG, pulse oximetry, and blood pressure monitoring 

5. Nasogastric (or orogastric) tube: should be placed in intubated patients unless contraindications (eg, cribriform 

plate fracture, other unstable midface fractures) are present. 

6. Bladder catheterization: place Foley catheter in unconscious or intubated patients unless contraindications (eg, 

blood at the urethral meatus, scrotal hematoma, or a high-riding prostate on rectal examination) are present. 

7. Trauma center transfer: consider need to transfer the patient to a designated trauma center or a hospital that 

can provide a higher level of trauma care. 

a. All trauma patients whose injuries exceed the management capabilities of their hospital should be 

transferred to an appropriate trauma center as quickly as possible (may be mandated in some states). 

b. A complete trauma evaluation, including imaging, beyond primary and secondary surveys (ie, ancillary 

tests and imaging) is not necessary and should not delay transfer of seriously injured patients. 

D. Secondary survey and final case management 

1. Obtain an "AMPLE" medical history and inquire about the mechanism of injury. 

2. Perform a complete physical examination. Consider performing a rectal examination, checking for sphincter 

tone, blood, high-riding prostate, and bowel-wall integrity. 

3. Order additional diagnostic studies as indicated, eg, radiographs of thoracolumbar spine and/or extremities, CT, etc. 

4. Assess and reassess laboratory data, response to fluids, vital signs, and overall stability of the patient. 

5. Administer tetanus booster and antibiotics when indicated. 

E. Additional information for pediatric patients 

1. Airway management 

a. Atropine may be considered when performing rapid-sequence intubation but is no longer routinely 

recommended. 

b. Cuffed or uncuffed endotracheal tubes are now acceptable in children. 

(1) Size: (16 + age in years)/4 

(2) If using cuffed tube, downsize ½ size. 

c. Needle cricothyrotomy is preferred in small children (60 mm Hg 

(2) 1 month to 1 year: >70 mmHg 

(3) > 1 year: 70 + 2(age in years) 

c. Children have robust compensatory mechanisms and maintain normal blood pressure for a longer time 

despite presence of significant hemorrhage and shock. 

3. Younger children (


Ill. HEMORRHAGIC SHOCK 

A. Hemorrhage-induced hypovolemia is the most common cause of shock in the trauma patient. 

B. The earliest signs of hemorrhagic shock are tachycardia and cutaneous vasoconstriction (prolonged 

capillary refill time). 

C. Once shock is identified, initial management is volume resuscitation with a warmed crystalloid solution; 

continued management is determined by the patient's response to initial therapy. 

D. The amount of blood loss in an average adult can be estimated based on the patient's initial clinical 

presentation as follows: 

Table 17: Classes of Hemorrhagic Shock 

Urine Output 

Class Pulse (beats/min) Blood Pressure CNS Status (ml/hr) Blood Loss 

30 120 Decreased Confused 5-15 30%-40% 

1,500-2,000 ml 

IV >140 Decreased Lethargic nil >40% 

>2,000 ml 

IV. COMMON INJURIES BY ANATOMIC LOCATION 

A. Traumatic brain injury (head injury) 

1. Overview 

a. Head injury is the leading cause of death and disability in trauma. 

b. The most frequent cause of death in patients sustaining severe head injury is uncontrolled intracranial 

hypertension and subsequent herniation. 

c. Assume a cervical spine injury exists in head-injured patients; if clinical assessment or the mechanism of 

injury suggests the possibility of neck injury, immobilize the cervical spine. 

d. Altered level of consciousness is the hallmark of brain injury. 

e. Indications for head CT in the injured adult patient and risk factors for abnormal findings on CT include: 

(1) Abnormal level of consciousness or sensorium (GCS


f. Considerations for head CT in children: The 2009 PECARN Guidelines identify children at low risk of 

clinically significant head injury in whom radiation-related risk of CT imaging may outweigh benefit (high 

negative predictive value). No CT indicated for: 

(1) 2 times 

+ 

Intoxication (drug/alcohol) + 

+ 

+ 

Anticoagu I ants/ 

coagulopathy 

+ 

+ 

Altered level of 

consciousness 

+ 

+ (implied by GCS


Table 18: Comparison of Decision Instruments for Head CT (continued) 

Criteria Nexus II Canadian New Orleans 

Sensitivity 

97% 

99% 

99% 

Specificity 

47% 

47% 

33% 

Inclusion criteria 

None listed 

Age2:16 years, GCS 13-15, 

no coagulopathy nor on 

anticoagulation, no obvious open 

sku 11 fracture 

Age> 18 years, GCS 15, blunt head 

trauma occurring within previous 24 

hours causing loss of consciousness, 

amnesia, or disorientation 

2. Specific types of head injuries 

a. Diffuse brain injuries (concussions, diffuse axonal injuries): usually do not have mass lesions necessitating 

emergent neurosurgical intervention 

(1) Cerebral concussion 

(a) Mechanism: head injury - 

brief loss of neurologic function 

(b) Clinical presentation: clinically variable; may range from minimal to severe and debilitating; 

rarely associated with any focal findings. Common symptoms include: 

i. Brief loss of consciousness (not necessary for diagnosis): results from impairment of the 

reticular activating system 

11. Antegrade amnesia (with perseveration) 

iii. Headache 

iv. Nausea and/or vomiting 

v. Abnormal sensorium (usually brief) 

vi. Difficulty with cognition 

(c) Imaging: CT of the head and/or MRI of the brain (if performed) are normal. 

(d) Management: cognitive rest and avoidance of repeated head injury while brain is recovering 

i. May take 7-14 days or longer 

ii. Symptoms lasting >2 weeks may be characterized as postconcussive syndrome 

(2) Diffuse axonal injury 

(a) Clinical presentation 

i. Prolonged coma (often lasting days to weeks)± posturing 

ii. ± Autonomic dysfunction (high fever, hypertension, sweating) 

(b) Results in widely scattered microscopic neuronal damage throughout the brain 

(c) Imaging: CT of head - 

matter 

no mass lesion; may show diffuse punctate hemorrhages throughout white 

(d) Management: patients require admission and neurosurgical consult (ICP monitoring often 

indicated); overall mortality 33%. 

(3) Cerebral contusion 

(a) Clinical presentation: similar to that of a concussion except: 

i. Neurologic dysfunction is more profound and prolonged; patients often demonstrate mental 

confusion, obtundation, or coma. 

11. Focal deficits may be present if contusions occur in the sensorimotor strip. 

(b) Imaging: these lesions are generally found in the frontal and temporal lobes and are visible on CT 

scan. They may be produced at the site of impact (coup contusions) or at the opposite pole of the 

brain (contrecoup contusions). 


1. Admit these patients for observation and obtain neurosurgical consult. Only supportive 

management is indicated unless complications develop. 

ii. Patients with temporal lobe contusions are at significant risk of progression of edema; the 

resulting mass effect may impinge directly on the brainstem. These patients should be closely 

observed in a neurosurgical ICU. 

309


(d) Complications: potential delayed complications (hours or days) include development of cerebral 

edema or an intracerebral hematoma at the site of the contusion, resulting in mass effect (best 

detected by repeating the CT 12-24 hours after the initial scan). 

b. Focal brain lesions (contusions, hemorrhages, hematomas): commonly cause mass effect and necessitate 

emergency neurosurgery 

(1) Epidural hematoma 

(a) Mechanism and clinical presentation: head injury causing sudden loss of consciousness 

(impairment of reticular activating system) as well as intracranial bleeding (usually arterial; most 

commonly middle meningeal artery) --,, brain may recover from initial cerebral concussion/ 

contusion, resulting in a lucid interval (.'.S30%). As bleeding causes increased ICP and mass 

effect, altered level of sensorium (coma), a fixed and dilated pupil on the side of the lesion, and 

contralateral hemiparesis develop. 

i. Transtentorial herniation compresses cranial nerve Ill and the corticospinal tract. 

ii. Classic presentation is not always present. 

(b) Imaging: CT scan demonstrates the classic lens-like, biconvex lesion. Associated parietal or 

temporal skull fracture is common (80%). Epidural hematomas do not cross suture lines but can 

cross midline. 


i. Immediate neurosurgical consult for surgical decompression 

ii. Manage increased ICP (see below). 

(d) Mortality is 0-20% depending on neurologic status: normal neurologic examination --,, 0%; coma 

--,, 20% without rapid detection and evacuation 

Courtesy of Dr. Colin Kaide 

(2) Subdural hematoma 

(a) More common than epidural hematomas and more often associated with significant primary 

brain damage (usually covering the entire surface of the hemisphere); subdural hematomas cross 

suture lines but not midline. 

(b) Risk factors: patients with brain atrophy (alcoholic patients, the elderly) are especially susceptible; 

brain atrophy --,, bridging veins spanning a greater distance and being more easily torn 

310


(c) Mechanism and clinical presentation 

i. Acute subdural hematoma: symptoms develop within 24 hours of injury. 

ii. Subacute or chronic subdural hematoma: symptoms may be delayed up to 2 weeks or more 

after injury. 

iii. Caused by "mass effect" of a venous hematoma bleed. 

iv. Symptoms range from a mild headache and confusion to lethargy and coma (with or without 

localizing signs). 

(d) Imaging: CT demonstrates the classic crescent-shaped lesion (be able to recognize on CT). 

(e) Management: same as for epidural hematoma; immediate neurosurgical intervention is usually 

required (except perhaps for mildly symptomatic chronic subdural hematomas). 

(f) 

Mortality rate for acute subdural hematomas ranges from 30% with early evacuation to 60% with 

later evacuation. 

i. Mortality is higher in patients who are unconscious from the time of injury. 

ii. Patients with a history of a lucid interval (50%-70%) have a better prognosis. 

c. Cerebral edema 

(1) Pathophysiology 

Courtesy of Dr. Sandra Werner 

SDH acute and chronic SL 

(a) Head trauma -s. brain swelling -s. increased ICP that can lead to brain herniation 

(b) Cerebral perfusion pressure= mean arterial pressure minus ICP (normal ICP


(h) Progression of neurologic symptoms 

(i) Development of signs of herniation 

i. Decreased level of consciousness 

ii. Posturing 

iii. lpsilateral pupil fixed and dilated, or both pupils are fixed (in midposition). 

iv. Loss of oculovestibular reflexes (doll's eyes/ice water calories) 

(3) Acute management of ICP 

(a) Raise the head of the bed 30°. 

(b) Ensure adequate sedation. 

(c) Maintain the pC0 2 

at ~32-35 mmHg. 

i. In the setting of acute herniation, hyperventilation to a pC0 2 

of 26-30 mmHg effectively 

lowers ICP by causing vasoconstriction but should be reserved for life-threatening situations 

as a bridge to more definitive therapy. 

11. Effects of hyperventilation are short-lived (1-24 hours) 

(d) Ensure adequate oxygenation (intubate early). 

(e) Osmotic therapy: administration of hyperosmolar solutions creates an osmolar gradient, drawing 

fluid across the blood-brain barrier out of the brain and into the systemic circulation, thereby 

reducing intracranial pressure. 

(f) 

1. Use caution in patients with decreased intravascular volume and hypernatremia; also 

controversial with mass lesions. 

11. Specific agents 

• Mannitol: 0.25-1 mg/kg IV bolus 

• Hypertonic saline (3%-23.4%): various dosing regimens (3-5 ml/kg IV bolus) 

Consult neurosurgery for consideration of ICP monitoring, seizure prophylaxis, and surgical 

intervention. 

d. Herniation syndromes 

(1) The addition of a mass to the closed cranial vault results in increased ICP which, if unchecked, can 

produce cerebral displacement (herniation). 

(2) Uncal herniation: occurs when a unilateral mass pushes the medial aspect of the temporal lobe 

(uncus) through the tentorial incisura. As the uncus herniates, the following clinical signs develop: 

(a) lpsilateral pupil dilatation and fixation (due to the compression of cranial nerve Ill) 

(b) Increased respiratory rate (or Cheynes-Stokes respiratory pattern) 

(c) Coma 

(d) Posturing (decorticate [not always seen], then decerebrate) 

(e) Apnea and death 

(3) Central herniation: occurs when a mass effect compresses the brainstem in a more symmetrical way; 

this results in a progressive loss of brainstem function: t level of consciousness+ t respiratory rate 

or Cheyne-Stokes (thalamic, upper brainstem compression)-> fixed midposition pupils (midbrain 

compression)-> posturing, loss of oculovestibular reflexes (pontine compression)-> flaccidity, apnea 

(medullary compression) 

(4) Cerebellar tonsillar herniation: downward displacement of the cerebellar tonsils through the foramen 

magnum, resulting in medullary compression-> pinpoint pupils and flaccid quadriplegia (most 

common motor deficit)-> apnea and circulatory collapse 

e. Skull fractures 

(1) Skull fractures help identify patients at high risk of having or developing an intracranial hematoma. 

(2) Imaging: routine skull radiographs are not indicated in the evaluation of patients with traumatic brain 

injury, because they do not evaluate the integrity of the underlying intracranial space. All significant 

head injuries require CT evaluation. 


(a) Most patients with skull fractures require neurosurgical consult and admission for observation. 

(b) Management is based on type of fracture and presence or absence of underlying brain injury. 

(4) Types 

(a) Linear, nondepressed skull fractures-> require no specific treatment. 

(b) Depressed skull fractures-> may require operative elevation of the bony fragment if fracture 

extends below inner table 

312


(c) Open skull fractures - 

(d) "Egg shell" skull fractures in children - 

(e) Basilar skull fractures 

(5) CSF leaks 

i. Clinical presentation 

require early operative intervention and prophylactic antibiotics. 

• Periorbital ecchymosis ("raccoon" eyes) 

• Retroauricular ecchymosis (Battle sign) 

• Hemotympanum or bloody discharge from the ear 

• Rhinorrhea or otorrhea 

require evaluation for nonaccidental trauma. 

• Cranial nerve deficits (I, II, VII, VIII); these signs may not develop for several hours after injury. 

ii. Commonly, the only radiographic sign of a basilar skull fracture is a blood-air interface in 

the sphenoid sinus; CT scanning (with thin cuts through the basilar skull) is indicated (but 

may not demonstrate the fracture). 

(a) May be seen from the ear or nose; associated with intracranial air in 20% of cases 

(b) Diagnostic evaluation (testing for CSF rhinorrhea) 

i. Place a drop of the fluid on filter paper; a clear halo ring suggests CSF. 

ii. Send a sample to the laboratory for glucose determination; if >30 mg/dL, CSF is present. (This 

test is accurate only if the fluid is clear; bloody fluid may yield a false-positive result). 

(c) The major complication is development of a CNS infection. 

(d) Most CSF leaks resolve spontaneously with conservative management. However, as many as 1 0% 

of patients develop a recurrent post-traumatic CSF leak that increases the risk of delayed bacterial 

meningitis. 

(e) Neurosurgical consult is indicated. 

3. Complications of head injuries 

a. Immediate (within 2 days) 

(1) Seizures: caused by traumatic neuronal depolarization; associated with low overall morbidity 

(2) "Talk and Deteriorate" syndrome 

(a) Most frequent neurologic findings are altered mental status and focal deficits. 

(b) Most frequent cause is epidural hematoma. 

b. Early (usually within 1 week) 

(1) Seizures (may indicate progressive injury) 

(2) Disseminated intravascular coagulation 

(3) Pulmonary edema (neurogenic) 

(4) Diabetes insipidus (loss of normal antidiuretic hormone secretion) 

(5) CSF leak 

(6) Cardiac dysrhythmias 

c. Late (after 1 week) 

(1) Delayed post-traumatic epilepsy 

(a) Acute intracranial hematomas 

(b) Depressed skull fractures 

(2) Recurrent CSF leak 

(3) Hydrocephalus 

(4) Subdural hygroma 

d. Postconcussion syndrome: symptoms may be noted on initial examination of the patient (or may appear 

later, eg, 1 week after the injury) and may persist for weeks, months, or years. 

(1) Headache (which may be severe) is the most common complaint. 

(2) Other signs/symptoms: irritability, insomnia, dizziness, anxiety, depression, fatigue, visual complaints, 

hearing problems, loss of memory, inability to concentrate, and sensitivity to alcohol 

e. Post-traumatic epilepsy 

(1) A high incidence is associated with 

(a) 

lntracranial hematoma 

(b) Depressed skull fracture 

(c) Seizures occurring within the first week of head injury 

313


4. Management 

(2) Anticonvulsant therapy 

(a) There is evidence that phenytoin reduces the incidence of seizures within the first week of injury, 

but not thereafter. 

(b) No consensus on best first-line antiepileptic agent for long-term management. 

a. ABCs and immobilize the cervical spine; measure pulse oximetry, analyze a rhythm strip, and measure 

bedside glucose level; all patients with a GCS :S8 should be intubated for airway protection. 

b. Assess the patient's level of consciousness using the GCS. A score of :S8 is associated with severe head injury; 

a score of 9-13 is associated with moderate brain injury; a score ?:14 is associated with mild head injury. 

Table 19: Glasgow Coma Scale 

Eye opening response 

Best verbal response 

Best motor response 

Spontaneous 

To voice 

To pain 

None 

Oriented 

Confused 

Inappropriate words 

Incomprehensible sounds 

None 

Obeys command 

Localizes pain 

Withdraws (pain) 

Flexion (pain) 

Extension (pain) 

None 

4 

3 

2 

5 

4 

3 

2 

6 

5 

4 

3 

2 

c. Assess pupillary function: both equality and response to light. The presence of a sluggishly reactive or fixed 

and dilated pupil is suggestive oft ICP and uncal herniation. 

d. In patients with a decreased level of consciousness, exclude other potential causes (hypoglycemia, 

hypoxia, drug overdose, sepsis, etc); administer oxygen, thiamine, D50W, and naloxone, as clinically 

indicated. Avoid administration of glucose to head-injured patients who are not hypoglycemic. 

e. Consider cervical spine injury if any of the following is present: 

(1) Unconsciousness or intoxication 

(2) Cervical pain or tenderness 

(3) Neurologic deficits 

(4). Facial fractures (especially LeFort II or Ill) 

(5) Mechanism of injury that can result in cervical injury 

f. Search for associated injuries; the finding of subhyaloid hemorrhages (preretinal bleeding) in children is 

suggestive of child abuse (shaking injuries or other trauma) or a bleeding disorder. 

g. Obtain CT scan and neurosurgical consult as clinically indicated. 

h. If signs oft ICP (eg, dilated pupil) are present: 

(1) Elevate head 30°. 

(2) Ventilate to a PaCO 2 

of 35 mmHg. 

(3) Obtain emergent CT and neurosurgical consult. 

1. Frequently reassess the patient's neurologic status (especially level of consciousness) looking for signs 

of evolution. 

314


B. Facial injuries (extensive facial injuries may necessitate a surgical airway) 

1. Midface fractures: the LeFort classification 

a. LeFort I: transverse through the maxilla above the roots of the upper teeth 

b. LeFort II: extends up into the midface and includes the maxilla, nasal bridge, lacrimal bones, orbital floors, 

and orbital rims 

c. LeFort Ill (craniofacial dissociation): extends from nasal bridge posteriorly along the medial and inferior 

orbital walls and laterally through the lateral orbital wall and zygoma; fractures extend back through the 

nasal bones to the sphenoid base; often associated with CSF leaks 

Le Fort Ill 

Le Fort II 

Le Fort I 

Le Fort I 

(Only Maxilla Moves) 

Le Fort II 

(Maxilla and Nose Move) 

Le Fort Ill 

(Entire Face Moves) 

2. Orbital wall fractures: orbital "blowout" fractures most commonly occur through the floor of the orbit but 

may also occur medially in the region of the lamina papyracea of the ethmoid bone. 

a. Orbital floor fractures 


(a) Pain and diplopia on upward gaze 

(b) Enophthalmos 

(c) Hypesthesia in the distribution of the infraorbital nerve (ipsilateral cheek and lip) 

(d) Limitation of upward gaze due to entrapment of the inferior rectus and inferior oblique muscles 

(e) Subcutaneous orbital emphysema 

(2) Radiographic findings (CT is imaging modality of choice; however, if plain radiographs are used, 

fractures are best seen on occipitomental, or Waters' view) 

(a) Air-fluid (blood) level in maxillary sinus 

(b) Prolapse of orbital tissue into the maxillary antrum ("tear-drop" sign) 

(c) Bony disruption of the orbital floor 

(d) Clouding of the maxillary sinus 

(e) Orbital emphysema 

315


b. Medial wall fractures 


(a) Epistaxis 

(b) Emphysema of the lids or conjunctiva 

(c) Limitation of lateral gaze due to entrapment of the medial rectus muscle (uncommon) 

(2) Radiographic findings (CT imaging) 

c. Management 

(a) Unilateral clouding of the ethmoid sinus 

(b) Orbital emphysema 

(1) Exclude associated ocular injuries (eg, rupture of the globe, hyphema), which occur in up to 30% of 

patients with these fractures; CT scanning may be helpful. 

(2) Prescribe decongestants and consider prophylactic antibiotics. 

(3) Advise patients to avoid Valsalva maneuvers such as blowing nose, which can worsen orbital emphysema. 

(4) Refer patients to an ophthalmologist and/or ENT surgeon or oral maxillofacial surgeon for follow-up; 

injuries usually heal without operative intervention, but surgical management is sometimes needed. 

(For further discussion of these fractures, see page 132 in HEENT Disorders.) 

3. N asa I fractures 

a. Imaging of clinically fractured nasal bones is rarely necessary. 

b. If all the following criteria are met, imaging is unlikely to affect urgent management, and patient may 

follow-up with an appropriate subspecialist in several days. 

(1) Tendernesss and swelling isolated to nasal bridge 

(2) Can breathe through both nares 

(3) No septal deviation 

(4) No septal hematoma 

4. Zygoma fractures 

a. "Tripod" fracture: involves zygoma, lateral orbital wall, and maxilla; usually caused by direct blow 

b. Displaced fractures usually require surgical repair 

5. Mandibular fractures 

a. Simple plain films poorly sensitive 

b. Imaging modality of choice: panoramic radiograph or CT 

c. Traditionally taught that mandible fractures occur in pairs, but more recent reviews suggest that single 

breaks relatively common 

6. Dental fractures: generally require antibiotics, analgesics, and referral 

a. Ellis classification: I= enamel only, II = enamel and dentin, Ill= enamel, dentin, and pulp 

b. Ellis Ill fractures generally require definitive follow-up and management within 48 hours of injury. 

C. Adult spinal trauma 

1. Spinal cord injury 

Table 20: Classification of Cervical Spine Injuries by Mechanism of Injury and Stability 

Injury Mechanism Stability 

Anterior subluxation Flexion Potentially unstable 

Bilateral facet dislocation Hexion Always unstable 

Simple wedge fracture Hexion Stable 

Clay-shoveler's fracture (C6, C7, T1) Flexion Stable 

Hexion teardrop fracture Flexion Extremely unstable 

Atlanto-occipital dislocation Flexion Unstable 

Anterior atlantoaxial dislocation Flexion Unstable 

Odontoid (C2) fracture Flexion/varied Unstable 

316


Table 20: Classification of Cervical Spine Injuries by Mechanism of Injury and Stability (continued) 

Injury Mechanism Stability 

Unilateral facet dislocation (C1-C2) Flexion-rotation Potentially unstable 

Rotatory atlantoaxial dislocation Flexion-rotation Unstable 

Pillar fracture Extension-compression Stable 

Jefferson fracture (burst of C1) Axial loading Extremely unstable 

Posterior atlantoaxial dislocation Extension Unstable 

Hyperextension-dislocation Extension Unstable 

Extension teardrop fracture Extension Unstable in extension 

C1 posterior neural arch Extension Potentially unstable 

Hangman fracture (C2) Extension Unstable 

Hyperextension-fracture/dislocation Extension Unstable 

Table 21: Memory Aid for Unstable Cervical Spine Fractures 

Letter 

Named Fracture 

Details 

Iefferson 

.B_it 

Qff 

A 

Hangman 

Ihumb 

Jefferson fracture 

Bilateral facet dislocation 

Odontoid 

Any atlanto-occipital 

Hangman fracture 

Teardrop fracture 

Burst fracture of C1 

Flexion injury 

C2 fracture: type II, type II unstable; type I (tip of the 

odontoid) is stable 

Flexion and flexion/rotation 

Bilateral C2 pedicle fracture (leads to C2 displacing 

anteriorly on C3) 

Flexion teardrop fracture is extremely unstable 

a. Incomplete cord lesions 

(1) Central cord syndrome 

(a) Usually occurs in older patients with spondylosis or congenital stenosis of the spinal canal 

whose necks are subjected to forced hyperextension injuries 

(b) Hyperextension - vascular ischemia of central cord (spinothalamic and corticospinal tracts) - 

weakness greater in arms than legs and variable loss of bladder control 

(c) Management is generally nonoperative. 

(d) Prognosis is excellent. 

Corticospi na I tract 

Spinothalamic tract 

317


(2) Anterior cord syndrome 

(a) Results from cervical flexion injuries 

(b) Flexion ----;, impingement of bony fragments on the spinal canal, cord contusion, or compression 

of the anterior spinal artery - loss of anterior cord function (complete motor paralysis and loss 

of pain and temperature sensation distal to the lesion) and preservation of posterior column 

function (vibration, light touch, position sense) 

(c) Immediate neurosurgical consult and emergent MRI or CT myelography 

Corticospinal tract 


(3) Brown-Sequard syndrome 

(a) Usually results from a penetrating injury (gun shot or knife wound) causing hemisection of the 

spinal cord 

(b) Hemisection of the spinal cord----;, ipsilateral motor paralysis, loss of proprioception, and vibratory 

sensation with contralateral loss of pain and temperature sensation 

Corticospinal tract 



(1) Suspect spinal cord injury in: 

(a) Patients with an altered or depressed mental status (including intoxicated patients with head or 

facial injuries) 

(b) Patients with any focal neurologic deficits 

(c) Significant mechanisms of trauma (especially high-speed motor vehicle collisions, falls, football 

injuries, and diving accidents) 

(d) Patients with unexplained hypotension and associated paradoxical (relative) bradycardia 

(spinal shock) 

(e) 

Elderly patients with suspected minor traumatic injuries 

(2) Examination findings highly suggestive of cervical cord injury 

(a) Flaccid areflexia 

(b) Loss of rectal sphincter tone 

(c) Diaphragmatic abdominal breathing 

(d) Priapism 

(e) 

Hypotension and relative bradycardia (spinal shock) 

(3) Physical examination 

(a) Neurologic examination should focus on identifying focal deficits and attempting to localize the 

injury to a specific spinal cord level. 

1. Sensory deficits should be localized to a specific dermatome if possible (Table 22). 

• Occipital sensation ----;, C2 

318


• The hold-up position (with the hands half closed) or the hands and arms flexed at the 

chest - C6 

• "Burning hands" syndrome (especially in football players) - 

11. Testing specific muscle groups may help localize injury (Table 22). 

iii. A strong handshake indicates an int act spinal cord down to Tl. 

C6-C7 

Table 22: Spinal Root Muscle and Sensory Distribution 

Root Motor Sensory 

C3 Diaphragm, trapezius Lower neck to clavicle 

C4 Diaphragm Clavicular area 

cs Biceps, deltoid, diaphragm Lateral arm at or above the elbow 

C6 Biceps Forearm and radial side of the hand 

C7 Triceps Middle finger 

cs Finger flexors Lateral aspect of hand 

Tl Hand intrinsics Medial side of forearm 

T4 

T12 

Anterior chest wall at level of nipples 

Abdominal wall at level of umbilicus 

L2-L3 

L3-L 

Hip flexion 

Knee extension 

LS 

Lateral lower leg and large toe 

S1 Ankle planter flexion Small toe and sole of foot 

(b) 

Other findings 

i. Anterior cord function is assessed by testing motor strength, pain, and temperature sensation. 

ii. Posterior cord function is assessed by testing light touch, position, and vibratory sensation. 

iii. Anal wink (bulbocavernous reflex): squeezing the penis or clitoris causes contraction of the 

anal sphincter; this is the last reflex to disappear in patients with spinal shock or a complete 

cord lesion and the first to return with improvement. 

Iv. Sacral sparing: preservation of sensation at the sacrum in a patient with a spinal cord injury (a 

good prognostic sign) 

v. Neurogenic shock (loss of sympathetic tone): hypotension associated with bradycardia, warm 

pink skin, and adequate urine output 

vi. Spinal shock: loss of motor and/or sensory function along with initial loss of reflexes below 

the level of spinal injury (differentiate from neurogenic shock) 

vii. Horner syndrome: unilateral ptosis, miosis, anhydrosis; indicates injury to the cervical 

sympathetic chain at the level of C7-T2. 


(1) Cervical spine radiographs 

(a) Cross-table lateral, open-mouth odontoid, and AP views have a high but imperfect diagnostic 

yield for fractures. 

(b) Reliance on the cross-table lateral view alone is unacceptable; 10%-15% of fractures, particularly 

those involving C7, are not visualized on this view. 

(c) "Swimmer's" view (lateral view with axial traction on the arms) or a transaxillary view may be 

necessary to visualize C7 and the C7-Tl i nterspace. 

(d) Pseudosubluxation of C2 on C3 (


(f) 

Flexion-extension radiographs: in the awake, alert patient, these may be helpful in evaluating for 

vertebral column ligamentous instability; rarely useful in acute injuries because associated softtissue 

injuries limit the patient's ability to adequately flex and extend neck. 

(2) CT scan: initial technique of choice in the evaluation of acute cervical injury in most emergency 

departments. 

(3) MRI: a useful examination when ligamentous or cord injury is suspected 

d. Cervical spine "clearance": refers to determination that a trauma patient is at very low risk of cervical spine 

injury and, therefore, radiographic imaging is not necessary. 

(1) Clinical decision rules to identify patients at very low risk of cervical spine injury in whom 

radiographic imaging is not necessary 

(a) NEXUS criteria: no midline cervical tenderness, no focal neurologic deficits, no intoxication, no 

abnormal sensorium/alertness, no distracting injuries 

(b) Canadian cervical spine rules: absence of any high-risk characteristics (age >65 years old, 

dangerous mechanism, extremity paresthesias) and presence of any low-risk characteristics 

(simple rear-end motor vehicle collision, ambulatory at scene, upright position in emergency 

department, no midline cervical tenderness, delayed onset of neck pain) 

(2) Patients with negative imaging (plain radiographs or CT scan) but persistent midline tenderness, 

abnormal sensorium, or abnormal neurologic examination should be maintained in a rigid cervical 

collar until more advanced imaging (MRI or flexion/extension radiographs) may be performed or until 

patient can be clinically evaluated by above criteria. 

e. Management 

(a) For the comatose trauma patient with normal CT imaging of the cervical spine, there is 

controversy on how to "clear" the cervical spine; some argue a normal CT is sufficient, while 

others advocate for MRI before removing collar. 

(1) Patients with either suspected or confirmed cervical spine injuries should be immobilized with a 

rigid cervical collar and supine positioning; any body movement that may cause manipulation of the 

injured spine should be minimized. 

(2) Advanced airway management (if indicated): options include nasotracheal intubation (if the patient is 

breathing), careful orotracheal intubation with in-line manual cervical immobilization (video-assisted 

laryngoscopy may be helpful), and cricothyrotomy (if intubation attempts are unsuccessful). 

(3) Complete primary and secondary trauma surveys to identify and manage other injuries. 

(4) Obtain immediate neurosurgical consult. 

(5) High-dose methylprednisolone no longer routinely recommended. Data suggest limited improvement 

in motor function at cost of significant increased risk of complications (infection). 

(6) Indications for early surgery 

(a) 

Failure to achieve closed reduction in patients with acute cord injury who have incomplete 

sensorimotor loss 

(b) Failure to maintain reduction 

(c) Continued bony encroachment despite reduction 

(d) Successful reduction but continued compression demonstrated on myelography 

2. Vertebral spine trauma 

a. Immobilize the entire vertebral column until unstable injuries are excluded. 

(1) Obtain plain radiographs while the patient is immobilized. 

(a) When evaluating the cross-table lateral cervical spine radiograph, be sure to visualize all 7 

cervical vertebrae (count them!) and the C7-Tl interspace. 

(b) Do not rely on the cross-table lateral radiograph alone to exclude cervical fractures; open-mouth 

odontoid and AP views must also be obtained or CT performed. 

(c) Detection of a cervical spine injury on plain radiographs usually necessitates radiographic 

evaluation of the entire cervical spinal column with CT. 

(2) CT scan: first-line imaging in many emergency departments; indicated if plain radiographs are not 

clearly negative or if the patient has neurologic complaints or findings associated with "normal" 

radiographs. 

(3) MRI: not routinely necessary 

(a) May be indicated if the patient is obtunded (neurologic examination not possible) or has 

neurologic complaints or findings with normal plain radiographs or CT 

320


(b) Can detect the following injuries 

i. Spinal epidural hematoma 

ii. Herniated disc 

iii. Spinal cord contusion/disruption 

iv. Paraspinal ligamentous/soft-tissue injury 

(4) CT myelography may exclude the presence of acute spinal cord compression caused by a traumatic 

herniated disc or epidural hematoma. It is indicated only if MRI is unavailable or contraindicated. 

b. Immediate neurosurgical consult is required for patients with positive radiographs as well as those with 

neurologic complaints or findings, eg, sensory or motor deficits 

c. Cervical spine injury 

(1) Should be suspected in any patient with: 

(a) An injury above the clavicle 

(b) A high-speed vehicular injury 

(c) A fall from >10 feet 

(d) An electrical injury 

(e) An altered level of consciousness 

(f) 

A diving accident 

(g) A football injury sustained while tackling 

(2) Common bony injuries 

(a) Jefferson fracture (C1 ring blowout): an axial loading injury, best seen on open-mouth odontoid 

view; associated C2 fractures are seen in ~40% of these patients. 

(b) Odontoid fracture: look for swelling anterior to C2 on the crosstable lateral view and for 

abnormalities on the open-mouth odontoid view; additional views including tomograms and CT 

are occasionally needed. There are three types of odontoid fractures: 

i. Type I is rare (involves tip of the dens). 

ii. Type II traverses the dens at the junction of the body of C2 (worst prognosis). 

iii. Type Ill involves the vertebral body of C2. 

(c) Hangman fracture (unstable bipeduncular fracture of C2): an extension injury 

(d) Facet dislocations: may be either unilateral or bilateral; unilateral dislocations result from flexionrotation 

injuries, whereas bilateral dislocations are produced by flexion injuries. The lateral view 

reveals ?:25% (unilateral) to ?:50% (bilateral) anterior displacement of the superior vertebral body 

relative to the adjoining inferior vertebral body. 

(e) Clay-shoveler's fracture: an avulsion fracture of the spinous process of C6-T3 (C7 most common); 

results from a flexion injury or a direct blow to the spinous process 

(f) 

Flexion teardrop fracture: associated with significant disruption of posterior ligaments and anterior 

cord syndrome 

d. Thoracic and lumbar injuries 

(1) Should be suspected in patients sustaining multiple traumatic injuries, particularly if the trauma was to 

the trunk and the patient complains of pain at these sites or has neurologic findings or complaints. 

(2) In patients undergoing chest and/or abdominal helical CT scanning, screening for thoracic or lumbar 

spine fractures can be performed on reformatted CT data, obviating the need for plain radiograph 

screening. 

(3) Specific injuries 

(a) Chance fractures: transverse fractures through the vertebral body caused by flexion about an axis 

anterior to the vertebral column (most frequently seen after motor vehicle collisions in which the 

patient was restrained only by a lap belt); may be associated with retroperitoneal and abdominal 

visceral injuries. These are unstable fractures and require operative stabilization. 

(b) Fracture-dislocations: caused by extreme flexion or severe blunt trauma to the spine - 

of the posterior elements (pedicles, facets, laminae) of the vertebra 

i. Because the thoracic spinal canal is narrow in relation to the spinal cord, fracturesubluxations 

of the thoracic spine commonly result in complete neurologic deficits. 

disruption 

11. Chance fractures and fracture-dislocations are extremely unstable and usually require internal 

fixation. 

321


(c) Compression fractures 

1. Most common thoracolumbar fracture 

ii. Characteristics associated with spinal instability: loss of 50% of vertebral height, compression 

fractures at multiple levels, rotational component of fracture, and significant kyphosis (>30%) 

D. Pediatric vertebral and spinal cord injuries 

1. Relatively rare compared with adults 

2. Children


(d) Management 

i. Immediate needle thoracostomy of the affected hemithorax (insert large-bore IV catheter 

perpendicular to the chest wall in second intracostal space along midclavicular line) 

followed by tube thoracostomy 

ii. Alternatively, the catheter can be placed in the usual location of a chest tube (4th intercostal 

space anterior to the midaxillary line); this is easier to do at this level and equally effective. 

(2) Simple pneumothorax 

(a) Clinical presentation 

i. Signs/symptoms range from asymptomatic to severe respiratory compromise depending on 

severity. 

ii. Decreased breath sounds and hyperresonance to percussion on the affected side 

iii. Dyspnea, pleuritic chest pain 

(b) Imaging 

i. Expiratory, upright chest radiograph is more sensitive than standard inspiratory view. 

ii. Ultrasound may be used to detect pneumothorax quickly at bedside. 

(c) Management: tube thoracostomy 

(3) Open pneumothorax ("sucking chest wound") 

(a) If the diameter of the defect in the chest wall is approximately two-thirds or more of the 

diameter of the trachea, air peferentially moves through the chest wall defect rather than the 

trachea with each breath - ineffective ventilation - hypoxia. 

(b) Management 

i. Cover the defect with a sterile occlusive dressing (petrolatum gauze, plastic wrap); tape it 

down on three of its four edges. 

ii. Place a chest tube in an area distant from the wound site. 

b. Pulmonary contusion 

(1) Mechanism of injury: usually results from blunt chest wall trauma (eg, motor vehicle collision with 

rapid deceleration) 

(2) Clinical presentation includes dyspnea, tachypnea, tachycardia, and chest wall tenderness/ 

ecchymosis at the site of injury. 

(3) Associated rib fractures may also be present (less commonly in children). 

(4) Arterial blood gases reveal hypoxemia and a widening alveolar-arterial oxygen gradient. 

(5) Chest radiograph findings 

(a) Localized to the site of injury 

(b) Range from patchy, irregular alveolar infiltrates to frank consolidation 

(c) May be delayed up to 6 hours 


(a) The goal is adequate ventilation/oxygenation and perfusion to promote healing and prevent 

complications (eg, pneumonia, pneumothorax). 

(b) Mild to moderate contusions (28% total lung volume or more than one lobe) are more likely to be 

associated with significant hypoxemia (p0 2 

200 ml of fluid to be evident on chest radiograph 


(a) Most hemothoraces are self-limited and need only tube thoracostomy. 

323


(b) Consider autotransfusion in patients with massive hemothoraces. 

(c) Thoracotomy is indicated for: 

i. Blood loss 2':1 1 

500 ml in the initial chest tube drainage 

ii. Persistent bleeding requiring serial blood transfusions 

iii. Refractory hypotension or cardiopulmonary decompensation 

iv. Blood loss >200 ml/hr for 2-4 hours 

v. 2':50% hemothorax 

3. Blunt cardiac injuries 

a. General principles 

(1) Usually result from high-speed blunt trauma to chest wall (eg, motor vehicle collisions, high-speed 

missile) 

(2) Associated with potentially fatal complications, including arrhythmias, wall motion abnormalities, 

anatomical ruptures, cardiogenic shock 

(3) Diagnosis 

(a) Cardiac enzymes have limited role in evaluation or management. 

(b) ECG is neither sensitive nor specific; however, presence of abnormalities on the initial ECG 

correlates with the risk of developing subsequent cardiac complications. Findings are variable 

and may include sinus tachycardia (most sensitive, least specific), premature ventricular 

contractions, atrial fibrillation, bundle-branch blocks (right bundle-branch block more 

common), ST-T wave changes. 

(c) 2-D echocardiographic findings: impaired regional systolic function (particularly right 

ventricular free wall dyskinesis), increased echogenicity ("brightness"), increased end-diastolic 

wall thickness 

(4) General management 

(a) Patients with conduction abnormalities (or other significant injuries) should be admitted to a 

critical care unit. 

(b) Asymptomatic patients with normal vital signs, a low-risk profile, and normal ECG may be 

released after a short period of observation. 

(c) Symptomatic patients with a low-risk profile and normal serial ECGs can probably be sent home 

after 6-12 hours of observation; if there is some concern after this time, consider ordering 2-D 

echocardiography. 

(d) Symptomatic patients with a moderate-risk profile and normal serial ECGs should have 

echocardiography performed; they may be sent home after a 12-hour observation period if the 

echocardiogram is clearly normal. 

(e) High-risk patients (or those with questionable findings on diagnostic evaluation) should be 

admitted for observation and cardiac monitoring, because they are at risk of developing 

dysrhythmias and cardiac dysfunction. 

b. Injury classification 

(1) Cardiac concussion (no permanent cell damage): commotio cordis 

(a) Mechanism of injury: a sharp, direct blow to the mid-anterior chest wall "stuns" the myocardium 

and results in a dysrhythmia 

(b) If the episode resolves (spontaneously or with treatment), there are no histopathologic changes. 

However, prolonged cellular dysfunction may lead to a nonperfusing rhythm (ventricular 

fibrillation, asystole) and irreversible cardiac arrest. 

(2) Cardiac contusion (permanent cell injury) 

(a) 

Mechanism of injury: high-speed deceleration - heart moves forward and forcibly strikes the sternum 

i. Injuries that occur during early systole or late diastole, when the ventricles are blood-filled, 

are the most damaging. 

ii. Right ventricle more commonly injured 

(b) Diagnosis may be difficult 

(3) Cardiac infarction (cell death) 

(a) 

Rare complication of blunt trauma 

(b) Mechanism of injury: usually results from coronary artery occlusion by arterial spasm, intimal tear, 

laceration, dissection, thrombosis, or compression from adjacent hemorrhage, and edema (which 

may occur with capillary bleeding in a contused heart); patients with preexisting coronary artery 

disease are at greatest risk. 

324


(c) Diagnosis: ischemic changes on ECG; increased cardiac enzymes (may be delayed) 

(d) Management: admission for cardiac monitoring and medical management of myocardial 

infarction 

(4) Cardiac tamponade (bleeding into the pericardium under pressure) 

(a) Penetrating trauma is the most frequent cause, but tamponade can also occur with blunt trauma 

or iatrogenic trauma (central venous pressure catheter placement, pacemaker insertion) 

(b) Mechanism of injury (in blunt injury): rapid deceleration with cardiac compression during early 

systole or late diastole when the ventricles are filled with blood and the myocardial wall is in the 

midst of contracting - rents/tears/lacerations in myocardial muscle - impending myocardial 

rupture - hemorrhage into pericardia! sac 

(c) Clinical presentation 

i. Beck's triad: hypotension, jugular venous distention, and muffled heart tones 

ii. Decreased pulse pressure 

iii. Rising central venous pressure (earliest response) 

iv. Kussmaul sign (distention of neck veins with inspiration) 

v. Pulsus paradoxus 

vi. A central venous pressure > 15 cm H 2 

0 in association with hypotension and tachycardia 

(most reliable sign) 

(d) Diagnostic evaluation 

i. Bedside echocardiography (FAST): preferred diagnostic test; presence of pericardia! fluid 

on ultrasound is highly suggestive of active bleeding in the pericardium in the setting of 

thoracic trauma. 

ii. ECG: electrical alternans is pathognomonic for tamponade but is rarely present in the acute 

scenario. 

iii. Pulseless electrical activity also occurs with tension pneumothorax, hypovolemia, etc. 


i. IV fluids 

ii. Pericardiocentesis 

iii. Open thoracotomy by a qualified surgeon (definitive treatment) 

(5) Myocardial rupture (exsanguination) 

(a) Death usually ensues within seconds to minutes of injury at the scene. 

(b) Mechanism of injury: compression of a blood-filled chamber (usually a ventricle); most commonly 

results from blunt thoracic injury 

(c) The patient is protected from immediate exsanguination if the pericardium is intact (tamponade). 

(d) Clinical presentation: usually one of pericardia! tamponade in a patient with other known or 

suspected thoracic injuries (eg, hemothorax, pneumothorax, aortic dissection/rupture) 

(e) Diagnostic evaluation 

(f) 

i. Chest radiograph is almost always abnormal (nonspecific). 

ii. Bedside FAST reveals pericardia\ effusion/tamponade physiology. 

Management 

1. Fluid resuscitation 

4. Traumatic aortic rupture 

ii. Immediate decompression of cardiac tamponade by pericardiocentesis (temporizing measure 

only) 

iii. If the patient's clinical status deteriorates in the emergency department, emergency thoracotomy 

and pericardiotomy may be required before definitive repair in the operating room. 

a. Mechanism of injury: sudden deceleration (2':45 mph motor vehicle collision impact, damaged steering 

wheel or 20-30 foot fall) 

b. Site of injury: most ruptures occur at the ligamentum arteriosum (the point of greatest aortic fixation) 

just distal to the left subclavian artery and progress from the intima outward toward the adventitia. 

c. 80%-90% of patients die at the scene, and as many as 50% of remaining survivors die within 24 hours if 

not diagnosed and treated expeditiously. 

325



(1) Retrosternal or interscapular pain (25%): most common 

(2) Dyspnea 

(3) Harsh systolic murmur over the precordium or in the interscapular area 

(4) Upper extremity hypertension in association with decreased or absent femoral pulses 

(pseudocoarctation syndrome) 

(5) Pulse deficits 

(6) Voice change or hoarseness (in the absence of laryngeal injury) 

(7) lschemic pain of the extremities 

(8) Paraplegia 


(1) Diagnosis is usually suspected from the history of a deceleration injury plus findings on chest 

radiograph (any, all, or none may be present): 

(a) Widening of the superior mediastinum (>8 cm) on an upright PA chest radiograph (most 

common finding) 

(b) Obliterated or indistinct aortic knob (most reliable finding) 

(c) Deviation of the trachea and/or esophagus (nasogastric tube) to the right 

(d) Depression of the left mainstem bronchus >40° below horizontal 

(e) Obliteration of the space between the pulmonary artery and the aorta 

(f) Left apical pleural cap (obliteration of the medial aspect of the left upper lobe apex) 

(g) Multiple rib fractures 

(h) Widening and/or displacement of the paratracheal stripe to the right 

(i) Widening of the left or right paraspinous stripe 

(j) Left hemothorax 

(k) Fractures of the first or second ribs or the scapula 

(2) Diagnosis is confirmed by: 

(a) Angiography is gold standard but invasive 

(b) Contrast-enhanced dynamic spiral CT is extremely accurate for demonstration or exclusion 

of direct aortic injury. If CT demonstrates traumatic aortic injury (or is not clearly negative), 

aortography should be performed. 

(c) Transesophageal echocardiography is a diagnostic alternative if both angiographic and CT 

findings are equivocal; however, results are highly operator-dependent and patient cooperation 

is required. 

f. Management 

(1) Prompt surgical repair 

(2) Medical management while awaiting surgery: goal is to minimize shear forces on intact adventitia of 

the aorta by decreasing both heart rate (


Table 23: Comparison of Diagnostic Peritoneal Lavage, Ultrasound, and CT Scan 

Diagnostic 

Study 

Indication 

Advantages 

Disadvantages 

Diagnostic 

peritoneal 

lavage 

Identify intraabdominal 

bleeding 

and/or signs of 

bowel perforation 

in hemodynamically 

unstable patients 

Early diagnosis 

Very sensitive 

Detects bowel 

injury (98% 

accurate) 

Invasive 

Does not detect injuries to diaphragm 

and retroperitoneum 

Less specific than ultrasound or CT 

May overdiagnose injuries 

Ultrasound/ 

FAST 

Identify free intraabdominal, 

pelvic, 

pericardia! fluid in 

hemodynamically 

unstable or stable 

patients 

Early diagnosis 

Noninvasive 

Easily repeatable 

86%-97% accurate 

Performed rapidly 

Operator dependent 

Does not detect diaphragm, bowel, 

and retroperitoneal injuries 

Bowel gas and subcutaneous air 

distortion 

CT scan 

Identify solid or 

viscus organ injury 

in hemodynamically 

stable patients 

Most specific for 

injury (92%-98% 

accurate) 

Cost, time, and radiation exposure 

Less sensitive for diaphragm, bowel, 

and some pancreatic injuries than for 

solid-organ injuries 

Usually requires transporting patient 

out of emergency department 

3. CT 

b. Should be used in combination with other diagnostic modalities and clinical assessment 

(1) Unstable patient+ positive ultrasound_,, laparotomy 

(2) Stable patient + positive ultrasound _,, CT (to exclude the need for operative intervention) 

(3) Unstable patient+ negative ultrasound _,, evaluate for other etiologies of hemodynamic instability+ 

serial repeat FAST examinations; or diagnostic peritoneal lavage 

(4) Stable patient+ negative ultrasound _,, observation or CT 

(5) A negative or equivocal ultrasound does not exclude significant injury or the need for further testing. 

c. Advantages 


(2) Detects the presence of intra-abdominal, pericardia!, or pelvic fluid (extended FAST also detects 

pleural fluid) 

(3) Rapid, safe, and portable (can be performed in the controlled environment of the trauma suite) and 

may be repeated as needed 

(4) Can be performed without interfering with resuscitative efforts 

(5) Does not require administration of contrast agents 

(6) No ionizing radiation exposure 

(7) Sensitivity 60%-95%, and specificity nearly 100% (serial examinations increase sensitivity) 

d. Disadvantages 

(1) Can miss bowel and retroperitoneal injuries 

(2) Cannot differentiate fluids, eg, ascites versus blood 

(3) Presence of >200 ml fluid in intra-abdominal cavity usually necessary for positive examination. 

(4) Imaging is impaired in patients who are markedly obese and in those with subcutaneous air/ 

emphysema or excessive bowel gas. 

(5) Operator-dependent 

(6) Less sensitive in evaluation of penetrating injuries 

a. The diagnostic study of choice for evaluating hemodynamically stable patients with blunt 

thoracoabdominal, genitourinary trauma, and/or suspected retroperitoneal injuries; often used in concert 

with the FAST examination (ie, initial evaluation with the FAST examination followed by CT) 

(1) Normal vital signs + normal ultrasound _,, CT may be deferred 

(2) Normal vital signs + positive ultrasound _,, CT may delineate extent of injuries 

327


b. Advantages 


(2) Provides information on specific organ injury; when liver or spleen injury is suspected, CT may 

reliably exclude injuries that require emergent operative intervention (ACEP Clinical Policy). 

(3) Can diagnose retroperitoneal and pelvic organ injuries 


(1) Usually necessitates administration of IV and sometimes oral contrast 

(2) Has a rather high false-negative rate (2%-25%); misses certain injuries, eg, diaphragm, pancreas, 

bladder, and bowel 

4. Diagnostic peritoneal lavage 

a. Used to identify intra-abdominal bleeding or bowel injury that requires immediate laparotomy in the 

unstable patient if a FAST examination is not available or is inconclusive; it is rapidly performed, readily 

available, and has a sensitivity of 98%. No longer recommended as a first-line diagnostic assessment 

because of the high rate of comp I ications. 

b. Indications 

(1) In blunt abdominal trauma, this includes: 

(a) Negative or equivocal FAST examination in unstable patient with suspected or known blunt 

abdominal trauma 

(b) Unstable patient with lap belt sign with suspicion of bowel injury 

(c) Unexplained hypo- or hypertension 

(d) Unstable patient who is unavailable for serial examinations (ie, requires anesthesia for 

management of other injuries) 

(2) In penetrating trauma, this includes: 

(a) Stab wounds with known or suspected peritoneal violation 

(b) Gunshot wounds when peritoneal violation is unclear 

c. Contraindications 

(1) The only absolute contraindication to diagnostic peritoneal lavage is an indication for laparotomy (eg, 

free air under the diaphragm, intraperitoneal bladder rupture). 

(2) Relative contraindications 

(a) Previous abdominal surgery 

(b) Morbid obesity 

(c) Advanced cirrhosis (ascites) 

(d) Severe coagulopathy 

(e) Gravid uterus 

d. The major disadvantages of diagnostic peritoneal lavage are that it can miss significant retroperitoneal 

bleeding and isolated hollow viscus perforation. 

e. Procedure 

(1) Closed, semi-open, or open technique; if performed during pregnancy, the open technique (or minilap) 

should be done using a supraumbilical approach when the gravid uterus is palpable above the 

umbilicus. 

(2) Stomach and bladder are decompressed (nasogastric tube and Foley catheter) before diagnostic 

peritoneal lavage. 

(3) A peritoneal lavage catheter is then placed, and aspiration of free intraperitoneal blood attempted. If 

blood is aspirated, diagnostic peritoneal lavage is considered positive and is terminated. 

(4) If no blood is obtained, 1 L (or 10 ml/kg in children) warmed normal saline or lactated Ringer's is 

instilled into the peritoneal cavity and allowed to drain back out. This effluent is then sent to the 

laboratory for analysis. 

f. RBC criteria for a positive lavage 

(1) 2:100,000 RBCs/mm 3 for blunt trauma and anterior abdominal stab wounds 

(2) >5,000 RBCs/mm 3 for stab wounds of the lower chest and abdominal gunshot wounds 

(3) The RBC count is the most accurate parameter for evaluating lavage fluid. Other criteria (WBC count, 

amylase, bile) are less reliable and increase only after a delay of several hours. 

(4) Presence of food particulate is specific for hollow viscus perforation. 

328


G. Pelvic and extremity injuries 

1. Because pelvic injuries are frequently encountered in major blunt trauma cases, an AP pelvic radiograph is 

traditionally included as part of the standard trauma evaluation (along with lateral cervical spine and AP chest 

radiographs). In stable patients in whom CT imaging is anticipated, plain radiographs are not necessary. 

2. During primary survey, extremity evaluation is limited to identifying (and managing) exsanguinating 

hemorrhage and to assessing perfusion. It is only during the secondary survey that a more detailed evaluation 

of the extremities is performed. 

3. Fractures should be immobilized with splints and/or traction, as appropriate, to control pain and bleeding, as 

well as prevent further injury. 

4. After appropriate radiographic evaluation, dislocations should be rapidly reduced. Reduction should not be 

delayed if there are signs of compromised perfusion distal to the injury. 

5. Distal neurovascular function should be assessed promptly and reassessed before and after all extremity 

manipulations (eg, joint reduction, application of splints, and/or traction). 

6. If open wounds/fractures are identified, the patient's tetanus immune status should be updated as appropriate. 

7. Systemic antibiotics should be administered to patients with open fractures and contaminated wounds. 

8. Fractured bones bleed extensively. Be prepared to transfuse packed RBCs. 

9. Compartment syndromes can occur later, especially in the lower leg and forearm. 

a. Classic signs of a compartment syndrome (the "6 P's") 

(1) Pain out of proportion to the injury and increased with passive stretching and active contraction of 

the involved muscles 

(2) Paresthesias 

(3) Paralysis 

(4) Pallor 

(5) Palpable tenseness and tenderness of the compartment 

(6) Pulselessness (a very late finding) 

b. Pain is the earliest finding and is followed by the development of paresthesias. (For specific bony injuries 

and further discussion of compartment syndrome, see Orthopedic Emergencies, pages 343-390.) 

V. UNIQUE SITUATIONS 

A. Electrical injury 

1. Three major insults result from electrical injury. 

a. Conduction system changes secondary to damage of the body's electrical system 

(1) Cardiac conduction (asystole, ventricular fibrillation, or other cardiac dysrhythmias) 

(a) Ventricular fibrillation is the most common cause of death in the acute phase of electrical 

injuries. 

(b) Asystole is the most common witnessed arrhythmia in lightning strikes. 

(2) CNS conduction of electricity occurs because the body's electrical system is the preferential path for 

current conduction (least resistance). 

(a) Results in respiratory problems, apnea, seizures, etc 

(b) Patients may have paralysis of respiratory muscles despite a perfusing cardiac rhythm. 

(c) Patients may have dilated, nonreactive pupils; these findings do not necessarily reflect overall 

neurologic status or prognosis. 

b. Thermal tissue damage 

(1) The passage of current generates heat - cutaneous burns and muscle injury 

(a) Conversion of electrical energy to thermal energy is proportional to the resistance of the tissue, 

ie, higher resistance results in more heat. 

(b) Tissue resistance is greatest in bone, followed in order by skin, muscle, and nerves. 

(2) Thermal burns are proportional to the time of exposure. 

(a) Lightning strikes deliver an incredible amount of energy for a very short time period. 

(b) AC electrical injuries deliver much less energy for a longer period of time. 

(3) Muscle injury - rhabdomyolysis - acute myoglobinuric renal failure 

329


c. Blunt trauma 

(1) An electric shock can throw the victim down or into the air _,. fractures (particularly long-bone 

fractures and spinal compression fractures) and dislocations 

(2) An electric shock delivered at a frequency of 40-110 Hz (AC current) _,. tetanic contractions _,. 

scapular fractures and shoulder dislocations 


a. Amount of voltage 

(1) Low voltage: 1,000 volts (high-tension power lines may be 100,000 volts; lightning may be in excess 

of 10 million volts) 

b. Type of electricity 

(1) AC: may cause repetitive muscle contractions and muscle tetany; may cause hand to grasp electrical 

source and prolong exposure 

(2) DC: generally causes a single muscle spasm that throws victim away from source; results in shorter 

duration of electrical current but more associated trauma from fall 

c. Type of injury 

(1) Direct injury: electrical current passes through the body, which acts as a circuit; there are usually 

entrance and exit wounds; the internal injuries are often much more severe than the skin wounds 

would suggest 

(2) Flash (arc) injury: current strikes the skin but does not enter the body; with flash lightning strikes, the 

classic finding is Lichtenberg figures (branching, "feathering" skin lesions) 

3. Management: focuses on ABCs: IV, oxygen, cardiac monitor, cervical spine precautions (if indicated) 

a. CPR should be initiated and continued despite prolonged periods of non-perfusing rhythms (usually 

ventricular fibrillation or asystole); cardiac arrhythmias should be managed according to standard ACLS/ 

ATLS protocols 

b. Return of spontaneous circulation and good neurologic outcomes are more common in victims of electrical 

injuries. 

c. Remember: patients may have apnea from paralysis of respiratory muscles despite a perfusing rhythm. 

d. Remember: victims of lightning strikes may have dilated, nonreactive pupils; these findings do not 

necessary reflect neurologic status. 

e. Begin fluid resuscitation with normal saline or lactated Ringer's. 

(1) If there are signs of shock (hypotension/tachycardia, diaphoresis, altered level of consciousness), a fluid 

bolus (20 ml/kg) is indicated. 

(2) The rate should then be adjusted as needed to maintain a urine output of at least 0.5-1 ml/kg/hr. 

(3) If there is evidence of myoglobinuria, the rate should be increased until urine output is 1.5-2 ml/kg/hr. 

f. Obtain an ECG. 

g. Laboratory tests: creatine kinase and urinalysis for presence of myoglobin as well as serum potassium and 

calcium levels (to exclude hyperkalemia and hypocalcemia). 

h. Check carefully for entrance and exit wounds; most common entrance sites are the hand and skull; most 

common exit site is the heel. 

i. Evaluate patients for evidence of blunt trauma. 

j. Wound care: cleanse cutaneous burns, and apply a topical antibiotic dressing (eg, silver sulfadiazine, 

mafenide acetate, bacitracin); do not debride soft-tissue injuries involving the hands, digits, or face. 

k. Administer tetanus prophylaxis as needed. 

I. Monitor for compartment syndromes. 

m. Evaluate patients who sustain electrical injuries of the head and neck for traumatic cataracts, and refer them 

to an ophthalmologist for follow-up; cataracts may develop shortly after injury, or they may be delayed 

months to years. 

n. Lip commissure burns require close observation and referral to a plastic or oral surgeon; delayed 

hemorrhage (3-14 days after injury) from the labial artery occurs in 10%-15 % of these patients. 


a. Hospitalization is indicated for all patients with high-voltage burns(> 1,000 volts) and for those patients 

with low-voltage burns (


b. Asymptomatic patients with low-voltage injuries may be discharged to home after a period of observation 

and cardiac monitoring in the emergency department if their ECG and physical examination are normal 

and if they have no evidence of cutaneous involvement or urinary heme pigment. 

5. Important differences between electrical injuries and thermal burns 

a. Electrical injuries cause extensive muscle damage - myoglobin release (physiologically, they are more like 

a crush injury than a thermal burn) 

b. In electrical injuries, the extent of cutaneous injury does not necessarily correlate with the amount of 

underlying tissue damage (neurovascular and musculoskeletal); it is often just the tip of the iceberg. (For 

further discussion of electrical injuries, see the chapter on Environmental Disorders, page 633.) 

6. Lightning injuries: a small but important subset of electrical injuries; see the chapter on Environmental 

Disorders, page 633. 

B. Rhabdomyolysis 

1. Pathophysiology: injury to muscle - release of myoglobin - damage to kidneys - acute renal failure (90% of 

patients recover) 

2. Commonly associated electrolyte abnormalities are hypocalcemia, hyperkalemia, and hypouricemia. 

3. Serial measurements of the creatine kinase level are used to monitor progress. 

4. Management 

a. Aggressive IV fluid (normal saline or lactated Ringer's) hydration; administer fluids at a rate sufficient to 

maintain urine output at 1.5-2 ml/kg/hr. 

b. Unproven and controversial therapy options 

C. Thermal burns 

(1) Mannitol: aids diuresis, which may help prevent heme-induced renal damage; no clear evidence of 

usefulness 

(2) Alkalinization of the urine with sodium bicarbonate 

(a) In theory decreases renal toxicity of heme; however, there is no clear evidence to support routine 

use. 

(b) May be a role for alkalinization in severe rhabdomyolysis 

(3) Loop diuretics: may exacerbate electrolyte abnormalities; limited role in fluid-overloaded patients only 

1. Start with the ABCs. Airway patency and fluid resuscitation are of prime importance. 

2. Inhalation injury should be considered in patients with facial burns, singed facial and nasal hair, evidence of 

oropharyngeal inflammation, carbon deposits in the oropharynx, carbonaceous sputum, and/or a history of 

fire exposure in a confined space. 

a. Treat with humidified oxygen and early intubation. 

b. Nasopharyngoscopy can be used to determine the extent of injury and the presence of posterior 

pharyngeal or laryngeal edema; if negative, need for intubation may be obviated. 

3. Early intubation is indicated in patients with: 

a. Circumferential burns of the neck 

b. Suspected airway/inhalation injury 

4. Early burn resuscitation requires fluid replacement based on the percent of body burned. 

a. Estimate the percent of body surface area (BSA) burned (second- and third-degree burns only) using one of 


(1) "Rule of Nines": head 9%, each arm 9%, chest, back, and each leg 18%, perineum 1 % 

(2) "Rule of Palms": surface area of victim's palm is -1 % of his or her BSA 

(3) Lund and Browder charts: more precise than the other two methods, particularly in children 

331


Rule of 9's 

Source: Dental Day (Wikispaces: http://dentalday.wikispaces.com/file/detail/ru1e_of_nines_2.jpg) 

b. There are many fluid replacement formulas; a general rule is to administer a crystalloid solution (eg, 

lactated Ringer's) in an amount equal to 2-4 ml/kg/% BSA burned/24 hours. Daily maintenance fluids 

should also be administered. 

(1) Parkland formula:% total BSA x weight (in kg) x 4 

(a) Give the first half of these fluids (plus maintenance fluid rate) over the initial 8 hours (from time 

of burn). 

(b) Give the second half of these fluids (plus maintenance fluid rate) over the next 16 hours. 

(2) Adjust fluid administration as needed based on urine output (goal 0.5-1 ml/kg/hr), heart rate, and 

mentation. 

For a more detailed discussion of burns and their management, see the chapter on Environmental 

Disorders, pages 633-669.) 

5. Indications for transfer to burn center (American Burn Association Criteria) 

a. ::::25 % total BSA partial-thickness burns (::::20% in children 40 years old) 

b. ::::10% total BSA full-thickness burns 

c. Burns involving eyes, ears, face, hands, feet, perineum, and any others that may result in significant 

cosmetic or functional disability 

d. Presence of associated major trauma or inhalation injuries 

e. High-voltage electrical burns 

D. Trauma in pregnancy 

1. Introduction 

a. Pregnant patients are fundamentally two patients. 

b. Trauma is the most common cause of nonobstetric maternal death during pregnancy. 

c. Because fetal survival depends entirely on maternal integrity, initial management should be directed at 

resuscitation and stabilization of the mother; prevention of maternal hypoxia and hypotension ensures the 

best outcome for both mother and fetus. 

d. Early obstetrical, pediatric, and trauma service consults should be obtained. 

2. Airway and breathing 

a. Use continuous pulse oximetry. 

b. Administer supplemental 100% oxygen by mask; because fetal blood functions in a lower portion of a 

left-shifted oxygen-hemoglobin dissociation curve, an increase in oxygen tension produces a significant 

increase in fetal blood saturation. 

332


c. If intubation is required in the breathing patient, standard rapid-sequence intubation with an induction 

agent (propofol, etomidate, ketamine, etc) and a neuromuscular blockage agent (succinylcholine, 

rocuronium) is recommended. 

d. Thoracostomy tube placement (when indicated) should be at the third or fourth intercostal space to avoid 

diaphragmatic injury. 

3. Circulatory status: hemodynamic parameters are misleading. 

a. An increased heart rate and decreased blood pressure may reflect the normal physiologic changes of 

pregnancy; flat, supine positioning (see below); or trauma-related shock. 

b. Total blood volume increases by 30%-50% during normal pregnancy. 

(1) As a result, a pregnant woman may lose 30%-35% of her blood volume (up to 1.5 L) before displaying 

clinical signs of hypovolemia. 

(2) Maternal blood loss results in decreased uterine blood flow and fetal hypoxia. Thus, the fetus may be 

in shock despite the presence of normal maternal vital signs. 

c. Supine hypotension syndrome: in flat, supine position, the gravid uterus compresses the inferior vena 

cava - decreased preload and cardiac output. 

(1) Prevention: patients >20 weeks gestation should be positioned on the left side. If a spinal injury is 

suspected, the backboard should be tilted 15 ° to the left. 

d. Lactated Ringer's solution is the preferred crystalloid fluid in late pregnancy; normal saline may cause 

hyperchloremic acidosis. 

4. Obstetric evaluation is conducted during the secondary survey and should include: 

a. Fundal height and tenderness 

b. Uterine contractions 

c. Fetal movement 

d. Fetal heart rate ( 160 beats per minute indicates fetal distress, which may be the first sign of 

maternal hemodynamic compromise) 

e. Inspection of the vulva and outer vaginal vault for blood and secretions (ferning and blue discoloration of 

nitrazine paper may aid in distinguishing alkaline amniotic fluid from urine) 

f. Pelvic (and rectal) examinations should be performed. 

(1) Perform a sterile speculum examination: inspect the cervix for dilation, effacement, and cloudy white 

or green fluid coming from the os (suggests prolapse of the umbilical cord, which is an obstetric 

emergency requiring immediate cesarean section). 

(2) Perform a bimanual examination (unless premature rupture of membranes is suspected) to determine 

fetal station, presence of contractions, or evidence of injury. 

5. Cardiotocographic monitoring: indicated in all pregnant trauma patients >20 weeks gestation; the fetus may be 

in jeopardy, even with minor maternal injury. 

a. Indications for immediate obstetrical consultation: uterine irritability, ruptured membranes, vaginal 

bleeding, abnormal fetal heart tones/rate (repetitive decelerations, absence of accelerations, beat-to-beat 

variability) or significant maternal injuries 

b. Usually 4-6 hours of monitoring is recommended (commonly performed in labor and delivery unit but 

should be initiated urgently in emergency department). 

6. A gestational age >24 weeks is considered to be viable. Estimate gestational age by reported history from 

mother if available, fundal height (uterine fundus >3-4 cm/2-3 fingerbreadths above the umbilicus), or 

ultrasonography (femur length or biparietal diameter). 

7. Traumatic uterine rupture (rare) 

a. Clinical presentation ranges from minimal signs and symptoms to maternal shock. 

b. Diagnosis 

(1) Ultrasonography is the diagnostic modality of choice; findings may include: 

(a) Disruption of the myometrium 

(b) Extra-uterine or free intraperitoneal fluid 

(c) Extra-uterine fetal anatomy 

(d) Anahydramnios 

(e) Fetal demise 

(2) Uterine rupture that is not identified on ultrasound may be diagnosed on MRI or CT. 

8. Placental abruption (abruptio placenta) is the most common cause of fetal death after blunt trauma. Late in 

pregnancy, abruption can occur after relatively minor injuries. 

333



(1) External vaginal bleeding (absent in up to 30% of cases) 

(2) Abdominal cramps/pain 

(3) Uterine tenderness/rigidity 

(4) Expanding fundal height 

(5) Maternal shock 

(6) Fetal distress 


(1) Cardiotocographic monitoring (most sensitive modality) 

(2) Uterine ultrasonography is only 25 %-50% sensitive. 

c. Because abruption may cause disseminated intravascular coagulation, clotting studies should be performed. 

9. Fetomaternal hemorrhage may occur in even minor blunt abdominal trauma. 

a. In an Rh-negative woman carrying an Rh-positive fetus, this can result in isoimmunization if not detected 

and treated. 

b. Rh-negative women who sustain abdominal trauma during pregnancy should be given Rh immune 

globulin within 72 hours of possible antigenic exposure. 

(1) 12 weeks gestation: administer standard dose (300 mcg). 

(3) Kleihauer-Betke test is not indicated in the emergency department. 

10. Peri mortem cesarean section 

a. Restoration of maternal circulation and thus fetal circulation is the optimal management goal. However, 

prolonged maternal resuscitation without improvement in maternal circulation may jeopardize the life 

of a potentially viable fetus. In this situation, decision to perform a perimortem cesarean section must be 

considered. 

b. Goal is to deliver fetus within 5 minutes of loss of maternal vital signs. Beyond 20 minutes, there is virtually 

no chance of survival with favorable neurologic outcome for the fetus. 

11. Prevention: use of seat belts significantly decreases the risk of serious and fatal maternal injuries; properly 

worn, three-point restraints (lap and shoulder) are the safest. 

E. Penetrating trauma 

1. Most penetrating injuries result from gunshot and stab wounds (rather than impalements); all but obviously 

superficial penetrating wounds require surgical evaluation. 

2. Gunshot wounds 

a. Bullets and other high-speed missiles can ricochet internally and cause much more extensive internal 

damage than is visible externally. 

b. Gunshot wounds to the lower thorax may involve the abdomen as well. The intraperitoneal cavity extends 

from the fourth intercostal space anteriorly to the 6th or 7th intercostal space posteriorly and laterally. 

c. Gunshot wounds of the abdomen are associated with a high incidence of peritoneal cavity penetration 

and intraperitoneal injuries; most require immediate laparotomy. 

3. Stab wounds 

a. Stab wounds of the abdomen have a relatively low incidence of intraperitoneal injuries (when compared 

with gunshot wounds). 

(1) Hollow viscus injuries most common. 

(2) Management based on clinical presentation. 

(a) Extremis: consider resuscitative thoracotomy and emergent laparotomy. 

(b) Hemodynamic instability, evisceration, impaled foreign body (eg, knife blade still present in 

wound), obvious peritonitis, etc: emergent laparotomy 

(c) Patients with no indication for emergent laparotomy: local wound exploration by a surgeon 

combined with advanced diagnostics (serial examinations, FAST, plain radiographs, CT, diagnostic 

peritoneal lavage, laparoscopy) is appropriate. 

1. Extraperitoneal wound only: patient may be discharged home. 

ii. Peritoneal violation: immediate operative management vs close observation for signs of 

peritonitis; only one-half associated with intraperitoneal injury require operative management. 

334


b. Stab wounds of the neck 

(1) Surgical zones of the neck 

(a) Zone I: clavicle to cricoid 

(b) Zone II: cricoid to angle of mandible 

(c) Zone Ill: angle of mandible to base of skull 

----------- -E7 --- 

ZONEIII 

F. Blast injuries 

(2) Evaluation 

(a) All penetrating wounds of the neck require surgical consultation unless determined to be 

superficial. 

(b) Airway management is first priority. 

(c) Physical examination, ancillary studies (chest radiograph, CT, bronchoscopy, 

esophagogastroduodenoscopy or barium swallow, CT angiography or color Doppler ultrasound), 

and/or surgical exploration are mainstay of emergency department evaluation; institutional 

protocols vary, and there is no consensus approach. 

1. Types and mechanisms of injury 

a. Primary blast injuries 

(1) The result of a pressure wave (caused by an explosion) as it passes through the body. Distance from 

the blast source determines magnitude of exposure. 

(2) The ears, lungs, and Cl tract are the most susceptible to injury (tissues with air-fluid interfaces). 

Commonly associated clinical findings include: 

(a) Tympanic membrane rupture (most sensitive indicator of a primary blast effect) 

(b) Air emboli on funduscopic exam 

(c) Petechial hemorrhages in the nasopharynx 

(3) Damage mechanisms 

(a) Spallation: occurs when a pressure wave passes from a dense to a less dense medium; results in 

particles of fluid to be thrown from a dense medium and fragmented into a less dense medium as 

the pressure wave (eg, explosion in water causes water on surface to splash into air); this affects 

organs containing both liquid and gas, eg, lungs. 

(b) Implosion: compression of gas pockets are produced by the pressure wave (such as occurs in the 

ear causing tympanic rupture, hearing loss, etc). 

(c) Pressure differentials: refer to the difference in pressure that develops between the skin and 

internal organs at the moment of impact of the shock wave; in the lung, this pressure differential 

can contribute to pulmonary hemorrhage. 

b. Secondary blast injuries are the result of rapid acceleration of small fragments (flying debris, glass, etc) 

caused by the explosion. 

c. Tertiary blast injuries are the result of the victim's collision with a hard surface (frequently a lethal event). 

d. Quaternary blast injuries are all explosion-related injuries not classified above; includes the exacerbation of 

existing conditions, eg, chest pain in a patient with known coronary artery disease. 

e. Qui nary: delayed hyperinflammatory response with fever and tachycardia 

335


2. Specific injuries 

a. Head and neck are the areas most vulnerable to injury. 

(1) Brain injury (primarily subarachnoid hemorrhage) 

(2) Skull fracture 

(3) Ocular injury (common) 

(4) Auditory injury 

(a) 

Hearing impairment 

i. May be conductive, sensorineural, or both 

ii. Very common in bomb victims (which may lead to an inaccurate assessment because they 

are unable to hear verbal commands and respond appropriately) 

iii. If associated with brain injury, skull fracture, vertigo, or dizziness, suspect ossicular damage. 

(b) Tympanic membrane perforation 

1. Mechanisms of injury 

• Inertia and pressure differentials - 

• Spalling - 

ii. Usual site of injury - 

large punched-out perforations 

linear or small perforations 

the pars tensa of the tympanic membrane 

(5) Facial injury - spalling in the ethmoid region - anosmia 

b. Lungs 

(1) Pulmonary edema and hemorrhage (most common in the intercostal spaces) are the predominant 

findings 

(2) Earliest signs: cough, tachypnea, hypoxemia ("blast lung syndrome") 

(3) ARDS may occur 24-48 hours after the blast. 

(4) Airway management 

(a) 

Unassisted ventilation (with the patient on oxygen) is best. 

(b) Assisted ventilation (with the patient intubated) carries a risk of tension pneumothorax; in 

addition, therapy with positive end-pressure ventilation should be avoided, because there is 

potential risk of air embolism associated with its use in these patients. 

(5) General anesthesia should be delayed 1-2 days (if possible\ because it is poorly tolerated in patients 

with primary blast injury; however, regional or spinal anesthesia may be used. 

c. GI tract 

G. Additional pearls 

(1) Air-containing organs (stomach, duodenum, colon) as well as solid viscera (liver, spleen, diaphragm) 

may rupture. 

(2) Delayed perforations may also occur (especially in the ileocecal region). 

(3) Intestinal injuries are common in underwater blasts. 

1. The spleen is the most common abdominal organ injured in blunt trauma, followed by the liver. 

2. The liver is the most common abdominal organ injured in penetrating trauma, followed by the small bowel. 

3. 

4. 

5. 

6. 

7. 

8. 

9. 

10. 

The most common cause of sudden death after a motor vehicle collision or fall from height is traumatic aortic 

rupture. 

A sternal fracture or chest wall contusion or first/second rib fractures may be associated with a potentially more 

serious injury, eg, myocardial contusion, traumatic aortic dissection. 

Pelvic fractures are associated with bladder injury; check for hematuria and do a urethrogram/cystogram if 

appropriate. 

Posterior knee dislocations may be associated with injury to the popliteal artery and/or nerve; arteriography 

may be indicated (in conjunction with surgical consult) even if pulses are present. If skilled in joint reduction, 

attempt one gentle reduction maneuver. 

Solitary lap belts are associated with small-bowel injuries and mesenteric lacerations in addition to Chance 

fractures. 

Up to 20% of patients with severe renal trauma do not have hematuria; if there is a high index of suspicion, 

perform a CT scan. 

The most common abdominal injury likely to present >24 hours after injury is a contused bowel (eg, duodenal 

hematoma); initial CT may be normal. 

Serial abdominal reexaminations of the trauma patient are important. 

336

TRAUMATIC DISORDERS: PRACTICE CLINICAL SCENARIOS 



Scenario A 

Presentation: A patient has sustained blunt thoracic trauma and presents with tachypnea and retractions. 

Physical examination: Pulse oximetry is 90% on 100% oxygen. Primary survey reveals a patent airway 

but decreased breath sounds on the affected side. The trachea is deviated to the contralateral side. The 

ipsilateral chest is hyperexpanded and hyperresonant on percussion. 


Scenario B 

Presentation: A 30-year-old man sustains a closed head injury from a 30-foot fall. He had a brief period 

of loss of consciousness immediately after the fall. He is now lucid but deteriorating neurologically. He 

progressively develops confusion, decreased level of consciousness, and coma. 


Scenario C 

Presentation: A patient arrives at the emergency department after a high-speed motor vehicle collision in 

which he was unrestrained and possibly ejected from the vehicle. He is tachycardic and hypotensive. 

Physical examination: The airway is secured, and no obvious signs of thoracic injury are found. A FAST 

exam reveals fluid in Morison's pouch. 


Scenario D 

Presentation: An elderly gentleman who is on supplemental oxygen at home presents after sustaining a 

flash burn while trying to light his cigarette. He is awake, alert, and talking, and has partial-thickness burns 

to his entire face. His nose hairs are singed, and there is soot in his oropharynx. His oxygen saturation is 

95% on a nonrebreathing mask. 


Scenario E 

Presentation: A 14-year-old presents with abdominal and back pain after a motor vehicle collision in 

which he was wearing only a lap belt, and the car rear-ended another vehicle at high speed. 

Physical examination: The patient is hemodynamically stable. On examination, there is a linear 

ecchymotic bruise or abrasion across the mid-abdomen, and the abdomen is tender. There is point 

thoracolumbar midline tenderness. 


337


Scenario F 

Presentation: A 35-year-old homeless man presents to the emergency department via EMS shortly after 

being struck by a motor vehicle while he was attempting to cross the street. 

Physical examination: The patient is agitated, combative, and smells of alcohol. He has gurgling upper 

airway sounds and shallow but equal breath sounds. He is moving all of his extremities but is not following 

commands. His heart rate is 110 beats/minute, blood pressure is 100/60 mm Hg, respiratory rate is 10 

breaths/minute, and SpO 2 

is 100% on 100% Fi 0 2 

• 

What is the most appropriate first step in management of this patient? 

Scenario G 

Presentation: A 3-year-old girl presents to the emergency department via EMS after a motor vehicle collision. 

She was an unrestrained rear-seat passenger in her mother's lap when the vehicle hit a tree at 35 mph. 

Physical examination: The child is awake and alert but crying and agitated. Her breath sounds are clear, 

and her SpO 2 

is 100%. Her heart rate is 190 beats/minute, systolic blood pressure is 80 mm Hg, and 

capillary refill time is 4-5 seconds. 


Scenario H 

Presentation: A 24-year-old G2P1 woman who reports that she is approximately 10 weeks pregnant 

presents to the emergency department reporting that she was the victim of domestic violence. She reports 

that her significant other kicked and punched her in the chest, back, and abdomen, and threw her down a 

flight of stairs. She complains of scattered painful bruises but has no other specific complaints and denies 

sexual assau It. 

Physical examination: The patient is tearful but in no distress. She is ambulatory. Primary survey does not 

reveal any life-threatening injuries. Her vital signs are normal. Secondary survey reveals scattered contusions 

but no other serious injuries. A social worker and a police detective are also present at the bedside. 

In addition to ensuring that the patient has a safe social environment, what other pregnancy-related 

considerations are appropriate? 

Scenario I 

Presentation: A 21-year-old man presents to the emergency department after being assaulted and 

robbed. He reports that he was stabbed in the abdomen with an unknown sharp object. He complains of 

abdominal pain but has no other complaints. 

Physical examination: The patient is brought back to an examination room in a wheelchair. He is awake, 

alert, and speaking. The primary trauma survey reveals normal airway, breathing, and circulation. His 

initial vital signs are normal. However, after the patient completely undresses, a 3-cm stab wound is seen 

on the anterior abdominal wall just superior to the umbilicus. There is evisceration of bowel loops through 

the wound. Complete secondary trauma survey is unremarkable. 

What is the appropriate management of this patient? 

ScenarioJ 

Presentation: A 30-year-old man presents to the emergency department via EMS after a motorcycle 

accident. He lost control on an icy road. He was wearing a helmet and did not lose consciousness. He 

complains of left leg pain only. 

Physical examination: The patient is fully immobilized with a cervical collar and long back board. He is 

awake, alert, and talking. This primary survey is normal. His initial vital signs are normal. Secondary survey 

reveals a swollen, tender left lower leg (mid-tibia region) but no obvious deformity. He complains of severe 

pain in his lower leg, foot, and toes. He also complains that his toes are tingling. 


338



Scenario A 

Diagnosis: tension pneumothorax 

Diagnostic evaluation: The diagnosis should be made immediately based on clinical presentation. No 

laboratory or radiologic studies should be necessary. 

Management: Immediate needle thoracostomy should be performed on the affected side, using 

a large bore over-the-needle catheter. The needle is inserted over the third rib (second intercostal 

space) perpendicular to the chest. A gush of air may be heard. After successful decompression, a tube 

thoracostomy should be performed. 

Scenario B 

Diagnosis: epidural hematoma 

Diagnostic evaluation: The diagnosis should be suspected based on the clinical history. It is confirmed by 

noncontrast head CT, which shows a classic lens-shaped convex hematoma, usually along the temporal bone. 

Management: Airway should be secured before head CT if the patient shows signs of neurologic 

deterioration. Standard management of increased ICP should be implemented. In the setting of acute 

herniation, hyperventilation is the most rapid measure to decrease ICP. Ultimately, neurosurgical 

decompression is definitive care. Consultation should be made early in course. 

Scenario C 

Diagnosis: intra-abdominal injury resulting in hemorrhagic shock 

Diagnostic evaluation: The key to diagnosis is identifying hemorrhagic shock (tachycardia and 

hypotension) and performing a FAST examination. The unstable patient should not leave the resuscitation 

bay for a CT. 

Management: Management in the emergency department focuses on restoring circulatory volume and 

oxygen-carrying capacity. Place two large-bore IV lines, and administer crystalloid fluids, 1-2 Lover 5 

minutes each. If the patient remains in shock, administer packed RBCs. Ultimately the unstable patient 

with intra-abdominal bleeding needs an exploratory laparotomy in the operating room. Consultation with 

trauma or general surgery early in the course is essential. 

Scenario D 

Diagnosis: burn with inhalational injury 

Diagnostic evaluation: The key to diagnosis is recognizing that this patient has an inhalation injury and is 

at very high risk of developing airway compromise and respiratory failure. 

Management: This is an airway emergency. This patient should be intubated immediately. A difficult 

airway should be anticipated, and advanced airway equipment, airway alternatives, and surgical airway 

equipment readily available. After intubation, partial-thickness burns should be treated by standard 

practice with fluid resuscitation, debridement of nonviable tissue, and wound cleansing. The patient 

should be transferred to a burn center. 

339


Scenario E 

Diagnosis: lap belt syndrome 

Diagnostic evaluation: The key to diagnosis is recognizing that this mechanism of injury combined with 

the examination findings is very suspicious of "lap belt syndrome" (abdominal wall hematoma/bruise, 

thoracolumbar Chance fracture, and small-bowel injury). FAST examination will likely be negative, 

because this is a hollow- rather than solid-organ injury. CT is most sensitive but may still not detect some 

hollow viscus injuries. Imaging of the thoracolumbar spine is essential. 

Management: Intra-abdominal injuries may be missed on initial evaluation, in which case, observation 

and serial abdominal examinations are essential. They are usually managed by exploratory laparotomy. 

Thoracolumbar Chance fractures are unstable. Spinal immobilization is essential during emergency 

department evaluation. These fractures are usually stabilized neurosurgically in the operating room. 

Scenario F 

Management: endotracheal intubation with in-line cervical spine immobilization 

The first step in the evaluation and management of every trauma patient is airway (followed by breathing 

and circulation). This pedestrian who was struck by a vehicle has altered mental status from a head injury, 

alcohol intoxication, hemorrhagic shock, or a combination of these factors. His gurgling airway sounds 

and altered mental status suggest that he cannot protect his airway and is at risk of aspiration. Therefore, 

the most appropriate initial step is endotracheal intubation. At the same time, it is important to consider a 

cervical spine injury. In-line cervical spine immobilization should be maintained to limit neck movement 

during intubation. Once the patient's airway is secured, the primary assessment should proceed to the 

patient's breathing, circulation, and disability, etc. 

ScenarioG 

Diagnosis: hemorrhagic shock 

Diagnostic evaluation: Children have very robust cardiovascular compensatory mechanisms. As a result, 

hypotension is a late finding in hypovolemic or hemorrhage shock in children. This child's systolic blood 

pressure is within the normal range (lowest 5th percentile normal= 70 + 2 x age in years). However, the 

child clearly has other signs of poor perfusion, including tachycardia, altered mental status (agitation), and 

delayed capillary refill time. 

Management: Because this child has signs of poor perfusion, it must be assumed that she is in 

hypovolemic/hemorrhagic shock. Initial resuscitation should begin with rapid IV crystalloid bolus infusions 

(20 ml/kg over 5 minutes x 2 if necessary). If the clinical response if inadequate, a packed RBC transfusion 

should be given (10 ml/kg). At the same time, an attempt should be made to identify the source of 

hemorrhage. This would likely include a chest radiograph, FAST examination, and pelvic radiograph. If the 

child responds to the resuscitative measures, a CT of the abdomen/pelvis may be considered. However, if 

the child remains in shock, exploratory laparotomy by a trauma surgeon may be the best next step. 

340


Scenario H 

Diagnosis: blunt abdominal trauma in pregnancy 

Diagnostic evaluation: Even minor blunt abdominal trauma in pregnancy can cause fetomaternal 

hemorrhage. In an Rh-negative woman carrying an Rh-positive fetus, this can result in isoimmunization 

if not detected and treated. Therefore, it is important to confirm the patient's Rh type. Rh-negative women 

who sustain abdominal trauma during pregnancy should be given Rh immune globulin within 72 hours of 

possible antigenic exposure. If gestation is estimated to be 12 weeks, the standard 300 mcg dose is recommended. Kleihauer-Betke test is not indicated in the 


Blunt trauma in pregnancy can cause placental abruption, uterine rupture, and fetal demise. These 

more commonly occur during the later stages of pregnancy. The initial assessment of the fetus includes 

measuring fetal heart tones. An ultrasound should be performed if there are concerns for fetal distress or 

uterine/placental abnormalities or if the gestational age is unknown. 

In major trauma resuscitation of the pregnancy patient, the first priority is always ensuring adequate 

cardiopulmonary function of the mother in an effort to maintain adequate fetal perfusion. 

Scenario I 

Diagnosis: stab wound to abdomen with evisceration 

Management: This patient requires emergent exploratory laparotomy. Indications for laparotomy in 

abdominal stab wounds include evisceration, signs of peritonitis, signs of hemodynamic instability/shock, 

and impaled foreign body. 

In patients without indications for emergency laparotomy, management is more complex. The wounds 

may be explored for signs of peritoneal violation. If there is no peritoneal violation, the patient may 

be discharged home. However, only about one half of patients whose wounds violate the peritoneum 

ultimately require laparotomy. Therefore, an approach that involves close observation, serial abdominal 

examinations, and selective laparotomy may be appropriate. 

ScenarioJ 

Diagnosis: acute compartment syndrome of the lower leg 

Diagnostic evaluation: Acute compartment syndrome most commonly develops in association with 

fractures. The lower leg is most commonly involved. Compartment syndrome develops when pressures 

within the extremity compartment increase as a result of soft-tissue swelling and hematoma formation and 

compromise perfusion. The first and earliest symptom is pain, usually out of proportion to the apparent 

injury. Other later findings include the "6 Ps": paresthesias, paralysis, pallor, pulselessness, palpable 

tenderness, in addition to pain. 

The initial evaluation should include radiographs of the affected extremity. Fractures and/or dislocations 

should be promptly reduced and splinted. If concerns for compartment syndrome persist, a surgeon skilled 

in performing fasciotomies should be consulted, if available. Compartment pressures may be measured, 

but it is not always necessary to make the diagnosis. Analgesic medications should be administered. 

Ultimately, the definitive and potentially limb-saving therapy is fasciotomy. 

341

342 

NOTES

ORTHOPEDIC EMERGENCIES 


General Principles of Fracture and Dislocation Management ................................................................................... 349 

Classification and Definitions ............................................................................................................................. 349 

Salter-Harris Classification of Epiphyseal Fractures ............................................................................................. 350 

Complications of Fractures/Dislocations ............................................................................................................. 351 

Upper Extremity Trauma ........................................................................................................................................... 352 

Shoulder Dislocations and Ligamentous Tears .................................................................................................... 352 

Scapular Fractures .............................................................................................................................................. 356 

Humeral Fractures .............................................................................................................................................. 357 

Elbow Injuries .................................................................................................................................................... 359 

Radial and Ulnar Injuries .................................................................................................................................... 362 

Hand and Wrist Injuries ..................................................................................................................................... 364 

Pelvis and Hip Injuries .............................................................................................................................................. 373 

Essential Anatomy of the Pelvis ........................................................................................................................... 373 

Pelvic Fractures .................................................................................................................................................. 3 73 

Hip Dislocations ................................................................................................................................................ 375 

Hip Fractures ...................................................................................................................................................... 377 

Pediatric Hip Disorders ...................................................................................................................................... 3 77 

Knee Injuries ............................................................................................................................................................. 379 

Essential Anatomy .............................................................................................................................................. 379 

Mechanisms of Knee Injury ................................................................................................................................ 379 

Hemarthrosis ...................................................................................................................................................... 380 

Physical Examination of the Knee ....................................................................................................................... 380 

Knee Dislocation ................................................................................................................................................ 380 

Rupture of the Quadriceps Mechanism .............................................................................................................. 381 

Patellar Subluxation/Dislocation ......................................................................................................................... 381 

Patellar Fracture .................................................................................................................................................. 382 

Tibial Plateau Fracture ........................................................................................................................................ 382 

Baker Cyst .......................................................................................................................................................... 382 

Osgood-Schlatter Disease ................................................................................................................................... 383 

Chondromalacia Patellae .................................................................................................................................... 383 

Lower Leg Injuries ..................................................................................................................................................... 383 

Soft Tissue .......................................................................................................................................................... 383 

Anterior Compartment Syndrome ....................................................................................................................... 384 

Stress Fractures of the Fibula ............................................................................................................................... 384 

Ankle Injuries ............................................................................................................................................................ 384 


Sprains (Ligamentous Injuries) ............................................................................................................................ 385 

Ankle Dislocations ............................................................................................................................................. 386 

Tendon Injuries ................................................................................................................................................... 387 

Ankle Injuries in Children ................................................................................................................................... 388 

Foot Injuries .............................................................................................................................................................. 388 


Fractures ............................................................................................................................................................. 388 

343

ORTHOPEDIC EMERGENCIES: SELF-ASSESSMENT QUESTIONS 


1. Which of the following statements regarding anterior shoulder dislocations is false? 

(a) A Hill-Sachs deformity is seen in up to 50% of anterior dislocations. 

(b) Associated neurovascular injury is nonexistent. 

(c) Subcoracoid dislocations are the most common type. 

(d) Treatment consists of reduction and immobilization in a shoulder immobilizer. 

2. Which of the following statements regarding posterior shoulder dislocations is accurate? 

(a) They are best visualized with an axillary or scapular "Y" view. 

(b) They are often associated with damage to the axillary nerve. 

(c) They are often associated with fracture of the anterior glenoid rim. 

(d) They are the most frequent type of shoulder dislocation. 

3. Which of the following muscles of the rotator cuff is tested with the lift off test 

(a) Subscapu laris 

(b) Supraspinatus 

(c) lnfraspinatus 

(d) Teres minor 

4. Which of the following statements regarding the rotator cuff is false? 

(a) All tears require surgical correction. 

(b) It may be torn in association with anterior shoulder dislocations. 

(c) It permits abduction and controls internal and external rotation of the shoulder. 

(d) The tendinous insertions of the rotator cuff are on the greater and lesser tuberosities of the humerus. 

5. Which of the following statements regarding humeral fractures is inaccurate? 

(a) Fractures through the anatomical neck of the humerus are associated with avascular necrosis of the humeral head. 

(b) Humeral shaft fractures are frequently associated with median nerve injuries. 

(c) Management of proximal humeral fractures is determined primarily by the amount of displacement present. 

(d) Proximal humeral fractures are classified according to the Neer classification system. 

6. Which of the following statements regarding supracondylar extension fractures is false? 

(a) They are associated with the development of Volkmann ischemic contracture. 

(b) They are commonly associated with median nerve injury. 

(c) They are more common in children than in adults. 

(d) They generally result from a fall on the outstretched arm. 

7. A proximal ulna fracture associated with a radial head dislocation is referred to as a ____ 

(a) Galeazzi fracture 

(b) Maisonneuve fracture 

(c) Monteggia fracture 

(d) Nightstick fracture 

8. Which of the following statements regarding the ulnar nerve is not accurate? 

(a) It passes through the Guyon canal. 

(b) It innervates the interosseous muscles. 

(c) It is frequently injured in association with Smith's fractures. 

(d) Loss of function results in a "claw hand" deformity. 

9. The second most commonly fractures carpal bone in a fall on the outstretched hand is the _____ 

(a) Lunate 

(b) Trapezoid 

(c) Scaphoid 

(d) Triquetrum 

344


10. The incidence of avascular necrosis in association with scaphoid fractures is highest in fractures of the ___ _ 

(a) Distal scaphoid 

(b) Proximal scaphoid 

(c) Tubercle of the scaphoid 

(d) Waist (middle third) of the scaphoid 

11. Which of the following injuries is most frequently associated with the development of acute carpal tunnel 

syndrome? 

(a) Lunate dislocation 

(b) Peri lunate dislocation 

(c) Scapholunate dislocation 


12. Which one of the injuries listed below does not typically occur by falling on the outstretched arm? 

(a) Proximal humeral fracture 

(b) Radial head subluxation 

(c) Rotator cuff tear 

(d) Supracondylar fracture 

13. The primary cause of death in patients with pelvic fractures is ___ _ 

(a) Associated injuries 

(b) Blood loss 

(c) Ruptured diaphragm 

(d) Sepsis 

14. Which of the following statements regarding posterior hip dislocations is true? 

(a) Avascular necrosis is an early complication of this injury. 

(b) The limb appears abducted, externally rotated, and flexed. 

(c) The mechanism of injury is a direct force applied to the extended knee. 

(d) They represent 15% of all hip dislocations. 

15. A rectal hematoma or tenderness that can be seen in patients with pelvic fracture is called the ___ _ 

(a) 

Destot sign 

(b) Earle sign 

(c) McMurray sign 

(d) Roux sign 

16. Which of the following are stabilizers of the lateral aspect of the knee? 

(a) 

Biceps femoris muscle iliotibial band 

(b) Cruciate ligaments 

(c) Semimembranosus muscle and medial collateral ligament 

(d) Vastus lateral is and rectus femoris muscles 

17. Which of the following statements regarding knee dislocations is not true? 

(a) 

Findings of a warm foot and palpable pulses exclude the presence of injury to the popliteal artery. 

(b) Findings of paresthesia along the dorsal aspect of the foot and foot drop signal the presence of associated 

peroneal nerve injury. 

(c) The incidence of associated popliteal artery injury is 30%-40%. 

(d) Vascular assessment is indicated for all patients with this injury. 

18. Which of the following is the earliest sign of compartment syndrome? 

(a) 

Absence of peripheral pulses 

(b) Pain with passive plantar flexion of the foot 

(c) Paralysis 

(d) Sensory loss distal to the compartment 

345


19. Which of the following findings is consistent with a third-degree sprain of the ankle? 

(a) Ability to bear weight 

(b) Moderate functional loss 

(c) Moderate swelling 

(d) Positive stress test 

20. Which of the following statements regarding calcaneal fractures is false? 

(a) A Bohler angle 75% PMNs), normal glucose, and needle-shaped crystals that are positively birefringent under 

polarized light. The most likely diagnosis is: 

(a) 

Gout 

(b) Osteoarthritis 

(c) Pseudogout 

(d) Rheumatoid arthritis 

25. A 40-year-old patient presents with low back pain and is noted to have a temperature of 38.4°C on examination. 

The most appropriate management of this case is: 

(a) 

Antibiotics for treatment of UTI and follow up with primary care provider in 3 days. 

(b) Bed rest for 2 days with appropriate analgesia and muscle relaxants plus primary care follow-up in 2 days. 

(c) Broad-spectrum antibiotics and admission for pyelonephritis. 

(d) Immediate MRI of the spine. 

346


26. A 62-year-old woman presents with severe shoulder and proximal arm pain after a fall. Radiograph reveals a 

proximal humeral fracture, with the lesser tuberosity displaced from the remainder of the humerus by >I cm, and the 

greater tuberosity minimally displaced by 2 mm. This type of proximal humeral fracture would most accurately be 

classified as a Neer ____ _ 

(a) One-part fracture 

(b) Two-part fracture 

(c) Three-part fracture 

(d) The Neer classification system does not pertain to this type of fracture. 

27. Which of the injuries listed below commonly occurs in association with the particular type of humeral fracture 

described in the question above (#26)? 

(a) Clavicular fracture 

(b) Posterior shoulder dislocation 

(c) Anterior and posterior shoulder dislocations 

(d) Anterior shoulder dislocation 

28. Which of the following statements regarding compartment syndrome is inaccurate? 

(a) A compartment pressure of 30 mm Hg makes a definitive diagnosis of compartment syndrome. 

(b) Initial management consists of removal of constricting dressings or casts (if present). 

(c) It can be caused by crush injuries, fractures, or constrictive dressings or casts. 

(d) The most commonly affected compartments are the anterior compartment of the lower leg and the volar 

compartment of the forearm. 

29. Which of the following is an absolute contraindication to reimplantation of an amputated digit? 

(a) Single-digit amputation other than the thumb 

(b) Serious underlying systemic illness 

(c) Severely damaged or contaminated part 

(d) Unstable patient with other life-threatening injuries 

30. While awaiting a decision from the vascular surgeon regarding reimplantation, what is the best method of 

preserving an amputated part? 

(a) 

Place it in a container of 10% povidone-iodine solution, and store this container in ice water. 

(b) Irrigate it with normal saline or lactated Ringer's to remove gross contamination, wrap it in sterile gauze 

moistened with normal saline, place it in a sterile, water-tight container, and store this container in ice water. 

(c) 

Irrigate it with normal saline or lactated Ringer's to remove gross contamination, wrap it in sterile gauze 

moistened with normal saline, and then place it on ice. 

(d) Irrigate it with 10% povidone-iodine solution to remove gross contamination, wrap it in sterile gauze 

moistened with normal saline, and place it between two ice packs. 

31. Which of the following statements regarding scapular fractures is inaccurate? 

(a) 

Associated injuries, some of which may be life- or limb-threatening, occur in up to 98% of these patients. 

(b) Most scapular fractures require orthopedic referral for open reduction and internal fixation. 

(c) The most common associated injuries are ipsilateral lung injuries, rib fractures, and clavicle fractures. 

(d) They typically occur in association with high-energy trauma. 

32. A segond fracture is associated with injury to which major ligament of the knee? 

(a) 

Anterior cruciate ligament 

(b) Medial collateral ligament 

(c) 

Lateral collateral ligament 

(d) Posterior cruciate 

33. A 48-year-old man presents with knee pain after a fall. Examination reveals a significant hemarthrosis, which you 

aspirate to make him more comfortable. The finding of fat globules in the aspirate is very suggestive of: 

(a) A fracture 

(b) A peripheral meniscus tear 

(c) A tear in the anterior cruciate ligament 


347


34. Innervation of the extrinsic flexor muscles of the hand is provided by: 

(a) The median nerve 

(b) The radial nerve 

(c) The ulnar nerve 

(d) The median and ulnar nerves 

35. The patellar grind tests is helpful in making the diagnosis of: 

(a) Chondromalacia patellae 

(b) Meniscal tears 

(c) A torn anterior cruciate ligament 

(d) A torn posterior cruciate ligament 

ANSWERS 

1. b 7. C 13. b 19. d 

2. a 8. C 14. b 20. d 

3. a 9. d 15. b 21. C 

4. a 10. b 16. a 22. C 

5. b 11. a 17. a 23. d 

6. b 12. b 18. b 24. a 30. b 

25. 

26. 

27. 

28. 

29. 

d 

b 

b 

a 

d 

31. b 

32. a 

33. a 

34. d 

35. a 



348


I. GENERAL PRINCIPLES OF FRACTURE AND DISLOCATION 

MANAGEMENT 

A. Classification and definitions 

1. Direct trauma (direct force over the fracture site) 

a. "Tapping" (nightstick) fracture 

(1) Linear fracture with two fragments 

(2) Little or no soft-tissue injury 

b. Crush fracture 

(1) Comminuted or transverse fracture 

(2) Extensive soft-tissue injury 

c. Penetrating fracture (often seen with missile wounds) 

(1) High-velocity injuries: fragmentation of bone - bone fragments act as secondary missiles - cavitation 

and extensive soft-tissue injury 

(2) Low-velocity injuries: mild fragmentation of bone 

2. Indirect trauma (forces acting at a distance from the fracture site) 

a. Traction (tension) fracture: bone is pulled apart - transverse fracture 

b. Angulation fracture: bending along the long axis of the bone - transverse fracture with concave surface 

often splintered 

c. Compression fracture: compression on the long axis of the bone - axial loading - "T" or "Y" fractures 

d. Spiral fracture: results from rotational stress (torque) 

(1) A pure rotational injury is rare. 

(2) When associated with an axial load - oblique fracture 

3. Incomplete fractures (torus and greenstick): only one cortex is interrupted; these fractures occur almost 

exclusively in children (because of their greater bone elasticity). 

a. Torus (buckle) fracture: characterized by a bulging (buckling) of one cortex; results from compressive forces 

and usually involves the metaphyseal region 

b. Greenstick fracture: characterized by a break in one cortex (convex side) and a bending (bowing) of the 

other cortex (concave side); results from an angular force applied to a long bone 

4. Complete fracture: involves both cortices 

5. Closed (simple) fracture: no communication with the external environment; overlying skin and soft tissue 

are intact. 

6. Open (compound) fracture: communication with the external environment through a break in the overlying 

skin and soft tissue; high risk of infection (osteomyelitis); considered an orthopedic emergency. Management 

includes: 

a. Early emergency department administration of IV antibiotics (a first-generation cephalosporin with or 

without an aminoglycoside) 

b. Tetanus prophylaxis 

c. Wound irrigation and debridement (usually accomplished in the operating room) 

7. Pathologic fracture: results from bone weakness secondary to an underlying disease process (cysts, tumors, 

osteogenesis imperfecta, scurvy, rickets, Paget disease, etc); should be suspected when trivial trauma results 

in a fracture 

8. Stress fracture ("march or fatigue fracture"): results from bone fatigue secondary to repeated or cyclical stress; 

often occurs in association with a sudden increase in level of training; usually located in the lower extremities 

(metatarsals, navicular, distal tibia/fibula, femoral neck); plain radiographs may be negative for ~2 weeks, but 

the fracture will be seen earlier on MRI. 

9. Dislocation: displacement of a bone from its normal position so that there is complete disruption of the 

articular surface 

10. Subluxation: a partial dislocation when there is incomplete disruption of the articular surface 

349


B. Salter-Harris classification of epiphyseal fractures (aids in determining prognosis: the higher the 

number, the poorer the prognosis) 

1. Type 1: fracture through the epiphyseal plate (physis), resulting in separation of the epiphysis; good 

prognosis. 

2. Type II: fracture of the metaphysis with extension through the epiphyseal plate (most common type); most 

common in children > 10 years old; a metaphyseal fragment called a "Thurston Holland sign"' is present; 

good prognosis. 

3. Type 111: fracture of the epiphysis with extension into the epiphyseal plate (an intra-articular fracture); open 

reduction is often necessary. 

4. Type IV: fracture through the metaphysis, epiphysis, and epiphyseal plate (also an intra-articular fracture); 

open reduction is usually necessary, and perfect reduction is essential; growth disturbance is common. 

350


5. Type V: crush fracture of the epiphyseal plate (opposite of Type 1 ): most commonly seen in the knee and 

ankle; radiographs may look normal; poor prognosis, because the blood supply to the epiphyseal plate is 

interrupted. 

C. Complications of fractures/dislocations 

1. Immediate complications 

a. Hemorrhage (can be extensive with pelvic fractures) 

b. Vascular injuries 

(1) Anterior shoulder dislocation - exclude axillary artery injury 

(2) Extension supracondylar fracture - exclude brachia! artery injury 

(3) Posterior elbow dislocation - exclude brachia! artery injury 

(4) Knee dislocation - exclude popliteal artery injury 

c. Nerve injuries 

(1) Anterior shoulder dislocation -a, exclude axillary and musculocutaneous nerve injury 

(2) Humeral shaft injury -a, exclude radial nerve injury 

(3) Extension supracondylar fracture - exclude median, radial, and ulnar nerve injury 

(4) Medial epicondylar fracture - exclude ulnar nerve injury 

(5) Posterior elbow dislocation - exclude ulnar and median nerve injury 

(6) Olecranon fracture - exclude ulnar nerve injury 

(7) Acetabular fracture - exclude sciatic nerve injury 

(8) Posterior hip dislocation -a, exclude sciatic nerve injury 

(9) Anterior hip dislocation -a, exclude femoral nerve injury 

(10) Knee dislocation - exclude peroneal and tibial nerve injury 

(11) Lateral tibial plateau fracture - exclude peroneal nerve injury 

d. Associated soft-tissue and visceral injuries 

2. Intermediate complications 

a. Compartment syndrome 

b. Fat embolism (usually originates from a long bone) 

3. Long-term complications 

a. Reflex sympathetic dystrophy (complex regional pain syndrome) 

b. Volkmann ischemic contracture 

c. Nonunion 

d. Avascular necrosis (femoral head, proximal scaphoid, capitate, and talus fractures are particularly 

predisposed to this complication) 

e. Angulation deformities, overgrowth or shortening 

f. Infection 

g. Joint stiffness 

h. Posttraumatic ossification or arthritis 

351


II. UPPER EXTREMITY TRAUMA 

A. Shoulder dislocations and ligamentous tears 

1. Sternoclavicular joint injuries 

a. Classification 

(1) First degree (sprain)_,. partial tear of the sternoclavicular and costoclavicular ligaments without 

associated clavicular subluxation 

(2) Second degree (subluxation)-,. complete tear of the sternoclavicular ligament plus partial tear of the 

costoclavicular ligament with subluxation of the clavicle from the manubrium 

(3) Third degree (dislocation)-,. complete tear of both the sternoclavicular and costoclavicular ligaments 

with dislocation of the clavicle from the manubrium; clavicle can dislocate either anteriorly (most 

common) or posteriorly (uncommon, but a true orthopedidvascular emergency). 

b. Mechanism of injury 

(1) Direct force over sternoclavicular joint-,. posterior dislocation 

(2) Fall onto the shoulder-,. anterior or posterior dislocation (large amount of force involved, often 

necessitating trauma evaluation and consideration of possible intrathoracic injuries) 


(1) Tenderness and swelling over the sternoclavicular joint 

(2) Pain with movement of the ipsilateral extremity and with lateral compression of the shoulders 

(3) With third-degree injuries, the medial clavicle is displaced (anteriorly or posteriorly) relative to 

the manubrium. 

(4) Shortness of breath, dysphagia, or choking (in patients with posterior dislocations associated with 

compression of mediastinal structures and risk of injury to the great vessels) 

d. Diagnostic evaluation: radiographs; dislocations best demonstrated with CT (obtain with IV contrast to 

exclude vascular injury) 

e. Treatment 

(1) First degree _,. arm sling for 3-4 days and analgesics 

(2) Second degree-,. arm sling, analgesics, and orthopedic follow-up 

(3) Third degree-,. immediate orthopedic consult and rapid reduction 

(a) Establish an IV line and administer analgesia; posterior dislocations often require general 

anesthesia in the operating room. 

(b) Place the patient in the supine position with a rolled sheet between the shoulders. 

(c) Extend, abduct, and apply traction to the ipsilateral arm while an assistant pushes (anterior 

dislocation) or pulls with a towel clip (posterior dislocation) the clavicle into its normal position. 

(d) Apply an arm sling, and refer for orthopedic follow-up. 

(e) Life-threatening injuries to adjacent structures (pneumothorax and compression or laceration of 

the esophagus, trachea, or great vessels) occur in up to 25 % of posterior dislocations and must 

be attended to promptly. 

2. Acromioclavicular separation 


(1) First degreerrype I (sprain)_,. partial tear of acromioclavicular ligament without subluxation of the 

clavicle; the coracoclavicular ligament is intact. 

(2) Second degreefrype II (subluxation) _,. complete tear of acromioclavicular ligament with subluxation 

of the clavicle; coracoclavicular ligament is stretched or incompletely torn. 

(3) Third degreefrype Ill (dislocation)-,. complete tears of both the acromioclavicular and 

coracoclavicular ligaments with dislocation of the clavicle 

(4) Fourth degreefrypes IV-VI (displacement) _,. significant displacement of the distal clavicle posteriorly 

(Type IV), superiorly (Type V), or inferiorly (Type VI), as well as associated injury/ interposition of the 

deltoid or trapezius muscle 


(1) Fall on the shoulder with the arm adducted (most common) 

(2) Fall on the outstretched arm 


(1) Tenderness and swelling over the acromioclavicular joint 

352


(2) Pain with movement of the affected extremity 

(3) With Type Ill injuries, the distal clavicle is displaced upward relative to the acromion when compared 

with the opposite shoulder. This is best visualized when the patient is examined in the sitting or 

standing position with the affected arm hanging at his or her side. 


(1) Radiographic evaluation 

(2) Obtain AP views of both clavicles 

(3) Stress views (taken with 10 lbs of weight suspended from each wrist) are no longer recommended 

because they: 

(a) Are associated with increased cost, radiation exposure, and patient discomfort 

(b) Provide little additional information and can be misleading 

(c) Do not usually alter the course of treatment, because most acromioclavicular separations are 

managed conservatively (nonoperatively), and most third-degree injuries are clinically obvious. 

(4) Findings depend on the degree of separation. 

e. Treatment 

(a) First degree - 

acromioclavicular joint is radiographically normal. 

(b) Second degree - due to upward displacement of the clavicle, the distance between the acromion 

and the inferior aspect of the distal aspect of the clavicle is increased by -S½ the width of the 

clavicle (or -S1 cm) on AP view. The distance seen between the clavicle and the coracoid process 

is normal. 

(c) Third degree - the distance between the acromion and the distal aspect of the clavicle is 

increased by> 1 /2 the width of the clavicle (or> 1 cm) on the AP view. The distance between the 

distal clavicle and the coracoid process is also increased. 

(1) Type I - sling for 1-2 weeks and analgesics, followed by early range-of-motion exercises 

(2) Type II - sling until acute pain has subsided; analgesics and orthopedic referral for further evaluation 

and rehabilitation 

(3) Type Ill - immobilization versus surgical fixation is controversial; immobilize in a sling, provide 

analgesics, and arrange orthopedic referral. 

(4) Types IV-VI - will likely require surgical fixation as definitive treatment; acute management is the 

same as that for Type 111. 

3. Shoulder dislocation (most common dislocation seen in the emergency department) 

a. Diagnostic evaluation: radiographic series 

(1) Standard views should always be ordered (AP shoulder, transcapular lateral or "Y" view, and axillary view) 

(a) 

In anterior dislocations, the AP view detects the most important associated fracture-the humeral 

neck; fracture of the lesser tuberosity suggests a posterior shoulder dislocation. 

(b) In posterior dislocations, the axillary view is diagnostic. The "Y" view can miss some posterior 

dislocations. 

(2) An axillary lateral view is ideal for differentiating anterior from posterior dislocations; it often reveals a 

compression fracture of the humeral head, but it may be difficult to obtain. 

(3) A modified axillary view (called the West Point view) allows visualization of the anterior glenoid 

rim; avulsion (Bankart) fractures in this area (that are associated with anterior dislocations) are not 

infrequent. 

b. Anterior (95%-97% of all shoulder dislocations) 

(1) Mechanism of injury: abduction, extension, and external rotation 

(2) Types (where the humeral head is) 

(a) Subcoracoid (most common) 

(b) Subglenoid (head of the humerus is anterior and inferior to the glenoid fossa) 

(c) Subclavicular (very rare) 

(d) lntrathoracic (very rare) 


(a) Examination of the shoulder reveals prominence of the acromion process and flattening of 

the normal contour of the shoulder. The affected arm is held in slight abduction and external 

rotation; the patient is unable to place his or her palm on the uninjured shoulder. 

(b) A clinical clue is resistance to internal rotation and adduction. 

353


(4) Complications/associated injuries 

(a) Recurrence is the most common complication and is age related; the younger the patient, the 

greater the likelihood of recurrence. 

(b) Bony injuries 

1. Hill-Sachs deformity 

• A compression fracture or "groove" of the posterolateral aspect of the humeral head 

Source: Hellerhoff (Wikimedia Commons: 

http://en. wi ki ped ia.org/wi ki/Fi le:D i slocated_shou Ider _X-ray _03. pn g) 

• Results from impaction of the humeral head on the anterior glenoid rim as it dislocates 

(or reduces) 

• Occurs in up to 50% of anterior dislocations and is particularly common in patients 

with recurrent dislocation; the humeral head is damaged by the sharp anterior rim of the 

glenoid, creating a lesion called the "hatchet sign," which is apparent on the reduction 

film. 

11. Avulsion of the greater tuberosity (more common in patients >45 years old and in those with 

subglenoid dislocations) 

iii. Fracture of the anterior glenoid lip (Bankart fracture) 

(c) Nerve injuries 

i. May occur when the shoulder is dislocated or reduced; therefore, it is important to check 

and document sensation both before and after reduction. 

11. Most injuries are neuropraxias and recover well over time. 

iii. Axillary nerve injury (most common): examination reveals sensory loss over the lateral 

aspect of the shoulder and weakness in shoulder abduction (deltoid muscle). 

iv. Musculocutaneous nerve injury: examination reveals weakness of forearm flexors and 

supinators, as well as sensory loss along dorsum of forearm. 

v. Brachia! plexus injuries: require atraumatic reduction 

(d) Rotator cuff tears (higher incidence in patients >40 years old) 

(e) Axillary artery injury is rare but should be suspected in an elderly patient with a weak/absent 

radial pulse or an expanding hematoma. 

c. Posterior (2%-4% of all shoulder injuries) 

(1) Mechanism of injury 

(a) Convulsive seizure and electric shock are most common mechanisms 

(b) Fall on a forward-flexed, adducted, and internally rotated arm 

(c) Significant direct blow to the anterior shoulder 

(2) The most commonly missed major dislocation of the body, it is often misdiagnosed as "bursitis" or 

"adhesive capsulitis." Radiographic diagnosis can be made with an axillary lateral or transscapular 

lateral "Y" view; an axillary lateral view is an excellent technique for visualization of a posterior 

dislocation, but may be difficult to obtain without adequate analgesia. (Be able to identify.) 

354


Courtesy oi Michael C. Bond, MD 

(3) Types 

(a) Subacromial (98%) 

(b) Subglenoid 

(c) Subspinous 


(a) Examination of the shoulder reveals anterior flatness, posterior fullness, and prominence of the 

coracoid process. The affected arm is internally rotated and is usually held in adduction. 

(b) A clinical clue is inability to abduct or externally rotate the arm. 

(5) Complications/associated injuries 

(a) Associated fractures of the posterior rim of the glenoid fossa, anteromedial aspect of the humeral 

head (reversed Hill-Sachs deformity), and lesser tuberosity. In fact, in the presence of an isolated 

lesser tuberosity fracture, a posterior shoulder dislocation should always be excluded. 

(b) Recurrence rate is 30%. 

(c) Neurovascular complications are uncommon. 

d. Treatment of shoulder dislocation is with reduction using traction, scapular manipulation, or leverage 

and often requires procedural sedation. Closed reduction can usually be accomplished in the emergency 

department. 

(1) Reduction techniques for anterior dislocations 

(a) Stimson or hanging-weight 

(b) Scapular manipulation 

(c) Traction-countertraction 

(d) External rotation (Hennipen technique) 

(e) Milch forward elevation 

(f) 

Spaso maneuver 

(g) Cunningham technique 

(h) The Kocher maneuver (a leverage technique) and the Hippocratic technique are associated with 

many complications and should not be used. 

(2) Reduction technique for posterior dislocations 

(a) Orthopedic consult should precede reduction attempts, because this injury is rare and the rate of 

complications (fractures) is high. 

355


(b) Axial traction is applied in-line with the humerus, and then the humeral head is pushed forward. 

(c) If this is unsuccessful, reduction may need to be accomplished under general anesthesia. 

(3) Shoulder dislocations with an associated fracture should be referred to an orthopedic surgeon for 

reduction (closed or open). 

(4) After reduction 

(a) 

4. Rotator cuff tears 

Recheck and document neurovascular examination. 

(b) Order radiographs to confirm reduction and exclude any associated injuries; humeral neck 

fractures are a known complication of anterior shoulder relocation, the result of which is often 

avascular necrosis of the humeral head. 

(c) Place patient in a shoulder immobilizer or Velpeau dressing. The length of immobilization 

will vary from 1 to 4 weeks, depending on the patient's age; the older the patient, the sooner 

mobilization should be started to avoid stiffness. 

(d) Refer for orthopedic follow-up. 

a. The rotator cuff is made up of tendinous insertions of the following muscles that attach to the greater 

and lesser tuberosities of the humerus. These muscles permit abduction and control internal and external 

rotation of the shoulder. 

(1) Subscapularis 

(2) Supraspinatus (most frequently injured/torn) 

(3) lnfraspinatus 

(4) Teres minor 

b. Mechanisms of injury 

(1) Acute tears usually occur in association with: 

(a) Forceful abduction of the arm against significant resistance (such as a fall on the outstretched arm) 

(b) Direct force such as a fall on the shoulder 

(c) Heavy lifting 

(2) Chronic tears (90% of all lesions) result from subacromial impingement and mechanical 

degeneration or a decreased blood supply to the tendons, both of which accompany advancing age; 

can be insidious in onset and can occur in the absence of trauma, particularly in the elderly. 


(1) Typical patient is a man 2:40 years old. 

(2) Pain over the anterior aspect of the shoulder is abrupt in onset and tearing in quality with acute tears; 

in chronic tears, the pain is more gradual in onset and is typically described as being worse at night. 

(3) Weak and painful abduction or, if the tear is large or complete, inability to initiate abduction; a 

positive "drop-arm test" (inability to hold the arm in 90° abduction) is present with significant tears. 

(4) Tenderness on palpation over the insertion site of the supraspinatus on the greater tuberosity 

d. Radiographs may be normal or show degenerative changes; in the presence of a complete tear, may 

demonstrate superior displacement of the humeral head (best seen on an external rotation view). 

e. Treatment 

(1) Acute tears 

(a) Sling immobilization, NSAIDs, early orthopedic referral 

(b) Complete tears require early surgical repair (


(2) Hemothorax 

(3) Pulmonary contusion 

c. Injuries to the shoulder girdle complex 

(1) Clavicle fractures 

(2) Shoulder dislocations with associated rotator cuff tears 

d. Neurovascular injuries (rare) 

(1) Brachia I plexus 

(2) Axillary artery or nerve 

(3) Subclavian artery 

(4) Suprascapular nerve 

e. Vertebral compression fractures 

3. Mechanism of injury 

a. Direct blow to the scapula 

b. Trauma to the shoulder 

c. Fall on an outstretched hand (FOOSH) 


a. Based on anatomic location 

b. Fractures of the body, neck, and glenoid are most common. 

5. Clinical presentation: The patient is frequently a man who was involved in a high-speed motor vehicle collision 

or had a significant fall. He presents with the affected arm and shoulder adducted against his body and 

complains of pain over the back of the shoulder. On examination, shoulder pain is increased with abduction of 

the arm. 


a. Radiographs 

7. Treatment 

(1) Routine shoulder radiographs demonstrate most scapular fractures. 

(2) Axillary lateral view is helpful in evaluating fractures involving the glenoid fossa, acromion, and 

coracoid process. 

(3) Chest radiograph to exclude associated pulmonary injury 

a. Once any associated injuries have been excluded, most scapular fractures can be managed with sling 

immobilization (for 2:2 weeks) and analgesia, followed by early range-of-motion exercises. 

b. Orthopedic referral for open reduction and internal fixation is usually reserved for severely displaced or 

angulated fractures. 

C. Humeral fractures 

1. Proximal humeral fractures (most commonly seen in the elderly) 

a. Mechanisms of injury 

(1) FOOSH - most common 

(2) Direct blow to the lateral aspect of the arm 

b. Clinical presentation: the patient is usually an older woman with osteoporosis who presents with severe 

upper arm and shoulder pain after a fall; she is likely to be holding the arm in adduction. 

c. Neer classification system 

(1) An anatomic classification system for proximal humeral fractures according to the amount of 

displacement of four segments (consider an additional part if fragment separation > 1 cm or 

angulation >45°). 

(a) Anatomic neck 

(b) Surgical neck 

(c) Greater tuberosity 

(d) Lesser tuberosity 

(2) Major categories 

(a) One-part fractures (minimally displaced) demonstrate no displacement (fragment separation > 1 

cm or angulation >45°). These fractures account for 80%-85% of all proximal humeral fractures. 

(b) Two-part fractures demonstrate displacement of only one fragment. 

357


(c) Three-part fractures demonstrate the displacement of two individual fragments from the remaining 

proximal humerus. 

(d) Four-part fractures demonstrate displacement of all four segments. 

Proximal Humerus Fractures 

Greater Tuberosity 

Lesser Tuberosity 

d. Treatment 

(1) In general, the amount of displacement determines how these fractures are managed. AP, lateral, and 

axillary (if possible) views are essential to make an accurate diagnosis. 

(2) One-part fractures_,. immobilize with shoulder immobilizer, sling and swathe or a Velpeau dressing, 

analgesics, and refer for orthopedic follow-up. 

(3) Two-, three-, and four-part fractures_,. immobilize as above and obtain emergent orthopedic referral. 

Many of these fractures require surgical repair. Four-part fractures may require insertion of a prosthesis. 

e. Complications and associated injuries 

(1) Adhesive capsulitis ("frozen shoulder") is the most common complication and can be minimized or 

prevented by early mobilization exercises. 

(2) Associated neurovascular injuries (brachia! plexus, axillary nerve, and axillary artery) should 

be excluded in all proximal humeral fractures, particularly surgical neck fractures and fracture 

dislocations. 

(3) Posterior shoulder dislocations frequently accompany fractures of the lesser tuberosity because of 

intense contraction of the subscapularis muscle, which inserts at this location. 

(4) Anterior and posterior dislocations occur in association with three- and four-part fractures. 

(5) Avascular necrosis of the humeral head frequently complicates anatomic neck fractures, four-part 

fractures, and fractures of articular surfaces. 

2. Humeral shaft fractures 


(1) Direct blow (most common) 

(2) FOOSH or fall on elbow 

(3) Pathologic fractures (particularly from metastatic breast cancer) are also common. 

b. Usually involves middle third of the humeral shaft 

c. Associated injuries 

(1) Most common is damage to the radial nerve_,. wrist drop (inability to extend the wrist, fingers, and 

thumb) and loss of sensation in the first dorsal web space 

(a) 

Nerve damage occurring at the time of injury is often due to neuropraxia and usually resolves 

spontaneously. 

(b) Nerve palsy occurring after manipulation or immobilization is generally due to nerve entrapment 

and requires immediate surgical exploration. 

(2) Ulnar and median nerve injury may also occur but are much less common. 

(3) Brachia! artery injury 

d. Treatment 

(1) Most of these fractures are managed nonoperatively with one of the following: 

(a) A coaptation ("sugar-tong") splint plus sling and swathe for nondisplaced fractures 

(b) A hanging cast for displaced or angulated fractures 

(2) Operative management is usually reserved for patients with neurovascular compromise, soft-tissue 

interposition, pathologic fractures, or transverse fractures. 

358



D. Elbow injuries 

1. Fractures 

(1) Delayed union is common and may necessitate prolonged immobilization. 

(2) Adhesive capsulitis (stiff/frozen shoulder) may be prevented by early initiation of circumduction 

exercises. 

a. Radiographic findings helpful in diagnosing occult elbow fractures that may be detected on the lateral view 

(1) Fat pad signs 

(a) Posterior fat pad sign: indicates distension of the joint capsule by effusion (hemarthrosis) and 

probable fracture; never seen on a normal elbow radiograph. 

(b) Anterior fat pad sign: not as useful diagnostically as the posterior fat pad sign, because a small 

one is present on many normal radiographs. However, superior and anterior displacement of this 

fat pad suggests a probable fracture. 

(2) Anterior humeral line: a line drawn along the anterior surface of the humerus and extending through 

the elbow that is helpful in detecting subtle supracondylar fractures; this line normally transects the 

middle of the capitellum but, with supracondylar extension fractures, transects the anterior third of the 

capitel lum or passes completely anterior to it. 

b. Supracondylar fractures 

(1) More common in children


c. Olecranon fractures 


(a) 

Direct blow to the olecranon 

(b) FOOSH with the elbow inflexion 


(a) Swelling and tenderness over the olecranon 

(b) Inability to extend the elbow against gravity or resistance due to inadequacy of the triceps 

mechanism 

(3) Associated injuries 

(a) Ulnar nerve injury (paresthesias and numbness in the ulnar nerve distribution or weakness of the 

interossei muscles) is common. 

(b) Usually secondary to ulnar nerve contusion and resolves spontaneously over time 

(4) Treatment 

(a) 

Nondisplaced fractures_,, elbow immobilization in 30° flexion 

(b) Fractures with >2 mm displacement_,, emergent orthopedic referral for surgical repair (open 

reduction with internal fixation) 

d. Condylar fractures 

(1) The distal humerus is composed of the medial and lateral condyles, each of which has an articular and 

nonarticular surface. 

(a) Articular surfaces 

i. Trochlea (on the medial condyle) 

ii. Capitellum (on the lateral condyle) 

(b) Nonarticular surfaces 

i. Medial epicondyle 

ii. Lateral epicondyle 

(2) Condylar fractures usually involve both the articular surface (trochlea, capitellum) and the nonarticular 

surface (epicondyle) of the distal humerus. 

(3) Fractures of the lateral condyle are more common than those of the medial condyle. 

(4) Treatment 

(a) Nondisplaced or minimally displaced fractures_,, immobilization in 90° elbow flexion with 

forearm supination (lateral condylar fracture) or pronation (medial condylar fracture) and 

orthopedic referral 

(b) Fractures with >3 mm displacement_,, surgical fixation 

e. Articular surface fractures (trochlea and capitellum) 


(a) Trochlea and capitellum fractures usually occur in association with posterior elbow dislocations. 

(b) Capitellum fractures can also result from FOOSH and may be associated with radial head 

fractures. 

(2) Treatment 

(a) 

Nondisplaced fractures_,, splint immobilization 

(b) Displaced fractures (even if minimal)_,, emergent orthopedic consult and surgical repair 

f. Epicondylar fractures 

(1) Most commonly seen in children 

(2) Medial epicondylar fractures 

(a) Avulsion fractures most often occur in association with posterior elbow dislocations in children 

and adolescents but can also occur as a result of repeated valgus stress of the elbow in 

adolescents ("little leaguer's elbow"), as well as from a direct blow. 

(b) Must evaluate for ulnar nerve injury (present in 60% of patients) 

(c) Treatment 

i. Nondisplaced (or minimally displaced) fractures---,, immobilization 

11. Displaced fractures_,, orthopedic referral and surgical reduction if fragment displaced >3-5 

mm or if they are intra-articular 

360


(3) Lateral epicondylar fractures 

(a) Rare; generally result from a direct blow 

(b) Generally nondisplaced and treated with immobilization 

2. Dislocations 

a. Posterior elbow dislocations 

(1) Most common type of elbow dislocations 

(2) Mechanism of injury: fall on the extended (or hyperextended) and abducted arm (FOOSH) 


(a) Marked swelling with 45° flex ion of the joint 

(b) Posterior prominence of the olecranon 

(4) Best demonstrated on the lateral surgical of the elbow 

Source: www.lifeinthefastlane.com. Used with permission. 


(a) Fractures about the elbow (30%-60% of cases) 

(b) Injuries to the ulnar and median nerves (common) 

(c) Brachia! artery injury (occurs in up to 8% of cases; should be suspect when a large opening 

between the tip of the olecranon and the distal humerus is palpated on examination or seen on 

radiograph) 

(6) Treatment is reduction. Orthopedic consultation is usually not necessary, and reduction should be 

done immediately if there is neurovascular compromise. 

(a) Provide procedural sedation. 

(b) Apply traction distally at the wrist, while an assistant immobilizes the humerus. 

(c) While maintaining traction at the wrist, flex the elbow and apply posterior pressure to the distal 

humerus. 

(d) A "clunk" will be heard or felt as the elbow is reduced and the articular surfaces mesh. 

(e) Move the elbow through its full range of motion to check stability, and then reassess 

neurovascular status. 

(f) 

Immobilize the elbow in a long-arm posterior splint in 120° (full flexion) or as much flexion as 

circulation permits and obtain radiographs (after reduction). 

(g) Patients can be discharged with instructions to apply ice, elevate, and watch for signs of vascular 

compromise. If the patient is not reliable, he or she should be admitted and observed for possible 

compartment syndrome. 

b. Anterior elbow dislocations (uncommon) 

(1) Mechanism of injury: a blow to the olecranon with the elbow inflexion 

(2) Clinical presentation: the forearm is elongated and supinated while the elbow is generally held in full 

extension 


(a) Incidence of vascular impairment is much higher than with posterior dislocations. 

(b) Associated avulsion of the triceps mechanism is common. 

361


(4) Treatment 

(a) Once neurovascular status has been assessed and procedural sedation provided, an assistant 

immobilizes the humerus while the physician applies in-line traction to the wrist (with one hand) 

and downward and backward pressure to the proximal forearm (with the other hand). 

(b) Orthopedic consultation should be obtained when possible before reduction of elbow 

dislocations with associated fractures. These are difficult or impossible to reduce and may have 

neurovascular sequelae. 

c. Brachia! artery injury may be present with a severe disruption of the elbow joint with any type of 

dislocation. Clues are a wide opening between the olecranon and distal humerus on palpation of the joint 

or seen on a lateral radiograph. 

d. Radial head subluxation (nursemaid elbow) 

(1) Subluxation of the radial head without associated ulnar fracture occurs with some regularity in 

children


e. Treatment 

(1) Nondisplaced fractures: sling immobilization followed by early range of motion exercises as tolerated. 

(2) Comminuted and displaced fractures: immobilization in a long-arm posterior splint and early (2-5 

days) orthopedic referral for screw fixation or radial head excision (with or without silastic implant) if 

one of the fol lowing exists: 

2. Galeazzi fracture 

(a) Marked comminution of the fracture 

(b) Angulation of the articular surface >30° 

(c) >2 mm offset in a two-part fracture 

(d) Fracture involving more than one-third of the articular surface 

a. Fracture of the distal radial shaft associated with a distal radioulnar dislocation (radiographic signs may 

be subtle) 


(1) Direct blow to the back of the wrist 

(2) FOOSH in forced pronation 

c. Treatment: open reduction and internal fixation 

3. Nightstick fracture 

a. Isolated fracture of the shaft of the ulna 

b. Mechanism of injury: a direct blow to the subcutaneous border of the ulna; usually occurs when a patient 

raises up the forearm to protect his or her face from a blow 

c. Treatment 

(1) Nondisplaced fractures: immobilization in a long-arm cast 

(2) Displaced fractures (those with> 10° angulation or displacement >50% of the diameter of the ulna): 

orthopedic referral for open reduction and internal fixation 

4. Monteggia fracture 

a. Fracture of the proximal third of the ulna combined with dislocation of the radial head (usually anterior) 


(1) Direct blow to the posterior aspect of the ulna 

(2) FOOSH with forearm in forced pronation 


(1) The ulnar fracture is often apparent on AP and lateral views of the forearm. 

(2) The radial head dislocation is missed in as many as 25% of cases. Avoid this by assessing the 

alignment of the radial head with the capitellum (radiocapitellar line on lateral radiograph); if the radial 

head is in its normal anatomic position, a line drawn through the radial shaft and head should intersect 

the capitellum in all views. 

d. Associated injury to the radial nerve is common; usually resolves spontaneously in 6-8 weeks. 

e. Treatment 

(1) In adults, open reduction and internal fixation of the ulnar fracture followed by closed reduction of the 

radial head dislocation is the preferred treatment and is associated with the best functional outcome. 

(2) Children can usually be treated with closed reduction under general anesthesia. 

5. Fractures of both the radius and ulna 

a. Usually displaced 

b. Mechanism of injury: most commonly a direct blow to the forearm 

c. Associated injuries 

(1) Peripheral nerve deficits (radial, ulnar, and median) occur infrequently with closed injuries but can be 

seen with open fractures. 

(2) Development of compartment syndrome is a major concern. 

d. Treatment 

(1) Nondisplaced fractures (rare): immobilization in a sugar tong splint 

(2) Displaced fractures: generally open reduction and internal fixation with compression plates is required 

(in adults); children can sometimes be treated with closed reduction. 

e. Complications: compartment syndromes (both anterior and posterior), malunion, and nonunion 

363


F. Hand and wrist injuries 

1. Essential anatomy 

a. Eight carpal bones 

b. Ulnar nerve 

(1) Runs deep to the flexor carpi ulnaris tendon and through Guyon canal 

(2) Innervates the following muscles: 

(a) Hypothenar eminence 

(b) lnterosseous muscles 

(c) Lumbrical muscles of the ring (4th) and little (5th) fingers 

(d) Adductor pollicis brevis 

(e) In the forearm, the flexor carpi ulnaris and ulnar aspect of the flexor digitorum profundus 

(3) Provides sensation to pal mar and dorsal aspects of the ulnar side of the hand, the little finger, and the 

ulnar half of the ring finger 

(4) Testing 

(a) 

Motor test of normal function __.,. abduction of fingers against resistance (patient can spread 

fingers apart) 

(b) Sensation__.,. best tested over the volar tip of the little (5th) finger 

(5) Loss of ulnar nerve function__.,. inability to hold a piece of paper between fingers (early) or claw 

hand (/ate) 

c. Median nerve 

(1) Runs through the carpal tunnel between the flexor carpi radial is and the palmaris longus 


(a) 

Pronator teres 

(b) Flexor carpi radial is 

(c) Flexor digitorum superficial is and profundus (radial part) 

(d) Flexor pollicis longus 

(e) Pronator quadratus 

(3) The thenar motor branch supplies the following: 

(a) Abductor poll icis brevis 

(b) Opponens pollicis 

(c) Flexor pollicis brevis 

(4) The common digital branches innervate the lumbrical muscles of the index (2nd) and middle (3rd) fingers 

364


(5) Provides sensation to the palm on the radial side of the hand and the pal mar aspect of the radial three 

and one-half fingers, as well as the dorsal aspect of the tips of the index (2nd) and middle (3rd) fingers 

and the radial half of the ring (4th) finger 

(6) Testing 

(a) Motor test of normal function - 

muscles for contractions 

(b) Sensation - 

opposition of the thumb to each finger while watching thenar 

best tested over the volar tip of the index (2nd) finger 

(7) Loss of median nerve function - carpal tunnel syndrome; with thenar atrophy in the late stages - 

monkey hand 

d. Radial nerve 


(a) Triceps 

(b) Brachioradialis 

(c) 

Extensor carpi radial is longus 

(d) Extensor carpi radialis brevis 

(e) Supinator 

(f) 

(g) 

Extensor digitorum communis 

Extensor digiti mini mi 

(h) Extensor carpi ulnaris 

(i) 

(j) 

(k) 

(I) 

Abductor pollicis longus 

Extensor pollicis brevis 

Extensor pollicis longus 

Extensor indicus proprium 

(2) Does not innervate any of the intrinsic muscles of the hand 

(3) Provides sensation to the dorsum of the radial aspect of the hand, the dorsum of the thumb, the dorsal 

aspect of the index (2nd) and middle (3rd) fingers, and the radial half of the ring (4th) finger as far 

distally as the proximal interphalangeal (PIP) joints 

(4) Testing 

(a) Motor test of normal function - 

(b) Sensation - 

extension of wrist and fingers against resistance 

best tested over the dorsal web space between the thumb and index finger 

(5) Primary function - extension of the wrist and metacarpophalangeal (MCP) joints 

(6) Loss of radial nerve function - wrist drop, loss of finger extension 

e. Intrinsic muscles of the hand 

(1) Thenar 

(2) Hypothenar 

(3) Abductor pollicis 

(4) Lumbricals 

(5) lnterossei 

f. Six groups of extrinsic extensor muscles 

(1) Abductor pollicis longus and extensor pollicis brevis 

(2) Extensor carpi radial is longus and brevis tendons 

(3) Extensor pollicis longus tendon 

(4) Extensor indices proprius and extensor digitorum communis 

(5) Extensor digiti minimi 

(6) Extensor carpi ulnaris 

g. Extrinsic flexor muscles 

(1) Flexor pollicis longus 

(2) Flexor digitorum superficial is 

(3) Flexor digitorum profundus 

(4) Flexor carpi ulnaris 

(5) Flexor carpi radial is 

(6) Palmaris longus 

365


2. Regional nerve blocks can be particularly useful when treating finger and hand injuries. 

a. Digital blocks 

(1) Digital blocks preferred to local infiltration for most finger injuries; local infiltration into the restricted 

space of the finger is very painful and can impair capillary refill. 

(2) Sensation to the finger (dorsal and volar surfaces and interphalangeal joints) is provided by the palmar 

and dorsal digital nerves, which run along the lateral aspects of each phalanx. 

(3) Digital blocks are performed by using one of three approaches (each of which has advantages and 

disadvantages). 

(a) 

Dorsal approach: needle is directed into the dorsum of the hand at the metacarpals. 

(b) Pal mar approach: needle is directed into the palm over the metacarpal head (very painful). 

(c) Web space approach: needle is directed into the interdigital web space. 

b. Nerve blocks (wrist) 

(1) Useful for extensive hand injuries (particularly the palm, which is very painful to inject into) and MCP 

joint injuries, but they require more time and training to learn and, therefore, are less commonly used. 

(2) Sensation to the hand is provided by the median, ulnar, and radial nerves; therefore, if complete 

anesthesia of the hand is needed, all three of these nerves must be blocked (requires multiple injections). 

(3) These blocks are performed on the volar aspect of the wrist at the proximal skin crease where the 

tendons are easily palpated and provide landmarks to guide the injections. 

(4) More detailed information on performing these blocks can be found in Roberts and Hedges Clinical 

Procedures in Emergency Medicine, 6th ed, page 541. 

3. Carpal injuries 

a. Scaphoid (navicular) fracture 

(1) Most common carpal fracture 

(2) Mechanism of injury: FOOSH 

(3) Initial AP, lateral, and scaphoid radiographic views of the wrist may not demonstrate a fracture in 

?:10% of cases. Repeat radiographs of the wrist in 2 weeks will often demonstrate the fracture. 


(a) Tenderness in the region of the anatomic snuff box 

(b) Pain referred to the anatomic snuff box with longitudinal compression of the thumb (axial 

loading) or with supination of the hand against resistance; if these findings are present, treat 

as a fracture. 

(5) Treatment 

(a) Nondisplaced and clinically suspected fracture: immobilization in a thumb spica splint and 

referral to an orthopedist/hand surgeon. Some hand surgeons immobilize the forearm in a 

coaptation (sugar-tong) splint to prevent supination/pronation, because this is thought to 

decrease rate of malunion/nonunion. 

(b) Displaced fractures usually require open reduction and fixation. 


(a) Avascular necrosis of the proximal fragment; the more proximal, oblique, or displaced the 

fracture, the greater the risk because the vascular supply enters the distal part of the bone. 

(b) Delayed union, malunion, and nonunion 

b. Triquetrum dorsal chip fracture 

(1) Second most common carpal fracture 

(2) Mechanisms of injury 

(a) FOOSH 

(b) Direct blow to the dorsum of the hand 

(3) Clinical presentation: tenderness immediately distal to the ulnar styloid on the dorsal aspect of the wrist 

(4) Best visualized on the lateral view of the wrist 

(5) Treatment: immobilization in a volar splint 

c. Lunate fracture 

(1) Third most common carpal fracture 

(2) Mechanism of injury: FOOSH 

(3) Clinical presentation: pain and tenderness over the mid-dorsum of the wrist that is increased by axial 

compression of the third metacarpal 

366


(4) Plain radiographs of the wrist are often normal; treatment should be started on clinical grounds alone. 

(5) Treatment: immobilization in a thumb spica splint and orthopedic referral 


d. Dislocations 

(a) Avascular necrosis of the proximal segment (Kienbock disease) is a serious complication. 

(b) Most often in patients with congenital shortening of the lunate, but it also results from inadequate 

immobilization. 

(1) Mechanism of injury: violent hyperextension 

(2) Refer all to a hand surgeon 

(3) Lunate dislocation 

(a) The lunate may dislocate either volarly (most common) or dorsally. 

Source: James Heilman, MD 

(Wi ki media: http://en. wi ki pedi a.orglwi ki/Fi le: Lunatedislocation L. j pg) 

(b) Clinical presentation 

1. Pain, swelling, and marked loss of flexion with the wrist, hand, and arm held in anatomic 

position 

ii. Occasionally, patient complains of tingling in the three radial digits (acute carpal tunnel 

syndrome). 

(c) Findings on wrist radiograph 

1. Best seen on the lateral view: the lunate is displaced volarly relative to the capitate and 

carpus, which remain in their normal alignment ("spilled teacup" sign). 

ii. On the AP view, the lunate is triangular ("piece of pie" sign). There is also foreshortening of 

the wrist and loss of the normal space between the capitate and the lunate. 

(d) Associated scaphoid injuries are common. 

(4) Perilunate dislocation (most common wrist dislocation) 

(a) May be associated with a fracture or dislocation of the scaphoid 

(b) The lunate remains in anatomic position relative to the forearm while the capitate is displaced 

dorsally because of disarticulation of the capitolunate joint. 

(c) Diagnostic evaluation: as with a lunate dislocation, a perilunate dislocation is best diagnosed by 

a true lateral film of the wrist. 

367


Source: Hellerhoff 

(Wi ki media: http://en. wi kipedi a .org/wi ki/Fi le: Peri I u naere_Luxation. jpg) 

(5) Scapholunate dislocation 

(a) Clinical presentation: pain with wrist hyperextension and a snapping sensation when the wrist is 

deviated in either the radial or ulnar direction 

(b) Diagnostic evaluation: radiologic signs 

4. Metacarpal injuries 

Source: Wikimanos 

(Wik i media: http://en. wi kiped i a.orglwi ki/Fi I e: Dynam i c_S-L-gri p. j pg) 

1. AP film: The scaphoid is foreshortened and has a dense ring-shaped image around its distal 

edge ("signet ring" sign). There is a widening >3 mm in the space between the lunate and 

scaphoid ("David Letterman" sign). 

11. Lateral film: the angle between the scaphoid and the lunate is increased (>60°). 

(c) Treatment: immobilize in a radial gutter splint or posterior mold for orthopedic referral. 

a. Metacarpal neck fractures 

(1) Result from a punch with a clenched fist 

(2) Almost all are unstable. 

(3) The proximal fragment angulates in the dorsal direction, while the distal fragment angulates in the 

volar direction. 

(4) The amount of angulation that is acceptable varies directly with the normal mobility of the involved 

metacarpal; the greater the mobility, the greater the degree of angulation that can be tolerated. 

368


(a) Metacarpal neck fractures of the ring (4th) and little (5th) fingers ("Boxer's fracture"); up to 20° 

and 40° of angulation, respectively, is acceptable. 

(b) Metacarpal neck fracture of the index (2nd) and middle (3rd) fingers; ::c15 ° of angulation 

is acceptable. 

(5) Rotational deformities, if present, must be completely corrected; look for malalignment of the plane 

of the fingernails when the fingers are viewed in the partially flexed position. 

Source:www.fpnotebook.com(http://www.fpnotebook.com/_media/OrthoHandPositionFistToScaphoid.jpg). 

Used with permission. 

b. MCP joint dislocations 

(1) MCP dislocations of fingers are rare, while those of the thumb are relatively common. 

(2) Usually dorsal and result from hyperextension forces 

(3) Types 

(a) Simple= subluxation 

(b) Complex= complete dislocation 

(4) Radiographs 

(a) Should be taken both before and after reduction to exclude associated fractures and confirm 

adequate reduction 

(b) The lateral view usually demonstrates an obvious dislocation. 

(5) Treatment 

(a) Simple dislocations can usually be managed with closed reduction with adequate anesthesia 

(often requires a wrist block of the ulna, median, and/or radial nerves, depending on which finger 

is involved), splinting inflexion, and referral to a hand surgeon. 

(b) Complex dislocations often cannot be reduced by closed reduction because of interposition of the 

volar plate in the MCP joint or entrapment of the metacarpal head between the lumbrical tendon 

and a flexor tendon. Irreducible MCP joint dislocations should be splinted and referred to a hand 

surgeon for open reduction and operative repair. 


(a) Volar plate injuries 

(b) Bony avulsions 

(c) Thickening and stiffness of the joint 

5. Bennett fracture/subluxation: an unstable fracture at the base of the first metacarpal, often caused by punching; 

it should be suspected when evaluating a "sprained thumb." 

6. Gamekeeper's or skier's thumb (torn ulnar collateral ligament) 

a. Mechanism of injury 

(1) Acute and forceful radial deviation of the thumb 

(2) Commonly occurs in skiing accidents when the ski pole forcefully abducts the thumb at the MCP joint 

as the hand hits the ground in a fall 

369



(1) Tenderness along the ulnar aspect of the thumb, which is most exquisite at the MCP joint 

(2) Thumb grasp and pinch are weak. 


(1) Obtain radiographs of the thumb to exclude associated fractures (present in up to 30% of cases). 

(2) Assess joint stability. 

d. Treatment 

(a) Apply a lateral stress (radial abduction) to the MCP joint of the injured thumb (after adequate 

anesthesia). 

(b) Stress the normal thumb in the same manner. 

(c) The presence of 10°-20° of laxity in the injured thumb when compared with the normal thumb is 

consistent with a complete tear. 

(1) Incomplete tear (some stability=


c. Examination of the flexor tendons 

(1) Flexor digitorum profundus tendon: immobilize the PIP and MCP joints in extension and ask the 

patient to flex the tip of the finger; inability to flex the distal interphalangeal (DIP) joint indicates a 

profundus tear that is usually associated with a volar plate slip at the PIP joint. 

(2) Flexor digitorum superficial is tendon: hold the uninjured fingers in extension and ask the patient to 

flex the injured finger; this blocks the action of the profundus tendon and allows an isolated test of the 

superficial is tendon. 

(3) Partial tears are detected by evaluating the strength of the flexor tendons against resistance. Patients 

with 90% full-thickness lacerations still have normal (although painful) range of motion. 

(4) Treatment of partial tendon lacerations is controversial and should be determined in consultation with 

a hand surgeon. Many are treated with protective splinting alone. 

d. Extensor tendon injuries are usually closed. (Be able to identify on pictorial.) 

(1) Mallet finger 

(a) Extensor tendon laceration or disruption at the DIP joint (may or may not be associated with 

avulsion chip fracture) 

(b) Clinical presentation: The patient is unable to extend the DIP joint. 

(c) Mechanism of injury: usually a blow to the tip of the extended finger producing sudden forced 

flexion 

(d) Treatment 

i. If there is no associated fracture-,, splint the DIP in full extension to slight hyperextension for 

6-8 weeks. 

11. If there is an associated fracture-,, the treatment is either splinting as above or surgical 

pinning of the avulsed fragment using Kirschner wire fixation. 

(e) Complications 

i. A delayed complication of an untreated mallet finger is the "swan neck deformity," in which 

there is hyperextension of the PIP joint in addition to the mallet flex ion deformity of the DIP 

joint. 

11. It is the result of increased extension forces on the PIP joint and is produced by proximal and 

dorsal migration of the lateral bands. 

Courtesy of Michael C. Bond, MD 

(2) Boutonniere deformity 

(a) Rupture of the central slip of the extensor tendon at the PIP. 

(b) Clinical presentation: characterized by flexion of the PIP joint and hyperextension of the DIP joint 

371


(c) Mechanism of injury: a direct blow to (or laceration of) the PIP joint or forced flexion of the PIP 

joint against resistance. 

(d) This deformity is not always present immediately after the injury, but rather often develops over 

time (1-2 weeks after the injury) because the lateral bands of the extensor tendon slip volar to the 

axis of the PIP joint and so become paradoxical flexors of this joint. 

(e) Treatment: splint the PIP in extension and then refer to a hand surgeon for possible operative 

repair. 

e. De Quervain stenosing tenosynovitis 

(1) An inflammation of the extensor tendons of the thumb 

(a) Abductor pollicis longus 

(b) Extensor pollicis brevis 


(a) Complaint of pain along the radial aspect of the wrist that is exacerbated with use of the thumb 

(b) Palpation reveals tenderness over the radial styloid. 

(c) A positive Finkelstein test (pain on ulnar deviation of the wrist while the thumb is flexed and held 

in the palm by the other fingers) confirms the diagnosis. 

(3) Mechanism of injury: overuse of the thumb 

(4) Treatment 

9. Amputated digits 

(a) Administer oral NSAIDs. 

(b) Place in thumb spica splint. 

(c) Inject the first dorsal compartment with a bupivacaine and triamcinolone combination; this can 

be done on the initial evaluation or reserved for those patients in whom conservative therapy has 

not been effective. (Repeated injections are associated with a risk of subsequent tendon rupture.) 

a. Preservation of the amputated part 

(1) After irrigating the amputated part with normal saline to remove gross contamination, wrap it in 

sterile gauze moistened with lactated Ringer's or normal saline and place it in a sterile, water-tight 

container. 

(2) Store the container in ice water. 

b. Criteria for reimplantation 

(1) Young, stable patient 

(2) Sharply incised wound with minimal associated damage 

(3) Thumb amputation 

(4) Multiple-digit amputation 

(5) Hand or forearm amputation 

(6) Amputation in a child 

c. Contraindications to reimplantation 

(1) Absolute 

(a) Unstable patient with other life-threatening injuries 

(b) Severe crush injury 

(2) Relative 

(a) Severely damaged or contaminated part 

(b) Single-digit amputation (other than the thumb) 

(c) Avulsion injury 

(d) Serious underlying systemic illness (eg, CHF, diabetes mellitus) 

(e) Prolonged warm ischemia (2:12 hours) 

(f) 

Prior injury/surgery to affected part 

(g) Emotionally unstable patient 

372


Ill. PELVIS AND HIP INJURIES 

A. Essential anatomy of the pelvis 

1. Pelvic bones: innominate (consists of the ilium, ischium, and pubis), sacrum, and coccyx 

2. On the AP view of the pelvis, the symphysis pubis is usually 5 mm wide, and the sacroiliac joint is normally 

2-4 mm wide. 

3. The lumbar and sacral nerves run through the pelvis. 

4. The ileopectalline divides the upper (false) pelvis and the lower (true) pelvis. Injuries to the true pelvis may be 

associated with injuries to the following structures: 

a. Bladder or urethra 

b. Descending colon 

C. Sigmoid colon 

d. Rectum 

e. Anus 

f. Nerve roots 

g. Vasculature 

B. Pelvic fractures 

1. Mechanism of injury 

a. Motor vehicle and motorcycle collisions (most common cause of injury in adults) 

b. Falls 

c. Crush injuries 

d. Pedestrian hit by motor vehicle (leading cause of injury in children) 

2. Classification: Several different systems have developed over the years to classify pelvic fractures. The 

central focus of most of these systems is the underlying stability of the pelvis. The Young-Burgess system is 

most favored by emergency physicians, because it is valuable in predicting hemorrhage related to pelvic 

fracture and local vascular injury. This system is based on the mechanism of injury (AP compression or lateral 

compression) as well as the degree of pelvic instability. 

3. Classification types: see page 374 for illustrations; arrow indicates direction of force. 

4. Lateral compression 

a. Type I: posteriorly directed force - sacral crushing and horizontal pubic ramus fractures ipsilaterally 

b. Type II: anteriorly directed force - horizontal pubic ramus fractures with anterior sacral crushing and 

disruption of the posterior sacroiliac joints or fractures through the iliac wing 

373


c. Type Ill: anteriorly directed force continued, causing external rotation of the contralateral side 

(1) Sacroiliac joint opened posteriorly 

(2) Sacrotuberous and spinous ligaments disrupted 

5. Anteroposterior (AP) compression 

a. Type I: symphysis disrupted but posterior ligamentous structures intact 

b. Type II: continues type I, with disruption of the sacrospinous and possibly the sacrotuberous ligaments and 

an anterior sacroiliac joint opening 

c. Type Ill: continued force disrupts the sacroiliac ligaments 

6. Vertical shear 

a. Vertical fractures in the rami; disruption of all posterior ligaments 

b. Equivalent to an AP type Ill or completely unstable and rotationally unstable fracture 

Ligamentous anatomy of the pelvis 

A, lateral compression 

II 

Ill 

8, anteroposterior 

(AP) compression 

t 

II 

t 

Ill 

C, vertical shear t 


a. Destot sign: a superficial hematoma above the inguinal ligament or on the scrotum 

b. Earle sign: on rectal examination, a large hematoma or tenderness along the fracture line or palpation of a 

bony prominence 

c. Roux sign: a diminished distance measured from the greater trochanter to the pubic spine on one side 

compared with the other (indicates an overlapping fracture of the anterior pelvic ring) 

8. Diagnostic evaluation: CT 

a. Superior to standard radiographs in evaluating the acetabulum, posterior (femorosacral) arch, and sacroiliac 

joint 

b. Often provides information on the degree of pelvic instability and the presence of a retroperitoneal 

hematoma 

374


9. Associated injuries: more common in children because the developing pelvis provides a lesser degree of 

protection 

a. Hemorrhage 

(1) Primary cause of death in patients with pelvic fractures; up to 6 L of blood can be accommodated in 

the retroperitoneal space. 

(2) Most common in patients with Type Ill and posterior fractures 

(3) Up to 50% of patients require transfusion. 

(4) Initial control obtained by application of a pelvic binder or tying a sheet across the pelvis, followed by 

external fixation and angiographic embolization in some patients. Resuscitative endovascular balloon 

occlusion of the aorta (REBOA) is a newer procedure to limit blood loss in hemodynamically unstable 

patients until hemorrhage can be more definitively controlled. 

b. Injuries of the urethra and bladder 

(1) Most common associated injury 

(2) Urethral injuries (particularly posterior urethral tears in men) are more common than bladder injuries. 

c. Vaginal laceration or rupture (relatively uncommon but may be seen with anterior pelvic fractures) 

d. Nerve damage (most commonly occurs in association with posterior pelvic fractures) 

e. Ruptured diaphragm (not uncommon and is often missed) 

f. Rectal injuries 

(1) Uncommon 

(2) Generally occur in association with ischial and urinary tract injuries 

(3) Prophylactic antibiotics should be administered without delay. 

g. Thoracic aortic rupture (traumatic aortic disruption): incidence is 8 times greater in patients with pelvic 

fractures than in patients with blunt abdominal trauma. 

10. Complications of pelvic fractures 

a. Sepsis 

b. Thromboembolic complications (pulmonary and fat emboli) 

c. Malunion or delayed union 

d. Chronic pain 

11. Specific pelvic fractures 

a. Pubic rami 

(1) A single pubic ramus fracture is the most common pelvic fracture. Common mechanism is a fall on 

the buttocks. Fracture may be missed on plain radiographs; order an MRI if in doubt or if it will change 

management. 

(2) A "straddle injury" is a fracture of all four pubic rami, such as occurs in a fall on the crotch with the 

legs apart. 

b. Iliac crest (result from impact collisions) 

(1) Duverney fracture (pelvic wing fracture) 

(2) Ilium fracture - pelvic ring disruption, visceral injuries 

c. Multiple pelvic fractures (Malgaigne fracture) 

(1) Involves the pubic rami bilaterally and the ilium or sacrum 

(2) Results from vertical shear forces (eg, fall from a height) 

C. Hip dislocations (an orthopedic emergency [in the absence of a prosthetic femoral head]) 

1. Anterior: 10% of hip dislocations (Be able to identify on pictorial.) 

a. Classified according to the final resting position of the femoral head 

(1) Superior iliac: femoral head is palpable in the area of the superior iliac spine. 

(2) Superior pubic: femoral head rests near the pubis. 

(3) Inferior (obturator): femoral head lies in the obturator foramen. 


(1) Extreme abduction causes the femoral head to be pushed out through a tear in the anterior capsule. 

(2) Causes include: 

(a) Motor vehicle collision 

(b) A fall 

(c) A blow to the back while squatting 

375



(1) Limb appearance (varies with the type of dislocation present) 

(a) With anterior superior dislocations, the limb is slightly abducted, externally rotated, 

and extended. 

(b) With anterior inferior dislocations, the limb is abducted, externally rotated, and flexed. 

(2) Associated physical findings 

(a) 

Diminishing femoral or distal pulse (or progressive swelling of the leg) indicates the need for 

immediate reduction of the hip. 

(b) If the femoral nerve is involved, the following will be diminished: 

i. Quadriceps function 

ii. Deep tendon reflexes at knee 

iii. Sensation on anteromedial thigh 

2. Posterior: 80%-90% of hip dislocations (Be able to identify on radiograph.) 

a. Mechanism of injury: most cases result from motor vehicle collisions in which a direct force is applied 

to the flexed knee (hitting the dashboard) that is transmitted to the femoral head, which is pushed out 

through the posterior capsule. 


Posterior Hip Dislocation 

Anterior Hip Dislocation 

3. Treatment 

(1) Limb appearance: shortened, adducted, internally rotated, and flexed 

(2) Associated physical findings 

(a) Evidence of acetabular/femoral fractures 

(b) Knee injury 

(c) Sciatic nerve injury results in loss of: 

i. Muscle function below the knee 

ii. Ability to flex the knee 

iii. Sensation on posterolateral leg and sole of the foot 

a. Early reduction is required; avascular necrosis of the femoral head increases in direct proportion to delay 

in reduction. 

b. Immediate closed reduction (using procedural sedation) should be attempted in the emergency 

department as soon as appropriate radiographs have been obtained to exclude associated injuries. If this 

is unsuccessful, closed reduction under general anesthesia is indicated. Neurovascular assessment should 

be performed before and after any reduction attempts. 


a. Early complications 

(1) Anterior dislocations _,. femoral artery, vein, and nerve injury 

(2) Posterior dislocation _,. sciatic nerve injury (10% of patients) 

b. Late complications (in addition to osteoarthritis) 

376


D. Hip fractures 

(1) Anterior dislocation - femoral artery/vein thrombosis - pulmonary embolism and avascular 

necrosis of the femoral head 

(2) Posterior dislocation - avascular necrosis of the femoral head (15 %-30% of patients) 


a. lntracapsular (femoral head and neck fractures) or 

b. Extracapsular (trochanteric, intertrochanteric, and subtrochanteric) 

c. This classification system has prognostic value in that intracapsular fractures are far more likely to result 

in a disrupted vascular supply and subsequent avascular necrosis than extracapsular fractures. 

lntracapsular lntertrochanteric Subtrochanteric 

2. Clinical presentations 

a. An elderly patient complains of hip pain after a fall. The patient limps when he or she walks or may be 

unable to walk. The affected leg is shortened, abducted, and in slight external rotation - femoral neck 

fracture 

b. A patient complains of hip pain after a fall. The leg is shortened and in marked external rotation - 

intertrochanteric fracture (fracture line between the greater and lesser trochanters) 

c. The ability to ambulate does not exclude a fracture; some patients with nondisplaced or minimally 

displaced fractures may be able to bear weight. 


a. Negative plain radiographs do not exclude a fracture. 

b. Patients with negative plain radiographs who are unable to ambulate require further evaluation (CT, MRI, 

or bone scan). 

4. Complications: most common is avascular necrosis (15 %-35 % of femoral neck fractures in the elderly) 

E. Pediatric hip disorders 

1. Classic clinical scenarios 

a. You are examining a female infant with some other condition. Because you routinely perform the 

Ortolani maneuver in all children


a history of trivial antecedent trauma. The affected leg is externally rotated and adducted (and may be 

shortened). Further evaluation reveals tenderness around the hip and decreased range of motion (internal 

rotation and abduction [full flexion] are limited). Radiographs (AP and bilateral frog-leg lateral views of the 

hips) confirm the diagnosis - slipped capital femoral epiphysis. 

2. Developmental dysplasia of the hip 

a. More common in females than males 

b. More common in first born, breech presentation 

c. Palpable click or clunk detected with range of motion of affected hip 

3. Septic arthritis 

a. Staphylococcus aureus most common organism 

b. Ultrasound of hip will often show an effusion 

c. Diagnosed by arthrocentesis of hip, usually under fluoroscopic guidance by orthopedics 

d. Synovial fluid analysis: WBC count 80,000-200,000/mm 3 with >75% PMNs 

e Treatment is antibiotics. 

4. Transient (toxic) synovitis 

a. Nonspecific inflammation of the synovium of the hip 

b. Often due to viral illness 

c. Diagnosis of exclusion: requires arthrocentesis to exclude septic arthritis 

d. Synovial fluid analysis: WBC count 5,000-15,000/mm 3 with


IV. KNEE INJURIES 

A. Essential anatomy 

1. There are five stabilizers (two static and three dynamic) of the lateral aspect of the knee. 

a. Static (ligamentous) stabilizers 

(1) Lateral collateral ligament (LCL) 

(2) Lateral joint capsule 

b. Dynamic (muscular) stabilizers 

(1) lliotibial tract 

(2) Popliteus muscle 

(3) Biceps femoris muscle 

2. There are four stabilizers of the medial aspect of the knee: 

a. Static stabi I izers 

(1) Medial collateral ligament (MCL): injury to this ligament is much more common than to the LCL 

(2) Medial joint capsule 

b. Dynamic stabilizers 

(1) Semimembranosus muscle 

(2) Pes anserinus 

3. The quadriceps tendon permits extension and is the primary dynamic stabilizer of the knee. It is formed by 

four muscles: 

a. Rectus femoris 

b. Vastus lateralis 

c. Vastus intermedius 

d. Vastus medialis 

4. The cruciate ligaments 

a. Two internal bands extending from the tibia to the femur (one anteriorly, the other posteriorly) 

b. Control anteroposterior and rotatory stability of the knee and prevent hyperextension 

c. Anterior cruciate ligament (ACL) is the most frequently injured ligament in the knee. It has a rich blood 

supply, which accounts for the high incidence of hemarthrosis when this ligament is injured. 

d. Posterior cruciate ligament (PCL) is significantly stronger than the ACL and collateral ligaments; thus, injury 

to it is rare and is usually associated with severe knee injuries. 

B. Mechanisms of knee injury 

1. Va Igus (abduction) stress: most common mechanism of injury 

a. Definition: outward stress on lower leg with angulation of the foot away from the midline 


(1) MCL (eg, ski injury): 61% 

(2) ACL: patient stumbled, caught himself or herself, and now cannot climb steps. 

(3) Medial meniscus: patient complains of knee "locking" in place or clicking (medial meniscus attached 

toMCL). 

2. Varus (adduction) stress: uncommon mechanism of injury 

a. Definition: inward stress on lower leg with angulation of the foot toward the midline 


(1) LCL (eg, skier fails to maintain a snow-plow and the tips of his or her skis cross): significant disruption 

__,. peroneal nerve injury 

(2) Lateral posterior capsule: knee buckling or "giving way" 

(3) Lateral meniscus: knee "locking" or clicking 

3. Hyperextension stress 

a. Definition: backward stress with the knee extended 

b. Usually results in injury to the cruciate ligaments 


(1) ACL: hyperextension of the knee 

379


(2) Rupture of the posterior capsule: knee buckling, collapsing, or "giving way" 

(3) Isolated PCL: blow to the anterior aspect of the tibia with the knee in extension or hyperextension 

4. Anterior and posterior forces of the tibia on the femur 

a. Usually occur with the knee in flexion 


(1) ACL/tibia is forced anteriorly relative to the femur. 

(2) PCL/tibia is forced posteriorly relative to the femur. 

5. Rotational stress 

a. Definition: rotation of the knee (tibia relative to femur) with the foot firmly planted on the ground 

(1) Internal rotation - ruptures the ACL 

(2) External rotation - disrupts the ACL and/or the medial capsular and MCLs 

b. Clinical presentation: a sudden stop and pivot while running; partial ligament ruptures are often more 

painful than complete tears, and cruciate ligament injuries are more common in women. 

C. Hemarthrosis in association with a negative radiograph indicates the presence of one of the following: 

1. Ligamentous tear 

a. Hemarthrosis usually develops within 2 hours of injury. 

b. Torn ACL is responsible for 75 % of all hemarthroses of the knee. 

2. Peripheral meniscus tear 

a. Effusion develops gradually (6-24 hours after injury). 

b. Usually occurs in association with rotational force to a weight-bearing knee 

3. Osteochondral fracture 

a. Hemarthrosis develops immediately. 

b. Usually occurs in children, particularly adolescent males 

4. When aspiration of a hemarthrosis reveals the presence of fat globules (lipohemarthrosis), a fracture is likely. 

D. Physical examination of the knee should include the following tests: 

1. Stability tests 

a. Va Igus stress in 30° of flexion - instability indicates rupture of the MCL. 

b. Valgus stress in extension - instability indicates rupture of the MCL as well as potential injury to the 

cruciate ligaments and posterior capsule. 

c. Varus stress in 30° of flexion - instability indicates rupture of the LCL. 

d. Varus stress in extension - instability indicates rupture of the LCL as well as potential injury to the iliotibial 

tract, popliteus muscle, and lateral capsule and cruciate ligaments. 

e. Anterior and posterior drawer signs: test the ACL and the PCL 

f. Lach man test: another test of the ACL; more sensitive and accurate than the anterior drawer sign 

g. McMurray and Ege tests: aid in diagnosing meniscal tears 

(1) McMurray test - joint line tenderness 

(2) Ege test - pain and/or a click on maximum rotation of the knee with the patient in a squatting 

position (external rotation - medial meniscus tear; internal rotation - lateral meniscus tear) 

2. Patellar compression and apprehension test: pain is elicited with chondromalacia patellae (an overuse 

syndrome often seen in young women). 

E. Knee dislocation (a true orthopedic emergency) 

1. Results from violent trauma, most commonly motor vehicle collisions, vehiclepedestrian collisions, and 

contact sports 

2. Knee dislocations are classified according to the direction of the tibial displacement relative to the femur 

a. 5 types: anterior, posterior, medial, lateral, and rotary 

b. Anterior and posterior dislocations are the most common (50%-60%). 


a. Diagnosis is essential because of the high incidence of associated injuries. 

b. The knee may relocate spontaneously, and the diagnosis of dislocation may be missed. Any patient who 

presents after trauma with a grossly unstable knee (a tear in three of the four major ligaments of the 

knee) should be assumed to have a spontaneously reduced dislocation until further evaluation excludes 

this injury. 

380


c. Complete disruption of all major ligaments plus meniscal injury 

d. Popliteal artery injury (21 %-32%) is particularly common with anterior and posterior dislocations 

(up to 40%). 

e. Peroneal nerve injury (25%-35%) 

(1) Paresthesia of the dorsal aspect of the foot 

(2) Diminished dorsiflexion of the foot (foot drop) 

(3) Decreased sensitivity between the first and second toes 

(4) Seen most often with medial and posterolateral dislocations 

f. Tibial nerve injury (plantar foot numbness/paresthesias and weakness with plantar flexion) is less 

common than peroneal nerve injury. 

g. Proximal tibial fractures 

h. The knee with complete disruption of all major ligaments (and the joint capsule) may exhibit less swelling 

and pain than the less severely injured knee with a tense hemarthrosis. 

i. Popliteal artery injury may be present even if the pulses are intact or the foot is warm. 

4. Treatment 

a. The dislocated knee should be reduced immediately in the neutral position (extension of the knee 

stretches the popliteal artery) by longitudinal traction in a sedated patient. Do not wait for radiographic 

confirmation. 

b. The popliteal, dorsalis pedis, and tibialis posterior pulses should be checked before and after reduction. 

c. After reduction, the knee should be immobilized in a posterior splint in 15° flexion. 

d. Doppler flow ultrasound, CT angiography, or standard angiography should be strongly considered in all 

cases in consultation with a vascular surgeon, even if pulses are present. At a minimum, ankle-brachia! 

indexes (ABls) should be obtained to ascertain if these is a vascular injury. 

(1) Distal pulses may still be present but a vascular injury (eg, intimal flap injury, pseudoaneurysm or 

partial intimal tear) may be present and lead to vascular complications if diagnosis is delayed. 

(2) If immediate surgical intervention is indicated, arteriography should be performed in the operating 

room, because performance in the radiology department is associated with an additional delay of 

1-2 hours before surgery. 

e. The peroneal and tibial nerves should be tested before and after reduction. 

f. Immediate orthopedic (and possibly vascular) surgery consult is indicated whenever this injury is 

suspected. 

g. Immediate surgical intervention is indicated for: 

(1) Popliteal artery injuries (arterial repair should be accomplished within 6 hours to avoid the 

complications of prolonged ischemia). 

(2) Open dislocations 

(3) Irreducible dislocations 

F. Rupture of the quadriceps mechanism 

1. May result from one of the following injuries: 

a. Quadriceps tendon rupture 

b. Patellar tendon rupture 

c. Patellar fracture 

d. Avulsion of the tibial tuberosity 


a. Complete disruption: the patient can stand but cannot walk or extend the knee; on physical examination, 

there is diffuse swelling around the knee and a palpable deficit. 

b. Incomplete disruption: active extension is weak and painful. 

3. Treatment 

a. Early orthopedic consult 

b. Complete ruptures_,. early surgical repair 

c. Partial tear_,. immobilization in full extension 

G. Patellar subluxation/dislocation 


a. Sudden flexion and external rotation of the tibia on the femur with concomitant contraction of the quadriceps 

b. Direct blow to the patella with the knee inflexion or extension 

381


2. Lateral subluxation!dis/ocation is the most common. 

3. Clinical presentation: adolescent females with chronic patellofemoral anatomic abnormalities such as 

genu valgum (knock-knees), patellae alta (high-riding patellae), a large Q (quadriceps) angle, or generalized 

joint laxity 

4. Diagnostic evaluation: obtain AP and lateral radiographs of the knee before and after reduction to exclude 

associated osteochondral fracture of the patellae or lateral femoral condyle. 

5. Treatment 

a. Patellar subluxations often reduce spontaneously. 

b. Reduction is accomplished by flexing the patient's hip and applying gentle, medially directed pressure over 

the lateral aspect of the pate! lae while extending the knee. 

c. Immobilize in full extension. 

d. Crutches: patient should be nonweight-bearing. 

e. Orthopedic referral for possible surgical intervention. 

f. Isometric quadriceps exercise should be started as soon as the patient can do them without pain. 

H. Patellar fracture 

1. One of several possible injuries to the extensor mechanism of the knee 


a. Direct blow (most common), eg, against the dashboard of a car 

b. Forceful contraction of the quadriceps muscles 

3. Transverse fractures are the most common (50%-80% of cases). 

4. Clinical presentation: patients typically present with tenderness and swelling over the patella and limited, 

painful knee extension (if the extensor mechanism is intact) or inability to extend the knee (if the extensor 

mechanism is torn). 

5. Diagnostic evaluation: radiographs, including AP, lateral, and sunrise (skyline) views 

6. Treatment 

a. Nondisplaced or minimally displaced and the extensor mechanism is intact 

(1) Immobilize in full extension, partial weight-bearing advancing to full weight-bearing as tolerated 

(2) Orthopedic referral 

b. If the fracture fragments are widely displaced (>3 mm) or there is loss of extensor function 

(1) Orthopedic referral for surgical intervention is required. 

(2) When fracture fragments are widely separated, associated concomitant knee joint injury is frequently 

present. 

I. Tibial plateau fracture (most common fracture of the knee) 

1. Most common mechanism of injury is a strong valgus stress with axial loading. 

2. Most condylar fractures (55%-70%) involve the lateral plateau. 

3. Vascular complications are common. 

a. Fracture fragments in the subcondylar area - popliteal artery 

b. Displaced fracture of the lateral condyle- anterior tibial artery 

4. An intra-articular fracture 

5. Treatment consists of placing the patient in a straight leg knee immobilizer or posterior leg splint. 

J. Baker cyst 

1. An inflammation of the semimembranosus or medial gastrocnemius bursa produced by protrusion of the 

synovial membrane through the posterior aspect of the knee capsule 

2. In adults, these cysts are usually due to an intra-articular abnormality of the knee, such as chronic inflammatory 

arthritis or a torn meniscus. In children, however, these cysts appear to be a primary lesion. 


a. History of intermittent swelling behind the knee and may complain of local discomfort 

b. Examination reveals a tense and occasionally painful fluid-filled sac in the medial aspect of the popliteal 

fossa. 

c. Rupture of the cyst with inferior dissection of the synovial fluid causes calf pain and swelling, often 

simulating thrombophlebitis or a deep vein thrombosis of the calf. 

382


4. Treatment 

a. In adults, management is directed toward correction of the underlying joint pathology. 

b. In children, treatment is generally unnecessary, because most of these cysts resolve on their own in 1-2 years. 

K. Osgood-Schlatter disease (traumatic tibial apophysitis) 

1. Inflammation of the apophysis of the tibial tubercle leads to partial avulsion and separation of the tibial tubercle 

2. Mechanism: repetitive microscopic injury to the tibial tubercle 


a. Commonly seen in adolescents (particularly males) who are active in sports 

b. Pain and swelling in the region of the tibial tuberosity that is increased with forceful leg extension (climbing 

stairs, running, jumping); often bilateral (25% of cases) 

4. Treatment: ice, NSAIDs, and decreased participation in sports 

L. Chondromalacia patellae (patellofemoral pain syndrome/patellar malalignment syndrome) 

1 . Most common cause of knee pain 

2. Usually occurs in young adults (particularly females) 

3. Often bilateral 

4. Causes include patellofemoral malalignment, recurrent patellar subluxation/dislocation, and excessive knee 

strain (athletes) 


a. Intermittent peripatellar pain that is exacerbated by prolonged sitting and climbing steps 

b. Pain with compression of the patellae into the femoral groove (patellar compression test) and with knee 

extended and quadriceps tightened 

c. Quadricep muscle contraction in anticipation of pain when the patella is displaced laterally while the 

knee is extended and relaxed (patellar apprehension test) 

d. Findings of patellar malalignment (Q angle >20°) may also be present. The Q angle is formed by the 

intersection of two lines: one drawn from the anterior superior iliac spine to the center of the patellae 

and the second drawn from the center of the patellae through the tibial tuberosity (the normal Q angle 

is 15°). 

6. Treatment: rest and NSAIDs, followed by isometric quadricep-strengthening exercises (quadricep contraction 

with adduction) 

V. LOWER LEG INJURIES 

A. The soft tissue surrounding the tibia and fibula is divided into four compartments. 

1 . Anterior compartment 

a. Dorsiflexor muscles of the ankle and foot (tibial is anterior, extensor digitorum longus, extensor hallucis 

longus, and peroneus tertius) 

b. Anterior tibial artery 

(1) Most frequently injured structure in this compartment 

(2) Injury occurs secondary to fractures of the: 

(a) 

Latera I tibial plateau 

(b) Proximal third of the tibia 

c. Deep peroneal nerve 

(1) Provides sensation to the first dorsal web space of the foot 

(2) May be injured because of fracture of the lateral tibial plateau 

2. Lateral (peroneal) compartment 

a. Everter and plantar flexor muscles of the foot (peroneus brevis and longus muscles) 

b. Superficial peroneal nerve 

(1) Provides sensation to the dorsum of the foot 

(2) Frequently injured because of fracture of the fibular neck or proximal shaft 

3. Deep posterior compartment 

a. Tibial is posterior, flexor digitorum longus, and flexor hallucis longus muscles 

b. Posterior tibial and peroneal arteries 

c. Posterior tibial nerve provides sensation to the sole of the foot. 

383


4. Superficial posterior compartment 

a. Gastrocnemius, plantaris, and soleus muscles 

b. Sural nerve provides sensation to the lateral aspect of the foot and the distal calf. 

B. Anterior compartment syndrome 

1. More common than the lateral or posterior compartment syndromes 

2. Usually occurs in association with proximal tibial fractures but can result from prolonged strenuous exercise 

(particularly in runners) or other causes 


a. Anterior tibial pain that is: 

(1) Out of proportion to the injury (one of the earliest findings) 

(2) Increased with active dorsiflexion of the foot (one of the earliest findings) 

(3) Increased with passive plantar flexion of the foot 

b. Decreased two-point sensory discrimination (most consistent finding) 

c. Paresthesia or hypesthesia in the distribution of the deep peroneal nerve (early finding) 

d. Weak dorsiflexion of the ankle and toes 

e. Palpable tenseness and tenderness of the compartment 

f. Pallor of the skin (late finding) 

g. Pulselessness or reduced distal pulses (a very late and frequently absent finding). The presence of 

peripheral pulses does not exclude increased intracompartmental pressure; pulses often remain intact. 

4. Treatment 

a. Remove constrictive dressing or cast (if present). 

b. Obtain immediate orthopedic consult and measure intracompartmental pressure. 

c. Surgical decompression via fasciotomy is indicated if the diastolic blood pressure minus the 

intracompartmental pressure is >30 mmHg. 

C. Stress fractures of the fibula 

1. Result from overtraining and usually occur at the distal fibula 

2. Patients present with pain exacerbated with ambulation. 

3. Initial radiographs are usually negative. 

4. Treatment is symptomatic. 

VI. ANKLE INJURIES 


1. Three groups of ligaments unify the bony structures of the ankle 

a. Medial collateral (deltoid) ligament 

(1) Provides medial support to the ankle 

(2) Originates from the medial malleolus and inserts on the navicular and talus 

b. Anterior talofibular, calcaneofibular, and posterior talofibular ligaments - provide lateral support. 

c. Ligaments of syndesmosis - bind the lower portions of the tibia and fibula together. 

(1) Anterior and posterior tibiofibular ligaments 

(2) Transverse tibiofibular ligament 

(3) lnterosseous ligament (provides the strongest bond between the tibia and fibula at the ankle joint) 

2. Four groups of muscles traverse the ankle joint 

a. Anteriorly - dorsiflexion of the ankle 

(1) Tibial is anterior 

(2) Extensor digitorum longus 

(3) Extensor hallucis longus 

b. Medially - inversion of the foot 

(1) Tibial is posterior 

(2) Flexor digitorum longus 

(3) Flexor hallucis longus 

384


c. Posteriorly----,, plantar flexion 

(1) Gastrocnemius 

(2) Plantaris 

(3) Soleus 

d. Laterally----,, eversion and plantar flexion 

(1) Peroneus longus 

(2) Peroneus brevis 

B. Sprains (ligamentous injury) 

1. Lateral collateral ligament (LCL) sprains 

a. Most common (85%-90%) 

b. Result from inversion and internal rotation of the plantarflexed foot 

c. Ligamentous injury occurs in sequence, starting anteriorly with the anterior talofibular ligament and 

progressing posteriorly to the calcaneofibular ligament, followed by the posterior talofibular ligament. 

d. The most frequently injured ligament ----,, anterior talofibular 

2. Medial collateral ligament sprains are uncommon. 

a. Result from eversion and external rotation of the foot 

b. Often associated with either a fracture of the fibula or a tear of the tibiofibular syndesmosis 

3. Distal tibiofibular syndesmotic ligament sprains (high ankle sprains) are also uncommon. 

a. Result from dorsiflexion and eversion forces with an axial load 

b. Have a prolonged recovery period 

4. Classification is based on the clinical presentation and the degree of instability present (as demonstrated by 

stress testing). 

a. First degree 

(1) Mild localized tenderness 

(2) Minimal swelling 

(3) No instability or functional loss 

(4) Able to beai- weight 

(5) No abnormal motion 

b. Second degree 

(1) Moderate swelling and tenderness 

(2) Moderate functional loss 

(3) Increased pain with stress testing 

c. Third degree 

(1) Marked tenderness 

(2) Egg-shaped swelling over the affected ligament(s) within 2 hours of injury 

(3) Significant functional loss 

(4) Inability to bear weight 

(5) Resistance to motion of the foot 

(6) Positive stress test 

5. Stress tests for ankle stability are useful in confirming specific ligamentous injury and in distinguishing second 

from third-degree sprains. 

a. Anterior drawer test: abnormal movement indicates a rupture of at least the anterior talofibular ligament. 

b. Inversion stress (or talar tilt) test 

(1) Needs to be done only if the anterior drawer test is positive 

(2) Abnormal movement indicates rupture of both the anterior talofibular and the calcaneofibular 

ligaments. 

c. External rotation test 

(1) Pain at the syndesmosis or a sensation of lateral talar movement indicates injury to the distal 

tibiofibular syndesmotic ligament. 

(2) Accurate results require the presence of good muscle relaxation obtained with application of ice or 

infiltration of a local anesthetic. 

385


6. Associated injuries 

a. Maisonneuve fracture 

(1) Proximal fibular fracture that occurs in association with rupture of the deltoid ligament or an 

avulsion fracture of the medial malleolus at the insertion site of the distal talofibular ligament 

(2) Should be suspected in patients presenting with a history of eversion injury and significant medial 

malleolar tenderness and swelling 

b. Osteochondral fracture of the talar dome 

c. Avulsion fracture of the fifth metatarsal (pseudo-Jones or dancer's fracture) occurs with flexioninversion 

injuries of the foot. 

d. Peroneal tendon dislocation or subluxation 

Fibula 

Tibia 

Anterior tibiofibular 

ligament 

Talus 

7. Treatment 

a. Determined by the degree of injury 

b. First- and most second-degree sprains 

(1) Ice, elevation, immobilization in a protective device (air cast, brace, splint, Unna boot), and crutches 

as needed. 

(2) As pain and swelling decrease, continue with graded exercises to increase dorsiflexion and peroneal 

strength, weight-bearing as tolerated, and reevaluation by the primary care provider. 

c. Severe second-degree sprains 

(1) Ice, elevation, splint immobilization (stir-up splint, air cast, or posterior mold), prolonged nonweightbearing, 

and crutches 

(2) Early orthopedic reevaluation for possible casting 

d. Third-degree sprains 

C. Ankle dislocations 

(1) Ice, elevation, splint immobilization, (stir-up splint, air cast, or posterior mold), prolonged nonweightbearing, 

and crutches 

(2) Referral to orthopedics 

(3) Some of these patients, depending on their level of athletic involvement and other associated injuries, 

may be considered for primary surgical repair. 

1. Described according to the direction of talar displacement relative to the tibia; five types: 

a. Anterior 

b. Posterior (common) 

c. Medial (common) 

d. Lateral 

e. Superior (diastasis) (uncommon) 

2. Pure ankle dislocations are uncommon; most occur in association with malleolar fractures. 

3. Treatment 

a. All ankle dislocations require immediate neurovascular assessment and emergent orthopedic consult. 

386


b. If there is any evidence of neurovascular compromise or skin tenting, reduction should be accomplished 

immediately (before radiographic evaluation). If these findings are absent, radiographs should be obtained 

before reduction to exclude the presence of associated fractures. 

c. After administration of adequate analgesia or procedural sedation, promptly reduce the dislocation with 

gentle in-line traction. 

d. Once reduction has been accomplished, reassess the patient's neurovascular status, order radiographs after 

reduction, and place the patient in a combination stir-up/posterior splint. 

D. Tendon injuries 

1. Achilles tendon rupture 

a. Common in sedentary, middle-aged men (mean age 35 years) engaging in weekend athletic activities 

b. Up to 25 % of cases are initially misdiagnosed as ankle sprains. 

c. Mechanism of injury 

(1) Forceful dorsiflexion of the foot with the ankle in a relaxed state 

(2) Direct trauma to a taut tendon 

(3) An extra stretch applied to a taut tendon 


(1) The patient gives a history of sudden excruciating pain at the back of the ankle that lessens instantly, 

and often reports having heard or felt a "pop" or "snap." 


(a) Swelling of the distal calf 

(b) A palpable defect in the tendon 2-6 cm proximal to its calcaneal insertion site 

(c) Weak plantar flexion when compared with the uninjured leg 


(1) Diagnosis is made with the Thompson test (also called Simmonds test), which is performed with the 

patient in the prone position. 

f. Treatment 

(a) Normal function: squeezing the calf produces plantar flexion of the foot. 

(b) With a complete tear, plantar flexion will not occur. 

(c) Bedside dynamic ultrasound is a quick easy way to confirm the diagnosis. 

(d) MRI can be used to confirm the diagnosis if doubt remains, but this is usually unnecessary. 

(1) Initial management 

(a) Ice, elevation, analgesia, immobilization in a posterior splint in passive equinus (plantar flexion), 

and crutches 

(b) Orthopedic consult within 48-72 hours 

(2) Definitive care (casting versus surgical repair) remains controversial; it is usually determined by 

the patient's age, activity level, and underlying medical conditions. Surgical repair appears to be 

associated with a better outcome (increased strength and mobility, and decreased incidence of rerupture) 

but is typically reserved for younger patients. 

2. Peron ea I tendon sub I uxation/dislocation 

a. Results from a tear of the superior peroneal retinaculum from its attachment on the fibula. This allows the 

peroneus brevis and longus tendons to sublux anteriorly over the lateral malleolus. 

b. Often misdiagnosed as an ankle sprain 

c. Mechanism of injury: forced dorsiflexion of the ankle with reflex contraction of the peroneal muscles 


(1) The patient typically complains of pain and a clicking or slipping sensation at the back of the ankle. 

(2) Diagnosis is made by physical examination. 

(a) Tenderness, swelling, and ecchymosis at the posterior aspect of the lateral malleolus 

(b) Tensing of the peroneal muscles intensifies the pain. 

(c) Eversion is weak. 

(d) Anterior subluxation of the tendons with the patient's foot dorsiflexed and everted against 

resistance confirms the diagnosis. 

e. Plain radiographs may reveal a small avulsion fracture of the lateral ridge of the distal fibula 

(pathognomonic for this injury) in 50% of cases. 

f. Treatment: splint in mid plantar flexion, and refer to orthopedist for possible surgical repair. 

387


E. Ankle injuries in children 

1. Because ligaments are stronger than bone in children, fractures at the epiphyseal plate are more common than 

ligamentous injuries. 

2. These fractures usually result from indirect forces and are classified according to the Salter-Harris classification 

system (see pages 350-351). 

3. Tillaux fracture 

a. A Salter Ill fracture of the lateral distal tibia commonly seen in adolescents participating in sporting events 

b. Consider this diagnosis if the history is suggestive and there is swelling over the anterior ankle. 

VII. FOOT INJURIES 


1. The foot is divided into three parts: 

a. Hindpart (calcaneus and talus) 

b. Midpart (navicular, cuboid, cuneiforms) 

c. Forepart (metatarsals and phalanges) 

2. The hindpart is separated from the midpart by Chopart joint; the mid part is separated from the forepart by 

Lisfranc joint. 

3. First metatarsal head bears twice the weight of the other metatarsals. 

4. During the push-off phase, the second and third metatarsals bear the most weight; hence, they are prone to 

stress fractures. 

B. Fractures 

1 . Calcaneus 

a. The calcaneus is the most frequently fractured tarsal bone. (The talus is the second most commonly fractured.) 

b. A calcaneal fracture is usually due to a compression injury (eg, fall from a height with the patient landing 

on his or her feet). 


(1) Examination reveals swelling, tenderness, and ecchymosis of the hindfoot and inability to bear 

weight on the fracture. 

(2) 10% are bilateral, and another 10% are associated with compression fractures of the dorsolumbar 

spine. 

(3) 26% are associated with other injuries to the lower extremities. 

(4) Whenever a calcaneal body fracture is diagnosed, the Bohler angle should be measured to determine 

whether or not the fracture is depressed. This is done by measuring the intersection of two lines 

on the lateral radiograph. One is drawn from the superior margin of the posterior tuberosity of the 

calcaneus and extended through the superior tip of the posterior facet. The other line is drawn from 

the superior tip of the anterior process and extended through the superior tip of the posterior facet. 

This angle normally measures 20°-40°. If the angle is


d. Treatment 

(1) Intra-articular or displaced calcaneal fractures: management remains controversial (nonoperative 

versus immediate surgical reduction); obtain emergent orthopedic consult in the emergency 

department. 

(2) Nondisplaced or minor extra-articular fractures: ice, elevation, immobilization in a posterior splint, 

crutches; obtain orthopedic consult and arrange for early follow-up on an outpatient basis. 

2. Lisfranc (tarsometatarsal) fracture/dislocation 


(1) Axial load: a fall on the plantar-flexed foot 

(2) Compressive forces: crush injury 

(3) Rotational forces: twisting of the body around a fixed foot 


(1) Examination reveals significant midfoot swelling and pain, decreased range of motion, and inability 

to bear weight. 

(2) Paresthesias of the midfoot may also be present. 

c. Diagnostic evaluation: radiographs 

(1) The key to making this diagnosis is to look for the normal alignment along the medial aspect of the 

middle cuneiform with the medial aspect of the base of the second metatarsal; any disruption of this 

alignment is indicative of a dislocation. 

(2) The second metatarsal functions as the primary stabilizing force of the joint; thus, a fracture through 

the base of the second metatarsal (Fleck sign) is indicative of a disrupted Lisfranc joint. 

(3) Separation between the base of the first and second metatarsals is highly suggestive of subluxation 

and is the most reliable finding. 

(4) Weight-bearing radiographs of the Lisfranc joint can help make the diagnosis if the initial plain 

radiographs are normal. 

d. Treatment 

(1) Involves either closed reduction under general anesthesia, or open reduction and surgical fixation 

(2) Early orthopedic consult in the emergency department is indicated. 

Lisfranc Injury 

Second metatarsal 

First metatarsal 

Lisfranc joint 

Second metatarsal 

Lisfranc joint 

389


3. Jones fracture (diaphyseal fracture of the fifth metatarsal) 

a. A transverse fracture of the proximal diaphysis of the fifth metatarsal 

b. In children, the proximal physis of the fifth metatarsal may be mistaken for a fracture. 

c. Mechanism of injury: a forceful load applied to the ball of the foot laterally (such as a pivot) 

d. Unlike avulsion fractures of the base of the fifth metatarsal (pseudo-Jones or dancer's fracture), these 

fractures are slow to heal and are associated with a high incidence of delayed union or nonunion. 

e. Treatment 

(1) Nondisplaced fractures are usually managed with immobilization in a nonweight-bearing 

short-leg cast. 

(2) Displaced fractures (and fractures in athletes) are typically managed surgically. 

(3) Orthopedic follow-up is required. 

390

ORTHOPEDIC EMERGENCIES: PRACTICE CLINICAL SCENARIOS 



Scenario A 

Presentation: An elderly man with a history of prosthetic hip replacement presents complaining of inability 

to walk or move the hip. The pain started with minimal trauma. 

Physical examination: On physical examination, the leg is shortened, abducted, and internally rotated. 


Scenario B 

Presentation: A middle-aged "weekend warrior" felt a snap or pop in his knee after a jump in a weekend 

game of basketball. 

Physical examination: On physical examination, the patient can stand but is unable to walk or extend the 

knee. The patella is high riding. 


Scenario C 

Presentation: The patient presents after a fall onto the foot or a twisting injury. Pain on the medial side of 

the ankle increases with weight-bearing. 

Physical examination: A careful examination of the proximal fibula elicits pain with compression of the 

fibula or palpation of the fibula head. 


Scenario D 

Presentation: A young football player is brought in from the field complaining of knee pain after taking a 

hit during the game. Bystanders and the patient report that the knee appeared deformed. 

Physical examination: An effusion is noted in the knee, along with multidirectional laxity (laxity with 

valgus, varus, anterior and posterior stress of the ligaments). 


Scenario E 

Presentation: Parents bring in a 3-year-old child, reporting arm pain. The child refuses to use the 

affected arm. 

Physical examination: The elbow is tender over the radial head, but there is no bruising, swelling, 

or deformity. 


391



Scenario A 

Diagnosis: posterior prosthetic hip dislocation 

Diagnostic evaluation: Pelvis and hip radiographs show the hip posteriorly dislocated. Care should be taken to 

ensure that there is no acetabular or pelvic fracture. 

Scenario B 

Diagnosis: quadriceps rupture 

Diagnostic evaluation: Radiographs of the knee may show a high-riding patella (can also be normal). A joint 

effusion can often be seen. 

Scenario C 

Diagnosis: Maisonneuve fracture 

Diagnostic evaluation: Ankle radiographs show a fracture of the medial malleolus, possibly with increased space 

between the malleolus and talar dome. Tibia/fibula radiographs demonstrate a proximal fibula fracture. 

Scenario D 

Diagnosis: knee dislocation 

Diagnostic evaluation: It is not unusual for the leg to look completely normal except for an effusion. Evaluation 

should consist of serial examinations of the leg with measurement of an ankle-brachia! index (ABI). Normally, AB ls 

do not definitively exclude arterial injury, because an intimal tear can initially be normal until a thrombosis forms 

and occludes the artery. Knee radiographs (AP and lateral) should be obtained to exclude fractures. These patients 

are at risk of compartment syndrome and injury to the popliteal artery. Consider obtaining Doppler ultrasound or a 

CT arteriogram (or angiogram) of the popliteal artery. 

Scenario E 

Diagnosis: nursemaid elbow (radial head subluxation) 

Diagnostic evaluation: There may be a history of the arm being pulled or yanked. Radiographs are generally 

not required; however, PA and lateral views of the elbow should be obtained if there is a concern for fracture or 

dislocation or if there is swelling, bruising, or crepitus on examination. 

Management: Treatment consists of reduction of the dislocated radial head by hyperpronating the forearm and, if 

necessary, flexing the elbow while applying some gentle pressure to the radial head. If pronation is not effective, 

reduction may be attempted by supinating the forearm and flexing the elbow. 

392

MUSCULOSKELETAL DISORDERS (NONTRAUMATIC) 


Arthritis ..................................................................................................................................................................... 396 

Classification ...................................................................................................................................................... 396 

Conditions Associated with Symmetric Polyarticular Joint Pain ........................................................................... 396 

Conditions Associated with Asymmetric Polyarticular Joint Pain ......................................................................... 396 

Conditions Associated with Monoarticular Joint Pain .......................................................................................... 397 

Conditions Associated with Migratory Arthritis ................................................................................................... 397 

Synovial Fluid Analysis ....................................................................................................................................... 398 

Tendinitis and Tenosynovitis ...................................................................................................................................... 398 

General Facts ..................................................................................................................................................... 398 

Stenosi ng Tenosynovitis or "Trigger Finger" ......................................................................................................... 3 98 

De Quervain Stenosing Tenosynovitis ................................................................................................................. 398 

Carpal Tunnel Syndrome .................................................................................................................................... 398 

Dupuytren Contracture ............................................................................................................................................. 399 

Ganglion Cysts .......................................................................................................................................................... 399 

Charcot Joint ............................................................................................................................................................. 399 

Back Pain ................................................................................................................................................................... 399 

Differential Diagnosis ......................................................................................................................................... 399 

General Facts ..................................................................................................................................................... 399 

Lumbar Disc Syndromes ..................................................................................................................................... 400 

Spondylol isthesis ................................................................................................................................................ 400 

Spinal Infections ................................................................................................................................................. 401 

Spinal Malignancy .............................................................................................................................................. 401 

Hand and Wrist Infections ........................................................................................................................................ 401 

Paronychia ......................................................................................................................................................... 401 

Felon .................................................................................................................................................................. 401 

Herpetic Whitlow ............................................................................................................................................... 402 

Human Bite Infections Involving the Metacarpophalangeal Joint ("Fight Bites") .................................................. 402 

Pyogenic Flexor Tenosynovitis ............................................................................................................................ 402 

Deep Pal mar Space Infection .............................................................................................................................. 403 

High-Pressure Injection Injuries .......................................................................................................................... 403 

Compartment Syndrome (Volkmann lschemia) of the Upper Extremity .................................................................... 403 

Rhabdomyolysis ........................................................................................................................................................ 404 

393

MUSCULOSKELETAL DISORDERS (NONTRAUMATIC): SELF-ASSESSMENT QUESTIONS 

MUSCULOSKELETAL DISORDERS (NONTRAUMATIC): 


1. Empiric antibiotic coverage from human bite cellulitis associated with involvement of the metacarpophalangeal 

joint (clenched fist injuries) should be selected to cover all the following pathogens except: 

(a) Anaerobic streptococci 

(b) Staphylococcus aureus 

(c) 

Eikenella corrodens 

(d) Pasteurella multocida 

2. Synovial fluid analysis with a WBC count of 3,500/mm 3 and PMNs of 60% is most likely related to which disease 

process? 

(a) Septic arthritis 

(b) Osteoarthritis 

(c) Pseudogout 

(d) Traumatic arthritis 

3. "Red flags" in a patient presenting with back pain that require further evaluation in the emergency department 

include all the following except: 

(a) History of breast cancer 

(b) Fever 

(c) Acute onset in a patient aged 30 

(d) Bladder retention 

4. A patient presents with finger pain and a red, swollen index finger with vesicles and itching for 3 days. This 

presentation is consistent with a diagnosis of: 

(a) 

Herpetic whitlow 

(b) Felon 

(c) Paronychia 

(d) Spider bite 

5. All of the following are Kanavel cardinal signs of flexor tenosynovitis except: 

(a) 

Pain with passive extension of the finger 

(b) Lack of capillary refill 

(c) Finger held in slight flexion 

(d) Fusiform swelling of the digit ("sausage digit") 

6. Al I of the fol lowing can lead to Volkmann ischemic contracture of the forearm except: 

(a) 

Arterial injection of drugs 

(b) Burns 

(c) 

Boxer's fracture 

(d) Extravasation of blood into the forearm 

7. Rhabdomyolysis may occur when ___ _ 

(a) ATP stores become depleted. 

(b) There is damage to the sarcolemma of the cell. 

(c) The calcium channels, pumps, and exchangers fail to function. 


(e) 

None of the above 

8. Treatment for rhabdomyolysis should be directed at: 

(a) Aggressive fluid repletion 

(b) Urine alkalinzation 

(c) Correcting electrolyte derangements 


394

MUSCULOSKELETAL DISORDERS (NONTRAUMATIC): SELF-ASSESSMENT QUESTIONS 

9. The most common pathogen responsible for epidural abscess is ___ _ 

(a) Pseudomonas spp 

(b) Escherichia coli 

(c) Staphylococcus aureus 

(d) Mycobacterium tuberculosis 

10. A patient presents with acute onset of back pain and complains of pain extending down the leg from the thigh to the 

medial aspect of the foot. A decreased knee jerk is present on examination. This correlates to nerve root involvement 

at which level of the spine? 

(a) 

L2 

(b) L3 

(c) L4 

(d) LS 

11. Which of the following statements about rheumatoid arthritis is true? 

(a) It causes symmetric monoarticular joint pain. 

(b) It affects al I joints of the hands, wrist and elbow in an additive manner. 

(c) It is a migratory polyarthritis. 

(d) It has a genetic predisposition to the HLA-DR4 haplotype. 

ANSWERS 

1. d 

4. 

a 

7. 

d 

10. C 

2. C 

5. 

b 

8. 

d 

11. d 

3. C 6. C 9. C 


answers for th is chapter. 

395


I. ARTHRITIS 

A. Classification 

1. Arthritis can be produced by many conditions and may be classified in several ways. 

2. Classification of arthritides by pattern of joint involvement (polyarticular, monarticular, migratory) is useful, but 

there is some overlap. 

B. Conditions associated with symmetric polyarticular joint pain 

1. Rheumatoid arthritis 

a. Most commonly affects women; there is a genetic predisposition related to HLA-DR 4 haplotype. 

b. Most commonly affects the hand (metacarpophalangeal and proximal interphalangeal joints, spares distal 

interphalangeal joints), wrist, and elbow in an additive manner 

c. Extra-articular complications may occur, including tenosynovitis, pericarditis, subcutaneous nodules, 

vasculitis of the skin, pulmonary fibrosis, mononeuritis multiplex, Sjogren syndrome, and Felty syndrome. 

Long-standing rheumatoid arthritis may lead to degeneration of the transverse ligament of the C1-C2 

junction, which requires precautions during endotracheal intubation. 

d. Treatment is with salicylates/NSAIDs, brief courses of corticosteroids or long-term with antimalarial 

agents, gold, and methotrexate. 

2. Systemic lupus erythematosus 

a. Women 15-40 years of age are most commonly affected. 

b. May be genetic (associated with HLA genotypes), environmental (exposure to UV light), or drug-induced 

c. Arthralgias and arthritis are the most common presenting complaints; both small and large joints are 

affected. 

d. An erythematous malar ("butterfly") rash is a typical feature and often accompanies joint involvement. 

3. Rheumatic fever 

a. A migratory polyarthritis 

b. Primarily affects the large joints of the extremities (knees, ankles, elbows, and wrists) 

c. Triggered by hyperimmune response after a group A streptococcal (GAS) infection 

d. Diagnosis requires evidence of prior GAS infection plus Jones criteria (two major or one major and two 

minor criteria). 

e. Treatment includes IM or PO penicillin to eradicate GAS and high-dose aspirin or IM or PO hydrocortisone 

for 2-4 weeks. 

4. Hepatitis B (migratory) 

5. Rubella 

a. Occurs with both natural and vaccine-induced rubella 

b. Most commonly affects young women 

c. Finger, wrist, and knee involvement is typical. 

C. Conditions associated with asymmetric polyarticular joint pain 

1. Reactive arthritis (previously called Reiter syndrome) 

a. Usually affects young males 15-35 years old; the HLA-B27 antigen is found in up to 75% of these patients. 


(1) Classic triad: urethritis, conjunctivitis, and arthritis 

(2) This syndrome has also been documented to occur after dysentery and cervicitis. 

(3) Oligoarthritis usually develops 1-6 weeks after an episode of urethritis (due to Chlamydia) or dysentery 

(due to Salmonella, Shigella, Yersinia, or Campylobacter). 

(4) The weight-bearing joints of the lower extremities are most commonly affected (usually four or five). 

c. Must be differentiated from gonococcal arthritis 

2. Gonococcal arthritis 

a. A migratory arthritis that primarily affects young adults, particularly women 


(1) The wrists, fingers, knees, and ankles are most affected. 

(2) An associated rash (erythematous macules or pustules with a necrotic or purpuric center), which is 

distributed primarily on the extremities, accompanies the arthritis in two-thirds of patients (arthritis/ 

dermatitis syndrome). 

396


c. Cervical, urethral, rectal, and pharyngeal cultures should be obtained. 

d. Initial treatment is with parental third-generation cephalosporins. 

3. Henoch-Schonlein purpura 

a. Most commonly occurs in children 4-11 years old 


4. Lyme disease 

(1) Classic triad: migratory arthritis, palpable purpuric rash on the lower extremities/buttocks, and colicky 

abdominal pain 

(2) Ankles and knees are most commonly affected. 

a. An oligoarthritis that typically affects the large joints (particularly the knees); it can be migratory and 

usually occurs in those patients not treated with appropriate antibiotics. 

b. Arthritic symptoms develop in Stage Ill of the disease (usually months after the initial infection). 

D. Conditions associated with monoarticular joint pain 

1. Septic arthritis (a medical emergency) 

a. Staphylococcus aureus is the most common cause. There is increasing incidence of methicillin-resistant 

S aureus (MRSA). 

b. In most adults, the knee is the most commonly affected joint. In IV drug abusers, however, the most 

common sites are the sacroiliac, sternoclavicular, and intervertebral joints. In children, the knee and hip 

are most commonly affected. 

c. High-risk populations: IV drug users, immunocompromised patients, diabetics, alcoholics, patients with 

chronic arthritis or skin infections, or after intra-articular injections or prosthetic implants. 

d. Treatment aimed at likely causative agents and adjusted according to Cram stain and culture results. 

Initial treatment in adults is a first-generation cephalosporin plus vancomycin for suspected gram-positive 

organisms and a third-generation cephalosporin for gram-negative bacilli. 

2. Gout 

a. A disease of middle-aged men and elderly adults 

b. Caused by deposition of uric acid crystals 

c. Usually affects the lower extremities, particularly the great toe ("podagra") 

d. Evaluation of synovial fluid reveals needle-shaped crystals that exhibit negative birefringence under 

polarized light. 

e. Acute treatment initially includes NSAIDs and colchicine orally, or prednisone for resistant cases. 

Corticotropin IM in a single dose may also be used, particularly in elderly and hospitalized patients in 

whom NSAIDs or colchicine may be problematic. 

3. Pseudogout 

a. Primarily affects men and women :::60 years old 

b. Caused by deposit of calcium pyrophosphate crystals 

c. Most commonly affected joint is the knee, followed by the wrist, ankle, and elbow. 

d. Treatment mirrors that of gout. 


(1) Evaluation of synovial fluid reveals rhomboid-shaped crystals that exhibit weakly positive 

birefringence under polarized light (appears yellow when light is perpendicular to the crystal). 

(2) Radiographs of the affected joint may reveal calcification of the cartilage (chondrocalcinosis). 

4. Osteoarthritis (degenerative joint disease) 

5. Trauma 

6. Aseptic arthritis 

7. Hemarthrosis 

8. Patients with monarticular joint pain should always be considered to have an infectious arthritis until proved 

otherwise. 

E. Conditions associated with migratory arthritis 

1. Rheumatic fever 

2. Bacterial endocarditis 

3. Hepatitis B 

4. Septicemia (gonococcal, meningococcal, streptococci, staphylococci) 

5. Henoch-Schonlein pupura 

397


6. Lyme disease 

7. Serum sickness 

8. Pulmonary infections (mycoplasmosis, histoplasmosis, coccidiomycosis) 

F. Synovial fluid analysis 

1. The most important diagnostic study in evaluation of acute arthritis 

2. Mnemonic for laboratory analysis: "CAPS" 

~ulture, cell count, crystals (If there is only enough fluid for one test, it should be culture and sensitivity.) 

Appearance 

frotein 

~ugar, stain (Gram stain) 

3. Crystals 

a. Gout: negatively birefringent (urate) and needle-shaped 

b. Pseudogout: positively birefringent (calcium pyrophosphate) and rhomboid-shaped 

4. WBC count 

a. 75% PMNs is septic. 

5. Glucose is significantly decreased (relative to serum glucose) in both septic and rheumatoid arthritis. 

6. Gram stain is usually positive in septic arthritis, except for gonococcal infection, in which it is positive in only 

25 % of cases. 

II. TENDINITIS AND TENOSYNOVITIS 

A. General facts 

1. Inflammation of flexor or extensor tendons of the hand from repetitive motion 

2. Indicated by tenderness on palpation or pain with active or passive range of motion 

3. Management is splinting in position of function, elevation, and NSA!Ds. 

B. Stenosing tenosynovitis or "trigger finger" 

1. Scarring or inflammation for prolonged periods of time causes nodules to form on the flexor tendon sheaths. 

2. Causes friction and "catching" of the finger at the A 1 pulley at the volar crease at the base of each digit 

3. Finger "snaps" into extension but may be locked inflexion. 

4. Treatment by depot steroid injection or surgical division of the A 1 pulley 

C. De Quervain stenosing tenosynovitis 

1. Due to excessive use of the thumb, the extensor pollicis brevis and abductor pollicis tendons become inflamed. 

2. Causes pain along radial aspect of the wrist that extends to the forearm 

3. Diagnosis is confirmed by a positive Finkelstein test (thumb is grasped in a closed fist and the wrist is ulnarly 

deviated, producing a sharp pain along the tendon). 

4. Management is immobilization of the thumb and wrist, range of motion exercises, and NSAIDs. 

D. Carpal tunnel syndrome 

1. Peripheral neuropathy involving the median nerve in the carpal tunnel 

2. Swelling of tendons in the tunnel causes compression of the median nerve, which triggers paresthesias in the 

pal mar aspect of the thumb, the index and long fingers, and the radial aspect of the ring finger. 

3. Symptoms include night pain, burning, and tingling in the above-mentioned distribution, and numbness when 

the wrist is in prolonged flexion. 

4. Typically is triggered by overuse syndromes but may occur with direct trauma, diabetes, rheumatoid arthritis, 

and edematous states such as pregnancy or heart failure. 

5. Tinel sign (paresthesias triggered by tapping over the flexor retinaculum) supports the diagnosis, but a positive 

Phalen sign (flexing the wrist maximally and holding it in this position for 1 minute) is more sensitive. 

6. Initial treatment is splinting in a volar splint with the wrist in neutral position and NSAIDs. 

7. Surgery may be necessary; emergent hand specialty consult is required for median nerve motor deficits. 

398

~ 


Ill. DUPUYTREN CONTRACTURE 

A. Fibroblastic changes of the subcutaneous tissues of the palm and volar aspects of the fingers 

B. Appears to have a genetic component 

C. May lead to joint contractures with thickened, nodular pal mar tissues 

IV. GANGLION CYSTS 

A. Cystic collection of synovial fluid within a joint or tendon sheath 

B. Presents as a tender, cystic swelling over or near a tendon sheath 

C. Management: pain control and NSAIDs 

D. One-third of ganglion cysts resolve spontaneously, but persistent cysts may be referred to a hand specialist 

for cyst aspiration, corticosteroid injection, or surgical excision. 

V. CHARCOT JOINT 

A. Most common presentation is a painful, swollen ankle 

B. Usual cause is diabetic peripheral neuropathy (not syphilis) 

C. Radiograph of the ankle reveals classic "bag of bones" appearance. 

VI. BACK PAIN 

A. Differential diagnosis 

1. Aortic aneurysm 

2. Peptic ulcer 

3. Pyelonephritis 

4. Pancreatitis 

5. Vertebral disc compression or fracture 

6. Osteoporosis 

7. Carcinoma (primary or metastatic) 

8. Ankylosing spondylitis (associated with inflammatory bowel disease) 

9. Infection 

10. Osteomyelitis 

11. Ectopic pregnancy 

12. Strain or sprain 

13. Pelvic inflammatory disease 

B. General facts 

1. Back pain is the most frequent (and the most costly) cause of workman's compensation claims/payments. 

2. 

3. 

4. 

5. 

6. 

Most back pain (including pain secondary to disc disease) is self-limited and resolves in :S6-7 weeks, regardless 

of treatment. 

Most back pain is benign (particularly in healthy, young- and middle-aged adults). 

A serious cause of back pain is more likely in patients 55 

years old (incidence of 20%). 

80% or more of low back pain occurs in the L4-S1 region; L5-S1 is the most frequent location. 

When radiographs are indicated (which they are not in most cases), AP and lateral views alone are usually 

sufficient. 

a. Most healthy patients 18-55 years old with atraumatic, nonspecific, mechanical low back pain can be 

managed initially without radiographic evaluation. 

399


b. Lumbosacral films should be obtained as part of the initial evaluation in the following circumstances: 

(1) Age 55 years (higher incidence of serious causes) 

(2) Trauma 

(3) Persistent, unremitting back pain >4-6 weeks duration 

(4) Prior referral 

(5) Suspicion of serious underlying pathology based on the patient's: 

(a) 

Past medical history (cancer, IV drug abuse) 

(b) Vital signs (fever) 

C. Lumbar disc syndromes 

(c) Atypical symptoms (night pain) 

1. Impingement of a herniated disc on the anterior nerve root produces pain in a dermatomal pattern. 

L 1: groin 

L2: upper thigh 

L3: mid thigh and medial knee 

L4: lower thigh, anterior knee, and medial foot 

LS: lateral lower leg, first interdigital web space, and dorsal foot 

Sl: posterolateral calf and lateral foot 

2. Clinical presentation: physical findings of nerve root involvement 

a. t Knee jerk= L3 and L4 

b. t Dorsiflexion of foot = LS 

c. t Ankle jerk (t plantar flexion) and numbness of lateral foot= Sl 

3. Cauda equina syndrome (neurosurgical emergency) 

a. A serious complication of lumbar disc disease 

b. Results from a massive midline lumbar disc herniation that compresses several nerve roots of the cauda 

equina 


(1) Patients complain of lower back/leg pain and incontinence (or retention) of bowel and bladder. With 

progression, the patient also develops numbness of the feet and trouble walking. 

(2) Examination reveals loss of sensation in the "saddle" distribution and loss of anal sphincter tone 

(S3, S4, S5). 

d. Diagnostic evaluation: an MRI or emergency myelogram may be used to confirm the diagnosis and locate 

the disc level but should not delay treatment. 

e. Management: immediate neurosurgical consult for operative disc decompression; decompression must be 

performed quickly (within several hours) if permanent disability is to be avoided. 

D. Spondylolisthesis 

1. Definition: displacement of a vertebral body on the one below (most commonly L4 on LS); causes include 

degenerative changes and trauma. 


a. Asymptomatic (only 25% of patients develop back or leg pain) 

b. Radiographic findings may be incidental and not necessarily the cause of the back/leg pain. 

c. Retrolisthesis, however, is almost always associated with back pain. 


a. Best seen on the lateral view of the I umbar spine series 

b. The amount of forward displacement is graded; the higher the grade, the worse the slippage. 

(1) Grade I: up to 25% 

(2) Grade II: 25%-50% 

(3) Grade Ill: 50%-75% 

4. Management 

(4) Grade IV: 75%-100% 

a. Outpatient protocol for patients with low back pain without neurologic findings ("lumbar strain") 

(1) Strict bed rest is no longer recommended for treatment of lumbar strain. Patients should be encouraged 

to do light activities, range of motion exercises, and stretches but should not be expected to do any 

prolonged walking, standing, twisting, or lifting of> 15 pounds. 

400


(2) Analgesics (including NSAIDs) 

(3) Muscle relaxants (offer some symptomatic benefit) 

(4) Follow-up in 7 days 

(5) Instructions to return immediately if problems develop (worsening pain, loss of motor strength, bowel 

or bladder incontinence) 

b. Inpatient management is indicated for patients with: 

E. Spinal infections 

(1) Cauda equina syndrome 

(2) Severe or progressive neurologic deficit 

(3) Multiple nerve root involvement 

(4) Unmanageable pain 

(5) Inadequate support system at home 

1. High-risk patients: IV drug users, immunocompromised patients, alcoholics, elderly, patients with prior blunt 

trauma or recent bacterial infection 

2. Epidural abscess 

a. True neurosurgical emergency 

b. 20% of patients may have no comorbid illness. 

c. Most common bacterial cause is S aureus. 

d. Classic presentation is fever with neurologic symptoms, although 50% of patients may have neither finding. 

e. Risk of misdiagnosis is high on initial presentation. 

f. Mortality is as high as 23%. 

g. Treatment should include vancomycin in addition to broad-spectrum IV antibiotics. Consider 

Pseudomonas coverage for IV drug users. 

3. Spondylitis (osteomyelitis of the vertebral bone) 

a. Typically starts as subtle hematogenous seeding of the disc space, causing discitis. Contiguous spread then 

leads to vertebral endplate erosion. 

b. Most common pathogen is 5 aureus. 

c. May see enteric gram-negative bacilli or Mycobacterium tuberculosis (Pott disease) 

d. Typically presents with more indolent course and subjective fevers. 

F. Spinal malignancy 

1. Typically >50 years old 

2. Presents with subacute or chronic back pain 

3. Pain is worse at night. 

4. Risk factors include a history of cancer, unexplained weight loss, persistent pain, and pain lasting> 1 month. 

5. Cancers that most commonly metastasize to bone include breast, lung, and prostate. 

VII. HAND AND WRIST INFECTIONS 

A. Paronychia 

1. Infection of the lateral nail fold that sometimes extends to involve the proximal nail fold (eponychium) 

2. Causative agents are usually 5 aureus or Streptococcus spp. 

3. Patients presenting early with cellulitis may respond to oral antibiotics (a penicillinase-resistant oral penicillin 

or a first-generation cephalosporin) and warm soaks alone. 

4. If purulent material is present, the nail fold should be incised and drained, followed by daily warm soaks; use 

antibiotics only if a surrounding cellulitis is present. 

5. If subungual pus is present, the adjacent portion of the nail should be removed. 

6. Chronic paronychia may develop in immunocompromised patients. Consider treatment directed at atypical 

bacteria or fungal infections (Candida a/bicans). 

B. Felon 

1. Infection of the pulp space of the fingertip 

2. Causative agent is usually S aureus. 

401


3. Management: incision and drainage at the point of maximum tenderness and fluctuance 

a. Make a central longitudinal incision starting 0.5 cm distal to the distal flexor crease (to avoid the flexor 

tendon sheath) or a unilateral longitudinal incision, and extend this incision into the pulp space. This 

approach is preferred because of fewer long-term complications. 

b. Pack the wound, splint the finger, and start the patient on an oral first-generation cephalosporin or 

antistaphylococcal antibiotic. 

c. Remove the packing in 48-72 hours, and start warm soaks. 


a. Flexor tenosynovitis and osteomyelitis 

b. Skin instability, loss of sensation, and a disrupted pad also may occur. 

C. Herpetic whitlow 

1. Viral infection of the distal finger 

2. Caused by herpes simplex virus (type I typically in children, or type II typically in adults) 

3. Typically occurs in healthcare providers with exposure to oral secretions and in patients with coexistent 

herpes infections. 


a. Localized burning, itching, and pain precede the development of the classic clear herpetic vesicles. 

b. Typically, only one finger is involved. 

5. Diagnostic evaluation: Diagnosis can usually be made clinically, but if doubt remains or the presentation is 

atypical, it can be confirmed with Tzanck smear (reveals multinucleated giant cells) or viral culture. 

6. Management 

a. Splinting, elevation, and analgesics for pain relief 

b. An oral antiviral agent effective against herpes simplex (eg, acyclovir, famciclovir) if patient is seen early 

in the course of the infection (or is immunocompromised) 

c. A dry dressing and instructions to prevent autoinoculation or transmission to others 

d. Surgical drainage is contraindicated; it can result in secondary infection and delayed healing. 

D. Human bite infections involving the metacarpophalangeal joint ("fight bites") 

1. Can result in severe complications, including deep palmar space infections, functional loss, and amputation; 

these wounds must be aggressively treated and associated tendon injuries must be excluded. 

2. Commonly result from punching someone in the mouth (initially denied by many patients) 

3. A common mistake is to suture a human bite laceration over the metacarpophalangeal joint; these lacerations 

should never be closed primarily but allowed to heal by secondary intention. 

4. Frequently found pathogens include anaerobes (especially Eikenella corrodens and anaerobic Streptococcus), 

S aureus, and Neisseria spp. Prophylaxis with amoxicillin-clavulanate may prevent this complication. 

5. Management 

a. Consult with a hand surgeon. 

b. Obtain radiographs to exclude fractures and retained foreign bodies. 

c. Obtain aerobic and anaerobic wound cultures. 

d. Irrigate the wound with normal saline. 

e. Splint and elevate the hand. 

f. Admit the patient for IV antibiotics (ampicillin/sulbactam). 

E. Pyogenic flexor tenosynovitis 

1. Typically results from a puncture wound 

2. Causative agents are usually S aureus or Streptococcus 

3. Diagnosis is based on the presence of Kanavel four cardinal signs of flexor tenosynovitis 

a. Finger held in slight flexion 

b. Symmetric swelling of the finger 

c. Tenderness along the flexor tendon sheath 

d. Pain with passive extension of the finger 

4. Management 

a. Hospitalization and emergent hand consult for surgical drainage 

b. IV antibiotics 

402


(1) If the tenosynovitis was caused by penetrating trauma - penicillinase-resistant antistaphylococcal 

penicillin or a first-generation cephalosporin 

(2) If there is no history (or evidence) of trauma in a sexually active adult, consider disseminated 

gonococcal infection and treat empirically with ceftriaxone until culture results are available. 

c. Elevation and splinting 

d. Tetanus prophylaxis as needed 

F. Deep pal mar space infection 

1. Characterized by swelling and tenderness localized to the pal mar space 

2. Management is incision and drainage in the operating room and IV antibiotics. 

G. High-pressure injection injuries (true surgical emergencies) 

1. Mechanisms 

a. A 1-3 mm wound caused by a grease or paint gun is the hallmark of a high-pressure injection injury. 

b. Fusiform swelling and mild pain on initial presentation evolves to a swollen, pale, and severely painful 

digit hours later. 

c. The fluid frequently travels down the tendon sheath and damages the flexor tendon, with tenderness 

typically present along the course of injection. 

2. Prognosis 

a. Poor, despite the deceptively normal appearance of the hand on initial presentation; amputation rates can 

range from 60% to 80%, but recent data demonstrate a 30% rate because of higher vigilance and early 

recognition of tissue injury. 

b. Factors affecting prognosis 

(1) Location of entry wound and the underlying anatomy affected 

(2) Physical and chemical qualities of the substance injected (viscosity, corrosiveness); substances that 

are low in viscosity and corrosive in nature (eg, paint solvents) produce the most damage. 

(3) Velocity of injection: the higher the velocity, the greater the penetration 

(4) Duration of exposure to the injected substance: the greater the duration of exposure, the worse the 

prognosis. 

3. Management 

a. Obtain a radiograph to determine the degree of spread of material injected; it may be radiopaque. 

b. Splint and elevate the extremity. 

c. Administer a parenteral broad-spectrum antibiotic. 

d. Update tetanus prophylaxis as indicated. 

e. Provide oral or parenteral analgesia. 

f. Digital blocks are contraindicated - increased tissue pressure ----;, vascular compromise 

g. Obtain immediate hand specialty consult for operative debridement. 

VIII. COMPARTMENT SYNDROME (VOLKMANN ISCHEMIA) 

OF THE UPPER EXTREMITY 

A. Usually involves the flexor (volar) compartment of the forearm 

B. Arises from increased pressure in the muscle compartment of the limb (forearm) that compromises the 

circulation to the muscles and nerves of that compartment 

C. Can be precipitated by an increase in compartment contents, a decrease in compartment size, or externally 

applied pressure; causes include: 

1. Supracondylar fracture of the elbow 

2. Fracture of the radius and ulna 

3. Forearm crush injury 

4. Extravasation of blood into the forearm 

5. Arterial injection of drugs 

6. Constrictive dressing or cast 

7. Burns 

403



1. Earliest finding is pain that is: 

a. Out of proportion to the injury 

b. Increased with passive stretching of the involved muscles 

c. Increased with active contraction of the involved muscles 

2. Paresthesia or hypesthesia of the nerves traversing the compartment (early finding) 

3. Paralysis or paresis of the involved muscles 

4. Palpable tenseness and tenderness of the compartment 

5. Pallor, cyanosis, or mottling of the skin (late finding) 

6. Pulselessness or reduced distal pulses: rarely present (late finding) 

E. Management 

1. Remove constrictive dressings or casts (if present). 

2. Obtain immediate orthopedic consult, and measure intracompartmental pressure. 

3. Surgical decompression via fasciotomy is indicated if the pressure is >30 mm Hg (normal pressure is


.. ~. F. Management 

1. Saline 

a. High volumes of normal saline 

b. Titrate to urine output of 200-300 ml/hour 

2. Mannitol 

a. Controversial 

b. May provide a better prognosis in early acute renal failure by increasing urine flow, which may help 

prevent obstruction by myoglobin casts 

3. Urine alkalinization 

G. Prognosis 

a. Increases solubility of myoglobin 

b. Goal is urine pH of 6.5 

c. May use 2 ampules of sodium bicarbonate in 1 L of half-normal saline or 5% dextrose in water 

1. Incidence of acute renal failure is unknown; may range from 13% to 50%. 

2. Outcome is good provided there is no renal failure. 

3. Incidence of renal failure is higher in patients who used illicit drugs or alcohol or have undergone trauma. 

Incidence is particularly higher in patients with more than one recognized cause. 

405

MUSCULOSKELETAL DISORDERS (NONTRAUMATIC): PRACTICE CLINICAL SCENARIOS 

MUSCULOSKELETAL DISORDERS (NONTRAUMATIC): 



Scenario A 

Presentation: A 58-year-old woman with a long history of rheumatoid arthritis presents with fever and left 

knee pain for the past 24 hours. 

Physical examination: Her knee is swollen, warm, and tender. 

Diagnostic evaluation: Laboratory evaluation reveals a leukocytosis and a markedly increased erythrocyte 

sedimentation rate. Aside from some soft-tissue swelling, radiographs are unremarkable. Arthrocentesis 

reveals purulent fluid(> 100,000 WBCs with a predominance of PMNs), a low glucose, and gram-positive 

cocci in clusters on Gram stain. 


Scenario B 

Presentation: An obese 48-year-old man presents with left knee pain. He states that the pain developed 

over a period of a few hours and is so bad that even the weight of a bedsheet on his knee is too much to 

bear. He denies recent trauma and prior injury to the knee but admits to overindulging in rich food and 

alcohol the past couple of days. His past medical history is remarkable only for hypertension, for which he 

is being treated with a loop diuretic. 

Physical examination: The patient's knee is erythematous, swollen, hot, and tender. 

Diagnostic evaluation: Radiograph evaluation reveals only soft-tissue swelling. Synovial fluid analysis 

demonstrates 20,000 WBCs with a predominance of PMNs, a negative Gram stain, and needle-shaped 

crystals that are negatively birefringent. 


Scenario C 

Presentation: A 68-year-old woman presents with left knee pain for the past 2 days. She denies acute 

trauma and prior injury to the knee. 

Physical examination: The patient's knee is erythematous, swollen, and tender. 

Diagnostic evaluation: Radiographs reveal presence of calcium deposits. Arthrocentesis demonstrates 

20,000 WBCs with a predominance of PMNs, a negative Gram stain, and rhomboid-shaped crystals that 

are positively birefringent. 


Scenario D 

Presentation: A 23-year-old IV heroin user presents after 2 days of back pain and fevers. She complains 

that she has tingling of the legs and cannot get comfortable regardless of how she moves or lays. 

Physical examination: The patient is tachycardic and febrile on arrival and has diffuse lumbar back pain on 

percussion. Rectal tone is normal. 


406


Scenario E 

Presentation: A 67-year-old woman with a history of breast cancer presents with 2 months of constant 

back pain that is worse at night. There is no history of trauma or fevers, but she also reports a 12-pound 

weight loss. 

Physical examination: There is midline tenderness over the upper lumbar spine without neurologic 

findings. Radiographs demonstrate a pathologic facture of the L 1 vertebral body with loss of height. 


Scenario F 

Presentation: A 77-year-old woman with a history of dementia and alcohol abuse was found lying in the 

bathroom by her daughter after a fal I the previous night. She complains of diffuse muscle aches, fatigue, 

generalized weakness, and dizziness. 

Physical examination: The patient has diffuse muscle tenderness and appears dehydrated. 

Diagnostic evaluation: A urine sample is dark brown. Laboratory studies show blood in the urine without 

RBCs present, and increased levels of potassium, BUN, creatinine, myoglobin, and total creatine kinase. 


407



Scenario A 

Diagnosis: septic arthritis 

Scenario B 

Diagnosis: gout 

Scenario C 

Diagnosis: pseudogout 

Scenario D 

Diagnosis: epidural abscess 

Diagnostic evaluation: An MRI demonstrates a large epidural fluid collection in the L2-L5 space. 

C-reactive protein and WBC levels are increased. 

Scenario E 

Diagnosis: spinal malignancy 

Scenario F 

Diagnosis: rhabdomyolysis 

408

NERVOUS SYSTEM DISORDERS 


Stroke ........................................................................................................................................................................ 412 

Seizures ..................................................................................................................................................................... 418 

Coma ........................................................................................................................................................................ 422 

The Altered Patient .................................................................................................................................................... 425 

Neuropathies ............................................................................................................................................................ 427 

Disorders of the Neuromuscular Junction ................................................................................................................. 429 

Myasthenia Gravis .............................................................................................................................................. 429 

Lambert-Eaton Syndrome ................................................................................................................................... 430 

Botulism (Food-Borne) ........................................................................................................................................ 430 

Myopathies ............................................................................................................................................................... 431 

Peripheral Neuropathies ........................................................................................................................................... 431 

Trigeminal Neuralgia (Tic Douloureux) ............................................................................................................... 431 

Bell's Palsy .......................................................................................................................................................... 432 

Mononeuropathies ............................................................................................................................................. 432 

Diabetic Neuropathies ....................................................................................................................................... 433 

Myelopathies (Disorders of the Spinal Cord) ............................................................................................................. 433 

Volkmann lschemic Paralysis ..................................................................................................................................... 433 

Vertigo ...................................................................................................................................................................... 434 

Headache .................................................................................................................................................................. 435 

Meningitis ................................................................................................................................................................. 438 

Hydrocephalus .......................................................................................................................................................... 440 

409

NERVOUS SYSTEM DISORDERS: SELF-ASSESSEMENT QUESTIONS 

NEUROLOGIC DISORDERS: SELF-ASSESSMENT QUESTIONS 

1. Symptoms of a vertebrobasilar artery stroke might include all of the following except: 

(a) Tinnitus 

(b) Vertigo 

(c) Monocular vision loss 

(d) "Locked-in syndrome" 

2. A 65-year-old patient presents with dizziness (vertigo), nausea and vomiting. On examination, he is noted to have 

lateralizing dysmetria and is unable to stand erect or ambulate without assistance. No other deficits are noted. The 

most likely diagnosis is: 

(a) Lacunar infarct 

(b) Vertebrobasilar artery occlusion 

(c) Middle cerebral artery occlusion 

(d) Cerebellar infarct 

3. Transient global amnesia is characterized by all of the following except: 

(a) 

It generally occurs in patients >60 years old. 

(b) It is characterized by loss of recent memory and inability to record new memory. 

(c) Motor, sensory, and speech functions are interrupted during the event. 

(d) In general, patients have no recollection of events that occur during the episode. 

4. The most appropriate therapy for refractory seizures secondary to isoniazid overdose is: 

(a) Thiamine 

(b) Pyridoxine 

(c) Magnesium sulfate 

(d) Lorazepam 

5. A patient presents with an intracranial hemorrhage and a blood pressure of 220/135 mm Hg. Which of the following 

is not a good choice for initial management? 

(a) Labetalol IV 

(b) Nicardipine IV 

(c) Nitroglycerin IV 

(d) ~-blocker 

6. Acute periodic paralysis generally occurs in males 7-21 years old and is associated with: 

(a) 

Hypokalemia 

(b) Normokalemia 

(c) Hyperkalemia 

(d) Hypocalcemia 

7. Which of the following syndromes generally occurs in association with malignancy? 

(a) 

Guillain-Barre 

(b) Eaton-Lambert 

(c) Myasthenia gravis 

(d) Polymyositis 

8. The most frequent initial symptoms of myasthenia gravis are: 

(a) 

Dysarthria and dysphagia 

(b) Muscle atrophy 

(c) Respiratory failure 

(d) Ptosis, diplopia, and blurred vision 

410

NERVOUS SYSTEM DISORDERS: SELF-ASSESSEMENT QUESTIONS 

9. Which of the following is a contraindication to IV tPA in an acute ischemic stroke patient? 

(a) Current warfarin therapy with an INR 100,000/mm 3 

(d) Cerebral infarction


I. STROKE 

A. Anatomy of cerebral blood flow 

1. Anterior circulation: 80% of cerebral blood flow originates from the carotid arteries, which supply the: 

a. Frontoparietal lobes 

b. Anterior aspect of temporal lobes 

c. Optic nerve and retina 

d. Many deep gray matter structures 

2. Posterior circulation: 20% of cerebral blood flow originates from the vertebrobasilar arteries, which supply the: 

a. Medial aspect of temporal lobe 

b. Visual occipital cortex 

c. Thalamus 

d. Brainstem 

e. Upper spinal cord 

f. Cerebellum 

g. Auditory and vestibular functions of the ear 

3. Circle of Willis: provides a connection between the anterior and posterior circulations; its integrity determines 

the clinical outcome of thromboembolic strokes because of the col lateral flow provided. 

B. Pathophysiology of cerebral ischemia and infarction 

1. lschemic strokes (may be caused by cerebrovascular thrombosis, emboli, or structural occlusion of a vessel) 

a. Cerebral in situ vascular occlusion (thrombosis) results from one of the following: 

(1) Atherosclerosis (most common cause in patients >50 years old) 

(a) Atherothrombotic infarcts are associated with plaques in the carotid and vertebrobasilar arteries or 

the middle cerebral artery. 

(b) Cerebral vessel branch points are common areas for thrombotic occlusion, because clot formation 

is prone to develop in areas of turbulent blood flow. 

(c) Patients of African-American descent and those with diabetes have a particularly high risk of 

intracranial thrombosis. 

(2) Hypercoagulable states (common cause in patients


2. Hemorrhagic strokes result from one of the following: 

Courtesy of Michael Abraham, MO 

CT scan showing right-sided temporoparietal intraparenchymal hemorrhage 

a. Spontaneous rupture of a congenital or berry aneurysm (subarachnoid hemorrhage) 

b. Spontaneous rupture of an AV malformation (less common cause of a subarachnoid hemorrhage) 

c. Spontaneous bleeding from arterioles (accounts for most cerebral hemorrhages) and are secondary to one 


(1) Chronic hypertension (arteriolar injury) 

(2) Ruptured mycotic aneurysm 

(3) Neoplasm (especially breast cancer, melanoma) 


d. Amyloid angiopathy 

(1) Common cause of intracerebral hemorrhage in the elderly 

(2) CT_,. distinctive location of the hemorrhage at the junction of gray and white matter 

e. Hemorrhagic transformation of an embolic (ischemic) stroke is: 

(1) Characterized by abrupt progression of neurologic dysfunction after a stroke and 

(2) Associated with fragmentation of an occluding embolus or administration of thrombolytics (there does 

not appear to be an increased risk of hemorrhage in patients on chronic ASA therapy). 

C. Incidence of stroke 

(3) Not always evident on CT; recent studies suggest that gradient recall echo MRI may be a better choice. 

1. Patients with a stroke frequently have a history of one or more of the following: 

a. Transient ischemic attack (TIA)-30%~35% of patients will have a stroke within 5 years, the highest 

incidence occurring within the first month and the earliest incidence within 2 days 

b. Hypertension (most common) 

c. Atherosclerosis 

d. Cardiac disease 

e. Migraine headaches 

f. Claudication 

g. Diabetes 

h. Hyperlipidemia 

1. Smoking 

j. Thrombocytosis 

k. Oral contraceptive use (high-estrogen formulas) 

I. E ryth rocytos is 

m. Sickle cell disease 

413


2. A carotid bruit 

a. Absence of a bruit does not exclude the presence of stenosis. 

b. Presence/absence of a bruit has no predictive value regarding the likelihood of stroke related to carotid 

artery disease; however, if >70% carotid stenosis is confirmed radiographically, there is a 26% risk of stroke 

within 2 years in patients who have had a TIA. 

D. Differential diagnosis of stroke (aka mimics) 

1. Seizure 

a. Although embolic strokes may present with seizures, a transient postictal neurologic deficit (such as Todd 

paralysis) is far more common. 

b. Patients with other intracranial pathology (post-traumatic hematoma formation, tumor, abscess) may also 

present with seizures and neurologic deficits. Patients with new focal deficits in the setting of seizure 

should undergo emergent CT scanning to look for structural CNS lesions. (ACE P Clinical Policy: Initial 

Approach to Patients Presenting with a Chief Complaint of Seizure Who Are Not in Status Epilepticus) 

2. Migraine 

a. The aura preceding migraine headache may include focal neurologic deficits (eg, weakness, numbness, 

aphasia, visual loss); a previous history of focal symptoms associated with migraine is required to make 

this diagnosis. Transient ischemia associated with migraine may also result in a stroke. 

b. MRI with diffusion-weighted imaging may help distinguish migraine from cerebral infarction. 

3. Trauma to the middle meningeal artery (epidural or extradural hematomas) 

4. Traumatic or spontaneous venous bleeding (subdural hematoma) 

5. Toxic/metabolic disorder (those listed below may cause focal neurologic deficits and, if present, may exclude 

a stroke) 

a. Toxic exposure (some drugs, poisons) 

b. Hypo/hyperglycemia 

c. Hypo/hypernatremia 

d. Hepatic encephalopathy 

E. lschemic stroke syndromes 

1. A TIA should be considered a warning sign of an impending thrombotic or embolic syndrome. It is a "red flag," 

heralding stroke in evolution. 

2. Differentiating thrombotic and embolic strokes 

a. Thrombotic syndromes are often characterized by a stuttering onset of symptoms. Some patients wake up 

with neurologic disability. 

b. Embolic syndromes are characterized by abrupt onset of symptoms with maximal deficit that improves 

slowly as the embolus breaks up and moves peripherally. Embolic strokes are more likely to occur when 

the patient is active. 

3. Occlusive stroke syndromes may be embolic or thrombotic. 

a. Middle cerebral artery 

(1) Most common site of intracranial cerebral artery thrombosis 

(2) Clinical presentation (frequently incomplete) 

(a) Contralateral hemiplegia, hemisensory loss, and homonymous hemianopsia 

(b) Upper extremity deficit that is more severe than lower extremity deficit 

(c) Aphasia (if the dominant hemisphere is involved) 

(d) Constructional apraxia and agnosia (if the nondominant hemisphere is involved) 

(e) Gaze preference in the direction of the lesion 

b. Anterior cerebral artery 


(a) Contralateral leg, foot, and arm paralysis 

(b) Sensorimotor deficit greater in the lower (rather than the upper) extremity 

(c) Loss of frontal lobe control 

i. Abulia (difficulty in responding to questions because of slowed mentation) 

ii. Gait apraxia (clumsiness) 

iii. Incontinence 

iv. Primitive grasp and suck reflexes 

414


c. Posterior cerebral artery 

(1) Affects blood supply to the occipital cortex and branches that supply upper midbrain structures 


(a) Contralateral homonymous hemianopsia (the patient may be unaware of this before clinical 

evaluation), hemiparesis, and hemisensory loss 

(b) Memory loss 

(c) lpsilateral cranial Ill nerve palsy (usually pupil-sparing) 

d. Vertebrobasilar artery (not all findings are present) 

(1) The vertebrobasilar arteries are affected by both atherosclerotic narrowing and embol ic events that 

may result in: 

(a) Cerebellar and cranial nerve deficits 

(b) Simultaneous deficits on both sides of the body 


(a) Pain and temperature deficits on one side of the face and on opposite side of the body 

(b) lpsilateral cranial nerve palsies 

(c) Cerebellar signs 

i. Those that suggest labyrinthitis 

• Vertigo 

• Severe ataxia 

• Nausea/vomiting 

11. Those that, along with cranial nerve palsies, are not present in patients with labyrinthitis 

• Vertical or bidirectional nystagmus 

• lpsilateral dysmetria (finger-nose-finger, heel-shin, past-pointing) 

• Dysdiakokinesis (rapid alternating movements) 

(d) Contralateral hemiplegia 

(e) Contralateral sensory deficits 

(3) Wallenberg syndrome (lateral medullary plate syndrome) 

e. Basilar artery 

(a) Occurs when occlusion of the proximal vertebral artery causes infarction of the lateral medulla 

(b) Clinical presentation 

i. Vertigo 

ii. Dysphagia 

iii. Horner syndrome 

iv. Facial pain/numbness 

v. lpsilateral clumsiness 

vi. Contralateral cool extremity (distally) 

(1) Characterized by severe bilateral signs 


(a) Quadriplegia 

(b) "Locked-in syndrome" (loss of all motor function except upward gaze) 

(c) Coma 

f. Cerebellar infarcts 


(a) Ataxia 

(b) Dizziness (vertigo) 

(c) Nausea/vomiting 

(d) Nystagmus (vertical or bidirectional) 

(e) Lateralizing dysmetria 

(f) 

g. Lacunar infarcts 

Dysdiadokokinesis 

(1) These small cystic infarcts are usually caused by a hypertensive vasculopathy (lipohyalinosis) but may 

occur in diabetic patients and can affect both the anterior and posterior cerebral vessels. Lacunar 

415


strokes involve penetrating cerebral arterial vessels lying deep in the gray matter (internal capsule) 

or brainstem. 

(2) There are four specific lacunar infarct states 

(a) The 11 dysarthria-clumsy hand syndrome" (midpons) 

(b) Pure sensory syndrome (thalamus) 

(c) Leg paresis and ataxia (pons or internal capsule) 

(d) Pure motor hemiplegia (pons or internal capsule): most common 

h. Transient global amnesia 

(1) Associated with ischemia to the temporal lobes or thalamus 

(2) Generally occurs in patients >60 years old, lasts from 30 minutes to 36 hours, and then resolves 

completely; has also been reported in association with therapeutic use of benzodiazepines (especially 

triazolam). 


(a) Sudden loss of recent memory and inability to record new memories; the patient usually has no 

recollection of events that occurred during the episode. 

(b) Preservation of long-term past memory and self-identity 

(c) 

F. Hemorrhagic syndromes 

Preservation of motor, sensory, and speech functions 

(d) The ability to carry out complex tasks (drive a car, give a speech) during the episode 

1. Characterized by abrupt onset of symptoms (usually headache, vomiting) and rapid progression of neurologic 

deficits. The patient may be lethargic or exhibit decreased mentation by the time he or she arrives in the 

emergency department. However, a more subtle presentation (not marked by a rapid clinical deterioration) is 

also common. Initial blood pressure is usually high in patients with significant hemorrhage. 

2. Subarachnoid hemorrhage (SAH): nontraumatic 

Courtesy of Michael Abraham, MO 

Classic CT scan of SAH 

a. Highest incidence in women 35-65 years old and in men



(1) CT of the brain is most sensitive in the first 6 hours after the bleed and is useful in differentiating SAH 

from other causes of severe headache. 

(2) ACEP/AHA guidelines suggest that if the scan is negative, a lumbar puncture should be done, because 

CT is ~96% sensitive. 

(3) MRI may be as accurate as CT in patients with focal signs or symptoms. 

(4) Lumbar puncture findings suggestive of SAH 

(a) Grossly bloody fluid 

(b) CSF does not progressively clear (unlike in a traumatic tap, in which the first tube of CSF taken 

immediately after the lumbar puncture shows higher RBC counts than the last tube) 

(c) Xanthochromia (takes up to 12 hours to develop and lasts 2 weeks): due to the degradation of 

RBC in the CSF 

(d) Normal (or ambiguous) CSF findings and a nondiagnostic CT in a patient with a high pretest risk 

of SAH do not exclude an unruptured (yet symptomatic) aneurysm. Angiography is indicated in 

these patients (CTA/MRA/DSA). 

(5) Angiography is not routinely indicated to exclude SAH for patients in whom the CT and lumbar 

puncture are both normal. (ACEP Clinical Policy: Critical Issues in the Evaluation and Management of 

Patients Presenting to the Emergency Department with Acute Headache) 

3. Hypertensive intracerebral hemorrhage 

a. Putamen hemorrhage (most common) 

(1) Similar in presentation to middle cerebral artery syndrome 

(a) Contralateral hemiplegia, hemianesthesia, and homonymous hemianopsia; gaze palsy may be 

present. 

(b) Aphasia (if the dominant hemisphere is involved) or hemineglect (if the nondominant hemisphere 

is involved) 

(2) Distinguishing feature: greater depression of consciousness with putamen hemorrhage than with 

middle cerebral artery occlusion 

b. Cerebellar hemorrhage 

(1) Sudden onset of ataxia, dizziness, occipital headache, repeated vomiting, and loss of ability to stand or 

walk is typical. 

(2) If diagnosed early, this condition is treatable with surgical decompression and hematoma evacuation. 

c. Thalamic hemorrhage 

(1) Contralateral hemiparesis and hemianesthesia 

(2) Sensory loss > motor loss 

(3) Restricted upward gaze or abnormal deviation of the eyes without a visual field defect (occasionally) 

(4) Coma (may resolve if associated with focal depression of reticular activating system) 

d. Pontine hemorrhage 

(1) Severe occipital headache with rapid progression to coma (associated with poor prognosis) 

(2) Decerebrate posturing 

(3) Hyperventilation 

(4) Pinpoint pontine pupils ("3 P's"); other causes of pinpoint pupils: 

(a) Narcotic overdose (associated with hypoventilation) 

(b) Cholinesterase inhibitor poisoning (pesticides) 

(c) Pilocarpine eye drops or systemic atropine 

(d) Clonidine overdose 

(5) Absence of oculovestibular reflexes on caloric testing and doll's head maneuver 

G. Treatment of stroke 

1. Intubation should be considered in any stroke patient with a depressed level of consciousness. 

2. Hypertension is commonly associated with acute stroke. Should it be treated? The general consensus in the 

neurology literature is not to treat hypertension in patients with acute thrombotic stroke unless they are 

candidates for thrombolysis. 

a. Is the patient going to receive thrombolysis? 

(1) If yes: lower the blood pressure to 220 mmHg. 

417


(3) Patients with chronic hypertension may suffer greater ischemia when the pressure is lowered. 

(4) Perfusion of the ischemic but still viable (ischemic penumbra) tissue around the stroke area may 

require a higher blood pressure. 

b. Treatment of patients with hemorrhagic stroke is less clear, but the neurosurgery literature suggests that 

significant increases in blood pressure be treated. The goal is to reduce the systolic blood pressure to 


B. Types 

(2) Extracranial pathology 

1. Partial seizures 

(a) Toxic (eg, alcohol withdrawal, cocaine, tricyclic antidepressant overdose) 

(b) Uremic or hypertensive encephalopathy 

(c) Eclampsia 

(d) Endocrine/electrolyte abnormalities, hypoglycemia 

a. Simple partial (focal) seizures-,, motor, sensory, autonomic symptoms depending on where the electrical 

discharge is coming from; no loss of consciousness 

b. Complex partial seizures (temporal lobe or psychomotor)-,, motor, sensory, autonomic, or psychic onset 

(may mimic functional psychosis) associated with impaired consciousness, automatisms (lip smacking, 

picking at clothes), and postictal confusion 

c. Secondary generalized partial seizures (tonic-clonic or grand mal)-,, motor, sensory, autonomic or 

psychic onset followed by a generalized seizure, coma, and slow return to consciousness; tongue biting or 

incontinence may occur. 

2. Generalized seizures 

a. Nonconvulsive: absence (petit mal) seizures-,, brief (-10 seconds) alteration in level of consciousness (eg, 

cessation of activity associated with staring in a school-aged child); motor tone may increase or decrease 

with mild clonic movements or automatisms, which may be precipitated by hyperventilation. 

b. Convulsive: tonic-clonic, grand mal 

3. Todd paralysis: a transient focal paralysis after a seizure that usually lasts 1-2 hours but can last 1-2 days 

C. Differential diagnosis 

1. Myoclonus (may be associated with a multitude of disorders that include hypotension, Creutzfeldt-Jakob 

disease, uremia, etomidate, or lithium toxicity) 

2. Narcolepsy/cataplexy 

3. Tetanus 

4. Syncope 

5. Psychogenic seizures (pseudoseizures) 

6. Strychnine poisoning (patients remain alert) 

Table 24: Historical Clues that Distinguish a Generalized Seizure from Syncope 

Generalized Seizure 

Occurs without warning 

Tonic-clonic movements 

Prolonged postictal period 

Syncope 

Prodrome of darkening vision, nausea 

May have brief clonic movements 

No postictal period after return of normal cerebral blood flow 

D. Diagnostic evaluation for a first-time seizure, questionable seizure, unusual seizure, or seizure that is 

complicated by injury, illness, or substance abuse 

1. The only routine tests that have a reasonable yield in the evaluation of a first-time seizure are a serum glucose 

and sodium; so-called baseline studies (CBC, urinalysis, electrolytes other than sodium, BUN/creatinine, etc) 

are only indicated by clinical assessment, so a good history and physical examination are essential. 

2. Other tests that may be useful (again, based on history and physical examination) 

a. Lumbar puncture 

b. Blood alcohol, toxicology screen 

c. Anticonvulsant levels (in patients taking them) 

d. Chest radiograph (if tumor or aspiration is suspected) 

3. Indications for neuroimaging 

a. Emergent CT or MRI 

(1) Postictal patients with: 

(a) Status epilepticus 

(b) Recent head injury 

419


(c) Prolonged postictal state 

(d) Severe headache 

(e) New focal deficit 

(2) Patients with new-onset seizures whose fol low-up for routine CT cannot be assured. (ACEP Clinical 

Policy: Initial Approach to Patients Presenting with a Chief Complaint of Seizure Who Are Not in Status 

Epi lepticus) 

b. Urgent CT (performed during emergency department evaluation) 

E. Status epilepticus 

(1) Suspected CNS lesion 

(2) New seizure (in patients at risk of neurocysticercosis or HIV, and those with a history of malignancy) 

1. Definition: seizures that persist for 2:5 minutes or repetitive seizures without a lucid interval; permanent 

neuronal damage may result within 1 hour in patients with uncontrolled seizures; mortality rate is as high 

as 30%. 

2. Treatment (adults) 

420


I 

Glucose 25-50 g (50% sol) 

(if bedside test positive) 

I 

Naloxone 2-4 mg 

(if drug overdose suspected) 

I 

I 

Thiamine 100 mg (if alcoholism or Magnesium sulfate 20 ml (10% sol) IV 

malnutrition is suspected) 

if patient is eclamptic (pregnant or 

I 

I 

postpartum), alcoholic, or malnourished 

Lorazepam 2 mg/min (0.1 mg/kg) IV, 

up to 10 mg as needed 

OR 

Diazepam 5 mg/min IV every 

5 min as needed, up to 20 mg 

(pediatric: 0.15 mg/kg, up to 1 0 mg) 

OR 

Midazolam 0.2 mg/kg IN or 0.5 mg/kg buccally 

I 

I 

I 

Pyridoxine 5 g (5 or 10% sol) IV 

(if isoniazid overdose suspected) 

Phenytoin* 18-20 mg/kg IV at a rate of 

25-50 mg/min; dissolve calculated dose Phenobarbital 8-20 mg/kg at a rate 

in normal saline and administer piggybacked 

of 60 mg/min (indicated in patients on 

via infusion pump into the main IV line while 

barbiturates and in those for whom phenytoin 

the benzodiazepine 

is contraindicated because of allergy or the 

is still being given; it is the long-acting agent of 

presence of AV block) 

choice for the treatment of 

status epilepticus. 

I 

I I I I 

I 

I 

Phenobarbital Phenytoin - a second Valproic acid 

10 mg/kg at a rate of infusion - 9 mg/kg 20-40 mg/kg 

100 mg/min (indicated at a rate of 50 mg/min at a rate not to exceed 

if seizures persist and up to 20 mg/min 

may be repeated up to 30 mg/kg (indicated in 

a maximum dosage of patients with a partial 

30 mg/kg for refractory response to the initial 

status) 

infusion) 

Levetiracetam 

2-4 gm infused over 

15 min 

*Fosphenytoin may be used instead. A prodrug that is metabolized to phenytoin, fosphenytoin has two 

advantages: a more rapid rate of administration IV and it can be given IM. Fosphenytoin is administered in 

phenytoin equivalents (loading dose is 15-20 mg PE/kg at 100-150 mg PE/min). 

Medications Administered in Initial Stabilization of Status Epilepticus 

421


3. Treatment (children) 

a. Airway management (intubation and oxygen) 

b. IV line followed by: 

(1) Rapid glucose determination - glucose 2-4 ml/kg 25% solution as needed (D10 in neonates) 

(2) Pyridoxine 50-100 mg slowly IV (for neonates) 

(3) Calcium gluconate 4 ml/kg IV (for neonates) 

c. See also "Medications Administered in Initial Stabilization of Status Epilepticus" (figure, above). 

Ill. COMA (PATIENT IS UNRESPONSIVE TO VERBAL AND 

PAINFUL STIMULI) 

A. Etiology: mnemonic "TIPS AEIOU" 

Irauma, Iemperature 

Infection 

forphyria, fsychiatric disorder 

.S_pace-occupying lesion, Subarachnoid hemorrhage, Stroke, Shock 

Alcohol (drugs and toxins) 

_Endocrine, _Exocrine and _Electrolyte disorders 

Insulin 

Qxygen, Qpiates 

!J.remia 

1. Trauma (primarily head injury) 

a. Subdural hematoma 

Courtesy of Michael Abraham, MD 

CT scan showing bilateral subdural hemorrhage 

b. Epidural hematoma 

c. Traumatic subarachnoid hemorrhage 

422


Courtesy of Michael Abraham, MD 

CT scan showing subdural, subarachnoid, and intraparenchymal hemorrhage from trauma 

2. Temperature 

a. Hypothermia: causes coma when temperature is 107.6°F (42°C) 

3. Infection 

a. Meningitis 

b. Encephalitis 

c. Sepsis 

4. Endocrine, exocrine, and electrolyte disorders 

a. Hypo/hyperglycemia 

b. Hypo/hypernatremia 

c. Hypo/hypercalcemia 

d. Hypo/hyperthyroidism 

e. Hepatic encephalopathy (t NH) 


1. Always check and stabilize the ABCs before any detailed evaluation. 

2. Because there is frequently little or no known history in these patients, perform a thorough physical 

examination, including completely exposing the patient. 

3. Smell the breath. 

a. Fruity (diabetic ketoacidosis) 

b. Feculent (bowel obstruction) 

c. Putrid (anaerobic infection) 

d. Garlic (organophosphate insecticide) 

e. Bitter almonds (cyanide): only 60%-80% of the population can detect this. 

f. Alcohols (ethanol, isopropyl alcohol); methanol and ethylene glycol are odorless. 

g. Ammonia (uremia) 

h. Wintergreen (methyl salicylate) 

i. Fetor hepaticus: a musty smell (liver failure) 

4. Observe the respiratory pattern; it may have diagnostic value. 

a. Cheyne-Stokes: periodic, regularly increasing breaths in a crescendo pattern, followed by decrescendo 

breathing and ending with short periods of apnea that are due to dysfunction (structural or metabolic) of 

both cerebral hemispheres or upper brainstem 

b. Hyperventilation: causes include: 

(1) Hypoxia 

423


(2) Metabolic acidosis 

(3) Salicylate overdose 

(4) Lesions of the midbrain 

(5) Hepatic coma 

(6) t lntracranial pressure (ICP) 

c. Apneustic breathing: an end-inspiratory pause that occurs in association with lesions of the pons in the area 

of cranial nerve V 

d. Cluster breathing: short bursts of breathing that are associated with lower pontine lesions 

e. Ataxic breathing: an irregular breathing pattern that precedes death and is associated with lesions of 

the medulla 

5. Look for any abnormal posturing. Both decorticate and decerebrate posturing may be seen in patients with 

hypoglycemia or severe hepatic encephalopathy. 

a. Decorticate posturing 

(1) Flexion of the upper extremities and extension of the lower extremities 

(2) Suggests a lesion in the upper midbrain or internal capsule 

b. Decerebrate posturing: extension of al I extremities; suggests a deeper, more severe dysfunction 

(1) Severe midbrain lesions 

(2) Posterior fossa lesions that compress or partially damage the midbrain and pons 

(3) Severe metabolic disorders (hepatic coma, drug overdose) that depress the function of the deep 

diencephalon and forebrain 

(4) Bilateral diffuse hemispheric abnormalities (postanoxic cerebral demyelination) 

6. Look at the skin. 

a. Needle tracks (IV drug abuse) 

b. Cyanosis (hypoxia, hemoglobinopathy) 

c. Pallor (anemia) 

d. Cherry red (carbon monoxide - late finding) 

e. Petechial or purpuric rash (meningococcemia, Rocky Mountain spotted fever) 

f. Diaphoresis (hypoglycemia, cholinergic/salicylate poisoning, sympathomimetic) 

g. Pressure bullae (barbiturates, carbon monoxide, meprobamate) 

h. Ecchymoses at common sites of insulin injection (hypoglycemia) 

7. Look for ocular signs. 

a. Pupillary reactivity (the most important physical sign in distinguishing metabolic from structural causes 

of coma) 

(1) Reactive (but sluggish) pupils are characteristic of a metabolic or toxic disorder. 

(2) Nonreactive pupils are associated with a structural lesion with the following exceptions: 

(a) Anoxia (fixed and dilated) 

(b) Atropine and scopolamine (fixed and dilated) 

(c) Hypothermia (may be fixed) 

b. Anisocoria (unequal pupils ;:,1 mm difference) 

(1) Found in 10%-20% of the normal population 

(2) Other causes 

(a) 

Local eye trauma (traumatic mydriasis) 

(b) Instillation of a cycloplegic agent in one eye 

(c) Prior eye surgery 

(d) Compression of cranial nerve Ill by an enlarging aneurysm 

(e) Uncal herniation 

c. Other pupillary abnormalities 

(1) Pupil initially constricts to direct light during the swinging light test but dilates paradoxically as the 

light swings back to it, because it perceives a less intense stimulus than the normal eye perceived - 

Marcus-Gunn pupil (retina/optic nerve pathology [unilateral]) 

(2) Large, irregular pupil constricts very slowly to direct light - Adie's pupil (diabetic neuropathy, alcoholism) 

(3) Dilated pupil unreactive to light (most commonly cranial nerve Ill [or cycloplegic]) 

424


(4) Small, unilateral pupil reacts to light__,. Horner syndrome (interruption of the sympathetic nerve 

supply, usually in the neck) 

(5) Small, bilateral pupils unreactive to light but reactive to accommodation__,. Argyll-Robertson pupil 

(suggests neurosyph i I is) 

d. Fundi 

(1) Spontaneous venous pulsations (normal ICP) 

(2) Papilledema ( ICP, chronic) 

(3) Subhyaloid hemorrhages 

e. Ocular reflexes 

(1) Corneal reflex tests cranial nerves V (sensory) and VII (motor); absent with lesions in the posterior fossa 

or brainstem. 

(2) Oculocephalic reflex (doll's eyes): if the cervical spine has been cleared, turn the head in either the 

horizontal or vertical plane; a normal response (intact brainstem in a comatose patient) is conjugate 

deviation of the eyes in a direction opposite to the head rotation. 

(3) Oculovestibular reflex (cold calorics): Elevate the head 30° by raising the head of the bed, and irrigate 

the ear canal with 10 ml cold water. 

(a) 

Horizontal nystagmus with the fast component away from the irrigated ear is a normal response, 

indicating that the brainstem and the cerebral cortex are intact and the patient is not comatose. 

(b) Slow conjugate ipsilateral eye deviation toward the irrigated ear occurs in the comatose patient 

whose brainstem is functioning. 

(c) No response indicates brainstem dysfunction and most commonly results from structural causes. 

C. Essential stabilization and assessment measures 

1. Airway management with cervical spine control 

2. IV line followed by administration of thiamine 100 mg, glucose 50 g of 50% solution (if hypoglycemic), and 

naloxone 2-4 mg 

3. Oxygen supplementation and pulse oximetry 

4. Cardiac monitor 

5. Brief history ("what happened"; go through personal effects, EMS history) 

6. Physical and neurologic examinations, including Glasgow Coma Score 

7. Complete history (including known allergies) 

8. Radiographic clearance of cervical spine (if trauma suspected) 

9. Laboratory studies and further radiographic evaluation as indicated 

IV. THE ALTERED PATIENT 

A. Classic clinical scenario 

1. A patient is brought to the emergency department by a concerned relative, friend, or neighbor who has noticed 

a behavioral change. There is a history of disorientation, forgetfulness, and hallucination. 

2. Your task is to determine whether there is organic disease (an underlying medical problem) or a functional 

(psychiatric) disorder. 

a. Recent onset of a behavioral change with rapid progression suggests an organic cause and can occur in any 

age group. 

b. The dementias tend to occur in the elderly, and there is a history of gradual onset with slow progression of 

a behavioral change; however, they can be exacerbated by organic causes. 

B. Etiology: organic causes of behavioral change 

1. Drug intoxication or withdrawal 

2. Metabolic disorders 

3. Toxic exposure 

4. Cerebrovascular disease 

5. Tumors 

6. CNS infections (meningitis, encephalitis, cerebral abscess) 

7. Anoxia 

425


8. Hypercapnia 

9. Uremia 

10. Hepatic encephalopathy 

11. Vitamin deficiency (B 121 

thiamine, niacin) 

12. Sepsis 

13. Neurosyphilis 

14. Infections in the elderly 

C. Psychiatric disorders 

1 . Causes of acute mental confusion 

a. Schizophrenia 

b. Mania 

c. Agitated psychosis 

d. Psychotic depression 

e. Severe adjustment reaction 

f. Posttraumatic/dissociative episodes 

2. Dementia: a syndrome of global and progressive deterioration of intellectual function as well as impairment of 

memory, language, and personality; some of the causes are medically correctable. 

a. Reversible causes (20%) 

(1) Drug toxicity (al most any agent should be suspect) 

(2) Emotional disorders (especially depression) 

(3) Metabolic disorders 

(4) Nutritional deficiencies (especially B 12 

) 

(5) Normal-pressure hydrocephalus 

(6) Tumors 

(7) Infection (including non-CNS, eg, pneumonia, urinary tract infection, diverticulitis) 

(8) Complications of arteriosclerosis 

(9) Wilson disease 

b. Irreversible causes (80%) 

(1) Alzheimer disease (50%) 

(2) Multi-infarct dementia (20%) 

(3) Mixed Alzheimer/multi-infarct dementia (10%) 

(4) Rare causes 

(a) 

Parkinson disease 

(b) Huntington chorea 

(c) Creutzfeldt-Jakob disease 

3. Delirium versus dementia 

a. Dementia 

(1) Global cognitive impairment 

(2) Insidious 

(3) Vital signs normal 

(4) Typically elderly 

(5) Progressive 

(6) Focused attention 

b. Delirium 

(1) Global cognitive impairment 

(2) Acute onset 

(3) Abnormal vital signs 

(4) Younger individual 

(5) Fluctuating 

(6) Impaired attention 

426


D. Clinical presentation: Evaluation requires screening evaluation consisting of history and physical and 

neurologic examinations, including the Mini-Mental State Evaluation; never"OMIT" it: 

1. Qrientation (time and place) 

2. Memory (recent and past) 

3. Intelligence (thought pattern) 

4. Ialk (speech pattern) 

E. Diagnostic evaluation (directed by physical examination and history) 


2. CBC and urinalysis 

3. Chemistries (glucose, electrolytes, BUN/creatinine) 

4. Liver and thyroid function tests 

5. Cultures (blood and urine) 

6. Toxicology screen (including drug and heavy metals) 


8. CT scan (head) 

9. Serum osmolality 

10. Serum ammonia 

11. Lumbar puncture and evaluation of CSF (if CNS infection suspected) 

12. B 12 

levels 

13. VDRL or FTA 

V. NEUROPATHIES (DISORDERS THAT AFFECT PERIPHERAL 

NERVES) 

A. Etiology (multiple, include toxic, metabolic, and hereditary) 

1. Toxins 

a. Heavy metals (lead, arsenic, thallium) 

b. Drugs (eg, amiodarone, dapsone, vincristine) 

c. Industrial solvents 

d. Organophosphates 

e. Diphtheria, tetanus 

f. Ethanol 

2. Medical disorders 

a. Guillain-Barre syndrome 

(1) Miller-Fischer variant (more cranial nerve involvement) 

b. Connective tissue disorders 

c. Thiamine or vitamin B 12 

deficiency 

d. Hypothyroidism 

e. Lyme disease or tick paralysis 

f. Amyloidosis 

g. Malignancy 

h. Diabetes 

1. Leprosy 

j. Uremia 


1. Most common 

a. Both motor and sensory signs are present. 

b. Weakness and sensory impairment are symmetrical but greater distally than proximally - stocking-glove 

distribution of sensory symptoms (pain, paresthesia, numbness) 

c. Reflexes are usually absent (Achilles reflex is first affected) 

427


2. Other 

a. A pure motor or sensory loss predominates or 

b. There is proximal (rather than distal) weakness, bu I bar symptoms, or asymmetry. 

C. Specific toxic neuropathies 

1. Diphtheria 


2. Tetanus 

(1) An acutely i 11 patient with fever, tachycardia, and vague history. 

(2) Membranous pharyngitis that bleeds when the membrane is pulled back 

(3) Mononeuritis of the eyes (ptosis, strabismus, accommodation problems) 

(4) Motor involvement in other areas (limbs, palate [usually the first to become paralyzed], urinary, and 

anal sphincters) may be present; sensory involvement is rare. 


(1) Symptoms ("4 T's"): trismus (most common), tetany, twitching, and tightness (tight back, arms, and 

face; a tight facial expression is called "risus sardonicus"); the patient is awake (consciousness is not 

impaired). 

(2) Signs of sympathetic nervous system hyperactivity (tachycardia, hypertension, hyperpyrexia, sweating) 

are generally present. 

b. Differential diagnosis 

(1) Dystonic reaction due to phenothiazine therapy 

(2) Poisoning with strychnine 

(3) Local trismus due to odontogenic infection 

c. Treatment 

(1) Human tetanus immune globulin, wound debridement, and antibiotics effective against anaerobes 

(eg, penicillin G, metronidazole, or a third-generation cephalosporin); clinical disease does not confer 

immunity, so give the first dose of tetanus toxoid vaccine series in the emergency department. 

(2) Sympathetic hyperactivity may be treated with labetalol. 

3. Thallium neuropathy _,, painful paresthesias, diffuse motor weakness, alopecia (1-2 weeks later) 

4. Arsenic neuropathy _,, polyneuritis (a late finding) with occupational exposure 

5. Lead neuropathy _,, peripheral motor neuropathy (chronic ingestion) 

6. Alcohol neuropathy (ethanol, methanol, ethylene glycol) _,, slowly progressive peripheral neuropathy that is 

predominantly sensory in a stocking-glove pattern 

D. Specific metabolic neuropathies 

1. Guillain-Barre syndrome 

a. The most common acute polyneuropathy, this syndrome is an ascending neuropathy preceded by a viral 

syndrome in 50% of cases. 

b. Clinical presentation: sensory abnormalities (especially paresthesias)....,. rapid, progressive, symmetrical 

weakness_,, paralysis with loss of deep tendon reflexes_,, respiratory failure 

c. Diagnostic evaluation: CSF reveals cytochemical dissociation (normal cells, t protein) 

d. Miller-Fisher variant: descending symmetrical neuropathy associated with cranial nerve abnormalities 

2. Diabetic neuropathy _,, paresthesias in stocking-glove pattern, poor sensation, muscle weakness 

3. Gout neuropathy _,, extremity neuropathy (particularly of the lumbar plexus) 

4. Porphyria neuropathy- polyneuropathy (similar to Gillain-Barre but associated with psychosis and abdominal pain) 

5. Tick paralysis....,. looks like Guillain-Barre syndrome; search for the tick, especially in hairy areas, or in children. 

428


VI. DISORDERS OF THE NEUROMUSCULAR JUNCTION 

A. Myasthenia gravis (most common disorder of neuromuscular transmission) 

1. Definition: an autoimmune disease that destroys acetylcholine receptors that leads to poor neurotransmission 

with subsequent proximal muscle weakness 


a. Group 1: localized, nonprogressive disease with perhaps only ptosis or diplopia when fatigued; responds 

well to anticholinesterase therapy (neostigmine, pyridostigmine); excellent prognosis 

b. Group 2: generalized disease that involves more than one group of striated muscles, both skeletal and 

cranial in origin, but without sensory involvement; usually amenable to drug therapy; good prognosis 

c. Group 3: acute fulminant disease with severe bulbar manifestations (dysarthria, dysphagia, respiratory 

failure); poor response to drug therapy and poor prognosis 

d. Group 4: late severe disease that develops at least 2 years after the onset of symptoms in Groups 1 or 2; 

poor prognosis 

e. Group 5: muscle atrophy that begins 2:6 months after the onset of generalized disease (Group 2); variable 

prognosis 


a. Muscle weakness that is exacerbated by activity, sleeplessness, or alcohol intake and is relieved by rest 

b. Ptosis, diplopia, and blurred vision are the most frequent initial symptoms and are the only manifestations 

of the disease in 20% of cases; the pupil is not involved. 


a. A double-blind edrophonium test produces transient subjective and objective improvement of symptoms by 

preventing rapid breakdown of acetylcholine at the myoneural junction. 

b. The electromyogram is diagnostic. 

c. Serologic testing for antibodies to acetylcholine receptors is useful when positive; however, a negative test 

does not exclude the disorder. 

5. Two forms of acute crisis in myasthenia gravis: myasthenic and cholinergic. Distinction between the two with 

an edrophonium test may be difficult and hazardous in the extremely weak patient with progressive respiratory 

insufficiency. 

a. Myasthenic crisis 

(1) Occurs in undiagnosed/untreated patients and those with acute exacerbation of their disease process 

(2) Due to a functional deficiency of acetylcholine 

(3) Can produce severe muscle weakness and respiratory compromise 

(4) Administration of edrophonium 1-2 mg IV (a test dose) followed by 5-8 mg IV - clinical improvement 

b. Cholinergic crisis 

(1) Occurs in patients being treated for myasthenia gravis who receive too much acetylcholinesterase 

inhibitor 

(2) Due to a functional excess of acetylcholine 

(3) Can produce severe muscle weakness and respiratory compromise. 

(4) Administration of edrophonium - increased muscle weakness. Note whether cardiopulmonary 

symptoms occur (hypotension, bradycardia, wheezing); if so, atropine 1 mg IV (repeated as needed) 

should be given but will not improve the signs of neuromuscular blockade. 

(5) Another clue is the presence of muscarinic effects: "SLUDGE" (also suggestive of cholinergic crisis) 

.S.alivation 

lacrimation 

l!rination 

Qiaphoresis 

_Gastrointestinal cramps 

J;mesis 

429


c. Schematic for differentiating the two "crises" 

Myasthenic crisis 

I 

Result of undertratment or no 

treatment 

I 

Cholinergic crisis 

I 

Result of overtreatment 

I 

Due to a functional 

Due to a functional excess of 

deficiency of acetylcholine 

acetylcholine 

I 

I 

Severe muscle weakness and respiratory compromise 

I 

Edrophonium 1-2 mg IV followed by 5-8 mg IV 

I 

I 

I 

I 

I 

I 

Clinical improvement 

Increased muscle 

weakness 


a. Lambert-Eaton syndrome 

b. Botulism 

c. Tick paralysis 

d. Familial periodic paralysis 

e. Sleep paralysis 

f. Amyotrophic lateral sclerosis 

g. Gui I lain-Barre syndrome 

h. Organophosphate poisoning 

B. Lambert-Eaton syndrome 

1. A disorder of neuromuscular transmission most often associated with small-cell cancer of the lung -- aching, 

weakness, and fatigability of pelvic girdle and thigh muscles 

2. Unlike in myasthenia gravis (which it closely resembles), cranial nerves are generally spared and grip strength 

increases with repeated stimulation. 

C. Botulism (food-borne) 

1. Etiology: ingestion of a preformed toxin from Clostridium botulinum growing in poorly prepared canned food 

2. Pathophysiology: the toxin prevents release of acetylcholine from nerve endings -- neurologic symptoms 


a. Symptoms occur within 24-48 hours: the more severe the poisoning, the earlier the symptoms appear. 

b. The earliest and most common neurologic symptoms (90%) are blurred vision, diplopia (cranial nerves Ill 

and VI), and photophobia. 

c. Other symptoms that occur within the first 24 hours are dry mouth, dysphagia, and dysarthria. 

d. Some symptoms may occur at any time but usually appear early in severe cases -- ophthalmoplegia, 

ptosis, symmetric impairment of cranial nerves and a descending pattern of trunk and extremity weakness; 

mentation and sensation are normal. 

e. Respiratory failure is the usual cause of death and can occur within 6-8 hours of onset of symptoms. 

4. Infant botulism ("floppy baby") can occur with the ingestion of raw honey in children


VII. MYOPATHIES 

A. Differentiating myopathies from neuropathies 

Table 25: Characteristics of Myopathies and Neuropathies 

Myopathies 

Proximal weakness (getting up from a chair, climbing 

steps, reaching overhead) 

Sensory symptoms absent 

Deep tendon reflexes intact 

Abnormal laboratory tests: 

f WBC count 

f erythrocyte sedimentation rate 

f muscle enzymes 

Neuropathies 

Distal weakness with proximal progression 

Paresthesias, t sensation (stocking-glove distribution) 

t Deep tendon reflexes 

Normal laboratory tests 

B. Myopathic syndromes 

1. Polymyositis____.. acute inflammation__,, muscle pain and weakness__,. f CPI


2. Treatment 

B. Bell's palsy 

a. Long-term medical therapy is with carbamazepine. 

b. Dosage adjustments are required to achieve therapeutic effect, and the patient also needs to be monitored 

for signs of toxicity; therefore, referral for follow-up is necessary. 

1. Definition 

a. Unilateral facial nerve paralysis (cranial nerve VII) that involves the muscles of the forehead, cheek, and lips 

b. Onset of facial weakness is rapid (within 1-2 days) and is frequently preceded by an upper respiratory 

infection and 1-2 days of retroauricular pain. 

2. It is important to determine if the lesion is located near the origin of cranial nerve VII (brainstem) or somewhere 

in its peripheral distribution (face only) to determine if a structural lesion or Bell's palsy is present; significant 

clues of an upper motor neuron lesion are sparing of the muscles of the forehead and slower onset of facial 

weakness (usually weeks). 


a. Other palsies may mimic Bell's palsy. 

b. Ramsay-Hunt syndrome 

(1) Caused by herpes zoster (Bell's palsy may be caused by herpes simplex) 

(2) Characterized by typical zoster eruptions on the affected side of the face and neck; if you don't see 

them on the skin, look for them in the external auditory canal and/or the tympanic membrane. 

(3) Cranial nerve VII palsy due to Lyme disease may occur; if it does, it is bilateral (Bell's is unilateral). 

4. Bell's palsy is differentiated from a stroke by involvement of the forehead and lower face, the absence of 

aphasia, hemiparesis, and other focal neurologic deficits. 

5. Treatment 

a. High-dose steroids in a short burst followed by gradual tapering with lower doses are effective if given 

within 48 hours (some say may even be effective if


3. Examination reveals wasting and tenderness of the involved muscles; associated sensory loss is variable. 

4. Oculomotor palsy (cranial nerve Ill) is the most common cranial neuropathy; the pupil is usually spared (which 

differentiates this neuropathy from one caused by a tumor or aneurysm). 

D. Diabetic neuropathies 

1. Usually present in lower extremities more often than upper extremities 

2. Classically described as a decreased sensation in the "stocking glove" distribution 

3. Can also present as painful neuropathies in the lower extremity 

IX. MYELOPATHIES (DISORDERS OF THE SPINAL CORD) 

A. Syringomyelia 

1. Characterized by development of fluid-filled cavity within the spinal cord 

2. Dissociated sensory loss; loss of pain and temperature sensibility with preservation of light touch, vibration, 

and position; may be impaired in a 11 capelike 11 

distribution 

B. Multiple sclerosis 

1. A demyelinating disorder with myriad potential CNS symptoms, women affected more often than men 

2. Spinal cord involvement results in: 

a. Upper motor neuron signs (weakness, hyperreflexia) 

b. Sensory abnormalities 

c. Bladder/bowel dysfunction 

d. lntranuclear ophthalmoplegia is pathognomonic 

C. Transverse myelitis 

1. A postviral or toxic inflammation of the spinal cord (includes radiation effects that may occur during cancer 

therapy) 

2. Sensation, pain, and temperature sensation are diminished below the level of cord involvement. Vibration and 

position sense may also be diminished. Patients may have weakness or paralysis of lower extremities. 

D. Epidural mass lesion 

1. Any patient with back pain and a neurologic deficit should be evaluated for an epidural mass lesion. Look for 

any "red flags" in the history: fever, cancer, extremes of age, incontinence, and IV drug abuse, which should 

prompt a more detailed evaluation, including imaging. 


a. Severe pain (may be the only presenting complaint initially) 

b. Radiating electrical sensations down the spine (Lhermitte sign) 

c. Progressive signs of cord compression, eg, cauda equina syndrome 

3. Nontraumatic acute presentations occur in patients with: 

a. Epidural hemorrhage (consider anticoagulants) 

b. Acute cervical disc syndromes 

c. Abscess formation (previous IV drug abuse should raise suspicion) 

d. Metastatic tumor 

E. Dorsal column disorders 

1. Selective injury to the dorsal columns (classically associated with syphilis, alcoholism, and vitamin B 12 deficiency). 

2. Results in loss of position sense, vibration, and light touch 

X. VOLKMANN ISCHEMIC PARALYSIS 

A. Pathophysiology: predisposing condition such as edema, circumferential burn, or tight cast (that results in a 

compartment syndrome) - ischemia of the nerves and muscles - paralysis with eventual contracture 

B. Clinical features of a compartment syndrome (all of which occur late) 

1. Pain out of proportion to the injury 

2. Increased pain with passive stretching of the ischemic muscle compartment 

3. Pallor, paresthesias, and pulselessness (associated findings) 

433



1. Diagnosis is confirmed by direct measurement of compartment pressures (which are increased). 

2. Normal compartment pressure is 0-8 mmHg. 

D. Treatment: fasciotomy of compartment will usually treat this complication. 

XI. VERTIGO 

A. Definition: the sensation of motion 

1. Subjective vertigo: The patient feels that he or she is moving. 

2. Objective vertigo: The patient feels that the environment is in motion. 

B. Types 

1. Central vertigo 

a. Due to lesions of the brainstem or cerebellum 

b. Accounts for ~10%-15% of cases and has a more ominous prognosis than peripheral vertigo 


(1) Sudden onset of mild, continuous dysequilibrium that lasts > 1 minute 

(2) Nausea and vomiting 

(a) Mild -,, pontine lacunar infarct or vertebrobasilar TIA 

(b) Severe -,, acute cerebellar hemorrhage 

(3) Hearing loss and tinnitus are rare. 

(4) Spontaneous nystagmus is increased by visual fixation and may be bidirectional or vertical. 

(5) Positional nystagmus: no latency, does not fatigue or adapt, is multidirectional 

(6) Associated neurologic abnormalities may be present. 

(a) Severe ataxia, lateralizing dysmetria, or dysdiadochokinesis -,, cerebellar injury 

(b) Dysarthria, dysphagia, diplopia, Horner syndrome, motor weakness, scotomata, or blindness -,, 

brainstem injury 

d. Etiology 

(1) Brainstem ischemia or infarction 

(2) Cerebellar hemorrhage or infarction 

(3) Vertebrobasilar insufficiency 

(4) Basilar artery migraine 

(5) Cerebellar or brainstem tumors 

(6) Multiple sclerosis 

(7) Temporal lobe epilepsy (cortical vertigo) 

(8) Posttraumatic or postconcussive syndromes 

e. These patients are admitted for further evaluation and treatment. 

2. Peripheral vertigo 

a. Due to disorders of the external/middle/inner ear or cranial nerve VIII 

b. Accounts for ~85% of cases and is generally self-limited 


(1) Sudden onset of intense, intermittent episodes of dysequilibrium associated with a spinning, whirling 

sensation (Benign positional vertigo lasts


(4) Vestibular neuronitis 

(5) Benign positional vertigo 

(6) labyrinthitis or labyrinthine concussion 

(7) Acoustic neuroma 

(8) Meniere disease (endolymphatic hydrops or cochlear hydrops) 

(a) Clinical presentation: Patient is usually 40-60 years old and presents with a history of vertiginous 

episodes accompanied by tinnitus, sensorineural deafness, and aural pressure. Associated nausea 

and vomiting are common. Episodes are abrupt in onset and last for minutes to hours. 

(b) Differential diagnosis 

i. Cerebellopontine angle tumor 

11. Acoustic neuroma 

• Vertigo may not be present because of CNS accommodation for impaired vestibular 

function. 

• Additional findings: headache, diplopia, decreased corneal sensitivity, facial weakness, 

positive radiologic findings, increased CSF protein 

iii. Tertiary syphilis 

e. Treatment: focus on cause 

(1) Remove inciting medication or treat infection. 

(2) Treat BPPV with otolith repositioning maneuvers (Epley). Medication will have limited benefits. 

(3) Outpatient with antihistamines or anticholinergics and antiemetics. 

(4) Benzodiazepines are effective for symptomatic relief in severe cases. 

XII. HEADACHE 

A. Screen for the diseases with highest morbidity and mortality. 

1. Infection (meningitis, encephalitis) 

2. Bleeding (ICH/SAH) 

3. Mass (tumor, abscess) 

4. Temporal arteritis 

5. Central venous thrombosis 

6. Glaucoma 

7. Carbon monoxide poisoning 


1. Pain-sensitive areas of the cranium are skin, fat, muscles, nerves, the large arteries at the base of the brain, the 

dural arteries, the falx cerebri, and the great venous sinuses. 

2. The major intracranial structures (brain parenchyma, most of the dura, arachnoid, and pia) have no pain fibers. 

3. Headache results from tension, traction, inflammation, distention, and dilation of pain-sensitive structures. 

C. Types of headache 

1. Migraine 

a. Pathophysiology 

(1) Previously thought to be due to vasoconstriction followed by vasodilatation; recent technological 

advances in biochemistry and pharmacology suggest that this theory is no longer viable. 

(2) Current theories include neurogenic inflammation and abnormalities of the following: 

(a) Serotonergic transmission (5-hydroxytryptamine) 

(b) Trigeminovascular neuronal transmission 

(c) Vascular structures 

(3) Types of auras (represent manifestations of brain dysfunction) 

(a) Visual phenomena (most common), scintillating scotoma, or visual field defects 

(b) Motor disturbances, hemiparesis, ophthalmoplegia, aphasia 

(c) Sensory abnormalities, dysesthesia 

(d) Brainstem disturbances, vertigo, ataxia 

435


b. Factors that provoke or intensify an attack 

(1) Menstruation (most common bodily change) 

(2) Changes in body rhythm (sleep or food deprivation) 

(3) Physical activity 

(4) Certain foods (chocolate, hard cheese), beverages (red wine or other alcoholic beverages), and 

chemicals (caffeine, MSG, nitrites) 

(5) Contraceptive estrogens 


(1) Migraine without aura (80% of cases) 

(a) The headache is unilateral (initially), pulsating, and usually severe enough to interfere with 

normal daily activities. 

(b) Associated findings: nausea and vomiting, photophobia, and phonophobia 

(c) A previous history of these attacks (at least five) is required to make the diagnosis. 

(2) Migraine with aura (20% of cases) 

(a) The headache usually follows the aura after a symptom-free period 4 minutes) or two symptoms that occur in 

succession 

iii. A single symptom that lasts


(2) Discharge therapy for patients who are having an exacerbation of cluster headache (if there are no 

contraindications) 

(a) Trial of prophylactic verapamil 80 mg three times per day, to be increased by follow-up 

physician, and 

(b) Tapering course of steroids over 1-2 weeks, which is the typical duration of a cluster headache 

3. Subarachnoid hemorrhage (SAH) 


(1) An unusual headache of sudden onset that may have been present for several days; physical 

examination may be normal, or there may be subtle signs of meningeal inflammation (eg, low-grade 

fever or mild nuchal rigidity); there may also be slightly abnormal vital signs (t blood pressure + 

t pulse + t respiration = a cerebral event unless proven otherwise) 

(2) Sudden onset of a severe "exploding" headache frequently described by the patient as "the worst 

headache I've ever had" is the classic presentation. Associated nausea and vomiting are common, 

which may lure the unwary clinician into the "migraine mentality;" a clinical clue is that this 

headache is unprecedented, ie, unlike any headache the patient has had before, and it is focal. 

(3) Neurologic deficits are frequently mild or absent, but nonfocal signs may be present (drowsiness, 

confusion, personality changes, dizziness, diplopia, or blurred vision). 

(4) Sudden, severe headache followed by loss of consciousness----,, patient presents with hypertension, 

hyperventilation, and neurologic devastation; subhyaloid hemorrhage may be found on funduscopic 

examination. 

b. An SAH is most commonly due to bleeding from a saccular (berry) aneurysm (~75%) or AV malformation 

(~10%) but may occur with trauma, vasculitis, and other causes. History often differentiates the two, but 

occasionally, the hemorrhage precedes a traumatic incident (eg, the patient loses consciousness and then 

falls, hitting his or her head, or the patient loses consciousness while driving, loses control of the car, and 

injures himself or herself). 


(1) Brain CT without contrast is the procedure of choice for diagnosing SAH and should be done in any 

patient with a new onset of a severe or persistent headache. It has a sensitivity of 95% for detecting 

SAH. 

(a) If the CT is negative, a lumbar puncture should be performed because some patients with SAH 

have a normal CT scan. A yellow supernatant liquid (xanthochromia) that may not be detected 

for 12 hours, obtained by centrifuging a bloody CSF sample, can help distinguish SAH from a 

traumatic tap (no xanthochromia). (ACEP Clinical Policy: Headaches) 

(b) If the diagnosis is still in question, angiography (or repeat lumbar puncture) may be required. 

(2) ECG changes (large, broad, or symmetrically inverted T waves, U waves, prolongation of the QRS, 

prolonged QT interval) may occur in association with SAH and mislead you into pursuing a cardiac 

diagnosis; dysrhythmias may also result from SAH. 

(3) Blood glucose should be determined very early in the evaluation process to exclude hypoglycemia as 

a cause of an altered mental status. 

d. Treatment 

(1) Directed toward stabilizing the patient and preventing vasospasm and rebleeding 

(2) Obtain immediate neurosurgical consult. 

(3) Keep the patient in a quiet room with the lights dimmed. 

( 4) Elevate the head of the bed 30°. 

(5) Start an IV with normal saline or lactated Ringer's (to maintain normovolemia), administer oxygen, 

place patient on pulse oximeter, and monitor. 

(6) If systolic blood pressure is > 140 mm Hg, consider labetalol or nicardine. 

(7) Provide analgesics and antiemetics (eg, ondansetron) as needed for control of pain, nausea, and 

vomiting. 

(8) Prophylactic treatment with an anticonvulsant (eg, fosphenytoin) to prevent seizures, which can 

t ICP, is controversial. 

(9) Other therapeutic modalities should be decided in consultation with the neurosurgeon. 

(a) Nicardipine may reduce the risk and severity of vasospasm. 

(b) Antifibrinolytics (aminocaproic acid) may prevent rebleeding; their use is decreasing because of 

the associated ischemic complications and the trend toward earlier surgical intervention. 

(c) Mannitol or hypertonic saline should be started if patient is showing signs of t ICP. 

437


4. Temporal arteritis (cranial arteritis) 

a. Definition: a granulomatous inflammation of one or more branches of the external carotid artery 

b. Classic clinical scenario: The patient is usually a woman, often >50 years old, who presents with a severe 

throbbing, burning headache on one side. Symptoms can include jaw claudication. There is often a past 

history of similar headaches that are especially excruciating at night. Associated complaints may include 

malaise, night sweats, weight loss, blurred vision, and polymyalgia rheumatica. Physical examination 

often reveals one or more of the following: 

(1) A tender, warm, and frequently pulseless temporal artery that can sometimes be rolled between the 

fingers and skull 

(2) Increased burning and decreased throbbing with vessel compression 

(3) Decreased visual acuity on the affected side 

(4) If some of these findings are absent, be careful not to tag this as "migraine," because failure to 

diagnose and treat cranial arteritis can result in permanent neurologic loss, especially blindness. 

Strokes may also occur. The sedimentation rate, by the Westergren method, is characteristically 

increased (at least >50 mm/hr, often >100 mm/hr); ~25% of patients have only mild increases of the 

sedimentation rate; temporal artery biopsy (when positive) confirms the diagnosis. 

c. Management 

(1) Diagnosis is made by temporal artery biopsy. 

(2) Therapy should be started when the diagnosis is suspected; blindness is the most common sequela 

and may develop rapidly secondary to ischemic papillitis. 

(3) Emergent consult with a rheumatologist is necessary to determine disposition and steroid therapy 

regimen (usually with prednisone in large doses_,. 60-80 mg/day) 

(4) Urgent consult with an ophthalmologist/neurologist or rheumatologist is recommended; if unilateral 

blindness occurs, loss of vision in the other eye will occur in 1-20 days in 75% of cases. 

(5) NSAIDs may be administered for pain relief. 

5. Muscle tension headache: pain is constant and feels like a tight band around the head. 

6. Space-occupying lesions (brain abscess, tumor): headache is nonthrobbing, prolonged, and constant; onset is 

gradual, worse in the morning. 

7. Ocular headache (orbital and/or periorbital pain): may be due to glaucoma, iritis, or corneal abrasion. 

8. Idiopathic intracranial hypertension (pseudotumor cerebri): affects women more often than men; the patient 

is usually obese, and headache is usually accompanied by blurred vision and papilledema. CT is negative, 

MRI excludes dural sinus thrombosis, and lumbar puncture showing t ICP is both diagnostic and therapeutic. 

XIII. MENINGITIS 


1. Acute (pyogenic) meningitis 

a. Rapid onset of symptoms (within 24 hours): fever, headache, photophobia, vomiting, confusion, and stiff 

neck 

b. Etiology: most commonly bacterial; incidence declining due to Haemophilus influenzae type Band 

7-valent pneumococcal conjugate vaccine 

c. Begin antibiotic therapy within 30 minutes of presentation, ie, do not wait for lumbar puncture to confirm 

diagnosis. 

2. Subacute (lymphocytic) meningitis 

a. Gradual onset of similar symptoms (1-7 days) 

b. Etiology: usually viral 

c. Begin appropriate therapy (usually supportive) within 2 hours of presentation. 

3. Chronic meningitis 

a. Insidious onset of symptoms (> 1 week) 

b. Etiology: TB, coccidiomycosis, and cryptococcus (most common in HIV patients) 

c. Begin appropriate therapy as soon as the diagnosis is made. 


a. Infants (especially neonates) and the elderly typically lack the usual signs and symptoms; in the elderly, the 

only clue may be an altered level of consciousness. 

438


b. Look for papilledema, focal neurologic signs (especially ophthalmoplegia), rashes (including purpura and 

petechiae), and sources of infection. 

c. Brudzinski sign: passive flexion of the neck results in flexion of the hips and knees. 

d. Kernig sign: with the hips flexed, passive extension of the knee (> 120°) produces pain. 


1 . CT scan of the head 

2. 

a. Done first to exclude a mass lesion in patients who have a depressed mental status, seizure, head injury, 

focal neurologic signs, or papilledema, regardless of whether fever is present. 

b. Antibiotic therapy should not be delayed in patients with suspected bacterial meningitis; antibiotics should 

be administered before the CT scan. 

CSF 

a. Characteristics 

Table 26: Characteristics of CSF in Different Types of Infections 

Test Normal Bacterial Viral Fungal TB* 

Pressure 300 200 

Glucose >40 40


C. Etiology and antibiotic therapy 

Table 27: Etiology and Therapy of Meningitis in Different Age Groups 

Age 

0-4 weeks old 

4-12 weeks old 

3 months 

to 18 years old 

18-50 years old 

>50 years old and 

alcoholic patients 

Etiology 

E coli, Group B streptococci, Listeria 

monocytogenes, gram-negative bacilli 

The neonatal pathogens, Streptococcus 

pneumoniae, Neisseria meningitides, and 


S pneumoniae, N meningitides, and 

H influenzae (decreasing incidence since 

H influenzae B vaccine) 

S pneumoniae, N meningitidis (decreasing 

incidence since H influenzae B vaccine) 

S pneumoniae, L monocytogenes, 

N meningitidis, gram-negative bacilli 

Antibiotic Therapy* 

Cefotaxime and ampicillin, or 

gentamicin and ampicillin** 


ceftriaxone and ampicillin** 

Ceftriaxone or cefotaxime 

Ceftriaxone 

Ceftriaxone and ampicillin** 

*If instituted early, reduces morbidity and sequelae; add vancomycin in any patient >30 days old when S pneumoniae resistance is 

possible. 

**If penicillin-allergic, use vancomycin ± rifampin. 

D. Steroid therapy 

1. The recommendations for steroids are controversial. When given simultaneously with (or before) the first dose 

of antibiotic, dexamethasone may reduce the incidence of sensorineural hearing loss associated with bacterial 

meningitis in children; it also decreases the risk of an unfavorable outcome in adults with bacterial meningitis. 

2. Indications 

a. Consider in children >6 weeks old with H inf/uenzae or 5 pneumoniae meningitis 

b. Adults with proven or suspected pneumococcal meningitis 

3. Dosage: 0.15 mg/kg IV 

XIV. HYDROCEPHALUS 

A. Definition: abnormality in formation, flow, or absorption of CSF that leads to excess accumulation of CSF in 

the ventricles of the brain 

B. Etiology 

1. Congenital malformations 

2. Mass effect 

3. Trauma 

4. SAH 

C. Clinical presentation: usually a bimodal distribution 

1. Children: due to congenital abnormalities; present with vomiting and developmental delay 

2. Adults: due to normal-pressure hydrocephalus 

D. Treatment 

a. Normal-pressure hydrocephalus is defined as a hydrocephalus that has normal opening pressure on lumbar 

puncture and normal funduscopic examination. 

b. Usually present with ataxia and urinary incontinence 

1. Children 

a. Immediate neurosurgical consultation for ventriculoperitoneal shunt placement 

b. ICP management (elevate head of bed), consider mannitol for temporizing measure 

2. Adults 

a. Decrease CSF production: acetazolamide or furosemide 

b. Repeated lumbar punctures: usually for SAH-induced hydrocephalus, because this may resolve spontaneously 

after the initial injury heals 

c. Surgical management: ventriculoperitoneal or ventriculo-atrial shunt 

440

NERVOUS SYSTEM DISORDERS: PRACTICE CLINICAL SCENARIOS 

NERVOUS DISORDERS: PRACTICE CLINICAL SCENARIOS 

Answers immediately follow practice clinical scenarios. 

Scenario A 

Presentation: A 22-year-old man presents with an acute onset of unilateral headache that awoke him from 

sleep and is occurring at night. 


Scenario B 

Presentation: An 78-year-old woman complains of right-sided headache and pain in her jaw when eating. 


Scenario C 

Presentation: A 2-week-old female infant presents with irritability, high fever, and vomiting. The 

fontanelle is full. 


441

NERVOUS SYSTEM DISORDERS: PRACTICE CLINICAL SCENARIOS 


Scenario A 

Diagnosis: cluster headache 

Diagnostic evaluation: If there are no associated neurologic deficits after a thorough neurologic examination, then 

no specific testing is necessary. 

Management: Oxygen, 100% via face mask, should help with symptoms. Oral carbamazepine should alleviate 

symptoms but not acutely. Facial nerve blocks may be considered for outpatients. 

Scenario B 

Diagnosis: temporal arteritis 

Diagnostic evaluation: Diagnosis relies heavily on the clinical scenario. In women with unilateral headaches 

and jaw claudication, suspicion for temporal arteritis should be high. The evaluation should include a thorough 

ophthalmologic examination and erythrocyte sedimentation rate. 

Management: Steroid therapy should be initiated in patients who have a diagnosis of temporal arteritis. Prednisone 

at 40-60 mg/kg per day should be sufficient and is customary. Good follow up with ophthalmology and 

rheumatology should be arranged. Admission is not necessary unless there are mitigating factors to discharge. 

Scenario C 

Diagnosis: bacterial meningitis 

Diagnostic evaluation: Neonates may present with fever and be inconsolable. In older patients, altered mental 

status may be the only symptom. A Gram stain of CSF obtained by lumbar puncture is the "gold standard." 

Performing a CT scan before lumbar puncture is not necessary if the patient has normal neurologic and 

funduscopic examinations. CT scan may identify alternative reasons for this presentation, such as intracranial 

abscess or SAH. 

Management: The patient should be treated with empiric antibiotics based on the most likely causative organism. 

Double coverage with vancomycin is warranted if there is suspicion of methicillin-resistant Staphylococcus aureus 

(MRSA). If clinical suspicion is high, treatment should begin before verification of diagnosis. Pretreating the patient 

with steroids is controversial, but it may help alleviate some of the long-term morbidity associated with the disease. 

Table 28: Etiology and Therapy of Meningitis in Different Age Groups 

Age 

0-4 weeks old 

4-12 weeks old 

3 months 

to 1 8 years old 

18-50 years old 

>50 years old and 

alcoholic patients 

Etiology 

E coli, Group B streptococci, Listeria 

monocytogenes, gram-negative bacilli 

The neonatal pathogens, Streptococcus 

pneumoniae, Neisseria meningitides, and 


S pneumoniae, N meningitides, and 

H influenzae (decreasing incidence since 

H influenzae B vaccine) 

S pneumoniae, N meningitidis (decreasing 

incidence since H influenzae B vaccine) 

S pneumoniae, L monocytogenes, 

N meningitidis, gram-negative bacilli 

Antibiotic Therapy* 


gentamicin and ampicillin** 


ceftriaxone and ampicillin** 

Ceftriaxone or cefotaxime 

Ceftriaxone 

Ceftriaxone and ampicillin** 

*If instituted early, reduces morbidity and sequelae; add vancomycin in any patient >30 days old when 5 pneumoniae resistance is 

possible. 

**If penicillin-allergic, use vancomycin ± rifampin. 

442

GYNECOLOGIC AND OBSTETRIC DISORDERS 


Bartholin Gland Duct Abscess .................................................................................................................................. 448 

Genital Ulcer Infections ............................................................................................................................................ 448 

Herpes Simplex Virus ......................................................................................................................................... 448 

Syphilis .............................................................................................................................................................. 449 

Chancroid .......................................................................................................................................................... 450 

Lymphogranuloma Venereum ............................................................................................................................. 451 

Genital Mass Lesions ................................................................................................................................................. 451 

Human Papillomavirus ....................................................................................................................................... 451 

Noninfectious Vaginitis ............................................................................................................................................. 452 

Bacterial Vaginosis ............................................................................................................................................. 452 

Foreign Body ...................................................................................................................................................... 452 

Infectious Vaginitis .................................................................................................................................................... 452 

Fungal Infections ................................................................................................................................................ 452 

Trichomoniasis ................................................................................................................................................... 453 

Cervicitis/Endocervicitis ........................................................................................................................................... 453 

Neisseria gonorrhoeae ........................................................................................................................................ 453 

Chlamydia trachomatis ....................................................................................................................................... 454 

Pelvic Inflammatory Disease ..................................................................................................................................... 455 

Ovary ........................................................................................................................................................................ 456 

Torsion ............................................................................................................................................................... 456 

Ovarian Cystic Masses ....................................................................................................................................... 457 

Uterus ....................................................................................................................................................................... 457 

Vaginal Bleeding ................................................................................................................................................ 457 

Cervical Bleeding ............................................................................................................................................... 458 

Endometriosis ..................................................................................................................................................... 458 

Pelvic Organ Prolapse ........................................................................................................................................ 458 

Tumors ............................................................................................................................................................... 459 

Emergency Contraception ......................................................................................................................................... 459 

Sexual Assault ........................................................................................................................................................... 459 

Normal Pregnancy .................................................................................................................................................... 460 

Drugs and Radiation Exposure in Pregnancy ............................................................................................................. 462 

Complications of Pregnancy ...................................................................................................................................... 462 

First Trimester Bleeding ....................................................................................................................................... 462 

Abortion ............................................................................................................................................................. 463 

Ectopic Pregnancy .............................................................................................................................................. 464 

Rh lsoimmunization ........................................................................................................................................... 466 

Infections in Pregnancy ...................................................................................................................................... 466 

Hyperemesis Gravidarum/Nausea and Vomiting of Pregnancy ............................................................................ 467 

Gestational Diabetes .......................................................................................................................................... 468 

Chronic and Gestational Hypertension ............................................................................................................... 468 

HELLP Syndrome ................................................................................................................................................ 468 

Preeclampsia ...................................................................................................................................................... 468 

Eclampsia ........................................................................................................................................................... 469 

Hemorrhage, Antepartum ................................................................................................................................... 469 

Abruptio Placentae ...................................................................................................................................... 469 

Placenta Previa ........................................................................................................................................... 470 

Thromboembolism ............................................................................................................................................. 470 

Aortic Dissection ................................................................................................................................................ 470 

Maternal Cardiac Disease ................................................................................................................................... 471 

443


Cardiac Arrest .................................................................................................................................................... 471 

Peri mortem Cesarean Section ............................................................................................................................. 471 

High-Risk Pregnancy ................................................................................................................................................. 471 

Assisted Reproductive Therapies ......................................................................................................................... 471 

Normal Labor and Delivery ...................................................................................................................................... 472 

Complications of Labor ............................................................................................................................................. 472 

Fetal Distress ...................................................................................................................................................... 472 

Premature Labor ................................................................................................................................................. 472 

Premature Rupture of Membranes ...................................................................................................................... 472 

Rupture of Uterus ............................................................................................................................................... 473 

Complications of Delivery ......................................................................................................................................... 473 

Mal position of Fetus ........................................................................................................................................... 473 

Nuchal Cord ...................................................................................................................................................... 473 

Prolapse of Cord ................................................................................................................................................. 47 4 

Postpartum Complications ........................................................................................................................................ 474 

Postpartum Fever ................................................................................................................................................ 47 4 

Postpartum Hemorrhage ..................................................................................................................................... 475 

Uterine Inversion ................................................................................................................................................ 475 

Pituitary Infarction .............................................................................................................................................. 475 

444

GYNECOLOGIC AND OBSTETRIC DISORDERS: SELF-ASSESSMENT QUESTIONS 

GYNECOLOGIC AND OBSTETRIC DISORDERS: 


1. Which of the fol lowing statements 1·egarding syphilis, chancroid, lymphogranuloma venereum, and genital herpes 

simplex is most accurate? 

(a) Treatment of these sexually transmitted infections should be withheld until laboratory confirmation has 

been obtained. 

(b) Doxycycline is the recommended drug of choice for each of these infections. 

(c) Patients with these infections commonly complain of a vaginal or penile discharge. 

(d) These infections are characterized by genital ulcers and/or inguinal lymphadenopathy. 

2. A female patient presents with the complaint of an itchy, malodorous vaginal discharge that is yellow-gray in color. 

On examination, her vaginal mucosa has a stippled appearance, and the vaginal pH is 6.0. Wet mount reveals 

motile pear-shaped organisms with flagella at one end. The patient tells you she is 5 weeks pregnant. What is the 

most appropriate treatment for this condition? 

(a) 

Doxycline 100 mg orally bid x 14 days 

(b) Fluconazole 150 mg orally once 

(c) Metronidazole 500 mg orally bid x 7 days 

(d) Metronidazole gel 0.75% vaginally x 5 days 

3. A 26-year-old woman presents with painful vesicles on an erythematous base on her vulva, which are also seen on 

the cervix during a speculum examination. Which of the following is an indication for intravenous treatment and 

hospitalization? 

(a) 

lmmunocompromised patient with severe infection 

(b) Initial episode 

(c) Pregnancy 

(d) Recurrent episode 

4. All of the following are long-term complications associated with pelvic inflammatory disease except: 

(a) Chronic pelvic pain 

(b) Ectopic pregnancy 

(c) Infertility 

(d) Pelvic organ prolapse 

5. Which of the fol lowing signs is most consistent with a diagnosis of tuba-ovarian torsion? 

(a) Bilateral adnexal tenderness 

(b) Coiled vessels, or a "whirlpool" sign on ultrasound 

(c) Free fluid within the pelvis on CT imaging 

(d) Vaginal bleeding 

6. Which of the following is correct regarding labor and delivery? 

(a) 

Braxton Hicks contractions turn into true labor. 

(b) The stages of labor are initial, true, and final. 

(c) The third stage of labor includes delivery of the placenta. 

(d) Cervical change occurs during the second stage of labor. 

7. All of the following statements regarding vulvovaginal candidiasis are accurate except: 

(a) Candida albicans is part of the normal vaginal flora in up to 20% of women. 

(b) Causes of colonization or overgrowth include diabetes mellitus, pregnancy, menstruation, and birth control pills. 

(c) Diagnosis is with a potassium hydroxide prep that reveals "clue cells." 

(d) Treatment of partners is generally unnecessary, because this is not a sexually transmitted infection. 

445


8. A young, sexually active woman presents with a history of right lower quadrant pain for the past several hours. Her 

last menstrual period was 6 weeks ago, but she says that is not unusual for her. Her vital signs are stable, but she 

looks visibly uncomfortable. On abdominal examination, you note tenderness confined to the right lower quadrant, 

and pelvic examination reveals right adnexal tenderness and fullness. Which of the following possible diagnoses is 

least Ii kely? 

(a) 

Ectopic pregnancy 

(b) Pelvic inflammatory disease 

(c) Hemorrhagic corpus luteum cyst 

(d) Adnexal torsion 

9. In the patient discussed in question #8, which of the following laboratory studies would be least likely to help you 

in narrowing the differential and establishing a definitive diagnosis? 

(a) 

~-human chorionic gonadotropin 

(b) CBC 

(c) Pelvic ultrasound 

(d) Wet prep and nucleic acid amplification tests 

10. The incidence of transmission of rubella from an infected mother to her fetus is greatest when maternal infection 

occurs: 

(a) 

In the first month of pregnancy 

(b) In the second month of pregnancy 

(c) In the third month of pregnancy 

(d) Is the same in the first 3 months of pregnancy 

11. The drugs considered to be safest for administration during pregnancy are those classified by the FDA as: 

(a) Category A drugs 

(b) Category C drugs 

(c) Category D drugs 

(d) Category X drugs 

12. A visibly pregnant woman presents to the emergency department in cardiac arrest. Correct management of this 

patient includes: 

(a) Continue CPR on the backboard, intubate, use ACLS drugs and protocols, place an internal jugular line, 

perimortem cesarean section after 5 minutes. 

(b) Continue CPR with manual displacement of the uterus, intubate, use ACLS drugs and protocols, place a 

subclavian or internal jugular line, perimortem cesarean section before 5 minutes. 

(c) Continue CPR with manual displacement of the uterus on the backboard, intubate, avoid ACLS drugs, place a 

femoral line, perimortem cesarean section after 5 minutes. 

(d) Continue CPR with the backboard at a 30° tilt, intubate, use ACLS drugs and protocols, place a femoral line, 

perimortem cesarean section after 5 minutes. 

13. Which of the following is not considered to be a risk factor for abruptio placenta? 

(a) Hypertension 

(b) Abdominal trauma 

(c) Primiparity 

(d) Smoking 

14. A patient is brought in by ambulance for evaluation. The paramedics state that she had been out shopping with a 

friend and had a grand mal seizure. A fingerstick done in the field showed a glucose level of 120 mg/dL. There is no 

known history of a prior seizure disorder. On evaluation, she looks to be about 17 years old and at least 8 months 

pregnant. She is lethargic and hyperreflexic (+¾)and has a blood pressure of 170/100 mm Hg. The most appropriate 

initial medication is: 

(a) 

Hydralazine 

(b) Diazepam 

(c) Furosemide 

(d) Magnesium sulfate 

446


15. Signs of magnesium toxicity include all of the following except: 

(a) Loss of deep tendon reflexes 

(b) Respiratory depression 

(c) Flushing 

(d) Bradydysrhythmias 

16. Appropriate initial evaluation of a woman with vaginal bleeding in the third trimester includes all of the 

following except: 

(a) 

Evaluation of the fetal heart tones 

(b) Immediate pelvic examination 

(c) CBC and type and Rh 

(d) Ultrasound 

17. A woman who is 34 weeks pregnant presents with right upper quadrant pain of several hours duration. On 

examination, she has a temperature of 100.4°F (38°C), a heart rate of 102 beats per minute, blood pressure of 

120/68 mm Hg, and a respiratory rate of 18 breaths per minute. She has diffuse right upper quadrant tenderness. 

CBC reveals a WBC count of 17,000/mm 3 • Alkaline phosphatase, platelets, and liver function tests are normal, and 

urinalysis reveals pyuria without bacteria. The most likely diagnosis is: 

(a) Ascending cholangitis 

(b) Salpingitis 

(c) Appendicitis 

(d) Preeclampsia 

18. A woman who is 4 days postpartum presents with vaginal bleeding. Examination reveals a temperature of 101 °F 

(38.3°C), a purulent discharge, and uterine tenderness. The most likely cause of the postpartum bleeding is: 

(a) Retained placental tissue 

(b) Endometritis 

(c) Uterine atony 

(d) Genital tract trauma sustained during delivery 

1 9. Al I of the fol lowing statements regarding the Klei hauer-Betke test are accurate except: 

(a) It can be used to detect and quantify fetomaternal hemorrhage. 

(b) It is useful in determining the amount of Rh immune globulin administered to an Rh-negative woman who has 

sustained fetomaternal hemorrhage. 

(c) Its use is generally limited to women who are at least 12 weeks pregnant. 

(d) A negative test means that no fetomaternal hemorrhage has occurred. 

ANSWERS 

1. d 

2. C 

6. 

7. 

C 

C 

11 . 

12. 

a 

b 

16. b 

17. C 

3. a 8. b 13. c 18. b 

4. d 9. b 14. d 19. d 

5. b 10. a 15. c 



447


I. BARTHOLIN GLAND DUCT ABSCESS 

A. Etiology: Barthol in gland or duct cyst can become infected with various organisms (Escherichia coli, 

Staphylococcus aureus, mixed anaerobes, and occasionally Neisseria gonorrhoeae or Chlamydia) 


1. Painful unilateral swelling of the posterior-lateral aspect of the vaginal opening 

2. Pain is increased with sitting and walking; associated swelling and erythema of the labia majora is common. 

C. Management 

1. Incision and drainage (on the mucosa! aspect of the vestibule) followed by sitz baths 

2. Antibiotics if cellulitis is also present 

3. Word catheter placement for 6-8 weeks (to facilitate healing and reepithelialization) 

4. Elective marsupialization 

II. GENITAL ULCER INFECTIONS 

A. Herpes simplex virus 

1. Etiology 

a. Most prevalent genital ulcer disease 

b. Two types: HSV-1 usually causes oral lesions, HSV-2 typically causes genital lesions. 

c. Transmission is generally by sexual contact with an infected individual; it may occur in the absence of 

visible lesions if viral shedding is present. 

d. Incubation period is 8-16 days. 


a. Recurring, painful genital lesions appear as clusters of vesicles on an erythematous base, which 

subsequently denude to form ulcers. 

b. The lesions may be found at any site, but the most commonly affected areas are: 

(1) The cervix and vulva in women (swelling of the vulva may be so severe that the patient may not be 

able to void urine) 

(2) The glans and prepuce in men 

c. Attacks are often heralded by a prodrome of pain, hyperesthesia, burning, or paraesthesia at the skin site. 

d. Headache, fever, arthralgias, and regional adenopathy may also be present, particularly with the first 

clinical episode. 

e. Newborns who acquire the virus at birth may develop devastating complications. 


a. The clinical findings are sufficient to initiate treatment. Do not delay treatment for testing. 

b. Laboratory diagnosis 

(1) The gold standard is tissue viral culture. Specificity is high, although sensitivity declines as lesions heal. 

(2) PCR testing and serologic type-specific antibody testing are also available and more sensitive than 

culture. 

c. The Tzanck smear used in the past for diagnosis of herpes simplex virus is no longer recommended because 

of its lack of sensitivity. 

4. Management 

a. Acyclovir (oral or IV) remains the antiviral agent of choice. 

(1) Accelerates healing 

(2) Shortens the duration of viral shedding 

(3) Provides partial control of symptoms 

(4) Topical acyclovir is not recommended. 

(5) Famciclovir and valacyclovir are acceptable alternatives. 

b. Indications for treatment with oral acyclovir 

(1) Patients with primary lesions 

(2) Patients with associated herpes cervicitis, urethritis, proctitis, stomatitis, or pharyngitis 

448


(3) Patients with recurrent genital herpes 

(4) Episodic infections in HIV-positive patients 

c. Indications for hospital admission and treatment with IV acyclovir 

(1) Patients with severe genital infections 

(2) lmmunocompromised patients with severe infections/disseminated disease 

(3) Patients who cannot tolerate or do not respond to oral medication 

(4) Neonatal herpes 

d. Prescribe analgesics as needed. 

e. If an associated cellulitis is present, prescribe antistaphylococcal antibiotics. 

f. Advise patients to avoid sexual contact when lesions are present. 


B. Syphilis 

a. Herpes simplex virus has been epidemiologically associated with both cervical cancer and cancer of the vulva. 

b. Genital herpes has been associated with an increased risk of acquiring HIV and other sexually transmitted 

infections. 

c. Cesarean section is indicated in term-pregnant patients with active genital herpes because of the high 

neonatal mortality rate (50%-80%) and morbidity associated with contraction of neonatal herpes during 

vaginal delivery. 

1. Etiology 

a. Caused by a spirochete (Treponema pallidum) that inhabits skin lesions, mucous membranes, saliva, 

semen, and blood. 

b. Transmission occurs primarily by direct contact with an infected lesion (usually genital). Syphilis may also 

be acquired congenitally or by a blood transfusion (if the donor was in a very early stage of the disease). 

2. Clinical phases and diagnostic evaluation 

a. Primary syphilis 

(1) A smal I papule develops at the site of inoculation and becomes a painless, indurated ulcerative 

chancre. Chancres develop after an incubation period of 10-90 days, are present for 3-6 weeks, and 

resolve spontaneously. 

(a) Scrapings obtained from the chancre and examined under darkfield microscopy reveal moving 

corkscrew-like treponemes. 

(b) Serologic tests (VDRL or rapid plasma reagin) are often negative early in the primary stage. 

(2) Inguinal lymphadenopathy (buboes) may be present. Nodes are enlarged, nontender, firm, and 

rubbery; they develop ~4 weeks after initial exposure. 

b. Secondary syphilis 

(1) Characterized by constitutional signs/symptoms and a rash 

(2) Rash and lymphadenopathy are the most common symptoms. 

(3) The rash of secondary syphilis emerges 4-8 weeks after the initial appearance of the chancre and 

lasts for several months. It may be difficult to distinguish from the rash of Rocky Mountain spotted 

fever, because both are seen on the palms and soles. Definitive differentiation is with serologic testing 

(screen with VDRL or rapid plasma reagin, followed by FT A-ABS if positive). 

(a) Erythematous (red) macules, papules, or plaques (condylomata lata) suggest syphilis. The classic 

rash is maculopapular, nonpruritic, and symmetric, and the palms and soles are commonly involved. 

(b) A fine pink (not red) rash interspersed with macules suggests Rocky Mountain spotted fever. 

c. Tertiary syphilis 

(1) Onset occurs after a latent (dormant) period of several years. 

(2) Characterized by development of cardiovascular and/or neurologic disorders such as thoracic 

aneurysm, dementia, and tabes dorsalis (syphilitic myelopathy) 

(3) Serology tests are positive. 

d. Neurosyphilis and ocular syphilis can occur at any stage and should be considered in the differential 

diagnosis of HIV-positive patients with neurologic or eye complaints. 

3. Management 

a. Exposed patients should be evaluated clinically with treatment initiated on a presumptive basis while 

serologic testing is pending. 

b. All patients who have syphilis should be tested for HIV infection. 

449


C. Chancroid 

c. Sexual partners should be notified and treated, which occurs at the state level. 

d. Primary, secondary, and early latent (


D. Lymphogranuloma venereum 

1. Etiology and epidemiology 

a. Uncommon sexually transmitted infection caused by Chlamydia trachomatis 

b. Usually seen in men 20-40 years old but can be seen in women as well 


a. A small, shallow, painless vesicle or ulcer appears 3-21 days after exposure. It usually goes unnoticed by 

the patient. 

b. Localized, tender inguinal (and/or femoral) lymphadenopathy that is unilateral develops 2-24 weeks after 

exposure. 

c. When the nodes enlarge, coalesce, and ulcerate, constitutional symptoms may develop. 

d. The "groove sign" may appear and is characterized by proliferation of inguinal lymphadenopathy above 

and below the inguinal ligament. 


a. The lymphogranuloma venereum complement fixation test (which has replaced the Frei skin test) is 

diagnostic but not available in many hospital laboratories. 

b. Culture is also diagnostic, but many laboratories do not have this capability. 

c. The diagnosis is usually made by identification of WBCs with intracellular inclusion bodies from aspirates 

of infected tissue. 

4. Management 

a. Treatment should be started as soon as the diagnosis is suspected, without waiting for laboratory 

confirmation. 

b. Doxycycline 100 mg orally bid x 3 weeks is the treatment of choice but should be avoided in pregnancy, 

while nursing, and in children 40 serotypes. 

b. Linked to development of genital warts as well as cervical cancer 


a. Frequently an asymptomatic infection, although clinical presentation depends on the serotype and location 

of infection. 

b. The virus may infect the oropharynx, genital, or anal tissue. 

c. Genital warts are usually flat papules or pedunculated and skin colored. 


a. Diagnostic evaluation should include genital examination in the emergency department for lesions. 

Emergency concerns are those of large, obstructing lesions. 

b. Serotyping is not required for routine diagnosis. 

c. Biopsy is not required unless coexisting neoplasia suspected. 

4. Management and prevention 

a. External lesions 

(1) lmiquimod 3.75% or 5% cream topical or 

(2) Podofilox 0.5% solution or gel or 

(3) Sinecatechin 15% ointment 

(4) Alternatively, the patient may be referred to a specialist for cryotherapy, trichloracidic acid, or surgical 

removal. 

b. Appropriate cancer screening and follow-up are recommended. 

c. Vaccination is recommended for children 11-12 years old to prevent development of cancer. (Vaccination 

is not typically done in the emergency department.) 

451


IV. NONINFECTIOUS VAGINITIS 

A. Bacterial vaginosis 

1. Pathophysiology: results from overgrowth of anaerobic vaginal flora (Cardnerella vagina/is, Ureaplasma 

urealyticum, etc) 

2. Clinical presentation: patients present with complaints of a fishy smelling discharge and mild itching. 


a. Homogeneous, grey-white, noninflammatory discharge that coats the vaginal wall rather than pooling on 

the vaginal floor 

b. "Clue cells" (vaginal epithelial cells covered with bacteria) on microscopic evaluation of vaginal secretion 

saline preparation (aka wet mount) 

c. Positive amine odor "whiff" test (fishy odor when potassium hydroxide is added to a sample of the vaginal 

secretions) 

d. pH of vaginal secretions >4.5 

e. DNA probe-based test available for point-of-care testing 

4. Management 

a. Metronidazole 500 mg orally bid x 7 days (Note: Metronidazole can produce a disulfiram ["Antabuse"] 

reaction if taken in conjunction with alcohol. Therefore, patients must be advised to avoid ingesting alcohol 

while taking metronidazole and for at least 24 hours after completion of therapy.) 

b. Metronidazole gel 0.75% intravaginally 5 glday x 5 days or 

c. Clindamycin cream 2% intravaginally 5 g at bedtime x 7 days or 

d. Other alternatives: oral clindamycin, clindamycin ovules, oral tinidazole 

e. For symptomatic pregnant women, oral regimens are preferred. 

B. Foreign body 

1. Children may insert any object; adults may forget tampons, pessaries, diaphragms, or condoms. 

2. Clinical presentation: a foul-smelling and sometimes bloody discharge 

3. Management 

a. Remove the object. 

b. Treat for any vaginitis and arrange for follow-up. 

c. Consider toxic shock syndrome if accompanied by fever, rash, etc. 

4. Consider the possibility of sexual abuse when vaginal foreign bodies are found in prepubertal girls. 

V. INFECTIOUS VAGINITIS 

A. Fungal infections 

1 . Pathophysiology 

a. Candida species, most commonly C albicans 

b. Normal vaginal flora in up to 20% of healthy women 

c. Symptoms due to overgrowth 


a. Extreme itching 

b. A thin watery to thick white discharge sometimes associated with dysuria or dyspareunia 

c. Physical examination: thick, white "cottage cheese" discharge, vulvovaginal erythema, and edema; may 

have satellite lesions on perineum 


a. Pseudohyphae and spores are seen on 10% potassium hydroxide preparation. 

b. pH of vaginal secretions is normal (::C:4.5). 

c. Latex agglutination testing is available for point-of-care testing. 

4. Classification of vulvovaginal candidiasis 

a. Uncomplicated: 90% of cases 

(1) Sporadic/infrequent 

452


(2) Mild to moderate 

(3) Likely to be C albicans 

(4) Nonimmunocompromised patients 

b. Complicated 

(1) Recurrent or severe (2:4 episodes per year) 

(2) Candidiasis not caused by C albicans 

(3) Pregnancy 

(4) Debilitated, diabetic, or immunocompromised patients 

5. Management 

a. Uncomplicated vulvovaginal candidiasis 

(1) Fluconazole 150 mg orally in one dose or 

(2) One of the following vaginal preparations every night x 3 days: 

(a) Butoconazole 2% cream or 

(b) Clotrimazole two (100 mg) vaginal tablets or 

(c) Miconazole 200 mg vaginal suppository or 

(d) Terconazole 80 mg suppository or 0.8% cream 

b. Complicated vulvovaginal candidiasis: longer course of treatment with oral fluconazole or intravaginal 

preparations 

B. Trichomoniasis 

1. Etiology: Trichomonas vagina/is, a flagellated protozoan 


a. Patients present with vulvovaginal itching and a foul-smelling discharge. 

b. Dysuria and lower abdominal pain may also be present. 

c. Symptoms usually develop after an incubation period of 4-28 days. 

d. Profuse, occasionally foamy, yellow-green discharge associated with diffuse vaginal erythema and a 

"strawberry cervix and vagina" (punctate hemorrhages) 


a. Wet mount demonstrates a flagellated, motile, tear-drop-shaped organism and many PMNs; sensitivity is 

60%-70%. 

b. Polymerase chain reaction testing is available for point-of-care testing and has higher sensitivity and 

specificity than wet mount. 

c. Vaginal pH 2:5.5 

4. Management 

a. Partner must also be treated. 

b. Recommended regimen (including for pregnant patients): metronidazole 2 g orally in one dose or 

tinidazole 2 g orally in one dose 

c. Alternative regimen: metronidazole 500 mg orally bid x 7 days (this regimen preferred for pregnant 

women) 

d. 90% of men with this infection are asymptomatic; therefore, sexual partners must be treated if reinfection is 

to be prevented. 

VI. CERVICITIS/ENDOCERVICITIS 

A. Neisseria gonorrhoeae 


a. The presenting complaint is frequently dysuria, a vaginal discharge, or both. The presence of abdominal 

pain should raise suspicion that the infection has spread to the uterus and fallopian tubes (pelvic 

inflammatory disease). 

b. Pharyngeal or anal infection may occur. Although generally asymptomatic, patients with anal infection 

may complain of discharge, rectal pain, tenesmus, and/or constipation. Patients with pharyngeal infection 

are rarely symptomatic. 

c. Gonococcal conjunctivitis is usually the result of inoculation of the eye by a contaminated finger. It 

presents with a unilateral copious purulent discharge and marked conjunctiva! injection. 

453


d. Hematogenous dissemination may produce any of the following complications and may present with 

a characteristic rash (erythematous macules or pustules with a necrotic or purpuric center) and/or 

petechiae. 

(1) Joint disease 

(a) Most common cause of septic arthritis in patients


b. Nucleic acid amplification test is more sensitive than culture. 

c. Chlamydia! cervicitis should be suspected if Gram stain reveals PMNs but no organisms. 

4. Management 

a. Start as soon as the diagnosis is suspected clinically or there is a history of exposure. Do not wait 

for culture results, because this may result in development of more advanced disease and continued 

transmission of infection. 

b. Antibiotic regimens 

(1) Azithromycin 1 g orally once or 

(2) Doxycycline 100 mg orally bid x 7 days (contraindicated in pregnancy) 

(3) Alternatives include erythromycin, levofloxacin, and amoxicillin. 

c. If untreated, may lead to infertility and ectopic pregnancy. 

d. Sexual partners need to be treated. 

VII. PELVIC INFLAMMATORY DISEASE (PID) 

A. Etiology 

1. Caused by infection of the upper reproductive tract organs that has spread from the cervix/lower tract 

2. Pathogenic organisms 

a. N gonorrhoeae and C trachomatis are the major pathogens; together they account for approximately 

80% of cases. 

b. Other pathogens include Trichomonas vagina/is and mycoplasmas. 


1. Normal host barriers (uterotubal cervical mucus, lysozymes, and local immunoglobulin lgA as well as the 

cervix itself) usually prevent infection. 

2. Menstruation is the most common cause of breakdown of these barriers. 

3. During pregnancy, fusion of the chorion and decidua forms another natural barrier, making PIO less common 

but higher risk if occurring during pregnancy. 


1. Criteria for diagnosing acute pelvic inflammatory disease 

a. CDC recommends empirical treatment for pelvic inflammatory disease in sexually active women with 

pelvic pain plus one of the following: 

(1) Cervical motion tenderness 

(2) Uterine tenderness 

(3) Adnexal tenderness (usually bilateral) 

b. Additional criteria helpful in increasing specificity but not required for diagnosis 

(1) Oral temperature > 101 °F (38.3°C) 

(2) Abnormal vaginal or cervical discharge 

(3) Abundant WBCs on wet prep 

(4) Increased erythrocyte sedimentation rate or C-reactive protein 

(5) Laboratory evidence of cervical infection with N gonorrhoeae or Chlamydia 

2. Ultrasonography may show tubo-ovarian abscess or pyosalpinx. 

D Management 

1. All regimens should cover N gonorrhoeae, Chlamydia, anaerobes, gram-negative rods, and streptococci. 

2. Outpatient 

a. Ceftriaxone 250 mg IM plus doxycycline 100 mg orally bid x 14 days ± metronidazole 500 mg orally bid 

x 14 days, or 

b. Cefoxitin 2 g IM and probenecid 1 g orally plus doxycycline 100 mg orally bid x 14 days is the traditional 

therapy, ± metronidazole 500 mg orally bid x 14 days. 

3. Inpatient 

a. Recommended admission indications for parenteral treatment 

(1) Temperature >38.3°C 

455


(2) Nausea and vomiting (unable to take antibiotics) 

(3) No response to outpatient therapy within 72 hours 

(4) Suspicion of a tubo-ovarian or pelvic abscess (which may require surgery) 

(5) Uncertain diagnosis (another surgical emergency cannot be excluded) 

(6) Young age (potential for future fertility issues) 

(7) WBC >15,000/mm 3 

(8) Timely clinical follow-up (within 72 hours of starting antibiotics) cannot be arranged. 

b. Drug therapy 

(1) Cefoxitin 2 g IV every 6 hours or cefotetan 2 g IV bid plus doxycycline 100 mg IV or orally bid, 

± metronidazole 500 mg orally, or 

(2) Ampicillin/sulbactam 3 g IV qid plus doxycycline 100 mg orally or IV bid 

c. Sexual partners should be evaluated and treated empirically to prevent reinfection. 

E. Complications 

1. Tubo-ovarian abscess 

a. Patients present with constitutional symptoms, unilateral pelvic pain, and vaginal discharge. The laterality 

is what differentiates tubo-ovarian abscess from PID. 

b. The infected fallopian tube adheres to the ovary, forming an abscess that can go on to rupture and cause 

peritonitis. 

c. Physical examination: unilateral adnexal tenderness and mass 

d. Ultrasound is preferred but can be seen on CT as well. 

e. Treatment: parenteral antibiotics with/without operative drainage if unruptured; ruptured tubo-ovarian 

abscess requires immediate surgery. 

2. Fitz-Hugh-Curtis syndrome (perihepatitis) 

a. Caused by inflammation of the liver capsule that leads to adhesions 

b. Sharp, pleuritic right upper quadrant pain that accompanies the pelvic pain of PID 

c. Pain may refer to the shoulder or upper arm. 

3. Chronic inflammation and scarring can lead ectopic pregnancy, infertility, and chronic pelvic pain. 

4. Obstetrical complications 

a. Intrauterine growth retardation 

b. Septic abortion 

c. Premature rupture of membranes/preterm delivery 

VIII. OVARY 

A. Torsion 


a. An abnormal ovary or fallopian tube twists around its vascular pedicle _,. blood supply is compromised _,. 

painful degeneration of the ovary or fallopian tube with eventual gangrenous necrosis 

b. Ovarian torsion usually occurs in association with an ovary that is enlarged because of a cyst or tumor or 

that is overstimulated (ovarian hyperstimulation syndrome) by use of fertility drugs; fallopian tube torsion 

usually occurs in association with hydrosalpinx, neoplasm, adhesions, trauma, or previous ligation. 

c. May occur at any age (although most common in the mid-twenties) and at any time during the menstrual 

cycle 


a. Vital signs: absence of fever, or tachycardia out of proportion to the fever (different from PID, tuboovarian 

abscess) 

b. History 

(1) Onset of pain is usually sudden (frequently during or immediately after sexual intercourse); the 

patient may even remember the exact moment. Pelvic infections have a more gradual onset. 

(2) The pain is usually unilateral (more commonly on the right), becomes increasingly severe but may 

subside and, if so, the patient may not appear to be acutely ill on presentation (not so with pelvic 

infections). 

(3) Often, there is a history of similar episodes in the past that resolved spontaneously. 

456


c. Pelvic examination 

(1) Unilateral adnexal tenderness ± mass 

(2) During early stages, significant tenderness or discomfort may not be elicited during examination. 


a. Routine laboratory studies are usually normal. Pregnancy testing should be done to exclude ectopic or 

concomitant intrauterine pregnancy. 

b. Ultrasound may reveal the adnexal mass when the physical examination does not. Color Doppler flow 

aids diagnosis. Coiled vessels or "whirlpool sign" is 88% accurate in diagnosing torsion. 

c. CT/MRI: thickened fallopian tube, enlarged ovary, ovarian mass, free pelvic fluid, edematous ovary, 

deviation of the uterus to the affected side, associated hemorrhage 

d. Laparoscopy: the definitive diagnostic procedure 

e. Negative imaging findings should be taken with caution when clinical suspicion of torsion is high. 

4. Management 

a. Surgical correction or resection is the definitive therapy of choice; however, laparoscopy alone is being 

used with increasing frequency, because "untwisting" may be possible if torsion is diagnosed early or is 

caused by the ovarian hyperstimulation syndrome. 

b. Although return of ovarian function is possible even with late presentation, pediatric patients taken to 

surgery within 8 hours have the best chance of recovery. 


a. Scarred tube - t fertility and t risk of tubal pregnancy 

b. Ovarian necrosis - peritonitis and shock, infertility 

B. Ovarian cystic masses 

1. Two major groups: functional ovarian cysts and ovarian cystic neoplasms 

2. Functional ovarian cysts 

a. Very common; subcategorized into follicular cysts or corpus luteum cysts 

b Originate from ovarian follicles, created by hormonal dysfunction during ovulation 

c. May become hemorrhagic 

d. Treatment: supportive/observational 

3. Ovarian cystic neoplasms 

a. Ovarian teratoma 

(1) Arises from a germ cell, containing any of the germ layers-ectoderm, mesoderm, endoderm-forming 

tissues that are disorganized in structure 

(2) Immature teratoma: malignant 

(3) Mature cystic teratoma (aka dermoid tumor): benign 

(4) 15% undergo torsion 

IX.UTERUS 

A. Vaginal bleeding 

1. Etiology 

a. Alterations in the endocrine system secondary to ovarian tumors, corpus luteum cyst, hypothyroidism, 

menarche or menopause, excessive exercise, poor diet, medications 

b. The most common medications implicated in "breakthrough" bleeding (ie, bleeding that occurs between 

periods) 

(1) Anticonvulsants 

(2) Some antibiotics 

(3) Anticoagulants 

(4) Exogenous estrogen or progesterone 

(5) Oral contraceptives (breakthrough and withdrawal bleeding) 

c. Coagu Iopa th ies 

d. Pelvic infections 

e. Neoplasms (Cervical polyps or carcinoma, leiomyomas, endometrial polyps or carcinoma, ovarian tumors) 

457


f. Postoperative (generally occurs when absorbable sutures dissolve) 

g. Trauma 

h. Foreign bodies 

1. Dysfunctional uterine bleeding 

2. Management 

a. Exclude life-threatening hemorrhage by evaluating hemodynamic stability. 

b. Stabilize patients with life-threatening bleeding (the minority) with IV fluids and blood products as needed; 

consider IV estrogens. 

c. Identify treatable causes through a careful history and physical; important points include: 

B. Cervical bleeding 

(1) Assume that any woman of childbearing age with abnormal vaginal bleeding is pregnant (intrauterine 

or ectopic) until proven otherwise; perform a pregnancy test. 

(2) Estimate the blood loss by determining the duration and amount of bleeding as well as the presence of 

clots. 

(3) In addition to performing a pelvic examination, check other potential sites of bleeding that might be 

confused with vaginal bleeding (perineum and rectum). 

(4) Order other appropriate laboratory studies as indicated. 

1. Mild to moderate - Mansel solution or silver nitrate 

2. Severe (postoperative or trauma-induced) - appropriate suturing 

3. Refer to a gynecologist for a complete investigation. 

C. Endometriosis 

1. Definition and clinical presentation 

a. Common gynecologic disorder defined as presence of endometrial glands and stroma outside the normal 

location; most commonly in pelvic peritoneum, ovaries, rectovaginal septum, and ureter; rarely found in 

bladder, pericardium, and pleura. 

b. Affects females of reproductive age; patients can be asymptomatic, subfertile, and/or have varying degrees 

of pelvic pain. 

2. Physical examination: the vagina and cervix usually appear normal. Occasionally, blue or red lesions can be 

seen on the cervix posterior vagina; these lesions can be tender or bleed with contact. Bimanual examination 

may reveal an adnexal mass representing ovarian endometrioma but is generally nonspecific. 

3. Diagnosis: diagnostic tests done in the emergency department include those to exclude other emergent causes 

of pelvic pain. Nonemergent diagnostic laparoscopy is the primary method used by gynecologists to diagnose 

endometriosis. 

4 Management 

a. Emergency department management: NSAIDs 

b. Gynecology: hormonal therapies (combination oral contraceptives, progestins, etc), surgical treatment 

D. Pelvic organ prolapse 

1. Definition and clinical presentation 

a. Descent of one or more of the following: anterior vaginal wall, posterior vaginal wall, uterus and cervix, 

the apex of the vagina after hysterectomy, or the perineum. Small bowel may be included in the presenting 

bulge, termed an enterocele. 

b. Patients present with complaints of pelvic pressure and vaginal bulging, and can also report urinary stress 

incontinence, frequency or urgency, and other voiding dysfunction. 

2. Physical examination: If no vaginal bulge is obviously present on visual inspection (before insertion of 

speculum), the patient should be directed to attempt a Valsalva maneuver. The prolapse may still not be seen 

with this maneuver, because it is a dynamic condition and frequently worsens at the end of the day or with 

physical activity. The gynecologist can perform a more extensive examination with a split speculum and 

measurements. 

3. Laboratory tests/imaging: diagnostic tests done in the emergency department include those to exclude other 

emergent causes of pelvic pain and/or urinary symptoms. 

4. Management: patients with minimal symptoms can be managed expectantly. For more significant symptoms, 

several nonsurgical (pessary, pelvic floor muscle exercise) and surgical (obliterative or reconstructive 

procedures) approaches can be managed by a gynecologist. 

458


E. Tumors 

1 . Leiomyoma 

a. Fibroid uterus is a common benign muscular tumor of the uterus. 

b. Incidence increases with age; affects >40% of women by age 35. 

c. Black American women are more likely to have fibroids. 

d. May cause anemia secondary to significant bleeding or become painful when large enough to become necrotic 

e. Diagnostic evaluation: ultrasound examination; however, the enlarged uterus may be palpable on bimanual 

examination. 

f. Management 

(1) NSAIDs to control pain 

(2) Iron supplementation and potentially blood transfusion for anemia 

(3) Hysterectomy, myomectomy, or embolization if indicated 

2. Gestational trophoblastic disease (molar pregnancy): see page 462. 

X. EMERGENCY CONTRACEPTION 

A. Definition: contraceptive care for women after consensual but unprotected sexual intercourse or after 

sexual assault. Substantially decreases the likelihood of an undesired pregnancy. 

B. Methods available for use as emergency contraception 

1. Progestin only 

a. Levonorgestrel 0.75 mg within 72 hours of intercourse, then 0.75 mg 12 hours later, or 

b. Levonorgestrel 1.5 mg once within 72 hours or up to 120 hours after intercourse 

2. Selective progestin-receptor modulator: ulipristal acetate 30 mg once up to 120 hours after intercourse 

3. Combination oral contraceptive pill: multiple regimens exist 

4. Insertion of copper-containing intrauterine device (although not a practical option in the emergency department) 

C. Patients should be counseled to use a barrier contraceptive technique until the next menses (because oral 

contraceptive methods will not prevent pregnancy resulting from subsequent episodes of intercourse), as 

well as obtain pregnancy testing if menstruation is delayed past its expected onset. 

XI. SEXUAL ASSAULT 

A. Purpose of evaluation is to diagnose and treat the victim's physical and emotional injuries, and to collect 

legal evidence. State and local protocols should be followed. Specialized, trained nurses commonly conduct 

this examination. 

B. History of the event 

1. Where and when did the assault occur? 

2. What happened during the assault? Document using the patient's own words with quotations. 

3. What happened after the assault? 

a. Did the patient bathe, void, defecate, brush teeth, or change clothes? 

b. Does she complain of pain or have any other symptoms? 

4. Has the patient had sexual intercourse in the last 72 hours? (If so, it may confuse the laboratory analysis of 

sperm and acid phosphatase.) 

C. Physical examination 

1. Perform a general physical examination, noting especially any signs of trauma. 

2. Perform a pelvic examination (unless protocol calls for trained sexual assault nurse), looking for evidence of 

trauma or infection. 

D. Laboratory and evidence collection 

1. Standard laboratory studies and radiographs when indicated for trauma, ~-HCG (to exclude preexisting pregnancy) 

459


2. Evidence 

a. Know what the police want before you examine the patient, or use a standard kit that contains supplies 

for the collection. Photographs are becoming increasingly important. Develop protocol for forensic 

admissibility and protect the victim's privacy. 

b. Maintain an unbroken chain of evidence. Specimens must always be in view or under lock and key. Sign 

the outside of each sealed container when transferring custody. 

E. Management 

1. Standard care for traumatic injuries 

2. Prevent infection 

a. Offer prophylactic antimicrobial therapy for syphilis, gonorrhea, Chlamydia, and Trichomonas. 

b. Offer prophylaxis for hepatitis B with vaccination. 

c. If assailant's HIV status is unknown, evaluate risks and benefits of postexposure prophylaxis on a case-bycase 

basis. 

d. Schedule follow-up visits for repeat serology and cultures. 

3. Prevent pregnancy: offer postcoital contraception as described above; refer for repeat pregnancy test as needed. 

4. Counseling: initial contact should be made while the patient is in the emergency department by an individual 

experienced in rape counseling; if this is not possible, early referral is essential. 

XII. NORMAL PREGNANCY 

ANY WOMAN OF CHILDBEARING AGE WHO PRESENTS TO THE EMERGENCY DEPARTMENT IS CONSIDERED 

PREGNANT UNTIL PROVEN OTHERWISE. 


1. Menstrual period: missed, light, or late 

2. Breast swel Ii ng and tenderness at 4 weeks 

3. Fatigue, nausea, and urinary frequency at 5-6 weeks 

4. Cervical softening (tip at 4 weeks, isthmus at 6-8 weeks) 

5. Chadwick sign (bluish discoloration of cervix at 6-8 weeks) 

6. Uterus enlarged and soft at 6-8 weeks 

B. Pregnancy tests 

1. All available tests detect ~-HCG with varying sensitivities and specificities. Production of ~-HCG begins at the 

time of implantation (8-9 days after conception). Levels of ~-HCG double every 2 days during the initial weeks 

of a normal pregnancy, peak at 8 weeks, and remain detectable up to 60 days after birth or abortion. With the 

newer assays, pregnancy can be detected as early as 23-25 days after the last menstrual period. Pregnancy tests 

that measure the ~-HCG subunit have the greatest specificity. 

2. Causes of false negatives 

a. Too early in pregnancy 

b. Dilute or old urine: if the specific gravity is below the recommended level set by your laboratory, get a 

serum qualitative. 

c. Ectopic pregnancy: although rare, ruptured ectopic pregnancies have been reported with very low or absent 

~-HCG. 

d. Incomplete abortion 

3. Causes of false positives (rare) 

a. Interference from non-~-HCG substances 

b. Exogenous HCG 

c. Trophoblastic neoplasm 

4. Ultrasound is frequently used in the emergency department to confirm that the pregnancy is intrauterine and to 

verify fetal heart rate. 

a. Fetal heart can be determined by using M-mode on ultrasound. 

b. Fetal age can be determined by measuring the gestational sac, the crown-rump length, the head 

circumference, or the femur length. The best measurement depends on the age and position of the fetus. 

c. Intrauterine pregnancy should be confirmed by visualization of an intrauterine yolk sac. 

460


d. Ultrasound should be performed only by trained personnel. 

Courtesy of Sarah Sommerkamp, MD 

M-mode ultrasound showing measurement of fetal heart rate 

Courtesy of Sarah Sommerkamp, MO 

Ultrasound showing crown-rump length measurement for gestational age 

C. Physiologic changes of pregnancy 

1. Cardiovascular changes 

a. Heart rate increases by 15-20 beats per minute above baseline (to an average of 80-90 beats per minute) 

by the third trimester. 

b. Blood pressure 

(1) Systolic and diastolic blood pressure decrease by 10-15 mm Hg in the second trimester (to an average 

of 102/55 mm Hg) and then gradually return to prepregnant levels in the third trimester. 

(2) After the 20th week of gestation, uterine compression of the inferior vena cava in the supine position 

can decrease venous return by as much as 30% and produce hypotension. This can be relieved by 

placing the patient in the left lateral decubitus position, inserting a wedge under the right hip, or 

manually displacing the uterus. 

c. Cardiac output increases by ~30% during the first trimester, increases further (~50%) in the second 

trimester and is maintained at this level for the remainder of the pregnancy. 

2. Respiratory changes 

a. Respiratory rate increases slightly (or not at all). 

b. Tidal volume increases by 40%. 

c. Functional residual volume decreases by 25% (due to elevation of the diaphragm). 

d. pCO 2 

decreases to 30-33 mm Hg. 

461


3. Hematologic changes 

a. Blood volume increases up to 50% at term 

b. Hematocrit decreases to the low 30% range by the 30th week. 

c. WBC count increases (due to an increase in PMNs); counts up to 18,000/mm 3 are normal in the second 

and third trimesters, while counts up to 25,000/mm 3 may be seen during labor. 

d. Fibrinogen level is increased (average level is 400-450 mg!dl). 

e. Prothrombin time (INR)/partial thromboplastin time are normal despite increases in factors VII, VIII, IX, X, and XII. 

XIII. DRUGS AND RADIATION EXPOSURE IN PREGNANCY 

A. Drugs 

1. The teratogenic risk associated with drugs is greatest during embryogenesis (the first trimester) and is usually 

dose-related. 

2. The FDA classifies drugs used in pregnancy into five categories (A, B, C, D, X) according to their safety. 

a. Drugs in category A have been studied in people and are considered safe for use in pregnancy. 

b. Drugs in category B have been studied in animals and are generally considered safe. 

c. Drugs in category C should be used with caution. 

d. Drugs in categories D and X should be avoided (if possible); studies have demonstrated use in pregnancy 

associated with risk to the fetus. 

B. Radiation exposure 

1. The risk of birth defects from a 1-rad exposure (1,000 mrads) is thousands of times smaller than the 

spontaneous risks of congenital malformations or genetic disease. If exposure to the fetus is 10 cm away from the fetus are 

not harmfu I. 

a. Plain radiographs of cervical spine, chest, and pelvis all deliver


(3) Vaginal passage of characteristic grapelike clusters of vesicles 

(4) Uterus large for dates 

(5) Anemia 

b. Diagnostic evaluation: ultrasound findings typically described as a "snow-storm" appearance 

B. Abortion 

Courtesy of Sam Hsu, MO 

Ultrasound showing a molar pregnancy 

c. Management 

(1) Uterine evacuation plus careful follow-up of ~-HCG titers to exclude chorionic carcinoma (2%-3% 

transform to carcinoma) 

(2) Rh immune globulin for Rh-negative women 

1. Threatened abortion is the most common cause of bleeding in a primigravida. 

a. Definition: any amount of bleeding without passage of products of conception or cervical dilatation 

b. Incidence: 30%-40% of clinically pregnant women have first trimester bleeding; 50% of these women 

ultimately miscarry. 

c. Management 

(1) Expectant management: pelvic rest (no douching, tampons, or intercourse until bleeding resolves) 


(3) Follow-up with obstetrician in 2-3 days 

2. Inevitable abortion 

a. Definition: the cervical os is open and vaginal bleeding is present. 

b. Management 

(1) Expectant management: dilation and evacuation, or dilatation and curettage 


(3) Consult obstetrics for brisk bleeding. 

3. Incomplete abortion 

a. Definition: the cervical os is open, vaginal bleeding is present, and products of conception are present at 

the cervical os or in the vaginal canal. 

b. Management 

(1) Visible products of conception should be removed with a ring forceps to control bleeding. 

(2) Expectant management: dilation and evacuation, or dilatation and curettage 

(3) Rh immune globulin for Rh-negative women. 

(4) Consult obstetrics for brisk bleeding. 

4. Complete abortion 

a. Definition: all products of conception have been passed, the cervix is closed, the uterus is firm and 

nontender, and the bleeding has almost stopped. 

463


b. Management 

(1) Up to 80% of first trimester miscarriages complete without intervention 

(2) Expectant management: curettage, or dilatation and curettage 

(3) Rh immune globulin for Rh-negative women. 

5. Missed abortion (more commonly called first or second trimester fetal demise) 

a. Definition: failure to pass products of conception beyond 2 months after fetal death; pregnancy test 

converts from positive to negative. 

b. Management: dilatation and curettage, Rh immune globulin for Rh-negative women 

C. Ectopic pregnancy 

1. Leading cause of maternal death in the first trimester 

2. Risk factors (~50% of ectopic pregnancies have no associated risk factors) 

a. Previous ectopic pregnancy, tubal surgery, or sterilization procedure 

b. Documented tubal scarring/pathology 

c. Diethylstilbestrol exposure in utero 

d. Presence of intrauterine device (prevents only intrauterine but not extrauterine pregnancies) 

e. History of pelvic inflammatory disease 

f. Infertility (in vitro) 

g. Multiple sex partners 


a. Patients classically present with a history of amenorrhea followed by abdominal pain and abnormal 

vaginal bleeding. Classic triad is present in only 15 % of patients and is neither sensitive nor specific. 

b. Ectopic pregnancy with hemorrhage may present with shoulder pain referred from an irritated diaphragm 

(Kehr sign). Only 20% of ectopic pregnancies present in extremis. May present with relative bradycardia. 

c. Pelvic examination findings 

(1) Vaginal bleeding (may be absent) 

(2) Unilateral adnexal tenderness± a palpable mass 

(3) Uterus normal in size or slightly enlarged 

(4) Fullness of cul-de-sac 

Table 29: Symptoms and Signs of an Ectopic Pregnancy 

Symptom/Sign 

Abdominal pain 

Amenorrhea 

Vaginal bleeding 

Dizziness 

Pregnancy symptoms 

Urge to defecate 

Passing tissue 

Adnexal tenderness 

Abdominal tenderness 

Adnexal mass 

Uterine enlargement 

Orthostatic changes 

Fever 

% of Women with Symptoms/Signs 

80-100 

75-95 

50-80 

20-35 

10-25 

5-15 

5-10 

75-95 

80-95 

50 

20-30 

10-15 

5-10 

464



a. Pregnancy tests: a benign course cannot be assumed with low f3-HCG levels; ruptured ectopic 

pregnancies that require surgery have been reported with very low or absent levels of f3-HCG. 

b. Pelvic ultrasound 

(1) Transabdominal ultrasound can be useful if it shows a clear intrauterine pregnancy in a patient who 

is not at risk of a heterotopic (concomitant intrauterine and extrauterine) pregnancy. Discriminatory 

zone is user dependent but around 5,000 for the transabdominal approach. 

(2) Transvaginal ultrasonography is a sensitive technique; it can identify landmarks consistent with a 

normal intrauterine pregnancy at 5 weeks of gestation and may occasionally identify the actual 

ectopic pregnancy. 

(3) Indeterminate ultrasounds (positive f3-HCG but no definite intrauterine pregnancy or extrauterine 

findings of ectopic pregnancy) occur in up to 20% of emergency department patients undergoing 

evaluation for first-trimester emergencies; 1,500: ultrasound, serial f3-HCG measurements to establish ectopic pregnancy or 

miscarriage. 

(2) f3-HCG 3,000 for transvaginal ultrasound. 

d. For patients in whom a ruptured ectopic pregnancy is a concern, check the right upper quadrant view/ 

Morison's pouch for free fluid. 

Courtesy of Sandra Werner, MD, ROMS, FACEP 

Left: Empty uterus with a yolk sac in the left adnexa (ectopic pregnancy) 

Right: Normal intrauterine pregnancy with a fetus surrounded by the uterus 

Courtesy of Sarah Sommerkamp, MD, ROMS 

Free fluid separating liver, kidney, and bowel in a patient with a ruptured ectopic pregnancy 

465


e. Ultrasound consistent with a known or expected ectopic pregnancy requires immediate obstetrics 

consultation. 

(1) Ruptured: emergent 

(2) Unruptured: consider methotrexate therapy versus surgery 

(3) Intrauterine pregnancy 

5. Management 

(a) Follow up with obstetrics. 

(b) Follow quantitative B-HCG for doubling every 2 days. 

(c) Repeat ultrasound. 

(d) Threatened miscarriage precautions 

a. Establish an IV line and provide fluid resuscitation as indicated. 

b. Obtain CBC, Rh typing as well as type and screen/crossmatch early in suspected cases, comprehensive 

metabolic panel, B-HCG, ultrasound. 

c. Administer Rh immune globulin to women who are Rh-negative. 

d. Definitive therapy 

(1) Stable patients with unruptured ectopic pregnancies measuring


2. Appendicitis 

(3) Admit pregnant patients with pyelonephritis to the hospital for IV antibiotics (a cephalosporin with or 

without an aminoglycoside) and hydration. These patients are at increased risk of developing preterm 

labor, bacteremia, and septic shock. Urine cultures should be sent and an obstetric consult obtained. 

a. The most frequent surgical emergency of pregnancy 

b. The incidence of appendicitis is not higher in pregnancy, but the development of complications (especially 

rupture) is more frequent because of delay in diagnosis. 

c. Clinical presentation: fever and right-sided pain. Diagnosis is difficult because the pregnant patient has 

baseline leukocytosis, and the appendix moves up the right side with uterine displacement. Can be 

confused with pyelonephritis. 

d. Management: obtain surgical and obstetric consultation. Ultrasonography, CT, and MRI have been used to 

assist with diagnosis. Additionally, laparoscopy or laparotomy is the definitive treatment. 

3. TORCH infections: toxoplasmosis, other (syphilis), rubella syndrome, cytomegalovirus, herpes simplex 

infection 

a. Toxoplasmosis (fetal: eye, ear, neurologic dysfunction, rash, prematurity) 

(1) Parasitic disease caused by Toxoplasma gondii 

(2) Linked with exposure to cats 

(3) Treatment: spiramycin in pregnancy 

b. Syphilis (fetal: fever, failure to thrive, saddle nose, rash) 

(1) Treatment: penicillin 

(2) If treated inappropriately, ~50% fatal. 

c. Rubel la syndrome (fetal: cataracts, deafness, patent ductus arteriosus) 

(1) Viral illness 

(2) Order a pregnancy test in all women of childbearing age with rubella. 

(3) If pregnancy test is positive, refer patient for genetic counseling. 

Time of Maternal Infection 

First month 

Second month 

Third month 

Fetal Infection 

50% 

25% 

10% 

d. Cytomegalovirus (fetal: neurologic dysfunction, chorioretinitis, hepatosplenomegaly, rash, microcephaly) 

(1) Viral ii lness; minimal maternal symptoms 

(2) No specific treatment; prevention 

e. Herpes simplex infection (fetal: eye, brain, and skin disease) 

(1) Women with primary mucous membrane infections in the third trimester have an increased risk of 

dissemination, which may be life threatening. 

(2) Most (if not all) of the complications associated with lesions during pregnancy can be avoided by taking 

antiviral medications in the third trimester. Famciclovir and valacyclovir are pregnancy category B. 

(3) Neonatal infection can be contracted via passage through an infected birth canal and is associated 

with significant mortality (50%) and morbidity (particularly neurologic sequelae). 

(4) Active infection at the time of delivery carries a 30%-40% risk of infecting the infant. 

(5) The presence of active lesions in a patient who is in labor is an indication for cesarean section. 

(6) Treatment with IV acyclovir for serious infections. 

F. Hyperemesis gravidarum/nausea and vomiting of pregnancy 

1. 50%-70% of women are affected, usually in the first trimester (probably due to increased ~-HCG levels). Some 

studies suggest a vitamin 8 6 

deficiency as the cause and recommend supplemental vitamin B 6 .) Persistence of 

symptoms past 14 weeks or presence of abdominal pain suggests the possibility of another cause. 

2. Management: frequent small meals (dry crackers before rising, toast and cereal when symptomatic) and 

supplemental vitamin B 6 

may be helpful with or without doxylamine. 

3. Hyperemesis gravidarum: persistent nausea and vomiting not caused by other medical conditions, ketonuria 

(as a marker of starvation), and at least 5% weight loss from pre-pregnancy weight. IV hydration (D5 lactated 

467


Ringer's or D5 normal saline) and antiemetics (vitamin B 6 

plus doxylamine, promethazine, metoclopramide, 

or ondansetron) are indicated. 

a. Hospitalization is indicated if emesis cannot be controlled with above measures. 

G. Gestational diabetes 

1. Diabetes in a pregnant woman who was not previously diabetic 

2. Places woman and fetus at risk of complications: both macrosomy and intrauterine growth restriction, difficult 

delivery, fetal hypoglycemia postpartum 

3. Initial steps in management are diet and exercise. 

4. Oral medications (metformin) or insulin may be required to maintain normoglycemia. 

H. Chronic and gestational hypertension 

1. Chronic hypertension is systolic blood pressure ?:140 or a disastolic blood pressure 90 mmHg identified before 

the 20th week of gestation and that persists for >6 weeks postpartum. 

2. Gestational hypertension is a blood pressure ?:140/90 mm Hg on two occasions in a patient who was 

normotensive before 20 weeks of gestation. There are no symptoms of preeclampsia or proteinuria. 

3. Management depends on severity of disease. 

a. Anti hypertensive medications are not routinely started for blood pressure


3. Management 

a. History, physical, and laboratory studies to confirm presence of preeclampsia and to exclude other 

pathology 

b. Consultation with obstetrics for further management (timing of delivery and steroids) and monitoring 

c. Antihypertensive therapy is not required unless systolic blood pressure> 160 mm Hg or diastolic blood 

pressure> 110 mm Hg. 

(1) Hydralazine is used most commonly, but other drugs also work well (eg, labetalol, nicardipine, sodium 

nitroprusside). 

(2) ACE inhibitors are contraindicated because of the possibility of fetal renal damage. 

(3) Prophylactic treatment with magnesium is also recommended to prevent seizures in the preeclamptic 

patient (loading dose of 4-6 g over 30 minutes followed by a 2 g/hour drip to maintain a serum level 

of 4-7 mEq/L). 

K. Eclampsia 

1. Diagnosis: preclampsia plus seizure 

a. Warning signs of impending seizure 

(1) Headache 

(2) Visual disturbances 

(3) Hyperreflexia 

(4) Abdominal pain (epigastric or right upper quadrant) 

2. Management 

a. Magnesium sulfate 

(1) Has both anticonvulsant and antihypertensive properties. 

(2) loading dose is 4-6 g IV over 5-15 minutes; then continuous IV infusion at 1-3 g/hour; patient 

should be placed on a cardiac monitor and have a Foley catheter in place. 

(3) Excretion is 100% renal, so urine output should be maintained at a rate of ~25 ml/hour. 

(4) Stop maintenance infusion if deep tendon reflexes disappear. 

(5) Watch for signs of magnesium toxicity: 

(a) Respiratory depression 

(b) Bradydysrhythmias 

(c) loss of deep tendon reflexes 

(6) Antidote: calcium gluconate (1 g slow IV push) 

b. If seizure continues, use typical anticonvulsant drugs (eg, benzodiazepines). Dilantin may be used in 

pregnancy. 

c. Additional medications may be needed for adequate control of blood pressure. IV labetalol or 

hydralazine are typically used. 

d. Delivery 

(1) Definitive treatment is delivery. Obtain obstetric consult. 

(2) Depending on patient specifics, this may be a vaginal or cesarean section delivery. 

e. Postpartum eclampsia can occur up to around 4 weeks postpartum. Consider in the differential for 

seizure patients. 

L. Hemorrhage, antepartum 

1. Abruptio placenta: 30% of cases of third-trimester bleeding 

a. Definition 

(1) Premature separation of a normally implanted placenta from the uterine wall causing visible or 

hidden bleeding 

(2) Significant unseen blood loss can occur before or without vaginal bleeding. 


(1) Painful uterine bleeding 

(a) Bleeding is typically light (but may be heavy) and is usually dark or clotted. 

(b) At times, only pain is present, and this can vary from mild to severe. 

(2) Uterine findings vary from soft and nontender to slightly tender to rock hard. 

c. Risk factors include hypertension, smoking, cocaine, abdominal trauma, multiparity, advanced maternal 

age, and prior abruption. 

469


d. Management 

(1) Establish IV access; draw blood for type and crossmatch, preoperative laboratory studies, and 

disseminated intravascular coagulation profile; establish cardiac and fetal monitoring. 

(2) Fluid resuscitation and blood replacement as needed 

(3) Obtain immediate obstetrics consult, and perform ultrasound to exclude placenta previa (ultrasound 

is not sensitive enough to exclude abruptio placenta). 

(4) Stable patients may be observed in the hospital under close surveillance if a surgical team is 

available. 

(5) If the patient is unstable - immediate delivery by cesarean section (unless patient is in advanced 

labor); place patient in left lateral decubitus position to relieve inferior vena caval compression (can 

increase cardiac output by 30%-40%). 

(6) Administer Rh immune globulin to Rh-negative women. 

2. Placenta previa: responsible for 20% of cases of third trimester bleeding 

a. Definition: implantation of the placenta in the lower uterine segment such that it covers all or part of the 

cervical os 


(1) Painless, bright red vaginal bleeding that is sometimes intermittent and progressively severe over a 

period of 1-2 weeks 

(2) On abdominal examination, the uterus is usually soft and nontender. 

c. Risk factors include prior cesarean section, prior previa, multiparity, multiple gestations, and advanced 

maternal age. 

d. Management 

(1) Establish IV access, draw blood for type and crossmatch and preoperative laboratory studies, and 

establish cardiac and fetal monitoring. 

(2) Obtain immediate obstetrics consult if patient is unstable and order ultrasound for placental location. 

(3) Pelvic examination (digital and speculum) 

(a) Should not be done unless ultrasound excludes placenta previa '-- 

(b) Should be done in the operating room by the obstetrician under "double set-up" conditions in 

patients who are bleeding rapidly, in labor, or are hemodynamically unstable. In this manner, an 

immediate cesarean section can be rapidly performed if uncontrolled bleeding results. 

(4) Administer Rh immune globulin to Rh-negative women. 

M. Thromboembolism 

1. Pregnancy is a hypercoagulable state. 

a. The synthesis of coagulation factors VII, VIII, IX, X, and XII is increased. 

b. Compression of the inferior vena cava by the enlarging uterus promotes venous stasis. 

2. The risk of thromboembolism is 5-6 times greater in pregnant women than in non pregnant women and is 

highest in the immediate postpartum period as well as those delivered by cesarean section. 

3. Initial diagnostic studies of choice 

a. o-dimer is often increased in pregnancy; however, a low o-dimer can reliably exclude clot in a low pretest 

probabi I ity patient. 

b. Doppler ultrasonography: a positive finding can potentially circumvent the need for CT angiography or a 

VQ scan. Does not reliably detect pelvic or calf deep venous thrombosis. 

c. Ventilation/perfusion scan or multidetector CT angiography can both be used to diagnose pulmonary 

embolism. CT angiography has more radiation directed at the woman (breast cancer concern) than the VQ. 

The VQ scan has a higher fetal dose of radiation. 

4. Treatment is with low-molecular-weight heparin or heparin, which does not cross the placenta. 

5. Warfarin is contraindicated in pregnancy. 

N. Aortic dissection 

1. Second most common cause of maternal death 

2. Imaging is required for diagnosis. 

a. Choice (CT, MRI, transesophageal echocardiography) depends on stability of the patient and resources 

available at the hospital. 

b. A transthoracic or transabdominal ultrasound cannot reliably exclude dissection but can potentially 

diagnose it. 

470


3. Treatment in pregnant women is similar to that in nonpregnant patients to reduce blood pressure and pulse: 

~-blockers as well as hydralazine and nitrates are commonly used. 

0. Maternal cardiac disease 

1. Frequency has increased because improvements in the care of congenital cardiac disorders has led to adults 

with significant cardiac history in the USA. 

2. Childhood and adult obesity, hypertension, hypercholesterolemia, and diabetes are increasing the rates of 

coronary artery disease. 

3. Chest pain and dyspnea are common symptoms in pregnancy. Cardiac disease can present as dyspnea on 

exertion, fatigue, and edema. 

a. Cardiomyopathy: possible etiologies are pregnancy, viral, alcohol, cocaine, and ischemia. 

b. Congestive heart failure: laboratory tests, chest radiograph, and B-type natriuretic peptide (BNP) may help 

discern acute heart failure. 

(1) Avoid ACE inhibitors in pregnancy. 

c. Acute myocardial infarction: ECG 

(1) Acute myocardial infarction is more commonly seen in pregnancy 

(2) Percutaneous coronary intervention is first-line intervention in pregnancy. 

(3) Aspirin, nitroglycerin, and heparin are safe. Clopidogrel is also considered safe, but keep in mind 

delivery plan when starting an anticoagulant. 

d. Dysrhythmias 

P. Cardiac arrest 

(1) Common and frequently benign; must exclude life-threatening arrhythmias. 

(2) ECG usually sufficient, may require further monitoring. 

(3) Supraventricular tachycardia: adenosine can be safely used. 

(4) Atrial fibrillation can be managed with rhythm control, rate control, or cardioversion. 

(5) Use low-molecular-weight heparin if onset is unclear and patient is stable before cardioversion. 

1. CPR: high-quality compressions 

a. Continue with chest compressions/airway/breathing with the understanding that the pregnant woman 

has lower reserve and increased airway edema and is at increased risk of aspiration due to the physiologic 

changes in pregnancy. 

2. Manual displacement of the uterus 

3. IV access above the diaphragm 

4. Defibrillation and drugs should not be withheld or delayed because of the gravid state. 

5. Consider the underlying cause of the cardiac arrest. 

a. Review H's and T's 

b. Ultrasound 

6. Prepare for perimortem cesarean section 

Q. Perimortem cesarean section 

1. Anxiety-provoking procedure: should be started within 4 minutes of cardiac arrest for all women with 

estimated gestational age of 20 weeks and beyond; may start earlier if no hope of maternal survival. 

2. Can be lifesaving for both mother and fetus 

3. Fetal and maternal survival have been documented up to 30 minutes after arrest, but improved neurologic 

outcome are linked with early intervention. 

4. Hospitals should prepare in advance a team/protocol for a perimortem cesarean section. 

XV. HIGH-RISK PREGNANCY 

A. Assisted reproductive therapies 

1. Increasing incidence 


a. Multiple gestations: larger than anticipated fundal height 

b. Heterotopic pregnancy: existence of an intrauterine and an ectopic pregnancy at the same time 

471


XVI. NORMAL LABOR AND DELIVERY 

A. Stages of labor 

1. Stage one 

a. From the onset of true labor (regular contractions with cervical change) to full dilation 

b. Consists of early, active, and transition 

2. Stage two 

a. From dilation of 10 cm until delivery of infant 

b. Support perineum, deliver head, check for nuchal cord, slight downward traction followed by upward 

traction to assist shoulder delivery support infant. May then place infant on mother's abdomen for 

clamping and cutting of cord. Routine suction of nose and mouth is no longer recommended. Deep suction 

for meconium only. 

3. Stage three 

a. From delivery of infant to delivery of placenta 

b. Avoid excessive tension on cord, because it may precipitate uterine inversion. 

XVII. COMPLICATIONS OF LABOR 

A. Fetal distress 

1. Ill defined and multifactorial 

2. Can be indicated by increased or decreased fetal heart rate, decreased fetal movement, repeated variable or 

late decelerations on fetal monitor 

3. Use and interpretation of electronic fetal monitors and tocodynamomoter should be done by appropriately 

trained staff. 

B. Premature labor 

1. Definition 

a. Onset of labor after 20 but before 37 weeks gestational age 

b. Contractions >30 seconds, regular contractions, 4 times every 20 minutes with changes in the cervix 

c. Braxton Hicks contractions: mild intensity and no cervical change 

d. Look for infection as cause (urinary tract infection, bacterial vaginosis, sexually transmitted infection, 

systemic infection 

e. Fetal fibronectin can be helpful to obstetrics to determine likelihood of delivery. 

2. Management 

a. Less than 34 weeks gestational age: corticosteroids for lung maturity 

b. Tocolytics: use with obstetrics consultation 

(1) Nifedipine 

(2) lndomethacin 

(3) Terbutaline 

(4) Magnesium 

C. Premature rupture of membranes 

1. Definition: rupture of fetal membranes before onset of labor 

2. Clinical presentation: history of watery vaginal discharge 

3. Diagnostic evaluation: after ultrasound to confirm placental placement if bleeding 

a. Perform a careful sterile speculum examination without using a lubricant (which can give a false-positive), 

and obtain sterile swabs of the posterior vaginal vault for: 

(1) A nitrazine test: amniotic fluid is alkaline (blood and semen give false-positives) and turns the yellow 

paper to blue-green. 

(2) Microscopic examination of a dried slide: amniotic fluid should show "ferning" (blood and 

inflammation give false-negatives). 

472


b. Obtain cervical cultures for N gonorrhoeae, Chlamydia, group B streptococci, aerobes, and anaerobes for 

patients with preterm (occurring before 3 7 weeks gestation) rupture of membranes. A digital examination 

should not be done in suspected or confirmed cases. 

4. Management is hospitalization. 

a. If gestational age is >37 weeks - delivery within 12-24 hours 

b. If gestational age


Courtesy of Wesley Fox 

C. Prolapse of cord 

1. Umbilical cord prolapse: typically occurs after rupture of membranes. 

a. Overt: cord lies below the presenting part and can be visualized or palpated. 

b. Occult: cord lies adjacent to the presenting part and can be detected by fetal monitoring (fetal heart rate 

changes with intermittent cord compression). 

2. Management 

a. Administer oxygen. 

b. Reposition the mother. 

c. Overt cord prolapse - knee to chest position (apply continuous upward pressure on the presenting part to 

relieve pressure on the cord until the fetus is delivered by cesarean section) 

d. Occult cord prolapse - lateral (or Trendelenburg) position 

(1) If fetal heart rate returns to normal with cord compression - vaginal delivery 

(2) Persistence of fetal heart rate change with cord compression - cesarean section 

XIX. POSTPARTUM COMPLICATIONS 

A. Postpartum fever 

1. Etiology: look for all usual causes of fever 

a. Wound infection (cesarean or episiotomy) 

b. Urinary tract infection (especially if history of catheterization or forceps delivery) 

c. Pneumonia 

d. Phlebitis 

2. Endometritis 

a. Clinical presentation: swollen, tender uterus with foul lochia 1-3 days after birth 

b. Management: hospitalization for broad-spectrum antibiotics IV 

3. Pelvic thrombophlebitis 

a. May mimic endometritis; suspect this diagnosis if patient does not respond quickly to antibiotics. 

b. Can cause pulmonary embolus 

4. Mastitis 

a. Etiology 

(1) Usually caused by Staphylococcus aureus 

(2) Usually occurs as a complication of breast-feeding (but can occur antepartum and in postpartum 

women who are not breastfeeding) 

(3) Usual mode of transmission is inoculation of breast milk from the infant's nasopharyngeal secretions; 

cracked nipples can also be a route of entry for organisms. 

b. Clinical presentation: painful swollen breast consistent with cellulitis, high fever, may result in abscess 

formation. Key is differentiating from blocked duct and abscess. 

474


c. Management 

(1) Simple mastitis 

(a) Warm compresses and analgesics for symptomatic relief 

(b) Breastfeeding should be continued to assure continued drainage; the infant will not be harmed 

because he or she is already colonized. 

(c) Oral antibiotics (penicillinase-resistant, eg, dicloxacillin or a cephalosporin) 

(2) Mastitis with abscess formation 

(a) 

B. Postpartum hemorrhage 

Refer to a surgeon for incision and drainage (in the operating room). 

(b) Continued drainage with a breast pump is indicated, because higher concentrations of bacteria 

may be harmful to the infant; some authors recommend discontinuation of breastfeeding until the 

infection has cleared. 

1. >500 ml blood loss in the first 24 hours 

2. Look for the 4 T's 

a. Tone: uterine atony 

b. Trauma: cervical laceration 

c. Tissue: retained placenta 

d. Thrombin: disseminated intravascular coagulation 

3. Management 

a. Resuscitation with crystalloid and blood as needed. Vital sign abnormalities occur late because of 

autotransfusion from placenta. 

b. Uterine massage 

c. Oxytocin 

d. Misoprostol 

C. Uterine inversion 

1. Traction on the umbilical cord during delivery can result in partial or complete uterine inversion. 


a. Partial inversion -a- crater-like depression over the suprapubic area and descended uterine fundus and 

cervix on vaginal examination 

b. Complete inversion -a- uterus is outside the body and associated with immediate life-threatening hemorrhage 

3. Management 

a. Immediate anesthesiology and obstetrics consult 

b. Begin resuscitation: two large-bore IV lines (crystalloid) and blood crossmatch 

c. Tocolytic drugs (terbutaline, ritodrine, MgS0 4 

) to relax the uterus so that manual reimplantation can be 

achieved 

d. Try to reimplant the uterus without removing the placenta (t risk of hemorrhage); must place back through 

cervix. 

e. Transport patient to OR for reimplantation and possible exploratory laparotomy. 

f. Broad-spectrum antibiotics 

D. Pituitary infarction (Sheehan's syndrome) 

1. Necrosis occurs because of decreased perfusion of the pituitary during delivery. 

2. Symptoms caused by failure of function of the hormones. 

a. Prolactin: agalactorrhea, amenorrhea 

b. Hypothyroid symptoms: cold, constipated, hair loss, bradycardia 

c. Adrenal insufficiency: hypoglycemia, hyponatremia 

3. Management: replace deficient hormones 

a. Patient may require acute steroid, electrolyte management, glucose, thyroid hormone 

b. Endocrine consultation 

475

GYNECOLOGIC AND OBSTETRIC DISORDERS: PRACTICE CLINICAL SCENARIOS 

GYNECOLOGIC AND OBSTETRIC DISORDERS: 



Scenario A 

Presentation: A 25-year-old woman presents with a painless rash that has been in the vaginal area for over 

a week. On examination, you see heaped-up edges surrounding a painless ulcer. 


Scenario B 

Presentation: A 23-year-old woman presents with copious amounts of gray vaginal discharge and a fishy 

odor. On physical examination, you see red spots on her cervix but no cervical motion tenderness. 


Scenario C 

Presentation: A sexually active young woman complains of bilateral lower abdominal pain for several days 

(often following menses) associated with an abnormal vaginal discharge. She has fever> 100.4°F (38°C), 

chills, and general malaise. 

Physical examination: On physical examination, there is lower abdominal tenderness, cervical motion 

tenderness, and bilateral adnexal tenderness. 


Scenario D 

Presentation: A 20-year-old woman presents with abrupt onset pain lateralized in the pelvis. The pain is 

10/1 0 and started after intercourse. She has had no other symptoms, discharge, or fever. 


Scenario E 

Presentation: A 28-year-old pregnant woman at 32 weeks gestational age presents complaining of 

right-sided chest pain and shortness of breath. She is tachycardic and tachypneic and has a low oxygen 

saturation. Her legs are swollen, and she has just taken a long car trip. 


Scenario F 

Presentation: EMS arrives with a visibly gravid woman who is actively seizing. 


476


ScenarioG 

Presentation: A woman at 35 weeks gestational age comes in feeling general malaise, mild headaches, 

nausea, and right upper quadrant pain. She is swollen. Laboratory studies show anemia and 

thrombocytopenia and an increased LOH, liver function tests, and uric acid. 


Scenario H 

Presentation: A 19-year-old Gl woman presents at 8 weeks with nausea and vomiting for a week. She 

states that she has not been able to keep anything down despite following all of her mother-in-law's 

recommendations. She tried the vitamin B 6 

but "it just came right back up." Her urinalysis shows large 

ketones. You give IV fluids containing glucose and antiemetics, but she continues to vomit and the ketones 

do not clear. 


Scenario I 

Presentation: A 35-year-old woman at 30 weeks gestational age presents for an upper respiratory infection. 

She is noted at triage to have a blood pressure of 145/86 mm Hg. She noted that her obstetrician said her 

blood pressure was a little high for the first time ever at her last OB visit. She has no headache, shortness of 

breath, chest pain, right upper quadrant pain, blurry vision, or change in mental status. She has not been 

taking over-the-counter medications other than acetaminophen. Laboratory tests were not believed to be 

indicated in this patient. 


ScenarioJ 

Presentation: A 21-year-old woman presents with right lower quadrant pain, fever, and vaginal discharge. 

She is febrile and slightly tachycardic with normal blood pressure, respirations, and oxygenation. Pelvic 

examination reveals right adnexal tenderness and mass. HCC is negative. 


Scenario K 

Presentation: A 74-year-old woman presents with intermittent pelvic pressure, stress incontinence, and 

multiple urinary tract infections over the past several months. Now she complains of a vaginal mass. 


477



Scenario A 

Diagnosis: syphi [is 

Scenario B 

Diagnosis: trichomoniasis 

Scenario C 

Diagnosis: pelvic inflammatory disease 

Key facts: 

This classic clinical scenario is seen in only one-third of cases. 

Constitutional symptoms (fever> 100.4 °F [38°C], chills, and general malaise) are frequently present. 

GI complaints, such as nausea and vomiting, may also be present but are less common. 

Scenario D 

Diagnosis: ovarian torsion 

Scenario E 

Diagnosis: pulmonary embolism 

Scenario F 

Diagnosis: eclampsia (preeclampsia and grand ma/ seizures or coma) 

Scenario G 

Diagnosis: HELLP 

Scenario H 

Diagnosis: hypermemesis gravidarum 

Scenario I 

Diagnosis: gestational hypertension 

ScenarioJ 

Diagnosis: tuba-ovarian abscess 

Scenario K 

Diagnosis: pelvic organ prolapse 

478

;,:~t,,:·, .. 

. 

Volume II 



Endocrine, Metabolic, and Nutritional 

Disorders 










Procedures and Skills Integral to the 

Practice of Emergency Medicine 

Other Components of the Practice of 

Emergency Medicine 

Ohio 1· 

·~/- · ACEP 

·"?:,:: '."\. American College of Emergency Physicians 

.. :/,,-· .•. , .. c..'

Dr. Carol Rivers' 

PREPARING FOR THE WRITTEN BOARD EXAM 

~, IN EMERGENCY MEDICINE 


Volume 2 

./--"' 

Ohio 

ACEP 

American College of Emergency Physicians 

Advocacy I Education I Leadership

Published by: 

Ohio Chapter, American College of Emergency Physicians (Ohio ACEP) 

3510 Snouffer Road 

Suite 100 

Columbus, Ohio 43235 

(614) 792-6506 

(888) OHACEP4 (642-2374) 

ohacep@ohacep.org 

www.ohacep.org 

Printed in the United States of America 


ISBN 978-0-9977410-0-l 

Date of original release: January 1992 

Most recent update: January 2017 

Copyright ©2017 Ohio Chapter, American College of Emergency Physicians. All 

rights reserved. No part of this publication may be reproduced or transmitted in 

any form, electronic or mechanical, including photocopying, recording, storage 

in any information retrieval system, or otherwise, without the prior written 

permission of the publisher. 

DISCLAIMER 

Ohio Chapter, American College of Emergency Physicians publishes information 

believed to be in agreement with the accepted standards of practice at the date 

of publication. Due to the continual state of change in diagnostic procedures, 

treatment, and drug therapy, Ohio ACEP and the writers and editors are not 

responsible for any errors or omissions. In the practice of medicine, the reader 

should confirm the use of any information with other sources.

The object of education is not learning, but discipline 

and enlightenment of the mind. 

Woodrow Wilson

Dr. Carol Rivers' Preparing for the Written Board Exam in 

Emergency Medicine, Eighth Edition 

EDITORS 

SENIOR ASSOCIATE EDITOR 

Ann M. Dietrich, MD, FAAP, FACEP 

Associate Professor of Primary Care (Lead), Ohio University Heritage College of Osteopathic Medicine; Pediatric 

Associate Medical Director, MedFlight of Ohio, Columbus, Ohio 

SECTION EDITORS 

Thomas Green, DO, MMM, MPH, CPE, FACOEP, FACEP 

Associate Dean, Clinical Affairs; Chief Academic Officer (interim)-HEARTLand Network OPTI and Associate Professor 

Family Medicine, Des Moines University College of Osteopathic Medicine; Associate Professor Emergency Medicine/ 

Family Medicine, Midwestern University-Chicago College of Osteopathic Medicine; Attending Physician, Emergency 

Department, Central Iowa Healthcare, Marshalltown, Iowa 

Joseph P. Martinez, MD, FACEP, FAAEM 

Associate Professor of Emergency Medicine and Medicine, Assistant Dean for Student Affairs, and Assistant Dean for 

Clinical Medical Education and Residency Programs Liaison, University of Maryland School of Medicine, Baltimore, 

Maryland 

Amal Mattu, MD, FACEP 

Professor and Vice Chair of Education, Co-Director, Emergency Cardiology Fellowship, University of Maryland School 


Victor J. Scali, DO, FACOEP-D 

Director of EM, Residency Education, and Associate Professor, Department of Emergency Medicine, Rowan University 

School of Osteopathic Medicine, Stratford, New Jersey 

Howard A. Werman, MD, FACEP 

Professor of Clinical Emergency Medicine, The Ohio State University Wexner Medical Center; Medical Director, 

MedFlight, Columbus, Ohio 

Sandra L. Werner, MD, RDMS, FACEP 

Operations Director, Emergency Medicine, Associate Director, Emergency Medicine Residency Program, MetroHealth 

Medical Center; Associate Professor, School of Medicine, Case Western Reserve University School of Medicine, 

Cleveland, Ohio 

CONTRIBUTORS 

Michael Abraham, MD, MS 




Rudd J. Bare, MD, MMEL 

Chief of Emergency Medicine; Faculty, Emergency Medicine Residency Program, Western Reserve Hospital, Cuyahoga 

Falls, Ohio; Summa Health System EM Residency, Akron City Hospital, Akron, Ohio; Masters in Medical Education and 

Administration, University of New England Medical School, Portland, Maine; Assistant Professor of Emergency Medicine, 

NEOMED, Rootstown, Ohio; Professor of Emergency Medicine, Ohio University, Athens, Ohio 


IV

Michelle Blanda, MD, FACEP 

Professor and Chair Emeritus of Emergency Medicine, Northeast Ohio Medical University, Akron City Hospital, 

Summa Health System, Akron, Ohio 


Michael C. Bond, MD, FACEP, FAAEM 

Associate Professor, Residency Program Director, Department of Emergency Medicine, University of Maryland School 


Orthopedic Emergencies 

Laura J. Bontempo, MD, MEd, FAAEM 

Assistant Professor, Emergency Medicine, University of Maryland School of Medicine, Baltimore, Maryland 


Brian Browne, MD, FACEP 

Professor of Emergency Medicine, Chair, Department of Emergency Medicine, University of Maryland School of 

Medicine, Baltimore, Maryland 


Luca R. Delatore, MD 

Medical Director of the James Emergency Department, Assistant Professor, Department of Emergency Medicine, 



Paul de Saint Victor, MD, FACEP, MHA, CPE 

Associate Director, Emergency Medicine Residency, Mercy St. Vincent Medical Center, Toledo, Ohio; President, 

Emergency Department Consultants 

Additional Tips for Good Performance, How to Take a Multiple-Choice Exam 

Sarah B. Dubbs, MD 

Clinical Assistant Professor, Assistant Residency Program Director, Department of Emergency Medicine, University 

of Maryland School of Medicine, Baltimore, Maryland 


Scott Felten, MD, FACEP 

US Acute Care Solutions Residency Director, Tulsa, Oklahoma 


William R. Fraser, DO, FACOEP-D 

Emergency Medicine Residency Director, Doctor's Hospital Ohio Health, Columbus, Ohio 


Hannah L. Hays, MD 

Assistant Professor, Department of Emergency Medicine and Pediatrics, The Ohio State University Wexner Medical 

Center and Nationwide Children's Hospital and Central Ohio Poison Center, Columbus, Ohio 


Colin G. Jaide, MD, FACEP, FAAEM 

Associate Pr fessor of Emergency Medicine, Attending Physician of Emergency Medicine and Hyperbaric Medicine, 

The Ohio St te University Wexner Medical Center, Columbus, Ohio 

Hematologi Disorders 

V

Jonathan Keary, MD, FACEP 

Staff Physician, Emergency Services Institute, Cleveland Clinic, Cleveland, Ohio 

Endocrine, Metabolic, and Nutritional Disorders 

Benjamin J. Lawner, DO, MS, EMT-P, FAAEM 

Assistant Professor, Department of Emergency Medicine, University of Maryland School of Medicine, Deputy EMS 

Medical Director, Baltimore City Fire Department, Baltimore, Maryland 


Le N. Lu, MD, MS 

Clinical Assistant Professor, Director, Pediatric Emergency Medicine Education, Department of Emergency Medicine, 

University of Maryland School of Medicine; Director, Pediatric Emergency Department, Upper Chesapeake Medical 

Center, Baltimore, Maryland 


Patrick J. Maloney, MD 

Director, Pediatric Emergency Services, Mission Hospital and Mission Children's Hospital, Asheville, North Carolina 


Laura Matrka, MD 

Assistant Professor, Otolaryngology-Head & Neck Surgery, The Ohio State University Wexner Medical Center, 



Stacy McCallion, MD 

Summa Health System, Akron City Hospital, Akron, Ohio; Associate Professor of Emergency Medicine, NEOMED, 

Rootstown, Ohio; Professor of Emergency Medicine, Ohio University, Athens, Ohio 


Michael J. McCrea, MD, FACEP, FAAEM 

Assistant Residency Director, Simulation Education Director, Emergency Medicine Residency, Mercy St. Vincent 

Medical Center, Toledo, Ohio 


Jillian L. McGrath, MD, FACEP 

Assistant Professor of Emergency Medicine, Department of Emergency Medicine, The Ohio State University Wexner 

Medical Center, Columbus, Ohio 


Colleen M. McQuown, MD, FACEP 

Director of Research Education, Department of Emergency Medicine, Summa Akron City Hospital; Associate Professor, 

Northeast Ohio Medical University, Rootstown, Ohio 

Other Components of the Practice of Emergency Medicine 

Siamak Moayedi, MD 



Sreeja M. Natesan, MD 

Assistant Professor, Duke University Medical Center, Durham, North Carolina 

Thoracic and Respiratory Disorders 

VI

Sarah K. Sommerkamp, MD, ROMS 



Matthew Tabbut, MD, FACEP 

Attending Physician, Department of Emergency Medicine, MetroHealth Medical Center; Assistant Professor, Case 

Western University School of Medicine, Cleveland, Ohio 

Procedures and Skills Integral to the Practice of Emergency Medicine 

Laura R. Thompson, MD, MS, FACEP 

Assistant Professor, Department of Emergency Medicine, The Ohio State University Wexner Medical Center, 



Mercedes Torres, MD 




Melissa Tscheiner, MD, FACEP 

Adjunct Assistant Professor, University of North Carolina School of Medicine-Asheville; Department of Emergency 

Medicine, Mission Hospital, Asheville, North Carolina 


Travis Ulmer, MD, FACEP 

Vice President, US Acute Care Solutions, Canton, Ohio; Clinical Assistant Professor of Emergency Medicine, 

Ohio University Heritage College of Osteopathic Medicine, Athens, Ohio 


PRODUCTION 

Laura L. Tiberi, MA, CAE 

Ohio ACEP Executive Director 

Holly J.F. Dorr, MBA, CAE 

Ohio ACEP Deputy Executive Director, Editorial and Production Coordinator 

Susan E. Aiello, ELS 

Medical Editor 

Sheryl Lazenby 

Designer 

vii

,~'

INTRODUCTION 

VOLUME I 

Foreword ........................................................................................................................................................................ x 

Introduction .................................................................................................................................................................. xi 

Recommended Study Plan ........................................................................................................................................... xiii 

Cardiovascular Disorders .............................................................................................................................................. 1 

Head, Ear, Eye, Nose, and Throat Disorders ................................................................................................................ 97 

Abdominal and Gastrointestinal Disorders ............................................................................................................... 169 

Thoracic and Respiratory Disorders .......................................................................................................................... 231 

Traumatic Disorders .................................................................................................................................................. 297 

Orthopedic Emergencies ........................................................................................................................................... 343 

Musculoskeletal Disorders (Nontraumatic) ............................................................................................................... 393 

Nervous System Disorders ........................................................................................................................................ 409 

Gynecologic and Obstetric Disorders ....................................................................................................................... 443 

VOLUME II 

Pediatric Emergencies ............................................................................................................................................... 489 

Toxicologic Disorders ................................................................................................................................................ 543 

Endocrine, Metabolic, and Nutritional Disorders ...................................................................................................... 591 

Environmental Disorders ........................................................................................................................................... 633 

Psychobehavioral Disorders ...................................................................................................................................... 673 

Hematologic Disorders ............................................................................................................................................. 711 

Oncologic Disorders ................................................................................................................................................. 743 

Systemic Infectious Disorders ................................................................................................................................... 759 

Immune System Disorders ........................................................................................................................................ 783 

Renal and Urologic Disorders ................................................................................................................................... 803 

Cutaneous Disorders ................................................................................................................................................. 829 

Emergency Medical Services ..................................................................................................................................... 869 

Procedures and Skills Integral to the Practice of Emergency Medicine ..................................................................... 883 

Other Components of the Practice of Emergency Medicine ...................................................................................... 941 

Mechanics of the Written Board Exam ....................................................................................................................... 975 

Additional Tips for Good Performance ....................................................................................................................... 979 

ix

PEDIATRIC EMERGENCIES 

Life-Threatening Cardiac Dysrhythmias .................................................................................................................... 495 

Cardiopulmonary Resuscitation ................................................................................................................................ 495 

Airway ................................................................................................................................................................ 495 

Breathing ............................................................................................................................................................ 497 

Circulation ......................................................................................................................................................... 498 

Chest Compressions ........................................................................................................................................... 498 

Defibrillation and Cardioversion ........................................................................................................................ 499 

Vascular Access .................................................................................................................................................. 499 

Life-Threatening Cardiac Arrhythmias ................................................................................................................. 500 

Unique Issues in Neonates and Infants ..................................................................................................................... 501 

Risk Factors Associated with Neonatal Cardiopulmonary Arrest.. ........................................................................ 501 

APGAR Scoring .................................................................................................................................................. 503 

Meconi um Staining ............................................................................................................................................ 503 

Neonatal Seizures .............................................................................................................................................. 503 

Congenital Diaphragmatic Hernia ...................................................................................................................... 504 

Tracheoesophageal Fistula .................................................................................................................................. 504 

Omphalocele and Gastroschisis ......................................................................................................................... 504 

Necrotizing Enterocolitis .................................................................................................................................... 505 

Cyanosis ............................................................................................................................................................. 505 

Congestive Heart Failure .................................................................................................................................... 506 

Jaundice in the Newborn .................................................................................................................................... 506 

Apparent Life-Threatening Event ......................................................................................................................... 507 

Sudden Infant Death Syndrome .......................................................................................................................... 508 

Congenital Heart Disease .......................................................................................................................................... 508 

Cyanotic Heart Lesions ....................................................................................................................................... 508 

Acyanotic Heart Lesions ..................................................................................................................................... 509 

Ductal Dependent Lesions ................................................................................................................................. 510 

Congestive Heart Failure .................................................................................................................................... 510 

Airway Emergencies .................................................................................................................................................. 511 

Upper Airway ..................................................................................................................................................... 511 

Lower Airway ..................................................................................................................................................... 513 

Pediatric Infectious Diseases ..................................................................................................................................... 518 

The Febrile Child ................................................................................................................................................ 518 

Bacteremia and Sepsis ........................................................................................................................................ 519 

Meningitis .......................................................................................................................................................... 520 

Pneumonia ......................................................................................................................................................... 521 

Pertussis (Whooping Cough) ............................................................................................................................... 524 

Otitis Media ....................................................................................................................................................... 524 

Urinary Tract Infection ........................................................................................................................................ 526 

Kawasaki Disease (Mucocutaneous Lymph Node Syndrome) .............................................................................. 527 

Pediatric Seizures ...................................................................................................................................................... 529 

Cerebrospinal Fluid Shunts ....................................................................................................................................... 531 

Pediatric Gastrointestinal/Genitourinary Emergencies .............................................................................................. 533 

Child Abuse ............................................................................................................................................................... 537 

Child Neglect ..................................................................................................................................................... 537 

Munchausen Syndrome by Proxy (Polle Syndrome) ............................................................................................ 537 

Sexual Abuse ...................................................................................................................................................... 538 

Physical Abuse ................................................................................................................................................... 538 

489

PEDIATRIC EMERGENCIES: SELF-ASSESSMENT QUESTIONS 


1. The appropriate endotracheal tube for a 6-year-old is: 

(a) 4.5 uncuffed 

(b) 4.5 cuffed 

(c) 5.5 uncuffed 

(d) 5.5 cuffed 

2. Relative to the location of the adult airway in the neck, the child's airway is: 

(a) More anterior and higher 

(b) More posterior and higher 

(c) More posterior and lower 

(d) More anterior and lower 

3. Which of the following drugs should not be administered via the endotracheal route? 

(a) Atropine 

(b) Calcium chloride 

(c) Epinephrine 

(d) Naloxone 

4. Which of the following is not considered a risk factor for sudden infant death syndrome? 

(a) Maternal age >35 years old 

(b) Low birth weight 

(c) Smoking and drug abuse by mother 


5. All of the following statements regarding congenital diaphragmatic hernias are accurate except: 

(a) Left-sided hernias are more common than right-sided hernias. 

(b) Associated polyhydramnios is common. 

(c) Treatment is intubation, orogastric tube placement, IV hydration, and surgical repair. 

(d) Right-sided hernias are called Bochdalek hernias. 

6. Which of the following is not a structural component of the tetralogy of Fallot? 

(a) Pulmonic stenosis 

(b) Ventricular septa! defect 

(c) Left ventricular hypertrophy 

(d) Dextroposition and overriding of the aorta 

7. Initial management of a hypercyanotic ("Tet") spell in a child with tetralogy of Fallot should include all of the 


(a) Administration of supplemental oxygen 

(b) Placement of the child in the prone knee-chest position 

(c) Morphine 0.1 mg/kg IV, IM, or SC 

(d) Propranolol 0.05-0.1 mg/kg IV 

8. Which of the lesions listed below is an acyanotic heart lesion? 

(a) Transposition of the great vessels 

(b) Aortic stenosis 

(c) Total anomalous pulmonary venous return 

(d) Tricuspid atresia 

9. Which of the following statements regarding necrotizing enterocolitis is least accurate? 

(a) Premature infants with very low birth weight are most commonly affected. 

(b) It typically develops during the first 2 weeks of life. 

(c) The first and most frequent clinical finding is abdominal wall erythema. 

(d) Pneumatosis intestinal is is the radiographic hallmark. 

490


10. The presence of biphasic stridor on examination localizes the airway obstruction __ _ 

(a) Above the larynx 

(b) At the larynx 

(c) Below the larynx 

(d) Below the carina 

11. The usual causative organism of bronchiolitis is: 

(a) Parainfluenza virus 

(b) Respiratory syncytial virus 


(d) Influenza B virus 

12. The usual causative organism of croup is: 

(a) Respiratory syncytial virus 

(b) Parainfluenza virus 


(d) Echovirus 

13. Anticholinergic agents (atropine, ipratropium bromide) produce their beneficial effects in asthma by: 

(a) Increasing cyclic GMP 

(b) Decreasing cyclic GMP 

(c) Increasing cyclic AMP 

(d) Decreasing cyclic AMP 

14. All of the following poisonings may be associated with hyperpyrexia except: 

(a) Atropine 

(b) Salicylates 

(c) Amphetamines 

(d) Acetaminophen 

15. Under normal land conditions, the greatest amount of heat loss from the body occurs via: 

(a) Radiation 

(b) Evaporation 

(c) Convection 

(d) Conduction 

16. The most common bacterial causative organism of otitis media is: 

(a) Streptococcus pneumoniae 

(b) Haemophilus influenzae nontypable 

(c) Moraxella catarrha/is 

(d) Staphyloccoccus aureus 

17. The pathogens most often responsible for the production of pneumonia in children :C:5years old are: 

(a) Haemophilus influenzae and Streptococcus pneumoniae 

(b) Haemophi/us influenzae and Mycoplasma pneumoniae 

(c) Mycop/asma pneumoniae and Streptococcus pneumoniae 

(d) Mycop/asma pneumoniae and viruses 

18. A 3-week-old infant is brought in for evaluation of a staccato cough. His mother states that he was born by normal 

spontaneous vaginal delivery and that, aside from some nasal congestion and eye inflammation over the past 

few days, he had been well until yesterday. On examination, the child is afebrile but quite tachypneic and has 

bilateral conjunctivitis. Pulse oximetry reveals a saturation of 94%, and chest radiograph reveals bilateral interstitial 

/~ infiltrates. The organism most likely to produce this constellation of signs and symptoms in an infant this age is: 

(a) Group B streptococci 

(b) Chlamydia trachomatis 

(c) Staphyloccoccus aureus 

(d) Mycoplasma pneumoniae 

491


19. The most common bacterial pathogen in all age groups beyond the newborn period is: 

(a) Streptococcus pneumoniae 

(b) Haemphilus influenzae type B 

(c) Staphyloccoccus aureus 

(d) Group B streptococci 

20. When evaluating a child who presents with pneumonia, findings on the CBC (although certainly not diagnostic) can 

suggest a particular etiologic agent. The classic WBC findings that occur in association with particular pathogens are 

listed below. Which of the following findings is inappropriately matched? 

(a) Normal WBC count and differential/Mycop/asma pneumoniae 

(b) High WBC count with a left shift/Streptococcus pneumoniae 

(c) Marked lymphocytosis/viruses 

(d) Eosinophilia/Ch/amydia trachomatis 

21. In children, cardiac arrest is most commonly secondary to: 

(a) A primary cardiac event 

(b) Respiratory arrest 

(c) Shock 


22. The easiest and most accurate method used in the selection of an endotracheal tube for pediatric intubation is: 

(a) A formula that estimates the tube size based on the child's age 

(b) A tube size that equals the diameter of the tip of the child's little finger 

(c) A tube size that approximates the size of the child's nostril 

(d) A length-based resuscitation tape 

23. You are attempting to defibrillate a child weighing 20 kg. What dose should be used for the initial attempt? 

(a) 20 joules 

(b) 40 joules 

(c) 60 joules 

(d) 80 joules 

24. When using the endotracheal route to administer epinephrine during pediatric resuscitation, the concentration of 

epinephrine should be ___ that administered when the IV route is used. 

(a) The same as 

(b) Half 

(c) Double 

(d) Ten times 

25. You have just delivered a baby in a rural emergency department. At 1 minute, the infant is limp, has a slow and 

irregular respiratory effort, a heart rate of 80 beats per minute, acrocyanosis, and some reflex irritability. The 

appropriate 1-minute APGAR score for this infant is: 

(a) 2 

(b) 3 

(c) 4 

(d) 5 

26. You are evaluating a 2-year-old child for possible retropharyngeal abscess and decide to obtain a soft-tissue lateral 

radiograph of the neck. For an accurate interpretation, the radiograph must be taken: 

(a) 

During inspiration with the neck in slight extension 

(b) During inspiration with the neck in slight flexion 

(c) During expiration with the neck in slight extension 

(d) During expiration with the neck in slight flexion 

492


27. Which of the following statements regarding bronchiolitis is inaccurate? 

(a) It usually affects infants 2 months to 2 years old. 

(b) The causative organism is generally respiratory syncytial virus. 

(c) Apnea is a serious complication, and premature infants


36. The drug of choice for the treatment of supraventricular tachycardia in children is: 

(a) Adenosine 

(b) Propranolol 

(c) Verapamil 

(d) Procainamide 

37. Which of the following statements regarding prostaglandin E, is inaccurate: 

(a) It is a potent dilator of the ductus arteriosus. 

(b) It can be used to maintain the patency of (or reopen) the ductus arteriosus in infants with ductal-dependent 

congenital heart lesions. 

(c) Significant adverse effects associated with its use include apnea and hypotension. 

(d) The initial infusion rate is 1 mcg/kg/min. 

38. The organism(s) most commonly responsible for causing CSF shunt infections are: 

(a) Staphylococcus spp 

(b) Klebsiel/a 

(c) Gram-negative organisms 

(d) Group A streptococci 

39. The sign/symptom most commonly present in association with CSF shunt infection is: 

(a) 

Headache 

(b) Lethargy 

(c) Fever 

(d) Meningismus 

40. A 10-day-old infant is brought in for evaluation of respiratory distress. His mother states that he was born by normal 

spontaneous vaginal delivery and that, aside from some nasal congestion and coughing over the past few days, he 

had been well until yesterday. On examination, the child is afebrile but quite tachypneic with moderate retractions. 

His pulse is 80 beats per minute, and pulse oximetry is 89% on 100% oxygen. What is the next step in management ,~ 

of this patient? 

(a) Chest radiograph 

(b) Positive-pressure ventilation 

(c) Begin chest compressions 

(d) Epinephrine 0.01 mg/kg IV 

41. A 14-day-old infant is brought in for evaluation of respiratory distress. His mother states that he was born by normal 

spontaneous vaginal delivery but has been having difficulty feeding over the past 24 hours. On examination, the child 

is afebrile but tachypneic with moderate retractions and cyanotic with pulse oximetry of 80%. After placing him on 

100% oxygen, an arterial blood gas is obtained and the Pa0 2 

is 160 mm Hg. Which of the following is least likely? 

(a) Sepsis 

(b) Congenital heart disease with right to left shunt 

(c) Pneumonia 

(d) Primary seizure disorder 

ANSWERS 

1. C 8. b 

2. a 9. C 

3. b 10. C 

4. a 11. b 

5. d 12. b 

6. C 13. b 

15. 

16. 

17. 

18. 

19. 

20. 

a 

a 

d 

b 

a 

C 

22. 

23. 

24. 

25. 

26. 

27. 

d 29. C 

b 30. b 

d 31. a 

C 32. C 

a 33. C 

d 34. b 

7. d 14. d 21. b 28. d 35. a 

36. a 

37. d 

38. a 

39. C 

40. b 

41. b 



494


A. Unlike in adults, in whom rhythm disturbances are primary cardiac disturbances, in children rhythm 

disturbances are frequently secondary problems. 

1. Children at risk of dysrhythmias may have congenital or acquired heart disease, systemic disease, intoxication, 

or acute hemodynamic alteration. 

2. Cardiac arrest is usually secondary to respiratory arrest. Circulatory failure (shock) is the second most common 

precipitating event. 

3. Symptomatic sinus bradycardia is generally the result of prolonged hypoxemia or increased vagal tone. 

4. Primary cardiac events (eg, ventricular fibrillation) are rare. 

B. Dysrhythmias by age 

Table 31: Most Common Clinically Significant Dysrhythmias by Age 

Age (years) 


(3) The mass of adenoidal tissue is greater and the nasopharyngeal angle is more acute in young 

children, making nasopharyngeal intubation more difficult and more likely to result in damage to the 

nasopharyngeal soft tissues; therefore, orotracheal intubation under direct visualization is the preferred 

method of establishing initial airway control in a child. 

(4) The trachea is shorter (5 cm at birth); this increases the potential for accidental intubation of the right 

mainstem bronchus. 

b. General approach 

(1) Determine the proper tube size. 

(a) 

Use a length-based resuscitation tape (eg, Broselow® tape). This will predict the tracheal tube 

size and is useful in determining drug dosages. Tracheal tubes 0.5 mm smaller or larger than the 

estimated size should be readily available. 

(b) If a tape is unavailable, use the following formulas in children >2 years old: 

i. Uncuffed endotracheal tube: tracheal tube size= (age [in years]/4) + 4 

ii. Cuffed endotracheal tube: tracheal tube size = (age [in years]/4) + 3.5 

(c) The appropriate size tracheal tube for premature infants is 2.5-3.0 mm; for newborns 3.0-3.5 

mm; for 1-year-olds 4.0-4.5 mm, and for 4-year-olds 5.0 mm. 

(2) Prepare to intubate. 

(a) 

Place the head in the sniffing position. 

(b) Use the chin-lift or jaw-thrust to move the hypotonic mandibular tissue out of the way. 

(c) If the respiratory effort is inadequate, preoxygenate with 100% oxygen for 5 minutes (if possible). 

(d) There is insufficient evidence to recommend routine cricoid pressure to prevent aspiration during 

endotracheal intubation in children. Cricoid pressure should be stopped if it interferes with 

ventilation or the ease of ventilation. 

(3) Rapid-sequence intubation 

(a) Definition: simultaneous administration of potent sedative agent and rapid-acting paralytic 

drug as well as medications to ameliorate potential adverse effects of laryngoscopy to facilitate 

endotracheal intubation; safe and effective in children when used properly 

(b) Medications 

1. Pretreatment (controversial) 

• Atropine 0.02 mg/kg IV push: no longer recommended according to 2015 AHA 

guidelines (if used, the minimum 0.1 mg dose is no longer necessary according to 2015 

AHA guidelines, maximum 0.5 mg); theoretically blunts vagal stimulation and prevents 

bradycardia associated with laryngoscopy 

• Lidocaine 1-1.5 mg/kg IV push: theoretically blunts increase in intracranial pressure 

associated with intubation 

ii. Induction 

• Midazolam 0.1 mg/kg IV push: variable dosing 

• Ketamine 1-2 mg/kg IV push: although previously believed to increase intracranial pressure, 

newer data suggest this may not be the case. 

• Thiopental 3-5 mg/kg IV push: may cause hypotension, laryngospasm 

• Etomidate 0.3 mg/kg IV push: hemodynamically stable; caution in septic shock secondary to 

adrenal suppression 

• Propofol 1-2 mg/kg IV push: may cause hypotension, may be used in some institutions 

iii. Paralytic agents 

• Rocuronium 0.6-1.2 mg/kg IV push 

• Succinylcholine 1-1.5 mg/kg IV push, infants may require 1.5-2 mg/kg; Contraindications 

include children with underlying muscular disorders or extensive burns. 

(4) Confirm tracheal tube placement after intubation by: 

(a) Observing the chest for symmetric movement 

(b) Listening over the axillae to confirm equal breath sounds 

(c) Listening over the stomach to assure absent breath sounds 

(d) Obtaining a chest radiograph; the tip of the tracheal tube should be located above the carina at 

the level ofT2. 

496


(e) End-tidal CO 2 

detection 

i. In patients with a pulse, this is the best adjuvant method (most sensitive/specific) for 

verification of tube placement; however, the most accurate means is observation of the tube 

passing through the vocal cords. 

(f) 

ii. A false-negative reading can occur with severe circulatory collapse; therefore, if the CO 2 

is not 

detected during CPR, take another look with a laryngoscope. 

Clinical deterioration in a previously stable intubated patient receiving positive-pressure 

ventilation can be remembered by the mnemonic "DOPE": 

,Qislodged tube 

Qbstructed tube 

Tension fneumothorax 

fquipment failure 

(5) Rescue airway devices: supraglottic devices, eg, the laryngeal mask airway, may quickly be inserted 

blindly in skilled hands. 

Table 26: Laryngeal-Mask Airway Sizes 

Age (weight) 

Size 

Newborn (0-5 kg) 

3 months to 1 year old (5-1 0 kg) 

1-4 years old (10-20 kg) 

4-8 years old (20-30 kg) 

>8 years old (30-40 kg) 

Adolescent and adult 

1.5 

2 

2.5 

3 

4 

3. Surgical airways in children 

B. Breathing 

a. Needle cricothyrotomy with jet ventilation 

(1) Indications: inability to ventilate and inability to intubate in children 8 years old as an alternative to needle cricothyrotomy. 

1. Each breath should be delivered slowly (over 1-1.5 seconds). 

,--.., 2. The appropriate volume of each breath is the volume that causes the chest to rise; this corresponds to a tidal 

volume of 6-8 mUkg with spontaneous breathing, 10-15 ml/kg with volume ventilation. 

3. Rate (breaths per minute) 

a. Neonates: 40-60 

b. Infants


c. Children 1-3 years old: 22-30 

d. Children >8 years old: 12 

4. Mechanical ventilation 

a. For children, use a volume-limited ventilator. Initial settings: 

(1) Tidal volume 10-15 ml/kg 

(2) FiO 2 

100% 

(3) lnspiratory time 0.5-1.5 seconds 

(4) Age-appropriate respiratory rate (adjusted to physiologic needs) 

(a) 20-30 breaths per minute in infants 

(b) 16-20 breaths per minute in children 

(5) Positive end-expiratory pressure 3-5 cm H 2 

O 

b. For infants 8 years old: 60-100 

2. Normal systolic blood pressure based on age (lowest 5th percentile) 

a. 60 mmHg 

b. 1 month to 1 year old: 70 mmHg 

c. > 1 year old: 70 + (2 x age in years) mm Hg (estimate) 

D. Chest compressions 

1. Should be started in: 

a. Children who do not have a pulse or have a heart rate


d. Children >8 years old 

(1) Rate= 100-120 per minute 

(2) Technique: heel of one hand with other hand on top located over lower half of sternum 

(3) Compression/ventilation ratio 15:2 (two-rescuer CPR) 

(4) Depth = at least 1 /3 the total depth of the chest or 2-2.5 inches (5-6 cm) in adolescents 

e. When only one provider is available, the universal 30:2 compression/ventilation ratio should be used. 

f. CPR with an advanced airway in place in infants, children, and adolescents: 10 breaths per minute and 

compressions at 100-120 per minute; in neonates, should continue at 3:1 compression:ventilation ratio 

E. Defibrillation and cardioversion 

1. Paddle size 

a. Infants (1 year old or >10 kg: adult paddles 8-13 cm 

2. Conducting medium 

a. Use electrode cream (or paste) or self-adhesive defibrillation pads. 

b. Do not use alcohol pads; they can produce significant burns. 

c. Do not allow the conducting medium under one paddle to come into contact with the conducting medium 

under the other paddle; this can result in "bridging" and delivery of an insufficient amount of current to 

the heart. 

3. Positioning 

a. Right upper-left lower anterior chest or anterior-posterior orientation: pads should not touch and should be 

positioned so that there is at least 3 cm between them. 

b. Infants may need anteriorposterior positioning. 

4. Defibrillation 

a. Initial dosage is 2-4 joules/kg; if unsuccessful, use 4 joules/kg for subsequent attempts, increasing up to 10 

joules/kg (maximum adult dosage). 

b. If unresponsive with shockable rhythm (ventricular fibrillation or pulseless ventricular tachycardia), 

initiate CPR before first shock and resume CPR immediately for 2 minutes before checking pulse. 

Administer epinephrine before proceeding with additional defibrillation attempts. 

5. Cardioversion: initial dosage is 0.5-1 joule/kg.; if unsuccessful, increase the dosage, up to 2 joules/kg. 

F. Vascular access 

1. Although the tracheal route may be used to administer a limited number of medications, the IV and 

intraosseous routes are preferable for drug delivery and are mandatory for fluid therapy. 

2. The preferred site of vascular access is the largest vein that can be rapidly cannulated without disrupting the 


a. Peripheral venous access (arm, hand, leg, foot) is usually attempted first. 

b. Central venous access has some advantages and should be used if already in place, but it is more difficult 

to accomplish in the arrest setting and may be associated with significant complications. 

c. Administration of drugs via the peripheral venous route should be followed by a saline flush of c::5 ml to 

promote movement of the drug into the central circulation. 

3. If peripheral venous access cannot be rapidly obtained (3 attempts or 90 seconds) in a child with a lifethreatening 

condition, intraosseous access should be considered. This route is usually easier (more successful 

and faster) than other types of access in volume-depleted children. In addition, intraosseous access is no 

longer restricted to young children; it is recommended for the entire spectrum of pediatric care. 

a. The anteromedial aspect of the proximal tibia (1-3 cm below the tibial tuberosity on the medial flat surface 

of the tibia) is the preferred site. 

b. Drugs, fluids, and blood products may be given by this route. The initial aspirate can also be used for blood 

typing and chemistries. 

c. Drug administration should be followed by a saline flush of 5 ml to promote movement of the drug into the 

central circulation. 

d. Alternative sites for intraosseous placement include distal femur, medial malleolus, proximal humerus, 

sternum, and anterior superior iliac spine. 

4. The tracheal route is less reliable and therefore less desirable; the kinetics of tracheal drug absorption do not 

favor this route. 

499


a. Medications that are safe and effective when given through the tracheal tube can be remembered by the 

mnemonic "LEAN": 

.!.idocaine 

_Epinephrine 

Atropine 

Naloxone 

b. When this route is used, the dosage administered should be greater than that given by the IV route. 

However, a specific tracheal dosage has been established only for epinephrine (0.1 mg/kg; 10 times venous 

dosage), and most authors recommend that the dosage be 2-3 times the IV dosage for other medications. 

c. Drugs administered by this route should be followed by a 2-5 ml saline flush (or diluted in 2-5 ml of 

saline) and followed by several positive-pressure ventilations. 

d. Drug administration should be switched to the IV route as soon as it becomes available. 

e. Sodium bicarbonate and calcium chloride should not be administered via the tracheal route. 

5. In the neonatal period, the umbilical vein is an excellent site of vascular access; it can be used up to 7 days 

after delivery. 

G. Life-threatening cardiac arrhythmias 

1. Unlike in adults, in whom rhythm disturbances are primary cardiac diseases, in children rhythm disturbances 

are frequently secondary problems. 

a. Most commonly secondary to respiratory (hypoxemia), metabolic/electrolyte, renal disturbances, or drug/ 

toxin effects 

b. Exceptions: children with congenital heart disease, structural heart disease, or acquired heart disease 

2. When evaluating and managing life-threatening dysrhythmias, always consider and treat causes and 

contributing factors ("6 H's and 5 T's") 

a. Hypovolemia 

b. Hypoxia 

c. Acidosis (hydrogen ion): sodium bicarbonate (1 mEq/kg IV or intraosseous) 

(1) No longer first-line agent for acidosis 

(2) Indicated for severe refractory acidosis (after adequate ventilation/oxygenation established and 

epinephrine ineffective) 

(3) In infants and children, use 8.4% solution (1 mEq/mL). 

(4) In neonates, dilute 8.4% solution to make 4.2%. 

d. Hypokalemia/hyperkalemia 

(1) Calcium chloride (for life-threatening hyperkalemia with dysrhythmia) 

(a) 20 mg/kg (0.2 ml/kg) slow IV or intraosseous 

(b) Preferably should be administered via a central line 

(c) Stabilizes cardiac membrane but does not decrease potassium 

(2) NaHCO 3 

, glucose and insulin, and albuterol are usually a part of the management of hyperkalemia. 

e. Hypoglycemia: glucose (0.5-1 g/kg IV or intraosseous) 

(1) 2 years old: 1-2 mUkg of D50 

f. Hypothermia 

g. Toxins, poisons, or drugs: naloxone 

(1) Dosage: 0.1 mg/kg IV push or intraosseous (2 mg IV push or intraosseous if >20 kg) for opioid intoxication 

(2) Use with caution in neonates, because it can precipitate life-threatening withdrawal in this age group. 

h. Cardiac tamponade 

i. Tension pneumothorax 

j. Thrombosis: acute coronary syndrome, pulmonary embolism 

k. Trauma 

3. Bradyarrhythmias (most common dysrhythmia seen in pediatric arrest) 

a. General principle: outside of the immediate neonatal period, only an emergency requiring intervention if 

causing cardiopulmonary compromise 

b. Evaluate and support ABCs, including supplemental oxygen. 

500


c. If pulse 180 beats per minute 

iii. Adenosine 0.1 mg/kg IV push (maximum 6 mg); if unsuccessful, 0.2 mg/kg IV push 

(maximum 12 mg) 

(2) Wide QRS (>90 milliseconds): ventricular tachycardia 

(a) Synchronized cardioversion: 0.5-1 joules/kg; if unsuccessful, increase dosage to 2 joules/kg. 

(b) Amiodarone 5 mg/kg IV over 20-60 minutes or 

(c) Procainamide 15 mg/kg IV over 30-60 minutes 

5. Pulseless arrest (ventricular tachycardia/ventricular fibrillation, pulseless electrical activity, asystole) 

a. Start CPR, including rescue breathing, cardiac monitor, IV access. 

b. Evaluate rhythm morphology. 

(1) Ventricular tachycardia/ventricular fibrillation 

(a) Defibrillation 

i. 2-4 joules/kg; if unsuccessful, then 4 joules/kg up to 10 joules/kg (maximum adult dosage) 

for all subsequent shocks. 

11. Always perform CPR for 2-3 minutes immediately after any defibrillation attempts before 

rechecking rhythm. 

(b) Epinephrine 

(c) Consider antiarrhythmic 

i. Amiodarone (5 mg/kg IV or intraosseous) 

ii. Lidocaine (1 mg/kg IV or intraosseous; may give second dose of 1.5 mg/kg if unsuccessful) 

iii. Magnesium (25-50 mg/kg IV or intraosseous) for torsades de pointes 

A. Risk factors associated with neonatal cardiopulmonary arrest 

1. Maternal factors 

a. Poor prenatal care 

b. Age (35 years old) 

c. Preeclampsia/eclampsia 

501


2. 

3. 

4. 

d. Hypertension 

e. Diabetes 

f. Drug abuse 

g. Medications (lithium, ~-blockers, magnesium) 

h. Anemia 

i. Renal disease 

j. Rh factor incompatibility 

k. History of prior perinatal morbidity/mortality 

I. Oligohydramnios 

m. HIV infection 

lntrapartum factors 

a. Premature or prolonged labor 

b. Abnormal presentation 

C. Precipitous or forceps delivery 

d. Cephalopelvic disproportion 

e. Cesarean section 

f. Cord prolapse or compression 

g. Analgesia and/or sedatives administered ::,2 hours before delivery 

h. Signs of fetal distress on fetal monitoring (late decelerations) 

i. Maternal shock 

j. Placenta previa/abruptio 

k. Premature rupture of membranes 

Fetal factors 

a. Prematurity and postmaturity 

b. Thick meconium 

C. Congenital infection 

d. Malformations identified by ultrasound 

e. Multiple gestations 

f. Bradycardia 

g. Acidosis 

h. Small fetus for maternal dates 

Precipitous/imminent delivery of newborn 

a. History: 3 questions currently recommended 

(1) Term gestation? 

(2) Prenatal care? 

(3) Single or multiple gestations? 

b. Equipment 

(1) Resuscitation bag 

(2) Neonatal resuscitation masks 

(3) Dry towels 

(4) Ambient warmer (if available) 

(5) Suction equipment (including meconium aspiration device) 

(6) Uncuffed entotracheal tubes (sizes 2.5, 3.0, and 3.5) 

(7) Laryngoscope (Miller size O and 1) 

"'·---·'/ 

502

~ 


B. APGAR scoring 

Table 33: APGAR Score 

Score 

0 2 

Activity (muscle tone) Limp Decreased flexion Good flexion 

Pulse (heart rate) Absent 100 beats per minute 

Grimace (reflex irritability, None Some motion Cry 

stimulus respiration) 

Appearance (color) Blue, pale Body pink, extremities blue Pink 

Respirations Absent Slow, irregular Good, crying 

1. The Apgar score is assigned to newborns 1-5 minutes after delivery. If the 5-minute score is


3. Management 

a. Assess ABCs: maintain airway, provide supplemental oxygen, establish an IV line (normal saline), and start 

appropriate monitoring. 

b. Correct underlying metabolic problems if present (hypoglycemia, hypocalcemia, electrolyte imbalance). 

c. Identify and treat associated problems (sepsis, acidosis, etc). 

d. Begin anticonvulsant therapy. 

(1) Phenobarbital is the initial anticonvulsant agent of choice in neonates. Dosage is 15-20 mg/kg IV over 

10 minutes; if this is ineffective, additional dosages of 5 mg/kg may be given every 5 minutes up to a 

total maximal dosage of 40 mg/kg. 

(2) If seizures persist or recur, follow with phenytoin. 

(a) Dosage is 20 mg/kg IV; dilute in normal saline and administer slowly at 0.5 mg/kg/min. 

(b) Fosphenytoin is another alternative. 

(3) If there is still no response, a benzodiazepine (lorazepam or diazepam) may be given. However, 

benzodiazepines are not first-line agents in this age group; they produce prolonged and profound 

respiratory depression (particularly if used in combination with phenobarbital), and they also displace 

bilirubin from albumin. 

(a) Lorazepam 0.05-0.1 mg/kg at a rate of 2 mg/min 

(b) Diazepam 0.2-0.3 mg/kg at a rate of 1 mg/min 

e. Administer pyridoxine 50-100 mg IV or IM for refractory seizures. 

E. Congenital diaphragmatic hernia 

1. Hernia results from developmental failure of the posterolateral or retrosternal portions of the diaphragm. 

2. Left-sided hernias (Bochdalek) are far more common (70%-85%) than right-sided hernias (Morgagni). 

3. Associated anomalies include congenital heart disease, GI and genitourinary anomalies, hydronephrosis, and 

cystic kidneys. 


a. History: respiratory distress and vomiting, which is caused by herniation of the abdominal viscera into the 

chest cavity 

b. Physical examination: scaphoid abdomen, absence of breath sounds on affected side of chest, auscultation 

of bowel sounds over affected side of chest 

5. Chest radiograph: air-filled loops of bowel in the chest, absence of diaphragmatic margin, displacement of 

heart and mediastinum, hypoplastic lungs 

6. Management 

a. Immediate intubation (avoid bag-mask ventilation) 

b. Placement of an orogastric tube, IV hydration, and surgery 

7. Mortality rate is 50% in severely affected infants; morbidity is even higher. 

F. Tracheoesophageal fistula 

1. One-third of affected infants are born prematurely. 

2. A proximal esophageal pouch and fistula between the trachea and the distal esophagus (tracheoesophageal 

fistula) is most common (84%). 

3. Associated anomalies and polyhydramnios are common. 

4. Infants may present with increased oral secretions, choking, or coughing with attempts at feeding or recurrent 

aspiration pneumonia. 

5. Inability to pass a catheter into the stomach confirms the diagnosis. 

6. Management: reverse Trendelenburg or semi-Fowler position, placement of suction catheter into esophageal 

pouch, IV fluids, and surgical correction 

G. Omphalocele and gastroschisis 

1. Abdominal wall defects resulting from developmental anomalies of the intestines 

a. Omphalocele 

(1) Defect in the umbilical ring with protrusion of the intestines (covered by the peritoneal sac) outside of 

the abdominal wall 

(2) Associated anomalies (particularly chromosomal ones) occur in one-third to one-half of these infants. 

b. Gastroschisis 

(1) Defect in the abdominal wall with antenatal evisceration of abdominal contents without a peritoneal sac 

(2) Occurs in association with intestinal atresia 

504


2. Management 

a. Keep the child warm. 

b. Place an orogastric tube to decompress the gut. 

c. Cover the eviscerated intestines with saline-soaked sterile gauze and place them in a plastic bag. 

d. Administer IV fluids and prophylactic antibiotics. 

e. Obtain immediate pediatric surgery consultation for operative repair. 

H. Necrotizing enterocolitis 

1. Primarily affects premature infants with very low birth weights, although may also be seen in term infants 

2. Characterized by variable degrees of mucosa! or transmucosal necrosis of the intestines 


a. Hypertonic feeding solutions or medicines 

b. Patent ductus arteriosus and apneic spells 

c. Infection 

d. lschemia after exchange transfusions 

4. Onset usually in first 2 weeks of life 


a. Feeding intolerance 

b. Abdominal distention with gastric retention (first and most frequent finding) 

c. Bilious emesis 

d. Guaiac positive or grossly bloody feces 

e. Abdominal wall tenderness or erythema 

f. Manifestations of associated sepsis 

(1) Metabolic acidosis 

(2) Apneic episodes 

(3) Temperature instability 

(4) Lethargy 

6. Radiographic findings on plain abdominal radiographs 

a. Pneumatosis intestinalis (radiographic hallmark) 

b. Separation of bowel loops (suggests mural edema) 

c. A fixed, dilated loop of bowel that fails to move on serial radiographs 

d. Air-fluid levels 

e. Portal vein gas (sign of severe disease) 

f. Pneumoperitoneum (indicative of perforation) 

7. Management 

I. Cyanosis 

a. Discontinue oral feedings. 

b. Place a nasogastric tube to decompress the bowel. 

c. Obtain cultures (blood, feces, urine, CSF). 

d. Administer IV fluids, parenteral feedings, and broad-spectrum antibiotics. 

e. Obtain surgical consult. 

1. Central 

a. Bluish discoloration of tongue, mucous membrane, and peripheral skin; unsaturated hemoglobin usually 5 g 

b. Pathologic if persists for >20 minutes after delivery 

c. Etiology 

(1) Cyanotic heart disease with a right-to-left shunt (the 5 "T's") 

(a) Truncus arteriosus 

(b) Transposition of the great vessels 

(c) Tricuspid atresia 

(d) Tetralogy of Fallot 

(e) Total anomalous pulmonary venous return 

505


(2) Primary lung disease 

(3) Hypoventilation due to a CNS lesion (eg, severe intracerebral hemorrhage) 

(4) Alveolar hypoventilation secondary to shock or sepsis 

(5) Methemoglobinemia 

d. The "hyperoxia test" (response of the PaO 2 

to the administration of 100% oxygen) can provide a 

diagnostic clue as to the underlying cause of the central cyanosis. 

2. Peripheral 

(1) Failure of the PaO 2 

to rise above 1 00 mm Hg suggests either cyanotic heart disease with a fixed 

right-to-left shunt or methemoglobinemia. 

(2) Improvement in the PaO 2 

suggests one of the other causes (eg, lung disease, sepsis, CNS disorder). 

a. Bluish discoloration of extremities only; oxygen saturation >94% 

b. Common in newborns in the first few days of life 

c. Generally due to vasomotor instability secondary to a cold environment 

J. Congestive heart failure 


a. Feeding difficulty (slow feeder, diaphoresis, and dyspnea on feeding) 

b. Tachypnea and tachycardia 

c. Rales and rhonchi 

d. Hepatomegaly and cardiomegaly 

e. Failure to thrive 

f. Peripheral edema rare 

2. Etiology 

a. Usually due to congenital heart disease, most commonly left-to-right shunts that present at 6-8 weeks 

b. Other causes include severe anemia, dysrhythmias (supraventricular tachycardia, ventricular tachycardia), 

sepsis, and arteriovenous malformation (hepatic, cerebral). 

3. Management 

a. Supplemental oxygen 

b. Semireclining position 

c. Restriction of fluid intake 

d. Digoxin 

(1) The oral digitalizing dosage is 10-20 mcglkg for preterm infants and 30 mcglkg for term infants; the IV 

dosage is three-fourths of the oral dosage. 

(2) Administer one-half of this dose initially, one-fourth in 8 hours, and the last one-fourth 8 hours later. 

(3) Contraindications: tetralogy of Fallot, idiopathic hypertrophic subaortic stenosis and myocarditis (a 

relative contraindication), and a heart rate



(1) Lethargy or irritability 

(2) Poor feeding 

(3) Dehydration 

(4) Hypotonia 

(5) Seizures 

d. Management 

(1) IV hydration 

(2) Treat any underlying pathology. 

(3) Phototherapy and exchange transfusion for severe hyperbilirubinemia: based on total serum bilirubin 

gestational age and hours of life (published guidelines exist) but concerning if >20 mgldL 

e. Complication of acute bilirubin encephalopathy (kernicterus): neurologically devastating sequelae of 

bilirubin crossing the blood-brain barrier, resulting in choreoathetoid cerebral palsy, sensorineural hearing 

loss, and gaze palsies 

L. Apparent life-threatening event (ALTE) 

1. Brief resolved unexplained events (BRUE) 

a. AAP Clinical Practice Guideline 2016 

b. Definition: an event occurring in an infant 60 days 

(2) Born >32 weeks gestation and corrected gestational age >45 weeks 

(3) No CPR by trained medical provider 

(4) Event lasted


b. Certain subgroups have higher rates of subsequent sudden infant death syndrome 

(1) Recurrent ALTEs requiring CPR 

(2) Premature infants 

5. Periodic breathing of infancy 

a. Normal breathing pattern of newborns (especially premature neonates) that is often mistaken for ALTEs 

b. Characterized by periods of rapid breathing followed by apnea of 3-20 seconds in duration 

c. Never associated with cyanosis or bradycardia 

M. Sudden infant death syndrome (SIDS) 

1. Although the incidence in the United States has been reduced by >50% (down to 3,700 deaths per year) as 

a result of the "back to sleep" initiative, which encouraged parents to place sleeping infants in the supine 

position, SIDS remains the leading cause of death in infants 1 month to 1 year old. 

2. Peak incidence is during the winter months during the hours of sleep (midnight to 9 AM) in infants 2-4 months 

old; boys are more commonly affected than girls. 

3. Although the exact cause(s) remains unclear, current pathologic data indicate that hypoxia (and possibly 

autonomic dysfunction) plays a role in the pathophysiology. 


a. Maternal 

(1) Age


(5) Loud, single second heart sound 

(6) Patients develop "hypercyanotic" ("Tet") spells with moderate to severe pulmonic stenosis. They are 

most common in the first 3 years of life and are brought on by exertion (feeding, straining, crying). 

These episodes are treated by placing the child in the prone knee-chest position and administering 

supplemental oxygen and morphine 0.1 mg/kg IV, IM, or SC. The morphine may be repeated if the 

child does not respond to the initial dose. If there is still no response, propranolol (0.05-0.1 mg/ 

kg IV) or phenylephrine (1 0 mcg/kg IV followed by 0.5-2 mcg/kg/min) may be given under the 

direction of appropriate pediatric consultation. 


(1) Chest radiograph findings 

(a) Boot-shaped heart 

(b) Diminished pulmonary vascular markings (due to decreased pulmonary blood flow) 

(2) ECG findings 

(a) Right axis deviation 

(b) Right ventricular hypertrophy 

3. Other causes of cyanotic heart disease 

a. Transposition of the great vessels (most common cause in newborns) 

b. Truncus arteriosus 

c. Tricuspid atresia 

d. Total anomalous pulmonary venous return 

e. Pulmonary atresia 

f. Ebstein anomaly of the tricuspid valve 

B. Acyanotic heart lesions 

1. Aortic stenosis (most common) 

a. A bicuspid aortic valve is the most frequent cause of significant valvular aortic stenosis in infancy and 

childhood; it is one of the most common congenital heart lesions identified in adults. 

b. Although generally seen in older children, severe lesions may present in infancy as left heart failure. Critical 

stenosis results in heart failure and cardiogenic shock when the ductus arteriosus closes. 


(1) Exercise intolerance 

(2) CHF 


(4) Syncope 

(5) Diamond-shaped systolic ejection murmur radiating to the neck 

(6) Systolic ejection click 

(7) An S 3 

is common; an S 4 indicates severe stenosis. 

(8) Palpable thrill over the base of the heart 

d. ECG findings: signs of left ventricular hypertrophy or strain may be present 


(1) Infectious endocarditis 

(2) Sudden death due to ventricular dysrhythmias 

2. Ventricular septa! defect 

a. Most common congenital heart anomaly 

b. Clinical presentation is determined by the size of the lesion. 

(1) Small defects: may be asymptomatic 

(2) Large defects: signs of CHF (tachypnea, grunting respirations, fatigue with feeding) typically develop 

after the first few weeks or months of life as the pulmonary vascular resistance falls and flow across the 

defect increases. 

(3) Physical findings 

(a) Holosystolic murmur at the lower left sternal border 

(b) Normal peripheral pulses 

509


3. Other causes of acyanotic heart disease 

a. Atrial septa! defect 

b. Patent ductus arteriosus (common in premature infants): characterized by bounding pulses, a continuous 

"machinery" murmur, and a suprasternal notch thrill 

c. Coarctation of the aorta: cardinal findings are hypertension in the upper extremities and decreased or 

absent pulses in the lower extremities. 

C. Ductal dependent lesions 

1. Cardiac lesions that manifest as outflow tract obstruction (severe coarctation of the aorta, critical aortic 

stenosis, hypoplastic left heart syndrome, and tricuspid atresia) 

2. Infants with these lesions usually present in profound shock with a classic skin color described as the 

"gray baby" within hours to days of delivery. 

3. Affected infants become symptomatic as the ductus arteriosus closes, because the systemic circulation 

(in left-sided lesions) or pulmonic circulation (in right-sided lesions) depends on shunting. 

4. Management 

a. ABCs, IV line, monitor 

b. Prostaglandin E 1 

, a potent dilator of the ductus arteriosus, can be life-saving in these infants. The infusion 

(0.05-0.1 mcg/kg/min) should be started, and the child monitored for apnea and hypotension (occurs 

with prostaglandin infusion). 

c. Obtain urgent cardiology consult. 

D. Congestive heart failure 

1. Primary cause in infants and young children is congenital heart disease. 

2. Etiology based on age of presentation: 

a. Newborn (noncardiac causes) 

(1) Anemia 

(2) Hypoxia 

(3) Acidosis 

(4) Hypoglycemia 

(5) Hypocalcemia 

(6) Sepsis 

b. Day 1 _.. patent ductus arteriosus 

c. First week_.. hypoplastic left heart syndrome 

d. 2 weeks _.. coarctation of the aorta 

e. 1 month __,. ventricular septa! defect 

f. 3 months _.. supraventricular tachycardia (the most common symptomatic dysrhythmia in infants and 

children) 

g. 1-2 years 

(1) Myocarditis 

(2) Cardiomyopathy 

(3) Severe anemia 

(4) Kawasaki disease 

h. 1 O years __,. rheumatic fever 


a. Right-sided CHF __,. hepatomegaly 

b. Left-sided CHF _.. tachypnea, dyspnea, diaphoresis, poor feeding 

c. Both_.. cardiomegaly, tachycardia, cyanosis, failure to thrive 

4. Diagnostic evaluation: chest radiograph typically shows cardiomegaly and increased pulmonary marking. 

5. Treatment: see management of newborn (see page 506) 

510


A. Upper airway (see also upper airway emergencies, page 150) 


a. Stridor 

(1) lnspiratory (obstruction at or above larynx) 

(2) Biphasic (obstruction below the larynx) 

(3) Expiratory (bronchial or lower tracheal obstruction) 

b. Expiratory wheezing (obstruction below the carina at the level of the bronchi) 

c. Tachypnea 

d. Nasal flaring 

e. lntercostal and substernal retractions 

f. Cyanosis 

g. Hoarseness 

h. Coughing 

i. Grunting and expiratory wheezing are signs of lower airway distress. 

2. Foreign body aspiration 

a. Most common cause of accidental home death in children


(b) Evaluation of the epiglottis by using a tongue blade (or a fiberoptic bronchoscope) can be safely 

done by experienced physicians, but it remains controversial and should be avoided in children 

with any respiratory distress. 

(c) Definitive diagnosis is ideally made in the operating room under controlled conditions by direct 

visualization of the "cherry-red" epiglottis. This is particularly true when severe respiratory distress 

is present. 

(3) Provide supplemental humidified oxygen, set up airway stabilization equipment at bedside (the patient 

can usually be adequately ventilated with bag and mask if total airway obstruction occurs), and obtain 

immediate ENT and anesthesia consultation. 

(4) Ideally, the child should be intubated under general anesthesia in the presence of an ENT surgeon. If 

unable to intubate, the surgeon will need to perform a tracheostomy. 

(5) Once the airway has been stabilized, draw blood for laboratory studies (including cultures); blood 

cultures are positive in 80% of patients. 

(6) Administer parenteral antibiotics. Acceptable regimens include a second- or third-generation 

cephalosporin (cefuroxime, cefotaxime, or ceftriaxone) or ampicillin-sulbactam. 

(7) Admitto ICU. 

d. Haemophilus influenzae type B cases caused by this organism have markedly decreased since the advent 

of the H influenzae B vaccine. Group A f3-hemolytic streptococci (followed by Streptococcus pneumoniae 

and Staphylococcus aureus) is responsible for an increasing number of cases. 

4. Croup (usual age group 6 months to 6 years old, peak incidence at 2 years old) 

a. Clinical presentation: The child has a barky, "seal-like" cough that is usually worse at night and may cause 

severe respiratory distress. The illness tends to come on gradually (usually in the late fall or early winter) as 

an upper respiratory infection. The cough, hoarseness, and stridor typically appear 1-2 days later. Croup 

symptoms peak on the third or fourth day of the illness (which is the first and second day of the croup 

symptoms) and generally resolve over a week. Fever is absent or low-grade, and the child is nontoxic in 

appearance. 


(1) Radiographs are not usually needed (diagnosis can often be made on clinical grounds alone) but are 

useful in excluding epiglottitis. 

(2) The PA neck radiograph reveals symmetric subglottic narrowing of the tracheal air column ("steeple 

sign"), and the lateral neck radiograph shows a distended hypopharynx and subglottic narrowing. The 

epiglottis and retropharyngeal space are normal. 

c. Management: supportive 

(1) Antibiotics are not indicated because the infecting organism is viral (usually parainfluenza virus). 

(2) Cool mist 

(3) Oxygen as needed 

(4) Hydration (orally or IV) 

(5) Racemic epinephrine aerosol (0.5 ml of a 2.25% solution diluted in 2.5 ml of saline) 

(a) Reserved for children with resting stridor and respiratory distress 

(b) Children who receive it should be observed in the emergency department for 2-4 hours after 

administration in case of return to their pretreatment stridorous state once the effect wears off. 

(c) If racemic epinephrine is unavailable, aerosolized L-epinephrine 1 :1,000 (5 ml) is equally 

effective and may be used. 

(6) Steroids (dexamethasone 0.3-0.6 mg/kg IM, IV, or orally as a one-time dose) 

(a) Should be administered to all children with croup (mild, moderate, or severe) and especially to 

those who receive racemic epinephrine 

(b) Hastens symptomatic improvement 

(7) Heliox (a mixture of helium and oxygen) 

(a) Decreases the work of breathing by improving laminar gas flow through the obstructed airway 

(b) Usually reserved for children with severe croup or refractory respiratory distress despite steroids 

and racemic epinephrine 

(8) Although most children can be discharged, admission should be considered for those who: 

(a) Have persistent stridor at rest 

(b) Are unable to tolerate oral fluids 

(c) Have an incomplete response to racemic epinephrine or require multiple doses 

(d) Present with severe croup (particularly those


5. Bacterial tracheitis (usual age


f. Differential diagnosis includes asthma ("reactive airway disease"), cystic fibrosis, recurrent aspiration, 

congenital heart disease, and foreign body aspiration. A careful history and chest radiographs are helpful ~/ 

in eliminating some of these diagnoses. However, differentiating between asthma and bronchiolitis can be 

difficult because of the similarity in presenting symptoms. 

g. Prevention: Prophylactic regimens using immune globulin (palivizumab) are available for high-risk infants 

(premature infants and those with lung or heart disease) to lessen the risk of subsequent severe respiratory 

syncytial virus infection. 

h. Risk factors for severe disease 

(1) Premature infants 

(2) Congenital heart disease 

(3) Respiratory syncytial virus subtype A 

(4) History of cyanosis/apnea 

(5) Age


(2) Serum lgE levels and the prevalence of asthma are closely related, lending support to the premise 

that asthma nearly always has an allergic basis. Further support comes from the fact that atopic 

individuals (those with a genetic predisposition for producing an lgE-mediated response to common 

environmental allergens) are at greatest risk of developing asthma. 

(3) "Triggers" that can precipitate an asthma attack 

(a) Viral respiratory infections (most frequent trigger in children


516 

1. Speak in complete sentences 

ii. Have only end-expiratory wheezing 

iii. Are generally not using accessory muscles 

iv. Do not have pulsus paradoxus 

v. Have a PEFR >80% of predicted/personal best and an SaO 2 

>95% on room air (at sea level) 

(b) Patients with moderate exacerbations 

i. Speak in phrases 

ii. Have wheezing throughout exhalation 

iii. Commonly use accessory muscles 

iv. May have a pulsus paradoxus of 10-25 mm Hg 

v. Have a PEFR 50%-80% of predicted/personal best and an SaO 2 

of 91 %-95% on room air 

(at sea level) 

(c) Patients with severe exacerbation 

i. Speak one or two words at a time 

ii. Commonly have loud wheezing throughout inhalation and exhalation 

iii. Are usually using accessory muscles 

iv. Frequently have a pulsus paradoxus of 20-40 mmHg 

v. Have a PEFR 95% in children and infants. 

(2) The initial treatment of choice is aerosolized therapy with a ~-adrenergic agonist; it is associated with 

fewer systemic adverse effects and better dilation than parenteral therapy, and it obviates the need for 

painful injections. 

(a) Albuterol 0.5% solution (5 mg/ml) is the preferred agent because of its ~ 2 

-agonist specificity. 

1. Administer 0.15 mg/kg (maximum dose is 5 mg; minimum dose is 2.5 mg) in 2-3 ml normal 

saline every 20 minutes for 3 doses, then 0.15-0.3 mg/kg up to 10 mg every 1-4 hours as 

needed. 

ii. Continuous nebulization using 0.5 mg/kg/hr (maximum 15 mg/hr) should be considered for 

children who do not respond to this regimen or who present with severe respiratory distress. 

iii. Albuterol administered by a metered-dose inhaler (90 mcg/puff) with a spacer is as effective 

as nebulizer therapy and can be used in children who are able to coordinate the inhalation 

maneuver (usually children >6 years old). The dosage is 4-8 puffs every 20 minutes up to 4 

hours, then every 1-4 hours as needed. 

(b) Alternative agents include terbutaline (parenteral formulation), bitolterol, and pirbuterol. 

These agents do not appear to provide any clear advantage over albuterol, although pediatric ,~ 

experience with bitolterol and pirbuterol is limited. Because of its lack of ~ 2 

-agonist specificity, 

metaproterenol is no longer recommended as a first-line agent. Albuterol is also available as an 

isomer (levalbuterol); compared with albuterol, less frequent dosing may be possible, and it may 

produce less direct effect on ~ 1 

-adrenergic receptors and/or fewer cardiac adverse effects, but 

these claims have not been consistently demonstrated in clinical trials.


(3) Parenteral adrenergic therapy is a useful adjuvant to ongoing aerosolized therapy for the very sick 

(those with a decreased level of consciousness) and the very young who may not be able to provide 

the necessary inspiratory effort or cooperate. Alternatives include: 

(a) Epinephrine (1 :1,000 solution) 

i. 0.01 mg/kg (up to 0.5 mg) SC every 20 minutes for 3 doses 

ii. IM route has more consistent and rapid absorption than SC route. 

(b) Terbutaline (1 mg/ml) 

i. Preferred agent because it is ~ 2 

-selective 

ii. 0.005-0.01 mg/kg (up to 0.4 mg) SC every 20 minutes for 3 doses, then every 2-6 hours 

as needed 

(4) Corticosteroids are useful in treating the inflammatory aspect of asthma. When administered early, 

they prevent progression of the illness and decrease the rate of relapse. 

(a) Administer these agents as soon as it is clear that they are indicated: 

i. All patients with moderate to severe exacerbations (administer them along with initial 

~ 2 -agonist therapy) 

ii. Those patients with mild exacerbations who: 

• Do not clear completely with initial ~ 2 

-agonist therapy 

(b) Dosage 

• Have recently discontinued an oral steroid preparation 

i. Methylprednisolone 1-2 mg/kg IV or orally or 

ii. Prednisolone 1-2 mg/kg orally or 

iii. Prednisone 1-2 mg/kg orally or 

iv. Dexamethasone 0.6 mg/kg IV, IM, or orally 

(c) Liquid prednisone/prednisolone/dexamethasone is absorbed rapidly; therefore, unless the 

patient is vomiting or in severe distress, there is no advantage to IV or IM administration of 

corticosteroids. 

(d) Patients who receive prednisone or prednisolone in the emergency department and are 

subsequently discharged should be continued on oral steroids at a dosage of 1-2 mg/kg/day x 5 

days. Patients who receive dexamethasone should receive one additional dose in 1-2 days 

(longer half-life). 

(5) lpratropium bromide is an inhaled anticholinergic agent that, when used in combination with a 

~-adrenergic agonist, exhibits an additive effect by reducing bronchoconstriction and decreasing 

mucus production. In patients with severe exacerbations, ipratropium should be added to the first 

three ~ 2 

-agonist treatments; dose is 250-500 mcg via nebulizer or 4-8 puffs via a metered-dose 

inhaler. 

(a) lpratropium bromide 0.25 mg/dose in 2 ml normal saline every 20 minutes for three doses, then 

every 2-4 hours (agent of choice) 

(b) Atropine is associated with a high incidence of adverse effects and is rarely used. 

(6) Magnesium sulfate acts as a smooth muscle relaxant and improves FEV 1 

by 10%; dosage is 25-75 

mg/kg IV over 20 minutes. 

(7) leukotriene modifiers are potent inflammatory mediators that play an important role in outpatient 

therapy but have not yet been shown to have a role in the acute exacerbation of asthma. Their 

bronchodilating effects are additive to those of ~ 2 

-agonists, but further research is needed to investigate 

their role in acute asthma management. 

(8) Methylxanthines are no longer recommended for routine management of acute asthma. 

(9) Heliox (a mixture of helium and oxygen) should be considered for children with severe exacerbations 

and/or impending respiratory failure. By virtue of its lower density than that of air, it reduces airway 

resistance and, in turn, the work of breathing. It can provide additional time for first-line agents to take 

effect and so may avert intubation in these patients. 

(10) High flow humidified oxygen via nasal cannula may also be used with similar results. 

(11) Noninvasive positive-pressure ventilation (CPAP or Bi PAP) may successfully avert the need for intubation. 

(12) Ketamine is the agent of choice for patients in respiratory failure who require intubation because of 

its bronchodilatory effects. 

(13) Ventilator settings for intubated asthmatics should reflect a strategy of "permissive hypercapnia" 

(controlled hypoventilation) to minimize airway pressures and reduce the potential for barotrauma; use 

a tidal volume of 5-8 ml/kg in these patients. 

517


518 

A. The febrile child 

1. Pathophysiology of fever production: exogenous agents (bacterial endotoxins, antigen-antibody complexes) -;, 

formation and release of endogenous pyrogens (interleukins, tumor necrosis factor) - prostaglandin synthesis 

- raises the body's thermostatic set point - chills - shivering, peripheral vasoconstriction, behavioral 

activities (cover with blanket, put on a coat, etc) - increase in body temperature 

2. Heat loss occurs secondary to 

a. Radiation (60%) 

b. Evaporation (25%) 

c. Convection (1 0%) 

d. Conduction (5%) 

3. Temperature assessment 

a. A rectal temperature is the most accurate and is, therefore, the gold standard and preferred route in almost 

all infants


c. Aspirin is also effective, but is associated with Reye syndrome and should, therefore, be avoided. 

d. A tepid water (not alcohol) sponge bath may also be helpful. 

B. Bacteremia and sepsis 

1. Occult bacteremia = fever and positive blood culture in a well-appearing child without a major focus of 

infection 

a. Most common organisms 

(1) Streptococcus pneumoniae 

(2) Neisseria meningitidis 

(3) Haemophilus influenzae 


(5) Group A streptococci 

(6) Salmonella spp 

b. Although children 3-36 months old are at risk of developing occult bacteremia, those 6-24 months old are 

most commonly affected; children 24 

months old are more immunocompetent. 

c. Since the introduction of the heptavalent pneumococcal conjugate vaccine in 2000 and the vaccine for 

H influenzae, the prevalence of bacteremia continues to decline (current risk ~ 1 %-2%). This is resulting in 

a reconsideration of occult bacteremia evaluation and management. 

d. Historically, the risk of occult bacteremia is increased in the presence of: 

(1) WBC count 2:l 5,000/mm 3 

(2) Temperature 2:102.2°F (39.4°C) 

(3) Absolute band count >1,500 

(4) Presence of toxic granulations or vacuolization of PMN leukocytes on peripheral smear 

e. Occult bacteremia is associated with a risk of progression to a major focus of infection (such as meningitis). 

(1) The risk of progression varies with the infecting organism. 

(2) It is much greater with H influenzae and N meningitidis than with S pneumoniae. 

2. Systemic inflammatory response system (SIRS)/sepsis/severe sepsis/septic shock 

a. Definitions 

(1) SIRS 

(a) Widespread inflammatory response secondary to infection or other physiologic stressor 

(b) SIRS criteria (must have two or more, at least one of which is temperature or WBC count) 

I. Temperature> 101 °F (38.5°C) or 95th percentile of normal for age; for children 10% immature neutrophils) 

(2) Sepsis: SIRS in the presence of or as a result of suspected or proven infection 

(3) Severe sepsis: sepsis plus one of the following: 

(a) Cardiovascular organ dysfunction 

(b) ARDS 

(c) Two or more organ dysfunctions 

(4) Septic shock: sepsis plus cardiovascular organ dysfunction 

b. Most common organisms 

(1) Neonatal period (0-4 weeks) 


(b) Escherichia coli 

(c) Listeria monocytogenes 

(2) Infancy and early childhood 

(a) 5 pneumoniae (declining due to vaccine) 

(b) N meningitidis 

(c) S aureus (methicillin susceptible and methicillin resistant) 

(d) H influenzae (almost eliminated because of vaccination) 

519


C. Meningitis 

c. Sickle cell disease/trait is associated with an increased risk of sepsis, particularly from encapsulated organisms 

such as 5 pneumoniae (400-fold increased risk), Neisseria, and H influenzae (5-fold increased risk). "-/ 

d. Septic infants (


,,--. 

(3) Children >2 months 

(a) 

Ceftriaxone 1 00 mg/kg IV, or 

(b) Cefotaxime 50 mg/kg IV 

(c) If gram-positive cocci are identified on Gram stain of the CSF and there is concern regarding 

the presence of cephalosporin and penicillin-resistant strains of 5 pneumoniae in the area, 

vancomycin 15 mg/kg should be added to the above regimens in this age group. 

b. Corticosteroid therapy 

(1) Steroids neutralize the host response to bacterial cell lysis (because of their anti-inflammatory properties). 

(2) When dexamethasone is administered early, it is controversial whether it effectively decreases the 

incidence of neurologic sequelae (eg, sensorineural hearing loss) in children with bacterial meningitis 

due to H inf/uenzae or S pneumoniae. 

(3) Dexamethasone (0.15 mg/kg) can be administered before antibiotic therapy in children 2:6 weeks old 

with suspected bacterial meningitis due to H influenzae or S pneumoniae (although there is no clearcut 

benefit of steroids in pneumococcal meningitis). 

c. Antiviral therapy: acyclovir (10 mg/kg IV every 8 hours) should be administered if there is any clinical 

suspicion that the infant has herpes meningoencephalitis, eg, maternal herpes, bloody CSF, focal seizures. 

d. Indications for antimicrobial chemoprophylaxis for meningococcal disease 

(1) All intimate contacts of patients 

(2) Prehospital and hospital personnel with direct exposure to respiratory secretions 

(3) All daycare/nursery school contacts of these children 

e. Chemoprophylaxis regimens 

D. Pneumonia 

(1) Rifampin 

(a) Infants 1 month: 10 mg/kg orally every 12 hours x 2 days 

(c) Adults: 600 mg orally every 12 hours x 2 days 

(2) Ciprofloxacin 500 mg orally once 

(3) Azithromycin 10 mg/kg orally once (maximal dose 500 mg) 

1. Epidemiology and pathophysiology 

a. Incidence is greatest in children 6-12 months old and decreases with age. 

b. Principal route of acquisition is aspiration of infectio~s particles into the lower respiratory tract. 

2. Etiology 

a. The principal organisms responsible for producing pneumonia in children vary with: 

(1) Age 

(2) Immunization status 

(3) Comorbid conditions 

(4) Daycare attendance 

b. Most pneumonias in children (60%-90%) are caused by viruses; it is only in the newborn period that 

bacterial pathogens predominate. 

(1) Respiratory syncytial virus is the most common viral agent. 

(2) 5 pneumoniae remains the predominant bacterial pathogen in all age groups beyond the newborn 

period (although the 13-valent protein-polysaccharide pneumococcal conjugate vaccine is changing 

this). 

(3) Introduction of the H inf/uenzae B vaccine has resulted in a significant decline in the incidence of 

infection due to H influenzae. 

c. Common causes of pneumonia in children by age (listed in decreasing order of frequency) are the 

following: 

(1) Newborns 0-2 weeks old 


(b) E coli 

(c) Klebsiella pneumonia 

(d) Listeria monocytogenes 

521


(2) Infants 2 weeks to 3 months old 

(a) Viruses (respiratory syncytial virus, parainfluenza, human metapneumovirus) 

(b) Chlamydia trachomatis 

(c) 5 pneumoniae 

(d) H influenzae 

(e) 5 aureus 

(3) Children 3 months to 4 years old 

(a) Viruses 

(b) 5 pneumoniae 

(c) H influenzae (non-type B where vaccine not prevalent) 

(d) Mycoplasma pneumoniae 

(4) Children 5-18 years old 

(a) Mycoplasma pneumoniae 

(b) Viruses 

(c) 5 pneumoniae 

3. Clinical pictures associated with specific infecting organisms 

a. Viral pneumonia: a child presents with a history of preceding upper respiratory infection symptoms (often 

with an exanthem), followed by gradual onset of lower respiratory tract symptoms and a low-grade fever. 

b. Bordetella pertussis: an afebrile infant with a 1-2 week history of mild upper respiratory tract symptoms 

and cough now presents with a severe paroxysmal cough and inspiratory whoop that is frequently 

followed by post-tussive emesis. 

c. Mycoplasma pneumonia: familial spread of a respiratory tract infection over a long period of time in a 

school-aged child with a nonproductive hacking cough, inspiratory rales, and multiple-organ involvement 

(pharyngitis, bullous myringitis, otitis media). 

d. Chlamydia pneumonia: an infant 2-16 weeks old has a "staccato" cough, is tachypneic, and usually 

afebrile; there is often a history of conjunctivitis and nasal congestion. 

e. Pneumococcal pneumonia: an older child with abrupt onset of high fever, cough, and tachypnea; chest 

radiograph often has focal findings. 

f. Staphylococcal pneumonia: a child with radiographic findings of pneumothorax and empyema (or 

pyopneumothorax) 


a. Pulse oximetry (to check for hypoxia) 

b. Chest radiograph (mainstay of diagnosis) 

(1) Useful in confirming the diagnosis and identifying complications 

(2) May provide a clue as to the underlying cause of the pneumonia. Although there is considerable 

variability, a diffuse interstitial pattern suggests a viral or chlamydia! infection, while alveolar infiltrates 

in a lobar distribution are more consistent with a bacterial infection. Pyopneumothorax suggests 

staphylococcal pneumonia. 

c. CBC (nonspecific) 

(1) High WBC count with a left shift suggests bacterial pneumonia. 

(2) Lymphocytosis is common with viral, chlamydia!, and pertussis pneumonia; a WBC count of 

15,000-40,000/mm 3 with a marked lymphocytosis is characteristic of pertussis. 

(3) Normal WBC count and differential is typical of mycoplasmal pneumonia. 

(4) WBC count


f. Apnea in infants 

g. Underlying medical problems, immunodeficiency 

h. Presence of complications (pneumatocele, pleural effusion, empyema, pneumothorax) 

i. Unresponsive to outpatient therapy 

j. Unreliable caregiver 

6. Management 

a. Viral pneumonia will resolve without specific antibiotic therapy and may be treated with supportive 

measures alone when the diagnosis is clear. 

b. Bacterial pneumonia necessitates specific antimicrobial therapy that is based on the child's age and the 

likely pathogens seen in that age group. Because it is difficult to exclude bacterial disease with certainty on 

initial presentation, antibiotics are usually prescribed if the clinical picture suggests a treatable etiology. 

c. Antibiotic therapy for bacterial pneumonia 

(1) Newborns


E. Pertussis (whooping cough) 

1. Etiology 

a. Bordetella pertussis (a gram-negative coccobacillus) is a highly contagious infection caused by inhalation of 

contaminated droplets. 

b. Incubation period is 6-20 days with a mean of 7-10 days. 


a. Pertussis is seen primarily in nonimmunized or partially immunized children and adolescents but is also 

seen in adults because the immunization series does not guarantee life-time protection. 

b. Boosters are recommended in adults who have close contact with infants


infection, and when it occurs in the presence of bacterial colonization of the nasopharynx, the stage is set 

for the development of middle ear infection. 

b. Obstruction of the eustachian tube----;. negative pressure in the middle ear and development of a sterile 

effusion - aspiration of nasopharyngeal secretions in the middle ear - acute otitis media 

c. Infants have short, more horizontal (and more easily collapsible) eustachian tubes than older children. 

These anatomic differences predispose infants to eustachian tube obstruction and reflux of oropharyngeal 

secretions, thereby placing them at greater risk of development of acute otitis media. 

2. Etiology 

a. Streptococcus pneumoniae (30%-40%) 

b. Moraxella catarrhalis (25%) 

c. Nontypeable Haemophi/us influenzae (20%) 

d. Streptococcus pyogenes group A (3%) 

e. Staphylococcus aureus, group B streptococci, and gram-negative enteric bacilli (may be seen as pathogens 

in the neonatal period but are otherwise uncommon) 

f. Viral infection is probably the most common cause. 


a. The most reliable sign of acute otitis media is decreased mobility of the tympanic membrane on pneumatic 

otoscopy. 

b. Other findings include abnormal erythema, distortion or bulging of the tympanic membrane, or loss of 

bony landmarks. 

4. Selection of antibiotics 

a. Some clinicians recommend withholding antibiotics in older children with mild signs and symptoms 

for 2-3 days when a virus is the suspected agent. Because most of these infections are self-limited, this 

reduces overtreatment and development of resistance. 

b. Amoxicillin 80-90 mg/kg/day (divided bid) is still the drug of choice. 

c. If J3-lactamase-producing H influenzae or M catarrhalis is suspected or documented, amoxicillinclavulanate 

or cefuroxime is preferred. 

d. Treatment failure with use of the above agents for 3 days necessitates the use of one of the following broadspectrum 

antibiotics: 

(1) Amoxicillin-clavulanate 40 mg/kg/day divided bid 

(2) Azithromycin suspension 10 mg/kg as a single dose on day 1, then 5 mg/kg on days 2-5 

(3) Cefuroxime axetil 30 mg/kg/day divided bid 

(4) Cefpodoxime proxetil 10 mg/kg/day divided bid 

(5) Cefdinir 14 mg/kg/day (can be divided bid) or clarithromycin 15 mg/kg/day divided bid 

(6) Ceftriaxone 50 mg/kg in a single IM dose is particularly useful if vomiting, compliance, or follow-up is 

a problem. 

Table 34: Recommended Antibiotics for Treatment of Otitis 

Initial Antibiotic Treatment 

Failure of Initial Antibiotic Treatment 

First-line 

Alternative 

(penicillin-allergy) 

First-line 

Alternative 

Amoxicillin 

Cefdinir or 

cefuroxime 

Amoxicillinclavulanate 

Ceftriaxone, cl i ndamyci n, 

with or without thirdgeneration 

cephalosporin 

Amoxicillinclavulanate 

Cefpodoxime or 

ceftriaxone 

Ceftriaxone 

Clindamycin plus thirdgeneration 

cephalospori n 

Tympanocentesis 

Consult specialist 

525


5. The possibility of systemic infection should be considered in infants with acute otitis media who have a fever 

and appear toxic (particularly those



a. Urinalysis 

(1) Specimen collection 

(a) In infants and young children, specimens should be obtained by bladder catheterization or 

suprapubic aspiration; bag specimens are often contaminated and are, therefore, unreliable. 

(b) In older children who are toilet-trained, an appropriately collected midstream clean-catch 

specimen is adequate. 

(2) Pyuria (> 10 WBCs per high-power field of spun urine) is suggestive of UT! but not diagnostic (also 

occurs in association with other inflammatory processes). 

(a) Renal causes 

i. Pyelonephritis (WBC casts on urinalysis) 

ii. Perinephric abscess 

iii. Acute glomerulonephritis (RBCs, RBC casts, and proteinuria) 

(b) Extrarenal causes 

i. Appendicitis 

ii. Vulvovaginitis 

iii. Vaginal foreign body 

iv. Gastroenteritis 

v. Dehydration 

vi. Sexually transmitted infections 

(3) Bacteriuria is a more reliable finding; there is a 95% probability of infection with 100,000 colonyforming 

units/ml. Presence of any bacteria on Gram stain of a noncentrifuged specimen is the best 

combination of high sensitivity and a low false-positive rate. 

(4) Nitrite test: detects nitrites produced by the reduction of dietary nitrates by urinary gram-negative 

bacteria (especially£ coli, Klebsiella spp, and Proteus spp) 

(a) 

Positive test is virtually diagnostic for UTI (high specificity). 

(b) False-negative results are common (low sensitivity). 

(5) Leukocyte esterase test 

(a) 

Detects esterases released from degraded leukocytes (an indirect test for WBCs) 

(b) Poor sensitivity and specificity for UTI 

b. Urine culture confirms the diagnosis and should be sent for: 

(1) Females


a. Infants and children are affected most commonly; 80% of cases occur in children 1.5 cm) that is usually unilateral occurs in 50%-75% 

of cases. 

c. Findings cannot be attributed to another disease process. 

4. Incomplete (atypical) Kawasaki disease 

a. Diagnostic criteria include fever for >5 days plus 

(1) Two or three of above characteristics 

(2) C-reactive protein >3 mg/dl, and erythrocyte sedimentation rate >40 mm/hr 

b. Management is determined by echocardiogram findings. 

5. Disease course is divided into three phases. 

a. Acute phase (days 1-11) 

(1) Characterized by fever and most of the other diagnostic features described above 

(2) Myocarditis is the most common cause of death during this time. 

b. Subacute phase (days 11-20) 

(1) Characterized by gradual resolution of fever, rash, and adenopathy, as well as the development of 

thrombocytosis and periungual desquamation 

(2) Risk of developing coronary artery thrombosis is greatest at this time. 

(3) Causes of death include myocardial infarction, aneurysm rupture, and myocarditis. 

c. Convalescent phase (days 21-60) 

(1) Begins when all signs and symptoms have disappeared and continues until the erythrocyte 

sedimentation rate and platelet count have normalized. 

(2) Death may occur from myocardial infarction secondary to thrombosis. 


a. ECG 

b. Echocardiography (to assess cardiac status) 

c. Chest radiograph 

d. CBC with platelet count 

(1) Moderate leukocytosis with left shift (acute phase) 

(2) Mild normochromic, normocytic anemia 

(3) Increased platelet count (subacute phase) 

e. Erythrocyte sedimentation rate increased 

f. C-reactive protein increased 

g. Serum transaminases mildly increased 

h. Urinalysis 

528


(1) Sterile pyuria (WBCs without bacteria) 

(2) Proteinuria 

1. Studies to exclude other diagnoses (streptococcal culture, blood culture, ASO titer, etc) 

7. Management 

a. Hospital admission (unit chosen depends on the extent of cardiac findings) 

b. Early consultation with a pediatric cardiologist 

c. IV immunoglobulin 

(1) Dosage is 2 g/kg over 1 0-12 hours. 

(2) When administered early in the illness (within 10 days of onset), it decreases systemic inflammation 

and the prevalence of coronary artery aneurysms. 

d. Oral aspirin 

(1) Anti-inflammatory dosage (80-100 mg/kg/day divided qid) during the acute phase 

(2) Antithrombotic dosage (3-5 mg/kg/day as a single dose) during the subacute and convalescent phases 

e. Steroids are not indicated and may increase the risk of coronary aneurysm development. 


a. Cardiovascular (most important) 

(1) A child's prognosis and outcome are primarily determined by the cardiac complications of Kawasaki 

disease. 

(2) Coronary artery aneurysms and ectasia develop in 20%-30% of untreated children; those


g. Treatment is directed at lowering the fever and identifying any underlying infection. 

h. Seizures recur in 30%-40% of children; more likely when the first febrile seizure occurs before 1 year old. 

i. Prophylaxis with phenobarbital is not routinely recommended; although it is the drug of choice, it has not 

been shown to be of significant benefit and interferes with cognitive functioning. 

2. Generalized tonic-clonic seizures 


(1) Both hemispheres are involved. 

(2) Motor involvement is bilateral. 

(3) Consciousness is impaired. 

(4) Patients are confused and lethargic during the postictal period. 


(1) Includes a directed history (description of the seizure and surrounding events, pertinent past medical 

history) and a complete physical examination 

(2) No role for routine laboratory or radiographic evaluation unless suggested by the history and physical 

examination. 

(3) Tests ordered should reflect the child's age and suspected cause of the seizure as suggested by the 

history and physical examination. 

(a) Electrolytes 

(b) Toxicology screening 

(c) Anticonvulsant medication serum levels (if applicable) 

(4) Indications for a CT scan of the head 

(5) MRI 

(a) Focal neurologic deficits 

(b) Signs of increased intracranial pressure 

(c) Infants 80% of seizures. Use one of the following: 

(a) Lorazepam 0.1 mg/kg IV is the preferred agent; it has a long half-life and the least effect on 

respiratory depression. 

(b) Diazepam 0.2-0.3 mg/kg IV may be used if lorazepam is unavailable; it has a much shorter halflife 

and produces a greater respiratory depression. 

(c) Midazolam 0.2 mg/kg IM or intranasal should be considered when IV access cannot be rapidly 

attained; it works as rapidly by this route as by the IV route but is very short acting. 

(d) Diazepam 0.5 mg/kg may also be given rectally if IV access cannot be attained and midazolam is 

unavailable; when administered via this route, its onset of action is ~5 minutes. 

(2) If seizure activity persists despite administration of a benzodiazepine, fosphenytoin (15-20 phenytoin 

equivalents [PE]lkg diluted in normal saline and infused at a rate ::'.50 mg/min) or phenobarbital (15-20 

mg/kg infused at a rate of 25 mg/min) should be administered. 

(3) Children presenting with their first afebrile, unprovoked seizure who make an uneventful recovery 

need not be treated with a long-term anticonvulsant unless they presented in status epilepticus. The 

rate of seizure recurrence in these children is quite variable; risk of recurrence within 1 year is ~25%; 

children with an underlying neurologic disease have a much higher recurrence rate (16%-62%), and 

the adverse effects associated with anticonvulsant therapy are significant. Therefore, it is recommended 

that anticonvulsant therapy be withheld until a second seizure occurs in these patients. 

(4) Most breakthrough seizures are a result of subtherapeutic drug levels or noncompliance. 

(5) Referral is generally indicated for ongoing monitoring. 

530


3. Infantile spasms 

a. Definition: convulsive disorders of infants and young children with onset between 3 and 9 months old and 

accompanied by developmental regression 


(1) Spasms last only a split second and are associated with flexion or extension of the head and trunk. 

(2) Spasms may occur as a single event or in groups of 5-20 at a time. 

c. Electroencephalogram is almost always abnormal with hypsarrhythmia (a slow irregular rhythm) being 

present in 50% of cases. 

d. Management includes admission and a neurologic consult. 

B. Differential diagnosis 

1. Syncope 

2. Pseudoseizure 

3. Breath-holding spells 

4. Movement disorders (eg, tics) 

5. Night terrors 

6. Cardiac dysrhythmias 

7. Complicated migraines 

C. Etiology 

1. Infectious 

a. Meningitis/encephalitis 

b. Herpes simplex virus 

c. Bacterial meningitis 

d. Parasitic encephalitis 

2. Metabolic 

a. Hypoglycemia 

b. Hypo- or hypernatremia 

c. Hypocalcemia 

d. Hypoxia 

e. Pyridoxine deficiency 

3. Inborn errors of metabolism 

4. Traumatic 

5. Neoplastic 

6. Drug-related (intoxication or withdrawal) 

7. Child abuse (eg, shaken baby syndrome) 

8. Miscellaneous 

a. Congenital malformations 

b. Ventriculoperitoneal shunt malfunction 

c. idiopathic 

D. Adverse effects of medications used in management of pediatric seizures 

1. Phenytoin: gum hyperplasia, hirsutism, and drug rashes (Stevens-Johnson syndrome) 

2. Phenobarbital: lethargy, hyperactivity, and behavioral disorders 

3. Carbamazepine: neutropenia, rashes, hepatic dysfunction, and cardiac toxicity 

4. Valproic acid: thrombocytopenia, pancreatitis, hepatic failure, and a bleeding diathesis when used in 

conjunction with aspirin 

VIII. CEREBROSPINAL FLUID SHUNTS 

A. Shunt systems 

1. Generally consist of a ventricular catheter, a valve device, and distal tubing 

2. Ventriculoperitoneal shunts are the most common type, accounting for >90% of the shunts currently in use. 

3. Ventriculoperitoneal shunts allow CSF to be diverted around obstructed areas in the subarachnoid space or 

ventricles. 

531


4. Conditions that result in hydrocephalus and require CSF shunt placement include: 

a. Congenital stenosis of the aqueduct of Sylvius 

b. Acquired aqueductal stenosis or scarring secondary to infection 

c. Malignancy or hemorrhage 

d. Dandy-Walker malformations 

e. Arnold-Chiari syndrome 

5. Shunt failure is common; it can result from: 

a. lntracranial infection or blockage 

b. Valve malfunction 

c. Distal tubal obstruction or disruption 

d. Pseudocyst formation or disruption 

B. Complications 

1. Shunt malfunction 

a. Obstruction 

(1) Most common cause of shunt malfunction 

(2) Results from blockage to flow anywhere along the shunt system and may be caused by kinking, 

thrombosis, disconnection, migration, or infection of the catheter. 

(3) Patients present with signs of increased intracranial pressure. 

(a) Headache with mental status changes and associated nausea and vomiting are the classic 

symptoms. Other clues include: 

i. Seizures while on therapeutic medication doses 

ii. Poor sucking or feeding 

iii. Paradoxical crying 

(b) Findings on physical examination 

i. Upward gaze palsy ("sunsetting" or "sundowning") 

ii. Diplopia 

iii. Bulging fontanelle 

iv. Enlarging head 

v. Cushing triad of bradycardia, hypertension, and respiratory ataxia (preherniation syndrome) 

(4) If left untreated, it can result in herniation. 

b. Slit ventricle syndrome 

(1) Results from chronic overdrainage of CSF with collapse of the ventricles and transient obstruction of 

CSF flow; overdrainage __,. col lapse of the ventricles and catheter obstruction __,. increased intracranial 

pressure__,. reexpansion of the ventricular system and relief of catheter obstruction 

(2) Symptoms are those of an intermittently increased intracranial pressure. 

(a) Episodic minor headache associated with reduced performance and intervening asymptomatic 

periods are characteristic. 

(b) Severe headache, nausea, vomiting, and bradycardia progressing to obtundation may occur with 

more severe presentations. 

(3) CT reveals small ventricles. 

(4) Placement of the patient in Trendelenburg position frequently relieves these symptoms. 

(5) Definitive treatment involves placement of an antisiphon device. 

c. Evaluation of shunt malfunction 

(1) Locate the shunt and trace its course, looking for evidence of infection and palpating for 

disconnections. 

(2) Obtain a shunt survey (plain radiographs of the entire shunt system) to exclude kinks and breaks in 

the catheter. 

(3) Compress the subcutaneous shunt reservoir and pumping chamber to evaluate ease of pump 

compression/refill (may be helpful but should not be used to exclude shunt dysfunction). 

(a) When functioning normally, the chamber refills in


(4) Determine ventricular size via CT scanning, and compare the results with those of prior studies to see 

if there has been a change. In infants with open fontanelles, ventricle size can also be assessed by 

ultrasound. Again, comparative studies are necessary. 

(a) Enlarged ventricles indicate obstruction. 

(b) Smaller or slit ventricles are consistent with overdrainage. 

(5) In difficult cases, radionuclide shunt clearance scans or MRI may be helpful. 


2. Shunt infections 

(a) Obtain urgent neurosurgical consult. 

(b) If seizures are secondary to increased intracranial pressure, manage as appropriate. 

a. 60% of the mortality that occurs in association with shunts is due to shunt infections. 

b. Most infections (75%) occur within the first 2 months after shunt placement and are caused by 

S epidermidis and 5 aureus. 

c. Resulting shunt obstruction that leads to increased intracranial pressure is common. 


(1) Fever is the most common symptom of shunt infection. 

(2) Other findings 

(a) Nausea, vomiting, headache, and feeding problems 

(b) Meningismus 

(c) A subtle change in behavior as detected by the parents 

(3) Signs of increased intracranial pressure 


(1) Examine the course of the shunt looking for evidence of infection; although this is very specific for 

shunt infection, it is not sensitive. 

(2) Obtain laboratory studies. 

f. Management 

(a) CBC with differential (may be normal) 

(b) Blood culture 

(c) CSF from the shunt (consult with neurosurgeon) for evaluation of samples for cell count and 

differential, glucose, Gram stain, protein, and culture and sensitivity 

(1) Obtain urgent neurosurgical consult, and admit these patients to the hospital for antibiotic therapy (IV 

and/or intraventricular) and externalization of the shunt. 

(2) Shunt removal and replacement is required in 50% of patients. 

IX. PEDIATRIC GASTROINTESTINAL/GENITOURINARY 

EMERGENCIES 

A. Abdominal conditions associated with rectal bleeding 

1. Infectious colitis: infection with the organisms listed below can result in bloody diarrhea. 

a. Shigella 

b. Salmonella 

c. Enteroinvasive E coli 

d. Campylobacter jejuni 

e. Yersinia enterocolitica 

f. C!ostridium difficile 

g. Entamoeba histolytica 

h. Enterohemorrhagic E coli serotype O157:H7 

2. Painless rectal bleeding 

a. Anal fissure (most common cause in infants) 

b. Swallowed maternal blood 

(1) Occurs in infants


c. Meckel's diverticulum 

d. Infectious gastroenteritis 

e. Juvenile polyps 

3. Meckel's diverticulum can produce a variety of signs and symptoms. 

a. It is a true diverticulum (all layers of the bowel wall are present) and can contain a variety of heterotopic 

tissue, of which gastric mucosa is the most common. 

b. Painless rectal bleeding (which can be massive) is the most common presentation of this congenital 

anomaly in children



(1) Plain radiographs should be obtained first. 

(a) Findings 

i. An abdominal mass or filling defect in the right upper quadrant 

ii. Signs of bowel obstruction 

iii. Free intraperitoneal air 

(b) Normal plain radiographs do not exclude the diagnosis. 

(2) Ultrasound evaluation is a quick and sensitive modality to identify an intussusception. However, air 

insufflation and barium enema are the preferred diagnostic and treatment studies. 

(a) Air-contrast is as effective as barium in reducing the intussusception and has replaced the 

barium enema as the study of choice in most major medical centers; successful reduction occurs 

in 60%-80% of cases. 

(b) If barium enema is performed, the classic finding of a "coiled spring" appearance may be seen 

on the evacuation radiograph. 

e. Operative intervention is required for patients in whom the intussusception cannot be reduced by air 

insufflation or barium enema. 

f. Recurrence rate is 5%-10% after barium enema reduction and 2%-5% after surgical reduction, with most 

recurrences occurring in the first 24 hours after reduction. 

B. Abdominal/genitourinary conditions not associated with rectal bleeding (these are all surgical mergencies) 

1. Incarcerated hernia 


(1) Common in children



(1) Nonbilious projectile vomiting after feeding, after which the infant usually hungrily re-feeds 

(2) Evidence of dehydration and failure to thrive 

(3) Prominent peristaltic waves (sometimes) 

(4) Palpable olive-shaped mass (the hypertrophied pylorus) in the right upper quadrant (pathognomonic) 

(5) Jaundice (~5% of cases) 


(1) When the "olive" can be palpated, the diagnosis is established and further diagnostic studies are 

unnecessary. 

(2) When the "olive" cannot be palpated, ultrasound is the diagnostic study of choice; a hypoechogenic 

ring with a hyperdense center that resembles a "doughnut" or "bull's-eye" can be seen. 

(3) If the ultrasound is unavailable or negative, an upper GI series should be performed. Findings include 


(a) Delayed gastric emptying 

(b) Indentation of the antrum by the "olive" 

(c) Elongation of the pyloric channel (the "string" or "beak" sign) 

(4) Hypochloremic, hypokalemic metabolic alkalosis 

e. Management 

4. Appendicitis 

(1) Correct dehydration and electrolyte imbalance. 

(2) Restrict oral feedings. 

(3) Obtain early surgical consult; definitive treatment (once fluid and electrolyte balance have seen 

restored) is pyloromyotomy. 


(1) Most common nontraumatic surgical emergency in children 

(2) Peak incidence 9-12 years old 

(3) Rare in children 10,000 cells/mm 3 ) is associated with the presence of appendicitis but 

has poor sensitivity and specificity and no clinical utility. Urinalysis may reveal sterile pyuria if the 

inflamed appendix is overlying the ureter. 

(2) Chest radiograph with supine and upright abdominal films are helpful in excluding pneumonia 

presenting as abdominal pain; abdominal radiograph may demonstrate a fecalith (10% of cases), loss 

of psoas shadow, localized ileus in right lower quadrant. 

(3) Ultrasound may be diagnostic but is highly operator dependent. 

(4) CT scanning is used to confirm the diagnosis. 

d. Findings suggestive of perforation 

(1) High temperature (>102°F [39°Cl) 

(2) High WBC count(> 15,000/mm 3 ) 

(3) Symptoms >36 hours 

e. Management 

(1) IV fluid resuscitation 

(2) Antibiotics (ampicillin, gentamicin, and metronidazole or clindamycin; piperacillin/tazobactam or 

cefoxitin; meropenem if perforation) 


536


5. Testicular torsion 

a. General 

(1) Annual incidence 4.5 in 100,000 males 1-25 years old 

(2) Cannot be diagnosed by physical examination alone 

(3) Salvage rate: classically 80%-1 00% within 6 hours of onset and


4. Clues to the diagnosis 

a. Laboratory results do not "fit." 

b. Signs and symptoms do not respond to appropriate medical management. 

c. Signs and symptoms resolve when the child is separated from the perpetrator. 

5. Management 

a. Admit to hospital with continuous camera monitoring to assure safety. 

b. Institute appropriate therapy. 

c. Involve counseling and social services. 

C. Sexual abuse 

1. 20% of all girls and 9% of boys are sexually abused. The abuse has often occurred over a long period of time 

and, in 90% of cases, the perpetrator is well known to the child (eg, family member, relative). 


a. Best performed with the child supine in the frog-leg position or prone in the knee-chest position; can be 

augmented by the use of a hand-held lens or colposcope 

b. Suggestive findings 

(1) Hymenal notches (concavities), scars, or tears 

(2) Vaginal discharge 

(3) Genital ulcers, warts, or vesicles 

(4) Anal fissures, hematomas, or tears; perinea! bruising 

(5) Immediate reflex anal dilatation (>20 mm) in the absence of feces in the ampulla 

c. The absence of physical findings does not exclude abuse; they are present in only 10% of cases of 

documented sexual abuse. 

3. Laboratory evaluation 

a. Cultures (not antigen assays) of: 

(1) Vagina or urethra-,, for Neisseria gonorrhoeae or Chlamydia trachomatis 

(2) Rectum -,, for N gonorrhoeae 

(3) Throat-,, for N gonorrhoeae 

b. Serologic testing for syphilis 

c. HIV testing (after counseling) if infection is suspected 

d. Pregnancy test if appropriate 

4. Management 

a. Gonoccoccal prophylaxis: indicated if abuse occurred


d. "Bucket handle" fractures 

e. Rib fractures 

f. Untreated healing fractures 

g. Shaken baby syndrome 

(1) Usually presents as unexplained seizures, abnormal behavior, unresponsiveness, or respiratory distress 

(2) Triad of severe intracranial bleeding (subdural, intraparenchymal, interhemispheric, epidurallt retinal 

hematomas (present in 70%-90% of casest and no or minimal external signs of trauma 

(3) Symptoms are the result of increased intracranial pressure. 

(4) Associated posterior rib fractures are common. 

h. Complex skul I fractures 

i. Duodenal hematomas from abdominal trauma 

j. Cigarette burns 

k. Immersion burns in a "glove-and-stocking" pattern 


a. Laboratory evaluation is guided by findings on examination and includes CBC platelet count and 

prothrombin time (INR)/partial thromboplastin time when the examination reveals multiple bruises and 

when there is any suggestion by the caregiver of easy bruisability. 

b. Radiographic evaluation 

(1) A skeletal survey when evidence of trauma is noted 

(2) CT of the head when retinal hemorrhages or an acute deterioration in neurologic status is present 

(3) Abdominal/pelvic CT for abdominal wall bruising, unexplained vomiting or abdominal pain, shock, 

anemia, or abnormal liver function tests 

6. Management 

a. Complete history and physical examination with verbatim quotations if possible 

b. Suspected cases must be reported to the police and/or child protection services. 

c. Hospitalization or placement in protective custody may be necessary to protect the child from further harm. 

Other children in the household must also be evaluated. 

d. Failure to report a suspected case may lead to misdemeanor charges and further harm or death to the child 

who is returned to the abusive environment. 

539

PEDIATRIC EMERGENCIES: PRACTICE CLINICAL SCENARIOS 



Scenario A 

Presentation: A 4-year-old unimmunized child is sitting upright with chin thrust forward, mouth open, and 

neck slightly extended. He appears toxic and apprehensive and, on closer inspection, is drooling, with 

difficulty swallowing and stridor. The mother relates that the child was well until just a few hours ago, 

when he started to complain of a sore throat and developed a fever. 


Scenario B 

Presentation: A 2-year-old child has a barky, "seal-like" cough that the mother says is usually worse at 

night and sometimes causes severe respiratory distress. The child had a recent upper respiratory infection, 

and the cough, hoarseness, and stridor appeared just a few days after. The child does not have a fever and 

is nontoxic in appearance. 


Scenario C 

Presentation: A 2-year-old child has a high fever, stridor, and appears toxic. His mother reports that he has 

had nasal congestion, barking cough, and stridor for the past few days and then suddenly took a turn for 

the worse over the past few hours. 


Scenario D 

Presentation: A young child has had a mild fever, rhinorrhea, and conjunctivitis for the last week or 

two. She is now having numerous episodes of unremitting paroxysmal coughing followed by a "whoop." 

Vomiting often occurs in association with these paroxysms. 


540



Scenario A 

Diagnosis: epiglottitis 

Diagnostic evaluation: If there is only slight respiratory distress, the diagnosis can be confirmed with 

a portable lateral soft-tissue radiograph of the neck. Findings include the "thumb print sign" and 

mild hypopharyngeal distention. Evaluation of the epiglottis by using a tongue blade (or a fiberoptic 

bronchoscope) should be avoided in children with any respiratory distress. Definitive diagnosis is ideally 

made in the operating room under controlled conditions by direct visualization of the "cherry-red" 

epiglottis. This is particularly true when severe respiratory distress is present. 

Management: Disturb the child as little as possible to reduce anxiety, because he is at high risk of 

complete airway obstruction. Allow him to assume a position of comfort (usually sitting upright) and 

remain with his parents. Do not force him to lie supine. 

Provide supplemental humidified oxygen, set up airway stabilization equipment at bedside, and obtain 

immediate ENT and anesthesia consults. Once the airway has been stabilized, draw blood for laboratory 

studies (including cultures), and administer parenteral antibiotics (cefuroxime, cefotaxime, ceftriaxone, or 

ampicillin-sulbactam). Admit to ICU. 

Scenario B 

Diagnosis: croup 

Diagnostic evaluation: The diagnosis can often be made on clinical grounds, but radiographs can be useful 

to exclude epiglottitis. The PA neck radiograph may reveal symmetric subglottic narrowing of the tracheal 

air column ("steeple sign"), and the lateral neck radiograph may show a distended hypopharynx and 

subglottic narrowing. The epiglottis and retropharyngeal space are normal. 

Management: Management is supportive, including cool mist, oxygen as needed, hydration (orally or 

IV), racemic epinephrine aerosol, steroids (one dose), and heliox if croup is severe or respiratory distress 

continues despite steroids and epinephrine. Consider admission if the child has persistent stridor at rest, 

cannot tolerate oral fluids, or has an incomplete response to epinephrine treatment. 

Scenario C 

Diagnosis: bacterial tracheitis 

Management: Provide supplemental humidified oxygen, and obtain immediate consult with ENT and 

anesthesiology for endoscopy. Secure the airway, and obtain appropriate laboratory studies (including a 

Gram stain and culture of tracheal secretions). Administer IV hydration and antibiotics effective against 

Staphylococcus aureus. Admit to ICU. 

Scenario D 

Diagnosis: pertussis (whooping cough) 

Diagnostic evaluation: A chest radiograph may show peribronchial thickening or a "shaggy" heart border. 

If the primary illness is complicated by pneumonia, infiltrates may be seen. The WBC count is 35,000/mm3 

with a marked absolute lymphocytosis. The organism can be cultured using nasopharyngeal or sputum 

specimens, or detected with fluorescent antibody staining (or PCR) of a nasopharyngeal swab specimen. 

Management: Begin erythromycin or azithromycin therapy and provide supplemental oxygen and 

postural drainage. Admit if the child has hypoxia and cyanosis during coughing spells or apnea. Monitor 

for pulmonary (eg, pneumonia, pneumothorax, hypoxia) and neurologic (eg, seizures, encephalitis) 

comp I ications. 

541

542 

NOTES

TOXICOLOGIC DISORDERS 


General Approach to the Poisoned Patient ................................................................................................................ 547 

History ............................................................................................................................................................... 547 

Physical Examination ......................................................................................................................................... 547 

Toxidromes ......................................................................................................................................................... 548 

Major Toxic Signs ............................................................................................................................................... 550 


General Treatment Measures .............................................................................................................................. 553 

Other Complications .......................................................................................................................................... 556 

Specific Overdoses and Poisonings ........................................................................................................................... 557 

Cyclic Antidepressants ....................................................................................................................................... 557 

Other Antidepressants ........................................................................................................................................ 558 

Lithium ............................................................................................................................................................... 559 

Sedative-Hypnotics ............................................................................................................................................ 559 

Phenothiazines ................................................................................................................................................... 561 

Phenytoin ........................................................................................................................................................... 562 

Opioids .............................................................................................................................................................. 562 

Cioni dine ........................................................................................................................................................... 563 

Alcohols ............................................................................................................................................................. 563 

Cocaine .............................................................................................................................................................. 566 

Amphetamines and Amphetamine-Like Drugs .................................................................................................... 567 

Hallucinogens .................................................................................................................................................... 568 

Salicylates .......................................................................................................................................................... 569 

Acetaminophen .................................................................................................................................................. 570 

Iron .................................................................................................................................................................... 571 

Hydrocarbons .................................................................................................................................................... 572 

Caustic Ingestions ............................................................................................................................................... 574 

Organophosphates ............................................................................................................................................. 576 

Mushroom Poisoning .......................................................................................................................................... 578 

Cyanide .............................................................................................................................................................. 579 

Digitalis .............................................................................................................................................................. 579 

f3-Blockers .......................................................................................................................................................... 580 

Calcium Channel Blockers ................................................................................................................................. 581 

Carbon Monoxide .............................................................................................................................................. 581 

Mercury ............................................................................................................................................................. 582 

Sulfonylureas ...................................................................................................................................................... 583 

543

TOXICOLOGIC DISORDERS: SELF-ASSESSMENT QUESTIONS 


1. All of the following are causes of a cholinergic toxidrome except: 

(a) Organophosphates 

(b) Sarin 

(c) Cyclic antidepressants 

(d) Carbamates 

2. Which is true regarding the end-organ damage associated with untreated methanol poisoning? 

(a) 

Renal failure can be permanent and develops soon after overdose. 

(b) Blindness can take over 24 hours to develop. 

(c) Renal damage associated with overdose is generally limited to acute tubular nephrosis and resolves after 

aggressive IV fluid rehydration. 

(d) Funduscopic examination may reveal petechial hemorrhages. 

3. GI hemorrhage is characteristic of which toxic ingestion? 

(a) 

Lithium 

(b) Iron 

(c) Lead 

(d) Household bleach 

4. The antidote for iron poisoning is: 

(a) 

Dimercaprol 

(b) Deferoxamine 

(c) N-acetylcysteine 

(d) Calcium disodium edetate (EDTA) 

5. Severe salicylate poisoning (serum level ~100 mg/dl) requires which of the following treatments immediately? 

(a) 

N-acetylcysteine 

(b) Acidification of the urine 

(c) Administration of chelator 

(d) Hemodialysis 

6. Clinical findings that indicate a serious overdose of a cyclic antidepressant include all of the following except: 

(a) Ventricular dysrhythmias 

(b) Wide QRS complex 

(c) AV block 

(d) Hypertension 

7. All of the following would be appropriate for treatment of symptomatic organophosphate poisoning except: 

(a) 

Physostigmine 

(b) Benzodiazepines 

(c) Pralidoxime 

(d) Atropine 

8. A homeless man arrives at the emergency department appearing intoxicated. As part of his diagnostic evaluation, 

the following laboratory studies are ordered. What is this patient's serum osmolarity? 

Sodium 125 mmol/L BUN 2.8 mg/dL 

Potassium 3.1 mmol/L Creatinine 1.8 mg/dl 

Chloride 100 mmol/L Glucose 360 mg/dL 

CO 2 22 mmol/L Ethanol 0.207 g/L 

(a) 294 

(b) 288 

(c) 261 

(d) 271 

544


9. The treatment of choice for ventricular dysrhythmias secondary to phenothiazine overdose is: 

(a) Acidification of the urine 

(b) Sodium bicarbonate 

(c) Phenytoin 

(d) Procainamide 

10. Seizures commonly occur after overdose of which of the following? 

(a) Morphine 

(b) Tramadol 

(c) Oxycodone 

(d) Fentanyl 

11. Early signs and symptoms of ethanol withdrawal include: 

(a) 

Hypertension, tachycardia, and irritability 

(b) Diaphoresis and dehydration 

(c) Hypotension, bradycardia, and fever 

(d) Visual hallucinations and paranoid ideation 

12. Cocaine-induced cardiac dysrhythmias should be treated with any of the following medications except: 

(a) Benzodiazepines 

(b) Sodium bicarbonate 

(c) Calcium channel blockers 

(d) P-blockers 

13. An elderly patient who presents with unexplained CNS dysfunction and arterial blood gases that reveal a mixed 

acid-base disturbance should be suspected of having: 

(a) Chronic lithium poisoning 

(b) Acetaminophen poisoning 

(c) Chronic salicylate poisoning 

(d) Iron poisoning 

14. Indications for hemodialysis in patients with acute salicylate toxicity include all of the following except: 

(a) Severe acid-base imbalance 

(b) Increasing serum ASA levels despite aggressive therapy 

(c) Urine pH


18. Seizures are an indication for hemodialysis in all of the following poisonings except: 

(a) Digoxin 

(b) Lithium 

(c) Theophylline 

(d) Methanol 

19. Which of the following is potentially harmful if given to a fire victim with suspected cyanide poisoning? 

(a) Hydroxocobalamin 

(b) Supplemental oxygen 

(c) Amyl nitrate 

(d) Sodium thiosulfate 

20. Which of the following is false regarding button battery ingestions? 

(a) 

Immediate surgical consult should be obtained if GI tract perforation is suspected. 

(b) If radiography demonstrates the battery is lodged in the esophagus, immediate endoscopic removal is 

indicated. 

(c) If radiography demonstrates the battery has entered the stomach, the patient should be monitored on an 

outpatient basis until the battery has passed. 

(d) If radiography demonstrates the battery has entered the stomach, immediate endoscopic removal is indicated. 

21. Which is least appropriate for the management of asymptomatic pediatric sulfonylurea ingestions? 

(a) 

Frequent blood glucose testing (every 15-20 minutes) 

(b) Empiric administration of glucose 

(c) Thorough physical examination, looking for signs of hypoglycemia 

(d) Hospital admission 

ANSWERS 

1. C 

2. b 

5. 

6. 

d 

d 

9. 

10. 

b 

b 

13. C 17. b 

14. C 18. a 

3. b 7. a 11. a 15. b 19. c 

4. b 8. d 12. d 16. c 20. d 

21. b 



546


I. GENERAL APPROACH TO THE POISONED PATIENT 

A. History 

1. Determine the involved poison. 

2. Determine route of exposure: ingestion, inhalation/insufflation, injection, dermal, etc. 

3. Determine how much was taken and inquire about extended-release preparations. 

4. Determine when it was taken. 

5. Determine whether the exposure was accidental or intentional 

a. Consider child abuse in patients 5 years old. 

6. Determine what the patient was doing at the time he or she became ill. Examples: 

a. Fumigating a ship --,, cyanide 

b. Working in a garage--,, carbon monoxide, pesticides, toxic alcohols 

c. Applying chemicals to crops --,, organophosphates/carbamates 


Table 35: Physiologic Effects Associated with Specific Poisons 

Poison 

Cyclic antidepressants 

Barbiturates 

Phenothiazines 

(eg, chlorpromazine, 

prochlorperazine) 

Digitalis 

Opioids 

Clonidine 

Ethanol, ethylene glycol, 

methanol, isopropanol 

Cocaine 

t pulse" 

t blood pressure 

t respiration 


t respiration 

t temperature 6 

t pulse 


t temperature 

t pulse" 

.j, blood pressure 

t pulse 

t blood pressure' 

.J, respiration 

.j, temperature 

Vital Signs 

.j, pulse' 

t blood pressure early (uncommon), 

then .j, blood pressure later 

.J, respiration (uncommon) 

.j, temperature 

t pulse 


t respirationa, c 

t temperature 6 

t pulse 


t or t res pi ration 

t temperature 

Level of Consciousness 

t (mostly in children) 

547


Table 35: Physiologic Effects Associated with Specific Poisons (continued) 

Poison 

Amphetamines 

Phencyclidine (PCP) 

Salicylates 

Iron 

Liquid petroleum distillates 

(gasoline, kerosene) 

Anticholinergics 

Organophosphates/carbamates 

Sedative-hypnotics 

a Earliest sign 

t pulse 


t temperature 

t pulse 


t temperature 

t res pi ration 

t temperature" 


t pulse 

t respirationa 

t temperature 

t pulse" 

t temperature 


Vital Signs 

t pulse early", then t pulse later 

t or t blood pressure 

t res pi ration 

t 0 2 

saturation 

t pulse 


t temperatureb 

Level of Consciousness 

b Poisoning can cause cutaneous vasodilation, resulting in poikilothermia. Because the ambient temperature is generally lower than 

body temperature, the more common clinical manifestation is hypothermia. Be aware that poisoning while exposed to high ambient 

temperatures (eg, unconscious victim in a hot car) can manifest hyperthermia by the same mechanism. 

c Depressed respiratory rate is an early sign associated with intoxication by various alcohols. In cases of ethylene glycol and 

methanol poisoning, when metabolic acidosis may occur, hyperventilation may occur as a compensatory mechanism and is 

expected to be a later finding. 

C. Toxidromes 

1. Cholinergic (wet manifestations) 


(1) "DUMBBELS" 

_!2.iarrhea 

.!lrination 

Miosis 

_!!radycardia 

_!!ronchospasm/bronchorrhea 

fmesis 

.!,_acrimation 

Salivation 

(2) Seizures, coma, and respiratory failure 

(3) Muscle fasciculations and weakness 

b. Examples 

(1) Organophosphates 

(a) Insecticides (eg, parathion, diazinon) 

(b) Nerve agents (sarin, soman, VX) 

548


(2) Carbamates 

(a) Insecticides (eg, carbaryl) 

(b) Physostigmine, pyridostigmine (mostly peripheral symptoms) 

(3) Muscarine-containing mushrooms (Clitocybe, lnocybe) 

2. Anticholinergic (dry manifestations) 


(1) Mad as a hatter (delirium), hot as a hare (hyperthermia), blind as a bat (loss of ability to accommodate 

near vision and mydriasis), dry as a bone (dry mucous membranes, full as a flask (urinary retention), 

bloated as a toad (decreased bowel sounds/ileus), red as a beet (flushing), tacky as a leisure suit 

(tachycardia) 

(2) Seizures 

b. Examples 

(1) Cyclic antidepressants 

(2) Atropine, scopolamine 

(3) Antihistamines 

(4) Jimsonweed 

3. Opioid drugs 


(1) Clinical triad: coma, respiratory depression, and miosis 

(2) Miosis does not always occur (eg, meperidine, propoxyphene, diphenoxylate and atropine). 

(3) Clonidine and other central alpha 2 

-agonists (guanfacine, tizanidine) can cause a syndrome identical 

to the opioid triad. 

4. Sedative-hypnotics 

a. Clinical presentation: CNS and respiratory depression 

b. Examples: barbiturates, ethanol, benzodiazepines, gamma hydroxybutyric acid, others 

5. Sympathomimetics 


(1) CNS stimulation 

(2) May lead to toxic psychosis; presence of abnormal vital signs (increased blood pressure, wide 

pulse pressure, hyperthermia), disorientation, and clouding of consciousness help differentiate from 

psychiatric conditions (schizophrenia). 

b. Examples: amphetamines, cocaine, PCP, bath salts 

6. Hallucinogens 


(1) Hallucinations or cognitive disorders, although patients remain oriented to person, place, and time 

(2) Tachycardia, hypertension, and mydriasis 

b. Examples: LSD, certain species of mushrooms (Psilocybe, Conocybe, etc), parotid secretions of Bufo sp 

toads (hallucinogenic component of secretions formerly thought to be bufotenine but is probably actually 

5-Me-0-DMT), DMT, designer drugs of tryptamine class (foxy methoxy, AMT), ketamine 

7. Extrapyramidal 

a. Clinical presentation: a 11 parkinsonian' 1 picture: "TROD" 

Iremor, torticollis, trismus 

Rigidity 

Qpisthotonos, oculogyric crisis 

Qysphonia, dysphagia 

b. Examples: all of the "-zines" (chlorpromazine, promethazine, etc), haloperidol, metoclopramide 

8. Serotonin syndrome (mimics neuroleptic malignant syndrome) 


(1) Altered mental status, seizures, coma 

(2) Neurologic findings: clonus (most important finding), tremor, hyperreflexia, muscle rigidity 

(3) Autonomic instability (hyperthermia, hypertension, tachycardia, tachypnea) 

b. Two sets of diagnostic criteria: Hunter's criteria and Sternbach's criteria 

c. Usually precipitated by overdose or drug-drug interaction between several serotonergic agents: SSRls, 

monoamine-oxidase inhibitors, lithium, meperidine, or dextromethorphan 

549


d. Treatment 

(1) Benzodiazepines 

(2) Cyproheptadine (first-generation histamine [H 1 

] blocker with nonspecific serotonin antagonism) 

9. Hemoglobinopathies 

a. Carboxyhemoglobinemia-clinical presentation 

(1) Headache 

(2) Nausea, vomiting, flu-like syndrome 

(3) Syncope, tachypnea, tachycardia, chest pain 

(4) Confusion, coma, convulsions 

(5) Cardiovascular collapse, respiratory failure 

b. Methemoglobinemia-clinical presentation 

(1) Cyanotic appearance (often more severe than would be expected based on degree of 

methemogl obi nem ia) 

(2) Chocolate-colored blood despite exposure to air 

(3) Asymptomatic (healthy patients with


(3) Differential diagnosis of anion gap metabolic acidosis: 

Methanol, metformin 

!J.remia 

Q_iabetic or alcoholic ketoacidosis 

faraldehyde, phenformin 

lsoniazid, iron, or inhalants (carbon monoxide, cyanide, hydrogen sulfide) 

lactic acid 

_Ethylene glycol (ethanol may produce a small gap) 

S.alicylates, solvents 

(4) Poisonings with a low anion gap (


6. Seizures 

a. Anticholinergics (cyclic antidepressants, antihistamines) 

b. Phencyclidine (PCP) 

c. LSD 

d. Stimulants (cocaine, amphetamines, theophylline) 

e. Sedative-hypnotic withdrawal 

f. Carbon monoxide 

g. Opioids (meperidine, tramadol) 

h. Disulfiram 

i. Organophosphates 

j. Camphor 

k. Phenothiazines 

I. lsoniazid (classic board scenario is status epilepticus) 

m. Monomethylhydrazine-containing mushrooms (Cyromitra) (classic board scenario is status epilepticus) 

n. Carbamazepine 

o. Monoamine-oxidase inhibitors (toxicity or drug/food interactions) 

p. Lindane 

q. Nicotine 

r. Gamma hydroxybutyrate 

7. Seizure mimics: strychnine, tetanus 

Note: These patients will have a normal level of consciousness despite abnormal, seizure-like movements; 

however, mental status may appear altered because of extreme pain. 

8. Pulmonary edema 

a. Opioids 

b. Salicylates 

c. Sedative-hypnotics 

d. Carbon monoxide 

e. Cardiac drugs: digoxin, ~-blockers, calcium channel blockers 

f. Toxic inhalations: chlorine, N 2 

O, phosgene, zinc chloride 

g. Cocaine 

h. Organophosphates 

9. Breath odor 

a. lsopropyl alcohol - fruit-like 

b. Phenols, creosol- disinfectants 

c. Cyanide - bitter almonds or silver polish 

d. Chloral hydrate-;, pear 

e. Organophosphates, arsine, phosphorus - garlic 

f. Nitrobenzene - shoe polish, aniline dye 

g. Turpentine-;, violets 

h. Carbon tetrachloride - cleaning fluid 

1. Ethchlorvynol -;, new vinyl shower curtain 

j. Hydrogen sulfide - rotten eggs 

k. Camphor, naphthalene, p-dichlorobenzene -- mothballs 

I. Phosgene - hay 

m. Methyl salicylate - wintergreen 

10. Skin findings 

a. Needle tracks: IV drug use 

b. Pressure sores and bullae: barbiturates, carbon monoxide, sedative-hypnotics (snake and spider bites also 

cause bullae) 

c. "Boiled lobster" skin: boric acid (roach tablets) 

d. Diaphoresis: salicylates, organophosphates, sympathomimetics, cholinergics, ethanol or sedative-hypnotic 

withdrawal 

552


e. Jaundice: acetaminophen, mushroom poisoning, arsine gas 

f. Alopecia: arsenic, thallium, cytotoxic agents 

g. Flushing: disulfiram, niacin, ethanol, monoamine-oxidase inhibitors, metronidazole, anticholinergics, 

scombroid fish poisoning 

h. Cyanosis (noncardiopulmonary, by way of methemoglobinemia): nitrates/nitrites, 11 -caine 11 anesthetics, 

aniline dyes, chlorates, dapsone, sulfonamides 

11. Alterations in motor tone 

a. Increased motor tone: lithium, levodopa, strychnine, phencyclidine (PCP), ketamine, extrapyramidals, black 

widow spider bite, serotonin syndrome, neuroleptic malignant syndrome 

b. Fasciculations: cholinergics, amphetamines, heavy metals, paralytic shellfish poisoning, scorpion, or 

pufferfish 

c. Flaccid: sedative-hypnotics, opioids, fasciculants listed above 

12. Bowel sounds 

a. Increased bowel sounds: cathartics (eg, sorbitol), cholinergics, heavy metals, mushrooms, withdrawal 

syndromes 

b. Decreased bowel sounds: opioids, anticholinergics, phenothiazines 


1. ECG -;, dysrhythmias and conduction blocks 

2. CBC - as indicated for specific poisons (eg, iron) 

3. Electrolytes-;, for calculating osmolar and anion gaps 

4. Glucose - hyper/hypoglycemia and osmolar gap determinations 

5. Serum osmolality - osmolar gap determination 

6. BUN/creatinine - osmolar gap determination (BUN), renal function 

7. Creatine kinase-;, as clinically indicated to evaluate for rhabdomyolysis 

8. Arterial blood gases - acid-base evaluation 

9. Specific drug levels: salicylate, acetaminophen, and ethanol, plus any other toxic agent that is suggested by the 

history and physical examination (findings uncovered in the history and physical examination frequently point 

to a specific toxic agent/class) 

10. Abdominal radiographs-;, look for radiopaque tablets ( 11 CHIPES 11 ); some poisons that can be radiopaque: 

.Chloral hydrate 

Heavy metals 

Iron 

fhenothiazines 

.[nteric-coated tablets 

.S.olvents 

11 . Urinalysis 

a. Urine pH as indicated for management of specific poisonings (eg, salicylates) 

b. Ketones-;, isopropanol, alcoholic/starvation ketoacidosis, salicylates 

c. Blood without RBCs-;, rhabdomyolysis (eg, cocaine) 

d. Crystal fluorescence-;, ethylene glycol (not reliable in practice) 

F. General treatment measures 

1. GI decontamination 

a. Activated charcoal 

(1) Action: binds (adsorbs) the toxic agent and prevents absorption 

(2) Dose: I g/kg or 10 g per gram of ingested toxin, whichever is greater 

(3) Not useful for the following ingestions (liquids and metals): 

(a) Lithium 

(b) Alkalis/acids (absolutely contraindicated) 

(c) Heavy metals 

(d) Iron 

(e) Alcohols 

(f) 

Hydrocarbons and solvents 

553


(4) Repeated doses of activated charcoal (0.5 g/kg every 4-6 hours) are used for poisoning due to 

salicylates, theophylline, barbiturates, valproic acid, carbamazepine, dapsone, and sustained-release 

preparations. 

(a) Should not be given to patients suspected of having a bowel obstruction or ileus (confirm 

presence of bowel sounds before administration) 

(b) Should not be accompanied by repeated doses of a cathartic (eg, sorbitol), which can cause 

severe fluid and electrolyte disturbances 

b. Whole-bowel irrigation (WBI) 

(1) Uses polyethylene glycol electrolyte lavage solution (PEG-ELS) to wash poisons from GI tract before 

they are absorbed 

(2) May be useful after ingestions of: 

(a) Lithium 

(b) Iron 

(c) Heavy metals 

(d) Sustained-release, highly toxic drugs (eg, verapamil, diltiazem, theophylline, buproprion) 

(e) 

Body packers 

(3) Must administer via nasogastric tube (volume required is too large for patient to drink independently): 

adults= 1,500-2,000 ml/hr; children= 25-40 ml/kg/hr 

(4) Activated charcoal can be used before and during WBI therapy. 

(5) End point is retrieval of all pills or packets from body packers/stuffers. Other commonly cited end 

points include presence of clear rectal effluent; however, WBI should continue despite clear rectal 

effluent if pills or packets are still present in GI tract. 

(6) Contraindications 

(a) 

Unprotected airway 

(b) Intestinal obstruction or ileus 

(c) Uncertainty regarding position of nasogastric tube 

(d) Intractable vomiting 

c. GI decontamination measures no longer recommended 

(1) Neutralization of acids or bases: produces exothermic reaction that can cause further tissue damage 

(2) Cathartics (to promote rapid transit of toxin through the GI tract): no proven benefit and can cause 

fluid and electrolyte imbalances 

2. Removal of unabsorbed poison assumes a secondary role and, in many cases, may not be performed. 

a. Induction of emesis 

(1) Not indicated for prehospital or in-hospital therapy 

(2) American Academy of Pediatrics no longer recommends ipecac be kept in the home. 

b. Gastric lavage 

(1) Indications 

(a) 

Known or suspected life-threatening ingestion and 

(b) Time of ingestion


3. Elimination of absorbed toxin 

a. Antidotes 

Table 36: Antidotes for Specific Poisons 

Antidotes 

N-Acetylcysteine 

Antivenin 

CroFab® 

Anascorp® 

Atropine sulfate 

Botulism antitoxin 

Calcium gluconate 

Calcium disodium EDTA 

Cyproheptadine 

Deferoxamine 

Dextrose 

Digoxin Fab 

Dimercaprol (BAL) 

Ethanol 

Flumazenil 

Folic acid 

Fomepizole (4-methylpyrazole) 

Glucagon 

Glucarpidase 

Hydroxocobalamin 

Insulin (high dose) 

ldarucizumab 

L-carnitine 

Leucovorin (folinic acid) 

Methylene blue 

Naloxone 

Nitrites (amyl nitrite, sodium 

nitrite) 

Octreotide 

Agents 

Acetaminophen 

Rattlesnakes, copperhead (rarely needed), water moccasin, Eastern 

coral snake, coral snake 

Black widow spider (Latrodectus) (antivenin rarely needed) 

Scorpion (Centuroides exilicauda) 

Organophosphates/carbamates 

C!ostridium botulinum 

Hydrofluoric acid (topical, intradermal, intravenous, intra-arterial), 

calcium channel blockers (intravenous) 

Lead 

Serotonin syndrome 

Iron 

Insulin/oral hypoglycemic agents 

Digoxin 

Cardiac glycoside plants (foxglove, oleander) 

Lead with encephalopathy (must be used with calcium disodium 

EDTA), mercuric salts and arsenic if GI tract compromised 

Ethylene glycol, methanol 

Benzodiazepines 

Methanol 

Ethylene glycol, methanol 

Calcium channel and ~-blockers 

Methotrexate 

Cyanide 

~-blockers, calcium channel blockers 

Dabigatran 

Valproic acid-induced hyperammonemia with mental status changes 

Methotrexate 

Nitrites, nitrates, aniline dyes (methemoglobinemia) 

Narcotics, diphenoxylate, propoxyphene 

Cyanide 

Su lfonyl ureas 

555


Table 36: Antidotes for Specific Poisons (continued) 

Antidotes 

Oxygen (normobaric and hyperbaric) 

Physostigmine 

Potassium iodide (Kl) 

Pralidoxime (2-PAM) 

Protamine sulfate 

Prussian blue 

Pyridoxine (vitamin B 6 

) 

Silibinin 

Sodium bicarbonate 

Sodium thiosulfate 

Succimer (2,3 dimercaptosuccinic 

acid, DMSA) 

Thiamine hydrochloride 

Vitamin K 

Agents 

Carbon monoxide 

Anticholinergic agents 

Radioactive iodine 

Organophosphates 

Heparin 

Thallium salts, cesium salts 

Ethylene glycol, INH, Gyrometra escu/enta (false morel) 

Amatoxin-induced mushroom poisoning (Amanita sp) 

Salicylates, tricyclic antidepressants 

Cyanide 

Lead, mercury, arsenic 

Ethylene glycol 

Warfarin, long-acting anticoagulant rodenticides 

b. Acidification of the urine is no longer recommended. 

c. Alkalinization therapy with IV sodium bicarbonate 

(1) Cyclic antidepressants and other sodium-channel blockers-;. alkalinization of the blood helps 

improve/prevent dysrhythmias/conduction blocks and improves hypotension 

(a) 

Use boluses of sodium bicarbonate 

(2) Alkalinization of the urine to a pH >7 (with a bicarbonate infusion) ionizes weak acids into ionized 

molecules, increasing excretion of the following toxic agents: 

(a) Salicylates 

(b) Phenobarbital 

(c) Chlorpropamide 

d. Charcoal hemoperfusion rarely used any longer 

e. Hemodialysis indications 

(1) Ethylene glycol, methanol 

(2) Methanol 

(3) Valproic acid 

(4) Lithium 

(5) Salicylates 

(6) Theophylline, caffeine 

G. Other complications 

1. Hepatotoxicity-;. acetaminophen, iron, carbon tetrachloride, cyclopeptide mushrooms (Amanita, Caterina, 

Lepiota), and pennyroyal oil 

2. GI hemorrhage 

a. ASA 

b. Iron 

c. Coumadin 

d. Mercuric salts 

e. Alkalis/acid caustics 

f. Long-acting anticoagulant rodenticides 

556


3. Renal failure - carbon tetrachloride, mercuric salts, acetaminophen, colchicine, ethylene glycol 

4. Dysrhythmias - cyclic antidepressants, cocaine, ~-blockers, calcium channel blockers, quinine, 

antidysrhythmics, chloroquine, propoxyphene, phenothiazine, theophylline, digoxin, chloral hydrate 

5. Hypertension - phencyclidine (PCP), monoamine-oxidase inhibitors, phenylpropanolamine, cocaine, 

amphetamines 

6. Hypotension - sustained-release calcium channel blockers 

7. Neurotoxicity - botulinum toxin, lithium, carbon monoxide, methanol, carbon disulfide 

8. Respiratory problems - nitrogen oxides, phosgene, paraquat 

II. SPECIFIC OVERDOSES AND POISONINGS 

A. Cyclic antidepressants 

1. Commonly prescribed agents 

a. lmipramine 

b. Desipramine 

C. Amitriptyline 

d. Nortriptyline 

e. Doxepin 

2. Pathophysiology (obtain cardiac monitoring and ECG early) 

a. Cardiac effects 

(1) Anticholinergic activity that can induce tachycardia 

(2) Quinidine-like activity (fast sodium channel blockade) that can induce intraventricular and AV blocks; 

avoid use of procainamide, quinidine, or other class IA and IC antiarrhythmics. 

(a) Bundle-branch and fascicular blocks are usually preceded by a widening QRS complex (wide 

QRS is a primary ECG finding). 

(b) AV blocks range from first degree to complete block. 

(c) Other ECG effects include tall R wave in aVR. 

(3) Hypotension due to peripheral a-adrenergic blockade, dysrhythmias, and norepinephrine depletion 


b. CNS effects 

(1) Confusion, agitation, and hallucinations with rapid progression to coma 

(2) Seizures are common and usually single. 

c. Anticholinergic effects are common; absence does not exclude toxicity. 

d. Signs that indicate a serious overdose 

(1) Ventricular dysrhythmias 

(2) lntraventricular conduction defects with a QRS complex> 100 milliseconds 

(3) Bradycardia and AV blocks 



(6) Seizures 

(7) Cardiac arrest 

3. Management 

a. Activated charcoal: use with caution because patients have the potential to rapidly decompensate. 

b. Consider orogastric lavage. 

c. IV boluses of sodium bicarbonate are the mainstay of therapy. 

(1) The most effective therapy for improving hypotension and abolishing dysrhythmias 

(2) Indications: if QRS complex :::100 milliseconds in the limb leads 

(3) Administration of sodium bicarbonate is usually via boluses: dosing 1-2 mEq/kg (1-2 ampules of 

NaHCOJ. 

(4) Avoid if arterial pH >7.55 or serum sodium> 150 mmol/L. 

557


d. Hypotension 

(1) Start with crystalloids and sodium bicarbonate. 

(2) If no or poor response, try vasopressors. 

e. Seizure control is important, because lactic acidosis can worsen cardiac toxicity. Therapeutic choices include: 

(1) Sodium bicarbonate 


(3) Phenobarbital 

(4) Propofol 

f. Therapies to avoid 

(1) Class IA (eg, procainamide) and IC (eg, flecainide) antidysrhythmics - can worsen the "quinidine-like" 

toxicity on the myocardium 

(2) Flumazenil --,, risk of precipitating seizures 

(3) Physostigmine--,, risk of cardiac toxicity and asystole 

(4) Hemodialysis--,, ineffective because cyclic antidepressants are highly protein bound 

(5) Hemoperfusion 

B. Other antidepressants 

1. Differ from the cyclic antidepressants in that their mechanism of action (inhibition of biogenic amine reuptake 

in the CNS) occurs without sodium channel blockade; therefore, life-threatening toxicity is less common. 

2. Common agents 

a. SSRls: selective inhibition of serotonin reuptake 

(1) Fluoxetine 

(2) Sertraline 

(3) Paroxetine 

(4) Fluvoxamine 

(5) Citalopram 

b. Venlafaxine: serotonin-norepinephrine reuptake inhibitor 

c. Trazodone, nefazodone: inhibit 5-hydroxytryptamine (5-HT) reuptake and block postsynaptic 5-HT 2 

receptors; trazadone has peripheral alpha effects that can result in priapism when taken therapeutically or 

in overdose. 

d. Bupropion: inhibits dopamine reuptake 

e. Mirtazapine: nonselective reuptake of biogenic amines inhibited and blocks postsynaptic 5-HT 2 

and 5-HT 3 

receptors 


a. SSRI overdose 

(1) Mild CNS depression, sinus tachycardia, GI symptoms (nausea, vomiting, diarrhea), and seizures (rare) 

(2) Serotonin syndrome 

b. Bupropion overdose: hallucinations, tachycardia, seizures (may be delayed up to 18 hours after overdose), 

status epilepticus, death 

c. Trazodone, nefazodone: prolonged QT interval 

4. Management 

a. Activated charcoal 

b. Monitor for 6 hours-longer for bupropion and extended-release preparations 

c. Benzodiazepines for seizures (rare) 

d. Serotonin syndrome 

(1) Critical care monitoring 

(2) IV crystalloid therapy 

(3) Active cooling therapy for hyperthermia 

(4) Cyproheptadine 4-8 mg orally every 8-12 hours 

(5) Muscle rigidity must be controlled quickly, because it contributes to the hyperthermia, rhabdomyolysis, 

and lactic acidosis. 

(6) Evaluate for underlying medical complications (including infections). 

(7) Watch for hyperkalemia and myoglobinuric-induced renal failure secondary to rhabdomyolysis. 

558


C. Lithium 

1. Primary therapeutic use is for bipolar disorder. 

2. Toxicity can develop after an acute overdose or in a patient taking the usual therapeutic dose who becomes 

dehydrated or develops renal insufficiency (chronic). 


a. Toxicity is characterized primarily by neurologic manifestations 

(1) Mild: fatigue, tremor, mild confusion 

(2) Moderate: increased tremor, slurred speech, ataxia, increased confusion, drowsiness, hyperreflexia 

(3) Severe: tremor, clonus, choreoathetosis, rigidity, hyperthermia, irritability, stupor, coma, seizures 

(4) The normal therapeutic blood level of lithium is 0.6-1.2 mEq/L. Signs and symptoms of toxicity 

often do not correlate with serum levels (especially with chronic toxicity, because the lithium has 

shifted into the CNS [tissue] compartment); the neurologic status of the patient is the most important 

determinant of toxicity. 

b. Other 

(1) Nausea, vomiting, diarrhea 

(2) Nephrogenic diabetes insipidus (chronic) 


a. Lithium level 

b. ECG 

(1) ST-T wave abnormalities 

(2) Prolonged QT interval 

(3) Bradycardia 

5. Management 

a. General measures 

(1) Cardiac monitor 

(2) Whole-bowel irrigation (acute overdoses, especially with sustained-release preparations) 

b. Specific therapy 

(1) The key to the treatment of lithium overdose is awareness of its mechanism of excretion. 

(a) 97% is excreted unchanged in the urine. 

(b) 75%-80% is reabsorbed by the proximal tubule along with sodium; volume depletion enhances 

lithium retention. 

(2) Restoration of sodium and water balance with normal saline. 

(a) The choice of fluid and rate of administration should be based on the degree of dehydration and 

hypotension as wel I as the serum sodium level. 

(b) Normal saline should be used unless the patient is severely hypernatremic. 

(c) Goal: correct dehydration and maintain urinary output at 1-2 ml/kg/hr. 

(3) Because lithium is reabsorbed in the proximal renal tubule, diuretics that act on the ascending limb of 

the loop of Henle (furosemide) or distal tubule (thiazides) will not increase lithium excretion and may 

promote reabsorption if they lead to volume depletion. 

(4) Indications for hemodialysis 

(a) Clinical signs of moderate to severe poisoning (eg, seizure) 

(b) Worsening clinical condition despite falling lithium levels 

(c) Onset of dysrhythmias 

(d) Decreasing urine output or renal failure (increased BUN/creatinine) 

(e) Serum level ?:4.0 mEq/L at least 6 hours after an acute ingestion (controversial) 

(5) Watch for a rebound in serum lithium levels after hemodialysis, because tissue (CNS) levels 

reequilibrate with the serum. Repeat hemodialysis may be necessary in chronic toxicity. 

(6) Failure to recognize or provide appropriate treatment may result in permanent neurologic sequelae. 

D. Sedative-hypnotics 

1. Barbiturates 


(1) Ultrashort acting 

(a) Methohexital 

(b) Thiopental 

559


(2) Short acting 

(a) Pentobarbital 

(b) Secobarbital 

(3) Intermediate acting 

(a) Amobarbital 

(b) Butabarbital 

(4) Long acting 

(a) Phenobarbital 

(b) Mephobarbital 

(c) Primidone 

b. Metabolism and major excretion mechanisms 

(1) Ultrashort-, short-, and intermediate-acting barbiturates are lipid-soluble and poorly ionized. 

(2) Long-acting barbiturates are not lipid-soluble, but they are ionized at an alkaline pH. 

(a) When ionized, drugs cannot enter neuronal cells or the resorptive cells that line the renal tubules. 

(b) This is why alkalinization of the urine is therapeutic in phenobarbital overdose. 


(1) Coma 

(2) Hypothermia 

(3) Respiratory depression 

(4) Shock 


(6) Absent corneal and deep tendon reflexes 

(7) Cutaneous bullae 

d. Management 

(1) General measures 

(a) Airway management 

(b) Fluid challenge if hypotension develops 

(c) Activated charcoal 

(2) Specific therapy of phenobarbital overdose 

2. Benzodiazepines 

(a) Alkalinization of the urine with sodium bicarbonate can increase the excretion of phenobarbital 

5- to 1 0-fold. 

1. Goal: urine pH 7.5-8 

ii. Use with caution, if at all, in patients dependent on phenobarbital (eg, those with alcohol 

dependence or seizure disorders). In these patients, supportive measures may be best. 

(b) One method of urinary alkalinization 

1. Begin therapy with a bolus of 1-2 mEq/kg (1-2 standard ampules; optional) 

ii. Follow with a continuous infusion of 150 mEq NaHCO 3 

(3 standard ampules) in 1,000 ml 

D5W and infuse at 1.5-2 times the maintenance fluid rate. 

iii. Adjust infusion rate as indicated to achieve goal urine pH. 

a. Agents include diazepam, lorazepam, midazolam, alprazolam, chlordiazepoxide, clonazepam, 

flurazepam, flunitrazepam ("roofies"), oxazepam, temazepam, and triazolam. 

b. Pathophysiology 

(1) Potency, duration of effects, and active metabolites vary widely. 

(2) Benzodiazepines enhance effects of gamma-aminobutyric acid (GABA) at central receptors. 


(1) Progressive depression of level of consciousness to coma 

(2) Hypothermia, pulmonary aspiration, and respiratory arrest 

d. Management 

(1) General supportive measures: careful monitoring with attention to airway potency, oxygenation, and 

ventilation support 

(2) Flumazenil: a competitive antagonist for benzodiazepines at the receptor level 

560


(a) Generally not recommended for emergency department management and has no role in 

management of multiple substance or unknown overdose 

(b) Generally reserved for iatrogenic overdoses in non-benzodiazepine-dependent patients or 

pediatric exposures requiring active airway intervention (uncommon) 

(c) Contraindicated in benzodiazepine-dependent patients, because it can induce withdrawal (may 

be severe and life-threatening) 

(d) Contraindicated when coingestion with cyclic antidepressants is a possibility, because seizures 

may occur. 

(e) Re-sedation is common (short half-life of the drug) 

3. Gamma hydroxybutyrate 


(1) Youth rave culture 

(2) Drug-facilitated sexual assault 

(3) Bodybuilders 


(1) Overdose 

(a) Bradycardia, respiratory depression 

(b) Lethargy, coma 

(c) Miosis, myoclonus, nystagmus, seizures 

(2) Withdrawal may resemble ethanol or sedative-hypnotic withdrawal (including delirium). 

c. Management 

(1) Overdose: supportive care, airway protection, intubation based on level of consciousness; typical 

course is abrupt awakening within a few hours. 

(2) Classic scenario: Comatose patient presents and is intubated; hours later awakes abruptly, pulls out 

endotracheal tube and flees the emergency department. 

(3) Withdrawal (seen after chronic use by body builders): benzodiazepines; pentobarbital for refractory cases 

E. Phenothiazines (eg, chlorpromazine, prochlorperazine) 


a. Erratic and unpredictable absorption after ingestion 

b. Half-life is 20-40 hours, and effects may persist for days. 

c. Metabolized in the liver 

2. Adverse effects seen with therapeutic doses and drug abuse 

a. Extrapyramidal reactions (most common) 

(1) Parkinsonian (rigidity, tremor) 

(2) Akathisia (incessant movement and restlessness) 

(3) Dystonic (grimacing, trismus, torticollis, dysphagia, dysarthria, oculogyric crisis); responds well to 

benztropine or diphenhydramine 

(4) Tardive dyskinesia (sucking, lip-smacking, perioral "rabbit" syndrome): appears late, after prolonged 

therapy. 

(5) Newer second-generation antipsychotics (eg, clozapine, risperidone, olanzapine) exhibit less 

dopamine2-receptor blockade and have a lower rate of extrapyramidal adverse effects. 

b. Orthostatic hypotension 

c. Hypo- or hyperthermia 

d. Neuroleptic malignant syndrome 

3. Acute overdose 


(1) Anticholinergic 

(2) a-adrenergic blockade (miosis, vasodilation, hypotension, "warm shock") 

(3) Sodium/potassium channel blockade and cardiodepressant effects are most common with thioridazine 

and mesoridazine. 

(a) Prolonged PR, QRS, and QT intervals 

(b) ST and T wave changes 

(c) Ventricular dysrhythmias (including torsades de pointes) and AV dissociation 

(4) Coma, rigidity, and seizures 

561


F. Phenytoin 

b. Management (conservative) 

(1) Activated charcoal 

(2) Respiratory compromise - airway management 

(3) Hypotension - IV fluids 

(4) Seizures - diazepam, lorazepam, phenobarbital 

(5) Extrapyramidal reactions- benztropine or diphenhydramine 

(6) Ventricular dysrhythmias 


(a) NaHCO 3 

should be tried first (see cyclic antidepressants). 

(b) Magnesium is indicated for torsades de pointes. 

(c) Do not use procainamide, quinidine, or other class IA or IC antidysrhythmics. 

a. Correlation of blood levels with evolution of clinical effects 

(1) 10-20 mcg/ml - therapeutic level 

(2) 20 mcg/ml - lateral gaze nystagmus 

(3) 20-30 mcglml - nystagmus and cerebellar excitation 

(4) 30-40 mcglml - nausea, vomiting, ataxia, dysarthria 

(5) >40 mcg/ml - confusion and lethargy 

(6) 50 mcglml - choreoathetosis, opisthotonus (rarely) 

(7) > 100 mcglml - potentially lethal level 

b. Cardiac actions 

(1) Decreased automaticity 

(2) Cardiac toxicity, especially ventricular dysrhythmias 

(a) May occur with IV loading of phenytoin (commonly attributed to too rapid infusion of the 

propylene glycol diluent) 

(b) Fosphenytoin is a water-soluble phenytoin pro-drug for parenteral use and does not contain 

propylene glycol; cardiac toxicity rare with fosphenytoin but has been reported. 

c. Miscellaneous effects 

(1) Osteomalacia (chronic use) 

(2) Gingival hypertrophy (chronic use) 

(3) Megaloblastic anemia 

(4) Fetal hydantoin syndrome 

(5) Skin rashes and the anticonvulsant hypersensitivity syndrome (fever, rash, lymphadenopathy, 

eosinophilia), which will recur if phenobarbital or carbamazepine are substituted 

2. Management of acute ingestion 

G. Opioids 

a. Repeated doses of activated charcoal may be useful. Use with caution, if at all, in patients dependent 

on phenobarbital (eg, those with alcohol dependence or seizure disorders). In these patients, supportive 

measures may be best. 

b. Supportive care until confusion and ataxia clear. 

1. Classic clinical scenarios 

a. Opioid withdrawal 

(1) Clinical presentation: abdominal cramping/pain, chills, sweating, nausea, diarrhea, and arthralgias; 

distinctive physical findings include yawning, lacrimation, rhinorrhea, and piloerection. 

(2) Onset is usually within 12-24 hours of the last dose but is longer with sustained-release opioids and 

methadone. 

(3) Symptoms peak 1-2 days after onset and subside within a week. 

b. Opioid intoxication and overdose 

(1) Clinical presentation: euphoria, drowsiness, decreased respiratory rate, miosis 

(2) Severe overdoses can cause coma and respiratory acidosis. 

(3) Seizures may occur after tramadol, propoxyphene, or meperidine overdose. 

562


2. Specific treatment of opioid overdose__,. naloxone 

a. Initial dose is 0.1-2 mg in adults and children and should be titrated carefully. It may be given IV, IM, 

SC, endotracheally, intranasally. It is effective within minutes. Higher doses may be needed to reverse the 

following agents: buprenorphine, propoxyphene, pentazocine, meperidine, fentanyl, and diphenoxylate. 

b. It should be used to reverse respiratory depression and dosed until respiratory depression has resolved. 

Note: Naloxone will precipitate acute withdrawal in opioid-dependent patients, which is the major 

complication of its use. 

c. The effect of naloxone decreases 15-30 minutes after injection, but the action of the opioid may last for hours. 

(1) Buprenorphine, methadone, controlled-release opioids, and diphenoxylate/atropine in particular last 

> 12-24 hours. 

(2) Repeated doses and prolonged observation may be required. 

(3) Patients who require naloxone after buprenorphine, methadone, sustainedrelease opioid, or 

diphenoxylate/atropine overdose need admission. 

(4) Patients may need a continuous infusion of naloxone. Titrate based on respiratory depression versus 

signs of withdrawal. 

3. Acute complications of opioid abuse 

H. Clonidine 

a. Seizures (meperidine, propoxyphene, tramadol, pentazocine, dextromethorphan) 

b. Pulmonary edema 

c. Rhabdomyolysis 

d. Aspiration pneumonia 


a. A centrally acting a2-agonist, clonidine reduces sympathetic stimulation to the heart and peripheral blood 

vessels. 

b. The initial effect is hypertension followed by an anti hypertensive effect that occurs up to 10 hours later. 

c. Withdrawal is associated with severe headache, rebound hypertension, anxiety, and tremors. 

2. Overdose 


(1) Mimics opioid overdose and includes apnea, altered level of consciousness (drowsiness__,. coma), 

seizures, and miosis; hypotension and bradycardia are prominent features. 

(2) Children are more severely affected than adults. 

b. Management 

(1) Supportive 

(2) Respiratory support, atropine, vasopressors, and GI decontamination 

(3) Naloxone has been used with variable success to reverse CNS and respiratory depression associated 

with clonidine poisoning. High doses may be needed (10-20 mg IV). 

I. Alcohols 

1. Methanol 

a. Sources and pathophysiology 

(1) Found in windshield washing fluids, solvents, paint thinners, and canned fuels. Suspect multiple 

victims if ingestion was recreational substitution for ethanol. 

(2) Converted by alcohol dehydrogenase to formaldehyde, which is then converted to formic acid. 

(a) The accumulation of formic acid correlates with the decrease in bicarbonate, the increase in 

anion gap, and the severity of metabolic acidosis. 

(b) Formic acid affects optic nerve function, producing optic papillitis and retinal edema __,. "blind 

drunk" 

b. Classic clinical scenario: A latent period of 8-30 hours is followed by the onset of abdominal pain, 

nausea and vomiting, blurred vision, and metabolic acidosis. The patient may have normal vision 

(and a normal eye examination) initially. As the formic acid accumulates, visual symptoms include 

photophobia, "snowstorm" vision, and blindness. The pupils dilate and react sluggishly, if at all, to light. 

The earliest funduscopic finding is hyperemia of the disc, followed by papilledema and optic atrophy. Late 

parkinsonism may result. 


(1) Anion gap metabolic acidosis associated with a low bicarbonate level 

563


(2) The osmol gap may be high, although a low or even "negative" gap does not exclude a toxic alcohol 

or glycol. 

(a) Osmolar gap: calculated osmolarity - measured osmolality 

(b) Calculated osmolarity 

(2 x Na) + 

BUN 

2.8 

+ 

Glucose 

18 

+ 

Ethanol 

4.6 

(c) Normal osmolar gap: 10-14 

(d) Osmotically active substances that may produce an osmol gap 

i. Methanol 

ii. Ethanol 

iii. lsopropyl alcohol 

iv. Glycerol 

v. Mannitol 

vi. Ethylene glycol 

(e) Osmol gaps can also be seen in lactic acidosis and alcoholic ketoacidosis, or with high serum 

ethanol concentrations (despite "correction" using the above formula). 

d. Management 

(1) General supportive measures, including airway management 

(2) Nasogastric aspiration of gastric contents if the patient is seen within the first 30-60 minutes after 

ingestion 

(3) Severe acidosis is treated with bicarbonate to reduce diffusion of formate into the CNS and protect 

the optic nerve. 

(4) Alcohol dehydrogenase inhibitor (ethanol or fomepizole) to block further metabolism of methanol. 

(a) Indications: methanol level >20 mg/dl (may start empirically while waiting for level) 

(b) Fomepizole (4-methylpyrazole) is the preferred agent. 

(c) Second-line agent: ethanol 

i. Difficult to find and to dose 

ii. Goal blood ethanol level: 100-150 mg/dl 

(5) Hemodialysis removes methanol and formic acid and is indicated for methanol level >50 mg/dl, 

metabolic acidosis (arterial pH :'c7.25), severe visual or CNS symptoms, or when ethanol is used 

for therapy. 

(6) Folic acid can be considered and may enhance metabolism of formic acid to nontoxic substances, 

which are then eliminated from the body. 

2. Ethylene glycol 

a. Source and pathophysiology 

(1) Found in antifreeze and brake fluids 

(2) Converted by alcohol dehydrogenase to glycolaldehyde, which is then metabolized to glycolic acid. 

(a) Glycolic acid is primarily responsible for the anion gap metabolic acidosis; it is ultimately 

metabolized to multiple metabolites, including oxalic acid. 

(b) Oxalic acid forms calcium oxalate crystals in the kidney, brain, and liver. 


(1) CNS changes suggesting ethanol intoxication 

(2) Progressive toxicity over 9-12 hours can lead to seizures, stupor, and coma. 

(3) As toxicity progresses, pulmonary edema and myocardial dysfunction can develop; death may occur. 

(4) Late toxicity is characterized by renal failure. 

(5) Cranial nerve (frequently facial) dysfunction can develop (late finding). 


(1) Anion gap metabolic acidosis 

(2) Positive birefringent calcium oxalate crystals in the urine 

(a) Often absent initially 

(b) Commonly described as "envelope-shaped" 

564


(3) Urine that fluoresces under a Wood's lamp may be evident if the patient recently ingested a 

fluorescein-containing antifreeze; however, this has been shown to be very unreliable, and falsepositives 

and false-negatives are common. 

(4) Osmol gap (absence does not exclude ingestion) 

(5) Hypocalcemia (not always present) 

d. Management 

(1) Gastric decontamination, IV ethanol or fomepizole, and hemodialysis (same indications as for 

methanol toxicity) 

(2) Thiamine and pyridoxine can be administered to decrease production of oxalic acid. 

(3) Calcium administration as needed (long QT interval) 

3. Ethanol 

a. Intoxication 

(1) Degree of intoxication varies according to the patient's tolerance. 


(a) Mild intoxication (euphoria, expansiveness, loss of self-control) 

(b) Moderate intoxication 

i. Slurred speech, ataxia, and nystagmus 

ii. Altered sensory perceptions that are dull, distorted, or obviously psychotic 

iii. Mild tachycardia is common. 

(c) Severe intoxication (the four "H's") 

i. t!.ypotension 

ii. t!.ypoventilation 

iii. t!.ypothermia 

iv. t!.ypoglycemia (more common in small children) 

(3) Care must be taken to consider coexisting disease, hypoglycemia, trauma (especially closed head 

injury), or drug ingestion. 


(a) Most patients with uncomplicated ethanol intoxication require only observation and basic 

supportive measures. 

(b) Gastric decontamination is indicated if polydrug ingestion is known or suspected. 

(c) Administer IV glucose, naloxone, and thiamine 100 mg, when necessary. 

(d) Hemodialysis is indicated only for life-threatening complications (refractory hypotension). 

b. Withdrawal 


(a) Early signs and symptoms: tremor, irritability, increased pulse, increased blood pressure 

(b) Delirium tremens (onset is 48-100 hours after cessation) 

i. Hypertension, tachycardia 

ii. Diaphoresis, dehydration 

iii. Visual hallucinations and paranoid ideation 

(c) Withdrawal seizures ("rum fits") 

i. Generally occur within 6-48 hours of last drink 

ii. Usually single or several brief generalized seizures with rapid recovery in between 

iii. lntracranial pathology must be considered in the presence of fever, prolonged postictal 

period, signs of trauma, or focality. 

(d) Wernicke-Korsakoff syndrome (thiamine deficiency)-two of the following signs: 

i. Dietary deficiencies 

ii. Cerebellar dysfunction 

iii. Oculomotor abnormalities 

iv. Altered mental state or mild memory impairment 


(a) IV fluids, thiamine, and glucose 

(b) Replacement of potassium, magnesium, and phosphorus when indicated 

565


4. lsopropanol 

J. Cocaine 

(c) Benzodiazepines for control of the withdrawal state 

a. Pathophysiology 

1. Enough medication should be administered to calm or lightly sedate the patient. For 

example, diazepam can be started at 5-10 mg and then doubled until desired effect; very 

large doses may be needed. 

11. Phenytoin is not effective for alcohol-withdrawal seizures. 

iii. Physical restraints should be used to temporarily control patients only until the 

pharmacologic treatment becomes effective. A patient should never be allowed to thrash 

uncontrollably in physical restraints, unattended, for a prolonged time. 

iv. Avoid antipsychotics (haloperidol, ziprasidone): may lower seizure threshold. 

v. Sedation with propofol or barbiturates may be necessary in severe refractory cases. 

(1) lsopropyl (rubbing) alcohol causes more intoxication/CNS depression but generally less severe 

sequlae than methanol and ethylene glycol. 

(2) 80% is absorbed from the stomach within 30 minutes and is then metabolized (by alcohol 

dehydrogenase) to acetone. 


(1) CNS depression 

(2) Hypotension (in severe cases) 

(3) Hemorrhagic gastritis/tracheobronchitis 


(1) Positive serum acetone and acetonuria 

(2) High osmolal gap 

(3) Anion gap metabolic acidosis is not a feature of isopropanol toxicity (unless hypotension with lactic 

acidosis is present). This finding should prompt a search for another cause (eg, sepsis, alcoholic 

ketoacidosis, ethylene glycol, or methanol coingestion). 

d. Management 

(1) Supportive care, including airway management 

(2) Nasogastric aspiration of gastric contents within initial 30-60 minutes 

(3) Alcohol dehydrogenase inhibitors (fomepizole, ethanol) are not indicated. 

(4) Search for any complication or concomitant condition (eg, trauma) 

(5) Indications for hemodialysis 


(a) Refractory hypotension 

(b) Serum levels >400-500 mg/dL 

a. Metabolized by the liver, plasma esterases, and spontaneous hydrolysis within a few hours, then excreted 

in the urine 

b. Causes euphoria with lack of fatigue, a sense of omnipotence, increased mental alertness, and sexual 

stimulation 


a. CNS stimulation__,. apprehension, twitching, seizures; coma can develop later. 

b. Cardiac stimulation 

(1) Hypertension, tachycardia, ventricular dysrhythmias, cardiac conduction blocks 

(2) Effects on coronary arteries and increased platelet aggregation can lead to an acute Ml; this finding in 

a young person should raise the suspicion of cocaine use. 

c. Respiratory depression/failure 


(2) Pneumothorax/mediastinal air 

(3) Crack lung (bronchospasm, infiltrates, eosinophilia hemorrhage) 

d. Hyperthermia (may occur suddenly and can be lethal) 

e. Rhabdomyolysis---,. hyperkalemia (can be life-threatening) 

f. Arterial vasospasm can lead to tissue infarction in various tissues, such as brain, lung, liver, and intestines. 

lntracerebral hemorrhages and aortic dissection can also occur. 

566


3. Cocaine-associated chest pain -s- acute Ml in 6% of patients 

a. Abnormal ECG is common (early repolarization, old and new nonspecific abnormalities) 

b. Management 

(1) Benzodiazepines are first-line treatment for hypertension and tachycardia. 

(2) Pharmacologic agents to control pulse rate and blood pressure (eg, phentolamine), along with 

benzodiazepines, should be started. 

(3) Angioplasty is preferred over systemic fibrinolysis for persistent ST-segment elevation Ml despite the 

above measures. 

4. Management 

(4) Patients without ischemic changes and negative cardiac markers over an appropriate observation 

period can usually be managed as outpatients. 

a. General supportive measures 

(1) Airway management and IV hydration to assure a urinary output of 1-2 ml/kg/hr. 

(2) Cardiac monitoring and repeat vital signs (including temperature) every few minutes. 

b. Seizures, agitation, and psychosis are best managed with benzodiazepines. Phenothiazines (eg, 

chlorpromazine) and haloperidol may lower the seizure threshold and prevent heat dissipation in the 

already hyperthermic patient; avoid when treating cocaine-induced psychosis. 

c. Cocaine-induced cardiac dysrhythmias should be treated with IV benzodiazepines. Sodium bicarbonate 

should be considered for dysrhythmias refractory to benzodiazepines (especially those with a wide QRS 

complex). Drugs that should be avoided include: 

(1) Lidocaine (may increase CNS toxicity -s- seizures) 

(2) ~-blockers (may precipitate cardiac ischemia or hypertension due to unopposed a-receptor stimulation) 

(3) a-blockers (eg, phentolamine) followed by use of a short-acting ~-blocker (or combination agents, 

such as labetalol) have been used in these patients to alleviate concerns for unopposed a-receptor 

stimulation and subsequent hypertensive crisis. 

d. Hyperthermia should be treated in the usual fashion. Aggressive measures may be needed. See page 649. 

e. Dialysis has no role in the management of cocaine poisoning. 

f. Body stuffers and body packers-specific management: 

(1) Activated charcoal for body stuffers 

(2) Whole-bowel irrigation for body packers 

(3) Observation 

(a) Body stuffers (nonprofessionally wrapped packets, eg, impromptu swallowing of baggies to avoid 

arrest) -s- until asymptomatic (6-12 hours) 

(b) Body packers (professionals) -s- until all packets have passed (may need to be confirmed with 

radiocontrast studies) 

K. Amphetamines/amphetamine-like drugs 

1. Commonly abused drugs 

a. Ephedrine (ma huang, herbal ecstasy) 

b. Methamphetamine (crank, ice)-can also be smoked 

c. MOMA (Ecstasy), MDEA (Eve), etc 

d. Cathinone (Khat) 

e. Synthetic cathinones ("bath salts") 

f. ADHD medications (eg, amphetamine, dextroamphetamine, lisdesamphetamine) 


a. Rapidly absorbed from GI tract 

b. Eliminated via liver (30%-45%) and kidneys (60%-70%) 


a. Prescription doses 

(1) Central effects (anorexia, hyperactivity, restlessness, and sleeplessness) 

(2) Peripheral effects (tachycardia, vasoconstriction, bronchodilation, and pupillary dilation) 

(3) Phenylpropanolamine was removed from OTC diet and decongestant preparations because of 

concerns with hypertension, seizures, intracerebral hemorrhage, and dysrhythmias. 

567


b. Withdrawal signs and symptoms 

(1) Headache 

(2) Increased appetite 

(3) Abdominal cramps and diarrhea 

c. Toxic signs and symptoms can be clinically indistinguishable from those of cocaine toxicity. 

4. Management 

(1) Cardiovascular: hypertension, tachycardia, dysrhythmias, Ml, intracerebral hemorrhage 

(2) Neurologic: diaphoresis, mydriasis, piloerection, extreme restlessness, psychotic behavior, seizures, coma 

(3) GI: nausea, vomiting, diarrhea 

(4) Other toxic signs 

(a) Hyperthermia 

(b) Rhabdomyolysis 

(c) Hallucinations (occur with designer amphetamines, eg, MOMA, MDEA) 

(d) Hyponatremia (due to syndrome of inappropriate antidiuretic hormone secretion with MOMA) 


(1) Quiet area to reduce hyperactivity 

(2) Cardiac monitor 

(3) Aggressive cooling measures for hyperthermia 

(4) Activated charcoal for ingestions 

(5) Correction of fluid and electrolyte disturbances 


L. Hallucinogens 

(1) Benzodiazepines for seizures and agitated psychosis 

(2) Nitroprusside, phentolamine, or labetalol for hypertension unresponsive to benzodiazepine sedation 

(avoid ~-blockers) 

1. Phencyclidine (PCP) 


(1) Most common findings are abnormal vital signs (hypertension, tachycardia, hyperthermia) and 

nystagmus (horizontal, vertical, or rotary) in a patient with bizarre behavior that can fluctuate between 

severe agitation and catatonic-like behavior. 

(2) Pupillary size is variable, but miosis is common. 

(3) Severe hyperthermia, seizures, coma, and rhabdomyolysis can occur with large ingestions. 

b. Management 

(1) Benzodiazepines for agitation and seizures 

(2) Aggressive cooling measures for severe hyperthermia 

(3) Hydrate with IV crystalloids to maintain a urinary output of 1-2 ml/kg/hr 

(4) Activated charcoal should be given; repeated doses may be efficacious because of the gastroenteric 

circulation of PCP. 

(5) Acidification of the urine is no longer recommended. 

2. Other hallucinogens 

a. LSD (psychedelic flashbacks are a prominent feature, especially in chronic users) 

b. Mescaline 

c. Psilocybin (see mushroom poisoning, page 578) 

d. Cannabinoids 

e. Jimsonweed (Datura) (anticholinergic toxicity) 

f. Morning glory plant (lpomoea) (anticholinergic toxicity) 

g. Nutmeg (large doses) 

h. Ketamine (vitamin K) 

i. Bufotenine (toad licking; 5-Me-0-DMT may be responsible chemical instead of bufotenine) 

j. Yohimbine 

k. Designer amphetamines (MOMA, MDEA, DOM/STP, "bath salts") 

568


3. General treatment of hallucinogens 

a. A quiet, semidarkened room 

b. Benzodiazepines for sedation (and seizures) 

c. Temperature monitoring and aggressive cooling for severe hyperthermia. 

M. Salicylates (includes ASA, oil of wintergreen, bismuth subsalicylate, liniments) 

1. Acid-base disorders occur in three phases 

a. First phase: primary respiratory alkalosis 

(1) Salicylate stimulates the respiratory center in cerebral medulla_,, respiratory alkalosis 

(2) May not be seen in children 

b. Second phase: primary metabolic acidosis, blood pH remains normal 

(1) Primary respiratory alkalosis also serves as compensation for this developing primary metabolic acidosis. 

(2) Salicylate uncouples oxidative phosphorylation, leading to anion gap metabolic acidosis. 

c. Third phase: overwhelming metabolic acidosis 

(1) Patient can no longer compensate for metabolic acidosis. 

(2) Acidemia and shock ensue. 

2. Acute versus chronic poisoning 

a. Acute ingestion 

(1) Mi Id toxicity (triad) 

(a) Ototoxicity (tinnitus, vertigo, and hearing distortion) 

(b) Tachypnea and hyperpnea 

(c) Nausea and vomiting, abdominal pain 

(2) Severe toxicity 

(a) 

CNS stimulation occurs initially, followed by CNS depression; can lead to stupor, convulsions, coma. 

(b) Definitive signs of severe toxicity 

i. Cardiac dysrhythmias 

ii. Noncardiogenic pulmonary edema 

iii. Acute renal failure 

iv. Hemorrhage 

v. Hypo- or hyperglycemia 

vi. Ketonemia, ketonuria 

(c) Other associated signs and symptoms 

i. Hyperthermia 

ii. Diaphoresis 

iii. Dehydration (especially in children) 

b. Chronic ingestion (most commonly seen in the elderly) 

(1) Suspect in any patient with unexplained CNS dysfunction, especially in the presence of a mixed acidbase 

disturbance 

(a) Change in mentation is the usual presenting complaint (confusion, disorientation, lethargy, or 

hal I ucinations). 

(b) Respiratory alkalosis with anion gap metabolic acidosis and a normal or increased pH is the most 

frequent presenting acid-base abnormality. 

(2) Noncardiogenic pulmonary edema 


a. Serum salicylate: a serum ASA level should be drawn at presentation and repeated every 4 hours until the 

serum level is clearly trending down and below 20 mg/dl. The Done nomogram has no use in assessing 

salicylate toxicity. 

b. Blood gases (venous or arterial) determine the type and degree of acid-base imbalance. 

c. Chemistries 

(1) Electrolytes_,, exclude 1 K+, 1 Na+, 1 HC0 3 

- 

(2) Glucose_,, exclude hypoglycemia, hyperglycemia; in salicylate-poisoned patients, CSF may be 

hypoglycemic despite a normal serum glucose. 

(3) BUN/creatinine _,, exclude renal failure 

569


570 

d. Urinary ferric chloride testing is littered with false-positives and false-negatives and cannot be reliably used 

to exclude salicylate poisoning. 

4. Management 

a. GI contamination: consider activated charcoal. Multiple doses of charcoal given every 2-4 hours can be 

given. Gastric lavage may be considered. 

b. Urine alkalinization 

(1) Renal excretion of salicylate (an acid) is enhanced by ionization; urinary excretion of salicylates 

increases 10- to 20-fold when urine pH is increased from 5 to 8. 

(2) Urinary alkalinization (see above) 

(3) Potassium replacement is necessary, because hypokalemia prevents urinary alkalinization due to 

exchange of H+ for K+ in the renal tubules. 


(a) Proven salicylate toxicity with salicylate >20 mg/dL 

(b) Caution: symptoms may be subtle. 

(c) Suspected toxicity based on history and/or physical examination (initiate before confirmatory 

laboratory results) 


(a) Urinary alkalinization with acetazolamide -- worsening of systemic acidosis - 

t ASA in CNS 

c. Hemodialysis is the most effective means of lowering the serum salicylate level and is indicated when one 

or more of the following conditions are present: 

(1) Serum ASA level >90-100 mg/dL in any patient regardless of symptoms. Some recommend 

hemodialysis in chronic salicylate poisoning when levels exceed 40-60 mg/dL. 

(2) Neurologic signs and symptoms (confusion, delirium, psychosis, stupor, coma, or seizures) 

(3) Renal or hepatic failure 


(5) Severe cardiac toxicity 

(6) Severe acid-base imbalance 

(7) Rising serum ASA levels despite urinary alkalinization 

5. Complications of salicylate toxicity 

a. Gastric dilation and ileus 

b. GI hemorrhage 

c. Platelet dysfunction 

N. Acetaminophen 

1. Phases of acetaminophen poisoning 

a. Phase 1-30 minutes to 24 hours after ingestion: anorexia, nausea, and vomiting; pallor and diaphoresis 

may also be present 

b. Phase 11-24-72 hours after ingestion: increased hepatic enzymes, INR, and bilirubin; right upper quadrant 

pain may be present but generally asymptomatic 

c. Phase 111-72-96 hours after ingestion: hepatic encephalopathy, coagulation defects, jaundice and renal 

failure; myocardial dysfunction may be present; anuria and coma are ominous signs 

d. Phase IV-4 days to 2 weeks after ingestion: if the pathologic effects of Phase Ill are reversible, hepatic 

dysfunction will completely resolve. 

2. Evaluation of toxicity 

a. Toxicity may occur with ingestions >200 mg/kg. 

b. The Ru mack Matthew nomogram is used to determine the need for treatment after a single, acute ingestion. 

3. Management 

(1) The first serum acetaminophen level should be drawn no earlier than 4 hours after ingestion. Only one 

level is required to determine the need for treatment. 

(2) If the measured concentration fal Is above the lower line on the nomogram, treatment with 

N-acetylcysteine (NAC) should be started. 

(3) If the level falls below the lower line, no treatment is needed. 

(4) IV and oral NAC are equally effective. 

a. Activated charcoal should be considered for patients presenting within 1 hour of a potentially toxic 

ingestion (200 mg/kg). Simultaneous activated charcoal and NAC is unlikely to cause consequential 

decrease in NAC availability (as was previously thought).


0. Iron 

b. N-acetylcysteine therapy is most efficacious when started within 8 hours of ingestion; however, therapy 

begun after 8 hours retains a high margin of efficacy and should therefore still be given to late-presenting 

patients. 

(1) Mechanism of action 

(a) Acetaminophen is converted to an intermediate reactive metabolite by the cytochrome p-450 

system. This metabolite (NAPQI) is normally detoxified by glutathione in the liver. 

(b) Excess acetaminophen depletes glutathione stores and the toxic metabolite damages hepatic 

cells, causing centrilobular hepatic necrosis. 

(c) The exact mechanism by which NAC prevents hepatotoxicity is uncertain and likely 

multifactorial. Possible mechanisms include the following: 

i. May act by increasing synthesis of glutathione 

ii. Functions as a glutathione substitute, combining directly with the toxic metabolite 

iii. Enhances the sulfonation pathway of acetaminophen metabolism (nontoxic) 

iv. Serves as a free-radical scavenger 

v. Converts NAPQI back to acetaminophen 

(2) Dosage schedule 

(a) Oral (72-hour) regimen 

i. Adverse effects: diarrhea, rash 

(b) 21-hour IV NAC: sick patients, usually those who present late after an acetaminophen overdose, 

may require extension of the protocol beyond 21 hours. 

i. Adverse effects: anaphylactoid reaction (ranging from rash to respiratory failure) 

ii. If an anaphylactoid reaction occurs during the initial IV load, stop the infusion and 

administer diphenhydramine; then reassess the need for NAC therapy and, if indicated, 

resume at a slower rate. This will resolve most anaphylactoid reactions; however, should 

it recur, the patient can be switched to the oral regimen. Anaphylactoid reactions are not 

reported with the oral regimen. 

c. NAC is also indicated for late-presenting patients who have already developed hepatotoxicity. The 

mechanisms by which NAC may ameliorate hepatotoxicity in these patients include: 

(1) Free-radical scavenger 

(2) Improved hepatic oxygen delivery and consumption 

(3) NAC therapy should continue in all hepatotoxic patients until recovery (patient is awake, serum 

acetaminophen undetectable, AST or ALT falling, and INR


(2) A potentially toxic ingestion of elemental iron is 20 mg/kg. More than 5 tablets of any iron preparation 

may be a toxic ingestion for a child. 

2. Clinical stages of iron poisoning (in severe poisoning, stages may overlap) 

a. Stage I: 30 minutes to 6 hours after ingestion: emesis, diarrhea, abdominal pain, hematemesis, and 

hematochezia; conversely, the absence of GI symptoms for 6 hours after ingestion excludes severe 

toxicity. 

b. Stage II: 4-12 hours after ingestion: GI symptoms improve, although patient status is not normal; 

subclinical hypoperfusion and metabolic acidosis manifest. Assess carefully for signs of early 

hypoperfusion and monitor arterial blood gases. 

c. Stage Ill: 6-72 hours after ingestion: coma, metabolic acidosis, coagulation problems, shock, and seizures 

d. Stage IV: 12-96 hours after ingestion: hepatic failure with jaundice, hypoglycemia, and coagulopathy 

e. Stage V: 2-4 weeks after ingestion: vomiting, abdominal pain and pyloric scarring, gastric outlet and 

small-bowel obstruction 


a. Serum iron concentration 

(1) A level >350 mcg/dl 3-5 hours after ingestion may indicate the need for chelation therapy. 

(2) Repeat levels should be obtained to be sure they are not rising. 

(3) Total iron binding capacity is not reliable in this setting, as was previously thought. 

b. Other studies 

(1) CBC, coagulation profile, glucose, electrolytes, and BUN 

(2) Blood gases are indicated if the patient is symptomatic. 

(3) Blood glucose and a WBC count, formerly thought to be predictive of serum iron levels >300 mcg/dl, 

are now known to be nonspecific. 

c. An abdominal radiograph can identify undissolved tablets but is not helpful if negative. 

4. Management 

a. Decontamination 

(1) Gastric emptying 

(2) Whole-bowel irrigation is indicated for a large ingestion, especially if radiopaque tablets are seen on 

abdominal radiograph. 

b. IV fluids are indicated if the patient is hypotensive or has severe gastroenteritis. 

c. Deferoxamine therapy 

P. Hydrocarbons 

1. Definitions 


(a) Serum iron concentration >350 mcg/dl and the patient has symptoms (including protracted 

vomiting) 

(b) Shock 

(c) Coma or seizures 

(d) Acidosis 

(2) Administration: 15 mg/kg/hr continuous IV infusion to a maximum of 6 g; hypotension is the main 

adverse effect. 

(3) The iron-deferoxamine complex is excreted in the urine and turns it an orange-red color (classically 

referred to as "vin rose"). 

(4) The deferoxamine challenge (IM deferoxamine) is no longer used diagnostically or therapeutically. 

a. Hydrocarbons are a broad group of organic compounds that contain carbon and hydrogen in various 

configurations. The halogenated hydrocarbons also contain halogens such as chlorine or fluorine. 

b. Petroleum distillates are hydrocarbons, but not all hydrocarbons are petroleum distillates. Petroleum 

distillates are the breakdown products remaining after processing crude oil. Hydrocarbons can also be 

derived from coal or plant sources. 

2. The aspirational hazard of a specific hydrocarbon depends on whether or not it has two physical properties: 

low viscosity and high volatility. Viscosity is by far the most important factor. 

3. Clinical presentation of hydrocarbon ingestion 

a. Signs and symptoms of aspiration include coughing, choking, and gagging. Cyanosis may be evident within 

minutes. 

572


b. Other signs 

(1) CNS (lethargy, seizures)_,. camphor, lindane, eucalyptus oil 

(2) Respiratory (wheezing, rales, rhonchi, decreased breath sounds, pulmonary edema); radiographic 

findings do not always correlate with physical signs. 

(3) Miscellaneous (tachycardia, fever, belching, vomiting, diarrhea) 

4. Management 

a. Asymptomatic patient 

(1) Indications for gastric aspiration (nasogastric tube) 

(a) Presence of a toxic, or "CHAMP," substance within the ingested agent: 

.Camphor 

.!::!.alogenated hydrocarbons 

Aromatics 

Metals 

festicides 

(b) Ingestion of a massive amount of a low-viscosity agent 

(2) Chest radiograph is controversial and generally not useful in asymptomatic, well-appearing patients. 

(3) Disposition 

(a) Children: observe and reassess for 6 hours in the emergency department. 

(b) Adults (responsible): discharge with specific instructions to return if symptoms develop. 

b. Symptomatic patient 


(2) Supportive care and airway management 

(3) Specific therapy 

(a) Bronchospasm---,, nebulized ~-agonists 

(b) Pulmonary edema---,, continuous positive-airway pressure/positive end-expiratory pressure 

(4) Precautions 

5. Aromatics (solvents) 

(a) Steroids are not useful. 

(b) Antibiotics should be used only for definite infection. 

a. Most exposures occur through inhalation, because aromatics evaporate readily at room temperature. 


(1) Benzene 

(a) Acute exposure causes CNS depression. 

(b) Chronic exposure causes bone marrow aplasia, leukemia. 

(2) Toluene, xylene 

(a) Respiratory tract irritation 

(b) A state of inebriation that can progress to CNS depression 

(c) Renal tubular acidosis (toluene) 

c. Management is symptomatic and supportive. The use of epinephrine for bronchospasm should be avoided, 

because aromatics sensitize the myocardium. 

6. Halogenated hydrocarbons (toxicity is by inhalation, and treatment is supportive and symptomatic) sensitize 

the myocardium, thus predisposing the patient to dysrhythmias. Signs and symptoms that differentiate specific 

agents are listed below. 

a. Carbon tetrachloride (tetrachloromethane) 

(1) Causes marked hepatic and renal toxicity 


(a) Immediate effects_,. nausea, vomiting, diarrhea, and abdominal pain 

(b) Exposure to high concentrations_,. dizziness, confusion, coma, respiratory depression, and 

hypotension 

(c) Prolonged exposure _,. polyneuritis, visual disturbances, and anemia 

(3) In addition to supportive and symptomatic treatment, NAC and hyperbaric oxygen therapy are also 

used for serious poisoning. 

573


b. Methylene chloride 

(1) Found in paint remover, degreasing solvents, aerosol solvents/propellants, and refrigerants. 

(2) On inhalation, pulmonary and CNS signs and symptoms dominate the clinical picture. 

(3) Methylene chloride is partially metabolized to carbon monoxide, so carboxyhemoglobin levels should 

be monitored. 

(a) 

c. Essential oils 

Patients may develop toxic carboxyhemoglobin levels after inhalation or ingestion of methylene 

chloride. 

(b) Peak levels may not be seen for ~8 hours. 

(1) Found in popular home remedies, liniments, and "aromatherapy." All have CNS effects and cause oral 

numbness/irritation and GI distress when ingested. 

(2) Specific toxicities 

Q. Caustic ingestions 

(a) Camphor - 

(b) Nutmeg - 


(c) Eucalyptus oil - 

(d) Pennyroyal oil - 

rapid onset of seizures 

hallucinations 

seizures, coma 

acetaminophen-like hepatotoxicity 

a. Alkali ingestion (eg, lye or sodium hydroxide) 

(1) The esophagus is injured more often than the stomach. 

(2) Injury results from liquefaction necrosis. 

b. Acid ingestion 

(1) The stomach is injured more often than the esophagus. 

(2) Injury results from coagulation necrosis. 

c. Degree of injury depends on: 

(1) Type of ingestion (alkali or acid) 

(2) Volume and concentration of ingested caustic 

(3) Presence or absence of food in the stomach 

(4) Tone of the pyloric sphincter 


a. Immediate 

(1) Result from caustic injury to the larynx, epiglottis, and occasionally the vocal cords. Immediate airway 

management may be needed. 

(2) Esophageal perforation is the most frequent complication in the first few days after ingestion. An alkali 

burn is more likely to cause esophageal perforation than an acid burn. 

(3) Gastric perforation and death can occur within hours of a large acid ingestion; metabolic acidosis, 

disseminated intravascular coagulation, and hemolysis can also occur with acid ingestion. 

b. Delayed 

(1) Esophageal strictures (alkali ingestion) 

(2) Pyloric strictures (acid ingestion) 


a. identify and treat life-threatening problems (airway obstruction and hemorrhage). Edema of the larynx, 

epiglottis, or vocal cords may necessitate cricothyrotomy. However, severe pain is the usual clinical 

presentation (not respiratory distress or shock). 

b. Assessment of GI injury 

(1) History of ingestion and any associated symptoms (dysphagia, pain in the mouth, chest, or abdomen) 


(a) 

Check the mouth for oral burns (not sensitive). 

(b) Check for signs and symptoms of overt or impending esophageal perforation. 

1. Pleuritic pain located in the chest, epigastrium or back is the single most reliable symptom of 

an esophageal injury and may be exacerbated by swallowing or neck flexion. 

574


11. Signs of mediastinal air 

• A nasal quality to the voice 

• A systolic, crunching heart sound (Hamman crunch) 

• Subcutaneous emphysema (although classic, may not be present) 

4. Diagnostic evaluation: indications for endoscopy 

a. Any adult patient with a history of alkali or acid ingestion 

b. Any pediatric patient with: 

(1) An acid ingestion 

(2) An alkali ingestion associated with stridor or two or more of the following: 

(a) Second- or third-degree oral burns 

(b) Drooling 

(c) Vomiting 

(3) Check for evidence of gastric perforation, which can occur within hours of an acid ingestion or 

massive alkali ingestion 

5. Management 

(a) Abdominal tenderness, rigidity 

(b) Decreased bowel sounds 

(c) Free air on abdominal radiograph (upright or lateral decubitus) 

a. Ensure airway is still patent, and treat hypovolemic shock if present. 

b. Treat pain. 

c. Use of diluents 

(1) The primary indication for the use of diluent (milk or water) is ingestion of solid alkali material (drain 

openers, automatic dishwashing detergents). Diluting a solid alkali may reduce the degree of tissue 

injury; in addition, solid alkali material that is adhering to the oropharynx and esophagus needs to be 

moved to the stomach, where it can be neutralized. 

(2) Diluents are of no value in the treatment of liquid alkali ingestion, because the tissue injury is immediate. 

(3) Diluents are of questionable value in the treatment of acid ingestions; although they have been 

recommended, no studies have demonstrated their benefit. 


(a) Liquid alkali ingestion 

(b) Vomiting 

(c) Signs of esophageal or gastric perforation 

(d) Shock 

(e) 

Upper airway obstruction 

(5) Neutralizers (eg, vinegar, sodium bicarbonate) should never be given, because the resulting 

exothermic reaction may worsen tissue damage. 

d. The usual postingestion removal measures are contraindicated in the treatment of caustic ingestions. 

(1) Lavage is contraindicated because of the risk of reexposure of the esophagus and possible perforation 

of the stomach. In addition, aspiration is a hazard. 

(2) Charcoal is contraindicated. 

(a) Alkali and acid are poorly absorbed by charcoal. 

(b) Charcoal does not prevent tissue injury, because the action of caustics is too rapid. 

(c) Charcoal interferes with endoscopic visualization of tissue injury. 

e. Steroid use is controversial and not currently recommended by major toxicology texts. 

f. Antibiotics should be used only for established infection or for perforation of the upper GI tract. 

g. Immediate surgical consult should be obtained if GI tract perforation is known/suspected or endoscopy 

reveals nonviable gastric tissue. 

6. Button battery ingestion 

a. If radiography demonstrates lodgement in the esophagus, immediate endoscopic removal is indicated. 

This is becoming more common with the shift to larger batteries (coin-sized or >20 mm in devices) 

b. If radiography demonstrates the battery has entered the stomach: 

(1) The patient can be followed as an outpatient to assure that the battery has passed within 4-7 days. 

575


(2) Endoscopic removal is indicated if the battery has not passed through the stomach after 48 hours or 

at any point that Cl symptoms develop. 

(3) Once the battery passes through the pylorus, the battery can take weeks to pass. The patient should 

be monitored on an outpatient basis until the battery has passed. 

R. Organophosphates 


a. Organophosphates inhibit acetylcholinesterase, which results in an excess of acetylcholine at the 

neuronal synapses and myoneural junctions. Excess acetylcholine initially excites-and then paralyzesneurotransmission 

at the motor endplate and stimulates CNS muscarinic and nicotinic sites. 

b. Carbamates have the same mechanism of action as organophosphates, except that they do not permanently 

bind to acetylcholinesterase; therefore, their mechanism of action is transient, and pralidoxime (2-PAM, the 

antidote) is not necessary. 

c. Clinical effects 

(1) Muscarinic effects 

(a) 

"DUMBBELS" 

_Qiarrhea 

Urination 

Miosis 

.B.radycardia 

.B.ronchorrhea/bronchospasm 

fmesis 

_Lacrimation 

.S.alivation 

(b) Hypotension and bradycardia 

(2) Nicotinic effects 

(a) 

Muscle fasciculations, cramps and weakness, paralysis 

(b) Hypoventilation and cyanosis 

(c) Diaphoresis 

(3) CNS effects 

(a) 

Restlessness, respiratory depression 

(b) Coma, convulsions 

d. Organophosphates bind with cholinesterase to form a diethylphosphate bond that can be broken with 

pralidoxime (2-PAM chloride). 


a. The classic clinical scenario is a farmer with profuse vomiting and diarrhea, pinpoint pupils, and 

diaphoresis who has a breath odor of insecticide or garlic. 

b. The "DUMBBELS" syndrome develops first, although patients are usually tachycardic initially and later 

develop bradycardia. Respiratory insufficiency and sudden respiratory arrest may occur. 


a. Should include a plasma or RBC cholinesterase (results will not be available immediately in the emergency 

department) 

b. It will be lower than normal in the presence of organophosphate poisoning (


(b) Large doses are frequently needed and should be repeated until tracheobronchial secretions dry up. 

i. In symptomatic adults, the minimum dose is 2 mg IV every 10-15 minutes as needed; the 

dose may be doubled every 10 minutes until secretions are controlled. 

ii. In symptomatic children, the dosage is 0.05 mg/kg IV every 15 minutes as needed. The dose 

may be doubled every 10 minutes until secretions are controlled. 

(2) Pralidoxime (2-PAM chloride) 

(a) A biochemical antidote that reactivates the cholinesterase that has been phosphorylated (bound) 

by the organophosphate 

(b) If this antidote is not given within 24-36 hours, the cholinesterase molecule may be irrevocably 

bound ("aging," ie, the antidote function becomes limited), and new cholinesterase will take 

weeks to regenerate. However, pralidoxime given later may still be beneficial and should be 

administered. 

(c) Patients with signs of cholinergic toxicity should be given pralidoxime as soon as possible even if 

the precise toxin is not yet known. 

i. In adults, the initial dose of 1 g IV over 15-30 minutes may be repeated in 1-2 hours as needed. 

ii. In children, the initial dosage of 25-50 mg/kg IV over 15-30 minutes can be repeated in 

1-2 hours. 


(a) Seizure prophylaxis (all severely poisoned patients) 

(b) Also help prevent rhabdomyolysis and discomfort associated with muscle fasciculations 

d. Drugs that should not be given to patients with organophosphate toxicity 

5. Nerve agents 

(1) Opioids (worsen respiratory depression) 

(2) Physostigmine/pyridostigmine (carbamates) 

(3) Succinylcholine - prolonged paralysis 

(4) Sympathomimetic agents (to treat bronchospasm, eg, aminophylline) 

a. Originally developed as insecticides prior to World War 11; they have been used by the military and, more 

recently, by terrorists. 

(1) Cyclohexyl methylphosphonofluoridate (CMPF or GF) 

(2) Soman (GD) 

(3) Tabun (GA) 

(4) Sarin (GB) 

(5) vx 

b. Nerve agents should be thought of as "potent organophosphates." Properties that distinguish nerve agents 

from conventional insecticides 

(1) High potential for multiple casualties presenting simultaneously, secondary to accidental release from 

military stockpiles, bioterrorist attacks, or chemical warfare 

(2) Highly potent (in severe exposures, death can occur within minutes) 

(3) More rapid "aging" than conventional insecticides, thus limiting the use of pralidoxime as an antidote. 

c. Management 

(1) Prehospital 

(a) Prepare for multiple casualties 

(b) Activate disaster plan 

(c) Assemble all appropriate available medications: atropine, glycopyrrolate, pralidoxime, 

benzodiazepines 

(2) Hospital decontamination area 

(a) Protect medical personnel and emergency department from secondary contamination. 

(b) Ensure surface decontamination of all affected patients before entering emergency department 

i. Remove clothing. 

ii. Surface washing as indicated. 

iii. Contain contaminated secretions. 

(3) Emergency department - pharmacologic therapy (same as above) 

577


S. Mushroom poisoning 

1. Distinct clinical classes based on mushrooms that contain: 

a. Cyclopeptides 

b. Monomethylhydrazine 

c. Muscarine 

d. Coprine 

e. Psilocybin 

2. Diagnostic information 

a. The most toxic classes have delayed onset of initial symptoms (nausea, vomiting, diarrhea). 

(1) Cyclopeptides - 6-10 hours after ingestion 

(2) Monomethylhydrazine - 6-10 hours after ingestion 

b. Identification of specific mushrooms is very difficult; assistance of the local poison center and a mycologist 

should be sought. 

3. Specific mushroom poisonings 

a. Cyclopeptide-containing mushrooms 

(1) Genera: Amanita phalloides, Calerina, Lepiota 

(2) Clinical effects are predominately renal, hepatic, and CNS. 

(a) Phase I: nausea, vomiting, and diarrhea, 6-10 hours after ingestion 

(b) Phase II: symptoms subside but liver function tests are increasing (24-48 hours) 

(c) Phase Ill: 1-6 days after ingestion: toxic hepatitis, renal failure, encephalopathy, seizures, coma 


(a) Early recognition, supportive care 

(b) The following therapies have been used with varying success: multidose activated charcoal, highdose 

penicillin G, N-acetylcysteine, milk thistle 

b. Monomethylhydrazine-containing mushrooms 

(1) Genus: Cyromitra escu/enta (false morel) 


(a) Nausea and vomiting (6-10 hours after ingestion) 

(b) Hepatorenal failure 

(c) Seizures 


(a) General supportive measures and activated charcoal 

(b) Benzodiazepines and pyridoxine (vitamin B6) 

c. Muscarine-containing mushrooms 

(1) Genera: Clitocybe and lnocybe (several varieties) 

(2) Pathophysiology and clinical effects: muscarinic ("DUMBBELS") 


(a) 

Activated charcoal 

(b) Management geared toward cholinergic toxidrome. 

d. Coprine-containing mushrooms 

(1) Genus: Coprinus atramentarious ("inky cap") 

(2) Pathophysiology: disulfiram-like effect 

(3) Clinical presentation: tachycardia, flushing, nausea, and vomiting within 0.5-2 hours of ingestion 


(a) Supportive care 

(b) Consider activated charcoal 

e. Psilocybin-containing mushrooms 

(1) Genera: Psilocybe, Cymnopilus, Conocybe, Panaeolus 

(2) Pathophysiology: act on the CNS in a manner similar to that of LSD 

(3) Clinical presentation: ataxia, hallucinations, hyperkinesis, seizures, nausea and vomiting, mydriasis, 

tachycardia (within 0.5-2 hours after ingestion) 

(4) Treatment: benzodiazepines for agitation and seizures 

578


T. Cyanide 

1. Sources of exposure 

a. Chemical laboratories--.. sudden collapse of a worker is suspicious 

b. Fires 

(1) Cyanide is a combustion product of wool, silk, polyurethane, synthetic rubber, and nitrocellulose. 

(2) Suspect in a fire victim/firefighter/paramedic with decreased level of consciousness, metabolic 

acidosis, and hypotension. 

c. Electroplating 

d. Precious metal refining 

e. Photography 

f. Ingestion of acetonitrile (artificial nail remover), which converts to cyanide 

g. Prolonged exposure to nitroprusside 

2. Pathophysiology: cyanide interacts with Fe+++ in cytochrome aa3 - blockage of electron transport chain-.. 

1 ATP production, 1 H+ consumption (acidosis), and t lactic acid 


a. Neurologic and cardiovascular signs and symptoms predominate the clinical picture. 

(1) Neurologic --.. agitation, seizures, 1 mental status, 1 respirations 

(2) Cardiovascular 

(a) Bradycardia 


(c) Pulmonary edema 

b. Odor of bitter almonds (only 50% of the population can detect this) 

c. Gastritis (with ingestions) 

d. Skin --.. cherry red color or cyanosis (late finding) 

e. Loss of color difference between retinal veins and arterioles on the funduscopic exam (arterialization due to 

high venous pO 2 

) 

4. Management 

U. Digitalis 


(1) IV line, oxygen, cardiac monitor 

(2) Decontamination (unless inhaled) 

(a) Lavage, activated charcoal 

(b) Remove clothing and wash skin (hospital personnel should avoid self-contamination; vomitus may 

give off hydrogen cyanide gas). 


(1) Hydroxocobalamin 5 g IV and repeat once; causes red discoloration of skin and urine; may be used 

safely in smoke inhalation victims 

(2) Cyanide antidote kit: contains a 3-step regimen that should be started as soon as cyanide poisoning 

is suspected. 

(a) Amyl nitrite pearls: until IV access is obtained, crush into gauze and have patient intermittently 

inhale. 

i. Nitrites: administration of nitrates induces methemoglobinemia; cyanide attaches to the 

methemoglobin. 

ii. Do not administer amyl nitrite or sodium nitrite to fire victims, because their hemoglobinoxygen 

carrying capacity may already be compromised by coexistent carbon monoxide 

toxicity. Use sodium thiosulfate. 

(b) 3% sodium nitrite IV at 2.5 ml/min; in anemic patients, dosage may need to be decreased. 

Mechanism of action is induction of methemoglobinemia; do not use in fire victims. 

(c) 25% sodium thiosulfate IV bolus: sodium thiosulfate uses rhodanase (enzyme ubiquitous in body) 

to convert cyanide and thiosulfate to thiocyanate, which is excreted in the urine. 

1. Pharmacology and mechanism of toxicity 

a. Cardiac glycosides have a large volume of distribution and a long half-life; elimination is through the 

kidney; they are not dialyzable. 

b. Toxicity is via Na+-K+ ATPase inhibition--.. changes in serum electrolytes and cardiac conduction 

579



a. Weakness, syncope 

b. Visual changes (yellow halos around lights, referred to as "xanthopsia," is classic) 

c. Nausea and vomiting (acute toxicity) 

d. Anorexia (chronic toxicity) 

e. Hyperkalemia (acute poisoning); hypokalemia (chronic poisoning) 

f. ECG changes 

(1) Bradycardia with AV block (most common finding) 

(2) Paroxysmal atrial tachycardia with block and bidirectional ventricular tachycardia (most characteristic 

findings) 

(3) Although digitalis does not precipitate atrial fibrillation, in patients with chronic poisoning, underlying 

atrial fibrillation can be regularized. 

3. Management 

V. ~-Blockers 

a. Gastric decontamination (charcoal) 

b. Indications for digoxin Immune Fab 

(1) Cardiovascular collapse 

(2) Conduction abnormalities 

(a) AV block (Mobitz II or third degree) 

(b) Ventricular dysrhythmias 

(3) Abnormal chemistries 

(a) 

K+ >5.5 mEq/L (some sources recommend use in patients with K+ >5.0 mEq/L) 

(b) Digitalis level >10 mg/ml 

c. Treatments to avoid 

(1) Routine supplementation with K+ or Mg+" 

(2) Transvenous pacing or cardioversion (may induce ventricular dysrhythmias) 

(3) Use of calcium is controversial. 

(4) ~-blockers and calcium channel blockers, as well as class IA and class IC drugs (specifically 

contraindicated; may worsen cardiac conduction) 

1. Produce toxicity through ~ 1 

- or ~ 2 -receptor blockade 


a. Coma/seizures 

b. Hypotension/bradycardia 

c. Hypoglycemia 

d. Varying degrees of AV blockade 

e. ECG changes can reflect sodium- or potassium-channel blockade 

(1) Widened QRS 

(2) Prolonged QT interval 

3. Management 

a. Gastric decontamination 

b. Specific therapy for cardiovascular collapse 

(1) Vasopressors 

(2) Atropine can be given but may be ineffective. 

(3) Glucagon 2-5 mg IV bolus, then a 2-5 mg/hr infusion 

(4) Calcium chloride 20 mg/kg bolus, then a 20 mg/kg/hr infusion 

(5) High-dose insulin therapy (see calcium channel blockers, below) 

(6) IV lipid emulsion (see calcium channel blockers, below) 

(7) Pacing at a modest rate to allow channels to recycle 

(8) Intra-aortic balloon pump 

c. Contraindicated drugs 

(1) Calcium channel blockers 

(2) Class IA and class IC agents 

580


W. Calcium channel blockers 

1. Inhibit calcium channel conduction in both smooth and cardiac muscle, including the cardiac conduction 

system. 


a. Hypotension and bradycardia, especially with diltiazem, verapamil; may have reflex tachycardia with the 

dihydropyridines 

b. Hyperglycemia 

c. Metabolic acidosis 

d. Pulmonary edema 

e. lleus 

f. ECG changes reflect conduction delay (AV dissociation is common) 

(1) Prolonged PR interval 

(2) Bradycardia, bradydysrhythmias 

3. Management 

a. Decontamination 

(1) Charcoal may be considered. 

(2) Whole-bowel irrigation (if sustained-release preparation) 

b. Specific therapies 

(1) Vasopressors (norepinephrine preferred) 

(2) Atropine (may be ineffective) 

(3) Clucagon 0.05-0.15 mg/kg bolus, then a 2-5 mg/hr infusion 

(4) Calcium 

(5) Pacing at a modest rate to allow channels to recycle 

(6) Invasive modalities: intra-aortic balloon pump, extracorporeal membrane oxygenation, cardiac bypass 

c. High-dose insulin (1-10 units/kg bolus, followed by 1-10 units/kg//hr) should be started in any patient 

not responding to IV fluids and calcium administration. 

d. Intravenous lipid emulsion (20% solution): 1.5 ml/kg bolus, followed by 0.25 ml/kg/min for 30-60 

minutes. 

e. Because of the prolonged absorption time of sustained-release preparations, 24-hour observation is 

mandatory. 

X. Carbon monoxide 

1. Primary mechanism of toxicity is carbon monoxide binding to cytochrome oxidase, disrupting oxidative 

phosphorylation, and interference with microvascular homeostasis. Of secondary importance is carbon 

monoxide binding to hemoglobin, which subsequently decreases the oxygen-carrying capacity of the blood. 


a. Mild to moderate poisoning 

(1) Weakness 

(2) Headache, dizziness 

(3) Nausea, vomiting 

b. Severe poisoning 

(1) Syncope 

(2) Visual complaints 


(4) Dysrhythmias 

(5) Coma, seizures 

(6) Cardiovascular collapse 

c. Flu-like symptoms are common, accounting for frequent misdiagnosis. Diagnostic clues: 

(1) Flu without fever 

(2) Multiple victims from same dwelling 

(3) Small household pets ill or dead from unknown cause 

(4) Recent vehicle travel 

(5) Early winter when furnaces are being turned on 

(6) Power outages in winter 

581


d. Delayed neuropsychiatric sequelae are seen in 10%-43% of cases after apparent recovery 

(1) Headache, dizziness 

(2) Memory deficits 

(3) Personality alterations 

(4) Parkinsonism 


a. Serum carboxyhemoglobin levels 

(1) May not correlate well with toxicity, especially if drawn after empiric oxygen administration 

(2) Venous levels may be used. 

b. Carbon monoxide neuropsychiatric screening battery is a sensitive indicator of toxicity in adults. 

c. CT or MRI may show bilateral hypodensity in the basal ganglia, diffuse white matter hypodensities, or 

cerebral edema. 

4. Management: oxygen therapy 

Y. Mercury 

a. 100% oxygen by tight-fitting mask for 4 hours; longer therapy is indicated for infants and pregnant patients. 

b. Hyperbaric oxygen should be considered if any of the following conditions are present: 

(1) Carboxyhemoglobin level >25% 

(2) Carboxyhemoglobin level > 10% if pregnant 

(3) Any neurologic symptom other than mild headache, including brief loss of consciousness, focal 

neurologic deficit, seizure 

(4) Coma 

(5) Myocardial ischemia 

(6) Worsening symptoms despite oxygen therapy 

c. Half-life of carbon monoxide during treatment with various oxygen sources 

1. Forms 

(1) Room air: 240 minutes 

(2) Nonrebreather: 90 minutes 

(3) Hyperbaric oxygen: 20 minutes 

a. Elemental (liquid mercury, quicksilver-"' thermometers, barometers, sphygmomanometers) 

b. Inorganic (mercuric chloride)-"' chemistry laboratories 

c. Organic (methylmercury)-"' fish and shellfish 


a. Elemental (CNS and lung) 

(1) Acute inhalation-"' pulmonary edema 

(2) Chronic exposure-"' tremor, acrodynia, neuropsychiatric changes 

(3) Contamination 

(a) 

Elemental mercury is most toxic when inhaled (especially if volatilized by heat). 

(b) Ingestions (eg, broken thermometer in mouth) are nontoxic unless extravasation into the 

peritoneum occurs. 

b. Inorganic (skin, GI tract, and kidney) 

(1) Corrosive to skin 

(2) Highly toxic when ingested 

(a) 

Hemorrhagic gastroenteritis -"' shock 

(b) Acute tubular necrosis 

c. Organic (chronic placental-fetal transfer-"' CNS): profound neurotoxicity to the developing brain 

3. Management 

a. Decontamination for ingestion of inorganic and organic mercury: despite the corrosiveness of inorganic 

mercury (and potential risk of perforation), the benefit of GI decontamination outweighs the risk. 

(1) If mercury has been ingested within the last 2 hours, lavage with a small orogastric (or nasogastric) tube. 

(2) When mercury is seen on plain radiograph of the abdomen, whole-bowel irrigation is indicated. 

582


b. Chelation for suspected ingestion (do not wait for blood levels) 

Z. Sulfonylureas 

(1) For all forms of mercury ingestion, may use dimercaptosuccinic acid (DMSA), administered orally 

(2) For significant, acute toxicity and/or inability to tolerate oral therapy, use BAL (dimercaprol) until the 

patient can tolerate DMSA. 

1. Examples (all are oral agents): glipizide, glimepiride, glyburide, chlorpropamide 

2. Pathophysiology: primary mechanism is binding to pancreatic f:\ cells and stimulating endogenous insulin secretion 


a. Signs and symptoms of hypoglycemia (eg, tachycardia, tremor, diaphoresis, confusion, agitation, seizures, 

coma) 

b. Can range from mild to severe and may be delayed 

c. May not manifest in children, the elderly, those taking f:\-adrenergic receptor blockers; must check blood 

glucose levels! 


a. Rapid bedside glucose determination 

(1) Can be unreliable at extreme hypo- and hyperglycemia 

(2) Check frequently (less often as clinical scenario evolves and stabilizes) 

b. Electrolytes: potassium and magnesium levels can also be depressed. 

5. Management 

a. Activated charcoal in the appropriate clinical conditions. 

b. Supplemental glucose 

(1) Should be administered only to hypoglycemic patients. In healthy patients with sulfonylurea poisoning, 

administration of prophylactic glucose can precipitate severe hypoglycemia, because these drugs may 

facilitate exaggerated insulin secretion in response to a glucose load. 

(2) Repeated boluses and/or initiation of a glucose infusion (with D5 or D10) may be necessary 

c. Octreotide 

(1) Synthetic, long-acting analog of somatostatin that antagonizes pancreatic insulin secretion 

(2) Indications: hypoglycemic sulfonylurea-poisoned patients whose serum glucose concentrations cannot 

be maintained with a dextrose infusion. Some recommend its use as a first-line agent along with 

glucose administration. 

(3) Available for administration by IV or SC routes only 

d. Alkalinization of the urine has been used to enhance renal elimination of chlorpropamide but is of no 

value for treatment of poisoning by other sulfonylureas. 

e. Admission or 24-hour observation due to long-acting nature of these agents 

583

TOXICOLOGIC DISORDERS: PRACTICE CLINICAL SCENARIOS 



Scenario A 

Presentation: A 36-year-old woman presents via EMS for evaluation of vomiting and lethargy. The 

paramedics report that the woman's family has been ill with flu-like symptoms. The patient has had no 

fever, diarrhea, or cough, and no significant past medical history. 

Physical examination: Vital signs are temperature 98.2°F (36.8°C), heart rate 85 beats per minute, 

respiratory rate 18 breaths per minute, blood pressure 122/60 mm Hg, and oxygen saturation of 94% 

on pulse oximetry. The patient appears sleepy and pale. Pupils are equal and reactive to light. Chest 

auscultation demonstrates clear lung fields and regular cardiac rate and rhythm. On neurologic 

examination, the patient is oriented to self and place but has some difficulty providing some details of the 

history. She has no focal deficits. An initial blood glucose level is 90 mg/dL. 


Scenario 8 

Presentation: A 2-year-old boy presents with his parents for evaluation of abdominal pain, vomiting, and 

copious bloody diarrhea. The father reports that the boy was found playing under the bathroom sink, where 

his mother's prenatal vitamins are stored. 

Physical examination: Vital signs are temperature 100°F (38°C), heart rate 144 beats per minute, respiratory 

rate 30 breaths per minute, and blood pressure 60/palp. The child weighs 44 pounds (20 kg). He is pale, 

diaphoretic, and barely responsive to stimuli. Chest auscultation demonstrates clear lung fields and regular 

cardiac rate and rhythm with no murmur. Capillary refill time is 5 seconds. Examination of the abdomen 

reveals mild, diffuse tenderness without peritoneal signs. Rectal examination is positive for gross blood. 

The child is somnolent, with no focal deficits. 

Diagnostic evaluation 

Arterial blood gases: 7.12 I 90 I 22 I 9 

WBC = 18,300/mm 3 , hemoglobin= 8.9 mg/dL, hematocrit = 26 

Na+= 135 mEq/L, Cl-= 98 mEq/L, K+ = 4.5 mEq/L, HCO 1 

- = 8 

Glucose: 54 mg/dl 

BUN: 38 mg/dL 


Scenario C 

Presentation: A 22-year-old woman presents after ingesting over 100 tablets of acetaminophen in a suicide 

attempt 4 hours before arrival. She denies coingestants and complains of nausea. She has no past medical 

history and denies pregnancy. 

Physical examination: Vital signs are temperature 98.7°F (37°C), heart rate 82 beats per minute, respiratory 

rate 14 breaths per minute, and blood pressure 123/71 mmHg. The patient is tearful but in no acute 

distress. Pupils are 3 mm and reactive to light, and mucus membranes are moist. Chest auscultation 

demonstrates clear lung fields and regular cardiac rate and rhythm with no murmurs. Bowel sounds are 

normal, and the abdomen is nontender on palpation. Neurologic examination is unremarkable. 


584


Scenario D 

Presentation: A 20-year-old man presents with a friend 1 hour after drinking a quart of windshield wiper 

solution in a suicide attempt. The patient denies coingestants, vision changes, abdominal pain, nausea, and 

vomiting. He has no past medical history. 

Physical examination: Vital signs are temperature 97.8°F (37°C), heart rate 79 beats per minute, respiratory 

rate 32 breaths per minute, and blood pressure 124/77 mmHg. The patient is intoxicated but in no distress. 

Pupils are equal and reactive to light. Chest auscultation demonstrates clear lung fields and regular cardiac 

rate and rhythm. Bowel sounds are normal, and the abdomen is nontender on palpation. On neurologic 

examination, visual acuity is 20/20 bilaterally, the patient is oriented to person and place, cranial nerves 

II-XII are intact, and no focal deficits are seen. 


Scenario E 

Presentation: An 82-year-old man presents for evaluation of "not feeling right." His wife states that he has 

become increasingly confused over the last 3 days. He has also been very irritable, unsteady on his feet, 

and seems to be breathing very rapidly and deeply at times. They deny a history of recent or past trauma. 

Past medical history includes hypertension, hyperlipidemia, and coronary artery disease, and medications 

include hydrochlorothiazide, simvastatin, aspirin, diltiazem, and nitroglycerin as needed. 

Physical examination: Vital signs are temperature 100.2°F (38°C), heart rate 99 beats per minute, 

respiratory rate 32 breaths per minute, and blood pressure 154/88 mmHg. The patient is alert, with no 

signs of trauma. His face is flushed, and mucous membranes are dry. His speech is slurred, but there is no 

facial drop. Pupils are equal and reactive to light. Chest auscultation demonstrates clear lung fields and 

regular cardiac rate and rhythm. Bowel sounds are normal, and the abdomen is nontender on palpation. 

On neurologic examination, motor strength is symmetric in upper and lower extremities. There is no 

clonus, and Babinski responses are down going bilaterally. Cranial nerves are intact. The patient appears 

to have ataxia with transfer into hospital bed; however, gait testing was not attempted because of his 

unsteadiness. Cardiac monitor shows normal sinus rhythm. 

What chronic poisoning can manifest in this fashion? 

Scenario F 

Presentation: A 42-year-old landscaper presents via EMS with profuse vomiting and diarrhea, lethargy, and 

diaphoresis. On their arrival at the scene, the paramedics note that the patient is very tachycardic and has 

pinpoint pupils. They report that the patient did not respond to naloxone before arrival in the emergency 

department. 

Physical examination: Vital signs are temperature 98.4°F, heart rate 55 beats per minute, respiratory rate 28 

breaths per minute, and blood pressure 105/65 mm Hg. The patient appears lethargic. Pupils are pinpoint, 

and eyes are tearing. The oropharynx is moist with excessive salivation, and the patient's breath has a 

strong odor of garlic. Chest auscultation demonstrates rhonchi bilaterally. 


Scenario G 

Presentation: A 25-year-old woman is brought to the emergency department by her family who notes that 

she has had abdominal pain, diarrhea, increasing tremor, confusion, slurred speech, and difficulty walking/ 

ataxia over the last 2 days. She has a history of bipolar disorder and has been hospitalized previously for 

suicide attempts. 

Physical examination: Vital signs are temperature 99.4°F, heart rate 95 beats per minute, respiratory rate 

22 breaths per minute, and blood pressure 118/70 mmHg. The patient appears very drowsy, and answers 

to your questions are slurred. Pupils are equal and reactive to light. Chest auscultation demonstrates clear 

585


lung fields and regular cardiac rate and rhythm. On neurologic examination, the patient is disoriented and 

has diffuse hyperreflexia and a fine tremor. She has no focal deficits. An initial blood glucose level is 85 

mg/dL, and ECG demonstrates QTc of 490 milliseconds. 


Scenario H 

Presentation: A 76-year-old man diabetic man presents with acute confusion and agitation after his wife 

cal led EMS. The paramedics noted that the patient was tremulous, diaphoretic, drowsy, and agitated on 

their arrival. An initial blood glucose level at the scene was 25 mg/dL. The patient was given 25 grams of 

dextrose before transport, after which mental status improved. 

Physical examination: Vital signs are temperature 98.2°F (36.8°C), heart rate 115 beats per minute, 

respiratory rate 24 breaths per minute, and blood pressure 146/88 mm Hg. The patient appears drowsy and 

diaphoretic. Pupils are equal and reactive to light. Chest auscultation demonstrates clear lung fields and 

tachycardic rate and rhythm. On neurologic examination, the patient is oriented to self only and has some 

difficulty providing any history. He appears to have no focal deficits. A repeat blood glucose level is 55 

mgldl. 


Scenario I 

Presentation: An 18-month-old, previously healthy baby boy is brought to the emergency department 

via EMS for evaluation of depressed mental status. His mother states that she found him playing in his 

older brother's pill holder 2 hours before the symptoms started, but she did not think any of the pills were 

missing. The brother takes medications for ADHD, but she is unsure of what they are called. 

Physical examination: Vital signs are temperature 96.8°F, heart rate 44 beats per minute, respiratory 

rate 10 breaths per minute, oxygen saturation 99% on room air, and blood pressure 72/48 mm Hg. The 

patient appears drowsy but responds to light touch. Pupils are pinpoint. Chest auscultation demonstrates 

bradycardia and regular rhythm, with no murmurs, rubs, or gallops; lung fields are clear bilaterally. On 

neurologic examination, the patient will follow simple commands after awakened with light touch but 

drifts back to sleep soon after. 


ScenarioJ 

Presentation: A 64-year-old female with a past medical history of hypertension and depression with 

multiple suicide attempts presents to the emergency department via EMS after she was found unresponsive 

by her family. 

Physical examination: Vital signs are temperature 96.2°F, heart rate 42 beats per minute, respiratory rate 6 

breaths per minute, oxygen saturation 87% on 6 L nasal cannula, and blood pressure 62/34 mmHg. She 

appears ill, has pale skin, and responds minimally to painful stimuli. Pupils are 3 mm bilaterally. Heart rate 

is bradycardic with regular rhythm. Breath sounds clear bilaterally. Skin is cool and pale. On neurologic 

examination, the patient cannot follow any commands or provide any history. 


586



Scenario A 

Diagnosis: carbon monoxide poisoning 

Diagnostic evaluation: A carboxyhemoglobin level is essential to the diagnosis of carbon monoxide 

poisoning. Arterial or venous blood samples may be used. Note that the SaO 2 

will be normal, because it 

measures both oxygen and carbon monoxide-bound hemoglobin. 

Management: The patient should be given high-flow oxygen, and hyperbaric oxygen should be considered. 

Hyperbaric oxygen therapy decreases the rate of delayed neurologic sequelae in carbon monoxidepoisoned 

patients and reduces the half-life of carbon monoxide to 20 minutes, versus a half-life of 240 

minutes when a patient is breathing room air. 

Scenario B 

Diagnosis: iron poisoning 

Diagnostic evaluation: Iron poisoning is classically described as occurring in five sequential "stages." 

• First stage: first few hours after ingestion; direct irritative effect of iron on GI tract causes GI upset, 

including vomiting and diarrhea (possibly bloody). The absence of these symptoms within 6 hours of 

ingestion essentially excludes the diagnosis. 

• Second stage: may last for up to 24 hours; GI symptoms improve, but patient will not become 

asymptomatic and may have abnormal vital signs and evidence of poor perfusion. 

• Third stage: may appear early or develop hours after the second stage; shock and metabolic acidosis 

develop, bleeding and hypovolemia may worsen, and hepatic dysfunction, cardiomyopathy, and 

renal failure may occur. 

• Fourth stage: 2-5 days after ingestion; transaminases increase and may progress to hepatic failure. 

• Fifth stage: 4-6 weeks after ingestion; involves gastric outlet obstruction secondary to corrosive 

effects of iron on pyloric mucosa. 

Management: A serum iron concentration should be obtained. Serum iron concentrations of 300-500 

mcg!dL correlate with mild symptoms, 500-1,000 mcgldl with moderate symptoms, and > 1 000 mcgldl 

with severe symptoms. GI decontamination with orogastric lavage can be considered. Whole-bowel 

irrigation can be performed in standard fashion. Iron does not adsorb to activated charcoal. Deferoxamine 

(IV infusion) is the chelator of choice for severe iron poisoning and can be repeated every 4-6 hours as 

needed. Deferoxamine removes iron from tissues and free iron from plasma and is safe in children and in 

pregnancy. Give empirically for critically ill patients. 

Scenario C 

Diagnosis: acetaminophen toxicity 

Diagnostic evaluation: An acetaminophen level should be obtained and plotted on the Rumack-Matthew 

nomogram (can be used only after a single acute ingestion). A 4-hour level > 150 mcg/ml is considered 

toxic; the nomogram will allow prediction of potentially toxic acetaminophen levels between 4 and 24 

hours after acute ingestion. 

Management: GI decontamination with activated charcoal is recommended by some in the appropriate 

clinical conditions (patient protecting airway). Many forgo administration of activated charcoal given the 

high efficacy of N-acetylcysteine (NAC). Its administration may be more important when the presence of 

coingestants is of concern. Administration of activated charcoal is not thought to significantly hinder the 

efficacy of oral NAC, and no dosing adjustments to either need be made. If the patient's acetaminophen 

level is above the treatment line on the Rumack-Matthew nomogram, NAC should ideally be administered. 

NAC is most effective when initiated within 8 hours of ingestion but is still very effective at reducing 

toxicity in later presenting patients and should not be withheld. 

587


Scenario F 

Diagnosis: organophosphate poisoning 

Diagnostic evaluation: For patients with significant fasciculations, a CK should be obtained. An RSC 

cholinesterase should be obtained (results will not be available immediately in the emergency department) 

and will be lower than normal in the presence of organophosphate poisoning (


Scenario I 

Diagnosis: exploratory ingestion of clonidine 

Management: Supportive care, including intravenous access, cardiorespiratory monitoring. Respiratory 

failure is uncommon but can occur. Intravenous fluid boluses are first-line treatments for hypotension, and 

atropine can be used for bradycardia. Vasopressors are sometimes needed. Naloxone has been used with 

inconsistent success; large doses (10 mg) are needed. 

Scenario J 

Diagnosis: ~-blocker overdose; this scenario could also occur after an overdose of calcium channel 

blockers. Both types of ingestion are treated in a similar fashion; many patients are on both types of agents, 

and the history is unclear on presentation. 

Management: Supportive care included intravenous access and cardiorespiratory monitoring. Activated 

charcoal can be used in the correct clinical situation. Consider whole-bowel irrigation for extendedrelease 

preparations. Respiratory failure can occur, and this patient may require endotracheal intubation. 

Intravenous fluid boluses are first-line treatments for hypotension, and atropine can be used for bradycardia. 

Other therapies for persistent bradycardia and hypotension include glucagon (traditional antidote for 

~-blocker poisoning but may work for calcium channel blocker poisoning), calcium (boluses followed by 

an infusion; hypercalcemia is well tolerated in these patients, and generous doses of calcium are needed 

to see an effect), high-dose insulin therapy (1 unit/kg bolus followed by an infusion of 1 unit/kg/hr, titrating 

upward; doses of 10 units/kg/hr have been used without complications), vasopressors (norepinephrine is 

recommended as first choice), lipid emulsion therapy, transcutaneous/transvenous pacing (may not capture), 

intra-aortic balloon pump, extracorporeal membrane oxygenation, and cardiac bypass. 

590

ENDOCRINE, METABOLIC, AND NUTRITIONAL DISORDERS 

ENDOCRINE, METABOLIC, AND NUTRITIONAL 

DISORDERS 

ADULT FLUID VOLUMES ......................................................................................................................................... 596 

Normal Values ........................................................................................................................................................... 596 

Patient Assessment .................................................................................................................................................... 596 

FLUID AND ELECTROLYTE DISORDERS .................................................................................................................. 596 

Basic Science Review ................................................................................................................................................ 596 

Total Body Water/Fluid Compartments ............................................................................................................... 596 

Water Regulation ............................................................................................................................................... 596 

Sodium Regulation ............................................................................................................................................. 597 

Potassium Regulation ......................................................................................................................................... 598 

Calcium Regulation ............................................................................................................................................ 598 

Magnesium Regulation ....................................................................................................................................... 598 

Chloride Regulation ........................................................................................................................................... 598 

Hydrogen-Potassium Exchange to Maintain Electrolyte Balance ......................................................................... 599 

The Anion Gap ................................................................................................................................................... 599 

Pathophysiology of Acid-Base Disorders ............................................................................................................. 599 

Electrolyte Disorders ................................................................................................................................................. 601 

Hyponatremia .................................................................................................................................................... 601 

Hypernatremia ................................................................................................................................................... 603 

Dehydration ....................................................................................................................................................... 604 

Hypokalemia ...................................................................................................................................................... 605 

Hyperkalemia ..................................................................................................................................................... 606 

Hypocalcemia .................................................................................................................................................... 607 

Hypercalcemia ................................................................................................................................................... 608 

Hypomagnesemia .............................................................................................................................................. 609 

Hypermagnesemia ............................................................................................................................................. 610 

Hypochloremia .................................................................................................................................................. 610 

Hyperchloremia ................................................................................................................................................. 611 

Key Concepts in Electrolyte Disorders ................................................................................................................ 611 

Acid-Base Disorders .................................................................................................................................................. 611 

General Approach to the Patient with an Acid-Base Abnormality ........................................................................ 611 

Metabolic Acidosis ............................................................................................................................................. 613 

Metabolic Alkalosis ............................................................................................................................................ 614 

Respiratory Acidosis ........................................................................................................................................... 614 

Respiratory Alkalosis .......................................................................................................................................... 615 

Lactic Acidosis ................................................................................................................................................... 615 

Important Points to Remember in the Management of Acid-Base Disorders ........................................................ 616 

Clinical Situations and Associated Laboratory Findings ....................................................................................... 616 

METABOLIC DISORDERS ......................................................................................................................................... 617 

Hypoglycemia ........................................................................................................................................................... 617 

Diabetic Ketoacidosis ................................................................................................................................................ 618 

Hyperglycemic Hyperosmolar Nonketotic Coma ...................................................................................................... 621 

Alcoholic Ketoacidosis .............................................................................................................................................. 622 

Thyroid Storm ........................................................................................................................................................... 623 

Myxedema (Hypothyroid) Coma ............................................................................................................................... 624 

Adrenal Insufficiency (Addison Disease) and Crisis ................................................................................................... 626 

591

ENDOCRINE, METABOLIC, AND NUTRITIONAL DISORDERS: SELF-ASSESSMENT QUESTIONS 

ENDOCRINE, METABOLIC, AND NUTRITIONAL DISORDERS: 


1. The major intracellular cation is: 

(a) Potassium 

(b) Calcium 

(c) Chloride 

(d) Sodium 

2. The weight of total body water in a 70-kg adult man is closest to: 

(a) 40 kg 

(b) 20 kg 

(c) 

60 kg 

(d) 30 kg 

3. All of the following are associated with an increased difference between the calculated and measured serum 

osmolality (osmolal gap) except: 

(a) An ethanol level of 200mg% 

(b) Administration of 100 grams of mannitol 

(c) Hyperglycemic nonketotic coma 

(d) Severe ketoacidosis 

4. All of the following are true about antidiuretic hormone (ADH) except: 

(a) 

It is released in response to decreases in serum osmolality. 

(b) It is released in response to decreases in intravascular volume. 

(c) It acts on the renal tubules to decrease free water excretion. 

(d) It is present in excessive amounts in syndrome of inappropriate ADH secretion (SIADH). 

5. All of the following may result in changes in the concentration of ionized calcium except: 

(a) Decreased serum albumin 

(b) Hyperventilation 

(c) Excessive parathyroid hormone 

(d) Vitamin D intoxication 

6. The regulation and function of magnesium are closely tied to: 

(a) 

Sodium 

(b) Chloride 

(c) Calcium and phosphate 

(d) Serum albumin 

7. Causes of an anion gap acidosis include all of the following except: 

(a) Salicylate poisoning 

(b) lsopropyl alcohol ingestion 

(c) Uremia 

(d) Methanol poisoning 

8. An increased anion gap(> 16 mEq/dL) and an increased osmolal gap(> 10 mOsm/dL) may be seen in all of the 


(a) 

Uremia 

(b) Ethanol intoxication 

(c) Methanol poisoning 

(d) Diabetic ketoacidosis 

592


9. The pulmonary excretion of CO 2 

(hyperventilation): 

(a) Increases the serum H+ concentration 

(b) Increases the serum pH 

(c) Decreases the renal excretion of bicarbonate 

(d) Increases the serum concentration of bicarbonate 

10. Physiologic compensation for metabolic acidosis occurs through all of the following mechanisms except: 

(a) Persistent vomiting 

(b) Pulmonary excretion of CO 2 

(c) Increased renal H+ excretion 

(d) Increased renal bicarbonate losses 

11. In human studies and experimental animal models, osmotic demyelination has been associated with all of the 


(a) Rapid correction of symptomatic hyponatremia (2 days duration at a rate >0.6 mEq/L/hour 

(c) Correction of hyponatremia >2 days duration at a rate >25 mEq over 48 hours 

(d) Correction of hyponatremia >24 hours duration at a rate >2.5 mEq/hour 

12. An 80-year-old woman is found unconscious in her Houston apartment, which is not air-conditioned, in August. Her 

serum sodium is 185 mEq/L. Blood pressure is 60 mmHg by palpation, and pulse 130 beats per minute. The most 

appropriate fluid regimen for her initial resuscitation is: 

(a) D5W at 500 ml/hour 

(b) D5/0.45% normal saline at 250 ml/hr 

(c) Normal saline or lactated Ringer's 1 L in the first hour 

(d) D5/0.33% normal saline at 500 ml/hr 

13. A 60-year-old man with a history of congestive heart failure presents to the emergency department complaining of 

pedal edema. His mental status is clear. Blood pressure is 120/80 mmHg, and pulse is 80 beats per minute. Lungs 

are clear, and neck veins distended. Serum sodium is 1 05 mEq/L. Of the fol lowing therapies, which is the most 

appropriate? 

(a) Infusion of 3% normal saline at 50 ml/hour and concomitant administration of furosemide 

(b) Infusion of normal saline at 200 ml/hour with concomitant administration of furosemide 

(c) Water restriction 

(d) IV administration of 40 mg of furosemide every hour until serum sodium is normal 

14. A 2-year-old child has been vomiting for 6 days. In the emergency department she is listless, with a pulse of 180 

beats per minute and capillary refill >4 seconds. Her weight is 10 kg. The serum sodium is 120 mEq/L. The most 

appropriate initial therapy is: 

(a) 

Infusion of 3% normal saline at 1 ml/kg/hour and concomitant administration of furosemide 

(b) Infusion of 3% normal saline at 1 ml/kg/hr 

(c) A rapid infusion of normal saline at 20 ml/kg 

(d) D5/0.45% normal saline at 125 ml/hr 

15. Of the following clinical scenarios, which patient has the most urgent need for rapid potassium replacement? 

(a) A 4-year-old with persistent vomiting, metabolic alkalosis, and a serum potassium of 3.0 mEq/L 

(b) A 56-year-old woman taking a diuretic and digoxin, with a serum potassium of 3.0 mEq/L 

(c) A 22-year-old insulin-dependent diabetic patient with an arterial pH of 6.9 and a serum potassium of 3.0 mEq/L 

(d) A 45-year-old man with delirium tremens and a serum potassium of 3.0 mEq/L 

16. A 60-year-old man presents with confusion, polyuria, and a serum calcium of 16 mg/dl. Of the fol lowing therapies, 

which is the least appropriate? 

.~ (a) Normal saline IV at 500 ml/hour 

(b) Salmon calcitonin 4 U/kg IM 

(c) Methylprednisolone sodium succinate 100 mg IV 

(d) Vitamin D 25,000 units IM 

593


17. A healthy 17-year-old woman suffers a cardiac arrest during an infusion of magnesium sulfate for treatment of 

eclampsia. In addition to starting CPR, the most appropriate initial treatment is: 

(a) 

Immediate hemodialysis 

(b) IV infusion of 1 g calcium chloride 

(c) 

IV infusion of 140 mEq of sodium bicarbonate 

(d) IV infusion of 10 mEq of potassium chloride 

18. A SO-year-old alcoholic patient presents with obtundation. Blood pressure is 150/100 mm Hg, and pulse is 120 beats 

per minute. He is treated empirically with 25 g of DS0W and 100 mg of thiamine. The pH is 7.2, pCO 2 

= 15, Na+= 

140 mEq/L, Cl-= 102 mEq/L, HCQ 3 

- = 6 mEq/L, K+ = 4 mEq/L, and glucose= 250 mg/dL. Urine ketones are negative. 

Ethanol is not detectable. The osmolal gap is 100 mOsm/L. The most urgent interventions are: 

(a) Administration of 1 mEq/kg of sodium bicarbonate, blood cultures, and broad-spectrum antibiotics, followed 

by observation in the ICU 

(b) Initiation of an ethanol infusion (or administration of 4-methylpyrazole) and arrangements for hemodialysis 

(c) Immediate head scan and neurosurgical consultation 

(d) Intubation and gastric lavage, followed by administration of 60 g of activated charcoal with sorbitol 

19. The mental obtundation seen in association with nonketotic hyperosmolar coma is most closely associated with: 

(a) 

Serum bicarbonate level 

(b) Serum osmolality 

(c) pH of the plasma 

(d) pH of the cerebrospinal fluid 

20. The nitroprusside test for ketones most accurately assesses the presence of: 

(a) 

Acetone 

(b) Acetoacetate 

(c) ~-hydroxybutyrate 

(d) It assesses all of the above equally we/ I. 

21. Which of the fol lowing drugs is not classically associated with producing drug-induced hypoglycemia? 

(a) 

Alcohol 

(b) Aspirin 

(c) 

NSAIDs 

(d) Disopyramide 

22. Expected findings in a patient with purely alcoholic ketoacidosis include all of the following except: 

(a) 

High anion gap acidosis 

(b) Markedly increased (>300 mg!dl) serum glucose 

(c) A nitroprusside test that may be only weakly positive 

(d) Nondetectable or low blood alcohol level 

23. The mainstay of therapy for patients in alcoholic ketoacidosis is IV hydration with: 

(a) 

A saline solution (normal saline or 0.45% normal saline) 

(b) A glucose solution (DSW) 

(c) A solution containing both glucose and saline (OS/normal saline or D5/0.45% normal saline) 

(d) The type of solution used is irrelevant. 

24. The acidosis seen in association with alcoholic ketoacidosis is primarily attributable to the presence of: 

(a) ~-hydroxybutyrate 

(b) Acetoacetate 

(c) Acetone 

(d) Lactate 

25. All of the following ingestions are associated with a high anion gap acidosis except: 

(a) 


(b) Paraldehyde 

(c) Aspirin 

(d) lsopropyl alcohol 

594


26. A patient presents with hypertension, tachycardia, a fever, and slight confusion. You suspect thyroid pathology. 

Which of the following drugs should be avoided? 

(a) Aspirin 

(b) Propranolol 

(c) Ibuprofen 

(d) Acetaminophen 

27. The role of propylthiouracil in the treatment of thyroid storm is most accurately described as that of: 

(a) Inhibiting conversion ofT 3 

to T 4 

(b) Retarding release of stored thyroid hormone 

(c) 

Blocking the synthesis of thyroid hormone 


28. Al I of the following statements regarding hypothyroidism are accurate except: 

(a) 

Primary hypothyroidism is more common than secondary hypothyroidism. 

(b) Patients with secondary hypothyroidism have increased levels of thyroid-stimulating hormone. 

(c) Treatment of Grave disease is the most common cause of primary hypothyroidism in adults. 

(d) Drugs that have been associated with development of primary hypothyroidism include lithium and 

phenylbutazone. 

29. After abrupt cessation of steroid therapy, a patient presents with vomiting, hypotension, and generalized malaise. All 

of the following laboratory findings would be suspected except: 

(a) 

Hyponatremia 

(b) Hypoglycemia 

(c) Hyperkalemia 


ANSWERS 

I. a 

2. a 

3. C 

7. 

8. 

9. 

b 

b 

b 

4. a 10. d 

13. 

14. 

15. 

16. 

5. a 11. a 17. b 

C 

C 

C 

d 

19. b 

20. b 

21. C 

22. b 

23. C 

6. c 12. c 18. b 24. a 

25. d 

26. a 

27. C 

28. b 

29. d 



595


ADULT FLUID VOLUMES 

I. NORMAL VALUES 

A. Extracellular fluid= 200 ml/kg 

B. Estimated blood volume= 70 ml/kg 

C. Plasma volume= 35.5 ml/kg (approximately half the blood volume) 

II. PATIENT ASSESSMENT 

A. Normal capillary refill (nail beds) ::;;2 seconds 

1. If delayed >2 seconds, an approximated volume deficit :C::15% is present. 

2. Capillary refill can also be delayed from poor pump function. 

B. Acute onset tachycardia from fluid loss 

1. > 100 beats per minute= 15%-30% volume deficit 

2. >120 beats per minute= 30%-40% volume deficit 

3. >140 beats per minute= >40% volume deficit 

4. These values may be decreased in elderly patients and in patients on ~-blockers or other medications that may 

impair the tachycardic response. For example, an elderly patient on ~-blockers may have a heart rate


c. At equilibrium, the concentration of molecules in the fluid of one compartment is equal to that in all 

the other compartments. When free water is lost from one compartment, its concentration of molecules 

increases; this causes water to diffuse into that compartment until the concentrations equalize. 

d. Normal serum osmolality is 275-295 mOsm/L. 

(1) The following equation may be used to calculate serum osmolality: 

(2 x Na) + 

BUN 

2.8 

+ 

Glucose 

18 

+ 

Ethanol 

4.6 

The calculated value should be within 10 mOsm/L of the measured value. The difference between 

the measured and calculated values is the osmolal gap. A high osmolal gap increases suspicion of an 

unidentified substance dissolved in the blood. 

(2) Causes of abnormal osmolar states: 

(a) 

Hyperosmolality = t measured serum osmolality 

i. t serum Na+ (no gap) 

ii. Alcohol ingestion: either ethanol or "toxic alcohols" (large gap) 

• Most common cause of coma+ t serum osmolality 

• t serum osmolality + t osmolal gap+ anion gap acidosis - 

• lsopropyl alcohol causes an osmolal gap but no acidosis. 

iii. Hyperosmolar hyperglycemic nonketotic coma (no gap) 

iv. Ketoacidosis (small gap) 

v. Uremia (small gap) 

(b) Hypo-osmolality - .j, serum Na+= .j, measured serum osmolality 

methanol or ethylene glycol 

(c) Remember that methanol or ethylene glycol causes anion gap acidosis and osmolal gap. lsopropyl 

alcohol does not cause an anion gap acidosis. 

3. Clinical pathophysiology 

a. The average adult requires about 2,000-3,000 ml of water per day (depending on losses). 

b. Water loss 

C. Sodium regulation 

1. Facts 

(1) The volume of water loss per day can be divided into two categories: 

(a) Insensible losses 

i. Respiratory tract (-600 ml) 

ii. Skin (-300 ml) 

iii. Feces(-100ml) 

(b) Urinary losses (-1,500 ml) 

i. Normal dietary intake produces -300 ml of solute/day. 

ii. A urine output of at least 0.5 ml/kg/hr indicates an adequate level of hydration and renal 

perfusion in adults with normal renal function. 

(2) Clinical manifestations of volume loss range from mild postural lightheadedness to resting tachycardia 

to a nondetectable blood pressure. 

(3) Flexibility in the body's handling of water intake is provided by two mechanisms. 

(a) Antidiuretic hormone (ADH) 

i. Increased body water - decreased serum osmolality - suppression of ADH secretion - 

diuresis of free water 

11. Decreased free water - increased serum osmolality - stimulation of ADH release - 

retention of free water 

(b) Aldosterone 

1. Released by the adrenal gland in response to renin release by the kidney in low-volume states 

ii. Stimulates retention of sodium by the renal tubules, which is followed by retention of water. 

a. Total body sodium= -40-50 mEq/kg. 

b. Distribution of major cations and anions 

597


2. Concepts 

(1) Na+ is the major extracellular cation (140 mEq/L) 

(2) Cl- and HCO 3 

are the major extracellular anions. 

(3) K+ and Mg++ are the major intracellular cations. 

a. When physiologic changes cause intracellular-extracellular osmotic dysequilibrium, corrections are not 

made by movement of solute across the cell membrane but, rather, by movement of water. 

b. Disorders of sodium regulation actually represent a disorder of water regulation in which either too little or 

too much water is present in the body relative to solute. 

c. What this means is that hyponatremia and hypernatremia can occur with normal, low, or high total body 

water content. 

D. Potassium regulation 

1. The normal serum concentration is 3.5-4.5 mEq/L. 

a. Although the serum potassium is only 2% of total body potassium, in most settings it is a good indicator of 

total body stores. 

b. Potassium is the primary intracellular cation. 

c. An increased potassium concentration is a potent stimulus for aldosterone release. 

2. Physiologic actions of potassium 

a. Maintains resting membrane potential 

b. Changes in the intracellular/extracellular gradient facilitate propagation of electrical impulses. 

c. Filters freely through the glomerulus, is reabsorbed in the proximal and ascending tubules, and is then 

secreted into the distal tubule in exchange for sodium 

E. Calcium regulation 

1. Calcium is the most abundant cation in the body, but 99% is bound in bone; the rest is in the extracellular 

fluid, half of which is bound to plasma proteins and half as free (active) ions. The calcium gradient between 

extracellular and intracellular spaces is highly regulated at 10,000:1. 

2. Total plasma calcium levels (8.5-10.5 mg/dl) are maintained by the function of vitamin D and parathyroid 

hormone. 

a. Protein-bound = 4.0-4.5 mg/dL 

b. Ionized = 4.2-4.8 mg/dL 

c. A laboratory value reported in mEq/L =½the amount in mgldl, eg, 4.2 mgldl = 2.1 mEq/L= 1.05 mOsm/L 

3. Physiologic actions 

a. Changes in H+ concentration result in changes of ionized calcium because Ca++ binds to protein in place of 

H+. Decreased H+, such as in hyperventilation - respiratory alkalosis - t protein-bound calcium+ 

t ionized serum Ca++ (relative hypocalcemia) 

b. The ionized fraction of calcium mediates physiologic effects. Clinical effects of hypocalcemia are seen 

when the ionized levels fall below 3 mg/dL. Clinical manifestations of hypercalcemia are noted at total 

serum calcium levels> 11 mg/dl. 

(1) Serum albumin level (a decrease of 1 gldl in albumin results in a decrease of 0.8 mg/dl in calcium) - 

no change in ionized fraction 

(2) Alkalosis (decreases the ionized fraction) - no change in total serum calcium 

(3) Acidosis (increases the ionized fraction) - no change in total serum calcium 

F. Magnesium regulation 

1. Magnesium is the second most abundant intracellular cation, and its regulation is closely related to calcium 

and phosphate. 

2. Total body content is 24 g (2,000 mEq), 60% of which is in bone; most of the remaining 40% is intracellular. 

Magnesium is also an essential element in the production of cellular energy, cardiac excitability, the clotting 

mechanism, and in neuromuscular activity. 

3. Dietary source is green vegetables; the usual daily requirement is ~25 mEq/day; normal serum level is 

1.4-2.2 mEq/L. 

G. Chloride regulation 

1. Chloride is an extracellular anion that increases or decreases in concentration whenever changes occur in the 

concentrations of other anions, eg, metabolic acidosis (due to bicarbonate loss) results in an increase in chloride. 

2. Functions of chloride 

598


a. Acid-base balance 

b. Osmotic balance 

c. Water balance 

3. A change in serum chloride is seldom a primary problem. 

H. Hydrogen-potassium exchange to maintain electrolyte balance 

1. A hydrogen-potassium exchange may also occur. The classic teaching is that when metabolic acidosis is 

caused by organic acids that do not freely cross the cell membrane (eg, ketoacids), H+ moves inside the cell 

to be buffered and is exchanged for K+. However, while hyperkalemia is commonly associated with diabetic 

ketoacidosis, it is not commonly seen in alcoholic ketoacidosis, suggesting that insulin may have a significant 

effect on potassium regulation. Increases in serum K+ do not occur when the metabolic acidosis is caused by 

other organic ions (such as lactate). This concept is important to help remember key clinical pearls for patient 

management. 

I. The anion gap 

1. The anion gap is the difference between serum anions and cations. In a physiologically normal person, 

measured serum anions are Cl- and HCO 3 

and unmeasured anions are the negative charges on serum albumin, 

phosphate, and sulfate. Measured serum cations are Na+, K+, Mg++, and Ca++. In the clinical setting, the anion 

gap is calculated from the predominant measured cation (Na+) and anions (Cl- and HCO -). 3 

Anion gap = Na+ - (Cl- and HCO 3 

-) 

Normal range= 8-16 mEq (A good rule of thumb is that both osmolal gap and anion gap are around 10.) 

2. A significantly increased anion gap signifies the presence of excessive unmeasured anions (usually due to 

metabolic acidosis). A small or negative anion gap is seen when there is: 

a. An excess of unmeasured serum cations or 

b. An increase in unmeasured positively charged proteins or 

c. A decrease in serum albumin or 

d. An increase in negatively charged particles that are mistaken for chloride (such as bromide or iodide) 

e. Decreased anion gap: lithium toxicity, myeloma patients 

3. Causes of anion gap acidosis (MUDPILES) 

a. Methanol 

b. 1/.remia 

c. Qiabetic ketoacidosis 

d. faraldehyde 

e. lron, isoniazid, inhalants, inborn errors of metabolism 

f. lactic acidosis 

g. S.alicylates, solvents, starvation 

4. If an abnormally high anion gap occurs in the presence of an abnormally high osmolal gap (> 10 mOsm 

difference between the measured and calculated serum osmolarity), ingestion of methanol or ethylene glycol 

should be suspected. 

5. If an abnormally high osmolal gap is seen in the presence of a normal anion gap, suspect the presence of one 


a. Ethanol 

b. lsopropyl alcohol 

c. Glycerol 

d. Sorbitol 

e. Mannitol 

f. Acetone 

J. Pathophysiology of acid-base disorders 

1. The body normally maintains a critical acid-base balance primarily by handling three types of acids: 

a. Fixed acids (W), which are normally produced from dietary intake (sulfates and phosphates) 

b. Acids produced from pathologic processes and abnormal metabolic pathways 

c. Exogenous acids (toxins, medications, iatrogenic administration) 

2. Approximately 15,000 mg of volatile acid (CO 2 

) is excreted from the lungs each day. 

3. Approximately 70 mEq/L of nonvolatile acids are produced each day. 

599


4. There are three mechanisms for renal excretion of these acids: 

a. Direct hydrogen excretion (~0.1 mEq/day) 

b. Excretion of urinary buffers (~20 mEq/day) 

c. Excretion with ammonia (~50 mEq/day) 

5. Hydrogen ion activity is clinically reported as pH. At normal body temperature, a system of buffers maintains 

the pH of blood at 7.4 (40 nMH+ concentration). 

[W] Halves for each 0.3 unit ~ 

rise in pH 

t ; 

[H+] Doubles for each 0.3 

unit fall in pH 

t 

Alkalinization 36 44 Acidification 

(alkalemia) 

(acidemia) 

10 16 20 26 32 50 63 80 100 

125 

160 

pH units 

8.0 7.8 7.7 7.6 7.5 7.3 7.2 7.1 7.0 

6.9 

6.8 

7.44 - 7.36 

Limited range of linearity between pH and [H+] 

(Li 0.1 pH unit= Li [H+] of 10 nM) 

Relationship of pH to H+ Concentration 

6. Minute-to-minute regulation of hydrogen ion concentration in the blood and interstitium is maintained 

primarily by the bicarbonatecarbonic acid system: 

~ ~ 

To maintain this equilibrium, reciprocal changes occur when a component of this equation is "out of balance." 

t HCO 3 

- """ t H+ 

t pCO 2 

_,. 

tW 

t pCO 2 

_,. 

tH+ 

; 

H+ = 24 x 

pCO 2 

HCO 3 

- 

7. When the balance between bicarbonate and carbonic acid is disrupted, compensatory mechanisms are 

stimulated. Metabolic compensation occurs in response to respiratory abnormalities, and respiratory 

compensation occurs in response to metabolic abnormalities. The following parameters can be used to predict 

the expected compensatory response with acute changes in the pCO 2 

: 

pH ! by 0.08 units for each 10 mmHg t in CO 2 

pH t by 0.08 units for each 10 mm Hg ! in CO 2 

a. Metabolic compensation for respiratory acidosis is facilitated by increased retention of bicarbonate by the 

kidney. In respiratory alkalosis, the kidney secretes bicarbonate. 

b. Respiratory compensation for metabolic alkalosis is limited by the development of hypoxemia that occurs 

during hypoventilation. 

c. Respiratory compensation for metabolic acidosis is rapid. Experimental observation of respiratory 

compensation for uncomplicated metabolic acidosis has determined the following: 

(1) The pH is never compensated to a normal level (>7.35). 

(2) The pCO 2 

almost never goes lower than 10. 

(3) The pCO 2 

approximates 1.5 x bicarb+ 8 ± 2. 

600


II. ELECTROLYTE DISORDERS 

A. Hyponatremia 

1. Definition: serum Na+ 25 mEq/48 

hours in cases of hyponatremia that has been present >2 days. 

(b) Avoid an increase in sodium of >9 mEq/L in 24 hours. 

(c) The sodium deficit can be calculated, but generally a change of 4-6 mEq/L within the first few 

hours will be safe. 

(d) There is no evidence that correction of very acute (


(2) Is the cause of hyponatremia evident on the basis of history and physical examination? If not, 

measurement of the serum osmolality will be very helpful. 

Electrolyte 

Normal 

nonelectrolyte 

Abnormal 

nonelectrolyte 

Serum 

osmolality 

2[Na+] mEq/L + 

I 

Effective osmoles 

(tonicity) 

mg!dL 

Ethanol 

lsopropanol 

/ 


[glucose] "' BUN 

+ -- Methanol 

18 2.8 Mannitol 

I 

Serum Osmolality Calculated and Measured 

Normal: 

Osmolal gap: 

calculated Osm - 10 mOsm/L = measured Osm (Na+, glucose, BUN) 

calculated Osm < measured Osm (nonelectrolyte solute other than glucose or urea, 

or pseudohyponatrem ia) 

(3) Categorize the hyponatremic patient into one of two groups, which will guide therapy (normal 

or high osmolality, low osmolality). Low osmolality is true hyponatremia and requires treatment. 

Pseudohyponatremia does not require treatment. 

(a) 

Pseudohyponatremia 

i. If the measured osmolality is normal and the calculated osmolality is low: 

• Cause: low water volume with high solute volume; the sodium concentration is normal in 

the aqueous phase. 

• Differential diagnosis: multiple myeloma, hyperlipidemia 

• Treatment: none 

ii. If the measured osmolality is high and the calculated osmolality is normal to high: 

• Cause: free water moves from the intracellular space to the high solute concentration in the 

extracellular space. 

• Differential diagnosis: hyperglycemia, mannitol, glycerol excess 

• Increased glucose is the most common cause of pseudohyponatremia in clinical practice. 

• Treatment 

0 Hyperglycemia_,. insulin and saline 

o Mannitol _,. saline 

(b) Low osmolality (most common) 

I. 

[ 

measured osmolality = low 

calculated osmolality = low 

> both equal 

J 

ii. The causes are classified and the treatments are based on evaluation of two parameters: 

• Volume status of the patient (hypovolemic, euvolemic, hypervolemic) 

• Measurement of urine sodium 

iii. Hypovolemic hypo-osmolar hyponatremia 

• Contracted effective intravascular volume_,. kidney avidly reabsorbs water_,. hyponatremia 

• Clinical examination reflects the presence of hypovolemia: postural hypotension, poor skin 

turgor, flat neck veins 

• Measurement of urinary sodium can help determine if the volume depletion is due to a 

renal or extrarenal source. 

602


B. Hypernatremia 

o Renal sodium loss (urine Na+ >20 mEq/L) 

-Diuretics 

-Mineralocorticoid deficiency 

-Salt-wasting nephropathy 

-Osmotic diuresis (hyperglycemia, mannitol) 

0 Extrarenal sodium loss (urine Na+ 20 mEq/L). 

iv. The diagnosis of SIADH is one of exclusion. 

• Typical laboratory data: t BUN, t urine osmolality (> 150 mOsm), t urine Na+ (>20 mEq/L) 

• Treatment is based on the severity of the disorder. For acute, severe, symptomatic 

hyponatremia, hypertonic saline or furosemide plus saline may be indicated for rapid 

correction. For less severe cases, the restriction of free water is appropriate therapy. 

(d) Hypervolemic hypo-osmolar hyponatremia (most common form) 

1. Volume status: clinically edematous (the extracellular volume is expanded but "ineffective"; 

the kidney perceives a low intravascular [extracellular] volume and resorbs excess salt and 

water; as a result, there is an excess of total body sodium and a greater excess of total body 

water) 

11. Measurement of urinary sodium 

• >20 mEq/L (renal): acute or chronic renal failure 

• 145 mEq/L (> 155 mEq/L = severe) 


a. Clinical presentation: t level of consciousness, dehydrated, ± seizures 

b. There are no classic ECG findings. 

c. Etiology: sodium and water loss 

(1) t water loss (hyperpnea, excessive sweating, vomiting) 

(2) t diuresis (diabetes insipidus, acute tubular necrosis, diuretics, and postobstructive diuresis) 

d. Hypernatremic states can be categorized into one of two groups: 

(1) Water loss (t intake or t output) 

(a) Patients who have a low or normal total body sodium 

1. Reduced water intake 

ii. Abnormal thirst mechanism 

603


iii. Inability to drink (physical, neurologic) 

iv. Osmotic diuresis 

• Diabetic ketoacidosis 

• Hyperosmolar nonketotic coma 

(b) Patients who have abnormalities in production of, or renal response to, ADH 

i. Diabetes insipidus (central, nephrogenic) 

ii. Drugs (lithium, aminoglycosides, phenytoin, fluoride) 

(2) Sodium gain (iatrogenic)-these patients have increased total body sodium. 

e. Management 

(a) Saline administration (including hypertonic saline) 

(b) Hypertonic dialysis 

(c) Hypertonic feedings 

(d) "Bicarb" administration 

(1) Guided by the rate of development of the hypernatremia, the presence of symptoms, and the absolute 

sodium level 

(2) Calculate the water deficit. (As a general rule of thumb, each liter of water deficit will cause an 

increase in serum sodium of 3-5 mEq/L.) 

water deficit (L) = 

( 

measured [Na+] 

normal [Na+] 

) -1 

C. Dehydration 

(3) The cornerstone of treatment is volume repletion, usually with 0.9% saline. 

(4) In patients with increased total body sodium due to sodium gain, it may be necessary to use a loop 

diuretic in conjunction with D5W. In severely ill patients, hemodialysis may be lifesaving. 

(5) Patients with prolonged hypernatremia have normal intracellular volume due to the acquisition of 

"idiogenic osmoles" that equalize intracellular and extracellular osmolarities. The rapid correction of 

hypernatremia may lead to excessive movement of water into these hyperosmolar cells, resulting in 

cerebral edema. Therefore, sodium levels should not be lowered faster than 10-15 mEq/L/day; only 

half of the water deficit should be corrected in the first 24 hours; in most clinical situations, the total 

deficit will require replacement over the next 24-48 hours so that the serum osmolality drops about 2 

mOsm/kg/hr. 

1. Three categories: hypotonic, isotonic, and hypertonic (Following is a summary of the information presented 

above on hypo- and-hypernatremia, which is important to understand the cause and type of dehydration in a 

particular patient.) 

2. Hypotonic dehydration 

a. Loss of sodium in excess of water 

b. Serum Na+ is low. 

c. Differential diagnoses 

(1) Diuretic excess 

(2) "Fluid space" losses 

(3) Vomiting 

(4) Adrenocortical insufficiency 

3. Isotonic dehydration 

a. Loss of sodium loss of water 

b. Serum Na+ is normal. 

c. Most commonly associated clinical condition is vomiting. 

4. Hypertonic dehydration 

a. Loss of water in excess of sodium 

b. Serum Na+ is increased. 

c. Differential diagnoses 

(1) Diarrhea 

(2) Lack of access to water 

604


D. Hypokalemia 

(3) Nonketotic hyperosmolar coma 

(4) Diabetes insipidus 

1. Definition: serum K+


E. Hyperkalemia 

1. Definition: serum K+ > 4.5 mEq/L (>6.5 mEq/L = severe) 


a. Acidosis: renal failure, diabetic ketoacidosis 

b. Cell lysis: chemotherapy, hemolysis, burns, rhabdomyolysis 

c. Mineralocorticoids (Addison disease) 

d. Medications (triamterene, spironolactone, ACE inhibitors, NSAIDs, f3-blockers) 


a. Signs and symptoms are multiple and often difficult to discern from those of the primary illness or condition 

that precipitated the hyperkalemia. 

b. Neuromuscular findings may begin with lethargy and weakness and progress to paralysis and areflexia. 

c. Cardiac findings 

4. Etiology 



(3) ECG changes progress as severity of hyperkalemia progresses: tall peaked T waves ___,, wide QRS 

complexes ___,, sine waves; however, ECG findings may be minimal, especially in renal patients. 

a. Factitious 

(1) Thrombocytosis 

(2) Leukocytosis 

(3) Prolonged tourniquet time 

(4) In-vitro hemolysis 

b. Decreased renal excretion 

(1) Renal insufficiency 

(2) Adrenal or aldosterone insufficiency 

(3) Drugs (eg, potassium-sparing diuretics, ACE inhibitors) 

(4) Type IV renal tubular acidosis (diabetes) 

c. Increased potassium load 

(1) Cellular breakdown (trauma, tumor lysis, rhabdomyolysis) 

(2) Potassium-containing salt substitutes 

(3) Hemolysis 

(4) GI bleeding 

(5) High-dose penicillin VK 

d. Decreased cellular uptake of potassium 

(1) Diabetic ketoacidosis (serum K+ level increases 0.6 mEq/L for every 0.1 decrease in pH) 

(2) Drugs (f3-blocker or digoxin overdose, succinylcholine) 

5. Management 

a. If there are no ECG signs, treatment can be restricted to methods that increase potassium excretion through 

the bowel or kidneys or decrease potassium intake (diet). 

b. Because the kidney is the major determinant of the serum potassium concentration, emergent treatment of 

hyperkalemia requires a method that either blocks the site of action of the excess potassium or shifts the 

excess potassium from one compartment to another. Hyperkalemia due to familial periodic paralysis is 

caused by potassium shifts (not total body depletion); therefore, overcorrection may occur in this setting. 

(1) Calcium chloride or gluconate antagonizes the effects of potassium in the myocardium, thus 

decreasing membrane irritability, which reduces the risk of developing a ventricular dysrhythmia. 

(2) Glucose and insulin, bicarbonate, and f3-adrenergic agonists redistribute excess potassium from the 

extracellular to the intracellular compartment. 

(3) Therapy with dialysis or an exchange resin (polystyrene sulfonate) should be started shortly after using 

any emergent treatment. 

606


Table 37: Treatments for Hyperkalemia 

Treatment 

Mechanism 

Dosage 

Onset 

Duration 

of Effect 

Calcium gluconate 

(10%) 

Membrane 

stabilization 

10-20 ml IV 

1-3 min 

20-50 min 

Sodium bicarbonate 

Redistribution of K+ 

1 mEq/kg IV 

5-10 min 

1-2 hours 

Albuterol 

Redistribution of K+ 

10-20 mg by inhaler 

30 min 

2-4 hours 

Insulin plus glucose 

Redistribution 

5-10 units of regular 

insulin with 1-2 

ampules 050 IV 

30 min 

4-6 hours 

Cation exchange resin 

(sodium polystyrene) 

Excretion 

25-50 g orally or per 

rectum with sorbitol 

1-2 hours 

4-6 hours 

Peritoneal or 

hemodialysis 

Excretion 

Within minutes 

after starting 

Until dialysis 

is completed 

Diuretics 

Excretion 

Furosemide 

40 mg IV 

With start of 

diuresis 

Until diuresis ends 

F. Hypocalcemia 

1. Definition: serum Ca++


f. Alkalosis (0.1 t in pH, 0.05-0.08 mEq/L 1 in Ca++) 

(1) Respiratory_,. hyperventilation 

(2) Metabolic_,. vomiting, diarrhea, malabsorption 

g. Rapid and massive blood transfusions 

h. Rhabdomyolysis (increased calcium binding to injured tissue) 

i. Sepsis and shock states 

j. Renal failure 

5. Management 

a. The ultimate goal of therapy is treatment of the underlying cause. 

b. Emergent treatment with IV replacement is indicated if the patient is acutely symptomatic: 10 ml CaC1 2 

(10% solution) IV push over 15-20 minutes (repeat as needed). 

c. Transfusion of citrated blood may result in hypocalcemia (which is transient) and does not require routine 

treatment unless signs of hyperreflexia develop. 

G. Hypercalcemia 

1. Definition: serum Ca++> 10.5 mg/dl (> 12 mg/dl severe) 

2. Clinical presentation: "groans, stones, psych overtones" 

a. Neuromuscular 

b. 

C. 

d. 

(1) Weakness, hyporeflexia, hypotonia 

(2) Apathy, confusion, depression 

(3) Lethargy, stupor, coma (if the hypercalcemia is the cause of the coma, serum Ca++ is> 13.5 mg) 

Cardiovascu Jar 

(1) Hypertension 

(2) Dysrhyth mi as 

(3) ECG abnormalities 

(a) Short QT interval 

(b) Coving of the ST segment and T wave 

(c) Widening of the T wave 

(4) Digitalis sensitivity (hypercalcemia enhances digitalis toxicity) 

GI 

(1) Anorexia 

(2) Nausea, vomiting 

(3) Abdominal pain 

(4) Constipation 

Renal 

3. Etiology 

(1) Nephrolithiasis 

(2) Renal failure 

(3) Polyuria 

a. Malignancy 

(1) Hematologic (Hodgkin, lymphomas, multiple myeloma) 

(2) Metastasis to bone (thyroid, lung, breast, kidney); a serum Ca++> 13.5 mg/dl suggests this diagnosis. 

(3) Parathyroid hormone-producing lung/kidney cancers 

b. Excess intake 

(1) Milk-alkali syndrome 

(2) Vitamin D (or vitamin A) toxicity 

c. Acute osteoporosis 

(1) Immobilization of young patients 

(2) Paget disease (especially with immobilization) 

d. Hyperparathyroidism (a serum Ca++> 11 mg/dl suggests this diagnosis) 

e. Drugs 

(1) Lithium 

(2) Thiazide diuretics 

608


4. Management 

a. Initiate for symptomatic patients or for Ca++> 14 mg/dl regardless of symptoms 

b. Saline hydration 

c. Furosemide 1 mg/kg as needed for fluid overload (thiazide diuretics contraindicated in patients with 

hypercal cem i a) 

d. Potassium replacement as needed 

e. Hydrocortisone 

f. Drugs that decrease bone absorption 

(1) Calcitonin 

(2) Glucocorticoids 

(3) B isphosphonates 

(4) Gallium nitrate 

g. Treatment of underlying neoplasm if present 

H. Hypomagnesemia 

1. Definition: serum Mg++


e. Drugs 

(1) Aminoglycosides 

(2) Amphotericin B 

(3) Diuretics 

(4) ~-agonists 

(5) Cyclosporine 

4. Management 

a. Check for hypocalcemia, hypokalemia. 

b. Treat the underlying cause. 

c. Replacement therapy 

I. Hypermagnesemia 

(1) For life-threatening problems (dysrhythmias, seizures): 1-2 g 10% MgSO 4 

IV in 1-5 minutes, fol lowed 

by an infusion of 1-2 g/hr. 

(2) For less urgent presentations: 1-2 g 10% MgSO 4 

IV over 3 hours or 2 g of a 50% solution IM every 

4 hours x 5 doses 

1. Definition: serum Mg++ >2 .2 mEq/L (>3 mEq/L = severe) 

2. Clinical presentation (usually does not occur until the serum level is >3 mEq/L) 

a. Neuromuscular 

(1) Weakness 

(2) Drowsiness/lethargy 

(3) Slurred speech 

(4) Hyporeflexia 

(5) Coma and respiratory failure (serum Mg++ >5 mEq/L) 

b. Cardiovascular 

(1) Bradycardia - AV block - asystole 

(2) Prolonged PR and QT intervals with extreme elevations of ST segments and T waves 

(3) Vasodilation and hypotension (serum Mg++> 10-12 mEq/L) 

c. Because magnesium is used to treat some clinical situations (eg, preterm labor), recognizing these findings 

is important in case of iatrogenic hypermagnesemia. 

3. Etiology 

a. Renal failure (particularly in patients who were given magnesiumcontaining drugs) 

b. Iatrogenic: preeclamptic and eclamptic patients who were treated with MgSO 4 

to reduce blood pressure 

and/or control seizure activity 

c. Untreated diabetic ketoacidosis 

d. Adrenal insufficiency 

e. Rhabdomyolysis 

4. Management 

a. Discontinue exogenous magnesium 

b. Diuretics 

c. Calcium 

d. Dialysis 

J. Hypochloremia 

1. Definition: serum Cl-


3. Management 

a. Treat underlying disorder 

b. Chloride replacement with NaCl is indicated if hypochloremia is severe or associated with hypokalemic 

alkalosis. 

K. Hyperchloremia 

1. Definition: serum Cl- >110 mEq/L (>120 mEq/L = severe) 

2. Etiology 

a. Dehydration 

b. Cardiac decompensation 

c. Bicarbonate loss (GI, renal) 

3. Management 

a. For GI bicarbonate loss - normal saline 

b. For renal bicarbonate loss - oral bicarbonate and renal consultation 

L. Key concepts in electrolyte disorders 

1. Potassium and pH are intrinsically linked in the body. As pH decreases, K+ increases. As pH increases, K+ 

decreases. 

2. Many disorders mimic each other. 

a. Hypomagnesemia and hypocalcemia both result in neuromuscular excitability and can both present with 

Chvostek signs. Both can cause prolonged QT interval. Hypomagnesemia classically causes torsades. 

b. Hypermagnesemia and hypercalcemia both cause neuromuscular depression. If mild, both are treated 

with IV fluids. 

3. Severe hyperkalemia and hypermagnesemia are both treated with IV calcium. 

Ill. ACID-BASE DISORDERS 

A. General approach to the patient with an acid-base abnormality 

1. Basic definitions 

a. alkalosis: a process leading to alkalemia 

b. acidosis: a process leading to acidemia 

c. alkalemia: pH >7.45 

d. acidemia: pH


(2) Respiratory acidosis (increased pC0 2 

) 

(a) Toxic: sedative hypnotics, opioids 

(b) Nontoxic: other causes of respiratory failure 

(3) Metabolic alkalosis (increased bicarbonate): volume depletion (any cause), Barter syndrome, 

hyper a I dosteron ism 

(4) Anion-gap metabolic acidosis (decreased bicarbonate) 

(a) Toxic: salicylates, phenformin, carbon monoxide, cyanide, isoniazid (seizures), iron, methanol, 

ethylene glycol 

(b) Nontoxic: seizures, shock, hypoxia, sepsis, ketoacidosis, uremia 

(5) Nonanion gap metabolic acidosis (decreased bicarbonate, increased chloride) 

(a) Toxic: chronic toluene exposure 

(b) Nontoxic: bicarbonate wasting conditions such as renal tubular acidosis or diarrhea, ketone-wasting 

(6) Mixed disorder 

(7) Remember: "Normal is not normal when it should be abnormal." For example, a person breathing 40 

times a minute should not have a pC0 2 

of 40. Even though this is a "normal" value, this is a sign of 

impending respiratory failure. 

c. If an anion gap is present, pinpoint the problem (see metabolic acidosis, page 613). 

(1) Consider causes (measurement of serum ketones, lactate, or glucose). 

(2) Consider an ethylene glycol, methanol, or salicylate level. 

(3) Consider causes of an anion gap other than metabolic acidosis. 

(a) Severe metabolic alkalosis 

(b) Anion infusion 

(c) Antibiotics 

(4) Causes of a decreased anion gap 

(a) 

Hypoalbuminemia 

(b) Bromide or iodide poisoning 

(c) Multiple myeloma 

(5) Measure the osmol gap (the difference between the measured and calculated osmolality). 

(a) The presence of an osmol gap suggests the laboratory is measuring an osmotically active 

substance that you are not using in your calculation. 

(b) Common causes of an osmol gap 

i. Ethanol 

ii. Methanol 

iii. Ethylene glycol 

iv. lsopropano 1 

v. Acetone 

vi. Glycerol 

vii. Mannitol 

viii.Uremia 

ix. Ketoacidosis 

(c) Of the alcohols, ethanol and isopropanol have an osmolal gap but a normal anion gap. 

(d) In uremia and ketoacidosis, the osmolal gap is usually 7. 

e. Questions to answer to determine if a mixed disorder is present: 

(1) Do the clinical rules for "pure metabolic acidosis" apply? Deviation implies the presence of a mixed 

disorder. 

(a) Respiratory compensation should not raise the pH to normal (>7.35). 

(b) The pC0 2 

approximates 1 .5 x bicarbonate+ 8 ± 2 

(c) For a pure anion gap acidosis, the increase in the anion gap should equal the decrease in the 

bicarbonate. 

612


B. Metabolic acidosis 

(2) Is the degree of respiratory compensation for metabolic acidosis- 

(a) Too much (pH 2: normal)= superimposed respiratory alkalosis; common clinical settings include: 

i. Salicylate poisoning 

ii. Sepsis 

iii. Early cyanide poisoning 

iv. Increased intracranial pressure with shock or seizure 

v. Normal renal compensation for primary respiratory alkalosis 

(b) Too little (change in pC0 2 

< 1.5 x bicarbonate+ 8) = superimposed respiratory acidosis; common 

clinical settings include: 

i. Sedative-hypnotic overdose with shock or seizures 

ii. Patient with primary ventilatory impairment and metabolic acidosis 

iii. Partial renal compensation for primary respiratory acidosis 

(3) Is the magnitude of the increase in the anion gap equal to the magnitude of the decrease in serum 

bicarbonate? If not, is it: 

(a) Greater? If the bicarbonate is relatively increased, this indicates a superimposed metabolic 

alkalosis. Common clinical settings include: 

i. Vomiting patient with diabetic ketoacidosis or alcoholic ketoacidosis 

ii. Administration of NaH 2 

C0 3 

to an acidemic patient 

(b) Less? If the chloride is relatively increased, this indicates an associated hyperchloremic metabolic 

acidosis. Common clinical settings include: 

i. Renal excretion of ketones with retention of chloride (especially during initial treatment of 

diabetic ketoacidosis) 

11. Resuscitation with chloride-containing solution and dilution of serum bicarbonate 

iii. Severe diarrhea, renal tubular acidosis, and any primary cause of metabolic acidosis 

(eg, shock, sepsis) 

1. Definition: t pH (


(4) faraldehyde 

(5) Iron, isoniazid, inhalants, inborn errors of metabolism 

(6) _lactic acidosis 

(7) Salicylates, solvents, starvation 

5. Management 

a. Controversial 

b. All agree that treatment of the underlying cause is paramount and clinically the most important. 

c. When the underlying cause is not readily reversed, some authors advocate administration of sodium 

bicarbonate to maintain a pH >7.10 or a serum bicarbonate >5 mEq/L. 

d. Bicarbonate can precipitate rapid electrolyte disturbances, resulting in symptomatic hypokalemia and 

hypocalcemia. 

e. Theoretically, paradoxical cerebral acidosis can occur because of the differential ability of CO 2 

and HCO 1 

- 

to cross the blood-brain barrier if bicarbonate is given too rapidly, ie, if CO 2 

crosses readily, HCO - 3 

crosses 

slowly. 

f. Specific therapy of the underlying cause 

(1) Insulin (diabetic ketoacidosis) 

(2) Pressors, antibiotics, and fluids (lactic acidosis) 

(3) Dialysis (renal failure, methanol, ethylene glycol, salicylates) 

C. Metabolic alkalosis 

(4) Ethanol or 4-methylpyrazole (methanol, ethylene glycol); 4-methylpyrazole (an alcohol dehydrogenase 

antagonist) is an alternative substitute for IV ethanol. 4-Methylpyrazole is the preferred current 

treatment if available. 

(5) Titrated HCO 3 

(renal tubular acidosis, according to type) 

(6) Benzodiazepines (status epilepticus) 

1. Definition: t pH (>7.45) and t HCO 3 

(>26 mEq/L) 

2. Most common reasons for a primary increase in blood bicarbonate concentration 

a. Vomiting and nasogastric suctioning 

b. Diuretic administration 

c. Adrenocortical hormone excess 

3. Metabolic alkalosis can be categorized as "chloride sensitive" or ''chloride resistant." 

a. Chloride-sensitive alkalosis (saline responsive): common 

(1) Diuretics - loss of K+ and Cl- - replace with saline and potassium 

(2) Vomiting and nasogastric suctioning - loss of H+, K+, and Cl- - (t renal excretion) - replace with 

saline. Vomiting is most likely the clinical scenario in a hypochloremic, hypokalemic metabolic 

acidosis. 

b. Chloride-resistant alkalosis (saline unresponsive): rare 

(1) Mineralocorticoid excess - t renal absorption of Na+ and HCO 3 

- with t renal excretion of K+, H+, 

and Cl- - replace with potassium 

(2) Large amounts of potassium are usually required to reduce renal excretion of H+ and treat the 

underlying cause. 

D. Respiratory acidosis 

1. Definition: t pH (45 mmHg) 

2. Primary cause is inadequate ventilation and/or increased dead space, both of which are associated with 

t excretion of pulmonary CO 2 

a. Etiology 

(1) Head or chest trauma 

(2) Oversedation 

(3) Metabolic coma 

(4) Neuromuscular disorders 

(a) 

Neuropathies 

(b) Myopathies 

(5) Chronic hypoventilation in obese patients 

(6) Obstruction 

614


(a) Foreign body 

(b) Bronchospasm or laryngospasm 

b. Cause of increased dead space (with or without inadequate ventilation)-;, COPD 

3. Full renal compensation requires 48 hours of steady state alteration. Compensation is not expected to be 

complete; however, the pH may "normalize" in some patients. 

4. Proceed with caution when treating the underlying disorder. 

a. The pC0 2 

should not be lowered more than 5 mm Hg/hr (especially in those with chronic compensated 

respiratory acidosis, eg, patients with COPD). 

b. Ventilator assistance: continuous positive-airway pressure (CPAP) or bi-level positive-airway pressure 

(BiPAP) may be necessary in selected patients. 

c. Low-flow oxygen should be given to Pickwickian patients. 

E. Respiratory alkalosis 

1. Definition: 1' pH (>7.45) and t pC0 2 

(4-5 mEq/L) 

and there is an associated high anion gap acidosis. Other causes of high anion gap acidosis must be 

excluded to confirm this diagnosis: 

(1) Ingestions 

(a) Alcohols (methanol, ethylene glycol) 

(b) Salicylate 

(c) Paraldehyde 

(d) lsoniazid, iron 

(e) Cyanide 

(2) l


(4) A mnemonic for causes of high anion gap acidosis is "A MUDPILES" and cyanide. 

Alcoholic ketoacidosis 

Methanol, Metformin 

.Uremia 

.!2iabetic (or alcoholic) ketoacidosis 

faraldehyde, Phenformin 

lsoniazid/lron/lnhalant (carbon monoxide, hydrogen sulfide) poisoning 

(mitochondrial injury caused by reverse transcriptase inhibitors [HIV treatment]) 

lactic acidosis - shock, hypoxia, seizures, cyanide, metformin, phenformin 

fthylene glycol 

S.alicylates 

2. Management 

a. The presence of clinically significant lactic acidosis indicates a serious underlying disorder that must be 

identified and corrected. 

b. IV sodium bicarbonate has traditionally been the mainstay of therapy, but it remains a controversial issue. 

In general, sodium bicarbonate should be given only when the pH is 9.1. The approximate dose in 

milliequivalents can be calculated from the following formula: 

HCQ 3 

- deficit= 25 measured HCO 3 

- x 0.5 (body weight in kg) 

c. Most do not favor the use of insulin (or glucose and insulin infusions) in the treatment of lactic acidosis. 

The exception is diabetic ketoacidosis with concomitant lactic acidosis. 

d. Thiamine should be given to alcoholic patients with lactic acidosis, because it is needed in the oxidation 

of pyruvate. 

G. Important points to remember in the management of acid-base disorders 

1. An acid-base abnormality due to mixed disorders may exist in the presence of a normal pH or CO 2 

• 

2. If you suspect that respiratory acidosis is due to opioid use, administer naloxone early in the clinical 

evaluation. 

3. If you suspect a toxicant as the cause of an acid-base abnormality, you need specific quantitative serum levels 

of ASA, methanol, ethylene glycol and, if isoniazid can be detected by your laboratory, a qualitative level of 

this drug, which may be helpful. (Broad, routine urine and serum toxicology screens are not helpful.) Consider 

general interventions such as decontamination measures and specific interventions such as dialysis in methanol 

toxicity early in the treatment process. 

4. Consider isopropyl ingestion in ketotic patients with a normal glucose and no anion gap; these patients have an 

osmolar gap. 

5. Pearls and pitfalls of anion-gap acidosis 

a. Nitroprusside tests (urine reagent strips, reagent tablets) measure only acetoacetic acid (not ~-hydroxybutyric 

acid), which means that patients with diabetic ketoacidosis or alcoholic ketoacidosis may register falsely 

low ketones or no ketones at all. 

b. Patients who have ingested methanol (eg, "Sterno," windshield wiper fluid) may present 24-48 hours after 

ingestion with abdominal pain, an intoxicated appearance (but no breath odor of alcohol), and blurred 

vision with a hyperemic optic disc ("blind drunk"). All cases of methanol toxicity should be treated with IV 

ethanol (or 4-methylpyrazole) and most require dialysis. 

c. Patients who have ingested ethylene glycol (antifreeze) present within 12-24 hours with an intoxicated 

appearance (but no breath odor of alcohol). Hypocalcemia and calcium oxalate crystals in the urine may 

be seen, but their absence does not exclude the diagnosis. 

(1) Calcium oxalate crystals can also be seen in nontoxic ingestions (eg, tea, cola, spinach, rhubarb). 

(2) In addition to IV ethanol (or 4-methylpyrazole) and dialysis, these patients also need thiamine and 

pyridoxine. IV calcium may also be indicated for symptomatic hypocalcemia. 

d. Repeat laboratory values may be of help. Laboratories make mistakes, too! 

H. Clinical situations and associated laboratory findings 

1. Starvation/dehydration (decrease in total body water but not extracellular fluid volume), eg, the stroke patient 

left unattended at home for several days 

a. Hypernatremia (excess water loss) 

b. Hypokalemia (continuing urinary losses) 

c. Increased serum osmolality (increased sodium, metabolic acids) 

616


d. Mild metabolic acidosis (ketones produced) 

e. Slightly increased anion gap 

2. Diarrhea/chronic laxative abuse 

a. Hyponatremia (fecal loss) 

b. Hypokalemia (fecal loss) 

c. Hypobicarbonatemia (fecal loss) 

d. Hyperchloremia (compensation for HCQ 3 

- loss) 

e. Hyperchloremic metabolic acidosis 

3. Vomiting 

a. Hypernatremia or hyponatremia or normal serum sodium 

b. Hypokalemia (potassium shifts intracellularly secondary to alkalosis; excess renal loss) 

c. HCQ 3 

- concentration >30 mEq/L 

d. Hypochloremia (Cl- loss) 

e. Metabolic' alkalosis (H+ loss) 

METABOLIC DISORDERS 

I. HYPOGLYCEMIA 

A. Definition 

1. Although there is significant individual variation, signs and symptoms of severe hypoglycemia do not usually 

occur until blood glucose falls below 50 mg/dL. 

2. Signs and symptoms 

B. Types 

a. Diaphoresis 

b. Tremulousness, nervousness 

c. Tachycardia 

d. Altered sensorium (confusion, agitation, unresponsiveness) 

e. Focal neurologic signs 

f. Seizures 

1. Although hypoglycemia can occur without diabetes (either insulin dependent or non-insulin dependent), it 

is most commonly seen as a result of treatment of diabetes. In the absence of diabetes, other diagnoses and 

medical conditions should be considered, but they are far less common than hypoglycemia seen as a diabetic 

emergency. These other illnesses are listed below: 

a. Medications such as ~-blockers 

b. Use of alcohol (usually excessive) 

c. Reactive hypoglycemia (delayed insulin release after a meal) 

d. Severe infection 

e. Cancers (eg, tumors such as hepatoma and mesothelioma can produce insulin-like factors) and insulinproducing 

tumors 

f. Renal insufficiency 

g. Liver failure 

h. Poor oral intake 

i. Congenital defects in metabolism 

j. Infants born to diabetic mothers, birth trauma, premature infants 

2. Hypoglycemia should be considered early in the management of any patient with altered mental status. 

Diagnosis is simple with bedside glucose testing. 

a. A blood glucose of


3. Hypoglycemia management is based on severity of symptoms and patient's ability to tolerate oral intake. 

a. Mild symptoms and able to tolerate oral fluids: complex carbohydrate intake (meal tray) 

b. More severe symptoms or inability to tolerate oral fluids: IV administration of dextrose. 

(1) For adults: 1-3 ampules of 50% dextrose in water (D50W [1 ampule is 25 g dextrose in 50 ml]) 

(2) For children: 0.5-1 g/kg IV of D25 or D10 

(3) Rule of 100: D25 dose is 4 ml/kg, D10 dose is 10 ml/kg. 

c. Additional treatment options 


(1) Glucagon can be given IM as an option when IV access cannot be obtained in an obtunded patient. 

This is not as effective in elderly or alcoholic patients (ineffective glycogen stores to make an effective 

increase in blood glucose). 

(2) Dose of glucagon in adults in 1 mg IM. 

a. Any patient with hypoglycemia from long-acting oral agents should be admitted to the hospital for 

observation because of continued risk of hypoglycemia. 

b. Patients with hypogylcemia requiring multiple doses of IV dextrose should be considered for observation in 

the hospital. 

c. Patients with straightforward hypoglycemia and no other significant factors such as infection, sepsis, etc, 

can be considered for discharge if only insulin is used for treatment of their diabetes. 

II. DIABETIC KETOACIDOSIS 

A. Etiology 

1. Metabolic derangements are due to a relative insufficiency of insulin and an excess of glucagon. 

a. Insulin insufficiency___,. cellular starvation ___,. release of stress hormones and glucagon ___,. increased 

gluconeogenesis, glycogenolysis, and lipolysis ___,. further hyperglycemia and increased free fatty acids___,. 

ketones (j3-hydroxybutyrate and acetoacetate) 

b. Glucagon has been implicated as the primary hormone responsible for hyperglycemia and ketonemia in 

diabetic ketoacidosis. 

2. Precipitating factors 

a. Lack of insulin 

b. Infection (a significant contributor to high mortality) 

(1) Pneumonia 

(2) Urinary tract infection 

c. Acute myocardial infarction (a significant contributor to high mortality) 

d. Cerebrovascular accident 

e. Trauma/surgery 

f. Pregnancy 

g. Alcohol/steroid use 


1. Hyperglycemia results in decreased total body water: 

a. Hypotension, tachycardia, and dehydration 

b. Decreased serum electrolytes with depletion of: 

(1) Sodium: the dilutional effect of hyperglycemia depresses the serum sodium still further (1.6 mEq/L 

for each 100 mg/dl increase of serum glucose). 

(2) Potassium (total body): Because of acidosis, the potassium measurement may be high due to the 

shifting of potassium as the acidosis increases. 

2. Ketogenesis results in: 

a. Acidosis with a decrease in sodium bicarbonate 

b. A fruity breath odor (from acetone) 

c. Hyperventilation (Kussmaul respirations) 

618


d. Hyperkalemia: potassium is initially increased, because the acidosis causes it to shift out of the cells in 

exchange for the hydrogen ion. However, correction of the acidosis may be associated with a profound 

hypokalemia. 

(1) As the acidosis improves, hydrogen ions will move out of the cells, allowing potassium to move back 

in and the serum potassium level to decrease. 

(2) Administration of insulin and glucose also allows potassium to move back into the cells, which 

further decreases serum potassium. 

(3) The average total body potassium deficit is -3-5 mEq/kg. 

C. Differential diagnosis of metabolic causes of coma in diabetic patients 

1. Diabetic ketoacidosis 

2. Hypoglycemia 

3. Hyperglycemic hyperosmolar nonketotic coma 

4. Alcoholic ketoacidosis 

5. Lactic acidosis 

6. Uremic acidosis 


1. Bedside testing (done immediately) 

a. Glucose reagent strip can rapidly differentiate hypoglycemia from hyperglycemia. 

b. Urine can be checked for: 

(1) Glucose: indicating hyperglycemia 

(2) Ketones with the nitroprusside test: a positive test is consistent with the diagnosis of diabetic 

ketoacidosis. However, this test primarily detects acetoacetate and will be falsely negative if most of 

the ketones are in the form of ~-hydroxybutyrate or acetone. 

2. Blood pH (arterial or venous blood gases) and serum CO 2 

content__,. confirms acidosis (1 pH and 

t bicarbonate) 

3. CBC (baseline) 

4. Glucose__,. hyperosmolarity secondary to hyperglycemia is the single most important determinant of the 

patient's mental status (serum osmolality >320 mOsm/kg = altered mental status) 

5. Serum ketones __,. the following are usually increased: 

a. Acetoacetate 

b. ~-Hydroxybutyrate 

c. Acetone (which is chemically neutral) 

6. Electrolytes__,. in addition to identifying abnormalities, you need to determine the anion gap. 

a. In the presence of a nondiagnostic ketone level, a wide gap suggests the presence of ~-hydroxybutyrate as 

the major ketone. 

b. In patients with mixed acid-base disturbances, the arterial pH may not accurately reflect the degree of 

acidosis; an anion gap does. 

7. Calcium, magnesium, phosphorus__,. if one is low, the other two generally are low as well. 

8. BUN/creatinine (baseline) 

9. Urinalysis, blood cultures, and chest radiograph __,. look for infection. Remember that any infection can cause 

diabetic ketoacidosis, including appendicitis, pyelonephritis, etc. 

10. ECG__,. look for evidence of acute myocardial infarction; estimate serum potassium level. 

11. Laboratory summary for diabetic ketoacidosis 

a. Blood glucose >250 mg/dL 

b. Serum acetone >2:1 dilution 

c. Bicarbonate


b. If the patient is severely dehydrated, use normal saline for the initial 2 L of fluid resuscitation, then 

switch to 0.45% normal saline. In all other cases, alternating normal saline and 0.45% normal saline is 

recommended. 

c. When the serum glucose level falls to ~250 mgldL, add glucose to the IV to prevent iatrogenic 

hypoglycemia and cerebral edema. 

2. Insulin administration 

a. Large doses are not usually required to reverse diabetic ketoacidosis. In addition, complications 

(hypoglycemia, hypokalemia) are more likely to develop with large-dose insulin therapy. 

b. Continuous IV infusion of low doses of insulin (5-10 units/hr in adults and 0.1 unit/kg/hr in children) is 

simple, safe, and effective. If a patient does not respond within 1 hour (about a 50 mg/dL drop in blood 

glucose), double the infusion rate or administer a bolus. 

c. Onset of action is almost immediate; a priming IV bolus is not required, and current evidence suggests that 

children do not need an IV bolus. In adults, an IV bolus is optional. 

d. Insulin should initially be held if potassium level is


d. Acute myocardial infarction 

e. Rhabdomyolysis 

2. Therapy-related comp I ications 

a. Hypoglycemia 

b. Hypokalemia, hypophosphatemia 

c. Paradoxical spinal fluid acidosis 

d. Cerebral edema 

e. Alkalosis (from too much bicarbonate replacement) 

f. Congestive heart failure (from overhydration) 

g. ARDS (from overhydration) 

G. Mortality from diabetic ketoacidosis 

1. Elderly: sepsis, cardiopulmonary complications 

2. Children and young adults: cerebral edema (onset usually


C. Diagnostic evaluation/laboratory findings 

1. Blood glucose >400 mg/dL (may be> 1,000 mg!dl) 

2. Serum osmolality >315 mOsm/kg 

A serum osmolality should always be ordered, but results may not be readily available. Calculate osmolality 

using the following formula: 

[2 x (Na+)] + Gl~~ose + 

BUN 

2-"il 

3. Negative serum ketones 

4. Blood pH - no acidosis 

D. Management 

1. Fluid resuscitation: saline is the preferred fluid. Administer bolus fluids until the patient is hemodynamically 

stable. 

a. 0.9% normal saline at a rate of 15-20 ml/kg/hr can be used during the first hour and 4-14 ml/kg/hr after 

the first hour. 

b. Once hypotension, tachycardia, and urine output improve, 0.45% saline can be used to replace the 

remaining free water deficit. 

c. The average fluid deficit in hyperglycemic hyperosmolar nonketotic coma is 8-12 L. 

d. When the blood glucose reaches ~250 mg/dl, add glucose to the IV. 

2. Insulin administration is not the mainstay of treatment. Volume repletion should precede insulin therapy. 

a. Regular insulin given by continuous IV infusion is the customary method; dosage is 0.05-0.1 unit/kg/hr. 

There is no benefit to an IV bolus of insulin. 

b. No insulin should be given after the blood glucose reaches ~300 mg/dL. 

c. Patients who are insulin-naive may experience a rapid drop in blood glucose; in these cases, periodic 

serum glucose determinations are important. 

3. Potassium replacement 

a. KCI (10-20 mEq/hr) should be given during the acute phase of therapy (24-36 hours). 

b. It should be started within 2 hours of IV fluid and insulin therapy, or as soon as adequate renal function has 

been confirmed. 

c. Total body potassium depletion in nonketotic hyperosmolar coma is usually greater than that in diabetic 

ketoacidosis. 

4. Magnesium replacement: MgSO 4 

(1-2 g) should be given in the first 2 L of fluid if the serum magnesium is low. 

IV. ALCOHOLIC KETOACIDOSIS 


Heavy ethanol consumption (or binge drinking) and decreased or no food intake for several days - 

} insulin and 

t glucagon and ethanol-induced inhibition of gluconeogenesis - lypolysis - t ketoacid production (acetoacetate 

and ~-hydroxybutyrate) by the liver - nausea, protracted vomiting, and abdominal pain that begins 24-72 

hours before presentation and usually terminates with consumption of any food or liquid (including alcohol) - 

tachypnea (ketoacidosis) and tachycardia (dehydration) 


1. A high anion gap acidosis is characteristic (Na+ - [Cl-+ HCQ 3 

-J = > 16) and is due primarily to high levels of 

~-hydroxybutyrate. 

2. Sometimes, ~-hydroxybutyrate cannot be detected with a urine test. If the patient has a high anion gap with a 

very low serum bicarbonate level, assume serum acidosis. 

3. The blood glucose level is not high (usually


C. Management 

1. Administration of IV fluids and glucose is the mainstay of therapy. 

a. A solution containing both saline and glucose (OS/normal saline alternating with D5/0.45% normal saline) 

should be used, because recovery is faster when glucose-containing solutions are used. 

b. Approximately 3-6 L of fluid are required over 24-48 hours. 

2. Thiamine 50-100 mg IV should be given before the IV fluids are started, because glucose administration can 

precipitate Wernicke disease in the alcoholic patient. 

3. Correction of hypokalemia is with 30 mEq KCI IV or 30 mEq potassium orally. 

4. Insulin is not indicated and may be dangerous, because these patients usually have a near-normal or low 

blood glucose. 

5. Sodium bicarbonate therapy is generally unnecessary and should be avoided unless: 

a. The pH is


c. Cooling blanket and acetaminophen to control fever 

d. Rate control of atrial fibrillation (may be refractory) and diuretics for CHF 

e. The order of treatment is very important to avoid iatrogenic injury. 

(1) Propranolol first 

(a) Decreases the life-threatening adrenergic activity 

(b) Can block the peripheral conversion ofT 4 

to T 3 

(c) Dosage: 1 mg/min IV with incremental increases of 1 mg every 10-15 minutes to a total of 10 mg 

(2) Propylthiouracil 

(a) Blocks the synthesis of thyroid hormone 

(b) Dosage: oral administration of a 600-1,000 mg load, followed by 250 mg every 6 hours 

(3) Iodide 

(a) Administer 1 hour after propylthiouracil because this can be used as a substrate in thyroid 

hormone production, worsening the disease process. 

(b) SSKI (potassium iodide) dosage: 3-5 drops orally every 8 hours 

(4) Dexamethasone 

(a) Prevents peripheral conversion ofT 4 

to T 3 

(b) Dosage: 2 mg IV every 6 hours 

2. Drugs to avoid in treating thyroid storm 

a. Aspirin: may t T 3 

and T 4 

levels 

b. Sedatives: interfere with CNS assessment during therapy 

c. Atropine: may accelerate heart rate and also counteract the effect of propranolol 

VI. MYXEDEMA (HYPOTHYROID) COMA 

A. An endocrinologic emergency with a 30%-40% mortality rate 

B. Pathophysiology of hypothyroidism 

1. Hypothyroidism may be primary (intrinsic failure of the thyroid gland to release T 3 

and T 4 

) or secondary to 

disease or destruction of the hypothalamus or pituitary gland. Primary hypothyroidism is far more common 

(95% of cases) than secondary hypothyroidism (5% of cases). 

a. Etiologies of primary hypothyroidism (TSH level is high) 

(1) Prior treatment of Grave disease with radioactive iodine or subtotal thyroidectomy (most common cause) 

(2) Autoimmune thyroid disorders (second most common cause) 

(a) Primary hypothyroidism secondary to autoimmune destruction of the thyroid - glandular atrophy 

- thyroid failure 

(b) Hashimoto thyroiditis 

i. The most common cause of goitrous hypothyroidism in areas with adequate iodine 

ii. Pathophysiologic mechanism may be defective hormone synthesis. 

(3) Rare causes of primary hypothyroidism 

(a) 

Iodine deficiency 

(b) Antithyroid drugs (lithium, phenylbutazone) 

(c) Spontaneous hypothyroidism from Grave disease 

(d) Congenital thyroid abnormalities 

b. Causes of secondary hypothyroidism (TSH level is normal or decreased) 

(1) Pituitary tumors 

(2) Postpartum hemorrhage - postpartum pituitary necrosis 

(3) Sarcoidosis 

(4) Dysfunction of the hypothalamus ("tertiary hypothyroidism") 

C. Evolution of hypothyroidism to myxedema and myxedema coma 

1. Myxedema is a rare and severe form of hypothyroidism seen in patients with undiagnosed or inadequately 

treated hypothyroidism. Like hypothyroidism, myxedema is most prevalent in older women and occurs most 

often in winter. 

2. The single most important factor in the evolution of myxedema to myxedema coma appears to be a physiologic 

stressor, including medications or another endocrine disorder. 

624



1. Overall, this is similar to a severe hypoadrenergic state and is classically characterized by hypotension, 

bradycardia, hypothermia, weakness, pseudomyotonic reflexes, alopecia, and a doughy, non-pitting edema. 

For the board exam, in the absence of an environmental insult: hypotension, bradycardia, and hypothermia is 

an endocrine problem (which can include sepsis). 

a. Hypothermia (80% of cases) without sweating or shivering is typical. 

b. Respiratory failure is also common and is characterized by hypercapnea, hypoventilation, and hypoxia. 

2. Key points to remember are that this is often associated with rhabdomyolysis and adrenal insufficiency. Key 

diagnostic findings include the following: 

a. Thyroid-stimulating hormone is usually increased. 

b. T 4 

is usually low. 

c. Glucose may be low. 

d. Serum cortisol may be low. 

e. Calcium level usually low. 

f. Creatine kinase is often increased. 

g. Look for effusions on chest radiograph and echocardiogram. 

h. ECG will often show bradycardia; may see prolonged QT interval or low voltage. 

1. Hyponatremia secondary to SIADH is a potentially grave finding that may lead to central edema. 

3. Evidence of hypothyroidism may be minimal or absent. 

a. A history of hypothyroidism should be sought in any comatose patient with hypothermia and respiratory 

failure. Historical clues: 

(1) Previous thyroid medication, radioactive iodine therapy, or subtotal thyroidectomy 

(2) Previous complaints of fatigue, weakness, cold intolerance, weight gain, menstrual irregularity, and 

muscle cramps 

(3) Previous evidence of neuropsychiatric abnormalities 

(a) Psychiatric disorders or personality changes 

(b) Seizures 

(c) Cerebellar signs (ataxia, intention tremors, nystagmus, difficulty with coordinated movements) 

(4) Previous history of paresthesias; a mononeuropathy is typical, with median nerve involvement (carpal 

tunnel syndrome) being the most common. 

b. Look for evidence of hypothyroidism on physical examination. 


(2) Thyroidectomy scar 

(3) Thin eyebrows and scant body hair 

(4) Dry, scaly, yellow skin and puffy eyes 

(5) Abdominal distention due to fecal impaction, ascites, ileus, or urinary retention 

(6) Pseudomyotonic reflexes (brisk upstroke, slow relaxation), especially at the ankle 

(7) Nonpitting edema, including periorbital 


1. Although thyroid function tests (TSH, thyroxine-binding globulin, free T 4 

) should be ordered and can confirm 

the diagnosis of hypothyroidism, results are not always available in a timely fashion; initial therapy must be 

based on clinical impression. 

2. Characteristic laboratory findings 

a. Arterial blood gases: t pO 2 

and t pCO 2 

b. Electrolytes: t Na+ and t CJ- (and t Ca++ in thyroidectomized patients) 

c. Glucose: normal or low 

d. CBC: a left shift in the differential (with or without an increased WBC count) may be present if infection is 

the precipitating event. 

3. Nonspecific associated laboratory findings 

a. t creatine phosphokinase, lactate dehydrogenase, and aspartate aminotransferase (occasionally) 

b. t cerebrospinal fluid protein> 100 mg/dL (in most hypothyroid patients), although this may not be routinely 

discovered in the emergency department. 

625


F. Management 

1. Supportive measures 

a. Levothyroxine 

(1) Dosage: 200-500 mcg IV 

(2) This is the most critical aspect of therapy, because clinical improvement will likely not be noticed 

with other measures until thyroid hormone is replaced. 

b. Slow rewarming of hypothermic patients 

c. IV fluids for hypotension 

d. Hydrocortisone 100 mg IV increments 

e 

If the patient is still hypotensive, consider pressors but usually a poor response. 

f. Correction of hyponatremia by fluid restriction (for dilutional hyponatremia) or hypertonic saline (for 

severe hyponatremia with altered mental state) 

g. Glucose infusion if there is hypoglycemia 

2. Identify and treat comorbid conditions (which are likely the inciting factor and are usually infectious). This may 

require empiric antibiotic therapy for infections. 

VII. ADRENAL INSUFFICIENCY (ADDISON DISEASE) AND CRISIS 


1. Adrenal cortex produces glucocorticoids and mineralocorticoids. 

a. The major glucocorticoid is cortisol, which is produced by the following mechanism: hypothalamus 

releases corticotropin-releasing factor____.. pituitary secretes adrenocorticotropic hormone (ACTH)____.. adrenal 

cortex produces and secretes cortisol 

b. The major mineralocorticoid is aldosterone, which is regulated by the renin-angiotensin system and by 

plasma potassium concentrations. 

2. Hypofunction of the adrenal cortex 

a. When the physiologic demand for glucocorticoids and mineralocorticoids exceeds the capacity of the 

adrenal cortex to produce them, adrenal insufficiency occurs. 

(1) Primary adrenal insufficiency (Addison disease) is due to disease/destruction of the adrenal cortex or 

adrenalectomy. 

(a) Idiopathic atrophy, usually autoimmune mediated, is the leading cause of chronic adrenal 

insufficiency (70%-75% autoimmune, and 25%-30% truly idiopathic). Associated diseases 

include: 

i. Diabetes mellitus 

ii. Hashimoto thyroiditis 

iii. Grave disease 

iv. Hypoparathyroidism 

v. Pernicious anemia 

vi. Primary ovarian failure 

(b) Infectious/infiltrative causes 

i. Tuberculosis 

ii. Protozoal/fungal 

iii. Sarcoidosis/amyloidosis 

iv. AIDS/cytomegalovirus/herpes simplex virus 

v. Hemochromatosis 

vi. Metastatic cancer 

(c) Pharmacologic causes 

i. Methadone 

ii. Rifampin 

iii. Ketoconazole 

(d) Causes of bilateral adrenal hemorrhage (adrenal apoplexy) that can lead to insufficiency or crisis 

i. Anticoagulant therapy (especially after myocardial infarction) 

626


ii. Fulminant neonatal sepsis (especially meningococcemia, ie, Waterhouse-Friderichsen syndrome) 

iii. Hemorrhage in the newborn 

(2) Secondary adrenal insufficiency due to dysfunction or destruction of the pituitary (and tertiary 

insufficiency due to hypothalamic dysfunction) leads to inability of the pituitary gland to secrete ACTH. 

(a) The most common cause of tertiary insufficiency (and crisis) is iatrogenic adrenal suppression 

from prolonged steroid use. 

(b) Causes of secondary insufficiency can include primary diseases of this pituitary axis, including 

tumors, hemorrhage, infarction, etc. 

b. When the adrenal reserve is exhausted (primarily of cortisol) in patients with chronic adrenal insufficiency 

who are subjected to stress or a concurrent illness, adrenal crisis occurs. 

(1) Most common cause is abrupt withdrawal of steroids in a patient whose adrenal function has been 

suppressed by prolonged steroid use. 

(2) Other causes include any physiologic stressor, which is a common theme in endocrine emergencies. 


1. Primary adrenal insufficiency (Addison disease) 

a. Overal I, the patient appears weak and lethargic and exhibits fatigue on exertion. Postural hypotension and 

syncope are common. Heart sounds may be soft or inaudible. 

b. Signs and symptoms of cortisol deficiency 

(1) Lethargy 

(2) Anorexia, nausea, vomiting 

(3) Hypoglycemia with fasting 

(4) Inability to withstand even minor stress without shock 

c. Signs of aldosterone deficiency 

(1) 1 Heart size with cardiac output - postural hypotension, syncope, and azotemia (due to renal blood flow) 

(2) Dehydration with sodium depletion and hyperkalemia 

d. Prominent GI symptoms 

(1) Anorexia, nausea, vomiting, and occasionally diarrhea with weight loss 

(2) Abdominal pain 

e. Cutaneous manifestations: brownish pigmentation over exposed areas of the body and over friction or 

pressure points such as the elbows, fingers, knees, toes, and nipples 

2. Adrenal crisis 

a. Classic clinical scenario: The patient appears very ill, profoundly weak, and possibly confused. 

Hypotension (especially postural) is typical. Circulatory collapse, when present, may be profound (feeble, 

rapid pulse, and soft heart sounds). Fever is common. GI signs and symptoms are almost always present: 

anorexia, nausea, vomiting, and abdominal pain. Delirium and seizures may occur. 

b. Laboratory findings are variable, but the following is a classic triad: 

(1) Serum sodium is decreased (usual) or may be normal. 

(2) Serum potassium is normal or slightly increased. 

(3) Hypoglycemia is characteristic and may be profound. 


1. Laboratory findings 

a. Electrolyte abnormalities 

(1) Hyponatremia (88%) 

(2) Hyperkalemia (64%) 

(3) Hypercalcemia (6%-33%) 

b. Hypoglycemia 

c. Azotemia (t BUN/creatinine) 

2. ECG changes 

a. Signs of hyperkalemia 

(1) Tai I peaked T waves 

(2) Prolonged PR and QT intervals 

(3) Absent P waves 

627


b. Nonspecific changes 

D. Management 

(1) Low voltage 

(2) Flat or inverted T waves (in the absence oft K+) 

(3) Depressed ST segment 

1. Adrenal crisis 

a. IV fluids: OS/normal saline with the first liter given over 1 hour. An additional 2-3 L may be needed during 

the first 8 hours of therapy. 

b. Glucocorticoid replacement 

(1) The drug of choice if adrenal insufficiency is not known and a corticotropin stimulation will be 

performed is dexamethasone (4 mg IV), because it does not interfere with measurement of steroids and 

it is long-acting (12-24 hours). Fludrocortisone should be added for mineralocorticoid effect. 

(2) If the diagnosis of adrenal insufficiency is known, hydrocortisone sodium succinate is preferred; the 

dose is 100-500 mg IV. This has mineralocorticoid activity, so additional medications are not needed. 

c. Hypoglycemia should be treated immediately. 

628

ENDOCRINE, METABOLIC, AND NUTRITIONAL DISORDERS: PRACTICE CLINICAL SCENARIOS 

ENDOCRINE, METABOLIC, AND NUTRITIONAL DISORDERS: 


Answers immediately follow the clinical practice scenarios. 

Scenario A 

Presentation: A 60-year-old man presents with altered mental status and a blood glucose of 1,100 mg/dL. 


Scenario B 

Presentation: A 45-year-old homeless person presents with an altered mental status. 

Diagnostic evaluation: Laboratory studies show an increased anion gap(> 16 mEq/dL) and an increased 

osmolar gap (> 10 mOsm/dL). 


Scenario C 

Presentation: A 25-year-old injects heroin IV and becomes apneic. 

What is expected on the laboratory studies? 

Scenario D 

Presentation: A 20-year-old multi system trauma patient receiving a massive transfusion develops a wide 

QRS complex on the cardiac monitor. 

What is the diagnosis, and what treatment should be given? 

Scenario E 

Presentation: A 40-year-old man presents with weakness, lethargy, and nausea/vomiting. You notice he has 

bronzed skin despite living in a cloudy climate. 

Diagnostic evaluation: The ECG shows peaked T waves. 

What electrolyte abnormalities are expected, and what is the treatment? 

Scenario F 

Presentation: A 30-year-old woman is in septic shock. 

Diagnostic evaluation: Arterial blood gas results show a pH of 7.15 and a pCO 2 

of 14. 

Does she have a mixed acid-base disorder? 

629


Scenario G 

Presentation: A 30-year-old, thin woman with no psychiatric history presents with tachycardia, 

diaphoresis, fever, agitation, and psychosis. Examination reveals hyperreflexia. 

What is the first medication that should be administered to treat the underlying disorder? 

Scenario H 

Presentation: A 20-year-old man with insulin-dependent diabetes presents 2 days after running out of 

insulin. He is vomiting, tachycardic, hypotensive, and lethargic. 

Why should insulin therapy not be initiated in this patient? 

Scenario I 

Presentation: A 60-year-old man with a chronic cough presents for weakness and confusion. While in the 

emergency department, he has a seizure. 

Diagnostic evaluation: The serum sodium is 110 mEq/L, and a chest radiograph shows a large mass in the 

right upper lobe. 

What findings are expected on a urinalysis? What treatment should be started? 

ScenarioJ 

Presentation: A 20-year-old woman with bipolar disorder presents for polydipsia and weakness. 

Diagnostic evaluation: The serum sodium is 150 mEq/L. 

What medication likely caused this patient's illness? What results are expected on a urinalysis? 

630



Scenario A 

Diagnosis: hyperosmolar nonketotic coma 

Diagnostic evaluation: Laboratory studies show hyperglycemia, ketoacidosis, and hypokalemia. 

Scenario B 

Diagnosis: isopropyl alcohol poisoning 

Diagnostic evaluation: Differential diagnoses include uremia, methanol poisoning, and ethylene glycol 

poisoning. 

Scenario C 

Diagnostic evaluation: Laboratory studies show respiratory acidosis, metabolic acidosis, and positive 

opiates on toxicologic screen. 

Scenario D 

Diagnosis: The diagnosis is hyperkalemia from massive transfusion, and potassium is leaking out of 

hemolyzed PRBCs. Treatment is calcium IV. 

Scenario E 

Diagnosis: The diagnosis is adrenal insufficiency/crisis. Hypoglycemia, hyponatremia, and hyperkalemia 

are expected. Treatment should include calcium for the ECG changes and a steroid such as hydrocortisone 

for the adrenal crisis. 

Scenario F 

A mixed acid-base disorder is unlikely given that the tenth and hundredth decimal points of the pH 

roughly estimate the pCO 2 

• 

ScenarioG 

The first medication to be administered should be a ~-blocker such as propranolol. 

Scenario H 

Insulin therapy should not be started until hypokalemia has not been excluded. If hypokalemia is 

discovered, it should be treated before starting insulin therapy. 

631


Scenario I 

Expected findings include a concentrated urine despite a hypo-osmolar/hyponatremic serum, because this 

is likely SIADH. Hypertonic saline should be started to treat the severe hyponatremia. 

ScenarioJ 

Lithium can cause diabetes insipidus. A very dilute urine is expected despite a hyperosmolar/ 

hypernatremic serum. 

632

ENVIRONMENTAL DISORDERS 


Burns ......................................................................................................................................................................... 639 

Pathophysiology ................................................................................................................................................. 639 


Management ...................................................................................................................................................... 640 

Inhalation Injuries .............................................................................................................................................. 642 

Chemical Injuries ............................................................................................................................................... 643 

Electrical Injuries ................................................................................................................................................ 643 

Lightning Injuries ................................................................................................................................................ 645 

Heat Disorders .......................................................................................................................................................... 647 

Cold Disorders .......................................................................................................................................................... 650 

Frostbite ............................................................................................................................................................. 650 

Hypothermia ...................................................................................................................................................... 651 

Bites and Stings ......................................................................................................................................................... 655 

Human Bites ...................................................................................................................................................... 655 

Dog Bites ........................................................................................................................................................... 656 

Cat Bites ............................................................................................................................................................. 657 

Venomous Snake Bites ....................................................................................................................................... 658 

Bee Stings, Ant Bites, and Other Insect Bites and Stings ...................................................................................... 659 

Black Widow Spider ........................................................................................................................................... 659 

Brown Recluse Spider ........................................................................................................................................ 660 

Scorpion Stings ................................................................................................................................................... 660 

Jellyfish Stings .................................................................................................................................................... 661 

Altitude Disorders ..................................................................................................................................................... 661 

High-Altitude Disorders ...................................................................................................................................... 661 

Acute Mountain Sickness ............................................................................................................................ 661 

High-Altitude Pulmonary Edema (HAPE) ..................................................................................................... 661 

High-Altitude Cerebral Edema (HACE) ........................................................................................................ 662 

Dysbarism .......................................................................................................................................................... 662 

Submersion Injury ..................................................................................................................................................... 664 

Other Environmental Hazards .................................................................................................................................. 668 

Radiation Injuries ............................................................................................................................................... 668 

Crush Syndrome ................................................................................................................................................. 668 

Volcanic Eruptions ............................................................................................................................................. 669 

633

ENVIRONMENTAL DISORDERS: SELF-ASSESSMENT QUESTIONS 


1. You are evaluating an adult burn victim of ideal body weight and find that he has partial-thickness burns of his 

entire right arm, anterior trunk, and one-half of his right leg. Using the "rule of nines," you estimate the total body 

surface area burned to be: 

(a) 27% 

(b) 31.5% 

(c) 36% 

(d) 54% 

2. The initial fluid of choice for the resuscitation of burn victims is: 

(a) 

D5/0.45% normal saline 

(b) OS/lactated Ringer's 

(c) Lactated Ringer's 

(d) Colloids 

3. Which of the following tissues has the least resistance? 

(a) Nerves, blood vessels 

(b) Bone and tendons 

(c) Fat 

(d) Skin 

4. Which of the following statements regarding electrical injuries is false? 

(a) Alternating current generally produces worse effects than direct current of the same voltage. 

(b) The dysrhythmia produced by direct current is usually ventricular fibrillation. 

(c) The exit wound produced by direct current is discrete. 

(d) Lightning behaves like direct current. 

5. All of the following statements regarding acclimatization are accurate except: 

(a) 

It is mediated by aldosterone. 

(b) It is a process through which an individual adapts to a warmer, more humid environment. 

(c) It results in a decreased concentration of sodium in the sweat and in the urine. 

(d) It results in decreased sweat volume. 

6. The mechanisms by which lightning produces injury include all of the following except: 

(a) Side flash ("splash") 

(b) Blunt trauma 

(c) Ground current 

(d) "Freezing" 

7. The appropriate method for rewarming a frostbitten extremity is to rewarm it rapidly in circulating water heated to: 

(a) 

100.4°-104°F (38°-40°C) 

(b) 104°-107.6°F (40°-42°C) 

(c) 107.6°-111.2°F (42°-44°C) 

(d) 111.2°-114.8°F (44°-46°C) 

8. All of the following ECG changes may be seen in association with hypothermia except: 

(a) Osborn waves 

(b) Prominent P and U waves 

(c) T wave inversion 

(d) Prolonged PR, QRS, and QT intervals 

9. The effect of hypothermia on the uncorrected arterial blood gas is to produce a falsely: 

(a) Low pH, high p0 2 

and pC0 2 

(b) High pH, low p0 2 

and pC0 2 

(c) Low pH, p0 2 

, and pC0 2 

(d) High pH, p0 2 

, and pC0 2 

634


10. Cat-scratch disease is caused by: 

(a) A gram-positive coccus 

(b) A gram-negative bacillus 

(c) A virus 

(d) The causative organism is unknown. 

11. A patient presents with the complaint of a cat bite to her hand. You choose an antibiotic to cover the most common 

pathogen associated with cat bites, which is: 


(b) Anaerobes 

(c) Eikenella corrodens 

(d) Pasteurella multocida 

12. What is the most venomous scorpion in North America? 

(a) Arizona bark scorpion (Centruroides genus) 

(b) Arizona hairy scorpion, aka desert hairy scorpion (Hadrurus arizonensis) 

(c) Stripe-tailed scorpion, aka "devil" scorpion (Hoffmannius genus) 

(d) Fat-tailed scorpion (Androctonus crassicauda) 

13. All of the following are appropriate antibiotic regimens for the treatment of a human bite wound except: 

(a) 

Dicloxacillin plus ampicillin or penicillin 

(b) Augmentin 

(c) Cefuroxime 

(d) Clindamycin 

14. The single leading cause of toxic death in the United States is: 

(a) Cyanide 

(b) Hydrogen sulfide 

(c) Carbon monoxide 

(d) Phosgene gas 

15. All of the following statements regarding "middle ear squeeze" are accurate except: 

(a) Symptoms (which include ear fullness and pain) develop on descent. 

(b) Divers usually begin to develop symptoms at 16-20 feet. 

(c) Symptoms result from failure to equalize the pressure between the middle ear and the water due to dysfunction 

of the eustachian tube. 

(d) Failure to abort the dive (or to return to the surface and then try a slower more controlled descent) will produce 

worsening pain and rupture of the tympanic membrane. 

16. All of the following statements regarding the treatment of black widow spider bites are accurate except: 

(a) The antivenin is equine-derived. 

(b) The mortality rate of these bites is rare. 

(c) Bites to the lower extremities or genitalia can produce pain simulating an "acute abdomen." 

(d) Antivenin should be administered to all patients. 

17. The organ system that is most resistant to the effects of ionizing radiation is: 

(a) GI system 

(b) CNS system 

(c) Hematopoietic system 

(d) Reproductive system 

18. The LD 50 

of whole body ionizing radiation is: 

(a) 250 rad 

(b) 350 rad 

(c) 650 rad 

(d) 850 rad 

635


19. Which of the following measures is not considered to be useful in the treatment of patients with heat stroke? 

(a) Removing the patient from the heat source and completely undressing him or her 

(b) Applying atomized tepid water to the skin and fanning the patient 

(c) Administering an antipyretic agent (aspirin, ibuprofen, acetaminophen) 

(d) Controlling shivering with a benzodiazepine or chlorpromazine 

20. When treating heat stroke, active core cooling measures should be abandoned when the patient's core temperature 

reaches: 

(a) 96.8°F (36°C) 

(b) 98.6°F (37°C) 

(c) 100.4°F (38°C) 

(d) 102.2°F (39°C) 

21. The antibiotic of choice for treating wound infections caused by Pasteurella multocida is: 

(a) 

Penicillin 

(b) Cephalexin 



22. Although all of the following burns may occur in association with a lightning strike, ____ burns are 

pathognomon i c. 

(a) 

Linear 

(b) Punctate 

(c) Fern-like 

(d) Thermal 

23. A 38-year-old man presents 48 hours after being bitten by a neighbor's dog and is clearly septic. He had not sought 

prior medical attention, because the wound was relatively superficial and the dog was known to him and appeared 

healthy. Except for a splenectomy 6 years ago (due to trauma), his past medical history is unremarkable. Gram stain 

of the wound reveals a gram-negative bacillus. The most likely organism responsible is: 

(a) 

Eikenella corrodens 

(b) Pasteure/la multocida 

(c) Capnocytophaga canimorsus 

(d) Rochalimaea henselae 

24. All of the following antibiotics would be effective in treating the patient in the dog bite question (above) except: 


(b) A cephalosporin 


(d) An aminoglycoside 

25. Permanent injury to the cochleovestibular system may occur in patients with: 

(a) 

Barotitis media 

(b) Barotitis interna 

(c) "Sinus squeeze" 

(d) Barotrauma of ascent 

26. The most common presentation of a pulmonary air embolism is a: 

(a) Neurologic event 

(b) Cardiovascular event 

(c) Pulmonary event 

(d) Psychological event 

636


27. A patient with glucose-6-phosophate dehydrogenase deficiency has been bitten by a brown recluse spider. Which of 

the following medications is contraindicated? 

(a) 

Erythromycin 

(b) Antihistamine 

(c) Corticosteroids 

(d) Dapsone 

28. The best predictor of survival after radiation exposure is: 

(a) The whole body dose of ionizing radiation 

(b) Timing of the onset of symptoms 

(c) The absolute lymphocyte count 48 hours after exposure 

(d) The organ system involved 

29. On physical examination, the most sensitive indicator of a primary blast effect is: 

(a) Air emboli on funduscopic examination 

(b) Tympanic membrane rupture 

(c) Petechial hemorrhages in the nasopharynx 

(d) Tachypnea 

30. Frequent metabolic derangements in submersion-injury victims include all of the following except: 

(a) Hypoxemia 

(b) Acidosis 

(c) Serum electrolyte abnormalities 

(d) Hypercapnia 

31. All of the following statements regarding submersion injury are accurate except: 

(a) Saltwater drowning is more common than freshwater drowning. 

(b) Males are more commonly affected than females, regardless of age. 

(c) Children


ANSWERS 

I. C 9. a 17. b 25. b 33. d 

2. C 10. b 18. b 26. a 34. d 

3. a 11. d 19. C 27. d 

4. b 12. a 20. d 28. C 

5. d 13. d 21. a 29. b 

6. d 14. C 22. C 30. C 

7. b 15. b 23. C 31. a 

8. b 16. d 24. d 32. C 



638


I. BURNS 


1. Application of heat or chemicals causes "burning" of the skin and underlying tissues. Loss of the normal skin 

barrier allows fluids and electrolytes "out" and bacteria "in." 

2. Pulmonary damage occurs from direct heat, especially with steam exposure, as well as from inhalation of 

products of combustion and particulate matter. 


1. Obtain the following information: 

a. Was the victim burned in an enclosed or open space? 

b. Were there any toxic products of combustion present at the burn site? 

c. Does the patient have any respiratory symptoms? 

2. Estimate the body surface area (BSA) burned (and chart it). Only second- and third-degree burns should be 

included in the estimation. 

a. The "rule of nines" is used for adults and children >4 years old. It should not be used for children


(2) Deep 

(a) 

Skin is white, with some erythematous areas, less blanching and moisture, tender 

(b) Deep reticular dermal injury 

(c) Causes: hot liquid or oil, steam, flame 

(d) Wound healing: 3-6 weeks (some scarring) 

c. Third degree (full thickness; dermal structures involved) 

(1) The skin is charred, pearly white, "leathery," and insensitive. 

(2) The entire skin layer and its nerve endings are destroyed and cannot grow back. 

(3) Causes: hot oil, steam, flame, high-voltage electrical burns 

(4) Wound healing: does not occur without surgical repair, skin grafting, or both (significant scarring) 

d. Fourth degree (musculoskeletal injury) 

(1) Extends below dermis to subcutaneous tissue (bone, muscle fascia) 

(2) Tissue is necrotic. 

(3) Causes: hot objects with high specific gravity (eg, molten metal), electrical burns 

4. Estimate the full extent of the burn (and chart it). 

a. Minor burns 

(1) Partial thickness 10% total BSA 

(3) Burns to the face, hands, major joints, feet, or perineum 

(4) Burns to an immunocompromised host 

(5) Burns and associated inhalation injury or major trauma 

(6) Electrical burns (high voltage) 

(7) Circumferential burns of the chest or extremities 

(8) Caustic chemical burns 

d. High-risk patients 

C. Management 

1. Prehospital 

(1) Younger than 10 or older than 50 years with minor to moderate burns 

(2) Concurrent medical illness or immunocompromised 

(3) Associated head injury, stroke, or psychiatric illness 

(4) Prolonged exposure in a confined space 

a. Stop the burning process. 

b. ABCs, including intubation if indicated, treatment with high-flow oxygen and IV fluids, followed by a 

head-to-toe survey looking for signs of trauma 

c. Cover the burn wounds with a clean dry sheet or sterile dressings. 

d. Severe pain may be lessened with frequent boluses of IV fentanyl or morphine as directed by medical 

protocol. 

2. Hospital (always use aseptic technique) 

a. ABCs: major pitfall is inadequate airway management 

(1) Make sure that the patient is receiving adequate supplemental oxygen; all patients with moderate 

to major burns should receive 100% oxygen via nonrebreather mask; place on pulse oximeter, but 

remember that the pulse oximeter may be inaccurate in the face of carbon monoxide and some other 

chemical inhalation injuries. 

(2) Early intubation is indicated if there are any signs of respiratory distress. 

(a) Unconscious or obtunded patients exposed to fire or smoke who were found in an enclosed 

space _,. consider possible cyanide poisoning (see page 579) 

640


(b) Evidence of airway edema (stridor, dysphonia, tongue or oropharynx swelling) progresses over 

several hours; failure to intubate early may lead to failed airway. 

(c) Moderate to severe respiratory distress (including tachypnea, stridor, or labored breathing) 

(d) Mild respiratory distress and signs of inhalation injury 

i. Facial burns 

ii. Sooty sputum 

iii. Singed facial/nasal hairs 

iv. Oropharyngeal erythema, swelling, carbon deposits 

(e) Abnormal laboratory parameters 

i. Hypoxia despite 100% oxygen 

ii. High carboxyhemoglobin 

iii. Low peak flow 

b. Fluid resuscitation 

(1) Patients with burns >20% total BSA require fluid resuscitation; start two large-bore IV lines (above 

waist level) with lactated Ringer's (the fluid of choice for the first 24 hours after burn). 

(2) Use a common fluid resuscitation formula (eg, the Parkland formula). A general rule is to administer 

2-4 ml/kg per % total BSA burned/24 hours. 

(a) Give the first half of these fluids over the initial 8 hours (from time of burn). 

(b) Give the second half of these fluids over the next 16 hours. 

(c) Daily maintenance fluids should be administered in addition to the fluids above, particularly in 

infants and small children. 

(3) The above formula represents only an initial estimate of the fluid requirements and should be 

adjusted according to the patient's response (urinary output, heart rate, and mentation); administer 

fluids at a rate sufficient to maintain the pulse 1 ml/kg/hr in children), and a clear sensorium. 

c. Patients with extensive burns also need a Foley catheter (to monitor fluid resuscitation and check urine 

for myoglobinuria) and a nasogastric tube (prophylaxis for ileus). 

d. Avoid excessive cooling; do not apply ice to wounds or cool compresses to extensive burns. 

e. Medications 

(1) IV narcotics for pain relief 

(2) Tetanus prophylaxis (the only medication given IM) 

f. Baseline studies for patients with major burns 

(1) Arterial blood gases with a carboxyhemoglobin level (persistent metabolic acidosis + 

t carboxyhemoglobin level - possible cyanide toxicity) 

(2) ECG 


(4) Hematology panel 

(a) CBC with differential 

(b) Prothrombin time/lNR and partial thromboplastin time 

(c) Type and screen 

(5) Chemistries 

(a) Glucose 

(b) Electrolytes 

(c) BUN/creatinine 

(d) Creatine kinase 

(6) Urine studies 

(a) Urinalysis 

(b) Myoglobin 

(c) Human chorionic gonadotropin (hCG) 

g. Burn care 

(1) Circumferential burns 

(a) Assess the respiratory status in patients with a circumferentially burned thoracic cage; signs of 

respiratory insufficiency warrant consideration of escharotomy. 

641


(b) Elevate circumferentially burned extremities, and monitor distal neurovascular status (sensation 

and pulses); loss of Doppler ultrasound signals mandates an escharotomy. 

(2) Major burns: cover burns with dry sterile sheets, and contact nearest burn center regarding any 

further management. 

(3) Minor burns 

h. Disposition 

(a) Apply cool compresses. 

(b) Administer pain medication. 

(c) Irrigate burn with sterile saline and gently cleanse with a mild soap. 

(d) Debride all loose tissue and broken blisters. 

(e) Large intact blisters (particularly tense ones) or blisters over very mobile joints can also be 

debrided or aspirated (controversial). 

(f) Apply a topical antibacterial agent (eg, bacitracin), and cover the wound with sterile dressing. 

Polymixin B is no longer recommended because of higher rates of contact allergic reaction. 

Silver sulfadiazine may be used but has fallen out of favor; it should be avoided in pregnant 

women in the late third trimester, because it may cause kernicterus and depigment skin (and 

because of cost). 

(1) Minor burns: discharge with pain medications and follow-up in 24 hours 

(2) Moderate burns: require hospital admission; patients with minor burns who are at high-risk or 

unreliable may also be appropriate for admission. 

(3) Major burns (see page 639): transfer to a burn center; patients with moderate burns who are highrisk 

or unreliable should also be considered for transfer. 

1. Contact the regional burn center early if transfer is contemplated, and tailor initial treatment to their 

standard regimen. In preparation for transfer, a protocol should be followed that includes: 

D. Inhalation injuries 

(1) Adequate resuscitation 

(2) Physician-to-physician contact 

(a) Do not delay initial airway management, fluid resuscitation, placement of catheters and lines, or 

diagnosis of associated life-threatening injuries. 

(b) Aggressive fluid resuscitation is especially important to maintain blood pressure and urine 

output to prevent renal failure; however, pulmonary edema and hypoxia can result from fluid 

overload (especially in elderly patients with inhalation injury). 

(3) A burn transfer checklist 

(4) A copy of the patient's completed chart 

1. Respiratory burns 

a. Intubate early, because subsequent edema may make this difficult or impossible later on. 

b. If at all possible, refer these patients to a regional burn center. 

2. Poisonous gas inhalation 

a. Phosgene gas or N 2 

O 2 

- immediate or delayed pulmonary edema 

b. Hydrogen sulfide (H 2 S) - rapid death from respiratory failure 

c. Carbon monoxide (CO) 

(1) The single leading cause of toxic deaths in the United States 

(2) A high index of suspicion is a must, because signs and symptoms are vague and multiple; any fire 

victim who was in an enclosed space should be evaluated for CO poisoning. 

(3) Treat all symptomatic patients because carboxyhemoglobin levels do not always correlate with severity 

of symptoms. 

(a) Minimum treatment is administration of 100% oxygen via a nonrebreather mask until the 

patient is asymptomatic and the carboxyhemoglobin level is 25%-40% at any time (level used varies with hospital policy and 

chamber accessibility) 

642


E. Chemical injuries 

iii. Coma (or a history oft level of consciousness) 

iv. Pregnant patients who are symptomatic or have a carboxyhemoglobi n level > 15 

v. Neonates 

vi. Severe metabolic acidosis (pH 1,000 volts) or low voltage (


(1) Current passing through the head and neck is more likely to induce cataract formation than current 

passing distal to these sites. 

(2) Current traversing the heart and thorax is associated with an increased likelihood of cardiac 

complications. 

5. Clinical presentation and physical examination 

a. Perform a head-to-toe survey looking for evidence of trauma. 

b. Look for entrance and exit wounds. 

(1) Electrical wounds are "bull's-eye" in appearance with a charred center; a grayish white area of 

coagulation necrosis is adjacent to the smrounding red, edematous tissue. 

(2) The true extent of underlying injury will not be apparent initially, so do not debride the wounds in 

the emergency department. Electrical injury may cause progressive intravascular thrombosis. 

6. Management 

a. Initial assessment and stabilization 

(1) ABCs 

(2) Monitor, IV access, and oxygen 

(a) Establish an IV line with a large-bore catheter; use lactated Ringer's or normal saline, and 

determine the rate based on the initial shock assessment (not the extent or degree of burn 

because most of the injury is internal); adjust the rate as needed to maintain a urine output of at 

least 0.5-1 ml/kg/hr. 

(b) Give oxygen to everyone (no exceptions). 

(c) Put the patient on a cardiac monitor. 

(3) Foley catheter (monitor urine output) 

(4) Nasogastric tube if injury is severe (increased risk of adynamic ileus) 


(1) ABGs 

(2) ECG 

(3) Creatine kinase (CK) + CK-MB 

(4) CBC 

(5) Prothrombin time/lNR and partial thromboplastin time 

(6) BUN/creatinine 

(7) Urinalysis (no RBCs but positive dipstick - presume myoglobinuria) 

(8) Serum electrolytes (including Ca++) 

(9) Urine myoglobin 

(10) Radiographic studies as indicated 

c. Treat myoglobinuria. 

(1) Administer fluids at a rate sufficient to maintain a urine output of 1.5-2 ml/kg/hr. 

(2) If this does not clear the pigment, administer mannitol as a bolus of 25 g, and add 12.5 g to each 

subsequent liter of fluids (at a rate of 1 L/hr) until the myoglobin is cleared. Furosemide (2 mg/kg IV) 

may also be administered to promote diuresis. 

(3) Alkalinization of the urine is suggested in some texts to be beneficial at CK concentrations >6,000 

IU/L; however, this has never been proved. 

d. Do not forget tetanus prophylaxis. 

e. Disposition 

(1) Hospitalization and cardiac monitoring are indicated for all patients with high-voltage burns and for 

those patients with low-voltage burns who are symptomatic (eg, chest pain, abnormal physical or 

laboratory findings). Those with severe electrical burns should be admitted to a burn center. 

(2) Asymptomatic patients with low-voltage injuries may be discharged to home after a period of 

observation and cardiac monitoring in the emergency department if their physical examination and 

diagnostic evaluation are unremarkable (no skin lesions, normal ECG, no urinary heme pigment). 

f. Delayed complications of major electrical burns 

(1) Myoglobinuric renal failure 

(2) Compartment syndromes 

(3) Gangrene (due to intravascular thrombosis) 


644


(5) Infection 

(6) Cataracts 

(7) Neurologic problems (peripheral nerve damage, trouble with memory/concentration, seizures, 

delayed spinal cord syndromes) 

7. Electrical lip burn 

a. Clinical presentation: usual history is a child bites on an electrical cord, and burns lips and commissures. 

b. Management 

(1) Do not debride these wounds. Cleanse and apply a petroleum-based antibiotic ointment. 

(2) These burns require close observation and referral to a plastic or oral surgeon for splinting and 

further care. 

c. Complications: Delayed hemorrhage from the labial artery may occur in 10%-15% of these patients 

3-14 days after injury, when the eschar separates. 

G. Lightning injuries 


a. Lightning injuries are extremely high-intensity bursts of direct current (10 million to 2 billion volts) that 

are very brief (0.1-1 milliseconds). Although one might compare lightning injuries to a massive DC 

countershock, the injuries that occur from a lightning strike are different from those that occur with manmade 

electricity, as is the treatment; unlike victims of high-voltage electricity, lightning victims rarely have 

deep burns or underlying tissue damage, and they do not generally require fluid resuscitation. 

b. Because of the brief duration, lightning rarely breaks down the skin; instead, it passes over the body 

surface, and if the victim's body is wet or sweaty, can cause burns in one of two ways: 

(1) Moisture can be vaporized and produce "steam burns." 

(2) Sudden expansion of water converting to steam can cause the clothes to "explode" off the body, 

burning it in the process. 


a. Direct strike: Lightning hits the victim directly and passes over or through him or her; morbidity and 

mortality are highest with this mechanism. 

b. Contact: lightning strikes an object that the victim is touching. 

c. Side flash or splash: lightning jumps from its initial strike site to a nearby person or object in its pathway. 

d. Ground current or step voltage: I ightning strikes the ground and spreads through it to the victim; if one of 

the victim's legs is nearer to the strike point than the other, a potential difference is created between them, 

resulting in the current passing through the legs and into the trunk. 

e. Thermal burns occur as a result of boiling sweat, burning clothes, or hot jewelry. 

f. Blunt trauma: lightning rapidly heating air followed by rapid cooling causes a blast effect that throws the 

victim; the organ affected most often by blast injury is the ear. 

3. Classic clinical scenario: An observed strike is obvious, but many are not observed. An important diagnostic 

clue in the unconscious patient is that clothes may be partially missing, especially the shoes. 

a. Clinical picture (minor lightning strike): patient appears "stunned," is somewhat confused, and has difficulty 

recalling events that transpired a few hours ago. He or she has no memory of the event described. Unless 

the lightning strike was witnessed, this diagnosis may be missed. Do not be fooled by the absence of 

entrance or exit wounds; they are rare. The patient has mild hypertension and tachycardia and is likely to 

complain of headache. There is frequently a history of temporary loss of vision or hearing. 

b. Possible physical findings (major lightning injuries) 

(1) Cardiopulmonary injuries 

(a) Cardiac arrest (asystole): most common cause of death 

(b) Respiratory arrest secondary to tetany of diaphragm muscles: may be more prolonged than 

cardiac arrest and can cause secondary ventricular fibrillation 

(c) Pulmonary edema 

(d) Transient hypertension 

(2) Neurologic injuries 

(a) Transient loss of consciousness (the most common neurologic event) 

(b) Confusion and amnesia (both anterograde and retrograde) are also common. 

(c) Peripheral nerve damage is another common finding. 

(d) Seizures result from hypoxia or concomitant head injury. 

645


(e) Transient flaccid paralysis (keraunoparalysis) of the lower extremities (which may initially 

appear cold, pale, pulseless, and insensitive) is generally due to vascular spasm and sympathetic 

instability; it usually resolves spontaneously over several hours. 

(3) Eye and ear injuries 

(a) Immediate or delayed cataract formation 

(b) Corneal injuries, uveitis, hyphema, vitreous hemorrhage, retinal detachment, optic nerve atrophy 

(c) Unreactive dilated pupils secondary to autonomic instability (do not misinterpret as an indication 

of brain death) 

(d) Ruptured tympanic membranes (>50% of cases) are caused by: 

i. The blast effect or 

ii. Basilar skull fractures or 

iii. Direct burn 

(4) Skeletal injuries (fractures) 

(a) Much less common than with manmade high-voltage injuries. 

(b) Common sites are skull, spine, or long bones. 

(5) Effects on fetus 

(a) Intrauterine death (25%) 

(b) Neonatal death (25%) 

(c) Healthy babies (50%) 

(6) Burns (four types) 

(a) Linear: superficial burns that occur in areas where sweat and moisture accumulate. 

(b) Punctate: small, discrete, circular burns that occur in clusters 

(c) Lichtenberg figures: superficial fern-like burns that are pathognomonic for lightning strike 

(d) Thermal: result from the ignition of clothing or the heating up of objects worn by the victim 

4. Management 

a. "Resuscitate the dead" (even if there are multiple victims) 

(1) Those who are in cardiac or pulmonary arrest need immediate attention if they are to have any 

chance of survival. 

(2) Those who are moving are OK on their own initially. 

b. ABC assessment and initial stabilization followed by a head-to-toe survey for signs of trauma. Standard 

ACLS and ATLS treatment protocols should be followed. Massive fluid resuscitation is seldom indicated, 

because lightning injuries rarely produce significant tissue destruction. 

c. Burns, if present, should be treated in the usual manner. Do not forget tetanus prophylaxis. 

d. Baseline laboratory and diagnostic evaluation 

(1) CBC 

(2) Electrolytes, BUN/creatinine 

(3) ECG and cardiac enzymes 

(4) Urinalysis and urine for myoglobin 

(5) Chest radiograph and other radiographs as indicated 

(6) Brain CT (and cervical spine radiographs) should be ordered for patients with an altered level of 

consciousness. 

5. Disposition: In almost all instances, these patients should be admitted with continuous cardiac monitoring for 

24 hours. 

6. Late sequelae 

a. Posttraumatic stress disorder/keraunophobia (an abnormal fear of thunder and lightning) 

b. Paresis 

c. Impaired mental function 

d. Memory deficits 

e. Insomnia 

f. Cataracts 

g. Peripheral neuropathy 

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II. HEAT DISORDERS 

A. Normal body temperature regulation (heat gain= heat loss) 

1. Heat gain is the result of: 

a. Metabolic activity 

b. Environmental heat 

c. Strenuous exertion 

2. Heat loss results from: 

a. Radiation 

(1) Cutaneous vasodilation increases the amount of heat that can be dissipated through the skin. 

(2) As ambient temperature approaches and surpasses body temperature, heat loss via radiation ceases 

and radiation becomes a source of heat gain. 

b. Convection: heat loss due to air or water circulating across the body (wind chill) 

c. Conduction: direct physical contact with a cooler object or immersion in water 

d. Evaporation 

(1) The degree of sweating is controlled by cholinergic and sympathetic activity. 

(2) The effectiveness of sweating is decreased in the presence of high humidity. 

3. The wet-bulb globe thermometer index 

a. Accounts for the effects of humidity and radiant heat on the ambient temperature 

b. The most accurate measure of environmental heat stress and the risk of heat illness 

4. Acclimatization 

a. A process over a period of 1-2 weeks in which an individual adapts to a warmer, more humid climate via 

hypothalamic and thyroid adaptation 

b. Mediated by aldosterone, which reduces the sodium concentration in sweat and urine; this preserves fluid 

volume, thus preventing the development of a heat illness. 

c. Characterized by an earlier onset of sweating, greater sweat volume, and a decreased concentration of 

sodium in the sweat and in the urine 

B. Heat illness 

1. Imbalance between heat production and loss 

2. Predisposing factors 

a. Physical activity (especially in a hot, humid environment) 

b. Extremes of age, poor physical condition, fatigue 

c. Inadequate indoor cooling (lack of or malfunctioning air conditioning) 

d. Excessive clothing 

e. Dehydration 

f. Preexisting cardiovascular disease 

g. Skin disorders 

h. Obesity 

1. Drugs 

(1) Phenothiazines (act centrally on the hypothalamus) 

(2) Anticholinergics: reduce the ability to sweat 

(a) Atropine 

(b) Scopolamine 

(c) Cogentin 

(d) Antihistamines 

(e) Cyclic antidepressants 

(3) [:)-blockers/calcium channel blockers (1 heat loss) 

(4) Diuretics (t heat loss) 

(5) Amphetamines (t heat gain) and sympathomimetics, including OTC pseudoephedrine and bath salts 

(6) LSD ( t heat gain) 

(7) Cocaine (t heat gain) 

(8) Monoamine oxidase inhibitors (t heat gain) 

647


(9) MDMNecstasy, "rave drugs" 

(1 0) Haloperidol (neuroleptic) 

(11) Alcohol withdrawal 


a. Heat cramps: inadequate replacement of salt from loss through sweating -> hyponatremia -> muscle cramps 

b. Heat tetany: hyperventilation -> respiratory alkalosis _,. paresthesias and carpopedal spasm 

c. Heat exhauston: salt water depletion from sweat loss-> hypovolemia and hypoperfusion, and normal 

mental status and neurologic examinations 

d. Heat stroke 

(1) Heat stress (classic) or endogenous heat production (exertional) -> a breakdown of central 

thermoregulatory control -> hyperpyrexia and neurologic symptoms ± absence of sweating. Sweating 

is usually absent in classic heat stroke and present in exercise-induced or exertional heat stroke. 

Cerebral edema is common. 

(2) Loss of sweating ability aggravates (but does not cause) the problem. 

(a) The exact mechanism by which the ability to sweat is lost is unknown, but a direct thermal 

effect on sweat glands is a contributing factor. 

(b) Anticholinergic drugs are the most frequent cause of impaired sweating in classic heat stroke. 

(c) Specific disorders such as congenital anhydrosis, cystic fibrosis, and quadriplegia are rare 

contributing factors. 

(3) Volume depletion and electrolyte imbalance are not usually prominent features, but central venous 

pressure is usually increased. 

(4) Patients with preexisting cardiovascular disease have a reduced capacity to cope with the 

hemodynamic changes of peripheral vasodilatation. 

(5) End-organ and systemic injury may occur. 

(a) Cardiac (CHF, pulmonary edema) 

(b) ARDS 

(c) Liver (marked increases of AST and ALT) 

(d) Kidney (hematuria, proteinuria, acute tubular necrosis) 

(e) Muscular (mild increase in creatine kinase -> rhabdomyolysis and acute renal faiure) 

(f) 

Hematologic (altered coagulation -> bleeding, disseminated intravascular coagulation) 

C. Classic presentation 

1. Heat cramps: The patient complains of severe muscle cramping typically involving the calves, thighs, and 

shoulders. Questioning reveals that the cramps developed after a bout of intense physical activity and profuse 

sweating, during which the patient had been replacing fluid losses with a hypotonic solution. Body temperature 

is normal. 

2. Heat tetany: The patient is hyperventilating and complains of tingling and spasms of the hands and feet. 

3. Heat exhaustion: The patient presents with extreme fatigue and profuse sweating. If the onset was fairly recent, 

he or she will complain of light-headedness, nausea, vomiting, and a dull headache. If the patient started 

feeling ill several hours ago, concerned family or friends may have brought the patient in because he or she 

"didn't look right;" this patient is tachypneic, tachycardic, and may be hypotensive. Body temperature in 

patients with heat exhaustion is normal or slightly increased. 

4. Heat stroke: a true medical emergency characterized by an altered level of consciousness and any neurologic 

finding and an increased temperature 

a. Classic heat stroke occurs most often in middle-aged or elderly patients who live a sedentary lifestyle 

and are taking medications for chronic illnesses. It is caused by environmental heat exposure. Do not be 

fooled if the patient is sweating; some do initially and, if not treated, will stop sweating and develop hot, 

dry skin. It may be difficult to exclude a cerebrovascular or CNS infection on physical examination. An 

accurate history is critical to the diagnosis; ataxia may be the initial (or presenting) complaint. Laboratory 

findings include: 

(1) Respiratory alkalosis and mild metabolic acidosis 

(2) Mild coagulopathy and increased creatine kinase 

(3) Normal glucose and calcium levels 

b. Exertional heat stroke typically occurs in young, healthy patients who have been engaged in strenuous 

exercise. These patients are usually diaphoretic on presentation. Characteristic laboratory findings 

include: 

648


D. Management 

(1) Respiratory alkalosis and marked lactic acidosis 

(2) Disseminated intravascular coagulation and rhabdomyolysis (urine specimen looks like "machine oil") 

(3) t BUN/creatinine (acute renal failure) 

(4) Hypoglycemia and hypocalcemia 

1. Heat cramps 

a. Oral or IV fluid and electrolyte replacement 

b. Rest in a cool environment with a gradual return to normal environment and activity 

2. Heat tetany 

a. Removal from heat 

b. Rebreathe expired air (bag-breathing) 

c. Exclude electrolyte abnormalities 

3. Heat exhaustion 

a. Bedrest in a cool environment 

b. Rapid IV fluid/electrolyte volume replacement, initially with normal saline 

c. Baseline studies: CBC, glucose, electrolytes, BUN/creatinine, liver profile, and urinalysis 

4. Heat stroke 

a. Management 

(1) Immediate, aggressive, rapid cooling down to 102.2°F (39°C). Morbidity is directly related to severity 

and duration of hyperthermia. 

(a) Remove patient from heat source, and undress him or her completely. 

(b) Apply atomized tepid water (not ice) to the skin, and fan the patient. 

(c) Apply ice packs to axillae and groin. 

(d) Iced gastric lavage is rarely used; if done, monitor ins and outs. 

(e) Immersion in ice water is also very effective but may precipitate seizures; monitoring and 

resuscitation are difficult with this technique. It is recommended, however, if above measures 

have failed to lower body temperature to 102.8°F (38.9°C) within 30 minutes. 

(2) Supportive measures 

(a) Administer high-flow oxygen to all patients, and monitor by pulse oximetry; intubate if there is 

obtundation, seizures, or a depressed gag reflex. 

(b) Establish IV access of normal saline. Young, healthy patients with exertional heat stroke are 

dehydrated and require aggressive fluid management. Those with classic heat stroke need IV 

fluids, but should not be rehydrated aggressively (fluid requirements are usually not large); rate 

of 250-300 ml/hr is generally adequate. Central venous pressure monitoring may be needed to 

guide fluid therapy in older patients and in those with cardiovascular disease. 

(c) Put the patient on a cardiac monitor. Tachydysrhythmias are common and respond to cooling 

(do not cardiovert); be careful not to insert the tip of the central venous pressure catheter into 

an irritable heart. 

(d) Establish continuous temperature monitoring via an esophageal or rectal probe. 

(e) Place a Foley catheter to monitor urine output. 

(f) Obtain baseline laboratory studies 

i. Arterial blood gases (corrected for temperature), lactate 

ii. CBC, glucose, electrolytes (including Ca++ and Mg++) 

iii. BUN/creatinine, prothrombin time/lNR and partial thromboplastin time, toxicology screen 

iv. Thyroid and liver function tests 

v. Urinalysis and urine myoglobin 

vi. ECG and chest radiograph (especially in older patients) 

b. Medications 

(1) Control shivering with a benzodiazepine or chlorpromazine as needed; induction of paralysis may 

be required. 

(2) Antipyretics (aspirin, ibuprofen, acetaminophen) are not useful. 

(3) Dantrolene has not been demonstrated to be effective. 

649


Ill. COLD DISORDERS 

A. Frostbite (local cold injury can occur at temperatures above and below freezing) 


a. Causes of tissue damage 

(1) Capillary stasis and thrombosis 

(a) Cooling to 59°F (15°C)-'> maximal vasoconstriction and a significant decrease in cutaneous 

blood flow 

(b) Continued cooling to 50°F (10°C) - cold-induced vasodilation (the "hunting response") in which 

vasoconstriction is interrupted in a cyclical fashion by periods of vasodilation in an effort to 

protect the extremity from the cold 

(c) When returning cold blood starts to decrease the core body temperature, blood flow to the 

extremity shuts down and the tissue temperature drops further-'> capillary endothelial damage-'> 

increased platelet affinity and plasma leakage from the intravascular space-'> increased viscosity, 

RBC stasis, and vessel thrombosis; frostbite occurs when the tissue temperature drops below 32°F 

(0°C). 

(2) Ice crystal formation in tissues 

(a) 

Extracellular ice contributes to intracellular dehydration and destruction of protein. 

(b) Intracellular ice destroys cell architecture and function. 

(3) Reperfusion injury: rewarming - return of blood flow to the injured extremity and release of 

arachidonic acid metabolites (thromboxane, prostaglandins) from the damaged endothelial cells-'> 

vasoconstriction, platelet clumping, and sludging of WBCs -'> progressive tissue loss 

b. Most likely sites of tissue damage because they are farthest from the body core: hands, feet, ears, face, 

and nose 

c. Factors that affect the severity of tissue injury 

(1) Temperature and duration of cold exposure: remember that wet skin and clothing freeze faster than dry 

skin and clothing. 

(2) Humidity: adds to correct evaporative heat loss. 

(3) Wind chill: moving air accelerates heat loss. 

(4) High altitude: hypoxia affects the CNS and one's judgment ability; dehydration results from the 

increased respiratory rate-'> decreased blood flow 

(5) Refreezing of a thawed extremity: greatly increases the severity of tissue damage and increases the 

likelihood of tissue loss 


a. Nonfreezing, wet - trench foot (immersion foot) 

(1) Requires prolonged exposure (hours to days) to a wet environment 

(2) Early symptoms include numbness, painful paresthesias, and leg cramps. 

(3) Initial evaluation reveals a cold, pale, and anesthetic extremity. 

(4) A hyperemic phase follows and is accompanied by severe burning pain. 

(5) Tissue loss is uncommon. 

b. Nonfreezing, dry - chilblains (pernio) 

(1) Results from exposure to cold, damp air 

(2) Lesions develop on exposed areas after a delay of 12-14 hours and are characterized by erythema, 

pruritus, and burning paresthesias. 

(3) Women with Raynaud phenomenon are at highest risk. 

c. Freezing, dry or wet-'> frostnip and frostbite 

(1) Frostnip is an early response to cold exposure and is reversible. 

(a) The first sign is pale, painful, itchy skin. 

(b) If this progresses to frostbite, the skin remains cold to palpation and appears pale and gray. 

(2) Frostbite 

(a) 

Superficial: under the frozen surface, skin is soft. 

1. Once thawed: large, clear, fluid-filled vesicles develop within 24-48 hours; when these are 

reabsorbed, the skin turns black and hard (carapace). 

650


3. Management 

ii. The skin takes weeks to demarcate, and the carapace sloughs slowly, leaving new pink 

hypersensitive skin. 

(b) Deep: under the frozen surface, skin is rock hard. 

i. Once thawed, the area is cold and has a purple or red discoloration; smal I hemorrhagic 

vesicles and edema develop within 1-3 weeks. 

ii. Weeks to months later, nonviable structures demarcate, become mummified, and slough off. 

a. Prevention is the most important aspect of treatment. Proper clothing and nutrition, good health, and 

avoidance of fatigue and alcohol seem to be the most crucial aspects of prevention. 

b. Frostnip 

(1) Rewarming may be initiated in the field (breath, body heat, other heat sources). No rubbing. 

(2) Return to work is possible after rewarming, but the patient should be cautioned about recurring symptoms. 

c. Frostbite 

(1) Rapid rewarming is key and should not be started until refreezing can be prevented. 

(2) Remove clothing and rewarm affected area in circulating water that is heated to 104°-107.6°F (40°- 

420C); rewarming with dry heat can be dangerous because the frozen (insensitive) skin cannot detect 

heat, and burns may result. 

(3) Initiate general rewarming measures (as appropriate) and rehydration to treat the systemic hypothermia 

and dehydration that frequently occur in association with frostbite. 

(4) Provide tetanus prophylaxis and analgesia as needed. 

(5) Local care after full thawing 

(a) Elevate the affected extremity. 

(b) Debride or aspirate white and clear blisters; they contain chemical mediators of ischemia (eg, 

prostaglandin F 2 

and thromboxane A2) that can further damage underlying tissue. 

(c) Leave hemorrhagic blisters intact, because debridement can result in extension of injury. 

(d) Apply a topical thromboxane inhibitor (eg, aloe vera). 

(e) Dress only open wounds and separate frostbitten digits with soft dressings; leave other frostbitten 

areas open to air. 

(f) 

(6) Administer 

Avoid early surgical intervention. 

(a) Ibuprofen 400 mg orally to inhibit the arachidonic acid cascade and promote fibrinolysis. 

(b) Penicillin G 500,000 units IV to prevent streptococcal infection. 

B. Hypothermia: core body temperature


(a) Blood pressure, pulse, and cardiac output all increase during the metabolic excitation phase 

(90°-95°F [32°-35°Cl), but they all decrease once the temperature falls below 32°C (metabolic 

slowing phase). 

(b) ECG changes 

i. Osborn or "J" waves 


ii. T-wave inversion 

iii. Prolonged PR, QRS, and QT intervals 

iv. Dysrhythmias: risk develops when core temperature is


3. Predisposing factors 

a. Environmental exposure 

(1) Non immersion hypothermia: most common presentation 

(2) Immersion hypothermia: water temperature


5. Staging and management 

Table 39: Staging and Management of Accidental Hypothermia* 

Stage 

HTI 

HT II 

HT Ill 

HT IV 

Clinical 

Symptoms 

Conscious, 

shivering 

Impaired 

consciousness, 

not shivering 

Unconscious, 

not shivering, 

vital signs 

present 

No vital signs 

Typical Core 

Temperature** 

35 to 32°C 


(2) Active external rewarming 

(a) Apply heat to the body surface with one of the following: 

i. Forced-air rewarming (eg, temperature management blanket) 

ii. Warming blanket 

iii. Immersion in warm water 

iv. Radiant heat 

(b) This is effective but has potential problems. 

i. Cold blood returning from the periphery causes further cooling ("core temperature 

afterdrop"), brings lactic acid with it ("rewarming acidosis"), and causes a relative 

hypovolemia from peripheral vasodilation ("rewarming shock"). 

ii. Metabolic demands in the periphery exceed perfusion capabilities. These complications can 

be minimized by applying the heat source to the trunk only, and by using this modality in 

combination with one or more of the active core rewarming methods described below. 

iii. Patients who are submerged in warm water are difficult to monitor. 

(3) Active core rewarming 

(a) Noninvasive methods 

,. Inhalation rewarming: warm humidified oxygen by mask or endotracheal tube at 

107 .6°-113°F (42°-45°C) 

ii. Heated IV fluids (DSNS is the preferred solution) 

(b) Invasive methods 

i. Gastric or colonic lavage with warm saline: rarely needed or used 

ii. Bladder lavage with warm saline using a Foley catheter: very poor heat transfer 

iii. Peritoneal lavage 

iv. Extracorporeal rewarming: usually accomplished by hemodialysis, cardiopulmonary bypass, 

or arteriovenous or venovenous rewarming 

v. Closed thoracic lavage (if extracorporeal membrane oxygenation unavailable): warm saline 

is infused through two thoracostomy tubes. 

(c) The advantage of active core rewarming is that preferential rewarming of the heart and internal 

organs results in improved function and avoidance of problems associated with peripheral 

vasodilatation. 

(d) Active core rewarming is the modality of choice for rewarming patients with HT Ill and IV and 

for those with cardiac instability. 

(4) Choice of rewarming method depends on the severity of the hypothermia, its cause and duration, 

and the patient's status on presentation to the emergency department. Guidelines follow: 

(a) Use multiple methods. 

(b) Patients who are still in the excitation phase probably do not need active rewarming. 

(c) Patients with life-threatening cardiac dysrhythmias need rapid rewarming; use both noninvasive 

and invasive active core rewarming techniques. 

(5) Outcome: the underlying or precipitating disease process and its severity are more important 

predictors of outcome than the degree of hypothermia on presentation. 

(6) Hypothermic patients should not be pronounced dead until after they have been rewarmed to 

95°F (35°C) and subsequent resuscitative efforts are still unsuccessful. "No one's dead until they're 

warm and dead." However, consider terminating resuscitation earlier for refractory cardiovascular 

unresponsiveness in patients with asphyxia (submersion or avalanche), lethal injuries, or serum K+ 

> 12 mEq/L. (See also hypothermia in the Dysrhythmia section, where the treatment focus is entirely 

on the degree of hypothermia and the patient's cardiovascular status, pages 9-10.) 

IV. BITES AND STINGS 

A. Human bites 

1. The most common aerobic pathogens are Streptococcus spp and Staphylococcus aureus. Most infections are 

polymicrobial and often involve both aerobes and anaerobes, especially Eikenella corrodens. 

2. Intact skin surrounding these bites should be cleansed with a broad-spectrum antimicrobial agent such as 

povidine-iodine; if there is a history of sensitivity/allergy to iodine, chlorhexidine may be used (but it is less 

655


effective and known to cause corneal ulcers if comes into contact with the eyes). The wound itself should be 

meticulously cleansed with copious amounts of sterile saline solution using a high-pressure irrigation technique. 

3. Inspect the wound for tooth fragments (from "fight bites") and sharply debride devitalized tissues. Hand 

wounds should be radiographed to exclude fractures, foreign bodies, and air in the joint spaces. 

4. Suturing 

a. Wounds of the head, face, and neck may be sutured (primary closure) if the patient presents within 24 

hours of injury and if there is no evidence of infection; if signs of infection are evident or the wound is >24 

hours old, it should be left open. 

b. All hand wounds should be left open initially; this includes closed fist/"fight bite" injuries (in which the 

extensor tendon and its sheath can be inoculated). 

c. Most wounds to other areas may be sutured as long as there is no evidence of infection or delay in treatment. 

5. Antibiotics are indicated for all human bites 

a. High-risk conditions 

(1) All hand wounds (strong evidence supporting infection prevention) 

(2) Any wound associated with comorbidity 

(a) Diabetes 

(b) Asplenia 

(c) Immune deficiency 

(d) Bite inflicted by a hospitalized or institutionalized person 

(3) Any wound with a poor blood supply, eg, anterior shin 

b. Wound type (laceration, puncture) does not influence the effectiveness of antibiotic prophylaxis (ie, same 

for cat, dog, and rabbit bites) 

c. Parenteral (IM or IV) antibiotics and possible admission 

(1) Wounds >24 hours old that are obviously infected 

(2) Wounds involving tendon, joint, or bone 

(3) Signs of systemic infection (tachycardia, fever, extensive cellulitis, lymphangitis, etc) 

d. Regimens for prophylaxis/treatment (3-5 days) 

(1) Provide coverage for 5 aureus, Streptococcus spp, Pasteure/la, Bacteroides, and Eikenella corrodens 

(2) E corrodens (a likely pathogen in hand wounds) is resistant to many agents including dicloxacillin, 

many firstgeneration cephalosporins, clindamycin, and the aminoglycosides. 

(3) Acceptable regimens (first two are best choices) 

(a) A second or third-generation cephalosporin (eg, cefuroxime, cefoxitin) 

(b) Dicloxacillin plus ampicillin or penicillin 

(c) Amoxicillin-clavulanate 

(d) Clarithromycin or clindamycin and TMP-SMX or doxycycline (in penicillin-allergic patients) 

(4) An aminoglycoside (eg, gentamicin) should be added to one of the above regimens in patients with 

diabetes, because these patients have a higher incidence of infection with gram-negative bacilli. 

6. Other appropriate measures 

B. Dog bites 

a. Provide tetanus prophylaxis as indicated. 

b. Consider administration of hepatitis B vaccine and immunoglobulin and testing for HIV when appropriate. 

1. Remember the mnemonic "RATS" 

Rabies 

Antibiotics 

Ietanus 

S.oap 

2. Common pathogens include a-hemolytic streptococci, 5 aureus, and (less often) Pasteurella multocida. A 

potentially lethal infection is caused by the organism Capnocytophaga canimorsus and occurs most often 

in immunocompromised patients (particularly the splenectomized and those with cirrhosis); mortality is 

secondary to sepsis, disseminated intravascular coagulation, or meningitis. 

3. Most lacerations (especially facial) that are seen within a few hours of injury should be closed primarily after 

meticulous irrigation and debridement. 

4. Wounds> 12 hours old and hand wounds should be left open initially with follow-up in 3-5 days for delayed 

primary closure; the exception is facial wounds, which should be closed primarily. 

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5. Management 

C. Cat bites 

a. Antibiotic regimens 

(1) Prophylaxis with cephalexin, dicloxacillin, or amoxicillin-clavulanate (erythromycin orTMP-SMX 

in the penicillinallergic patient) is indicated for all hand wounds and recommended for all puncture 

wounds, lacerations, and patients with comorbid conditions. 

(2) Treatment for infected wounds is determined by the probable pathogen involved, as follows: 

(a) Cephalexin, dicloxacillin, or amoxicillin-clavulanate (erythromycin orTMP-SMX in the penicillinallergic 

patient) is indicated for infections occurring >24 hours after injury (Streptococcus or 

Staphylococcus are most likely pathogens). 

(6) Penicillin VK (TMP-SMX, ciprofloxacin, or clarithromycin in the penicillin-allergic patient) is 

indicated for wound infections occurring within 24 hours of injury (Pasteure//a multocida most 

likely pathogen). 

(c) Penicillin or a cephalosporin (erythromycin in the penicillinallergic patient) is appropriate for 

suspected infection with C canimorsus. 

1. lmmunocompromised patient who presents with gangrene or severe systemic manifestations 

such as sepsis, endocarditis, or cardiopulmonary or acute renal failure 

ii. Because this is a potentially life-threatening infection, highrisk patients should be given 

prophylactic treatment. 

b. Indications for admission and empirical, parenteral antibiotic therapy with penicillin G and nafcillin 

(pending culture results) 

(1) Wound infection plus any of the following: 

(a) Lymphangitis/lymphaden itis 

(b) Tenosynovitis 

(c) Septic arthritis 

(d) Osteomyelitis 

(2) Systemic signs (fever, tachycardia, etc) 

(3) Injury to tendons, joints, or bone 

c. Tetanus prophylaxis should be administered as indicated. 

d. Rabies prophylaxis should be considered but is rarely indicated in the United States. 

1. Most common pathogen is Pasteure/la multocida; other, less commonly encountered organisms, are similar to 

those associated with dog bites (including C canimorsus). 

2. Wound closure 

a. Puncture wounds and lacerations


4. Cat scratch disease 

a. Etiology and epidemiology 

(1) Most commonly affects children and adolescents 

(2) Causative oraganism is Bartone/la henselae, a small, pleomorphic, gram-negative bacillus 

(3) Incubation period is ~ 1 week (range 3 days to 6 weeks). 

b. Clinical presentation: characterized by persistent regional lymphadenitis that is often unilateral and 

typically involves the lymph nodes of the arms or legs 

c. Management 

(1) Most cases resolve spontaneously over a period of weeks to months and require only symptomatic 

treatment. 

(2) Antibiotics are usually reserved for patients with severe or persistent disease. Acceptable choices 

include TMP-SMX, gentamicin, ciprofloxacin, and erythromycin. 

D. Venomous snake bites 

1. Most venomous snake bites in the United States (>98%) are inflicted by pit vipers, and 95% of the bites 

involve the extremities. 

2. Management 

a. The mainstay of therapy is administration of antivenin IV (described below). 

b. Establish monitoring and begin aggressive supportive therapy as appropriate. 

c. Immobilize the affected extremity to delay systemic absorption of venom; application of a loosely 

constricting band proximal to the bite site within 30 minutes of envenomation may also be helpful. Local 

therapy (mechanical, suction, wound excision/incision, elastic wrap) is not recommended. 

d. Cleanse the wound, and administer tetanus prophylaxis (if indicated). 

3. Pit vipers (Crotalidae family) 

a. Crotalid venom produces both local and systemic effects; its major effects occur in local tissue, blood 

vessels, and blood components. 

b. The severity of envenomation and the severity of the bite (rattlesnake > cottonmouth > copperhead) 

determine both the need for and the amount of antivenin to be administered. 

Table 40: Clinical Parameters Used to Assess Need for and Amount of Antivenin 

Parameter Dry Bite Minimal Moderate Severe 

Signs Puncture wound Swelling, erythema, Evidence of Entire area or 

± swelling ecchymosis spreading limb involved 

Symptoms 

Focal Slight pain Minimal pain Progressive pain Severe pain 

Systemic None None or minimal Present Fulminant 

Coagulation Normal Normal Abnormal Abnormal 

tests but no bleeding and bleeding 

c. The antivenin Crotalidae Polyvalent Immune Fab Ovine not only demonstrates clinical efficacy but 

appears to be associated with fewer allergic symptoms and reduced incidence of serum sickness. 

However, because it has a short half-life, venom effects can recur, and a repeat dose regimen must 

be used. 

(1) Minimal to moderate signs/symptoms: 4-6 vials diluted in 100 ml normal saline administered IV 

over 1 hour 

(2) Moderate to severe signs/symptoms: 6 vials diluted in 100 ml normal saline administered IV over 

1 hour 

(3) Progression of signs/symptoms: 2 vials in 100 ml normal saline administered IV over 20-30 minutes 

(4) Recurrent signs/symptoms 2 vials in 100 ml normal saline every 6 hours x 3 (6 vials total) 

d. Patients with dry bites (no signs/symptoms of envenomation and normal laboratory studies) may be 

discharged after 8-12 hours of observation (possibly longer depending on the species); all others should 

be admitted. One of every five bites is a dry bite. 

658


4. Coral snakes (Elapidae family) 

a. Coral snakes may be confused with king snakes and milk snakes. Coral snakes have wider bands of black 

and have red directly next to a yellow stripe. Remember "Red on yellow, kill a fellow. Red on black, 

venom lack." 

b. Elapid venom is largely neurotoxic; it has a curare-like effect on neuromuscular transmission and can 

produce total flaccid paralysis. It does not cause local edema. 


(1) Signs and symptoms of envenomation may be delayed up to 12 hours. 

(2) A change in mental status and cranial nerve dysfunction (eg, diplopia) are the earliest findings to develop. 

(3) Respiratory paralysis is the major life threat. 

d. Antivenin is available and should be administered early (even in the absence of any signs or symptoms) in 

patients who clearly have been bitten. 

(1) Because the antivenin is equine-derived, precautions for a possible allergic reaction during 

administration must be observed. However, in the case of a positive skin test, antivenin should 

be withheld because these patients do well with aggressive supportive measures (eg, prolonged 

intubation and ventilation) alone. 

(2) Begin with 3 vials; administer 3-5 additional vials if signs and symptoms develop or worsen. 

e. All patients with suspected or known envenomation should be admitted for observation or definitive care. 

f. Delayed onset of serum sickness, 1-2 weeks after treatment, is the most frequent reaction to both types 

of antivenin. 

E. Bee stings, ant bites, and other insect bites and stings 

1. Immediate concerns: upper airway obstruction, anaphylaxis, and toxic reactions from multiple stings 

2. If stingers are present, remove them immediately by whatever means possible. While it has been traditionally 

recommended that stingers be removed by scraping rather than forceps, evidence refutes the benefit of this 

technique. 

F. Black widow spider (Latrodectus mactans) 

1. The female spider is more poisonous than the male. The female has a red hourglass shape on the thorax. The 

male is much smaller and has a blue, yellow, or white hourglass on the thorax. 

2. Clinical presentation (symptoms often wax and wane) 

a. Local - a dull, muscle cramping sensation 

(1) Upper extremity bite: chest pain 

(2) Lower extremity or genitalia bite 

(a) Abdominal pain that may simulate an "acute abdomen"; a differentiating feature is the presence 

of abdominal rigidity with little or no associated tenderness. 

(b) Rectal spasm with normal bowel sounds 

b. Systemic - neurotoxic effects (diffuse CNS and peripheral nervous excitation) 

(1) Diffuse muscle pain and stiffness 

(2) Dizziness and restlessness 

(3) Profuse sweating (which may be uniquely focal to one area) and weakness 

(4) Difficulty in speaking and ptosis 

3. Management 

(5) Hypertension and tachycardia 

a. First aid: ice pack to the bite area 

b. Treatment 

(1) Cleanse with soap and water (look for fang marks and halo lesions) 

(2) Tetanus toxoid 

(3) Disposition 

(a) 

1 hour if the spider not positively identified and the patient remains symptom-free during this time 

(b) 4 hours if the spider positively identified but the patient remains symptom-free during this time 

c. Specific therapeutic measures 

(1) Signs and symptoms may be treated with: 

(a) 

Narcotic analgesics (the mainstay of therapy and pain relief) 

(b) Benzodiazepines (relieve muscle spasms) 

659


(2) Use of antivenin (one vial is usually sufficient) 

(a) 

Antivenin is not used in all cases because: 

1. The effects of black widow spider bites are self-limited with a low mortality rate; because use 

of antivenin has been associated with death, most patients are not given antivenin. 

ii. The antivenin is equine-derived (pretesting for horse serum sensitivity is advised) and can 

therefore produce anaphylaxis. Serum sickness can also occur but is uncommon, because so 

little antivenin is used. 

iii. The antivenin, when combined with -adrenergic blockers, can produce anaphylactic 

reactions that are refractory to treatment. 

(b) Indications for antivenin 

i. Patients 65 years old 

ii. Patients with severe pain (despite analgesics) or severe envenomations 

iii. Patients unable to stand the stress of the envenomation (due to concurrent illness) 

iv. Patients with dangerous hypertension 

v. Pregnant women 

G. Brown recluse spider (Loxosceles reclusa) 

1. The brown recluse is the size of a penny, and the head has a fiddle-shaped black marking. 


a. Local pain develops at the site in 3-4 hours. 

(1) The lesion starts with a halo of vasoconstriction, which then develops a central bleb (the classic bull'seye 

lesion), which may continue to spread over several days. 

(2) Tissue necrosis is a major complication that may require surgical consultation. 

b. Systemic (\oxoscilism): thought to be an allergic reaction 

(1) Develops over 24-72 hours 

(2) Fever, chills, petechial rash, nausea, vomiting, weakness 

(3) May progress to hemolysis, shock, renal failure, disseminated intravascular coagulation 

(4) Most fatalities are in children. 

3. Local tissue necrosis is a major complication that may require surgical consultation. 

4. Management 

a. Wash wound with soap and water. 

b. Apply ice compresses locally to decrease pain and diminish the evolution of cutaneous inflammation. 

c. Administer tetanus toxoid. 

d. Observe the patient in the emergency department if elapsed time since the bite is


I. Jellyfish stings 

(1) Symptomatic therapy (ice packs to area, analgesics, sedation) alone is adequate for grades I and II. 

(2) Antivenin may be required for grades Ill and IV; the antivenin is goat-serum derived, carries the risk 

of anaphylaxis and serum sickness, and is available only in Arizona (the Arizona bark scorpion is the 

most deadly scorpion in North America); skin testing is advised. 

1. Jellyfish envenomate their victims via stinging cells called nematocysts (cnidocysts). 

2. Victims of many severe toxic jellyfish stings (especially the Inda-Pacific box jellyfish) do not survive to shore; 

some succumb to the direct effects of the venom, but many drown due to the cardiopulmonary complications 

from the envenomation. Problems with survivors include removal of nematocysts, pain control, and prevention 

of infection. 

3. Treatment is controversial and unproven (therefore, less likely to be on the exam). 

a. Remove patient from the water. 

b. Wash the area with sea water; do not use fresh water, because it may cause the nematocysts to discharge, 

which may then cause severe pain. 

c. Do not rub the area with sand, because this worsens the condition. 

d. Remove tentacles with forceps or a thickly gloved hand. 

e. Any nematocysts that remain after washing should be fixed by pouring vinegar (or isopropyl alcohol) 

over the wound area for at least 30 minutes. Next, dust the area with talcum powder or cover with shaving 

cream. The nematocysts, now adherent to the powder or cream, can be scraped off with a knife or razor 

blade. 

f. Wash the area with sea water once again and then apply a topical anesthetic/antihistamine or low-potency 

steroid cream (which may be soothing). 

g. Administer tetanus toxoid. 

h. Allergic reactions are common and should be treated in the usual manner. 

4. Hospitalize patients who sustain severe envenomation or develop an allergic reaction. 

V. ALTITUDE DISORDERS 

A. High-altitude disorders (can be avoided by proper acclimatization or use of acetazolamide 1-2 days before 

ascent) 

1. Acute mountain sickness 


(1) Onset of symptoms is within a few hours; duration is 3-4 days. 

(2) Symptoms include bifrontal headache, anorexia, nausea, and sleeping difficulties. The headache is 

usually worsened with the Valsalva maneuver and with stooping over; it is most severe during the 

night and in the morning on awakening. 

b. Management 

(1) Symptomatic treatment and a halting of the ascent for 12-36 hours until acclimatization has 

occurred is usually all that is needed in mild cases. 

(2) Effective agents include NSAIDs or acetaminophen for headache and prochlorperazine for nausea and 

vomiting. Prochlorperazine also has the advantage of increasing the hypoxic ventilatory response. 

(3) Supplemental low-flow oxygen is useful in relieving symptoms, especially at night, during sleep. 

(4) Acetazolamide 125-250 mg orally bid speeds acclimatization and is also effective for treatment of 

acute mountain sickness; it is contraindicated in patients allergic to sulfa. 

(5) Dexamethasone 4 mg orally, IM, or IV qid is also effective for prophylaxis as well as treatment of 

acute mountain sickness but, because of adverse effects and problems with rebound when the drug 

is stopped, it is recommended only as treatment (not prophylaxis) and is reserved for moderate to 

severe cases. 

(6) Descent is the definitive therapy and is rapidly effective but is not necessary unless symptoms 

progress or are prolonged and debilitating. 

2. High-altitude pulmonary edema (HAPE) 

a. This is noncardiogenic (wet lungs and normal heart size) in origin; it should not be confused with CHF. 


661


(1) Onset of signs and symptoms is 1-4 days after ascent and often preceded by exertion. 

(2) Symptoms include weakness, headache, cough, shortness of breath, cyanosis, and rales. 

c. Management 

(1) Bedrest, oxygen, increased positive-airway pressure (via CPAP, BiPAP, or endotracheal intubation) 

and descent 

(2) If descent is impossible: 

(a) The Gamow bag (portable hyperbaric chamber) simulates descent to a lower altitude. 

(b) Nifedipine may be helpful, because it reduces pulmonary artery pressure through its vasodilatory 

effect. 

3. High-altitude cerebral edema (HACE) 

B. Dysbarism 

a. Can result in permanent neurologic injury or even death 


(1) Common signs/symptoms: confusion, ataxia, retinal hemorrhages, hallucinations, and headache 

(2) Can progress to coma if untreated 

c. Management 

(1) Oxygen, head elevation, descent, and dexamethasone; hyperbaric therapy is also effective if available. 

(2) Loop diuretics (eg, furosemide, bumetanide) may be helpful in the treatment of both HAPE and HACE, 

but hypoperfusion is a significant risk so they should be used cautiously, if at all. 

1. Barotrauma of descent ("squeeze") based on Boyle's Law: the volume of a gas varies inversely with the pressure. 

a. Symptoms develop because of compression of air that is trapped in various parts of the body during 

descent. Divers can develop symptoms in water as shallow as 4.5-6.5 feet. 

b. Barotitis externa ("external ear squeeze") 

(1) Occurs when the external auditory canal is occluded (eg, by cerumen, foreign bodies, exostoses, ear 

plugs, or a too-tight fitting wet suit hood) 

(2) Compression of the enclosed air with descent produces pain and/or bloody otorrhea (from bloodfilled 

cutaneous blebs along the canal or tympanic membrane rupture). 

(3) Management: keep canal dry; no diving (or swimming) until healed. 

c. Barotitis media ("middle ear squeeze") 

(1) Most common type of aural barotrauma 

(2) Results from failure to equalize the pressure between the middle ear and the water; this occurs 

because of occlusion or dysfunction of the eustachian tube. 

(3) Predisposing factors 

(a) Mucosal congestion secondary to an upper respiratory infection, allergies, or smoking 

(b) Mucosal polyps 

(c) Excessively vigorous autoinflation maneuvers 

(d) Previous maxillofacial trauma 

(4) As the pressure differential increases, the diver experiences ear fullness or pain (which will worsen 

until the tympanic membrane ruptures, unless the dive is aborted); if the tympanic membrane does 

rupture, the diver may become disoriented because of severe nausea and vertigo that result from the 

caloric stimulation of cold water entering the middle ear. 

(5) The severity of the injury can be assessed from the amount of hemorrhage associated with the 

eardrum; a grading system may be used, with "O" signifying no hemorrhage (only symptoms) to "5" 

indicating tympanic membrane rupture with gross hemorrhage. 

(6) Management: no diving and nasal decongestants until healed; if the tympanic membrane is ruptured, 

antibiotics are indicated; resolution occurs within 1 week. 

d. Barotitis interna ("internal ear squeeze") 

(1) Permanent injury to the cochleovestibular system may occur. 

(2) Results from sudden pressure differences between the internal and middle ear, which may occur 

after an overzealous Valsalva maneuver or extremely rapid descent. 

(3) Clinical presentation: classic symptomatology - tinnitus, deafness, and vertigo 

(4) Mechanisms of injury: inner ear hemorrhage, rupture in Reissner membrane - mixing of endolymph 

and perilymph, round or oval window fistulation, or a combination of these insults 

662


(5) Management: bed rest with the head elevated, sedentary activities as tolerated, symptomatic therapy, 

and ENT referral; early surgical intervention is indicated for patients with total (or near total) hearing 

loss. 

e. "Sinus squeeze" 

(1) Hemorrhage or sensation of fullness, pressure, or pain in the affected sinuses 

(2) The maxillary and frontal sinuses are most often affected. 

(3) Antibiotics are usually indicated if the frontal sinuses are involved; otherwise, the treatment is the 

same as for barotitis media. 

2. Barotrauma of ascent (Boyle's Law) 

a. Symptoms develop because of expansion of air that is trapped in bodily spaces during ascent. 

Bare's (Scuba) law: Mr. Boyle Breaths out on ascent Before Bubbles in Bad places cause Barotrauma by 

Bursting Big organs and little eardrums. 

b. Examples 

(1) Middle ear and sinus barotrauma of ascent ("reverse squeeze") 

(2) Barodontalgia 

(3) Aerogastralgia (air in the gut) 

(4) Pulmonary barotrauma (Boyle's Law) 

(a) Mediastinal or subcutaneous emphysema (most common) 

(b) Pulmonary interstitial emphysema 

(c) Alveolar hemorrhage 

(d) Pneumothorax 

(e) Pulmonary air (arterial gas) embolism 

i. The most severe complication of pulmonary barotrauma 

ii. Immediately after ascent, air bubbles enter the systemic circulation through ruptured 

pulmonary veins. 

iii. Arterial occlusion from an air embolus can occur at any site, including the coronary arteries 

(Ml, cardiac arrest). However, the most common presentation is a neurologic event, eg, 

level of consciousness, blindness, deafness, vertigo, confusion, seizures, monoplegia, or 

asymptomatic multiplegia. 

iv. Symptoms develop within 10 minutes of surfacing from a dive, and often much sooner. 

v. Treatment of air embolism (pulmonary, coronary, or cerebral) is recompression in a 

hyperbaric chamber as soon as possible. During transport, the patient should be given 

oxygen and placed in the supine position. Placement in Trendelenburg is no longer 

recommended, because it may worsen cerebral edema and respiratory distress. 

3. Barotrauma of descent or ascent is the result of a direct effect of pressure changes on the body (Boyle's 

Law). Nitrogen narcosis and decompression sickness, on the other hand, are the result of an indirect effect of 

pressure changes on the body (Henry's and Dalton's Laws). 

a. Henry's Law: The amount of gas dissolved in a liquid is proportional to the partial pressure of the gas in 

contact with the liquid. 

b. Dalton's Law: The partial pressure of a gas increases with increasing pressure. 

c. Nitrogen narcosis and decompression sickness (DCS) occur secondary to breathing gases (usually 

nitrogen) at higher than normal atmospheric pressure. 

(1) Nitrogen narcosis occurs as the diver descends to depths >70 feet. The clinical picture resembles 

alcoholic intoxication and can impair judgment; the condition clears with resurfacing. 

(2) DCS occurs if the diver ascends too quickly. Symptoms result from dissolved inert gas (nitrogen) 

bubbles reentering tissues and blood vessels; it can involve any organ system. There are two main 

types of DCS: 

(a) DCS type 1 

1. Cutaneous - "skin bends" 

ii. Musculoskeletal, most frequently affected ----,► "the bends" 

• Delayed and insidious in onset 

• Often symptoms may not manifest for hours to days 

(b) DCS type 2: more serious and involves cardiopulmonary and nervous symptoms 

i. Pulmonary --;, "the chokes" 

663


II, CNS 

• Spinal cord, most frequently affected - 

• Cerebellar - 

• Cerebral 

"the staggers" 

acute paraplegia 

(c) Treatment is recompression in a hyperbaric chamber as soon as possible. During the transport, 

100% oxygen should be administered to provide a favorable gradient for nitrogen washout and 

improved oxygenation of injured tissues. No flying for at least 3 days with DCS type 1, and no 

flying for 3-4 weeks after treatment of DCS type 2. 

VI. SUBMERSION INJURY 


1. Drowning is defined as a process resulting in primary respiratory impairment from submersion in a liquid 

medium. A liquid-air interface must be present in the victim's airway. 

2. The outcome of drowning may include: 

a. Delayed morbidity 

b. Delayed death 

c. Life without morbidity 

3. Immersion syndrome is sudden death after submersion in very cold water (presumed to be due to vagally 

mediated asystole or ventricular fibrillation). 

4. Postimmersion syndrome is delayed deterioration of a patient who is initially relatively asymptomatic; 

deterioration is generally due to respiratory insufficiency and may be delayed several hours to several days 

(ARDS). This is the major complication of submersion injury. 

B. Epidemiology 

1. Drowning is the second leading cause of death in children and the third most common cause of accidental 

death in the United States, claiming 8,000-9,000 lives/year, with brain injury being the major cause of death 

from drowning. 

2. Freshwater submersion injury (particularly in swimming pools) is more common than saltwater submersion 

injury, but the type of water has no bearing on morbidity and mortality. 

3. Age distribution is bimodal, two-thirds under the age of 30, with peaks occurring in children


C. Pathophysiology 

1. Sequence of events (are essentially the same for freshwater and saltwater submersion) 

Panic and air hunger 

• 

Breath-holding 

• 

Air hunger 

+ 

• 

Involuntary inspiratory effort forcing victim 

to inhale and swallow 

I 

+ 

Aspiration ("wet drowning") 

85%-90% 

t 

•Direct pulmonary injury 

•Surfactant loss-+ atelectasis, 

V/Q mismatch, alveolar capillary 

membrane breakdown 

(Fresh water also changes surfactant 

surface tension) 

• Inflammatory contaminants 

(bacteria, emesis, chemical irritants) 

•Cerebral hypoxia 

+ 

Noncardiogenic pulmonary edema 

Laryngospasm and glottis closure 

without aspiration 

("dry drowning") 

10% - 15% 

I 

i 

Profound hypoxemia 

(final common pathway) 

t 

Cardiac arrest 

Sequence of Events in Submersion Injury 

2. Other pathophysiologic characteristics of submersion injury 

a. Metabolic acidosis (lactic acidosis type A) develops in many patients and is due to hypoxemia (anaerobic 

metabolism) and poor perfusion. 

(1) It is usually well tolerated in children and may be reversed with adequate ventilation and oxygenation. 

(2) It is less well tolerated in adults. 

665


(a) 

In addition to ventilation and oxygenation, small doses of NaHCO 3 

may be considered for 

refractory acidosis. 

(b) Lactic acidosis persists if severe hypoxemia is not corrected. 

b. Most victims do not aspirate enough fluid to cause life-threatening changes in blood volume or serum 

electrolyte concentrations. 

c. Renal failure occurs infrequently in submersion injury. 

(1) Acute tubular necrosis may develop secondary to hypoxemia. 

(2) In freshwater submersion injury, acute renal failure may result from hemolysis and hemoglobinuria. 

d. Cerebral edema may develop (usually within 6-12 hours) from generalized neuronal death. Cerebral 

edema-"' i intracranial pressure -"' t cerebral perfusion pressure and t cerebral blood flow -"' further 

ischemic neurologic injury 

D. Prehospital care 

1. Ineffective and potentially dangerous procedures 

a. In-water CPR (but can do airway management in water) 

b. Attempts to remove fluid from the lungs via postural drainage or the Heimlich maneuver 

2. Initial assessment and stabilization 

a. If patient is conscious, safer to throw flotation device to the victim than to jump in: "throw, tow, row, go." 

b. Start CPR in the pulseless, apneic victim even if there is only a remote possibility of success. 

c. Airway maintenance and supplemental oxygen are of primary importance. 

d. An IV line should be started if possible. 

e. Immobilize the cervical spine and look for signs of spinal injury: 

(1) Paradoxical respirations 

(2) Unexplained hypotension 


(4) Flaccidity 

(5) Priapism 

f. Prevent onset or worsening of hypothermia: remove wet clothes, dry the patient, and wrap in dry blankets. 

3. Transport all submersion-injury victims to the hospital. 

E. Emergency department 

1. Remember that submersion injury is an airway problem first. Evaluate airway patency, adequacy of cervical 

spine immobilization, and mental status; naloxone and glucose (if hypoglycemic) are indicated if there is an 

altered level of consciousness. 

2. Assess respiratory status, looking for signs of pulmonary insufficiency: 

a. Tachypnea 

b. Dyspnea 

c. Use of accessory muscles 

d. Wheezing, rales, or rhonchi 

3. Provide supplemental oxygen. 

a. Always use 100% oxygen. 

b. Avoid prolonged suctioning, steroids, prophylactic antibiotics, and early extubation. 

c. Intubation is indicated if the pO 2 

is


6. Correct shock (if present) with fluid boluses; if this is unsuccessful, use an inotrope (eg, norepinephrine). 

7. Maintain cervical spine immobilization until cervical and first thoracic vertebra have been cleared by imaging. 

8. Decompress the stomach with a nasogastric tube. 

9. Place Foley catheter to monitor urine output. 

10. Conduct a thorough search for associated injuries. 

11. Assess the patient's temperature to exclude hypothermia (which is not uncommon and changes the therapeutic 

approach). 

a. Use a rectal thermometer that is specially calibrated to record low temperatures; most clinical 

thermometers only read down to 95°F (35°C). 

(1) Patients who have been submerged in icy cold water (:S41 °-50°F [5°-10°C]) for >40 minutes have 

survived with a good neurologic outcome. 

(2) Cold water slows the metabolic rate and shunts blood to the brain, heart, and lungs (diving reflex). 

b. Institute appropriate rewarming measures for hypothermia (see page 654-655). 

c. Extracorporeal membrane oxygenation (if available) is indicated for patients with severe hypothermia and/ 

or hypoxia. 

d. Continue resuscitation efforts until a near-normal core temperature (95°F [35°C]) is attained. 


a. Cervical spine imaging should be done if there is any suspicion of possible cervical injury. 

b. Arterial blood gases 

c. Chest radiograph (50% of patients with abnormal radiographs will require intubation). Typically, one of 

three patterns is seen: 

(1) Normal (although this does not necessarily mean there is no lung pathology) 

(2) Perihilar pulmonary edema 

(3) Generalized pulmonary edema 

d. CBC and urinalysis 

e. Glucose, electrolytes, prothrombin time (INR)/partial thromboplastin time 

f. Blood alcohol level and drug screen 

g. ECG 

13. Do not administer prophylactic antibiotics or steroids; neither has been shown to change the course of 

aspiration pneumonia in submersion-injury victims. 

F. Predicting outcome 

1. The most reliable predictors of outcome are the duration of both submersion and resuscitation. 

a. Prognostic indicators of a good outcome 

(1) Short submersion time 

(2) Basic and/or advanced life support at the scene 

(3) Favorable response to initial resuscitative efforts (return of spontaneous respiration) 

(4) Alert on admission 

(5) Older child (c::3 years old) or adult 

(6) Water temperature 41 °-50°F (5-1 0°C) 

b. Prognostic indicators of a poor outcome 

(1) Submersion duration >25 minutes 

(2) Cardiac arrest requiring>25 minutes advanced life support 

(3) Ongoing CPR in the emergency department 

(4) Fixed, dilated pupils in the emergency department 

(5) pH


c. Patients who are comatose and have an abnormal response to pain and abnormal respirations have a more 

variable outcome; although some survive intact if appropriate care is provided, many die or survive with 

anoxic encephalopathy. These patients were generally submerged for a prolonged period of time. 

3. Pulmonary injury and hypoxia are the primary pathophysiologic determinants of outcome. 

G. Disposition 

1. Asymptomatic patients should be observed for 6 hours. If they remain asymptomatic, are oxygenating normally 

on room air, and have a normal chest radiograph, they may be discharged. Early follow-up should be arranged. 

2. Hypoxemic and/or symptomatic patients should be hospitalized. 

H. Postimmersion syndrome risk factors 

1. Severe transient hypoxia 

2. History of unconsciousness in the water 

3. Presence of symptoms such as dyspnea, coughing, and tachypnea 

4. Underlying cardiopulmonary disease 

VII. OTHER ENVIRONMENTAL HAZARDS 

A. Radiation injuries 

1. Pathophysiology: radiation - ionization - formation of free radicals from water - breakage of DNA and 

RNA strands 

2. The LD 50 

of whole-body ionizing radiation (the dose that will kill 50% of those exposed to it) is 350 rad (3.5 Gy). 

3. The whole-body dose of ionizing radiation determines the timing of the onset of symptoms, severity of the 

illness, and organ systems involved. 

a. The higher the exposure, the earlier symptoms develop: 400 rads), >6 hours (500 rads 

(3) The CNS is the most resistant to radiation effects; exposure >5,000 rads is required to damage this 

system. 

4. The best predictor of survival is the absolute lymphocyte count 48 hours after radiation exposure. 

a. > 1,200/mm 3 = good prognosis 

b. 300-1,200/mm 3 = fair prognosis 

c.


C. Volcanic eruptions 

1. Mortality 

a. Immediate: ash in the upper airways - suffocation 

b. Delayed: ash (or other particulate matter) in the lungs - ARDS 

2. Morbidity 

a. Increased incidence of new-onset asthma 

b. Prolonged inhalation of volcanic ash - silica pneumoconiosis 

669

ENVIRONMENTAL DISORDERS: PRACTICE CLINICAL SCENARIOS 



Scenario A 

Presentation: A middle-aged antique dealer presents complaining of hand discoloration and weakness. His 

symptoms started after using a rust and glass cleaner on some newly purchased glass sculptures and metal 

etchings. Laboratory studies are normal except for hypocalcemia. 

Source: Dr. Watchorn (Wikimedia Commons: http://en.wikipedia.org/wiki/File:61569264_jamesheilman-224x2991.jpg) 


Scenario B 

Presentation: A 4-year-old boy bites a household electrical cord and receives burn care at a local urgent 

care that day. Three days later, his parents bring him to the local emergency department with profuse lip 

bleeding with arterial pulsations. ABCs are started, and an emergent plastic surgery consult is obtained. 


670


Scenario C 

Presentation: A grandfather flys a kite with his grandson on a warm summer day when a storm rolls in. 

The grandfather attempts to rapidly bring down the kite when he is hit by lightning. He thinks he tripped 

while bringing the kite down but only recalls waking up on a grassy knoll. He is asymptomatic other than 

Lichtenberg figures. 

Source: United States Department of Health and Human Services (Wikimedia: http://commons.wikimedia.org/wiki/File:Rear_ 

view _of _a_l ightn i ng-stri ke_su rvivor,_di spl ayi ng_Lichten berg_figu re_on_ski n .png) 


Scenario D 

Presentation: A licensed California marijuana farmer brings in a dead snake. He states the snake bit him 

on the hand while he was trying to harvest his crop. The snake has wide red bands next to narrow black 

bands. 


Scenario E 

Presentation: An emergency medicine physician from Ohio takes a morning flight into Denver after 

working all night. He and his wife drive immediately to a large ski resort a few hours outside of Denver. He 

begins to notice severe headache and nausea as he rides up the chairlift. His symptoms seem to improve as 

he descends the slope and recur as he rides back up the chairlift. 


671



Scenario A 

Diagnosis: hydrofluoric acid burn 

Scenario B 

Diagnosis: electrical lip burn 

Management: Acutely, do not debride these wounds. Cleanse and apply a petroleum-based antibiotic 

ointment. Observe closely and refer to a plastic or oral surgeon for splinting and further care. 

Complications include delayed hemorrhage from the labial artery (10%-15% of patients) 3-14 days after 

injury, when the eschar separates, which is what occurred in this patient. 

Scenario C 

Diagnosis: lightning strike 

Scenario D 

Diagnosis: snake bite: "red on black, venom lack" 

LOUISIANA MILK 

TEXAS CORAL 

SNAKE 

Red and Black 

VENOM LACK 

' 

■ 

■ 

, 

red I black I yellow I black I red 

Red and Yellow 

KILL A FELLOW 

I 

yellow I red I black I red I yellow 

Scenario E 

Diagnosis: acute mountain sickness 

672

PSYCHOBEHAVIORAL DISORDERS 


Clinical Approach to the Psychiatric Patient ............................................................................................................. 677 

Recognition ........................................................................................................................................................ 677 

Triage ................................................................................................................................................................. 677 

Safety ................................................................................................................................................................. 677 

Medical Evaluation ............................................................................................................................................. 678 

The Psychiatric Interview .................................................................................................................................... 680 

Treatment .................................................................................................................................................................. 681 

Management of the Agitated Patient ................................................................................................................... 681 

Crisis Intervention .............................................................................................................................................. 685 

Psychopharmacology ......................................................................................................................................... 686 

Specific Behavioral Disorders ................................................................................................................................... 692 

Psychosis ............................................................................................................................................................ 692 

Depression ......................................................................................................................................................... 693 

Suicide ............................................................................................................................................................... 6 94 

Mania and Hypomania ....................................................................................................................................... 696 

Catatonia ............................................................................................................................................................ 697 

Panic Attacks/Disorder ........................................................................................................................................ 698 

Somatoform Disorders ........................................................................................................................................ 699 

Insomnia and Sleep Disorders ............................................................................................................................ 700 

Eating Disorders ................................................................................................................................................. 701 

Intoxication and Withdrawal .............................................................................................................................. 703 

Delirium and Dementia ...................................................................................................................................... 705 

"Medical Mimickers" of Psychiatric 11 lness ......................................................................................................... 707 

673

PSYCHOBEHAVIORAL DISORDERS: SELF-ASSESSMENT QUESTIONS 


1. Which of the following is not an adverse effect of anti psychotics? 

(a) Hypotension 

(b) Bradycardia 

(c) Dystonic reactions 

(d) Lowered seizure threshold 

2. A depressed 20-year-old woman arrives in the emergency department complaining of headache, chest tightness, 

and palpitations. Examination reveals tachycardia, increased blood pressure, and diaphoresis. She mentions that 

she is taking a medication for depression but cannot recall its name. She states that she started to feel ill shortly after 

taking an OTC decongestant/cough suppressant for her cold symptoms. These would be signs of a potentially lethal 

drug-drug interaction if the patient's antidepressant were a: 

(a) 

(b) SSRI 

Benzodiazepine 

(c) Monoamine oxidase inhibitor 

(d) Tricyclic antidepressant 

3. The patient most likely to benefit from crisis intervention is the patient with: 

(a) An acute grief reaction 

(b) Delirium 

(c) Agoraphobia 

(d) Seasonal affective disorder 

4. Which of the following statements regarding conversion reactions is inaccurate? 

(a) They have a sudden onset and are often triggered by an emotionally charged event. 

(b) The process is unconscious; the patient is not malingering. 

(c) Symptoms attributed to conversion reactions are often later found to be due to an occult general medical disorder. 

(d) The symptoms often involve involuntary muscle functions. 

5. Which of the following medications has depression as an adverse effect? 

(a) 

Propranolol 


(c) Sumatriptan 

(d) Atorvastatin 

6. A 55-year-old man presents to the emergency department with depression and suicidal threats. He recently had a 

cholecystectomy. He is a veteran and has a history of drug abuse, and has chronic low back pain due to an injury. 

His brother committed suicide 10 years ago. He lives at home with his wife. Which of the following is not a risk 

factor for suicide for this patient? 

(a) 

Recent surgery 

(b) Drug and alcohol abuse 

(c) Chronic pain 

(d) Family history of suicide 

7. A 28-year-old man presents to the emergency department by police after being picked up on the street where he 

was walking around on a crowded sidewalk threatening other pedestrians. He has been handcuffed and is carried 

in while he tries to kick and bite the police who are escorting him. The most appropriate medical treatment for his 

behavior is: 

(a) Chlorpromazine and diazepam 

(b) Haloperidol and lorazepam 

(c) Thioridazine and midazolam 

(d) Droperidol and clonazepam 

674


8. Unlike the hallucinations that occur in patients with delirium due to an underlying medical condition, those 

occurring in patients with a psychosis (eg, schizophrenia) are usually: 

(a) Tactile and painful 

(b) Auditory and frightening 

(c) Visual and colorful 

(d) Olfactory and noxious 

9. Which of the following is not considered a symptom of depression? 

(a) 

Feelings of worthlessness or guilt 

(b) Pressured speech 

(c) Sleep disturbances 

(d) Weight loss, weight gain, or change in appetite 

10. Which of the following statements regarding antidepressants is accurate? 

(a) 

Routine prescription of these agents to patients evaluated in the emergency department for depression is 

appropriate. 

(b) SSRI antidepressants produce significant cardiotoxicity. 

(c) SSRls may influence other drug levels through cytochrome P450 pathways. 

(d) Second-generation antidepressants (venlafaxine, duloxetine, mirtazapine) exert their mechanism of action 

through dopamine and norepinephrine effects. 

11. An otherwise healthy 23-year-old woman presents to the emergency department with palpitations, shortness 

of breath, and feeling of panic associated with pain in her chest. Which of the following is false regarding her 

condition? 

(a) Symptoms include apprehension, shortness of breath, difficulty swallowing, chest tightness, and palpitations. 

(b) Patients often believe they have a medical problem. 

(c) Attacks are sudden in onset and last, on average,


15. A 20-year-old woman presents with agitation, hallucinations, and abdominal pain. Her abdominal examination is 

benign, but she continues to be preoccupied with the pain. Her physician made a psychiatric referral and prescribed 

clonazepam for her anxiety, but her condition rapidly worsened and she became increasingly distressed by her 

abdominal pain before the psychiatric evaluation could be arranged. The most likely diagnosis is: 

(a) Manic psychosis 

(b) Acute intermittent porphyria 

(c) Somatoform pain disorder 


ANSWERS 

1. b 4. d 7. b 10. c 13. a 

2. c 5. a 8. b 11. d 14. d 

3. a 6. a 9. b 12. d 15. b 



676


I. CLINICAL APPROACH TO THE PSYCHIATRIC PATIENT 

A. Recognition 

1. A psychiatric emergency arises when a patient poses a danger to others/self or is gravely disabled. The situation 

is complex and often characterized by intense symptoms, a sense of urgency, and perceived danger. 

2. The patient's primary problem (depression, psychosis) may be identified by himself/herself, family or friends, or 

others who are aware of the patient's abnormal behavior. 

3. Patients may present with physical symptoms that are manifestations of a psychiatric disorder, eg, a depressed 

patient may present with insomnia, weight loss, and somatic complaints. 

4. Patients may present with psychiatric complaints that are caused or exacerbated by general medical syndromes 

or medications/substances (eg, psychosis due to corticosteroids or phencyclidine [PCP] ingestion). 

5. Patients may present with a general medical problem or injury that was caused by an underlying psychiatric 

disorder (eg, dystonic reaction or a suicide attempt). 

6. Patients may also present with a general medical condition that has been exacerbated by neglect or with 

symptoms that are masked or distorted by their psychiatric disorder. 

B. Triage: determine the need for immediate treatment. 

1. Psychiatric patients should be seen in accordance with guidelines established for all patients (by severity of 

illness, then "first come, first served"). Patients should be categorized as emergent, urgent, or nonurgent and 

seen in order of priority. 

a. Emergent: ask yourself "Does this patient's condition pose a physical threat to himself or herself or others?" 

The answer is "yes" if: 

(1) Vital signs are abnormal. 

(2) A life-threatening illness or injury is present, even though the chief complaint is psychiatric (eg, the 

suicidal patient with a potentially lethal overdose or the combative patient who is hypoglycemic). 

(3) The patient is suicidal, violent (or potentially violent), or unable to care for himself or herself. 

b. Urgent: patient does not meet emergent criteria, and there is: 

(1) Agitation 

(2) Overwhelming anxiety 

(3) Suicidal or homicidal ideation 

(4) An inability on the part of the patient to explain the problem coherently 

(5) Extremely concerned family/collaterals 

(6) Intoxication 

c. Non urgent: patient requests psychiatric help but does not meet criteria for emergent or urgent treatment. 

2. All patients need a medical (as well as psychiatric) evaluation before leaving the emergency department, 

including a complete set of vital signs and a mental status examination. People with psychiatric illness may 

have comorbid medical/surgical conditions that may be overlooked because staff has labeled the patient and/or 

chief complaint as psychiatric ("anchoring" phenomenon). 

3. Patients with psychiatric problems must not be permitted to leave the emergency department without being 

evaluated as potentially harmful to self and/or others, incompetent to care for self, intoxicated, or psychotic 

and grossly disorganized. 

C. Safety: determine the need for seclusion/restraints. 

1. Attending to the safety of the patient, physician, and staff is a primary concern when managing a patient with 

agitation and/or thoughts of harm to self or others. 

2. Many emergency departments have rooms designed with this population in mind. The room should be devoid 

of medical equipment that could be used to harm oneself (eg, IV tubing that could be used to strangulate 

oneself) or others (eg, equipment that could be used as projectiles). 

3. Patients who are reporting active suicidal ideation should be placed on a direct-observation status (eg, use of a 

one-on-one sitter). 

4. Early warning signs indicating that a patient is a risk for violent behavior should be addressed immediately. 

5. Maintain a safe distance between you and the patient, and allow for you and the patient to both have an easy 

egress from the room. 

6. Keep in mind that the behavior of a patient with psychosis can be unpredictable, because the patient may be 

responding to thoughts (delusions) or perceptions (hallucinations) that are not based in reality. 

677


D. Medical evaluation 

1. The goal is to recognize and distinguish general medical ("organic") from psychiatric ("functional") illness. If 

a general medical illness is identified or suspected, evaluate and treat appropriately before or while obtaining 

a psychiatric consult. 

a. Profile of a general medical disorder presenting as a behavioral emergency 

(1) Classic presentation: sudden or recent onset of a behavioral change in an older person without 

previously diagnosed psychiatric disorder 

(2) The patient may retain insight (but not always). 

(3) Specific findings 

(a) Sudden onset or change in symptoms 

(b) Recent diagnosis of a medical illness 

(c) Recent change in prescribed or OTC medications 

(d) Visual, tactile, or olfactory hallucinations are more common than auditory hallucinations. 

(4) Abnormal cognitive function including: 

(a) Altered level of consciousness (sedation or hyperarousal) 

(b) Disorientation (confusion is usually present) 

(c) Memory impairment 

(d) Poor attention 

b. Profile of a psychiatric disorder 

(1) Past history of behavioral problems in a younger patient 

(2) The patient lacks insight (but not always). 

(3) Specific findings 

(a) Auditory hallucinations are more common than other hallucinations. 

(b) Normal vital signs, physical examination, and laboratory studies 

(c) Disordered or illogical thinking, especially in the face of normal cognitive function. The patient 

should be oriented and can complete routine cognitive tasks (eg, spelling "world" backward). 

c. Specific medical illnesses presenting as psychiatric emergencies 

(1) Common "behavioral" presentations 

(a) Adverse effects of medications 

(b) Hyponatremia 

(c) Hypoglycemia or hyperglycemia 

(d) Alcohol intoxication or withdrawal 

(e) Illicit drug intoxication (eg, cocaine, bath salts, LSD, phencyclidine [PCP]) 

(f) Drug withdrawal 

(g) Urinary tract infection leading to delirium 

(h) Pneumonia leading to delirium 

(i) COPD leading to hypoxia or hypercapnia 

(j) Liver disease, which may be accompanied by hyperammonemia 

(k) Chronic renal disease 

(I) Hypothyroidism or hyperthyroidism 

(2) Less common but potentially life-threatening "behavioral" presentations 

(a) Subarachnoid or intracranial hemorrhage 

(b) Encephalitis 

(c) Metastatic carcinoma or intracranial tumor 

(d) Malignant hypertension/hypertensive encephalopathy 

(e) Hypocalcemia/hypercalcemia 

(f) Steroid-induced psychosis 

(g) Autoimmune diseases 

2. Medical history 

a. All history must be corroborated. 

(1) Compare the patient's version with that of family, friends, and other sources (eg, police, paramedics). 

(2) Obtain old medical and psychiatric records. 

(3) Contact current or recent primary care physician. 

678


b. Include medications, especially pain relievers, sedatives, and psychiatric medications. (Remember that 

many OTC and prescription drugs, as well as herbal supplements such as St. John's wort and ginseng, 

have psychiatric adverse effects.) 

c. Ask about drug and alcohol use (often overlooked in the professional, executive, "nice person," elderly, 

and children!) 


a. If the patient is unable to cooperate, physical or chemical restraints may be required before examination. 

b. If the patient refuses to cooperate, procedures for involuntary commitment and/or emergency assessment 

should be followed. Do not permit the patient to leave the emergency department before adequate 

medical and psychiatric assessments have been completed. 

c. Patients must be disrobed and gowned, but first conduct search for possible weapons or concealed pills/ 

other substances. 

(1) Proactively seek assistance from hospital security personnel and/or police. 

(2) If the patient has a weapon, security personnel are required; they must disarm him or her before any 

further evaluation or treatment can be safely conducted. 

d. Make sure vital signs have been taken and recorded (abnormalities suggest a possible medical problem). 

e. Neurologic examination: note particularly any signs of nonpsychiatric illness, eg, dysarthria, aphasia, 

dyspraxia, ataxia, dyskinesias, tremor, nystagmus, incontinence, paresis, paresthesias, and lateralizing 

neurologic signs. 

f. Documentation should include vital signs as well as signs of: 

(1) Trauma or exposure-related injuries 

(2) Previous suicide attempts 

(3) Thyroid, liver, or renal disease 

(4) Toxidromes (anticholinergics, cholinergics, sympathomimetics, opioids, etc) 

(5) Withdrawal syndromes (opioids, benzodiazepines, alcohol, etc) 

4. Mental status examination 

a. Level of consciousness: alert/somnolent/stuporous, fluctuating, or stable 

b. General appearance 

(1) Activity level: agitation, hyper-, normo-, hypomotor 

(2) Grooming and hygiene: appropriate, inappropriate, disheveled 

(3) Movements: tremor, tics, stereotypes, chorea, dyskinesias 

c. Orientation 

(1) Time, place, person, situation 

(2) Orientation to time is most sensitive: ask about day, date, month, season, and year. 

d. Memory 

(1) Immediate, short- and long-term 

(2) Give the patient three words and ask him or her to repeat them (immediate recall). 

(3) Ask the patient to repeat the words again after 3 minutes (short-term recall). 

(4) Long-term recall can be inferred in the course of history-taking. 

e. Mood and affect 

(1) Mood is self-reported ("sad," "angry"), whereas affect is observed (flat, irritable, tearful). 

(2) Affect ranges from flat to labile and can be described as mood-congruent or mood-incongruent (eg, 

inappropriate laughter). 

f. Speech: rate, rhythm, fluency 

g. Thought process: may be described as linear and logical, circumstantial, tangential, derailed, loose 

associations, thought blocking, illogical 

h. Thought content 

(1) Delusions ("fixed false beliefs") 

(a) Paranoid, persecutory, grandiose, self-deprecatory, erotic 

(b) Mood congruent/incongruent 

(c) Bizarre (impossible in real life) versus nonbizarre 

(2) Suicidal or homicidal ideation 

(3) Depressive cognitions: hopelessness, worthlessness, inappropriate guilt 

679


1. Perceptual abnormalities 

(1) Hallucinations: visual, tactile, auditory, olfactory 

(2) Illusions: misperceptions of visual stimuli 

(3) Dissociative phenomena: flashbacks, deja vu, depersonalization 

j. Cognitive function: ask the patient to spell a word backward (such as "world" or "earth") and subtract 7 

from 100 serially (93, 86, 79, etc). 

k. Judgment and insight: can usually be inferred in the course of history-taking 

5. Screening diagnostic studies are not required to medically clear all patients with psychiatric complaints. The 

history, physical examination, and clinical judgment should direct appropriate diagnostic evaluation. 

a. "Medical clearance" is a controversial term used to communicate that the patient is stable for transfer to 

a psychiatric facility where medical resources may not be readily available. 

b. The history and medical examination may indicate the need for diagnostic evaluation, including 

electrolytes, BUN, creatinine, urinalysis, CBC, glucose, total CK, ECG, and chest radiograph. 

c. Tests such as an ethanol level or urine drug screen may aid psychiatric consultants in making an 

appropriate diagnosis and referral, particularly in a setting where dual diagnosis admission/treatment is 

available. 

d. Drug levels, including lithium, valproic acid, and carbamazepine, are useful in determining medication 

compliance. Trough levels are preferred for therapeutic monitoring. 

e. Be suspicious of suicidal patients who may not disclose an ingestion, and consider ordering 

acetaminophen, toxic alcohols, and salicylate levels; these ingestions are best discovered early. 

E. The psychiatric interview 

1. General approach 

a. Psychiatric conditions, like all medical problems, are biopsychosocial disorders. Evaluation should focus 

on signs and symptoms (onset, severity, and progression), the patient's physical and behavioral coping, and 

also the availability of therapeutic and/or supportive resources. 

b. Stages of the interview 

(1) Begin by asking open-ended questions and be silent afterward; the patient will fill in the silence. 

(2) Progress to structured, directive questioning to explore symptoms and circumstances. 

(3) Finish with a psychiatric "review of systems" to continue to consider or exclude covert, comorbid 

syndromes. 

(4) All history must be corroborated. In addition to the sources listed under the medical evaluation, 

contact with the patient's current treating psychiatrist and psychotherapist is essential to rapid, accurate 

diagnosis and treatment planning. 

(5) Collateral information is essential, particularly when planning to discharge a patient with safety 

concerns. It is considered standard of care. 

c. Pay attention to your emotional response to the patient. 

(1) The interviewer's emotional response will often mirror the patient's mood and thus is a valuable 

diagnostic instrument. 

(2) Maintain a calm demeanor and nonjudgmental approach with even difficult patients. Arguing with an 

agitated patient may exacerbate the situation; a better approach is to agree with the patient or "agree 

to disagree." 

2. The goals of the interview are to determine the: 

a. Nature of the problem: "What is wrong?" What is the patient upset or worried about, and how is he or she 

having difficulty functioning? 

b. Precipitant: "Why now?" What change in symptoms or circumstances has led to the current emergency 

department visit, and how did the patient come to the emergency department today? 

c. Progression, including course and duration: How long has the problem been going on, how has its nature 

and severity changed, has there been any prior treatment, and if so, to what effect? 

d. Patient's expectations: What is he or she (or the patient's family) hoping to have done at this time? 

e. Disposition: Has an appropriate plan, such as medical admission, psychiatric admission, outpatient 

psychiatric, and/or medical follow-up been decided? 

3. The interview: in addition to asking questions to determine the patient's mental/emotional stability, ask 

specifically about: 

a. Suicidal or homicidal ideation or threats 

b. Availability of firearms 

680


c. Hallucinations, delusions 

d. Drug, alcohol, and prescription medication abuse 

e. Current (or past) physical or sexual abuse 

f. Any inconsistencies between the histories given by the patient and collaterals, or between the history given 

and your examination findings. 

4. Determining disposition 

a. Inpatient versus outpatient management is determined by whether the patient presents immediate danger to 

himself/herself or others, whether the patient is able to care for himself/herself, and what social supports are 

available at home. 

b. At the end of the interview, discuss your understanding of the psychiatric problem and any medical/surgical 

problems, and explain treatment recommendations. 

c. If immediate psychiatric hospitalization is indicated but unavailable (on site or by transfer), some 

hospitals will admit the patient to a medical service with appropriate supervision ("sitter") and psychiatric 

consultation, while other hospitals will have the patient "board" in the emergency department. 

d. There is a growing trend toward psychiatric observation units or psychiatric crisis units with the goal of


emergency room. I would be upset, too, if I spent two hours waiting for a prescription and then was told 

that I would not get it. However, it is our policy not to give prescriptions for that medication." 

e. Do not argue with the patient or raise your voice in reaction to the patient. Yelling will make the patient 

more defensive, and the agitation will increase. Patients who remain agitated or become threatening 

should be informed that such behavior is not allowed, is scaring others (you, staff, other patients), and 

that restraints (either physical or chemical) may be required to control the behavior. 

f. The physician's body language should communicate confidence and calmness. Arms should be relaxed at 

the sides. Arms crossed in front of you can communicate that you feel afraid or closed off, whereas hands 

on the hips communicate that you are controlling and may be threatening. 

g. Always keep clear a lane of egress from the room when evaluating a psychiatric patient with the potential 

for violence and/or inappropriate behavior. Also consider having security nearby if there is concern the 

conversation may become violent. 

h. Verbal de-escalation is particularly likely to be successful in a patient who is cognitively intact. 

5. Pharmacologic management of agitation 

a. Use of medications to treat agitation is sometimes called "chemical restraint." Medications can be useful 

in obtaining behavioral control and should be considered once the initial evaluation has been completed 

or if the patient becomes agitated. 


(a) Agitation that would otherwise interfere with safe medical management 

(b) Treatment of the underlying cause of agitation (eg, giving an antipsychotic medication to a 

psychotic patient will decrease his or her agitation and also treat the psychosis) 

(c) If the patient requests a medication that was previously effective for safety 

(2) Goal: a calm patient in behavioral control (not a patient who is too sedated to interview, although 

sleep may result from these medications) 

(3) Relative contraindications 

(a) Incomplete assessment 

i. Medication may obscure diagnostic signs and symptoms. 

ii. Overmedication may delay completion of evaluation by several hours. 

(b) Unknown dosage of preexisting medication or overdose 

(c) For patients with dementia or other cognitive disorders, sedating medication (especially 

benzodiazepines) may cause disinhibition, potentially worsening agitation or confusion. 

(4) Protocols 

(a) Administration of the oral concentrate form is preferred if the patient is willing because: 

i. Consent is thereby implied. 

ii. Therapeutic alliance with the patient is furthered. 

iii. Absorption and efficacy are almost as rapid as with IM dosing. 

(b) "Rapid tranquilization" is well researched as safe and effective when using haloperidol, 

lorazepam, or both. This combination is considered by many to be the safest and most effective 

protocol for the severely agitated or violent patient. 

b. Classes of medication 

(1) Medications should be chosen to target the underlying cause of the agitation. 

682


Based on response to interventions, 

medication is now required 

I 

I 

I 

I 

Ethanol or 

benzodiazepine 

withdrawal 

not suspected 

I 

Agitation associated 

with delirium 

Identify and correct any 

underlying condition 

Avoid benxodiazepines 

Oral second-generation 

anti psychotics 

(eg, risperidone, 

olanzapine) 

Oral first-generation 


(eg, haloperidol)# 

Parenteral secondgeneration 

antipsychotics 

(cg, olanzapine, 

ziprasidone) 

Parenteral first-generation 


(eg, haloperidol)#' 

#There is strong evidence 

that doses above 3 mg/day 

in patients with delirium 

are associated with 

significant risk of 

extrapyramidal side effects. 

'See FDA guidelines 

I 

Ethanol or 

benzodiazepine 

Oral benzodiazepines 

(eg, lorazepam, 

chlordiazepoxide, 

diazepam) 

Parenteral 

benzodiazepines 

(eg, lorazepam) 

I 

I 

CNS 

stimulant 

I 

Agitation due to 

intoxication 

I 

I 

CNS depressant 

(eg, ethanol) 

Avoid benzodiazepine 

if possible 

Oral first-generation 


(eg, haloperidol) 



(eg, haloperidol) 

Agitation 

associated 

with psychosis 

in patient with 

known 

psychiatric 

disorder 

Oral second-generation 


(eg, risperidone', olanzapine') 

Oral first-generation antipsychotics 

(eg, haloperidol with 

benzodiazepine) 

Parenteral second-generation 


(eg, olanzapine', ziprasidone') 



(eg, haloperidol with 

benzodiazepine') 

' If an antipsychotic alone does not 

work sufficiently, add lorazepam 

(oral or parenteral). 

I 

Undifferentiated 

agitation or 

complex 

presentation 

I 

No psychosis evident 

Same as agitaiton due 

to withdrawal 

Psychosis evident 

Same as for primary 

psychiatric disorder 

Protocol for Treatment of Agitation 

Source: Wilson MP, Pepper D, Currier GW, Holloman GH Jr, Feifel D. The psychopharmacology of agitation: consensus statement of the 

American Association for Emergency Psychiatry Project BETA Psychopharmacology Workgroup. Western j Emerg Med. Vol XIII, No. 1; Feb 

2012:31. 

(2) If a patient is violent or at imminent risk of violent behavior, then medications may be given IM 

against the patient's consent. Hospital security should be present to restrain the patient while the 

medication is administered to decrease risk of staff or patient injury. 

(3) Haloperidol and lorazepam are frequently considered agents of choice and may be used orally, IM, 

or IV (alone or in combination). They may be given together in the same syringe. In the absence of 

contraindications, combined dosing tends to reduce adverse effects as well as promote a synergistic 

drug effect. Lorazepam effectively prevents dystonia, while haloperidol permits the use of lower 

doses of lorazepam, thereby minimizing lorazepam's dose-dependent adverse effects (excessive 

sedation, respiratory depression). 

683


(4) First-generation (typical) antipsychotics 

(a) Haloperidol 2-5 mg orally, IM, or IV every 30 minutes as needed up to 40 mg total for adults 

(0.5-1.0 mg every 30 minutes as needed in the elderly or children). Major complication is acute 

dystonias (may be prevented or treated with diphenhydramine 25-50 mg or benztropine I mg). 

Haloperidol is relatively contraindicated in patients with parkinsonism because of its potent 

dopamine D2 blockade. 

(b) Chlorpromazine 25-50 mg orally or IM every 30 minutes as needed. Hypotension may result 

with use of low-potency antipsychotics, particularly with concomitant use of a benzodiazepine. 

(5) Second-generation (atypical) antipsychotics 

(a) Medications in this class are being used increasingly in psychiatric emergency services, because 

they are less likely to cause extrapyramidal symptoms than older antipsychotics. 

(b) Olanzapine 5-10 mg orally or IM every 30 minutes, up to a total dose of 30 mg. It is also 

available in a rapidly dissolving wafer that can be useful in emergency situations in which the 

patient is somewhat cooperative. Do not give IM olanzapine along with IM lorazepam because 

of the risk of oversedation and hypotension. 

(c) Ziprasidone 10-20 mg orally or IM every hour, up to a total dose of 40 mg; may cause 

QT prolongation in some patients. Do a baseline ECG to measure QT interval before drug 

administration to avoid dangerous additive effect. 

(d) Risperidone does not have an immediate-acting IM formulation, but its oral preparation may still 

be helpful in treating agitation. 


(a) Lorazepam 1-2 mg orally, IM, or IV every 30 minutes (0.25-0.5 mg every 30 minutes as needed 

in the elderly or children). Lorazepam is the only benzodiazepine with reliable and rapid IM 

efficacy. 

(b) Duration of action is intermediate (~6 hours). 

(c) Respiratory depression may occur, particularly in COPD, preexisting sedative-hypnotic 

ingestion, or in IV use. (IV administration requires availability of intubation and respiratory 

support.) 

(d) Disinhibition and agitation may occasionally occur, particularly in geriatric patients with/ 

without underlying dementia. 

(e) In cases of substance abuse, particularly cocaine intoxication, benzodiazepines alone are 

preferable choices for chemical restraint. 

6. Seclusion 

a. The Centers for Medicare and Medicaid Services mandate detailed documentation of indications and 

procedures when restraints are used: "Seclusion or restraint can only be used in emergency situations ... 

only when less restrictive measures have been found to be ineffective to protect the patient or others 

from harm." Restraints may be ordered only for limited periods, and continuous face-to-face or audiovideo 

monitoring must be implemented. Transfers to other facilities are also subject to documentation of 

"least restrictive available" and "face-to-face monitoring" by trained staff. 

b. A seclusion room is designed and located to provide: 

(1) Safety: no potential weapons, minimal furnishings 

(2) Reduced stimulation: soundproofed, dimly lit, private 

(3) Continuous observation: by audio-video or in direct view of staff 

(4) Security staff and resuscitation area nearby 

(5) Clearly controlled entrance and exit 

c. Vital signs and triage should be done before leaving a patient in the seclusion room. 

7. Physical restraints (frequently required for violent or severely agitated psychotic, delirious/demented, or 

intoxicated patients) 

a. Advantages 

(1) Minimal adverse effects 

(2) Immediately reversible 

(3) Clearly visible reminders to staff and patient 

(4) Permits search for weapons and drugs (never, however, a primary indication) 

(5) Legally, it is appropriate medical treatment that is clearly established (Youngberg v. Romeo). 

684



(1) Patient is a danger to self or others. 

(2) Patient is unable to cooperate with assessment of a life-threatening condition. 

(3) Patient requests restraints for safety (rare). 

c. Contraindications 

(1) Unstable orthopedic injury 

(2) Unstable cardiovascular status 

(3) Use as punishment or solely for staff convenience 

d. Protocol should be clearly established, in written form, and institution-specific, with all emergency 

department personnel well trained. 

(1) Call for help immediately; the presence of a "show of force" is frequently very helpful in 

de-escalating such situations. 

(2) A team approach is required, with a leader and five helpers (one takes the head and each of the 

others an extremity). 

(3) Use leather (not cloth) restraints on all four extremities. 

(4) Restrain the patient so he or she can be examined and rolled onto his or her side quickly, if needed, 

to protect the airway. The patient should not be left restrained in the prone position because of the 

risk of positional asphyxia. 

(5) Tell the patient why restraints were applied. 

(6) Search for weapons and drugs. 

(7) Perform a physical examination. 

(8) Monitor continuously, face-to-face, or by audio-video. 

(9) Frequently (every 15 minutes or less) reassess the patient for safety and the need for continued 

physical restraints. Consider using medications if necessary to help the patient calm down and to 

allow for removal of physical restraints. 

(1 O) Document in the chart why restraints were required (to protect the patient and/or staff from harm) 

and the frequency and results of reassessments. Have an institutional policy and follow it. 

(11) Remove restraints only when the patient's behavior improves and he or she is no longer a threat. Don't 

bargain for removal. If a patient is calm and in behavioral control, do not keep him or her in restraints 

longer than needed as a form of punishment or prophylaxis against future episodes of agitation. 

B. Crisis intervention 

1. A patient with or without a psychiatric illness may present to the emergency department "in crisis," eg, after 

a trauma or in bereavement. The emergency physician can follow guidelines for crisis intervention to help the 

patient manage the crisis. 

2. Trauma may result in a severe psychological reaction. When the traumatic event is so severe or occurs so 

suddenly that patients are unable to master the resulting emotions, the patient experiences a crisis. Crisis 

intervention involves understanding the patient's view and assisting patients to change their perception of the 

problem in such a way that they are no longer overwhelmed by their own reaction. 

a. Goals 

(1) Stabilize the patient's emotional and behavioral reaction. 

(2) Prevent psychological sequelae and screen for pathologic reactions. 

(3) Assist the patient in developing mastery of the traumatic situation, thereby creating growth, maturation, 

and a long-term improvement in coping skills. 

b. Prerequisites 

(1) The traumatic event must be identified and must have ended. 

(2) The patient must have sufficient self-reliance and social support. 

c. Patients most likely to benefit are those with a prior history of adequate functioning. 

d. Technique 

(1) Develop rapport. Be supportive of the patient but avoid glib reassurance; mobilize hope by 

communicating an expectation for improvement. Reassure the patient that it is good that he or she is 

seeking help and that the catastrophe has indeed ended. 

(2) Let the patient talk about his or her feelings; be a sympathetic, nonjudgmental, active listener. 

(3) Help the patient to reassess the situation, survey critical issues, and develop a solution. 

685


(4) Activate natural support systems in family and community. 

(a) 

If possible, access community resources (eg, government agencies, caseworker, minister, 

responsible family member, etc) before discharging the patient from your care. 

(b) Medical/surgical issues (eg, chronic pain) must be addressed. 

e. Warning signs of poor coping include dissociation, reexperiencing the traumatic event, hyperarousal 

(including hypervigilence or severe sleep disturbance), or avoidance of reminders of the trauma. These 

symptoms may suggest the need for referral to a counselor or psychiatrist. 

f. Debriefing (ie, discussion of the event in detail, often in a group of individuals who had witnessed the same 

trauma) was previously recommended as a method to help individuals process a traumatic event. However, 

recent evidence suggests that group debriefing may increase the risk of developing an acute stress reaction 

or post-traumatic stress disorder and should be avoided. 

3. Bereavement ("acute grief reaction") 

a. Etiology: awareness of a sudden loss, eg, sudden infant death syndrome, accidental death or suicide of a 

family member or close friend, spousal abandonment, job loss, etc 

b. Clinical stages of grief and mourning have been described, some or all of which the patient may evidence. 

(1) Shock and denial (may be accompanied by screaming/collapse) 

(2) Anger 

(3) Bargaining 

(4) Depression (feeling of powerlessness over the event) 

(5) Acceptance (in which loss and its consequences are constructively integrated into the patient's psyche 

and life) 

c. Exclude "pathological grief reaction" ie, depressive mood disorder. 

(1) Features characteristic of major depression (eg, pervasive sadness with insomnia, anorexia, agitation, 

impaired concentration, etc) may be found during the course of normal bereavement. 

(2) Some symptoms are abnormal (even in severe bereavement) and warrant a diagnosis of "depressive 

disorder" and psychiatric treatment. 

(a) 

Persistence of significant symptoms beyond 2 months 

(b) Suicidal ideation (other than wishing to be with the deceased) 

(c) Morbid preoccupation with worthlessness 

(d) Marked slowing of thought and movement ("psychomotor retardation") 

(e) 

(f) 

d. Treatment 

Prolonged and severe debilitation 

Hallucinations other than hearing the voice of, or transiently seeing the deceased (these 

experiences are common-and normal-in survivors) 

(g) Substance abuse or an increase in use of alcohol, pain medications, sedatives 

(1) Help patients identify the loss and encourage them to express their feelings about it; defuse blame, 

suspicion, and guilt. 

(2) The severity of the grief reaction is directly related to the suddenness and importance of the loss; signs 

of severe depression, psychosis, or other inappropriate response warrant psychiatric referral. 

(3) Most people will not require counseling; however, referral information should be provided, because 

some individuals may decide to use it later on. 

C. Psychopharmacology 

1. Anti anxiety agents 

a. Benzodiazepines 

(1) Useful for short-term management of anxious, agitated patients in crisis and for initial treatment of 

patients with panic disorder. They are also used to treat seizures, muscle tension, alcohol withdrawal, 

and catatonia. 

(2) When used in conjunction with antipsychotic agents, they have synergistic effects. 

(3) Sedation with low doses reduces anxiety; occasionally, disinhibition ("paradoxical excitation") occurs. 

(4) Lorazepam 

(a) 

0.5-2 mg may be repeated every 30-60 minutes as needed. 

(b) Onset of action varies with route of administration; 20-40 minutes when administered orally or 

IM and


(5) Chlordiazepoxide 25-100 mg is sometimes given for alcohol withdrawal, particularly in a patient 

without liver dysfunction. Its long half-life provides a self-taper. 

(6) Diazepam 5-10 mg can be administered orally or IM. Diazepam is highly distributed in fat, and will 

(along with several active metabolites) accumulate after repeated administration. 

(7) Adverse effects 

(a) Dose-dependent sedation, impairment of motor coordination and reaction time 

(b) Impairment of consolidation of short-term memory (learning); at higher doses, ataxia/dysarthria 

and amnesia ("blackouts") may occur. 

(c) Respiratory depression is found at higher dosages but is essentially benign in oral and IM use for 

healthy individuals who are not taking other respiratory depressants. IV use, comorbid COPD 

(or other respiratory compromise), and interactions with other medications/substances can cause 

lethal apnea. Therapeutic use under these circumstances requires caution, less aggressive dosing, 

and the immediate availability of intubation and ventilatory support. 

(8) Tolerance may develop over time. 

(9) A withdrawal syndrome may occur with insomnia, agitation, increased vital signs, and withdrawal 

seizures. 

(10) These drugs have abuse potential and can be addictive. Diazepam and alprazolam are well-known 

offenders. 

(11) Benzodiazepines are very safe in oral and IM use. 

b. Buspirone 

(a) Lorazepam in particular has minimal cardiovascular effects, no active metabolites, and does not 

inhibit/induce cytochrome P450 isoenzyme catabolism of other substrates. 

(b) Although these drugs are frequently ingested in suicide attempts, a fatality is rare unless they are 

taken in combination with alcohol or other drugs. 

(1) A nonbenzodiazepine anxiolytic that is not subject to withdrawal or addiction 

(2) Requires 2-3 weeks for efficacy and therefore is not indicated in the emergency department 

c. Antihistamines 

(1) Diphenhydramine and hydroxyzine can be useful as mild oral antianxiety agents. 

(2) Dosage is 25-50 mg every 4 hours orally or IM (may also be given IV). 

(3) If a hypnotic is indicated for brief outpatient use after emergency department discharge, these agents 

are preferred because of their low incidence of adverse effects and safety. 

2. First-generation antipsychotic agents 

a. First-generation ("typical") antipsychotics have largely been replaced by second-generation ("atypical") 

antipsychotics for routine control of psychiatric symptoms. However, the first-generation agents continue 

to be used in some patients, including some who need long-acting injectable formulations. Antipsychotic 

medications are also called neuroleptics. 

Table 41: Characteristics of First-Generation (Typical) Neuroleptic Agents 

Potency Dystonia Drug 

Equivalent 

Dose (mg) 

Anticholinergic 

Sedation 

high high low low 

Haloperidol 2 

I I I I 

Droperidol 2 

Fl uphenazi ne 2 

Perphenazine 10 

low low Chlorpromazine 100 high high 

b. Mechanism of action is dopaminergic receptor blockade in the mesolimbic area of the CNS. This may result 

in reduced hallucinations, delusions, anxiety, impulsivity, and aggression. 

c. Al I anti psychotics cause some orthostatic hypotension and reflex tachycardia; these adverse effects 

(which are due to a-adrenergic blockade) are more common and severe with low-potency neuroleptics 

(chlorpromazine). 

d. The seizure threshold is lowered with use of antipsychotics. 

687


e. Haloperidol is the neuroleptic agent of choice in many emergency departments; it reduces agitation, has 

benign cardiovascular (and minimal anticholinergic) effects, is not very sedating, and has a rapid onset. 

3. Second-generation antipsychotic agents 

a. Characteristics 

(1) Enhanced mechanism of action: postsynaptic antagonism of both serotonin and dopamine receptors 

(2) Less likely to cause extrapyramidal symptoms but more likely to produce metabolic syndrome than 

first-generation agents 

(3) Also used to treat bipolar disorder and to augment treatment of depression 

b. Clozapine 

(1) Very low risk of extrapyramidal symptoms, increased risk of seizures 

(2) Risk of agranulocytosis requires weekly CBC monitoring. Its use is limited to psychotic disorders 

unresponsive to standard agents or to patients with severe extrapyramidal symptoms. It should never 

be started in the emergency department. 

c. Risperidone, paliperidone, ziprasidone, olanzapine, quetiapine, and aripiprazole are other second-generation 

anti psychotics. These agents may cause sedation, weight gain, hyperlipidemia, and hyperglycemia. 

4. Adverse effects of anti psychotic agents 

a. Extrapyramidal symptoms: occur more often with high-potency neuroleptics but can also occur with 

second-generation agents 

(1) Dystonias 

(a) Painful clonus of voluntary muscles; they usually involve muscles of the face, neck, and tongue, 

but any muscle group can be affected. 

(b) Laryngospasm occurs rarely and can be life threatening. 

(c) Oculogyric crisis involves involuntary eye movements, usually in the upward direction. 

(d) Torticollis is a painful contraction of the sternocleidomastoid muscle. 

(e) These reactions generally occur within the first month of treatment (or after dose increases). 

(f) Treatment is with anticholinergic agents, followed by a maintenance prescription of 

anticholinergics prescribed twice daily to prevent recurrence. 

(2) Parkinsonism 

i. Benztropine 1-2 mg orally, IM, or IV 

ii. Diphenhydramine 25-50 mg orally, IM, or IV 

(a) One or more of the following: shuffling gait, bradykinesia or akinesia, resting tremor, cogwheel 

rigidity, masked fades, drooling 

(b) Dosage reduction and/or anticholinergic agents are usually effective. 

(3) Akathisia 

(a) An unpleasant and disturbing feeling of restlessness with an almost uncontrollable desire to 

move; easily mistaken for agitation 

(b) Reactions begin several days to weeks after start of therapy and are worsened by increases in dosage. 

(c) Treatment 

i. Propranolol 10-20 mg orally is the drug of choice for managing anti psychotic medicationinduced 

acute and chronic akathisia, and relief is usually seen within 20-40 minutes; if not, 

the dose may be repeated. Ongoing treatment is necessary to prevent recurrence. 

ii. For acute akathisia in the emergency department, treat with anticholinergics (eg, 

diphenhydramine) and/or lorazepam IV or IM. 

(4) Tardive dyskinesia 

(a) A disorder of abnormal, involuntary movements that develops after a period of antipsychotic use 

(b) Oral-buccal muscle involvement is common and characterized by lip smacking and tongue 

protrusion. Limb and truncal muscles can also be involved. 

(c) The patient can voluntarily suppress the movements temporarily. 

(d) There is no definitive treatment. The offending agent should be discontinued. This should be 

coordinated with the treating psychiatrist to prevent recurrence of psychosis. Discontinuation 

of the antipsychotic may also lead to a transient increase in the movement severity but a greater 

chance of improvement over time. 

b. Anticholinergic effects (occur more often with low-potency neuroleptics) 

(1) May be central (sedation, agitation, delirium/psychosis) and/or peripheral (eg, dry mucous 

membranes, flushed skin, mydriasis, tachycardia, urinary retention) 

688


(2) Treatment is supportive, and the offending agent should be discontinued. Use of physostigmine 

should be avoided. 

c. Cardiovascular effects 

(1) The major cardiovascular adverse effects (seen more often with low-potency neuroleptics) are 

hypotension (usually managed with IV fluids) and tachycardia. The mechanism of action is through 

noradrenergic blockade. 

(2) Antipsychotics may result in QTc prolongation. Cases of torsades have been reported with use of IV 

haloperidol. Of the newer antipsychotics, ziprasidone is most associated with QTc prolongation. 

d. Hyperprolactinemia and its clinical consequences (galactorrhea, amenorrhea) may result from use of 

antipsychotics, especially risperidone. 

e. Neuroleptic malignant syndrome 

(1) This uncommon (0.5 %-1 %) idiosyncratic reaction (usually occurring in the first weeks of treatment 

or after a dose increase) constitutes a medical emergency. Mortality rates up to 30% can be 

improved to 10% with early recognition and aggressive supportive treatment. 

(2) More commonly associated with high-potency neuroleptics, it can also be associated with the lowpotency 

agents or withdrawal of anti-Parkinson agents (eg, discontinuation of L-dopa). 


(a) Generalized muscle "lead pipe" rigidity. Occasional patients may also have a superimposed 

tremor or a cogwheel phenomenon. 

(b) Mental status change, often presenting as confusion, agitation, or coma 

(c) Hyperthermia with temperatures often >104°F (40°C), often with diaphoresis 

(d) Autonomic instability with tachycardia and labile or high blood pressure 

(4) Laboratory abnormalities 

(a) Leukocytosis 

(b) Increased creatine phosphokinase: typically >1,000 IU/L, can be as high as 100,000 IU/L 

(5) Findings cannot be explained by a medical or neurologic disorder (eg, viral encephalitis), a mental 

disorder (eg, psychosis), or substance abuse (eg, phencyclidine). 

(6) Treatment 

(a) ICU admission is often required. 

(b) Supportive measures, including IV fluid hydration. Some patients may require mechanical 

ventilation. 

(c) The offending agent should be discontinued. Other psychotropic medications (eg, lithium or 

antidepressants) should also be held. 

(d) Anticholinergic agents should be avoided; they are not effective and may worsen the reaction by 

interfering with temperature regulation. 

(e) Benzodiazepines (eg, lorazepam 1-2 mg) can be used as needed for muscular rigidity or agitation. 

(f) 

5. Antidepressants 

Dantrolene may reduce rigidity and temperature. Its use is controversial and may cause 

hepatotoxicity and as monotherapy may increase mortality. 

a. Starting antidepressants in the emergency department is not recommended without a high certainty of 

reliable follow-up. These medications can be dangerous in overdose, and in the short-term may increase 

suicidal thoughts. 

b. SSRls (fluoxetine, sertraline, paroxetine, citalopram, escitalopram, fluvoxamine) are the current first-line 

agents for depressive disorders, premenstrual dysphoric disorder, and anxiety disorders (including panic, 

obsessive-compulsive, and post-traumatic stress disorders). 

(1) Adverse effects are generally mild and include nausea, headache, sleep disturbance, and sexual 

dysfunction. 

(2) Many of these agents inhibit cytochrome P450, causing drug-drug interactions. 

(a) Fluoxetine, paroxetine, and venlafaxine (a serotonin norepinephrine-reuptake inhibitor [SNRI]) 

are P450 2D6 inhibitors and prolong/increase tricyclic antidepressant (TCA) levels, thereby 

potentiating their cardiotoxic effects. Risperidone, codeine, dextromethorphan, and class IC 

antidysrhythmics (eg, encainide, flecainide) levels are also increased via this mechanism. 

(b) Fluoxetine, fluvoxamine, and citalopram are P450 3A4 inhibitors (as is grapefruit juice) and 

prolong/increase levels of alprazolam, triazolam, clonazepam, and verapamil. 

(3) Toxicity develops only with large overdoses or when combined with other agents. 

689


c. SNRls: inhibit reuptake of both serotonin and norepinephrine, a mechanism of action similar to that of the 

TCAs without the cardiotoxicity of the TCAs. 

(1) Venlafaxine: can cause hypertension or orthostatic hypotension 

(2) Duloxetine: often prescribed for patients with depression or anxiety and a comorbid pain disorder; 

should not be used in patients with hepatic dysfunction or active alcohol abuse 

d. Other newer antipsychotics 

(1) Trazodone: may increase serum digoxin and phenytoin levels; orthostasis and rarely priapism can occur. 

(2) Bupropion: increases norepinephrine and dopamine; causes seizures in overdose and in the 

predisposed (notably bulimic patients and those with seizure disorders) 

e. TCAs (eg, amitriptyline, nortriptyline, imipramine, and others) were the standard of care through the early 

1990s. They have been replaced by the SSRls because of their many adverse effects: 

(1) Anticholinergic effects (both peripheral and central) 

(2) a-adrenergic effects: TCAs act therapeutically by presynpatic norepinephrine reuptake inhibition; 

sympathetic adverse effects can include both hypertension and orthostatic hypotension with fal Is 

(particularly in older patients). 

(3) Cardiac effects: TCAs are type IA (quinidine-like) antidysrhythmics and delay conduction. In overdose, 

this causes nonspecific T-wave changes, AV block, t QT interval, and ventricular tachdysrhythmias, 

including torsades de pointes and fibrillation. 

(4) Increased seizure risk 

(5) Lethality in overdose 

f. Monoamine oxidase inhibitors (MAOls), eg, phenelzine, tranylcypromine, isocarboxazid, selegiline) 

(1) Use of MAOls has largely been replaced by newer antidepressants; however, emergency physicians 

should be aware of potential drug-food and drug-drug interactions with these agents. 

(2) Patients on an MAOI should be on a tyramine-free diet. Consumption of tyramine-containing foods 

(aged cheeses, cured meats, fava beans, red wine) can lead to a hypertensive crisis. 

(a) 

Clinical presentation of impending hypertensive crisis may include severe occipital headache, 

hypertension, palpitations, chest pain, tachycardia, dilated pupils, diaphoresis, nausea, and 

vomiting. 

(b) Treatment 

i. Phentolamine, an a-antagonist (2.5-5 mg slow IV push, which may be repeated every 10-15 

minutes as needed), or sublingual or IV nifedipine 

11. ~-blockers are contraindicated, because they may worsen hypertension by producing 

vasoconstriction. 

(3) Ingestion of an MAOI and other serotonergic agents can lead to life-threatening serotonin syndrome. 

Patients taking an MAOI should avoid SSRls, SNRls, tricyclics, meperidine, dextromethorphan, and 

MOMA. 

(4) The antibiotic linezolid is pharmacologically an MAOI. Patients should not be continued on 

serotonergic agents while taking linezolid. 

6. Serotonin syndrome 

a. May occur with drug-drug interactions between SSRls, MAOls, and other serotonergic agents 

(sumatriptan, meperidine, tramadol) or in overdose. 

b. By Hunter Criteria, serotonin syndrome is diagnosed if the patient took a serotonergic agent and has one 


(1) Spontaneous cl onus 

(2) Inducible clonus plus agitation or diaphoresis 

(3) Ocular clonus plus agitation or diaphoresis 

(4) Tremor and hyperreflexia 

(5) Hypertonia and temperature > 100.4°F (38°C) plus ocular or inducible clonus 

c. In addition to the Hunter Criteria, the patient may have additional symptoms including: 

(1) Altered mental status: confusion, hallucinations, delirium 

(2) Autonomic instability: diaphoresis, hyperthermia, orthostasis 

(3) GI signs: nausea, vomiting, diarrhea 

(4) Neuromuscular instability: tremor, myoclonus, hyperreflexia 

(5) Life-threatening seizures and cardiovascular collapse may occur. 

690


d. Management 

(1) Discontinue all serotonergic drugs. 

(2) Supportive care, including IV fluid hydration and cardiac monitoring 

(3) Benzodiazepines (eg, lorazepam 1-2 mg) can be used to treat agitation. 

(4) Cyproheptadine is a serotonin and histamine antagonist that may be used if supportive care does not 

result in clinical improvement. 

(5) Patients with severe symptoms may require ICU admission. Patients with moderate symptoms may be 

admitted with cardiac monitoring until symptoms resolve. 

7. Mood stabilizers 

a. Mood stabilizers are not usually started in the emergency department given their complications and 

requirements for close monitoring. 

b. Lithium 

(1) First used in the late 1800s and a very effective mood stabilizer. It has been shown to reduce risk of 

suicide in patients with bipolar disorder. 

(2) Narrow therapeutic index: therapeutic level is 0.8-1.2 mEq/L; signs of toxicity can be evident at levels 

as low as 1 .5 mEq/L. 

(3) Acute toxicity 

(a) Can be precipitated by dehydration, diuretics, ACE inhibitors, and NSAIDs 

(b) Early signs of lithium toxicity include nausea, vomiting, and diarrhea. Patients then develop 

sluggishness, confusion, ataxia, and an irregular coarse tremor or myoclonic jerks, followed by 

seizures and nonconvulsive status epilepticus. 

(c) Hemodialysis is indicated for a lithium level >4 mEq/L regardless of clinical status, or for a level 

>2.5 mEg/L if severe symptoms are present. Otherwise, hydration with IV fluids will help facilitate 

excretion. 

(4) Chronic toxicity 

(a) Renal toxicity: chronic use of lithium can cause nephrogenic diabetes insipidus, nephrotic 

syndrome, and chronic interstitial nephritis. Occasionally, this progresses to end-stage renal 

disease. Creatinine should be monitored in patients taking lithium. 

(b) Hypothyroidism also develops as a result of chronic lithium use. 

c. Divalproex/valproic acid 

(1) Indicated for use in bipolar disorder, seizure disorders, and migraine prophylaxis 

(2) Contraindicated in pregnancy given high risk of neural tube defects 

(3) Targettrough level 50-125 mcg/ml 

(4) Valproic acid toxicity 

(a) Signs of toxicity are present at levels> 180 mcg/ml. 

(b) Symptoms include CNS suppression, respiratory depression, hyperammonemia, cerebral edema, 

tremors, and myoclonus. 

(c) May also result in a dose-related hepatotoxicity 

(5) Patients on divalproex may develop hyperammonemia and encephalopathy even with normal valproic 

acid and transaminase levels. 

(6) Rare but severe complications include hepatic failure and pancreatitis. 

d. Carbamazepine and oxcarbazepine 

(1) Indicated for maintenance treatment of bipolar disorder 

(2) Oxcarbazepine is used as an alternative to carbamazepine given its better tolerability but has an 

increased risk of hyponatremia. 

e. Lamotrigi ne 

(1) Indicated for treatment of bipolar depression 

(2) Risk of Stevens-Johnson syndrome, toxic epidermal necrolysis, and drug reaction with eosinophilia 

and symptoms (DRESS) syndrome, usually occurring in the first 2-8 weeks of therapy; therefore, slow 

titration of dose is required. 

691


Ill. SPECIFIC BEHAVIORIAL DISORDERS 

A. Psychosis 

1. Definition: loss of contact with reality 


a. Delusions: a "fixed false belief" that is not accepted by the patient's cultural group and that is firmly 

sustained despite what others believe, and in spite of incontrovertible evidence to the contrary (eg, "The 

FBI implanted radio transmitters in my heat ducts"). 

b. Hallucinations: a false perception experienced in a sensory modality (usually auditory) occurring while 

the individual is fully conscious; if they are visual, olfactory, or tactile, suspect a medical- or substanceinduced 

("organic") disorder. 

c. Disorganized speech: the patient does not make sense, rapidly jumps from one topic to another, or takes 

long pauses before answering, which is suggestive of thought blocking. 

d. Crossly disorganized behavior: purposeless behavior that does not make sense in context, eg, spreading 

one's wardrobe across the lawn or masturbating in the emergency room 

e. Catatonia: a neuropsychiatric syndrome characterized by decreased responsiveness to one's environment 

and either hypo- or hyperactivity 

(1) A classic presentation includes "waxy flexibility," whereby the examiner can move the patient's limbs 

and they will stay fixed in the new position. 

(2) Catatonic excitation resembles phencyclidine (PCP) intoxication and can be extremely dangerous to 

others, including emergency department staff. 

f. Negative symptoms: flat affect, poverty of speech, loss of volition, interpersonal withdrawal, minor 

cognitive deficits (acutely psychotic patients are usually oriented) 

3. Treatment 

a. Determination of the underlying cause of an acute psychotic episode may not be possible in the emergency 

department, but initial treatment and evaluation are the same. 

b. Establish safety first. 

(1) Search for weapons (involve security personnel as indicated). 

(2) For patients who are violent or at imminent risk of becoming violent, manage their acute agitation. 

c. After behavioral stabilization, proceed immediately to exclude treatable general medical causes of the 

acute episode (including substance- or medication-induced disorders). 


a. Anatomic: head trauma, stroke, tumor, seizures 

b. Metabolic: hypoxia, hypoglycemia, ketoacidosis, hyper- or hypocalcemia 

c. Endocrinologic: hyper- or hypothyroid, hypoparathyroid 

d. Autoimmune: multiple sclerosis, systemic lupus erythematosus, Hashimoto encephalitis (rare) 

e. Infectious: HIV, syphilis, encephalitis/meningitis 

f. Toxic: anticholinergic delirium 

g. Medications: steroids 

h. Substances: alcohol intoxication/withdrawal, stimulants, hallucinogens, cocaine 

5. Major psychiatric disorders that can present as an acute psychotic episode 

a. Schizophrenia 

(1) A chronic disorder affecting~ 1 % of the population 

(2) Onset usually in late adolescence/early adulthood 

(3) Diagnosis requires: 

(a) 

At least two of the positive symptoms of psychosis for c::1 month ("positive symptoms" include 

hallucinations, delusions, disorganized speech, disorganized behavior, or catatonia) 

(b) Severe impairment in level of functioning 

(c) Duration of c::6 months of some signs of the disorder 

(d) Exclusion of substance abuse, medications, or a general medical condition as the cause of the 

signs and symptoms 

b. Major depression with psychotic features ("psychotic depression"): a psychosis occurring solely during the 

course of a depressive episode 

692


c. Mania with psychotic features: a psychosis occurring solely during the course of a manic episode 

d. Schizoaffective disorder: a psychosis that is chronic and often associated with mood symptoms, but it also 

occurs for significant periods without mood symptoms 

e. Schizophreniform disorder: a psychosis lasting


(c) Hypo- or hyperthyroidism 

(d) Diabetes (and its complications) 

(3) Other general medical conditions: HIV encephalitis, mononucleosis, renal failure, pancreatic cancer 

3. Focal points of the psychiatric history 

a. Previous psychiatric illness, including history of psychiatric hospitalizations, suicide attempts, and suicidal 

ideation 

b. Recent acute or chronic illnesses (especially life-threatening ones) 

b. Recent life changes 

d. Existing social supports or lack thereof 

e. Always ask about suicidal or homicidal ideation 

4. Treatment and disposition 

a. The primary goal in evaluating depression is to determine the patient's suicidal potential. An adaptation of 

the "SAD PERSONS" score correlates well with the need for hospitalization. 

Table 42: SAD PERSONS Score 

£ex (male) 

Age (45 years old) 

Points 

Q.epression (or signs and symptoms of) 

2 

frevious attempts or psychiatric care 

l;xcessive alcohol or drug use 

Rational thinking (loss of) 

2 

Separated/divorced/widowed/single 

Qrganized plan or serious attempt 

2 

~o social support 

Stated future intent, plan, or mechanism 

2 

Score: >8 = high risk, 6-8 

intermediate risk, 8: almost all patients require admission 

(2) 6-8: psychiatry consult with follow-up or possible admission 

(3)


2. Risk assessment for suicide 

a. Anyone who attempts or threatens suicide must be taken seriously and evaluated for suicide risk potential. 

(1) Ask the patient how he or she feels about having survived an attempt and assess his or her reaction 

(eg, angry, doesn't care, relieved). 

(2) Ask directly about the suicidal intent; patients do not find this insulting and it will not "put ideas in 

their head." 

(3) Confirm all patient reports with collaterals. 

b. What is the content of the suicidal thoughts? Consider the following in your evaluation: 

(1) Expressed intent 

(2) Lethality of the method 

(3) Likelihood of rescue: was rescue a foregone conclusion, or purely fortuitous? 

(4) Suicidal thoughts can range from a passive death wish (eg, "I wish I would go to sleep and not wake 

up, but I would never hurt myself" to having a suicide plan with intent and means to act on this plan. 

The more detailed the plan, the greater the risk. For a patient who has had a self-injurious act, has 

anything changed as a result of the act, eg, improved ("I didn't realize people cared") or worsened 

("I'm so inadequate, I couldn't even commit suicide successfully"). 

c. What are this patient's risk factors for suicide? 

(1) History of previous suicide attempts conveys the highest risk. 

(2) Age and ethnicity: white men >65 years old are the demographic group most likely to complete 

suicide. 

(3) Gender: men are 3-4 times more likely to complete suicide, whereas women are 3-4 times more 

likely to attempt suicide. Men are more likely to attempt suicide by a more lethal means (firearms, 

hanging) than women (ingestion, cutting). 

(4) Family history of completed suicide 

(5) Major psychiatric illness, including major depressive disorder, schizophrenia, bipolar disorder, and 

borderline personality disorder 

(6) Marital status: those who are separated, divorced, or single are at higher risk 

(7) Medical illness, particularly chronic illnesses (multiple sclerosis, HIV) 

(8) Hopelessness: an individual in a personal crisis who sees "no way out" or no recovery from mental 

illness is at high risk of acting on these thoughts. 

(9) Recent loss (of job, of relationship, recent death) 

(10) Alcohol abuse: one-third of completed suicides occur when the individual had consumed alcohol. 

(11) Additional risk factors include panic attack, agitation, insomnia, and physical pain. These can be 

addressed while the patient is in the emergency department. 

(12) In adolescents, the ratio of attempts to completions is 25:1 in girls and 3:1 in boys. Risk is increased 

with a history of running away, previous suicide threats or attempts, psychiatric disorder, alcohol or 

substance abuse, and being a lesbian/gay/bisexual/transexual teen. The presence of a firearm in the 

household markedly increases (by 5-10 times) the suicide risk. 

d. What factors mitigate suicide risk? 

(1) Caring for dependent children 

(2) Strong religious beliefs that deter suicide 

(3) Evidence of planning for the future (being "future-oriented") 

(4) The ability to put in place an action plan for what to do if the suicidal thoughts return 

e. Is there access to lethal means? 

(1) Firearms are used in 53% of all completed suicides in the United States. Their presence in the home 

constitutes an independent risk factor for completed suicide. All suicidal patients should be asked 

about access to firearms. 

(2) Inquire as to whether the family can safely remove sharp objects and lock up medications. 

f. Consider less obvious presentations. 

(1) Repeated medical emergencies due to noncompliance with treatment may indicate silent suicide, the 

act of killing oneself slowly by nonviolent means. This is often unrecognized and is most common in 

the elderly. 

(2) "Unintentional" overdoses, wrist lacerations, self-inflicted gunshot wounds, falls from heights, and 

single-automobile collisions may represent occult suicide, ie, self-destructive acts disguised 

as accidents. 

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3. Treatment 

a. Patients at high risk of committing suicide should be hospitalized, and safeguards must be put in place 

to limit a patient's ability for self-harm while in the hospital. In-hospital suicides are the second most 

commonly reported sentinel event and occur at a rate of 5-15 per 100,000 admissions. 

b. After a suicide attempt, medical stabilization of toxicity or trauma is required, followed by the identification 

and treatment of any comorbid medical condition. Once the patient is medically stabilized, placement in a 

psychiatric hospital can be considered. 

c. While in the emergency room: 

(1) Search for weapons and pills with assistance of security personnel. 

(2) Constant observation of the patient must be provided, eg, through use of 1 :1 sitters. 

(3) Patients must not be permitted to leave before their assessment has been completed, and if found to 

be at risk of suicide or to lack decision-making capacity, they must not be permitted to leave against 

medical advice. 

(4) Involuntary admission may be required. 

d. Disposition 

(1) If the patient's suicide intent is serious, or you are unsure how serious the potential suicide risk is after 

your evaluation, obtain an emergent psychiatric consultation. 

(2) While mental health professionals may assist in the evaluation, the emergency physician is required 

to make an independent judgment and retains final responsibility for medical decisions. In particular, 

"denial of medical necessity" by a managed care organization or third-party payer does not override 

the physician's duty to render appropriate and adequate medical care, including, if necessary, 

involuntary admission. 

(3) Admission may be required if: 

(a) The patient will not (or cannot) cooperate with assessment 

(b) The crisis is ongoing or unresolved 

(c) After your evaluation (or a psychiatrist's), the patient is still considered a suicide risk 

(d) When in doubt, err on the side of caution. 

(4) Discharge to outpatient treatment may be considered if: 

(a) The patient is perceived to be at low risk of acting on suicidal thoughts (eg, if the patient has only 

passive thoughts of suicide, has no history of attempts, and is able to agree to a "safety plan") 

(b) The patient has adequate social support, and 

(c) 

Referral for close outpatient follow up has been arranged. 

(5) Patients who present after an actual suicide gesture (not just thoughts) are almost always referred 

for inpatient psychiatric treatment. Those with a gesture that is "low lethality" (eg, ingesting a small 

number of OTC tablets or superficial cuts on the dorsal surface of the arm) and "high rescue" (eg, 

took the ingestion in front of a family member) might be considered for potential discharge only if 

the above criteria are already met and the patient's family and outpatient providers are prepared to 

manage outpatient care. 

(6) Patients deemed high risk may decline voluntary hospitalization and may require an involuntary 

hold to protect their safety. State laws determine the specific criteria for involuntary hospitalization, 

the duration of time a patient can be held, and the process for court proceedings for extending the 

hospitalization. 

D. Mania and hypomania 

1. A "manic episode" is defined as an excessive, persistently elevated, expansive, or irritable mood and 3 or more 

of the fol lowing symptoms for ::,:1 week duration: 

a. Grandiosity or inflated self-esteem 

b. Decreased need for sleep (without fatigue) 

c. Pressured speech or increased talkativeness 

d. "Flight of ideas" (repeatedly jumping from one topic to another loosely related topic in conversation, or a 

subjective feeling that the mind is "racing") 

e. Distractibility 

f. Agitation or increase in goal-directed activity 

g. lmpulsivity ("excessive involvement in pleasurable activities that have a high potential for painful 

consequences," eg, spending sprees, hypersexual behavior, fights, foolish behavior at work; psychosis is 

possible, often with paranoid, grandiose, or religiose features) 

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2. A hypomanic episode is of less intense severity, has less impact on the patient's ability to function, and may 

last


f. Waxy flexibility: the examiner can move the patient's body position and the patient assumes the new position 

g. Negativism: the patient actively resists the examiner's attempts to move the patient 

3. Both medical and psychiatric etiologies 

a. Major depression 

b. Mania 

c. Chronic psychoses such as schizophrenia 

d. Stroke 

e. Cerebral tumors 

f. Encephalitis 

4. Malignant catatonia: catatonia accompanied by autonomic instability (hyperthermia, tachycardia, hypertension, 

or labile blood pressure); can be life threatening 

5. Treatment 

a. Benzodiazepines (particularly lorazepam) are the treatment of choice. An initial trial of lorazepam 1-2 mg 

can be administered orally, IM, or IV. Response should be seen within 1-2 hours. A second dose should be 

administered if there is no response after 3 hours. 

b. An initial positive response to lorazepam can confirm the diagnosis in many patients. 

c. If no response to benzodiazepine treatment, electroconvulsive therapy is the next recommended treatment 

of choice. 

d. If the catatonia is associated with an underlying psychiatric disorder, the patient responds to lorazepam, 

and his or her vital signs remain stable, psychiatric admission may be appropriate. 

e. Patients with malignant catatonia require medical hospitalization and may require treatment in the ICU. 

f. Antipsychotics should not be given while the patient is catatonic, because they may increase the likelihood 

of precipitating neuroleptic malignant syndrome. (Neuroleptic malignant syndrome and catatonia are 

believed to be related syndromes.) 

F. Panic attacks/disorder 


a. Common: apprehension, tremor, sweats/flushing/chills, shortness of breath, chest tightness or pain, 

palpitations or tachycardia, difficulty swallowing, nausea, lightheadedness, paresthesias, and a sense of 

depersonalization, derealization, and feelings of impending doom 

b. Patients believe that they are suffering from an acute medical problem (and physicians are required to 

believe that these patients are suffering from an acute medical problem until proven otherwise). 

c. Attacks usually begin suddenly, sometimes without provocation, and last


c. Immediate interventions aimed at reducing hyperventilation (such as having the patient lock his hands 

behind his neck) improve hypocapnia and respiratory alkalosis, and thus help to resolve paresthesias, 

lightheadedness, and derealization/depersonalization, as well as provide a reassuring sense of self-control. 

d. The most useful intervention is the communication to the patient that any potentially life-threatening 

medical disorder has indeed been excluded. During a panic attack, the patient feels that he or she is about 

to die (and, indeed, symptoms can be indistinguishable from an acute Ml). This is itself frightening, and the 

emotional reaction to the perceived life threat causes further sympathetic arousal, thus further exacerbating 

symptoms. 

G. Somatoform disorders 

1. Somatoform disorders include conversion disorder, somatization disorder, hypochondriasis, and pain disorder. 

These disorders are all characterized by psychological conflict that manifests either as physical symptoms or as 

concern about symptoms or illness. 

a. The link between psychological distress and physical symptoms may be apparent to the physician but is not 

realized by the patient. 

b. This is not malingering. Malingering is an intentional faking of symptoms for conscious personal gain such 

as obtaining drugs, avoiding legal responsibility, or gaining shelter in the hospital. 

c. This is not a factitious disorder in which symptoms are intentionally produced or feigned but with no 

motivation or incentive other than to assume the "sick role" (primary gain). 

d. Psychiatric consults may be of limited use for somatoform patients. The patient will not want (and may 

resent) this suggestion, because the somatoform symptom serves the purpose of masking a psychological 

conflict. 

2. Conversion disorder 

a. A psychological conflict "converts" into an acute loss of neurologic function that allows the patient to 

avoid or resolve the conflict; typical examples include loss of voluntary motor or sensory function (eg, 

paralysis of one or both legs), blindness, or nonepileptic seizures ("pseudoseizures"). 

b. Diagnostic criteria 

(1) Symptom(s) or deficit(s) of voluntary sensory or motor function suggesting a neurologic (or other 

medical) condition, eg, stroke 

(2) These symptoms/deficits are judged to be due to psychological factors, because conflicts or stressors 

precede their onset/exacerbation. 

(3) They are not intentionally produced or "faked." 

(4) No demonstrable source from a general medical disorder, substance use/abuse, or culture-specific 

pattern (This is a diagnosis of exclusion and should not be made without an appropriate medical 

evaluation to exclude physiologic causes of the symptoms.) 


(1) The patient appears healthy and may be less concerned about his or her symptoms than you would 

expect ("la belle indifference"). 

(2) The physical symptoms typically developed suddenly and involve a voluntary muscle function (most 

common) or loss of sensation. They also tend to have a relationship to the conflict they "solve" (eg, 

a man who hates his manual labor job develops "paralyzed" legs at home Sunday night). Ask the 

patient what it is that he or she cannot do now and what it was that he or she was doing when the 

symptoms began. 

d. Treatment 

(1) Perform a detailed history and physical examination, and obtain diagnostic studies as indicated to 

exclude medical/surgical pathology. 

(2) Once the evaluation is completed, assure the patient that a serious medical problem has not been 

discovered and suggest that the symptom will resolve. Most cases of conversion disorder resolve 

without intervention. 

(3) About 25%-50% of patients initially diagnosed with conversion disorder are eventually found to 

be suffering from significant medical pathology (systemic lupus erythematosus, multiple sclerosis, 

polymyositis, thyroid disease, porphyria, hypo- or hyperparathyroidism); therefore, referral for 

thorough evaluation and ongoing follow up is a must. 

3. Somatization disorder 

a. Patients present repeatedly to medical practice settings, including the emergency department, with multiple 

physiologic complaints. Psychologic conflict is manifest as physical complaints that gain the focus of the 

patient's attention. The review of physical systems will have positive findings in multiple organ systems. 

699


b. To meet diagnostic criteria, patients must have pain complaints on four body sites, two GI symptoms, one 

pseudoneurologic symptom, and one sexual symptom. 

c. Treatment is coordinated through an involved primary care physician. Appointments are scheduled at 

regular intervals, and discussions restricted to a limited number of complaints. 

d. Medical evaluation of physical symptoms should be thoughtfully selected and guided by objective findings. 

4. Hypochondriasis 

a. The patient intensely believes that he or she has a specific disease such as cancer or HIV. The patient 

presents with "evidence" of the disease and repeatedly requests testing. 

b. In hypochondriasis, the patient is concerned with disease, while in somatization disorder, the patient is 

concerned with symptoms. 

5. Somatoform pain disorder 

a. A patient presents with one or more pain symptoms that cause clinically significant distress or impairment. 

b. Psychological factors are believed to have an important role in the onset, severity, exacerbation, or 

maintenance of the pain. The patient may also have an underlying physiologic reason for the pain, but the 

pain is usually disproportionately more than what would be expected. 

c. The patient is experiencing real pain (ie, it is not faked) and usually believes it is due to a physical problem. 

d. This is difficult to detect in the emergency department. The physician may be concerned that the patient is 

"drug seeking" because of the disproportionate level of pain. Arranging continuity of care with a primary 

care provider may be of assistance to the patient. 

6. Psychophysiologic reactions 

a. A physical condition brought on by an event that is associated with a heavy emotional overlay, eg, nausea 

and diarrhea that occur before a performance. This is not a somatoform disorder but another example of a 

link between psychological factors and physical symptoms. 

b. Symptoms are real although engendered unconsciously; physiologic illness develops to express or resolve 

emotional conflict without the patient realizing it. These reactions can also be understood as "overflow" 

autonomic activation in response to a stimulus. 

c. Treat the medical condition without confronting the patient with the psychogenic cause. 

d. The reactive condition is not produced voluntarily or intentionally and is, in fact, realistically distressing/ 

handicapping to the patient. Gently suggest a stress-related emotional-physical connection. It may be 

possible to illustrate this by having the patient reenact the situation. 

e. These patients may benefit from psychotherapy or biofeedback. 

7. Techniques that distinguish neurologic from psychogenic deficits 

a. Bowlus-Currier test (sensation): Have the patient extend his or her arms, crossing them at the wrists, so the 

palms are facing each other; then have him or her interlock the fingers and rotate the hands inward toward 

the chest. In this position, false responses to sensory testing are difficult. 

b. Hoover test (motor): Cup your hands under the heels of the patient, and ask him to raise his or her normal 

leg. With pseudoparalysis, the other leg will push downward. 

c. Gray test (pain): Patients with abdominal pain that is psychological in origin will close their eyes on 

palpation of the abdomen (most patients with organic pain watch your hand in anticipation of pain). 

d. Bell phenomenon (coma): In true coma, the eyes remain neutral when the lids are opened; in conversion, 

the eyes are diverted upward. 

e. Corneal reflex: intact with pseudoseizure 

f. Optokinetic drum: nystagmus in pseudoblindness 

H. Insomnia and sleep disorders 

1. Insomnia is one of the most common medical complaints. Patients report difficulty falling or staying asleep, or 

not feeling rested the following day. 

2. Myriad causes of sleep disturbance exist and include the following: 

a. Psychophysiologic insomnia (also called primary insomnia): the patient becomes increasingly concerned 

about the delay in falling sleep, which leads to an increase in anxiety and greater delay in sleep onset. 

b. Extrinsic factors 

(1) Poor sleep hygiene (eg, TV and lights remain on at night) 

(2) Shift-work sleep disorder 

(3) Jet lag 

c. Psychological contributors include mood disturbances (eg, mania or major depression) and anticipatory 

anxiety (eg, about an exam). 

700


d. Alcohol and other substances directly disrupt the sleep-wake cycle. 

e. Medical problems can impair sleep, eg, obstructive sleep apnea, restless legs syndrome, orthopnea, 

physical pain. 

3. Treatment 

a. Treatment of insomnia focuses on identification and treatment of the underlying pathology (eg, obstructive 

sleep apnea, depression). However, this is not always possible in the emergency room setting. 

b. Sleep hygiene education should be provided. Patients should avoid caffeine, exercise, and alcohol in the 

evening, and they should go to bed and rise at the same time every day. The bedroom should be restricted 

to use for sleep and sex, and televisions should be removed from the room. 

c. Sleep aids can be useful for acute insomnia. They generally should not be used for >2 weeks, because 

tolerance and withdrawal can develop. 

(1) Zolpidem 5-10 mg is often used to treat insomnia. Adverse effects include increased risk of 

parasomnias (eg, sleep walking). 

(2) Long-acting benzodiazepines are used for those with middle-of-the-night insomnia. 

(3) Melatonin, a hormone produced by the pineal gland that triggers natural onset of sleep, is often 

recommended for jet lag. It is available OTC. 

(4) OTC sleep aids (eg, diphenhydramine) have limited effectiveness and make use of sedating, 

antihistamine effects. 

d. Patients presenting to the emergency department with insomnia should follow up with their primary care 

provider. 

I. Eating disorders 

1 . Anorexia nervosa 

a. Prevalence is approximately 1 % in Western societies; women are most commonly affected (95%), 

particularly those from middle and upper socioeconomic classes. 

b. Onset generally occurs between 12 and 18 years of age and usually follows an episode of severe dieting or 

other weight loss. 

c. The central characteristic is a preoccupying fear of being overweight that does not diminish with weight loss. 

It may or may not be associated with purging behaviors (self-induced vomiting, or laxative or diuretic abuse). 

d. Prognosis improves with earlier onset, diagnosis, and treatment. Chronicity increases morbidity. 

e. Mortality at 10-year follow-up is 7%; at 30-year follow-up, 18%. 

f. Diagnostic criteria 

(1) Weight 15% ideal body weight is sufficient to 

hospitalize) 

701


(b) Hypokalemia 

(c) 

Hyponatremia 

(d) Bradycarclia with heart rate


(5) Diuretic abuse can cause: 

(a) 

Dehydration 

(b) Hypokalemia, hypercalcemia, hyperuricemia, hypomagnesemia, and hyponatremia 

(6) Binge eating after a period of starvation has further complications. 

h. Treatment 

(a) Acute gastric distention (even rupture) 

(b) Acute pancreatitis (mortality 10%) 

(1) Normotensive, hypokalemic, hypochloremic metabolic alkalosis is a typical manifestation of chronic 

purging. The patient has usually adapted physiologically to this state. Overzealous efforts at treatment 

frequently lead to overcorrection and fluid overload (which can be dangerous). 

(2) Nutritional rehabilitation: normalization of the eating pattern is the primary consideration. 

(3) Medical admission is indicated for: 

(a) Vital sign abnormalities 

(b) Hypokalemia 

(c) Hyponatremia 

(d) Comorbid medical disorder (eg, diabetes, particularly in a patient who is withholding insulin as a 

means of losing weight) 

(4) Psychiatric admission may be indicated when: 

(a) Severe psychiatric illness or comorbid suicidality 

(b) Worsening ability to control self-induced vomiting, binge eating, or diuretic/laxative use, which 

may be life threatening 

(c) The patient's binging, purging, or obsessive thoughts leads him or her to be uncooperative with 

lower levels of treatment. 

(5) Definitive treatment after medical stabilization requires cognitive-behavioral psychotherapy and/or 

antidepressant medication (an SSRI); combining both psychotherapy and medication may enhance 

treatment efficacy. 

J. Intoxication and withdrawal 

1. Intoxication: impairment of judgment, perception, attention, emotional control, and psychomotor activity 

produced by recent ingestion of a drug 

a. Clinical presentation is predominately impaired judgment and motor coordination. With increasing 

severity, delirium, stupor, coma, and death may occur. 

b. Intoxication should be included in the differential diagnosis of any patient with an altered state of 

consciousness. 

2. Urine drug screens do not have perfect sensitivity. Watch for false-negatives (oxycodone and methylphenidate 

are often not detected) or false-positives (eg, pseudoephedrine showing positive for amphetamines). 

3. Treatment should be guided by the following principles: 

a. Provision of general supportive measures that include the ABC priorities 

b. Specific measures to remove toxic substances or substances that have been ingested in toxic amounts 

c. Exclusion of other serious medical, surgical, or psychiatric disorders 

d. Appropriate referral-substance abuse is a chronic and episodic disorder, and effective treatment is available. 

4. Alcohol or other sedative-hypnotics (benzodiazepines) 


(1) Symptoms include an initial feeling of euphoria and disinhibition, followed by slurred speech and 

ataxia. New memories are not encoded into memory (anterograde amnesia). More severe intoxication 

may present with either agitation or sedation. 

(2) Degree of impairment depends on total alcohol consumption and also previous exposure (tolerance). 

"Legal limit" for driving in most states is a blood alcohol level of 0.08 gldl. 

(3) If tranquilization is required, use of additional sedativehypnotic medications (such as lorazepam) 

should be avoided. An antipsychotic (eg, haloperidol 5 mg or chlorpromazine 25-50 mg orally or IM 

every 30-60 minutes) is a safer choice because these contribute little to respiratory depression. 

(4) Treatment of alcohol intoxication requires placement in a secure setting and allowing time to pass 

for the patient to metabolize the alcohol. If large quantities of alcohol have been rapidly ingested, 

intubation may be required for airway protection. 

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b. Withdrawal 

(1) For a person with an average rate of alcohol metabolism, the blood alcohol level will drop by ~0.02 

g/dl per hour. 

(2) A seasoned alcoholic may begin to show alcohol withdrawal with a blood alcohol content well above 

the "legal limit." 

(3) Withdrawal symptoms: 6-24 hours from the last drink, patients experience a high-amplitude tremor 

and autonomic hyperactivity (nausea, tremor, hypertension, tachycardia, hyperreflexia, sleep 

disturbances, and anxiety) 

(4) Withdrawal seizures: generalized tonic-clonic seizures that usually occur 12-48 hours from last 

drink. Indications for CT of the head in patients who have seizures: 

(a) New-onset seizure 

(b) Focal seizure 

(c) Focal neurologic deficit 

(d) Status epilepticus 

(e) With significant head trauma 

(5) Alcohol withdrawal delirium (delirium tremens): delirium (characterized by an altered level of 

consciousness, disorientation, confusion, and often visual hallucinations) with onset 3-5 days after 

last drink. Autonomic instability with gross tremor, fever, incontinence, mydriasis, and frightening 

visual hallucinations may occur, leading to substantial mortality and often requiring ICU admission. 

(6) Alcohol withdrawal is treated with benzodiazepines. Lorazepam is metabolized by hepatic 

glucuronidation and does not require metabolism by hepatic oxidation and, therefore, is preferred 

for patients with hepatic dysfunction. Patients with liver disease and the elderly have decreased 

ability to oxidize benzodiazepines. Longer-acting agents (chlordiazepoxide or diazepam) are also 

used. Benzodiazepine dosages are based on the patient's Clinical Institute Withdrawal Assessment 

(CIWA) score. 

(a) These patients are generally volume-depleted, hypomagnesemic, malnourished, and 

hypoglycemic. Provide IV hydration (D5NS), thiamine 100 mg, and magnesium 2-4 g. 

(b) Do not administer glucose or other carbohydrate before replacing thiamine (IV); doing so can 

precipitate Wernicke encephalopathy and/or Korsakoff syndrome with brain damage that is 

frequently permanently disabling. 

(7) Disposition is determined by the patient's stage of withdrawal and history of complicated withdrawals. 

(a) Patients in early withdrawal (autonomic hyperactivity) who respond to emergency department 

treatment can often be managed as outpatients or in a dedicated detoxification/substance abuse 

center. These patients may require 1-2 days of therapy with a long-acting benzodiazepine. This is 

controversial, because these medications may mask symptoms of a medical problem or may be 

sold on the street. Close follow-up is required. 

(b) Patients may require medical admission for alcohol withdrawal if they have a history of 

complicated withdrawals (including delirium or seizures) or if their presenting symptoms cannot 

be controlled with oral benzodiazepines. The presence of seizures, hallucinations, delirium, or 

signs of Wernicke encephalopathy merits a medical admission. 

5. Opioids (including heroin, oxycodone, hydrocodone, hydromorphone, morphine, meperidine, opium, 

methadone) 


(1) Toxidrome includes somnolence, decreased respiration rate, decreased tidal volume, decreased bowel 

sounds, and miotic pupils. The absence of miotic pupils does not exclude opioids as the cause of a 

change in mental status. 

(2) Usual presentation in the emergency department is of a person who has overdosed and may have 

received naloxone in the field. Accidental overdose of opioids is rising rapidly as a cause of death in 

the United States. 

(3) Naloxone is a competitive opioid antagonist that quickly reverses the effects of opioid intoxication. It 

can be given IV, IM, SC, or by nasal spray. Usual doses are 0.4-2 mg, and it can be repeated up to 10 

mg. Effects of naloxone last for 30-60 minutes, so repeated dosing may be needed. 

(4) Opioid-addicted individuals may also present to the emergency department with medical 

complications of their drug use, eg, cellulitis or abscesses from "skin popping" (injecting heroin 

subcutaneously). 

704


b. Withdrawal 

(1) Unlike alcohol withdrawal, opioid withdrawal is unlikely to be life threatening. 

(2) Symptoms include muscle aches, abdominal cramps, malaise, nausea, yawning, rhinorrhea, 

piloerection, diarrhea, sweats, and chills. 

(3) Vital signs are often normal, although the patient may be tachycardic or hypertensive due to physical 

discomfort or pain. 

(4) Opioid withdrawal is treated symptomatically, for example: 

(a) Clonidine to decrease adrenergic tone, which results in many withdrawal symptoms 

(b) Ibuprofen for muscle aches 

(c) Dicyclomine for abdominal cramps 

(d) lmodium for diarrhea 

(e) Buprenorphine (sometimes)-Caution should be used in giving buprenorphine too soon after 

last opioid use, in particular with long-acting opioids such as methadone. Because it is a partial 

agonist that binds strongly to the mu receptor, buprenorphine may precipitate withdrawal if 

given too soon. 

(5) Medical admission is usually not warranted. 

6. Cocaine, bath salts, and other psychostimulants (amphetamine, methamphetamine, methylphenidate 


(1) Cocaine can be snorted as powder, injected, or smoked as crack-cocaine. Effects usually last


2. Patients with dementia are predisposed to bouts of delirium. For these patients, differentiating between delirium 

and dementia requires knowledge of the patient's baseline mental state. 

3. Delirium 

a. Diagnostic features 

(1) Disturbance of consciousness with reduced ability to focus, sustain, or shift attention. 

(2) Cognitive impairment (eg, memory deficit, disorientation, dysphasia) or perceptual disturbance 

(3) Acute onset (hours to days) with diurnal fluctuation of symptoms 

(4) Physiologic result of a general medical condition 


(1) Fluctuating level of consciousness and alertness 

(2) Trouble paying attention; ask the patient to state the days of the week backward (a delirious patient 

will often state them forward) 

(3) May be characterized by hyperactive or hypoactive motor activity 

(4) Visual hallucinations (common) 

c. Search for underlying cause. 

(1) Metabolic disorders 

(2) CNS injury or mass lesion 

(3) Infection (CNS or elsewhere) 

(4) Medication effects/interactions 

(5) Drugs, heavy metals, toxins, poisons 

d. Treatment revolves around correction of underlying cause. 

(1) Patients with delirium are hospitalized in a medical facility because of their underlying medical illness. 

(2) If the cause of delirium is not determined in the emergency department, these patients are 

hospitalized to determine the underlying cause. 

4. Dementia: a global and progressive impairment of cognitive function without an alteration of consciousness 

a. Diagnostic features: multiple cognitive deficits with both 

(1) Memory impairment (either ability to learn or recall) and 

(2) At least one other cognitive disturbance 

(a) Aphasia (language deficits) 

(b) Apraxia (inability to perform known tasks) 

(c) Agnosia ("not knowing") 

(d) Impaired executive function (planning, organizing, sequencing, abstracting) 


(1) Gradual onset (months or years) 

(2) Disturbance of recent memory may be the first sign. 

(3) Dementia may become acutely worse in response to another illness, change in living situation, or 

medications. 

(4) Common causes of reversible dementia 

c. Treatment 

(a) Metabolic and endocrine disorders 

i. Hypothyroidism 

ii. 8 12 

deficiency 

(b) Normal pressure hydrocephalus 

(c) Depression (depressive "pseudodementia") should be suspected if onset was relatively acute 

and accompanied by vegetative signs of depression (eg, loss of appetite and weight, sleep 

disturbances, etc). Reversible medical/surgical causes must be excluded. 

(d) Medication effects 

i. Anticholinergic medications 

ii. Polypharmacy 

iii. Incorrect medication usage (demented patients may take medications incorrectly) 

(1) Initial treatment focuses on correcting reversible causes of dementia and reviewing the drug regimen 

to identify medications that may exacerbate the cognitive symptoms. 

706


(2) The progression of the dementia may be slowed by modulating risk factors (eg, treating hypertension in 

vascular dementia) or use of anticholinesterase inhibitors (eg, donepezil). 

(3) Discussions about advance directives, power of attorney, code status, and long-term care wishes 

should be started (if not done already) at the onset of the diagnosis, while patients still have capacity to 

make these decision for themselves. 

L. "Medical mimickers" of psychiatric illness (medical illnesses that manifest psychiatric symptoms) 

1. Acute intermittent porphyria 

a. Presents as episodic psychosis (with agitation and hallucinations) and acute abdominal pain 

b. Neurologic symptoms are due to accumulation of early heme precursors due to a deficiency of 

porphobilinogen deaminase. 

c. Attacks are precipitated by drugs, hormones, and diet that stress the hepatic aminolevulinic acid synthase 

and cytochrome P450 systems. Offenders include barbiturates and other anticonvulsants, sulfonamide 

antibiotics, low-calorie and low-carbohydrate diets, alcohol abuse, progesterone/progestins, and 

nonspecific severe stress. 

d. Diagnosis is made by laboratory quantification of urinary aminolevulinic acid and porphobilinogen, 

which are markedly increased during attacks and between recurring attacks. Urine dipstick urobilinogen 

tests are nonspecific, and urine exposed to sunlight turns dark or red in color. 

e. Treatment is primarily supportive. Patients may be admitted and observed for neurologic complications. 

2. Hyperthyroidism 

a. Symptoms include anxiety, emotional !ability, weakness, tremor, palpitations, heat intolerance, increased 

perspiration, and weight loss despite a normal or increased appetite. 

b. Physical examination may be notable for hyperactivity, rapid speech, and lid retraction, which may make 

the patient appear to be staring. 

c. Diagnosis is made on the basis of thyroid function tests. Thyroid-stimulating hormone is usually

PSYCHOBEHAVIORAL DISORDERS: PRACTICE CLINICAL SCENARIOS 

PSYCHOBEHAVIORAL DISORDERS: PRACTICE CLINICAL 

SCENARIOS 


Scenario A 

Presentation: A 48-year-old man is brought in by EMS after he was found crawling in the hallway of 

his apartment building toward his door, and then laying against the wall. He admits to alcohol use and 

smoking marijuana. He is given IV fluids and thiamine. His alcohol level is 0.39 gldL. The patient is given 

IV fluids, a meal tray, and observed. He is on the monitor, and the nurse comes to you noting that the 

patient is becoming agitated and tachycardic. As you walk toward the room, the patient begins to seize. 


Scenario B 

Presentation: A 21-year-old law student presents to the emergency department the night before his final 

exams with inability to move his fingers. On discussion with the patient, you find he will not be able to 

take his computer-based final exam tomorrow because of this paralysis. 


Scenario C 

Presentation: A 24-year-old male patient with a history of depression and psychosis presents to the 

emergency department with his mother. She says that he has been having excited outbursts at home over 

the last few days. Today, he is stuporous and is not engaging in the history or physical examination. When 

you perform a neurologic examination, the patient resists any movement of his extremities. 


Scenario D 

Presentation: A 66-year-old physician is brought to the emergency department with fatigue, sadness, 

difficulty concentrating, and suicidal ideation. His symptoms started about 6-9 months ago. He is an avid 

hunter. He has recently lost his practice because of questions from the medical board about his prescribing 

habits. His wife left him last year, because she couldn't handle the investigation by the medical board. He 

admits to alcohol use and is drinking at least a bottle of wine daily. 

What is the diagnosis, and what are the patient's risk factors for suicide? 

Scenario E 

Presentation: A 54-year-old woman is brought to the emergency department by her husband. She has a 

history of bipolar disorder and takes daily medications. Lately, she has been more tired, confused, and 

has had nausea and diarrhea. She was recently started on furosemide by her primary care provider for 

hypertension. On examination, she has a coarse tremor. 


708

PSYCHOBEHAVIORAL DISORDERS: PRACTICE CLINICAL SCENARIOS 


Scenario A 

Diagnosis: alcohol withdrawal seizures 

Management: Administer IV benzodiazepines (lorazepam is the preferred agent) and titrate to response, 

and consider scheduled dosing of IV benzodiazepines in addition to following the patient's symptoms 

of withdrawal for as-needed dosing. Also consider giving thiamine (100 mg), magnesium (2-4 g), and IV 

hydration with dextrose-containing fluids. 

Scenario B 

Diagnosis: conversion disorder 

Management: Provide reassurance that there is no serious medical problem, and suggest that the symptoms 

will resolve. Refer for medical evaluation, because 25%-50% of patients diagnosed with conversion 

disorder are found later to have medical illness that requires treatment, even if it does not require emergent 

care. 

Scenario C 

Diagnosis: ca ta ton ia 

Management: Administer IV benzodiazepines, in particular lorazepam 1-2 mg every 3 hours for 2 or 3 

doses and observe for response. If the patient responds to the benzodiazepines, he would still require 

admission for further treatment. If the patient does not respond to medical management, ECT is the secondline 

therapy. 

Scenario D 

Diagnosis: major depressive disorder 

Diagnostic evaluation: This patient's risk factors for suicide include access to guns, male sex, age, marital 

status, recent loss of job license, and alcohol abuse. Evaluation in the emergency department includes a 

drug screen in most cases, observation by a sitter, and search for weapons and/or pills with the assistance 

of security if needed. Remember that the second most common sentinel event resulting in in-hospital 

mortality is in-hospital suicide. 

Management: Admit for in-patient treatment of depression. 

Scenario E 

Diagnosis: lithium toxicity, likely caused by recent initiation of diuretic 

Diagnostic evaluation: Laboratory tests include a lithium level, serum biochemical screen, and urinalysis. 

A creatinine level is key, because lithium is renally excreted. 

Management: Administer IV fluids, and hold lithium and diuretic. If the lithium level is >4 mEq/L 

(regardless of symptoms) or >2.5 mEq/L with symptoms, the patient should have emergency dialysis. 

709

710 

NOTES

HEMATOLOGIC DISORDERS 


Recognition of Bleeding Disorders ............................................................................................................................ 714 

Pathophysiology of Hemostasis .......................................................................................................................... 714 

Laboratory Tests for Evaluation of Hemostasis .................................................................................................... 714 

Bleeding Disorders and Their Clinical Parameters ............................................................................................... 717 

Bleeding Disorders Associated with Platelet Function Problems and/or a Decreased Platelet Count ........................ 718 

Platelet Disorders .............................................................................................................................................. 718 

Heparin-Induced Thrombocytopenia .................................................................................................................. 721 

Disseminated lntravascular Coagulation ............................................................................................................. 723 

Bleeding (Coagulation) Disorders Associated with an Increased Partial Thromboplastin Time and Normal 

Prothrombin Time ..................................................................................................................................................... 724 

Hemophilia ........................................................................................................................................................ 724 

von Willebrand Disease ..................................................................................................................................... 725 

Sickle Cell Disease .................................................................................................................................................... 725 

Anemia ...................................................................................................................................................................... 728 

General Approach .............................................................................................................................................. 728 



Nonhereditary Anemia: Hemolytic Anemia ........................................................................................................ 731 

Acquired Nonhemolytic Anemias ....................................................................................................................... 731 

Hereditary Anemia ............................................................................................................................................. 732 

Blood Transfusions .................................................................................................................................................... 733 

Transfusion of Specific Blood Products ............................................................................................................... 733 

Transfusion Methods .......................................................................................................................................... 734 

Complications .................................................................................................................................................... 734 

Reversal of Drug-Induced Anticoagulation ............................................................................................................... 735 

Reversal ofWarfarin-lnduced Coagulopathy ....................................................................................................... 735 

Reversal of Heparin and Low-Molecular-Weight Heparin ................................................................................... 737 

Reversal of Newer Anticoagulants ...................................................................................................................... 738 

Reversal ofThrombolysis .................................................................................................................................... 738 

711

HEMATOLOGIC DISORDERS: SELF-ASSESSMENT QUESTIONS 


1. All of the following factors are vitamin K-dependent except: 

(a) 

II 

(b) VII 

(c) 

IX 

(d) XI 

2. Isolated prolongation of the prothrombin time may be seen in each of the following patients except: 

(a) Patients taking warfarin 

(b) Patients with liver disease 

(c) Patients with vitamin K deficiency 

(d) Patients with hemophilia 

3. The test that is most appropriate for evaluating the tissue factor pathway (extrinsic) is: 

(a) Platelet aggregation studies 

(b) Prothrombin time 

(c) Thrombin time 

(d) Partial thromboplastin time 

4. All of the following laboratory findings are consistent with disseminated intravascular coagulation except: 

(a) 

Increased fibrinogen level 

(b) Decreased platelets 

(c) Fragmented RBCs and anemia 

(d) Increased fibrin split products 

5. The laboratory test that distinguishes hemophilia A and B from von Willebrand disease is: 

(a) 

Partial thromboplastin time 

(b) Platelet function studies 

(c) Prothrombin time 

(d) Platelet count 

6. Which of the following is effective in treating hemophilia A, hemophilia B, and von Willebrand disease (although 

not necessarily the therapy of choice)? 

(a) 

Cryoprecipitate 

(b) DDAVP 

(c) Prothrombin complex 

(d) Fresh frozen plasma 

7. Which of the following labile clotting factors are most depleted in a stored unit of blood? 

(a) 

Factors VIII and I 

(b) Factors VIII and V 

(c) Factors VII and V 

(d) Factors IX and XI 

8. Al I of the following statements regarding cryoprecipitate are true except: 

(a) It is effective in treating all types of von Willebrand disease. 

(b) It contains large quantities of factors I, VIII, and IX. 

(c) Use of this product is associated with risk of transmission of the AIDS and hepatitis viruses. 

(d) Although not the therapy of choice, it is effective in treatment of hemophilia A. 

9. Which of the following statements about aplastic crisis in sickle cell patients is inaccurate? 

(a) It is frequently precipitated by an infection. 

(b) Patients complain of abdominal pain, and physical examination reveals splenomegaly. 

(c) The diagnosis is suggested by the presence of a decreased reticulocyte count and a low hemoglobin. 

(d) Patients are usually shocky and require oxygen, folic acid, fluid resuscitation, and transfusion. 

712


10. The most accurate test for evaluating the adequacy of anticoagulation in a patient on chronic warfarin therapy is: 

(a) Prothrombin time 

(b) Partial thromboplastin time 

(c) INR 

(d) The prothrombin time and INR are of equal accuracy in such a patient and can be used interchangeably. 

11. A 7-year-old white boy is brought in from summer camp for evaluation of a head injury. The counselor 

accompanying him reports that the boy was accidentally struck in the head with a bat. The injury occurred about 30 

minutes ago and according to the counselor, the boy now seems somewhat more lethargic. The counselor also states 

that the child has hemophilia A. Examination reveals a frontal hematoma and a resolving hemarthrosis of the left 

knee. You decide to immediately administer factor VIII concentrate to this child in whom you suspect CNS bleeding. 

The most appropriate dosage of factor VI II concentrate is: 

(a) 

18 units/kg 

(b) 26 units/kg 

(c) 50 units/kg 

(d) Cannot be determined from the information given 

12. A 40-year-old woman presents with easy bruising, gingival bleeding when she brushes her teeth, and menorrhagia. 

Examination reveals multiple purpuric lesions that are particularly prevalent on the lower extremities, but there 

is no active bleeding. Laboratory findings include a platelet count of 25,000/mm3, a hemoglobin of 12.8 g!dL, a 

BUN of 15 mg/dL, a creatinine of 0.8, and a normal prothrombin time (INR)/partial thromboplastin time. The most 

appropriate initial therapy is: 

(a) Platelet transfusion 

(b) Plasmapheresis 

(c) Corticosteroids 

(d) Immediate splenectomy 

13. A 50-year-old-man presents with profuse rectal bleeding. He is currently on warfarin, and his INR is 5.2. His 

hemoglobin is 10.2 g/dl. The most appropriate initial therapy is: 

(a) Platelet transfusion 

(b) IV vitamin K 

(c) DDAVP 

(d) Cryoprecipitate 

14. Which of the following statements about anticoagulation reversal is false? 

(a) Owing to the risk of anaphylaxis, vitamin K should not be given IV. 

(b) Prothrombin complex concentrate (PCC) is indicated for the reversal of warfarin in patients with an increased 

INR who are bleeding. 

(c) Although not FDA approved, factor Vil inhibitor bypassing activity (FEIBA) has been shown in small studies to 

reverse the anticoagulant effects of dabigatran and rivaroxaban. 

(d) Protamine can partially reverse the effects of low-molecular-weight heparin (LMWH). 

15. A patient presents with progressive fatigue and shortness of breath. Laboratory studies show a hemoglobin of 8 g/dl, 

WBC count of 8.3 x10 9 /L, and a platelet count of 21 0/mm 3 . Her reticulocyte count is increased, and her serum 

haptoglobin is low. She has a total bilirubin of 4 and a direct bilirubin of 1.2. What is the most likely cause of the 

anemia? 

(a) Hemolysis 

(b) Iron deficiency 

(c) Thrombotic thrombocytopenia purpura 

(d) Bone marrow failure 

ANSWERS 

I. d 4. a 7. b 10. C 13. b 

2. d 5. b 8. b 11. c 14. a 

3. b 6. d 9. b 12. c 15. a 



713


I. RECOGNITION OF BLEEDING DISORDERS 

A. Pathophysiology of hemostasis 

1. Hemostasis is a balance between excessive bleeding and thrombosis. It occurs when four components (listed 

below) interact synergistically with one another. If a component is not functioning normally, or it fails to 

interact appropriately with another component, excessive bleeding or clotting occurs. 

Contact Activation Pathway 

(Intrinsic) 

Deficiency = 

Hemophilia A 

• 

. 

. 

Deficiency = 

Hemophilia B 

Tissue Factor Pathway 

(Extrinsic) 

COMMON PATHWAY 

Thrombin (II) 

Thrombin 

Fibrin 

Ogen (I) 

Coagulation Very Simplified 

Courtesy of Colin Kaide, MD 

2. Components of hemostasis 

a. Vascular integrity: primary 

b. Platelet function: primary 

c. Coagulation factors: secondary 

d. Fibri nolysis 

3. Bleeding disorders result from a defect in one or more of the components of hemostasis. 

a. Inflammation of blood vessel walls, or a defect in the vessel supportive connective tissue, causes increased 

aggregation of platelets at the vessel site but does not affect the total number of circulating platelets. 

Bleeding, therefore, is localized to the vessel site. 

b. Platelet function depends on an adequate number of circulating platelets, as well as normally functioning 

platelets. Bleeding results when either the count is low or the function is abnormal. 

c. Coagulation factors are activated by substances in injured tissue that set off a series of steps that terminate 

in the formation of a fibrin clot. If there is an inadequate amount of one or more factors, or if a factor is 

abnormal, this series of steps is disrupted, thus preventing formation of a fibrin clot. 

d. Fibrinolysis normally results in dissolution of the fibrin clot as the vascular defect is repaired. Excessive 

fibrinolysis causes bleeding by functionally altering coagulation factors or by inducing excessive 

consumption of coagulation factors. 

B. Laboratory tests for evaluation of hemostasis 

1 . Platelet count 

a. Normal range: 150,000-400,000/mm 3 

b. Decreased in any condition that causes destruction, sequestration, or decreased production of platelets: 

714


(1) Idiopathic (autoimmune) thrombocytopenic purpura (ITP) 

(2) Thrombotic thrombocytopenic purpura (TTP) 

(3) Leukemia 

(4) Bone marrow suppression/replacement 

(5) Drug/toxic effect 

(6) Hypersplenism 

(7) Disseminated intravascular coagulation (DIC) 

(8) HIV infection 

(9) Sepsis (especially gram-negative sepsis) 

(10) Aplastic/hypoplastic anemia 

c. Post-traumatic bleeding occurs if the platelet count falls below 50,000/mm 3 ; spontaneous, lifethreatening 

hemorrhage can occur when the platelet count falls below 10,000-20,000/mm 3 • 

d. As many as 50% of patients with unexplained thrombocytosis (t platelet count) have an underlying 

malignancy. 

2. Testing of platelet function 

a. Bleeding time is no longer used clinically and is mentioned here only for historical purposes. It measures 

the time between skin incision and cessation of bleeding. Duration of this type of bleeding depends on 

the integrity of primary hemostasis (platelets, von Willebrand factor) and is independent of coagulation. 

b. Platelet function testing is not routinely used and has limited utility in the emergency department. 

(However, the emergency physician may come across these tests and their results and should at 

least be familiar with the concept.) It has replaced bleeding time as the test of choice for evaluating 

platelet activity. Platelet aggregation studies can confirm the inhibitory effects of ASA, thienopyridines 

(ticlopidine, clopidogrel), 13-lactam antibiotics, and other factors on platelet function. 

c. Platelet function tests measure platelet aggregation after exposure to a panel of agonists, which may 

include ADP, epinephrine, collagen, arachidonic acid, ristocetin, and thrombin. The pattern obtained 

allows for the diagnosis and classification of the platelet defect. 

3. Prothrombin time (PT) 

a. Tests the factors of the tissue factor (extrinsic) pathway (primarily factor VII) and the common pathway 

(X, V, II, and I). 

b. Normal control values are 10-12 seconds. 

c. Prolongation of PT c':2 seconds is considered significant. 

d. Increased PT (with a normal PTT) results from a deficiency of factor VI I. Causes of factor VII deficiency are: 

(1) Hereditary (rare) 

(2) Acquired secondary to: 

(a) Vitamin K deficiency 

(b) Warfarin use 

(c) Liver disease 

(3) Although the PT is very useful in evaluating patients with hemostatic abnormalities, it should not 

be used to monitor the adequacy of anticoagulation with warfarin. The response of the PT to a 

dose of warfarin is very dependent on the thromboplastin used in the assay, which varies from 

laboratory to laboratory. Thus, reliance on the PT alone in these patients can result in excessive or 

suboptimal anticoagulation and an increased risk of bleeding complications. For this reason, it is now 

recommended that the international normalized ratio (INR) be used to monitor these patients. 

4. INR 

a. The INR is the PT ratio that would be obtained if the World Health Organization's reference 

thromboplastin had been used. 

b. It is the test of choice for monitoring the adequacy of anticoagulation in patients taking warfarin. 

c. An INR of 1 is normal. 

d. An INR of 2-3 is considered to be therapeutic for most patients, while an INR of 2.5-3.5 is recommended 

for patients with mechanical prosthetic valves and recurrent embolization. 

5. Partial thromboplastin time (PTT) 

a. Essentially tests all of the factors except VII and XIII but is used primarily to evaluate the factors of the 

contact activation (intrinsic) pathway; it tests components of both the contact activation (intrinsic) and 

common pathways. 

b. Normal control values range from 25 to 35 seconds. 

715


c. A prolongation of 8-1 0 seconds above normal is considered significant. 

d. Increased PTT (with a normal PT) is seen with: 

(1) Factor VIII, IX, or XI deficiency (primarily) 

(2) Factor XII deficiency (asymptomatic) 

(3) Heparin therapy 

e. It is common to see the PTT reported as "aPTT," which stands for activated partial thromboplastin time, 

called this because an "activating" agent (kaolin) was added to the plasma before the test was run. 

f. When laboratory tests reveal an increased PT and increased PTT, this indicates an abnormality primarily 

in the common pathway (associated abnormalities of the intrinsic and extrinsic pathways may also be 

present). 

(1) Heparin overdose (factors X and 11 are primary sites of action) 

(2) Warfarin overdose (inhibits factors II, VII, IX, and X) 

(3) Vitamin K deficiency and moderate to severe liver disease (inhibit production of factors II, VII, IX, 

and X) 

(4) DIC (consumes factors I, V, VIII, and XIII) 

(5) Functional abnormality or deficiency of fibrinogen (factor I) 

(6) Massive transfusion of stored blood (deficient in factors V, VIII) 

(7) Thrombolytic therapy 

6. Thrombin time 

a. Tests the ability of fibrinogen (factor I) to convert into a fibrin clot. This is a useful screening test for both 

qualitative and quantitative abnormalities of fibrinogen. 

b. Increased thrombin time is seen with: 

(1) Hypofibrinogenemia 

(2) Myeloma, macroglobulinemia (interferes with fibrin polymerization) 

(3) Heparin therapy (inhibits fibrinogen formation) 

(4) DIC (consumes fibrinogen) 

(5) Liver disease 

(6) Uremia 

7. Fibrinogen degradation products test for specific degradation products of fibrin. Increased levels are seen 

with consumption coagulopathies (eg, DIC) and thrombolytic agent therapy. 

716


C. Bleeding disorders and their clinical parameters 

Table 43: Clinical Parameters of Hemostatic Disorders 

Hemostatic 

Platelet 

Function 

Disorder Clinical Findings Studies Platelets PT PTT Fibrinogen Clinical Disorder 

Primary hemostasis: platelet mediated 

Thrombocytopenia Purpura; petechiae; Normal Normal Normal Normal ITP, TTP, hemolytic 

epistaxis; GI, GU, 

uremic syndrome, 

and menstrual 

heparin-induced 

bleeding 

thrombocytopenia 

(abnormal PTT if 

still on heparin), 

others 

Platelet dysfunction Purpura; petechiae; Abnormal Normal Normal Normal Normal ASA, clopidogrel, 

epistaxis; GI, GU, 

ticlopidine, 

and menstrual 

inherited disorders, 

bleeding 

others 

von Willebrand Purpura; petechiae; Abnormal Normal Normal Normal Normal von Willebrand 

disease epistaxis; GI, GU, to t' disease 

and menstrual 

bleeding; 

hemarthrosis and 

muscular bleedinga 

Secondary hemostasis: coagulation 

Warfarin therapy Normal Normal Normal Normal Warfarin therapy, 

to fb 

rat poison 

(brodifacoum, 

others) 

Heparin Normal Normal Normal Normal Heparin therapy 

Low-molecularweight 

heparin 

(LMWH) 

Intramuscular, 

intracranial, GI, 

postoperative, and 

traumatic bleeding 

Normal Normal Normal Normal to Normal Enoxaparin, 

mildly t' 

dalteparin, 

fondaparinux, 

tinzaparin 

Hemophilia A Normal Normal Normal Normal Factor VIII levels 

decreased 

Hemophilia B Normal Normal Normal Normal Factor IX levels 

(Christmas disease) 

decreased 

Combined disorders of platelets and coagulation 

Disseminated Thrombosis, Normal td Sepsis, trauma, 

i ntravascu lar microangiopathic burns, acute 

coagulation hemolytic anemia, promyelocytic 

bleeding (purpura; 

leukemia, amniotic 

petechiae; epistaxis; 

fluid embolism, 

GI, GU, menstrual, 

placental 

intramuscular, 

abruption, snake 

i ntracran ial, 

bites (pit viper), 

postoperative, and 

liver disease 

traumatic bleeding) 

0 

In type 3 and type 2N (abnormal binding of von Willebrand factor to factor VIII, resembling hemophilia A) 

b 

' 

If INR/PT is sufficiently prolonged by warfarin, PTT will also be prolonged, owing to warfarin's effect on the common pathway. 

LMWH is monitored using antiXa levels. 

" Fibrin split products and d-dimers are increased as the result of concomitant thrombolysis during DIC. 

717


II. BLEEDING DISORDERS ASSOCIATED WITH PLATELET FUNCTION 

PROBLEMS AND/OR A DECREASED PLATELET COUNT 

718 

A. Platelet disorders 

1. Thrombocytopenia (the most common platelet abnormality) 

2. ITP 

a. Etiology 

(1) Decreased bone marrow production 

(a) Malignant infiltration of bone marrow 

(b) Myelofibrosis 

(c) Aplastic anemia 

(d) Drug suppression (ethanol, thiazide diuretics, chemotherapeutic agents) 

(e) Radiation therapy 

(f) 

Viral infections 

(g) Vitamin 8 1 

/folate deficiency 

(2) Hypersplenism (cirrhosis, uremia, sequestration) 

(3) Increased platelet destruction 

(a) ITP 

(b) TTP 

(c) Drug-related destruction (eg, penicillin, sulfonamides, quinine, furosemide, heparin, ASA, gold 

salts, cimetidine, digoxin) 

(d) Hemolysis, elevated liver enzymes, and low platelet count (HELLP) syndrome 

(e) Sepsis 

(f) 

Viral infection: HIV, mumps, varicella, Epstein-Barr virus 

(g) Collagen vascular diseases (especially lupus erythematosus) 

(h) Hemolytic uremic syndrome 

(i) 

Post-transfusion (middle-aged woman previously sensitized to the P1 Al antigen during pregnancy 

who received a transfusion 1 week ago) 

b. Classic clinical scenario 

(1) A patient (usually a woman) presents with easy bruising, epistaxis, gingival bleeding, hematuria, 

menorrhagia, and/or GI bleeding. The bleeding may be spontaneous or secondary to trauma and is 

usually controlled by local pressure. When secondary to trauma, the bleeding has immediate onset. In 

some cases, the patient may also relate that she was recently started on a new medication. 

(2) Examination reveals multiple petechiae and purpura on the mucous membranes and skin, particularly 

on the dependent parts of the body. 

(3) Laboratory findings include a low platelet count and a normal PT(INR)/PTT. 

c. Indications for platelet transfusion (6 units of random donor platelet concentrate increases the platelet 

count by 50,000/mm 3 ) 

(1) Platelet count


(3) Emergency treatment for severe bleeding (platelets


von Willebrand Multimer 

Schistocytes 

Q Platelet 

von Willebrand factor 

Courtesy of Colin Kaide, MO 

f. Mortality is 80% if untreated. 

g. Early diagnosis is a key factor in survival. 

h. Clinical presentation 

(1) It is rare to see all of these findings in TTP, especially if the patient presents early in the course of the 

disease. Later in the course, more findings may be present. 

(a) Fever: least common finding in TTP 

(b) Anemia: microangiopathic hemolytic anemia 

(c) Thrombocytopenia 

(d) Renal abnormalities: less common in TTP and more common in hemolytic uremic syndrome 

(e) Neurologic abnormalities: found in two-thirds of patients with TTP 

(2) Most patients in this era do not have all five features, because it is now treated before progression to 

its natural end; untreated, the mortality is ~80%. 

(3) All that is needed for diagnosis is thrombocytopenia and microangiopathic hemolytic anemia 

(produces schistocytes). Schistocytes (> 1 %) are damaged and fragmented RBCs. They are never 

normal on a peripheral smear. 

(4) Neurologic symptoms in two-thirds of cases; global or focal via CNS thrombosis. The pattern of CNS 

symptoms can be confusing. Owing to microvascular plugging that can come and go in constantly 

varying locations, the patient may experience odd, transient atypical complaints. They can range 

from transient speech problems, to patchy areas of numbness, to focal weakness. It is important to 

ask about waxing and waning symptoms over the preceding few days. 

(5) Renal failure is more common in hemolytic uremic syndrome but can also happen in TTP. 

(6) Fevers are less common. 

(7) Mortality rate is high if untreated. 

(8) An increased lactate dehydrogenase and a decreased haptoglobin are usually seen in TTP and are 

markers of hemolysis. 

1. TTP versus DIC 

(1) DIC is a "consumptive coagulopathy." 

(a) Low platelets 

(b) Low coagulation factors (high PTT and INR) 

(c) Low fibrinogen 

(d) Microangiopathic hemolytic anemia and fibrin plugs 

(2) TTP is a platelet problem 

(a) Low platelets 

(b) Normal coagulation factors (normal PTT and INR) 

(c) Normal fibrin 

(d) Microangiopathic hemolytic anemia and platelet plugs 

720


j. Treatment 

(1) Begin steroids: methylprednisolone 125 mg 

(2) Dialysis may be needed if renal failure. 

(3) Plasma exchange transfusion is the key. 

(4) Give fresh frozen plasma (FFP) if plasma exchange will be delayed for any reason (extended transfer 

times, equipment issues, etc). This gives back the missing ADAMTS13 from someone else's blood and 

can transiently improve TTP symptoms until definitive care can be initiated. 

(5) Avoid platelet transfusions. 

B. Heparin-induced thrombocytopenia (HIT) 


a. Up to 5% of heparinized patients 

b. Develops in 5-10 days 

c. Can develop earlier if the patient has had prior HIT episodes 

d. Late presentation (>10 days after heparin) is also possible but less common. 

e. Occurs as the result of an lgG antibody that forms against heparin when it is bound to platelet factor 4 

f. HIT can develop after heparin doses as small as those used for repetitive heparin flushes. 

g. HIT can develop in patients who are heparinized repeatedly for dialysis. 

h. Regular heparin > LMWH 

1. Surgical > medical > obstetrics patients 

j. Female > male 

Heparin 

Platelet Removal 

Thrombocytopenia 

Thrombosis 

Heparin-induced thrombocytopenia 


2. Clinical presentation (4 T's) 

a. Ihrombocytopenia (


3. Treatment: The 3 Do's 

a. Stop heparin or LMWH! 

b. Start alternative anticoagulant. This should be a direct thrombin (factor Ila) inhibitor. Don't delay! These 

drugs include argatroban, lepirudin, and bivalirudin. 

c. Reverse warfarin. If INR is increased, warfarin reversal should be done with vitamin K 10 mg orally. There 

is no need to use other reversal agents such as FFP, prothrombin complex concentrates (eg, nonactivated 

factor IX complex), or recombinant coagulation factor Vila, because there is no active bleeding and 

reversal is not time dependent. (Warfarin reversal seems counterintuitive; why would you want to reverse 

anticoagulation in someone who is now hypercoagulable? Disturbance in procoagulant-anticoagulant 

balance is the reason for the need to reverse warfarin. Warfarin has two major effects. First, it causes 

an immediate decrease in protein C-mediated anticoagulation. This means that warfarin initially has 

a procoagulant effect. After a few days of use, warfarin also inhibits the production of active forms of 

factors II, VII, IX, and X. This is its anticoagulant effect. After a few days, the net balance of these two 

effects is to cause anticoagulation. When protein C levels are decreased by warfarin and HIT antibodies 

are present [procoagulants], the balance shifts toward the formation of clots.) 

4. Treatment: The 2 Don'ts 

a. Avoid warfarin: reverse with vitamin Kif INR increased. 

b. Avoid platelet transfusions: may worsen the hypercoagulability. 


a. Investigate for lower-limb deep-venous thrombosis (duplex ultrasonography). 

b. Test for HIT antibodies. This looks for lgG antibodies to the heparin-platelet factor 4 complex. This is not 

a useful test for the emergency physician. It is worth sending the test for the purpose of confirming the 

diagnosis for the inpatient physicians. The test will take a while to complete and will probably be a "send 

out" test for most emergency departments. 


Bleeding at LMWH injection site with HIT 


Clotting in extremity with HIT 

722


C. Disseminated intravascular coagulation (DIC) 

1. Definition: life-threatening bleeding disorder resulting from loss of platelets and coagulation factors, 

fibrinolysis, small vessel occlusion, and RBC destruction from fibrin deposition 


a. Patients usually present with diffuse bleeding from multiple sites (skin, mucous membranes, and viscera) 

that is not control led by local measures. 

b. At times, acrocyanosis, thrombosis, and pregangrenous changes of fingers, toes, genitalia, and nose are 

presenting symptoms (purpura fulminans). 

3. Etiology 

a. Trauma (including burns, crush injuries, and brain trauma) 

b. Pregnancy complications (placental abruption, amniotic fluid emboli, fetal death in utero) 

c. Sepsis and a host of infectious diseases 

d. Transfusion and drug reactions 

e. Carcinoma and acute leukemias 

f. Liver disease 

g. Snake bites 

h. Prosthetic devices (especially peritoneovenous shunts) 

1. Heat stroke 


a. Clinical and laboratory triads 

(1) Purpura (petechiae) --.. decreased platelets 

(2) A bleeding tendency--.. increased PT(NR)/PTT 

(3) Signs of organ injury--.. decreased fibrinogen 

b. Additional laboratory findings 

5. Treatment 

(1) j Fibrin split products (the earliest sign) and j o-dimer (most specific sign) 

(2) i Thrombin time 

(3) Fragmented RBCs (schistocytes): evidence of microangiopathic hemolytic anemia 

a. Primary therapy is directed toward the underlying cause when it is easily identifiable (sepsis, pregnancy, 

drug or transfusion therapy) and correction of hemodynamic instability (IV fluids and packed RBCs). 

b. Specific therapy is based on the clinical presentation. 

(1) If hemorrhage predominates the clinical picture, then blood component therapy is indicated. (All three 

should be given.) 

(a) 

Platelets 

(b) FFP (coagulation factors and fibrinogen) 

(c) Cryoprecipitate (factors I and VIII) 

(2) If fibrin deposition and thrombosis predominate the clinical picture, then low-dose IV heparin is 

indicated. Disease states in which this occurs include: 

(a) Gram-negative sepsis in pregnancy 

(b) Retained dead fetus 

(c) Chronic DIC (eg, carcinoma) 

(d) Purpura fulminans 

(3) Antithrombin Ill concentrates may also be used to treat DIC, either alone or in conjunction with 

heparin. Antithrombin Ill is an endogenous inhibitor of coagulation that binds to and inactivates 

thrombin and several other factors. 

723


Ill. BLEEDING (COAGULATION) DISORDERS ASSOCIATED WITH 

AN INCREASED PARTIAL THROMBOPLASTIN TIME (PTT) AND 

NORMAL PROTHROMBIN TIME (PT) 

A. Hemophilia 

1. Characteristics of both hemophilia A and hemophilia B 

a. Bleeding history 

(1) Delayed and protracted bleeding after mild trauma or dental extractions 

(2) Spontaneous hematuria 

(3) Hemarthrosis and muscle hematomas (~90% of all bleeding) 

(4) lntracranial hemorrhages (a major cause of death in patients with hemophilia A) 


(1) Prolonged PTT 

(2) Normal PT and platelets 

2. Hemophilia A (classic hemophilia) 

a. A sex-linked recessive disorder due to a deficiency in the production of factor Vlll:C 

b. Although a sex-linked disorder with women being carriers and men being affected, spontaneous 

mutations can produce female hemophiliacs. Additionally, if a female carrier reproduces with a 

male hemophiliac, the predicted offspring can include a carrier daughter, a hemophiliac daughter, a 

hemophiliac son, and an unaffected son. 

c. In addition to a prolonged PTT, assay of factor Vlll:C is abnormal. 

d. Treatment 

(1) Factor VIII concentrate: the treatment of choice for those with moderate to severe disease. The 

products that are now available are all free of the risk of transmission of AIDS and hepatitis (types B 

and C) and include: 

(a) Heat-treated factor VIII concentrate (hepatitis A and parvovirus transmission is still possible) 

(b) Monoclonal antibody purified factor VIII concentrate 

(c) Recombinant factor VIII concentrate (an ultrapure product) 

(d) Dosing: primarily determined by the type/location of bleeding 

1. Mild bleeding (hematuria, early hemarthrosis, deep laceration) - 12.5 units/kg 

ii. Moderate bleeding (oral lacerations, dental extraction or minor surgery, late hemarthrosis) 

- 25 units/kg 

iii. Severe bleeding (CNS, GI, intra-abdominal or retroperitoneal bleeding; major trauma or 

surgery, documented or potentially serious head injury) - 50 units/kg 

iv. Each unit of factor VIII infused per kg of body weight increases the plasma factor VIII level 

by 2%. In a suspected bleeding emergency, a hemophiliac patient's present level of factor 

VIII is assumed to be zero unless previously known. 

(2) Cryoprecipitate carries a risk of hepatitis and AIDS viruses as well as of allergic reactions and, for 

this reason, its use has declined; it is no longer considered first-line therapy. (One bag equals 80-100 

units of factor VIII). 

(3) Desmopressin (DDAVP) is effective in increasing the levels of factor VIII in patients with mild 

hemophilia and is the treatment of choice for these patients; dosage is 0.3 mcg/kg. There is no risk of 

infectious disease transmission. 

(4) FFP: volume constraints generally limit its use to patients with mild hemophilia. Infectious disease 

transmission can occur. (1 unit of FFP raises the factor level only 3%-5%) 

3. Hemophilia B (Christmas disease) 

a. A sex-linked recessive disorder caused by a deficiency of factor IX 

b. In addition to a prolonged PTT, assay of factor IX is abnormal. 

c. Treatment 

(1) Factor IX concentrate is currently the treatment of choice for patients with hemophilia B. The 

monoclonal concentrates are free from the risk of transmission of hepatitis and AIDS. 

724


(2) Prothrombin complex concentrates contain factors II, VII, IX, and X, which are also effective but have 

thrombogenic adverse effects and may transmit hepatitis. 

(3) FFP is effective too, but carries the risk of infectious disease transmission. 

B. von Willebrand disease (vWD) 

1. This is an autosomal (usually dominant) disorder affecting both males and females. 

2. vWD is the most common genetic bleeding disorder. There are three major types: 

a. Type I (most common): decreased von Willebrand factor (vWF) 

b. Type II: abnormal or dysfunctional vWF 

c. Type Ill (rare): almost no vWF if present (serious disease) 

3. Depending on the specific type of vWD present, these patients have a deficiency or abnormality of one or 

more of the fol lowing: 

a. vWF: promotes platelet adhesion; this is the primary deficiency found in vWD. 

b. vWF: Ag 

c. FactorVlll:C: protected by vWF 


a. Mucocutaneous bleeding (especially epistaxis, menorrhagia, and GI bleeding) predominates; hemarthroses, 

therefore, are rare. 

b. Bleeding episodes are usually milder than with hemophilia (particularly hemophilia A, which is typically 

associated with the most severe bleeding). 


a. Increased PTT 

b. Abnormal platelet function studies 

c. Normal platelet count and PT 

d. Abnormal assay of one or more of the following: vWF, vWF:Ag, or factorVlll:C 

6. Management is determined by the type of vWD present. 

a. DDAVP: use is restricted to patients with mild to moderate type I vWD; it is the treatment of choice in these 

patients and has no risk of infectious disease transmission. 

b. Factor VIII concentrates containing large amounts of vWF (Humate-P and Koate-HS) are currently the 

treatment of choice for patients with type II and type Ill disease. Both products have been treated to 

eliminate the risk of transmission of infectious diseases. 

c. Cryoprecipitate (usual dose= 10 units/kg) is effective for all types of vWD but carries risk of transmission of 

hepatitis and HIV infection. 

d. FFP is also effective for all types of vWD but carries risk of transmission of infectious diseases. FFP may be 

used to treat all forms of hemophilia (hemophilia A and Band vWD), because it contains all factors. The 

major limitation to its use is volume overload; compared with factor VIII concentrate, factor IX concentrate, 

prothrombin complex, and cryoprecipitate, the concentration of factors in FFP (1 unit/ml) is low. Therefore, 

excessively large volumes would be required to treat patients with moderate or severe disease. FFP is most 

appropriate for patients in whom the exact nature of their hemophilia is unknown. 

IV. SICKLE CELL DISEASE 

A. A genetic disorder found predominantly in people of African ancestry that is due to an abnormal 

hemoglobin molecule (hemoglobin S). The normal hemoglobin molecule is hemoglobin A. Hemoglobin 

S induces red cell deformation (sickling). These sickled cells have two properties that account for their 

pathologic manifestations: 

1. Sickled RBCs are unable to pass freely through the systemic microvasculature. This leads to thrombosis 

(ischemia, infarction). 

2. Sickled RBCs hemolyze more easily than normal RBCs. This leads to chronic hemolytic anemia and increased 

susceptibility to infection. 

725


Table 44: Sickle Cell Hemoglobin (Hb) 

Phenotype Genotype Hemoglobin Abnormality 

Sickle trait HbNS a2 bl sl Valine for Glu at 6th position 

Sickle cell disease HbS a2 s2 Valine for Glu at 6th position 

Sickle thalassemia Hb S/A-thal* a2 s2/a2b2-thal thal=decreased production of Hb A 

Sickle eel I disease Hb S + Hb C** a2 s2/a2 c2 Lysine for Glu at 6th position 

* In thalassemias, Hb A is produced in decreased amounts. 

** In sickle cell disease, both forms of hemoglobin exist (Hb Sand Hb C). 

B. Sickle cell trait (heterozygous hemoglobin AS) 

1. When hemoglobin S is inherited from one parent and hemoglobin A from the other, RBCs will contain both 

hemoglobin A and hemoglobin S (


3. Sequestration crisis (most common precipitating cause of acute anemia) 

a. Seen in young children (6 months to 6 years old) 

b. Clinical presentation: patient presents with abdominal pain and distention, pallor, shock, and 

splenomegaly. 


(1) As above 

(2) Hemoglobin very low (may be as low as 1-2 g) and pancytopenia 

d. Treatment: as above and consultation with a pediatric surgeon for possible splenectomy 

4. Aplastic crisis 

a. Usually precipitated by an infection (most often human B19 parvovirus) that suppresses erythropoiesis; 

folate deficiency is rarely the underlying cause. 

b. Clinical presentation: patient is pale, lethargic, and in shock. 


(1) As above and appropriate cultures 

(2) Decreased reticulocyte count (secondary to severe bone marrow depression) is pathognomonic and 

associated with a very low hemoglobin. 

d. Treatment 

(1) Support shock and transfuse blood. 

(2) Administer oxygen, folic acid, and antibiotics as indicated. 

E. Other potential complications and sequelae of sickle cell disease 

1. Infections (most common cause of death) 

a. Sepsis, meningitis, pneumonia, and osteomyelitis occur with increased frequency due to functional 

asplenia, poorly migrating neutrophils, and decreased opsonin activity. 

b. Children (particularly those 103°F [39.4°C]) and a WBC count 

>20,000/mm 3 should be promptly treated with broad-spectrum IV antibiotics, and cultures should be done. 

2. Priapism 

a. Definition: a painful, sustained, pathologic erection 

b. Occurs in 10%-40% of men and can result in impotence 

c. Treatment 

(1) Obtain immediate urologic consult and administer terbutaline 0.25-0.5 mg SC. 

(2) Subsequent measures 

(a) Hydration 

(b) Transfusion of packed RBCs 

(c) Hyperbaric oxygen 

(d) Analgesia (appropriate for treatment of pain but ineffective in relieving priapism) 

3. Acute chest syndrome 

a. Most commonly affects older children, adolescents, and adults 

b. Patients present with fever, cough, chest pain, and shortness of breath. 

c. Cause is multifactorial and includes both infection and infarction of pulmonary tissue. 

d. Diagnostic evaluation: hypoxia and new chest radiograph abnormalities 

e. Treatment 

4. Strokes 

(1) Supplemental oxygen, hydration, and antibiotics 

(2) Exchange transfusion to reduce the proportion of hemoglobin S may also be needed. 

a. May be thrombotic or hemorrhagic (intracranial or subarachnoid) 

b. Clinical presentation: patients usually present with abrupt onset of aphasia, hemiparesis, change in vision, 

and/or seizures. 

c. Diagnostic evaluation: baseline laboratory studies and CT or MRI of the brain 

d. Treatment: immediate exchange transfusion to decrease the amount of hemoglobin S to


8. Potential sequelae 

a. CHF (chest radiograph - bibasilar congestion) 

b. Renal insufficiency/nephrotic syndrome 

c. Leg ulcers (particularly on the malleoli) 

d. Retinal infarction/detachment 

e. Avascular necrosis 

(1) Digits (children) 

(2) Femoral head (young adults) 

9. Caution with any eye trauma. There is a significant risk of hyphema, which tends to rebleed. 

V. ANEMIA 

A. General approach 

1. Decide how emergent and prioritize decision making. 

2. Profound nontraumatic anemia causing severe compromise to the patient's physiologic functions: attention 

should be focused first on resuscitation, then on diagnosis of underlying causes. 


1. History 

a. Symptoms of anemia: chest pain, exertional dyspnea, syncope 

b. Bleeding diathesis 

(1) Bleeding after trauma, surgery, tooth extractions, or injections 

(2) Spontaneous bleeding: epistaxis, menorrhagia 

(3) Spontaneous purpura, petechiae 

c. Intermittent jaundice/dark urine 

d. Dietary history: vegetarian diet or poor nutrition 

e. Drug use/toxin exposure 

f. Family history and racial background: African-American, Middle Eastern 

g. Underlying disease 

(1) Renal or liver disease 

(2) Hypothyroidism 

(3) Chronic disease states: cancer, rheumatic or renal disease 


a. Skin: pallor, purpura, petechiae, angiomas, ulcerations 

b. HEENT 

(1) Conjunctiva! jaundice/pallor/hemorrhage, funduscopic hemorrhage 

(2) Tongue atrophy, papillary soreness 

c. Cardiopulmonary 

(1) Heart size, murmurs, extra-cardiac sounds 

(2) Wheezing, rales, other signs of pulmonary edema 

d. Abdomen: hepatomegaly, ascites, splenomegaly, masses, rectal/pelvic 

e. Neurologic: altered position or vibratory sense, peripheral neuritis 


1. Basic laboratory studies should be obtained: CBC with differential, platelet count, mean corpuscular volume 

(MCV), reticulocyte count, peripheral smear 

2. Other tests can be ordered as indicated. 

a. Suspect hemolytic anemia: direct Coombs' test, serum free hemoglobin and haptoglobin 

b. Suspect microangiopathic hemolytic anemia (MAHA) or DIC: PT/PTT, o-dimer, fibrin degradation products, 

fibrinogen 

728


Table 45: Differential Diagnosis of Anemia 

Mechanism/Type 

Blood loss 

Examples 

Traumatic 

Nontraumatic 

GI/GU bleeding, menorrhagia, aneurysmal rupture, hemoptysis 

Decreased production 

Hypochromic/microcytic 

Macrocytic 

Normocytic 

Iron deficiency, thalassemia, sideroblastic anemia or lead poisoning, 

chronic disease (cancer, renal, inflammatory diseases) 

B 1 

/folate deficiency, liver disease, hypothyroidism 

Primary bone marrow involvement: aplastic anemia, myelofibrosis 

Underlying disease: hypoendocrine state (thyroid, adrenal, pituitary), 

uremia, liver disease, chronic inflammation 

Increased destruction (hemolytic anemias) 

Intrinsic 

Extrinsic 

Enzyme defects: pyruvate kinase deficiency, G6PD deficiency 

Membrane abnormality: spherocytosis/el I iptostomatocytosis, 

paroxysmal nocturnal hemoglobinuria, spur cell anemia 

Hemoglobin abnormality: hemoglobinopathies, thalassemias, unstable 

hemoglobin, hemoglobin M 

Immunologic: allo/autoantibodies 

Mechanical: microangiopathic hemolytic anemia, prosthetic heart 

valves 

Environmental 

Drugs/toxins 

Infections 

Thermal 

Abnormal sequestration: hypersplenism 

729


All cell lines affected 

or reticulocytes


D. Nonhereditary anemia: hemolytic anemia 

1. Acquired anemias 

a. Precipitating factor is extrinsic to the body. 

b. Result of exposure to some immunologic, toxic/infectious, or mechanical problem 

2. Autoimmune hemolytic anemia 

a. The direct Coombs' antiglobulin test is used to demonstrate lgG or complement (C3) attached to the 

surface of the RBCs: positive only in immune-mediated hemolytic anemias. 

b. Indirect Coombs' test looks for free-circulating antibodies and is used in pretransfusion screening. 

c. Warm and cold antibody hemolytic anemia exist. 

d. Drug-induced hemolytic anemias 

(1) Many drugs have been linked with induction of hemolytic anemias via various mechanisms. 

(2) The prototype drugs for each reaction are alpha-methyldopa, procainamide, penicillin, and quinidine. 

(3) Hemolysis generally resolves when the drug is stopped. 

3. Fragmentation hemolysis: MAHA 

a. Thrombotic thrombocytopenic purpura/hemolytic uremic syndrome 

b. Pregnancy-associated hemolysis 

(1) Preeclampsia, eclampsia, or placental abruption can result in MAHA. 

(2) Preeclampsia (even with minimal signs and symptoms) can be associated with the HELLP syndrome, 

which untreated can lead to liver failure, DIC, or CHF . 

.!::!.emolysis 

_!;levated liver enzymes 

low flatelets 

4. Toxic hemolysis 

a. Infectious agents 

(1) Malaria, babesiosis, and bartonel losis can cause hemolysis via parasitization of the RBCs. 

(2) Hemophilus influenzae type B can alter RBC membranes, which leads to their destruction by the 

immune system. 

(3) C/ostridium perfringens releases enzymes that break down RBC membranes. 

(4) Mycoplasma and mononucleosis induce cold agglutinins. 

b. Other toxins: insect and snake bites (especially cobras) can induce hemolysis; American pit vipers usually 

cause coagulopathies. 

5. Mechanical destruction: heat, repetitive trauma to hands or feet and shearing by passage of blood through 

oxygenators or artificial heart valves can induce breakage of RBC membranes. 

E. Acquired non hemolytic anemias 

1. General 

a. Problems with production of RBCs because of absent components (iron deficiency) or marrow disease 

b. Characterized by a decreased reticulocyte count 

c. The MCV and iron studies can help to further classify and differentiate anemias. 

2. Aplastic anemia 

a. Disease of stem cells in the bone marrow that results in a pancytopenia 

b. Most cases are idiopathic, but up to 20% are associated with drug or chemical exposure. 

(1) Benzene 

(2) Phenylbutazone, gold, o-penicillamine 

(3) Anticonvulsants 

(4) Sulfonamides, chloramphenicol 

(5) Clozapine (antipsychotic) 

(6) Chemotherapeutic agents 

c. 10% are due to viral infections, especially hepatitis, Epstein-Barr virus, cytomegalovirus 

d. Management 

(1) Best handled by a hematologist; is often supportive but can include bone marrow transplant, 

immunosuppression, and transfusions 

(2) Fever in a neutropenic patient (absolute neutrophil count


3. Iron-deficiency anemia 

a. Results from blood loss (often GI or menstrual), increased iron requirements (pregnancy, lactation), or 

malabsorption of iron 

b. Typically a microcytic anemia; a normal MCV may be seen early on. 

c. Iron studies rarely help the emergency physician but are often requested by consultants. 

(1) Serum ferritin 

(a)


d. Treatment: expectant but the key is to avoid drugs that may exacerbate the condition, eg, sulfa, 

antimalarials, phenazopyridine, nitrofurantoin 

5. Hereditary spherocytosis 

a. The cytoskeleton of the RBCs is abnormal, causing them to have a spherical shape. 

b. The RBCs become trapped in the spleen and are destroyed. 

c. Most patients have mild, chronic anemia. 

d. The cure is splenectomy. 

VI. BLOOD TRANSFUSIONS 

A. Transfusion of specific blood products 

1 . Packed RBCs 

a. Indicated for red cell repletion (not volume repletion) 

b. Transfusion of packed RBCs coupled with crystalloid fluid resuscitation has become the standard of care for 

the treatment of the acutely hemorrhaging patient. 

c. Type O negative (universal donor) should be given for exsanguinating hemorrhage if type-specific blood is 

not immediately available, ie, if you ordered it, and you are losing the patient, don't wait for it; as soon as 

type-specific blood is ready, you can switch infusions if need be. 

d. One unit of packed cells is 250 ml volume; standard practice is to administer at least two units in adults, 

15 ml/kg in children. 

e. Packed RBCs can be leukocyte-reduced, washed, irradiated, or frozen for specific needs. Consider 

leukocyte-reduced packed cells for: 

(1) Protecting immunocompromised patients 

(2) Preventing sensitization 

(3) Preventing nonhemolytic febrile reactions 

2. Fresh frozen plasma (FFP) 

a. Contains all the coagulation factors except platelets 


(1) Correction of clinically significant depletion of clotting factors, eg, patient on warfarin therapy who 

is actively bleeding or requires emergent surgery 

(2) Treatment of an acute undiagnosed bleeding disorder 

c. Requires ABO matching and carries risk of infectious disease transmission 

d. Typical dosage is 4 units (250 ml/unit) for adults, 15 ml/kg for children. 

3. Platelets 

a. Indicated for spontaneous bleeding resulting from thrombocytopenia or inadequate platelet function 

b. A platelet pack of 6 units (typical adult transfusion) raises the platelet count ~50,000/mm 3 • 

Ordering Platelets Made Simple 

• Platelets are ordered in packs, not individual units. 

• Some hospitals use 4 packs and some use 6 packs. This equals either 4 or 6 individual units of platelets, 

usually from random donors. 

• The 4 or 6 pack raises the platelet count by about 50,000. 

• Platelets can also be ordered as an apheresis unit. This is made from one single donor. A lot of blood is 

taken from this one donor, and a certain amount of platelets are removed from the blood; the rest of the 

blood and plasma is returned to the donor. 

• This should raise the platelet count by about 50,000 and expose the patient to fewer antigens and fewer 

possible transmissible infections. 

Courtesy of Colin Kaide, MO 

733


734 

c. ABO matching is preferred; platelets may also be leukocyte-reduced. 

d. Transfusion is associated with risk of infectious disease transmission. 

e. Contraindications: TTP and HIT 

4. Cryoprecipitate 

a. Contains large quantities of factor VIII:C, vWF, vWF:Ag, and fibrinogen (factor I) 

b. Effective in bleeding due to: 

(1) vWD: effective for all types of vWD but is not the treatment of first choice 

(2) Hemophilia A (not the therapy of first choice) 

(3) Hypofibrinogenemia (congenital or acquired) 

c. Does not require ABO matching 

d. Use is associated with risk of transmission of both hepatitis and AIDS. 

5. Factor concentrates/plasma coagulation factors (contain no fibrinogen) are used in management of coagulation 

factor deficiencies. 

a. Contain high concentrations of the deficient factor and therefore are particularly useful in patients with 

hemophilia 

(1) Hemophilia A_,. factor VIII concentrate 

(2) Hemophilia B _,. factor IX concentrate 

(3) vWD _,. factor VIII concentrate containing large amounts of vWF 

b. Almost completely free of the risk of transmission of both the hepatitis and AIDS viruses 

6. Albumin and plasma protein fraction are no longer used because of the lack of proven efficacy of volume 

resuscitation; crystalloid administration is preferable. 

B. Transfusion methods 

1. Blood products should be infused with warmed normal saline (hypotonic saline solutions; solutions containing 

calcium or glucose should not be used). Whole blood and packed RBCs should be typed and crossmatched. In 

certain situations, however, untyped or non-crossmatched blood must be given: 

a. When type-specific blood is not available in a patient with exsanguinating hemorrhage, type 0-negative 

blood should be given. 

b. Type-specific blood is indicated for: 

(1) Progressive hypovolemic shock in spite of aggressive shock management (lactated Ringer's or normal 

saline 2 Lover 10-15 minutes) 

(2) Profound hypovolemic shock unresponsive to aggressive shock management in the first 10-15 minutes 

of therapy 

2. Autotransfusion 

a. This is a patient-specific source of blood for the patient in urgent need who has a traumatic hemothorax. 

(Blood collected from the chest does not have normal levels of fibrinogen nor does it have normally 

functioning platelets.) 

b. Technique: blood is drained through a chest tube, screenfiltered to remove clots and debris, then reinfused 

through a micropore filter. 

C. Complications of transfusions 

1. Complications associated with massive transfusions: defined as the transfusion of a volume of blood equivalent 

to the patient's entire blood volume within a 24-hour period or the transfusion of the equivalent of one-half of 

the patient's blood volume at one time. 

a. Coagulopathies 

(1) May result from dilution of clotting factors, platelet destruction, or DIC 

(2) Administration of FFP should be reserved for the massively transfused and bleeding patient who is in 

shock. Routine prophylactic use of FFP is unwarranted. 

(3) Platelets should be administered to patients who receive a massive transfusion in


c. Microembolization 

(1) Occurs when microaggregates form in refrigerated blood from the degeneration products of platelets, 

leukocytes, and fibrin 

(2) Embolization of these aggregates is thought to be associated with development of ARDS. 

(3) Use of micropore filtration will decrease the incidence of this complication. 

d. Hypocalcemia (citrate toxicity) 

(1) Decreased Ca++ can occur, because citrate chelates ionized calcium until all the citrate is metabolized. 

(2) Routine prophylactic calcium supplementation, however, is not recommended. 

(3) Calcium supplementation should be reserved for those patients who develop evidence of myocardial 

impairment. 

2. Complications associated with any transfusion 

a. Immediate reactions 

(1) Hemolytic reaction (most worrisome): an antibody-mediated reaction characterized by the 

development of fever, chills, burning at the infusion site, joint and low back pain, chest tightness, 

bleeding, hematuria, and shock 

(2) Febrile reaction (most common and least worrisome): characterized by fever, chills, and malaise, but 

patients may occasionally go on to develop blood pressure and respiratory distress 

(3) Allergic reaction (rare): characterized by development of urticaria skin flushing, laryngeal edema, 

and/or shock 

(4) Altered hemoglobin function: storage of blood --;, t 2,3 diphosphoglycerate levels - increased 

affinity of hemoglobin for oxygen --;, decreased delivery of oxygen to tissues 

(5) Hyperkalemia and acidosis: may occur in association with massive transfusions 

b. Delayed reactions 

(1) Infections: many different blood-borne infections may be transmitted by transfusions, including 

hepatitis, AIDS, human T-cell lymphotropic viruses, cytomegalovirus, Epstein-Barr virus, and malaria. 

Hepatitis C (formerly non-A, non-B) is currently the most common infection acquired from blood 

transfusions. 

(2) Extravascular hemolysis: most commonly manifests as an unexplained decrease in the hemoglobin 

level 7-1 0 days after transfusion 

(3) Graft versus host disease 

VII. REVERSAL OF DRUG-INDUCED ANTICOAGULATION 

A. Reversal of warfarin-induced coagulopathy 

1. General 

a. Increased IN Rs


Contact Activation Pathway 

(Intrinsic) 

• 

. 

. 

Tissue Factor Pathway 

(Extrinsic) 

COMMON PATHWAY 

2 Thrombin 

Fibrin 

Ogen (I) 

Warfarin Effects (2, 7, 9, 10) 


2. Reversal agents 

a. Warfarin-induced anticoagulation is reversed by adding back into the system the missing factors (II, VII, 

IX, and X) and by providing additional vitamin K to allow the liver to produce new factors. 

b. Vitamin K is given orally or IV. SC or IM injections are not recommended, because absorption is erratic. 

The risk of serious or life-threatening reactions from IV vitamin K is very low. INR correction begins in 2 

hours and is usually completed within 24 hours (see Table 46 for dosing recommendations). 

c. HP is given to replace the missing factors II, VII, IX, and X. The minimum dose should be 4 units. With 

FFP, the lowest attainable INR is 1.5. This is because the IR of HP is 1.5. 

d. Prothrombin complex concentrates (PCC) are now recommended as a first-line reversal agent for 

warfarin-induced coagulopathy. PCCs have been used in Europe and other parts of the world for years 

as reversal agents. PCCs are highly purified concentrates of the vitamin K-dependent clotting factors 

II (prothrombin), VII, IX, and X. They are pooled from plasma and although purified, do carry a very 

small risk of viral transmission. Product formulations vary in concentrations of each factor. They can be 

3-factor preparations with minimal VII activity or 4-factor with good VII levels. In the United States, 

two PCC products are available: Profilnine SD® and Bebulin VH®. They both have very low factor VII 

activity and are 3-factor preparations. A new 4-factor preparation is now also available in the United 

States (Kcentra®). It contains protein C and S to limit the risk of inducing inappropriate clotting. It is FDA 

approved for use as a reversal agent in warfarin-associated bleeding. 

(1) All factors are referenced against 100 U of factor IX activity. 

(2) All preparations are dosed based on the amount of factor IX. 

(3) There are reports of thrombosis with PCC preparations; however, the risk appears low. 

(4) Onset is very fast (15 minutes), and IN Rs can return to normal in 10 minutes. 

e. Factor eight inhibitor bypassing activity (FEIBA) 

(1) FEIBA is used in patients with hemophilia who develop antibodies to factor VIII after receiving factor 

VIII replacement for a prolonged time. 

(2) It is an activated form of PCC. It contains mostly activated factor VII and mostly nonactivated factors 

II, IX, and X. 

(3) It has been shown to be an effective reversal agent for warfarin-induced anticoagulation. It may have 

a thromboembolic risk greater than that of PCC and is not routinely recommended as a reversal 

agent for warfarin. 

(4) There is no FDA-approved indication for FEIBA as a warfarin reversal agent. 

736


f. Activated factor VI I 

(1) A very large thrombin burst is theoretically possible to create by directly activating factor X using 

recombinant factor VII (rVlla). 

(2) The INR can be rapidly normalized, although redosing is needed every few hours. 

(3) Despite normalizing the INR, studies have called into question the effects of rVlla on actual clinical 

reversal of bleeding, and it is no longer recommended for warfarin bleeding. 

(4) There is no FDA-approved indication of rVlla as a warfarin reversal agent. 

Table 46: Recommendations for Managing Increased IN Rs or Bleeding in Patients Receiving Vitamin K 

Antagonists 

Condition 

INR above therapeutic range 

but


c. Protamine may have some effect on LMWH. Only 60%-75% of the anti-Xa activity of LMWH is 

neutralized by protamine. Effectiveness depends on which LMWH is used. 

d. There is a real concern when using protamine with LMWH-protamine when given by itself has 

anticoagulant effects. If there is reversal of the non-Xa activity and only partial (but not enough) reversal of 

the Xa activity, the net result will point to anticoagulation. 

C. Reversal of newer anticoagulants 

1. Data supporting the reversal of the newer anticoagulants rivaroxaban, apixaban, and dabigatran is largely 

limited to ex vivo and in vitro studies. There are very few randomized, controlled trials supporting the reversal 

of these agents. 

2. Rivaroxaban, apixaban, and edoxaban are direct factor Xa inhibitors, ie, they bind directly to factor Xa without 

usingATIII. 

3. Dabigatran is a direct factor II inhibitor, ie, it binds directly to factor II without using ATIII. 

4. These agents attack at the most critical part of the clotting cascade, making reversal difficult. 

5. Information on reversal with the following agents is not FDA approved, but it does appear on many written 

protocols. It represents the best information available at the time of this publication, until accepted protocols 

become standard. The exception to this is the newly released antibody to dabigatran, idarucizumab, which was 

FDA approved in fall 2015. 

6. Strategies that have been tried involve overwhelming the factor inhibition by introducing a large amount of 

replacement factors into the system. PCC and aPCC (FEIBA) have been tried for both agents. FEIBA thus far has 

shown promise in reversal of both agents. These studies have been conducted in volunteers and in animals and 

are not definitive. 4 factor PCCs are currently the preferred reversal agent for the Xa inhibitors. Activated PCC 

(FEIBA) is recommended as the reversal agent of choice for dabigatran, if idarucizumab is not available. 

7. In theory, rVlla may also work to reverse the effect of factor X inhibition by direct inhibitors. The possible 

reversal of rivaroxaban by rVlla has been suggested because of its ability to reverse the indirect Xa inhibitor 

fondaparinux. However, there is no convincing human clinical data as of yet to support the use of rVlla. 

D. Reversal of thrombolysis 

1. General 

a. Thrombolytics (rTPA and others) work by catalyzing the conversion of plasminogen to plasmin. Plasm in 

cleaves cross-linked fibrin into d-dimers and fibrin degradation products. 

b. Reversal is not an accurate term in that the best that can be done is to mitigate the effects as best as 

possible. 

2. Agents to "reverse" thrombolytic-induced bleeding 

a. E-Aminocaproic acid 

(1) Blocks fibrinolysis by reversibly blocking plasminogen, which then cannot be cleaved to plasm in; 

plasm in cleaves crosslinked fibrin and lyses clots. 

(2) Enhances hemostasis when fibrinolysis contributes to bleeding; used for bleeding in patients with 

hemophilia after dental procedures 

(3) There are no data on the use for rescue of rTPA (or other thrombolytics) for bleeding in the brain or 

other sites when rTPA is used for stroke, Ml, or pulmonary embolism. 

(4) Not FDA approved for this use 

b. Cryoprecipitate 

(1) Contains a significant amount of fibrinogen (see above for details) 

(2) Gives back the fibrinogen that is degraded by the action of tPA 

738


Table 47: Anticoagulant Reversal Agents 

Anticoagulant 

Warfarin 

Heparin 

LMWH 

Synthetic 

pentasacchari de 

(fondapari n ux) 

Direct thrombin 

inhibitors 

Direct Xa inhibitors 

Platelet inhibitors 

(eg, clopidogrel) 

Thrombolytics 

Mechanism of Anticoagulation 

Interferes with the production of II, VII, IX, X 

Potentiates the action of antithrombin, 

inactivating Xa and thrombin 

Acts via antithrombin to inactivate Xa and 

thrombin. Activity varies but mostly anti-Xa 

activity 

Indirectly inhibits Xa via antithrombin 

Inhibit thrombin without using antithrombin 

Inhibit Xa without using antithrombin 

Block various mechanisms by which 

platelets aggregate and degranulate 

Catalyze plasminogen to plasmin, causing 

clot lysis 

Reversal Agents 

Vitamin K, FFP, PCC, aPCC 

Protamine 

Protamine (partial), rVlla 

rVlla, PCC, aPCC may be 

effective but limited data 

aPCC may be effective but 

limited data; idarucizumab 

4-factor PCC 

Platelets(?), DDAVP (?), rVlla 

(?) 

Aminocaproic acid, 

cryoprecipitate 

739

HEMATOLOGIC DISORDERS: PRACTICE CLINICAL SCENARIOS 



Scenario A 

Presentation: A patient presents to the emergency department with altered mental status. He is confused 

and lethargic. 

Laboratory studies: Platelet count is 75,000/mm 3 , and hemoglobin is 9.5 mg/dL. There has been no 

heparin exposure. The laboratory reports schistocytes on the peripheral blood smear. 


Scenario B 

Presentation: A patient with sickle cell disease presents with complaints of chest pain. He complains of 

discomfort with breathing, shortness of breath, and fever. 


Scenario C 

Presentation: A patient presents 3 days after being discharged from the hospital after a left knee 

replacement. The patient is on a LMWH 40 mg/day (prophylactic dosage). 

Physical examination: The patient has what appears to be bleeding at the sites of the LMWH injections. 

She also has a painful, pulseless lower extremity on the right side (the opposite side from the knee 

replacement). 


Scenario D 

Presentation: A patient with hemophilia A comes in with swelling and pain in his knee after a minor injury. 

He took some of his factor at home but still complains of increased swelling and worsening pain. 


Scenario E 

Presentation: A patient is on warfarin and was started on TMP-SMX. She presents with a massive GI bleed. 

Laboratory studies: The patient's INR is 9. Her INR before starting an antibiotic was 2.4. Her hemoglobin is 

9 mg/dL. 


740



Scenario A 

Diagnosis: thrombotic thrombocytopenic purpura (TTP) 

Diagnostic evaluation: Never ignore schistocytes on a peripheral smear; they are always bad! If> 1 % is 

reported, consider a microangiopathic hemolytic anemia. This patient meets the three most important 

criteria for TTP: thrombocytopenia, neurologic symptoms (due to microthrombi), and schistocytes on the 

peripheral blood smear (due to breakage of cells flowing through platelet plug debris). Fever and renal 

abnormalities are less common. Two-thirds of patients with TTP have some neurologic symptoms due to 

microthrombi in the CNS. 

Management: The main treatment is plasma exchange transfusion, which is done by a hematologist. 

Additional management includes steroids to decrease production of the pathologic antibody (against 

ADAMTS13) and FFP to replete ADAMTS13. 

Scenario B 

Diagnosis: sickle cell with chest pain and shortness of breath 

Diagnostic evaluation: The patient's oxygen saturation is 90%. Chest radiograph shows a patchy lower lobe 

infiltrate on the right side. Although this could be nothing more than a community acquired pneumonia, 

you must be concerned about acute chest syndrome, which is seen in SS, SC, sickle-thalassemia. The 

criteria for diagnosis are new pulmonary infiltrate involving at least one complete lung segment consistent 

with alveolar consolidation but excluding atelectasis, plus at least one or more clinical findings of cough, 

wheezing, tachypnea, temperature >38.5°C (101.3°F), dyspnea/hypoxia, or chest pain. 

Management: Testing should include a radiograph to look for infiltrate. Treatment is aimed at treating 

infection and maximizing symptom control and respiratory function. This can include bronchodilators, 

transfusions, pain medications, and respiratory support as needed. 

Scenario C 

Diagnosis: heparin-induced thrombocytopen ia 

Diagnostic evaluation: Although the patient has a platelet count that is seemingly normal (130,000/mm 3 ), 

postoperative platelet counts should be increased. Her platelet count on the last known laboratory study is 

600,000/mm3, which would be normal in the postoperative state. She has had a drop of >50%. Remember 

the T's: The patient has thrombocytopenia (relative), thrombosis, and no other explanation. The timing is 

within the appropriate range of 5-1 0 days. 

Management: Stop the LMWH (or regular heparin). An alternative form of anticoagulation is needed. 

Because the patient will be admitted, start a drug like argatroban. If the patient had been on warfarin, 

vitamin K therapy would be needed. There is no need for fresh frozen plasma. 

Scenario D 

Diagnosis: hemophilia 

Key facts: 

• Bleeding history in a hemophiliac 

• Bleeding after mild trauma or dental extractions 

• Spontaneous hematuria 

• Hemarthrosis and muscle hematomas (90% of all bleeding) 

• lntracranial hemorrhages (a major cause of death in patients with hemophilia A) 

741


Management: Treatment includes replacement of the missing factor. Factor VIII concentrate is the treatment 

of choice. Check the patient's record or ask the patient how much factor he would normally get in the 

situation. Patients with hemophilia very likely know a lot more about it than you do, because they have 

lived with it their entire life, whereas you may not see it very often. Dosing is determined by whether the 

bleeding is mild, moderate, or severe. 

• In mild bleeding (hematuria, early hemarthrosis, deep laceration), the goal is to increase factor levels by 

25% _,. 12.5 units/kg. 

• In moderate bleeding (oral lacerations, dental extraction or minor surgery, late hemarthrosis), the goal is 

to increase factor levels up to 50%. _,. 25 units/kg. 

• In severe bleeding (CNS, GI, intra-abdominal or retroperitoneal bleeding; major trauma or surgery; 

documented or potentially serious head injury), the goal is to increase factor levels up to 100% _,. 

50 units/kg. 

Scenario E 

Diagnosis: warfarin over-anticoagulation 

Alternative presentation: A patient on warfarin is sent over from his family doctor's office for an 

asymptomatic INR of 6. 

Diagnostic evaluation: Determine the need for reversal of anticoagulation. Severe bleeding with an 

increased INR almost always needs to be treated. Caution should be exercised in patients with a left 

ventricular assist device or mechanical artificial valve; these are not absolute contraindications to reversal, 

but consider discussing with the cardiovascular surgeon to establish a target final INR. In cases when the 

acute bleeding can be controlled (cauterized epistaxis, banded varices, etc), reversal of warfarin should be 

followed by cross-anticoagulation with heparin. Patients with increased IN Rs who are asymptomatic may 

be treated by holding a dose of warfarin ± smal I doses of vitamin K. 

Management: If needed, administer vitamin K orally or IV. Replace missing factors when indicated. Fresh 

frozen plasma or PCC can be used. 

742

ONCOLOGIC DISORDERS 


Upper Airway Obstruction ........................................................................................................................................ 746 

Tamponade Secondary to Malignant Pericardia( Effusion .......................................................................................... 746 

Superior Vena Cava Obstruction ............................................................................................................................... 747 

Acute Spinal Cord Compression ................................................................................................................................ 748 

Hypercalcemia Secondary to Malignancy ................................................................................................................. 748 

Syndrome of Inappropriate ADH Secretion (SIADH) ................................................................................................ 749 

Acute Tumor Lysis Syndrome ..................................................................................................................................... 750 

Hyperviscosity Syndrome .......................................................................................................................................... 751 

Adrenal Insufficiency ................................................................................................................................................ 752 

Granulocytopenia, lmmunosuppression, and Overwhelming Infection in the Presence of Malignancy .................... 752 

Leptomeningeal Carcinomatosis ............................................................................................................................... 753 

743

ONCOLOGIC DISORDERS: SELF-ASSESSMENT QUESTIONS 


1. All of the following statements regarding cardiac tamponade secondary to malignant pericardia I effusion are 

true except: 

(a) 

ECG findings of low QRS voltage and electrical alternans are consistent with this diagnosis. 

(b) Suggestive physical findings include hypotension with a narrow pulse pressure, jugular venous distention, 

and muffled heart tones. 

(c) Supportive measures include fluid restriction and diuretics. 

(d) The diagnosis may be confirmed by echocardiography or Swan-Ganz catheterization. 

2. All of the following statements regarding superior vena cava obstruction are accurate except: 

(a) 

Patients present with headache, swelling of the face and upper extremities, and shortness of breath. 

(b) Common causes of this syndrome are lung cancer and lymphoma. 

(c) Useful therapeutic measures include administration of oxygen, diuretics, and corticosteroids. 

(d) Initially, symptoms occur in the evening. 

3. The ECG finding most consistent with a diagnosis of hypercalcemia is: 

(a) Shortened QT interval 

(b) Prolonged PR interval 

(c) 

Prolonged QT interval 

(d) Hyperacute T waves 

4. Which of the fol lowing signs and symptoms is/are not consistent with the diagnosis of hypercalcemia? 

(a) 

Lethargy/decreased level of consciousness 


(c) Constipation 

(d) Anorexia/nausea/vomiting 

5. In a patient presenting with the triad of unexplained stupor or coma, anemia, and rouleaux formation on peripheral 

blood smear, the most likely diagnosis is: 

(a) Acute adrenal insufficiency 

(b) Hypercalcemia 

(c) Hyperviscosity syndrome 

(d) Superior vena cava syndrome 

6. Which of the fol lowing findings is inconsistent with the diagnosis of adrenal insufficiency? 

(a) 

Hyperkalemia 


(c) Hyponatremia 

(d) Hyperglycemia 

7. The most common presenting symptom in patients with leptomeningeal carcinomatosis is: 

(a) 

Headache 

(b) Incontinence 

(c) 

Back pain 

(d) Facial nerve palsy 

8. Common causes of the hyperviscosity syndrome include all of the following except: 

(a) Chronic myelocytic leukemia 

(b) Lymphomas 

(c) Multiple myeloma 

(d) Waldenstrom macroglobulinemia 

744


9. The most appropriate initial therapy for malignancy-induced hypercalcemia consists of: 

(a) Administration of glucocorticoids 

(b) Administration of plicamycin (mithramycin) 

(c) Fluid hydration with IV normal saline followed by administration of furosemide 

(d) Administration of calcitonin 

10. Infection in the cancer patient is most commonly ___ in etiology. 

(a) Viral 

(b) Bacterial 

(c) Fungal 

(d) Protozoa! 

11. A reasonable antibiotic regimen for the cancer patient who presents with a history of fever and abdominal pain 

associated with peritonitis on physical examination is: 

(a) An antipseudomonal aminoglycoside plus an antipseudomonal penicillin 

(b) A fluoroquinolone and an antipseudomonal aminoglycoside plus an antipseudomonal third- or fourthgeneration 

cephalosporin 

(c) Metronidazole or clindamycin 

(d) A combination of A+ C or B + C 

ANSWERS 

I. c 4. b 7. a 10. b 

2. d 5. c 8. b 11. d 

3. a 6. d 9. c 



745


I. UPPER AIRWAY OBSTRUCTION (AT THE LEVEL OF THE 

MAINSTEM BRONCHI OR ABOVE) 

A. Signs and symptoms 

1. Voice change or hoarseness (indicates a slow process of local tumor compression or obstruction) 

2. Laryngeal stridor from a rapidly growing tumor 

3. Acute upper airway obstruction secondary to infection, tumor hemorrhage, or inspissated secretions; 

respiratory arrest is imminent. 

B. Etiology 

1. Carcinoma 

a. Laryngeal 

b. Thyroid 

c. Pulmonary metastases 

2. Lymphoma (especially Burkitt) 


1. Immediate assessment 

2. Palpation of mass 

3. Lateral soft-tissue radiograph of the neck 

4. Direct laryngoscopy 

5. Fiberoptic laryngoscopy 

6. CT if stable 

D. Management 

1. Establish an airway if there is airway compromise. 

a. Fiberoptic laryngoscope-assisted intubation can be very useful in securing the difficult airway. 

b. A surgical airway may be necessary. 

2. ENTconsult 

3. Treat the underlying neoplasm. 

II. TAMPONADE SECONDARY TO MALIGNANT PERICARDIAL 

EFFUSION 


1. Related to the volume of fluid, its rate of accumulation, and the tempo of cardiac compressions 

2. Hypotension with narrow pulse pressure 

3. Shortness of breath and extreme anxiety and apprehension 

4. Jugular venous distention 

5. Pulsus paradoxus > 10 mm Hg (may be absent) 

6. Other signs that may by present 

B. Etiology 

a. Auscultation: diminished heart sounds ("muffled") 

b. ECG: low QRS voltage and electrical alternans 

c. Chest radiograph: enlargement of the cardiac silhouette in association with clear lung fields and a normal 

vascular pattern (no CHF) 

1 . Most common 

a. Carcinoma of the lung and breast 

b. Hodgkin and non-Hodgkin lymphoma 

c. Leukemia 

d. Malignant melanoma 

746


2. Others 

a. Mesotheliomas and sarcomas of the pericardium and other metastatic tumors 

b. Postradiation pericarditis 


1. Massive pulmonary embolus 

2. Acute superior vena cava obstruction 

3. CHF 

4. Anxiety 


1. Echocardiography is the diagnostic study of choice; it is sensitive, specific, and noninvasive. 

2. Swan Ganz catheterization is performed if diagnostic confirmation is required; a positive finding is diastolic 

equalization of pressures (pulmonary artery= right ventricle= right atrial= intrapericardial) 

E. Management 

1. Supportive measures include IV fluids, inotropic support with dobutamine or isoproterenol, and 

supplemental oxygen 

2. Definitive therapeutic measures 

a. Pericardiocentesis (with ultrasound guidance if possible) 

b. Pericardia! stripping/window surgery 

c. Radiotherapy/ chemotherapy 

Ill. SUPERIOR VENA CAVA OBSTRUCTION 


1. Reflect slow, progressive tumor development; initially, the symptoms occur in early morning. 

2. Most common complaints are edema and venous distention of the face and upper extremities plus shortness 

of breath. 

3. Headache or feeling of fullness/congestion in head 

4. Facial plethora and telangiectasia 

5. Papilledema (signifies a critical increase of intracranial pressure) 

6 Cough, difficulty swallowing 

B. Etiology 

1. Carcinoma of the lung (small-cell or squamous cell): bronchogenic carcinoma is the most common cause of 

superior vena cava obstruction (usually on the right side). 

2. Lymphoma 


1. Chest radiograph: wide mediastinum and/or mass 

2. Contrast-enhanced chest CT confirms the diagnosis. 

3. MRI is indicated if neck pain is present to exclude coexistent spinal cord compression (Rubin syndrome). 

4. Immediate consultation for tissue diagnosis, followed by radiation and/or chemotherapy 

5 Intravenous stents becoming more common 

D. Management 

1. Administer supplemental oxygen. 

2. Begin measures to decrease cerebral edema if symptoms are present. 

a. Elevate head to 30° midline position. 

b. Diuretics (eg, furosemide) 

c. Corticosteroids (eg, methylprednisolone) 

747


IV. ACUTE SPINAL CORD COMPRESSION 


1. Back pain (most commonly thoracic) is the initial symptom in 95 % of these patients. 

2. Pain occurs at the site of tumor metastases; it may be localized or radicular in nature and is usually worsened 

by percussion over the affected vertebral bodies. 

3. Other symptoms include lower extremity weakness, difficulty with ambulation, sensory deficits, paralysis, 

and urinary incontinence (acute urinary retention may also occur). 

4. Thoracic spine is most commonly affected, followed by lumbar spine. Can be life-threatening in the cervical 

spine because of potential respiratory depression. 

B. Etiology 

Multiple myeloma 

2. Lymphoma (Hodgkin or non-Hodgkin) 

3. Carcinoma 

a. Lung (most common cause) 

b. Breast 

c. Prostate 


1. Plain radiographs: identify the level of vertebral collapse 

2. MRI of spine (diagnostic modality of choice) 

3. Myelography 

a. Associated with significant morbidity resulting from lumbar puncture and dye insertion 

b. Should be done if MRI is unavailable or if the MR images were of poor quality 

4. CT of the spine, in conjunction with myelography, enhances detection of small areas of spinal destruction. 

D. Management 

1. Steroids (consider high-dose dexamethasone (100 mg); otherwise 4-6 mg every 6 hours) - t inflammation 

and edema 

2. Radiation (the definitive therapy) and surgery (decompression laminectomy) improve neurologic function. 

3. Early recognition is critical for preserving neurologic function. 

V. HYPERCALCEMIA SECONDARY TO MALIGNANCY 

(MOST COMMON LIFE-THREATENING METABOLIC DISORDER 

ASSOCIATED WITH CANCER) 


1. Early presentation 

a. Anorexia, nausea, vomiting 

b. Fatigue, weakness 

c. Decreased level of consciousness 

d. Constipation 

e. Hypertension 

f. Back pain 

g. Polydipsia, polyuria 

2. Late presentation 

a. Oliguria 

b. Renal failure 

c. Stupor/coma 

d. lieus 

e. Heart blocks 

748


3. Remember the symptoms as: 

Stones (kidney stones) 

Bones (osteitis fibrosa cystica: results in pain and pathologic fractures; also can see osteoporosis, osteomalacia, 

and arthritis) 

Groans (abdominal groans: GI symptoms of constipation, indigestion, nausea, and vomiting; hypercalcemia 

can lead to peptic ulcers and acute pancreatitis) 

Moans (psychic moans: lethargy, fatigue, depression, memory loss, psychosis, ataxia, delirium, and coma) 

B. Etiology 

1 . Bone destruction 

a. Carcinomas of lung, breast, and prostate 

b. Multiple myeloma 

2. Parathyroid hormone-like substance (squamous cell carcinoma of the lung) 

3. Osteoclast-activating factor (calcitriol overproduction) 

a. Non-Hodgkin lymphoma 

b. AdultT-cell lymphoma or leukemia 

4. New hormonal therapy in patients with breast cancer (that is not related to the underlying malignancy) 


1. Serum levels of the following: 

a. Calcium (t): check ionized Ca++ levels 

b. Phosphorus (normal or !) 

c. Alkaline phosphatase (normal or t) 

d. Chloride (


4. Urinary sodium >40 mEq/L and urine osmolality > 100-150 mOsm/L associated with a urine specific gravity 

>1.002 

5. Normal renal, adrenal, and thyroid functions 


1. Depends more on the rate of decrease in serum sodium than on the absolute serum sodium concentration 

2. Weakness, malaise 

3. Headache, dizziness 

4. Subtle changes in mental status 

5. Coma, seizures 

C. Etiology: malignancies (medications for malignancies, eg, cyclophosphamide, vincristine, can also cause 

SIADH) 

1. Lung: most common (small cell) 

2. Brain 


1. Blood 

a. EI ectro I ytes 

b. Serum osmolality 

c. Thyroid function studies 

d. Adrenal function studies (if myxedema or Addison disease is suspected) 

2. Urine 

a. Urinalysis 

b. Sodium 

c. Creatinine (1' in adrenal disease) 

d. Osmolality 

E. Management 

1 . Water restriction 

2. Furosemide 0.5-1 mg/kg with concomitant normal saline results in net free water clearance while 

maintaining euvolemia. 

3. 3% saline (for seizures/dysrhythmias) 100-250 ml over several hours to lower the risk of central 

demyelination: 0.5 mEq/L increase in sodium _,, 10-12 mEq in 12-24 hours 

4. Treat underlying tumor. 

5. Demeclocycline: longer-term benefit 

VII. ACUTE TUMOR LYSIS SYNDROME 

A. Etiology 

1. Most commonly occurs 1-5 days after chemotherapy for a hematologic malignancy such as leukemia and 

lymphoma (particularly Burkitt lymphoma) but can happen in any malignancy. 

2. Other factors that make acute tumor lysis syndrome more likely include small-cell lung cancer, a high tumor 

burden, and highly chemosensitive tumors. 

3. Results in the release of intracellular products into the circulation. 

4. Overwhelms the normal homeostatic mechanisms that control potassium, calcium, phosphorus, and uric acid 

5 Biochemical hallmarks include hyperuricemia (DNA breakdown), hyperkalemia (cytosol breakdown), 

hyperphosphatemia (protein breakdown), and hypocalcemia secondary to hyperphosphatemia. 

6. The integrity of renal function is a critical factor, because the kidney provides the primary mechanism for 

excretion of uric acid, potassium, and phosphate. 

a. Acute tumor lysis syndrome is more likely to be seen in patients with preexisting renal insufficiency, and 

the subsequent metabolic derangements are more likely to be severe than in those with normal renal 

function. 

b. Acute renal failure may also be precipitated by hyperuricemia and hyperphosphatemia (even in patients 

with preexisting normal renal function, especially in the presence of rapid tumor lysis). 

c. Hyperuricemia with resultant urate nephropathy is the most common metabolic cause of renal insufficiency. 

750



1. Paresthesia 1 altered mental status, seizures, nausea, vomiting, anorexia, flank pain, oliguria 1 

hematuria, edema 

2. Acute renal failure (t uric acid and/or t PO 4 

) 

3. Ventricular dysrhythmias, sudden death (t K+ or 1 Ca++) 

4. Neuromuscular instability (1 Ca++) 

C. Management 

1. Control preexisting hyperuricemia _,. hydration, allopurinol 

a. The primary means of reducing hyperuricemia is hydration and diuresis to maintain adequate urinary 

flow (at least 100 ml/hr). 

b. Alkalinization is no longer routinely recommended. 

2. Rasburicase is now widely used to treat tumor lysis syndrome. It is a recombinant version of a urate oxidase 

enzyme that is found in many mammals but not people. It catalyzes the conversion of uric acid to allantoin. 

Discuss with oncologist first, but an empiric dose should be considered in a patient with hyperuricemia and 

renal insufficiency. 

3. Hemodialysis should be considered a potentially life-saving measure. 

4. Frequent monitoring of electrolytes, calcium, and phosphorus. 

VIII. HYPERVISCOSITY SYNDROME 

A. The degree of viscosity reflects the flow-resisting characteristics of bodily fluids. This syndrome is 

characterized by marked increase in serum proteins, WBCs, or RBCs, which result in sludging and reduction 

in microcirculatory perfusion. 

B. Classic clinical scenario 

1. The patient presents with headache, fatigue, and somnolence or coma. Persistent bleeding from mucosa! 

surfaces is common (and the platelet count is normal). Focal signs of microthrombosis may be present and 

include deafness, blindness, and seizures. 

2. On funduscopic examination, 11 sausagelinked 11 retinal vessels, hemorrhages, and exudates may be seen. 

3. A clinical clue to this diagnosis is the patient with unexplained stupor or coma who is anemic and 

demonstrates "rouleaux cells" on the peripheral smear. The laboratory may tell you the chemical tests cannot 

be performed because of serum stasis in the analyzers, ie 1 the blood is too thick. 

C. Etiology 

1. Dysproteinemias 

a. Waldenstrom macroglobulinemia 

(1) Most common cause of hyperviscosity syndrome 

(2) Produces high-viscosity lgM 

b. Multiple myeloma (lgA and lgG myelomas): second most common cause 

2. Leukemias with blastic transformation, eg, chronic myelogenous leukemia 

3. Polycythemia vera, essential thrombocytosis 


1. Increased serum viscosity (>4-5 times the viscosity of water) 

2. Increased serum proteins on electrophoresis 

3. WBC count> 100,000/mm 3 in chronic myelogenous leukemia 

4. Urinalysis_,. Bence Jones protein in multiple myeloma 

E. Management 

1. Dysproteinemias 

a. Immediate rehydration followed by emergency plasmapheresis 

b. Phlebotomy of two units and replacement of the patient's RBCs with physiologic saline is appropriate for 

patients in coma due to hyperviscosity syndrome. 

c. Chemotherapy 

2. Leukemias with blastic transformation 

a. Immediate rehydration followed by leukapheresis 

b. Hydrea 

c. Chemotherapy 

751


IX. ADRENAL INSUFFICIENCY 

A. Classic clinical scenario 

1. Sudden vasomotor collapse is classic. 

2. On physical examination, the patient is hypotensive with signs of dehydration. 

3. Laboratory findings are hypoglycemia, hyponatremia, hyperkalemia, and increased eosinophils. 

B. Etiology 

1. Carcinoma of the lung or breast 

2. Withdrawal of chronic steroid therapy 

3. Malignant melanoma 

4. Retroperitoneal malignancies 

C. Management (draw blood for a serum cortisol level first) 

1. Aggressive IV fluid therapy with D5 normal saline (1 Lover the first hour) 

2. Hydrocortisone 100 mg IV initially and every 6 hours; could use dexamethasone as an alternative if planning 

ACTH stimulation test. 

3. Correct precipitating factors (especially infection). 

X. GRANULOCYTOPENIA, IMMUNOSUPPRESSION, AND OVER 

WHELMING INFECTION IN THE PRESENCE OF MALIGNANCY 

A. Significance 

1. Infection is the most common cause of death in the cancer patient and may be subtle in presentation. 

2. Fever is usually the initial clinical manifestation of the infectious process and may be the only sign present. 

3. The risk of infection increases as the number of granulocytes decreases and is particularly pronounced in the 

granulocytopenic patient (PMN count



1. CBC with platelet count 

2. Urinalysis 


4. Cultures from all appropriate sites 

5. Electrolytes 

6. Prothrombin time (INR)/partial thromboplastin time 

7. Lactate 

F. Management 

1. Emergency therapy with IV fluids and antibiotics is recommended. 

2. Because infection may be life-threatening, antibiotics should be started as soon as cultures are drawn. 

Possible regimens include: 

a. Monotherapy options: cefepime, ceftazidime, imipenem/cilastatin, meropenem, or piperacillin/ 

tazobactam 

b. Dual therapy: monotherapy agent and gentamicin, tobramycin, or amikacin 

c. The above regimens should be modified as follows if specific infections are suspected. 

(1) Add vancomycin and ceftazidime or cefepime if a gram-positive infection is likely (a clinically 

obvious catheter related infection, severe mucositis, quinolone prophylaxis), if infection with 

methicillin-resistant S aureus (or S epidermidis) is suspected, or if the patient is hypotensive. 

(2) Add clindamycin or metronidazole if an anaerobic infection is probable (patients with abdominal or 

gynecologic complaints). 

d. Consider granulocyte macrophage colony-stimulating factor (CM-CSF) after oncology consult; generally 

will decrease length of chemotherapy-induced neutropenia by one day (may be important in critically ill 

patients). 

XI. LEPTOMENINGEAL CARCINOMATOSIS 

A. Etiology 

1. Solid tumors in adults (breast, lung, GI carcinomas/melanoma) 

2. Hematogenous malignancies in children 

3. Tumor cells reach the meninges by hematogenous spread or by direct extension from preexisting lesions. 


1. Headache is the most common presenting complaint. 

2. Cranial nerve deficits are common. 

3. Spinal symptoms also occur (weakness, numbness, and pain that is frequently radicular in nature). 


1. Contrast CT or MRI 

2. Lumbar puncture: CSF t pressure, t protein, t glucose, positive cytology 

D. Management 

1. Emergency department treatment with steroids and osmotherapy (mannitol) is indicated only in the presence of 

impending herniation. 

2. Early diagnosis and therapy are critical to preserve neurologic function. 

753

ONCOLOGIC DISORDERS: PRACTICE CLINICAL SCENARIOS 



Scenario A 

Presentation: A 45-year-old man with colon cancer presents 10 days after starting chemotherapy, with 

the sole complaint of fever. He denies chest pain, cough, sputum, shortness of breath, upper respiratory 

symptoms, dysuria or urinary frequency, diarrhea, and vomiting. He has some nausea and decreased oral 

intake. 

Physical examination: Temperature is 102 .3°F (39°C), pulse is 110 beats per minute, respiration rate is 16 

breaths per minute, and saturation on room air is 98%. Physical examination is unremarkable except for 

dry mucous membranes. 


Scenario B 

Presentation: A SO-year-old woman with breast cancer complains of being tired, weak, anorectic, 

nauseous, and constipated. Other than breast cancer, past medical history is negative, including for GI 

disorders or kidney stones. 

Physical examination: Temperature is 98.9°F (37.2°C), pulse is 96 beats per minute, respiration rate is 

18 breaths per minute, oxygen saturation on room air is 96%. Physical examination is unremarkable, 

including a nontender, nondistended abdomen with normal bowel sounds. Neurologic exam is nonfocal 

and within normal limits. Her family reports she is a little confused (slow to answer) but is oriented to 

person, place, and time. 


Scenario C 

Presentation: A 65-year-old man with lymphoma presents with back pain that worsens when he lies flat. 

The pain is located in the mid upper back and is a radicular pain. He also complains of some difficulty 

with urination but no dysuria. 

Physical examination: Temperature is 98.3°F (36.8°C), pulse is 68 beats per minute, respiration rate is 

14 breaths per minute, and saturation on room air is 95%. Physical examination reveals tenderness on 

percussion over the thoracic spine in the area ofT9-T10. There is no swelling or skin abnormalities. He has 

decreased sensation on the left lower leg to light touch and some weakness of the left lower extremity. 


Scenario D 

Presentation: EMS arrives with a SO-year-old man with a known history of lung cancer and reports that 

the patient complains of shortness of breath and seems very anxious. The patient says that he feels dizzy 

with standing. He has noticed that he has needed more oxygen at home over the past week. He denies 

associated chest pain or pressure. 

Physical examination: Temperature is 99.0°F, blood pressure is 90/69 mm Hg, and pulse is 110 beats per 

minute and regular. Respiratory rate is 18 breaths per minute, and oxygen saturation on 4 Lis 95%. On 

examination, the patient has a chronically ill appearance, seems anxious, and has diminished breath 

sounds at the bases bilaterally. Some venous distention is noted, and heart sounds are diminished. 


754


Scenario E 

Presentation: A 60-year-old woman with a history of lymphoma presents for progressive headache and 

shortness of breath. Headache onset has been gradual for 1 week. She reports that the shortness of breath 

has worsened over the past month. She has a history of right upper extremity edema following previous 

lymph node biopsy. The family reports they have noticed more swelling in her arm and face. 

Physical examination: Temperature is 98.0°F, blood pressure is 145/90 mm Hg, pulse is 100 beats 

per minute, respiratory rate is 15 breaths per minute, and oxygen saturation is 96%. Examination is 

remarkable for facial plethora, swelling of the eyelids, and telangiectasia. She is also noted to have a slight 

nonproductive cough. Her right upper extremity is nontender and edematous compared with the left. 


Scenario F 

Presentation: A 30-year-old man with HIV and Burkitt lymphoma presents 5 days after chemotherapy for 

nausea, vomiting, and flank pain. He reports that he has been urinating less and that his urine has been 

dark despite drinking adequate water. His spouse reports that he has a history of mild renal insufficiency 

but has never required treatment beyond hydration. 

Physical examination: Temperature is 100.0°F, pulse is 105 beats per minute, respiratory rate is 14 breaths 

per minute, blood pressure is 110/70 mm Hg, and oxygen saturation is 97%. On physical examination, the 

patient is noted to be thin and in no distress. Mucous membranes are dry. He has mild tenderness in his 

lower abdomen and bilateral flank. Minimal edema is seen in both lower extremities. His urine sample is 

dark in color. 


Scenario G 

Presentation: A 65-year-old woman presents via EMS for evaluation of witnessed generalized seizure and 

altered mental status. She has a history of chronic myeloid leukemia. No past history of seizure is noted. 

Laboratory studies from the nursing facility could not be performed because the "blood was too thick." 

Physical examination: Temperature is 99.0°F, pulse is 110 beats per minute, respiratory rate is 12 breaths 

per minute, blood pressure is 140/80 mmHg, and oxygen saturation is 98% on 2 L nasal cannula. On 

examination, the patient is confused and moving all extremities spontaneously. Oral examination shows 

evidence of bleeding from the tongue and mucosa! surface. Funduscopic examination reveals "sausagelinked" 

retinal vessels. 


Scenario H 

Presentation: A 70-year-old man with a history of metastatic colon cancer presents for generalized 

weakness, vision changes, and headache. Symptoms have gradually progressed over the past month. He is 

scheduled to see his oncologist, and laboratory studies obtained yesterday were within normal limits. No 

trauma or injury is reported. 

Physical examination: Temperature is 98.9°F, pulse is 90 beats per minute, respiratory rate is 14 breaths per 

minute, blood pressure is 120/80 mmHg, and oxygen saturation is 97% on room air. On examination, the 

patient appears well and is in no acute distress. Neurologic examination is positive for double vision, mild 

lack of coordination, and equal generalized weakness of the extremities. The remainder of the examination 

is unremarkable. 


755



Scenario A 

Diagnosis: fever and neutropenia 

Diagnostic evaluation: Chest radiograph and urinalysis are within normal limits. The WBC count is 

500/mm 3 with 10% neutrophils. Other laboratory studies include a metabolic panel (BUN, creatinine, 

electrolytes, etc), blood cultures, urine culture, and chest radiograph. The patient is examined for other 

sources of fever/abscess, including skin (eg, cellulitis), ears, nose, throat, rectal area, etc. 

Management: Normal saline is administered IV for mild dehydration. Because the patient has recently 

been on ciprofloxacin (a quinolone), imipenem and vancomycin are started for broad-spectrum antibiotic 

coverage, including for methicillin-resistant Staphylococcus aureus (MRSA). He is admitted to oncology. 

Scenario B 

Diagnosis: hypercalcemia 

Diagnostic evaluation: A CBC and urinalysis are within normal limits. The calcium concentration is 

14 mgldL. The ECG shows a short QT interval but no dysrhythmias. An abdominal radiograph shows a 

stone in the renal parenchyma. 

Management: The patient is placed on a cardiac monitor and 1 L of normal saline is administered IV 

immediately. After a second liter of normal saline is administered, she is given 40 mg furosemide and 

60 mg pamidronate (both IV) over 3-4 hours while waiting for a bed on the oncology floor. 

Scenario C 

Diagnosis: acute spinal cord compression 

Diagnostic evaluation: Laboratory studies, including a CBC, metabolic panel, and urinalysis, are 

unremarkable. 

Management: A consult with radiation oncology is obtained immediately. The patient is given 

dexamethasone 100 mg IV, and the diagnosis is confirmed by MRI. His oncologist is notified, and the 

patient is admitted. A consult with the spine surgeon is obtained. 

Scenario D 

Diagnosis: tamponade secondary to malignant pericardia! effusion 

Diagnostic evaluation: The WBC count is 1,400/mm 3 , and hemoglobin is normal. Mild renal insufficiency 

is noted on the serum chemistry panel. The ECG shows sinus tachycardia with low voltage QRS and 

electrical alternans. Chest radiograph shows a left lung mass, an enlarged heart, and bilateral pleural 

effusion. Bedside ultrasonography shows a large pericardia! effusion. 

Management: IV fluids are administered and inotropic support is provided. A consult with cardiology or 

cardiothoracic surgery is obtained for ultrasound-guided pericardiocentesis or pericardia! window. 

756


Scenario E 

Diagnosis: superior vena cava obstruction 

Diagnostic evaluation: Laboratory studies show mild renal insufficiency but are otherwise normal. Chest 

radiograph shows a mass in the right upper lung and anterior mediastinum. CT scan of the chest with 

contrast shows a large obstructing mass compressing the superior vena cava. 

Management: Measures to control symptoms are instituted, and the head is elevated to 30°. Administration 

of diuretics and steroids is considered. A consult is obtained with radiation oncology and interventional 

radiology for possible radiation or intravenous stent placement. 

Scenario F 

Diagnosis: tumor lysis syndrome 

Diagnostic evaluation: The CBC shows mild anemia and an increased WBC count of 30,000/mm 3 • Serum 

creatinine is 5.0 mg/dl, and potassium is 5.4 mEq/L. The urine is positive for protein and is concentrated 

without evidence of infection. Uric acid is increased. 

Management: The patient is monitored for further hyperkalemia, and an ECG is obtained. IV fluids are 

administered for hydration with strict measurement of intake and output. Urinary flow should be at 

least 100 ml/hour, and diuresis may be necessary. Allopurinol or rasburicase can be considered after 

consultation with oncology and nephrology. 

ScenarioG 

Diagnosis: hyperviscosity syndrome 

Diagnostic evaluation: Emergent noncontrast CT scan of the brain shows no obvious infarct or bleed. 

Laboratory studies show a WBC count of 110,000/mm3, and pathology has been consulted to review a 

peripheral smear. Chest radiograph and ECG show no acute process. 

Management: Symptoms should be controlled and monitored. Immediate hydration, line placement, 

and consultation for emergent plasmapheresis. Hydroxyurea and chemotherapy can be considered after 

plasmapheresis has been arranged. 

Scenario H 

Diagnosis: leptomeningeal carcinomatosis 

Diagnostic evaluation: Laboratory studies are repeated and within normal limits. CT scan of the brain 

shows no evidence of mass or herniation. MRI of the brain and spine shows a cluster of cells concerning 

for cancerous lesion. 

Management: A consult is obtained with oncology for possible radiation therapy and to discuss the need 

for lumbar puncture for cytology. 

757

758 

NOTES

SYSTEMIC INFECTIOUS DISORDERS 


Sepsis and Septic Shock ............................................................................................................................................ 762 

HIV/AIDS .................................................................................................................................................................. 763 

Tetanus ...................................................................................................................................................................... 766 

Rabies ....................................................................................................................................................................... 768 

Vector-Borne Infections ............................................................................................................................................ 769 

Lyme Disease ..................................................................................................................................................... 769 

Rocky Mountain Spotted Fever ........................................................................................................................... 771 

West Nile Virus ................................................................................................................................................... 772 

Malaria ............................................................................................................................................................... 773 

Biological Warfare Agents ......................................................................................................................................... 774 

Smallpox ............................................................................................................................................................ 774 

Anthrax .............................................................................................................................................................. 775 

Other High-Priority Biologic Agents ................................................................................................................... 777 

Legionella pneumophila ........................................................................................................................................... 777 

Toxoplasmosis ........................................................................................................................................................... 778 

Ebola ......................................................................................................................................................................... 778 

759

SYSTEMIC INFECTIOUS DISORDERS: SELF-ASSESSMENT QUESTIONS 


1. Classically, the rash of Rocky Mountain spotted fever: 

(a) Begins on the wrists and ankles, spreads to the palms and soles, and then progresses centripetally 

(b) Is coincident with the onset of fever 

(c) Appears initially at the site of the bite 

(d) Begins on the chest, face, and neck and spreads to the extremities 

2. The vector for spread of Rocky Mountain spotted fever is 

(a) The male lxodes tick 

(b) The female lxodes tick 

(c) The male Dermacentor tick 

(d) The female Dermacentor tick 

3. All of the following statements regarding erythema migrans are true except: 

(a) It is tender and painful. 

(b) It is seen in Stage I. 

(c) It is warm to the touch. 

(d) It is nonpruritic. 

4. Antibiotics that may be used in treating children with Lyme carditis include all of the following except: 


(b) Tetracycline 

(c) Amoxicillin 

(d) Ceftriaxone 

5. The animals most commonly associated with the transmission of rabies in the United States are: 

(a) Rodents, lagomorphs, and cats 

(b) Skunks, bats, and raccoons 

(c) Cats, dogs, and foxes 

(d) Cattle, foxes, and rabbits 

6. Characteristic features of anthrax on chest radiograph include all of the following except: 

(a) Widespread edema 

(b) Diffuse hemorrhagic lymphadenitis 

(c) Lobar pneumonia 

(d) Mediastinal widening 

7. Initial antibiotic therapy for inhalational anthrax is: 

(a) Ciprofloxacin or doxycycline 

(b) Levofloxacin or a third-generation cephalosporin 

(c) Ofloxacin or vancomycin 

(d) Streptomycin or clindamycin 

8. Al I of the following are characteristic of primary HIV except: 

(a) Positive HIV ELISA 

(b) Fever 

( c) Sore throat 

(d) Increased HIV viral load 

9. A minor criteria required for the diagnosis of smallpox is: 

(a) A febrile prodrome 

(b) "Belly-button" lesions 

(c) Lesions at the same stage of evolution 

(d) Centrifugal distribution of the rash with the greatest concentration of lesions on the face and distal extremities 

760


10. A suspected case of smallpox is one that: 

(a) Is epidemiologically linked to a laboratory-confirmed case 

(b) Does not meet the clinical criteria but is clinically consistent with smallpox 

(c) Is characterized by fever that precedes development of the rash 

(d) Meets the clinical criteria of smallpox 

11. CSF findings in patients with West Nile virus include: 

(a) PMNs + t protein+ pleocytosis 

(b) Lymphocytes+ t protein+ pleocytosis 

(c) Lymphocytes + t protein + pleocytosis 

(d) PMNs + t protein + pleocytosis 

12. Which of the following statements is true regarding the role of steroids in the treatment of Pneumocystis jerovici 

(PJP) pneumonia? 

(a) They have no role. 

(b) They are beneficial as adjunctive therapy in patients with moderate to severe PJP pneumonia. 

(c) They are beneficial as adjunctive therapy in patients with mild PJP pneumonia. 

(d) They should be used as a primary therapeutic modality in all patients with PJP pneumonia. 

13. Severe malaria is defined by: 

(a) Parasitemia > 1 % 

(b) Pulmonary edema 

(c) Thrombocytosis 

(d) High fever 

14. All of the following features define systemic inflammatory response syndrome (SIRS) except: 

(a) Mean arterial pressure 90 beats per minute 

(c) Respiratory rate >20 breaths per minute or PaCO 2 12,000/mm 3 , 10% bands 

ANSWERS 

I. a 

2. d 

5. 

6. 

b 

C 

9. 

10. 

3. a 7. a 11. b 

4. b 8. a 12. b 

d 

C 

13. b 

14. a 



761


I. SEPSIS AND SEPTIC SHOCK 


1. Sepsis is defined as a life-threatening organ dysfunction caused by dysregulated host response to infection 

2. For ICU patients, a sequential organ failure assessment (SOFA) score of 2 or more points meets the criteria 

for sepsis (associated with in-hospital mortality> 10%). Because the SOFA score requires multiple laboratory 

tests, the following bedside clinical score, termed quickSOFA, has been proposed for use in the emergency 

department (2 or more of the following): respiratory rate c':22 breaths per minute, systolic blood pressure 

::;100 mm Hg, or altered mental status 

3. Septic shock is defined as requirement of a vasopressor to maintain a mean arterial pressure c':65 mmHg 

despite adequate volume resuscitation and a serum lactate level >2 mmol/L. 

4. The term "severe sepsis" is no longer used. 

5. These new sepsis definitions abandon the concept of systemic inflammatory response syndrome (SIRS) because 

those symptoms occur in a large majority of hospitalized patients and are often associated with benign 

conditions. SIRS is defined by two or more of the following: 


a. Temperature > 101 °F (38.3°C) or 90 beats per minute 

c. Respiratory rate >20 breaths per minute or PaCO, 12,000 cells/mm 3 , 10% bands 

1. Age >65 years old 

2. lmmunosuppression (AIDS, chronic steroid therapy, chemotherapy, transplant medicines, diabetes) 

3. Bacteremia 

4. Chronic indwelling lines and tubes (Foley catheters, central lines) 

C. Pathogens 

1. Gram-positive cocci are most common, followed by gram-negative rods (in the United States). 

2. Hospital-acquired pathogens are more likely to be resistant to multiple drugs and result in higher mortality rates. 

3. Pathogens from a urinary source result in a lower mortality rate than those from pulmonary, GI, or unknown 

sources. 


1. History and physical examination for source, such as intra-abdominal infections (cholecystitis, appendicitis, 

or peritonitis), skin examination (cellulitis, evidence of IV drug abuse), indwelling catheters (dialysis catheter, 

urinary catheters, central Ii nes), endocarditis 

2. Complementary diagnostic studies: chest radiograph, urinalysis, urine culture, blood culture, CBC, serum 

chemistries, lactate 

E. Management 

1. Early aggressive resuscitation 

a. Focused on reversing end-organ hypoperfusion/hypoxia by aggressive fluid administration, early broad 

antibiotic administration, and vasopressor support 

b. Administration of broad-spectrum antibiotics within 1 hour of recognition of septic shock 

c. An initial fluid bolus of 30 ml/kg of normal saline 

2. Supplemental oxygen therapy and intubation/mechanical ventilation as indicated by patient's clinical status 

(increased work of breathing, hypoxia, altered mental status, inability to protect airway) 

3. Norepinephrine is vasopressor of first-choice. Epinephrine or vasopressin can be added as needed to maintain 

mean arterial pressure >65 mmHg. 

4. Dopamine is not recommended except in highly select circumstances (eg, patients with low risk of 

tachyarrhythmias and absolute or relative bradycardia). 

5. Corticosteroids are only used to treat adult septic patients with shock if adequate fluid resuscitation and 

vasopressor therapy are unable to restore hemodynamic stability. 

6. Antibiotic therapy 

a. Community-acquired urinary tract infection: fluoroquinolone or third-generation cephalosporin 

b. Community-acquired pneumonia (non-ICU): ceftriaxone + macrolide 

c. Pneumonia, recently hospitalized: fourth-generation cephalosporin or piperacillin/tazobactam + vancomycin 

762


d. Unknown source: broad spectrum covering gram-positive, gram-negative and anaerobic organisms with 

special consideration for methicillin-resistant Staphylococcus aureus (MRSA), eg, piperacillin/tazobactam 

+ vancomycin 

II. HIV/ AIDS 

A. Etiology and pathogenesis 

1. Disease complex resulting from an incompetent immune system. It begins when a patient becomes infected 

with HIV, a retrovirus. 

2. CDC estimates that in the United States, over 1.2 million people are HIV positive, and 50,000 people are 

newly infected yearly. 

3. HIV reduces the number of normally immunocompetent cells (especially T-helper lymphocytes). 

4. AIDS is defined by CD4 count 95% after 6 months). 

6. HIV antibody screening with ELISA confirmed by Western blot assay. 

E. AIDS-related diseases 

1. Pneumocystis jiroveci pneumonia (PJP) 


(1) The causative organism is P jiroveci (formerly P carinii), a genus of unicellular fungi found in the 

respiratory tract. 

(2) Seen almost exclusively in immunosuppressed patients 

(a) Patients with AIDS 

(b) Patients receiving immunosuppressive therapy for cancer (especially corticosteroids) or organ 

transplantation 

(c) Premature and malnourished infants 

(d) Children with primary immunodeficiency disease 

(3) Most common opportunistic infection seen in HIV patients; the leading cause of death in these patients 

(a) 80% of HIV patients acquire PJP at some time during their illness. 

(b) It is the initial opportunistic infection in 2:60% of those who are not receiving prophylactic therapy. 

(c) In adults, infection generally does not occur until the CD4 lymphocyte count is



(1) Signs and symptoms develop in a slow and insidious fashion in AIDS patients; most have been 

symptomatic for 2-3 weeks at the time of diagnosis. Abrupt onset of signs and symptoms with rapid 

progression occurs more commonly with oncology patients. 

(2) Patients usually present with dyspnea, nonproductive cough, and fever. Decreased exercise tolerance 

is also common. Other more variable complaints include weight loss, night sweats, chest pain, fatigue, 

and chills. 

(3) Typical physical findings are cyanosis with tachypnea, tachycardia, and a moderately increased 

temperature. 


(1) Arterial blood gases (or pulse oximetry as substitute) are frequently abnormal. 

(a) Decreased pO 2 

(b) Increased alveolar-arterial (A-a) oxygen gradient 

(c) 

Low oxygen saturation or desaturation with 10 minutes of exercise 


(a) May be normal in up to 20%-30% of patients; this is more common early in the disease process. 

(b) Classically demonstrates bilateral diffuse interstitial or alveolar infiltrates beginning in the perihilar 

region and extending in a "bat-wing" pattern. 

(c) PJP is the most common cause of pneumothorax in patients with AIDS. 

(3) Lactate dehydrogenase: increased levels in the setting of clinical suspicion and normal chest 

radiograph are helpful in making the diagnosis. Degree of increase correlates with prognosis. 

(4) A high-resolution CT scan that reveals patchy nodular densities suggests the diagnosis. 

(5) The diagnosis in the emergency department is a clinical one. Inpatient evaluation may include 

bronchoscopy/lavage and sputum monoclonal antibodies. 

d. Treatment 

(1) Oxygen 

(2) Antibiotics 

(a) TMP-SMX 

1. Initial drug of choice in patients who can tolerate sulfa drugs. It has the advantage of providing 

coverage for some bacterial pneumonias and is well tolerated in non-AIDS patients. 

ii. Dosage is trimethoprim at 15-20 mg/kg/day and sulfamethoxazole at 75-100 mg/kg/day IV or 

orally divided in four doses x 14-21 days. 

iii. Adverse reactions include nausea and vomiting, fever, rash, increased liver enzymes, and 

neutropenia. 

(b) IV Pentamidine 

1. May be used as an alternative drug for patients with a history of severe allergy or adverse 

reactions to sulfonamides. 

ii. Dosage is 4 mg/kg/day IV over 1 hour x 14-21 days. Blood pressure must be carefully 

monitored during infusion, because hypotension is a common adverse effect. 

iii. Adverse reactions include hypotension, syncope, tachycardia, fever, facial flushing, pruritus, 

renal toxicity, increased liver enzymes, hypoglycemia, rash, thrombocytopenia, neutropenia, 

pancreatitis, and hallucinations. 

(3) Steroids 

(a) Beneficial as adjunctive therapy in patients with moderate to severe PJP. They limit oxygen 

deterioration, decrease mortality and respiratory failure, and accelerate recovery. 

(b) Administer them to all children and to adult patients with a p0 2 

35 mmHg. 

(c) Start before the antibiotic is given, because hypoxemia may worsen. 

(d) Dosage 

i. Prednisone is administered at a starting dosage of 40 mg bid x 5 days, followed by 40 mg/ 

day x 5 days, followed by 20 mg/day x 11 days. 

ii. Methylprednisolone may be substituted for prednisone at 75% of the above dosages if IV 

therapy is preferred. 

764


e. Disposition 

(1) Hospitalization is indicated for most patients, especially children and those with a prior history of PJP, 

because the mortality rate increases with subsequent episodes. 

(2) Patients with mild disease and favorable respiratory parameters can be treated on an outpatient basis if 

close follow-up can be assured. 

f. Prophylaxis 

(1) Recommended for the following patients: 

(a) Those with a prior episode of PJP pneumonia (the recurrence rate is 60% in AIDS patients) 

(b) HIV-infected patients with a CD4 count 3 weeks for esophageal 

candidiasis 

765


6. Herpes zoster (shingles) 

a. Can be a severe and recurrent problem at any stage of HIV infection 

b. Acyclovir orally (in large doses) or parenterally is the treatment of choice. 

7. Cytomegalovirus retinitis 

a. Most common ocular complication of AIDS and, if untreated, leads to blindness 

b. Funduscopy: small, white perivascular infiltrates (early); hemorrhagic necrotizing retinitis (late) 

c. Treatment with foscarnet or ganciclovir is indicated. 

8. A host of other AIDS-related diseases can affect one or more organ systems, including tuberculosis (see 

Thoracic and Respiratory Disorders, pages 231-291 ). The management of AIDS and associated opportunistic 

infections is rapidly evolving; early consult with an infectious disease specialist regarding therapeutic options is 

highly recommended. 

F. Postexposure prophylaxis 

1. Risk of HIV transmission: 0.3% for percutaneous inoculation 

a. Risk greatest if hollow-bore needle in contact with infected blood 

b. Splashes on mucous membranes or broken skin 0.09% risk of transmission 

2. Fluids that can transmit HIV: blood, seminal/vaginal, breast milk (feces, nasal, saliva, sweat, tears, urine, and 

vomit are not infectious unless bloody) 

3. Nonoccupational exposure 

a. Risk greatest with receptive anal intercourse (1 %-30%), insertive anal or receptive vaginal (0.1%-10%), 

and insertive vaginal (0.1 %-1 %). 

b. Risk of needle sharing for IV drug abuse is 0.67% per contact. 

4. Management 

a. Start as soon as possible. 

b. Three-drug regimen: emtricitabine (FTC), tenofovir DF, and raltegravir 

c. 28-day duration unless the source patient is found to be HIV-negative 

d. Adverse effects: nausea/vomiting, diarrhea, headache 

e. Renal toxicity possible with tenofovir DF 

f. 24-hour postexposure prophylaxis hotline (PEPline): (888) 448-4911 

Ill. TETANUS 

A. Etiology 

1. Tetanus is a potentially fatal neuroparalytic disease caused by tetanospasmin, which is an exotoxin produced 

by Clostridium tetani, a gram-positive anaerobic rod found chiefly in soil and the feces of many animals 

(including people). 

2. The organism cannot invade healthy tissue, because it requires an anaerobic environment to convert the spores 

into toxin-producing vegetative forms. The toxin enters peripheral nerve endings and ascends to the spinal 

cord and brain. The major effect occurs in the spinal cord where the toxin prevents release of the inhibitory 

neurotransmitters, thereby producing neuromuscular irritability and generalized spasms. 

3. High-risk patients 

a. The elderly (inadequate immunization) 

b. IV drug abusers 

c. Patients with decubiti or diabetic ulcers 

4. In 10%-20% of cases, no causative wound or injury is ever determined. 


1. The toxin has no effect on the sensorium, and patients are alert and oriented. 

2. Trismus ("lockjaw") is the presenting symptom in >50% of cases. 

3. The longer the incubation period (range 1 month), the less severe the disease. 

4. Four forms of clinical tetanus 

a. Local tetanus 

(1) Muscle rigidity close to the site of injury 

(2) Resolves in weeks to months without sequelae 

(3) May progress to the generalized form 

766


b. Generalized tetanus (most common form) 

(1) Pain and stiffness in the jaw and trunk muscles - facial rigidity (trismus and risus sardonicus) - 

spasms and tonic contractions - dysphagia, opisthotonos - glottal spasm (with respiratory distress 

that may lead to arrest) and painful convulsive spasms (arms flexed, fists clenched, legs extended). This 

may be confused with seizures. 

(2) Autonomic nervous system dysfunction (occurs during the second week of clinical tetanus) - signs 

of catecholamine excess (hyperpyrexia, sweating, tachycardia, and labile hypertension) - t blood 

pressure, pulse, and temperature - high morbidity and mortality rate 

c. Cephalic tetanus (may occur in fully immunized patients) 

(1) Head injury or otitis media - cranial nerve dysfunction (cranial nerve VII most common) and trismus 

(2) Poor prognosis 

d. Neonatal tetanus 

(1) Secondary to inadequate maternal immunization 

(2) Usually results from an infected umbilical stump 

(3) Extremely high mortality rate 


1. Strychnine poisoning (strychnine is detectable in the urine) 

2. Dystonic reactions to phenothiazines (improves with diphenhydramine) 

3. Hypocalcemic tetany 

4. Early rabies (unlike tetanus, trismus is uncommon) 

D. Management 

1. Maintain an adequate airway to prevent asphyxia. 

2. Use a benzodiazepine to control muscular spasms. 

3. If the patient needs aggressive airway management, neuromuscular blockade with vecuronium. Concomitant 

sedation is mandatory; use a benzodiazepine, barbiturate, or propofol. 

4. Autonomic dysfunction, manifested by sympathetic overactivity, can be treated with labetalol. 

5. Meticulous surgical debridement of the causative wound is critical. Theoretically, this decreases continued 

toxin production. 

6. Give human tetanus immune globulin 500 IU IM to neutralize any unbound toxin. 

7. The antibiotic of choice is IV metronidazole. 

8. Clinical disease does not produce immunity, so give the first dose of tetanus toxoid in the emergency 

department. 

9. A quiet room is essential to prevent precipitation of generalized spasms. 

E. Tetanus prophylaxis protocol 

Table 48: Tetanus Immunization Protocol 

Previous Immunization 

Uncertain or 5 years ago 

c::3 doses with last dose > 10 years ago 

Minor Wound 

Vaccinate 

Vaccinate 

All Other Wounds 

Vaccinate + tetanus 

immune globulin 

Vaccinate 

Vaccinate 

1. Complete primary tetanus immunization for adults consists of three IM injections ofTd 0.5 ml; the second 

dose is given 6 weeks after the first, and the third is given 6 months later. 

2. Contaminated (tetanus-prone) wounds 

a. Those contaminated with feces, soil, or saliva 

b. Punctures, crush wounds, avulsions 

c. Burns and frostbite 

d. Those from missiles 

e. Those >6 hours old or infected on initial presentation 

767


3. Patients >60 years old and immigrants are most likely to have inadequate prior tetanus immunization. If a 

patient's vaccination status is unknown or uncertain, he or she should receive the complete vaccination series. 

4. Give human tetanus immune globulin to individuals with a tetanus-prone wound who have not completed a 

primary immunization series or who have a contraindication to receiving Td. 

5. The CDC recommends that emergency physicians offer tetanus prophylaxis routinely to all patients 

(regardless of the presenting complaint) who have not been immunized within the last 10 years. 

IV. RABIES 

A. Etiology 

1. A rhabdoviral infection of the CNS with an incubation period that usually ranges from 30 days to years 

2. Extremely rare in the United States (22 cases from 1980 to 1997) 

3. Transmitted primarily by the saliva of an infected animal through a break in the victim's skin or mucous membrane. 

4. In the United States, ~90% of animal rabies is found only in wildlife (raccoons, skunks, bats, foxes, coyotes, 

and bobcats). Almost all cases of rabid domestic animals have been reported in rural areas; rabies is prevalent 

in local wildlife species. 

a. Major wildlife reservoir is the raccoon, with> 60% of all reported cases (most prevalent in the eastern states). 

b. Skunk rabies is predominant in the central and western states. 

c. Since 1980, 78% of documented rabies cases have had no history of exposure. 


1. The prodromal period may resemble "viral illness." Symptoms are variable and include fever, headache, 

malaise, sore throat, dry cough, anorexia, and nausea and vomiting; back pain is common. The patient may not 

tell you about the bite or the associated tingling, pain, or numbness if other symptoms are more distressing. 

2. The excitement phase of clinical presentation is variable and includes thought disturbances with lucid intervals, 

hypersensitivity to light/sound/touch, agitation, confusion, hallucinations, restlessness, or even seizures. 

3. Finally, evidence of brainstem dysfunction becomes apparent. If the patient is lucid, check for diplopia, facial 

palsies, and dysphagia (which leads to the characteristic hydrophobia). From this point, the patient lapses into a 

coma. Involvement of the respiratory center follows, and an apneic death ensues. 

C. Postexposure prophylactic management 

1. Thoroughly irrigate the wound; this can decrease the amount of virus at the wound site and is an important 

step in rabies prevention. 

2. Tetanus prophylaxis as indicated. 

3. Vaccine selection 

a. Active immunization with human diploid cell vaccine (HDCV) is indicated after a bite from an animal in 

the suspected group; 1 ml is given IM on day 0 and repeated on days 3, 7, and 14. 

b. Passive immunization with human rabies immune globulin (HRIG) is advised if the animal is (or may 

be) rabid; 20 IU/kg, with as much as possible infiltrated at the site of the bite, and the remainder given 

IM at a site near to the wound (avoid gluteal administration because vaccine deposited in fat is poorly 

immunogenic). 

D. Management 

1. Report the incident to the public health department. 

2. Domestic animals (cats and dogs) 

a. If the animal is secured/captured, its behavior is normal, and it remains normal for a 10-day observation 

period, no treatment is necessary. 

b. If the animal is secured/captured and exhibits abnormal behavior or becomes ill during the 10-day 

observation period, the animal should be euthanized, the head/brain placed in a plastic bag, and 

sent refrigerated (not frozen or fixed in formalin) to the state public health department for direct 

immunofluorescent antibody studies. 

(1) If laboratory analysis is negative for rabies, no treatment is needed. 

(2) If laboratory analysis is positive for rabies, treatment with HRIG and the HDVC series is indicated and 

should be started as soon as possible. 

c. If the animal cannot be found and captured, pub I ic health officials should be contacted regarding the 

prevalence of rabies in the involved species in your locality and the need for treatment. 

768


3. Wild animals (skunks, bats, etc): assume they are rabid unless proved negative by direct immunofluorescent 

antibody testing. 

a. If the wild animal cannot be found and captured, begin treatment with HRIC and the HDCV series. 

b. Wild animals that are captured should be tested immediately. 

(1) If laboratory analysis is negative for rabies, no treatment is needed. 

(2) If laboratory analysis is positive for rabies, administer HRIC and the HDCV series. 

c. Consider postexposure prophylaxis for those who were in the same room as a bat and might be unaware of 

bite or contact. 

4. Bites from rodents, squirrels, and rabbits almost never require postexposure prophylaxis. 


1. Performed on a specimen of brain tissue obtained postmortem or by biopsy 

2. Fluorescent antibody testing is the procedure of choice (both sensitive and specific). 

3. Staining for Negri bodies: although these intracytoplasmic inclusion bodies are pathognomonic for rabies, they 

are absent in up to 25% of cases (unacceptably high falsenegative rate). 

V. VECTOR-BORNE INFECTIONS (SPREAD BY MOSQUITOES, 

TICKS, AND FLEAS) 

A. Lyme disease 

1. Etiology and epidemiology 

a. This tick-borne illness has been reported on every continent in the world except Antarctica; in the United 

States, the highest frequency is in New England and the middle Atlantic and upper Midwestern states. 

b. The lxodes tick (deer tick) harbors the spirochete Borrelia burgdorferi. 

c. The most common tick- and vector-borne disease in the United States; most cases occur between May and 

August (when tick and human outdoor activity are greatest) and where deer populations are increasing. 


a. Early localized disease (within 1 month) 

(1) History from patients who have been in or near wooded areas 

(a) Fever and fatigue 

(b) Malaise and myalgia 

(c) Headache 

(2) Physical examination: erythema migrans is the hallmark of early Lyme disease---;,. circular skin lesions 

that begin as a macule or papule at the site of the tick bite and gradually enlarge, at times attaining 

diameters of c::25 cm. Classically, erythema migrans has a bright-red to blue-red border with a pale 

interior; it is warm to the touch and is neither tender nor pruritic. Erythema migrans is absent in 20% 

of cases. Note: For pictures of erythema migrans and further specifics on treatment guidelines, see the 

Centers for Disease Control website (http://www.cdc.gov/lyme). 

Source: http://phil.cec.gov/phil ID #9875 

Content provider: CDC/James Cathany 

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b. Early disseminated disease (weeks to months) 

(1) Neurologic abnormalities predominate the clinical picture. 

(a) 

Fluctuating meningoencephalitis (most common) 

(b) Cranial neuropathy (especially Bell's palsy) 

(c) Peripheral neuropathy (mononeuritis, radiculitis, brachia! plexitis) 

(2) Myocarditis is the most common cardiac abnormality; it occurs transiently and is associated with 

varying degrees of AV block. 

c. Late disease (months to years later-,, chronic infection) 

(1) Migratory oligoarthritis of the large joints is characteristic. 

(a) The knee is most often affected and may be associated with an effusion. 

(b) A clue to the diagnosis is the intermittent nature of the joint pain and swelling that occurs for 

weeks or months; then it completely disappears and recurs sometime later. 

(2) Neurologic symptoms include a wide range of manifestations that may mimic other neurologic 

conditions and, at this stage of disease, may be the only presenting complaint. Be especially suspicious 

of any of the following: 


(a) Subtle encephalopathy (disturbances in mood, memory, sleep) or polyneuropathy (spinal/radicular 

pain or numbness/tingling in the hands and feet) 

(b) Cognitive dysfunction (confusion -,, dementia) 

(c) Incapacitating fatigue 

a. Clinical suspicion is of utmost importance, because laboratory testing may be inaccurate or misinterpreted. 

A history of tick bite (or exposure in an endemic area) followed by a flu-like syndrome and a rash 

(erythema migrans) suggests the possibility of Lyme disease. Unfortunately, 66% of patients do not recall a 

tick bite, and 20%-40% never develop or notice the rash. 

b. Cerebrospinal fluid (CSF) is almost always abnormal but is frequently confused with viral meningitis, 

because lymphocytes and monocytes are the dominant cell types; however, when associated with an t CSF 

protein, the diagnosis should be suspected. 

c. The two-test approach is recommended. 

(1) Initial positive ELISA screen is followed by Western blot. ELISA has a high false-positive rate but good 

sensitivity. PCR is not recommended because of poor sensitivity and specificity. There is no value in 

testing in early localized disease. 

(2) lgM antibodies develop within 1-2 weeks; lgG antibodies develop within 2-6 weeks. Antibodies may 

be present for years after Lyme disease treatment. 

(3) Antibiotics in early Lyme disease may prevent seroconversion. 

d. ECG for evaluation of AV block 

4. Post-tick exposure prophylaxis 

a. Deer tick exposure with tick engorgement for >36 hours is treated with one dose of doxycycline (200 mg) 

given orally. 

b. Ticks that are embedded in the skin must be removed ensuring that there is no compression of the gut by 

using fine tweezers. Grasp the tick as close as possible to the head and pull straight out. 

5. Management 

a. Early localized disease: erythema migrans treated with doxycycline or amoxicillin for 10-14 days 

b. Early disseminated disease 

(1) Neurologic 

(a) Isolated facial palsy: oral doxycycline or amoxicillin for 14 days 

(b) Other neurologic: IV therapy for 14-21 days 

(2) Cardiac 

c. Late disease 

(a) Cardiac monitor and temporary pacing if needed 

(b) IV therapy until cardiac symptoms resolve up to 21 days 

(1) Arthritis: 28-day course of oral antibiotics 

(2) Neurologic: 28-day course of IV antibiotics 

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d. Medication 

(1) Oral 

(2) IV 

(a) Doxycycline 100 mg twice daily (contraindicated in children 102.2°F [39°C]). 

b. Although rash is the hallmark of RMSF, it is absent in 5 %-15 % of cases. 

(1) An erythematous blanching rash (with 2-3 mm macules) appears initially on the flexor surfaces of 

the wrists and ankles, spreads to the palms and soles, and then moves rapidly (centrally) to cover 

most of the body. 

(2) In the next 2-3 days, the rash becomes maculopapular, darker red, fixed, and finally petechial. 

c. A diagnostic clue on physical examination is extreme tenderness of the gastrocnemius muscle. 

4. Diagnostic evaluation (usually useful only retrospectively) 

a. Because serologic tests are often negative in the early phase of illness (results are not usually available 

during emergency department assessment and availability of specific tests vary from hospital to hospital), 

the diagnosis of RMSF is a clinical one. The triad of fever, headache, and rash, occurring late spring to early 

fall, is presumptive evidence for treatment and should not await positive serologic testing. The mortality rate 

remains high because of delay in starting appropriate antibiotic therapy. 

(1) Laboratory findings of neutropenia, thrombocytopenia, increased liver function studies, and 

hypernatremia are suggestive. 

(2) Indirect fluorescent antibody assay 

(a) The most sensitive and specific test 

(b) A titer> 1 :64 is diagnostic 

(3) Indirect hemagglutination (second most sensitive and specific) 

(4) The Weil-Felix, complement fixation, and latex agglutination tests are much less sensitive. 

771


b. Skin biopsy: immunofluorescent antibody staining of a rash specimen 

(1) 70% sensitivity, 1 00% specificity 

(2) The best rapid diagnostic test; if available, it may provide rapid diagnosis (as early as the third day 

of illness). 

5. Management 

a. Early antibiotic therapy significantly reduces the mortality rate so, if you suspect RMSF, start doxycycline 

therapy. 

(1) Adults: 100 mg orally or IV bid 

(2) Children 102.2°F [39°(], headache, and myalgias). 

(1) Signs of meningitis: nuchal rigidity 

(2) Symptoms of early encephalitis: mental status changes (confusion, disorientation, t level of 

consciousness) 

(3) Signs of severe encephalitis: stupor or coma, some degree of paresis (including flaccid paralysis) or 

proximal muscle weakness 

(4) These are typically older and/or debilitated patients. Patients with neuroinvasive illness have a 

mortality rate of approximately 10%. 

772



a. CSF: lymphocytes+ t protein+ pleocytosis (30-100 cells/mm 3 ) and no bacterial pathogens 

b. Radiologic studies 

(1) CT rarely shows signs of CNS inflammation. 

(2) MRI demonstrates enhancement of leptomeninges and/or periventriular areas in 30% of patients. 

c. Differential diagnosis 

5. Treatment 

(1) Herpes simplex virus 1 meningoencephalitis 

(a) Predominance of PMNs (not lymphocytes), RBCs, and possibly glucose 

(b) Electroencephalography: temporal lobe focus 

(2) Bacterial meningitis: positive Gram stain and culture 

a. Empiric treatment for bacterial meningitis and/or herpes simplex viral encephalitis is appropriate until 

results of testing for West Nile virus-lgM are clarified. 

b. Symptomatic and supportive measures are the mainstay of therapy; there is no specific therapy for the 

treatment of West Nile virus. 

6. Prevention 

a. No human vaccine is currently available. 

b. Reduce mosquito breeding. 

(1) Drainage of standing water 

(2) Chemical spraying (to reduce vector transmission) 

c. Avoid mosquito exposure. 

D. Malaria 

1. Etiology 

a. Plasmodium fa/ciparum (only one that can cause severe disease) 

b. P malariae 

c. P vivax and P ovale can develop dormant stage for years. 

d. Vector: Anopheles mosquito 


a. Consider malaria in all febrile travelers from areas where malaria is endemic. 

b. Incubation 7-30 days (month with inadequate prophylaxis) 

c. 1-2.7 million related deaths per year (75% African children) 

d. Leading cause of death in children worldwide 

e. Leading reason for blood transfusion worldwide 


a. Classic malaria 

(1) Cyclic stages of rigors, fever, headache, vomiting, myalgias, seizures (infants), sweats, fatigue 

(2) Every 2 days (P falciparum, P vivax, P ovale) 

(3) Every 3 days (P malariae) 

(4) Splenomegaly 

(5) Anemia 

b. Severe malaria (P fa/ciparum) 

(1) Severe anemia (parasitemia >5%) 

(2) Cerebral malaria: confusion, coma, seizures, permanent deficits (deaf, blind, palsies) 

(3) Pulmonary edema, ARDS 


(5) Shock 

(6) Acute renal failure 

4. Diagnostic evaluation: thin and thick smears 

5. Management 

a. Infectious disease consult (for latest chloroquine sensitivities) 

b. Chloroquine sensitive (Middle East, Central America west of Panama Canal) 

c. Chloroquine-resistant strains: quinine plus doxycycline or atovaquone/proguanil 

d. Severe anemia requires parenteral therapy: quinidine + doxycycline, or artesunate 

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VI. BIOLOGICAL WARFARE AGENTS 

A. Smallpox 

1. Overview 

a. Variola (smal I pox) is an orthopoxvirus. Formerly used as a weapon in the biological warfare program of 

the Soviet Union, smallpox is one of the most feared potential bioterrorist agents because of the high 

mortality rate in unvaccinated patients. A single case, anywhere in the world, would constitute a global 

health emergency. 

b. Flu-like symptoms (mild to severe) precede the onset of rash by 1-4 days. 

c. Characteristic clinical features 

(1) Febrile prodrome (> 101 °F [38.3°C]) and at least one of the following: 

(a) Headache 

(b) Backache 

(c) Chills 

(d) Vomiting 

(e) Severe abdominal pain 

(f) 

Prostration 

(2) Smallpox lesions: distinct well-circumscribed vesicles or pustules that may become umbilicated or 

confluent as they evolve 

(3) High mortality rates (30%) in unvaccinated patients primarily because of lack of specific therapy 


a. There are no known animal or insect vectors. The virus is spread person to person by droplet nuclei or 

aerosols expelled from the oropharynx; it can also be spread by direct contact (skin lesions or contaminated 

clothing or bedding). 

b. Risk of transmission occurs during the prodrome but maximizes with onset of the rash, which usually 

begins in the mouth and throat and lasts 7-10 days. The risk of infectivity is significantly decreased when 

the lesions scab over. When the scabs fall off the skin, there is no longer any risk of transmission from the 

individual, but the scabs remain infectious. 

3. Clinical presentation (depends on the evolutionary stage of the illness) 

a. Incubation period (7-17 days): not contagious 

b. Prodrome (2-4 days): sometimes contagious 

Initial symptoms include fever (usually high [101 °-1 04°F; 38.3 °-40°C]), head/body aches, malaise, 

± vomiting; patients usually feel too sick to carry on normal activities. 

c. Early rash (-4 days): most contagious 

Fever and red spots in the mouth - spread to face - arms and legs - hands and feet. Rash develops to 

bumps with a thick, opaque fluid and that look like a bellybutton (a major distinguishing characteristic of 

smallpox). 

d. Pustular rash (-5 days): contagious 

The bumps become pustules (sharply raised, round, and firm to the touch) often described by patients as a 

feeling of BB pellets embedded under the skin. 

e. Pustules and scabs (-5 days): contagious 

The pustules form a crust and then scab; by the end of the second week (after the appearance of the rash), 

most of the sores have scabbed over. 

f. Resolving scabs (-6 days): contagious 

As the scabs fall off, they leave marks on the skin that eventually become pitted scars; most of the scabs are 

gone by 3 weeks after the rash appeared. 

g. Scabs resolved: not contagious 

Smallpox remains contagious until al I of the scabs have fallen off. The scabs continue to remain infectious. 


a. Suspicious setting: unexplained fever and a rash in a patient with small red spots or sores on the tongue 

and buccal mucosa 

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b. Clinical diagnosis 

(1) Major criteria 

(a) Febrile prodrome with temperature > 101 °F (38.3°C) 

(b) Classic "belly-button" lesions 

(c) All lesions in the same stage of evolution 

(2) Minor criteria 


(a) Centrifugal distribution of the rash on the face and distal extremities 

(b) Lesions appeared first on the oral mucosa and/or palate, face, or arms 

(c) Patient appears toxic or moribund 

(d) Slow evolution of lesions (macules-;, papules-;, pustules), each type over a period of 1-2 days 

(e) Lesions on the palms and soles 

a. Chickenpox (varicella) is the most likely infectious disease to be confused with smallpox; however, 

chickenpox has distinctive features that should make the diagnosis easier. 

(1) Varicella lesions tend to be more superficial, appear in crops, and are present in different stages of 

development at any given time, ie, papules, vesicles, and scabs all appear together. 

(2) Varicella lesions tend to be more on the abdomen and back and less on the extremities. 

b. Disseminated herpes zoster is more likely in an immunocompromised host. 

6. Specific treatment 

B. Anthrax 

a. Smallpox vaccination: if administered within 4 days of the first exposure, attenuates the course of the illness 

and protects against a fatal outcome. 

b. Vaccinia immunoglobulin: antibodies against a similar virus may shorten duration of disease. 

c. Postexposure isolation and infection control practices: critical to limiting transmission of smallpox to 

populations outside the target source. 

1. Overview 

a. lnhalational anthrax is a rare and rapidly fatal disease. A potential biological warfare agent, it is often 

difficult to diagnose early; a high index of suspicion is required. 

b. Clinical presentation: mild flu-like symptoms progress rapidly to respiratory distress-;, septic shock-;, 

multiple organ failure 

c. Characteristic features on chest radiograph 

(1) Diffuse hemorrhagic lymphadenitis 

(2) Widespread edema 

(3) Mediastinal widening 

d. Management 

(1) Fluoroquinolones 

(2) Adequate management of respiratory distress and septic/hemorrhagic shock in an ICU setting 

(3) Vaccination programs 

e. Morbidity/mortality rate is high despite above measures. 


a. The distribution of Bacillus anthracis is worldwide and most prevalent among herbivores (cattle, sheep, 

horses, and goats) that contaminate soil and water holes with 8 anthracis (which may subsequently 

sporulate and persist in the environment). 

b. While aggressive animal vaccination has lowered the incidence of anthrax among livestock in the United 

States, the microorganism remains endemic in the soil ofTexas, Oklahoma, and the lower Mississippi valley. 

c. Most human cases of anthrax are due to agricultural or industrial exposure. Shepherds, farmers, and 

workers in manufacturing plants using infected animal products (particularly contaminated hide, goat hair, 

wool, or bone) are at highest risk. 

d. There are three predominant clinical forms of anthrax: 

(1) Cutaneous anthrax (>95% of cases) from entry of spores through skin abrasions 

(2) lnhalational anthrax 

(3) GI anthrax (contaminated meat) 

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3. Microbiology 

a. 8 anthracis is a large, square-ended, nonmotile, aerobic, gram-positive rod with a centrally located spore. 

b. On gram stain, the spore appears as an "unstained" area. 

c. Spores are highly resistant to drying, boiling for 10 minutes, and most disinfectants. 

4. Clinical presentation (depends on route of inoculation) 

a. Cutaneous anthrax (most common form; recognition is important because its presence could possibly 

herald the more serious inhalational anthrax) 

(1) Through cuts, abrasions, or biting flies, spores of B anthracis are introduced into the skin; within hours, 

they germinate, and vegetative cells multiply and produce anthrax toxin, which causes edema and 

necrosis. 

(2) Within 5 days of exposure, small painless (but pruritic) papules appear; 24-48 hours later, the papules 

enlarge and become vesicular. Edema out of proportion to the size of the vesicle surrounds the lesion 

and is often associated with fever, malaise, and regional adenopathy. 

(3) Near the end of the first week, the vesicle usually ruptures, and the remaining ulcer progresses to a 

black eschar. If recognized and treated promptly, cutaneous anthrax is rarely fatal. 

b. Pharyngeal and GI anthrax 

(1) After ingestion of contaminated undercooked meat, pharyngeal ulcers and edema of the neck develop 

as the anthrax bacilli multiply. 

(2) After intestinal absorption, bacteria are transported to mesenteric and regional lymph nodes---,, 

multiplication and dissemination---,, hemorrhagic adenitis, ascites, and bacteremia 

(3) Within 5 days of ingestion of contaminated meat, the patient experiences severe abdominal pain 

associated with hematemesis and hematochezia. Early diagnosis is difficult, resulting in high mortality. 

c. lnhalational anthrax 

(1) Aerosolized anthrax spores >5 µm in size are usually trapped in the upper airway (pharynx, larynx, 

trachea) or cleared by the mucociliary system. 

(2) Spores between 2 and 5 µm in size are able to reach the alveolar ducts and alveoli, where they are 

engulfed by pulmonary macrophages and transported to mediastinal and hilar lymph nodes. 

(3) After a period of germination, a large amount of anthrax toxin is produced. Regional lymph nodes are 

quickly overwhelmed, and the toxin finds its way into the systemic circulation. 

(a) 

Because the organisms are initially transported to mediastinal lymph nodes, a major site of 

involvement is the mediastinum, which leads to massive hemorrhagic mediastinitis (a typical 

outcome). 

(b) Widespread dissemination of the toxin, leading to edema, hemorrhage, necrosis, and septic shock 

is an ominous sign; death soon follows. 

d. Disease progression 

(1) Incubation period (up to 6 days): insidious onset of malaise, myalgia, fatigue, nonproductive cough, 

fever, and an occasional sensation of retrosternal pressure (continues for ~4 days) 

(2) Sudden onset acute respiratory distress, cyanosis, and hypoxemia. Stridor suggests partial tracheal 

compression from enlarged mediastinal lymph nodes. The patient may be diaphoretic, with crackles 

heard on auscultation of the lungs. This stage lasts 24-36 hours and often culminates in death. 

(a) Chest radiograph: widened mediastinum and pleural effusions are characteristic; lung parenchyma 

may appear normal. 

(b) Meningeal involvement: seen in up to 50% of cases; usually bloody and may be associated with 

subarachnoid hemorrhage 

5. Diagnosis and treatment of inhalational anthrax 

a. "Suspicion" is the key to diagnosing and treating inhalational anthrax in the first stage. Guidelines: 

(1) Do an epidemiologic profile that includes a history of exposure, occupation, and where the victims 

have been (to identify a possible "hot zone" where anthrax has been found). 

(2) Has the patient been exposed to someone who has the flu? (lnhalational anthrax is not spread person 

to person.) 

(3) Clinical findings suggesting anthrax rather than flu 

(a) 

Nausea and vomiting without sore throat, nasal congestion, or rhinorrhea 

(b) Chest discomfort or pleuritic pain 

(c) Stuttering, onset of dyspnea, and nonproductive cough 

(d) Abnormal chest radiograph; consider chest CT if pleural effusion or mediastinal abnormalities 

are present. 

776


(4) Gram stains and cultures should be obtained on blood samples of patients in whom anthrax is 

suspected; suspicious results should be reported to the CDC for further evaluation. 

b. Antibiotics and supportive care in an ICU setting are the mainstays of therapy. 

(1) Consensus recommendations include fluoroquinolones, irrespective of age. Nontoxic victims with 

cutaneous anthrax can be treated as outpatients with oral ciprofloxacin or doxycycline for 7-10 days. 

Victims with inhalational, cutaneous, or GI disease and toxicity require IV therapy with ciprofloxacin 

or doxycycline plus at least two other antibiotics (eg, rifampin, clindamycin, imipenem, or an 

aminoglycoside). 

(2) The ICU setting is especially useful for hemodynamic monitoring and management of septic/ 

hemorrhagic shock; also, progressive respiratory insufficiency may necessitate use of ventilatory support. 

c. People with a credible history of exposure (based on results of forensic investigation by law enforcement 

agencies) or contact with a known or suspected environment contaminated with B anthracis (regardless of 

laboratory results) should be offered antimicrobial prophylaxis. Oral ciprofloxacin (500 mg) or doxycycline 

(1 00 mg) twice a day is recommended. 

d. For images of cutaneous anthrax and chest radiographs, see http://en.wikipedia.org/wiki/Anthrax. 

C. Other high-priority biologic agents (can be easily disseminated or transmitted person to person) 

1. Pneumonic plague (Yersinia pestis) 

2. Botulism (Clostridium botulinum) 

3. Tularemia (Francisella tularensis) 

4. Viral hemorrhagic fevers (Ebola, Marburg, Lassa, and Argentine viruses) 

VII. LEG/ONELLA PNEUMOPHILA 


1. L pneumophila is a gram-negative facultative intracellular bacillus that lives in natural and manmade water 

systems. It is implicated in as many as 6% of community-acquired pneumonia cases. 

2. Transmission occurs via inhalation of contaminated aqueous aerosols from equipment such as cooling towers, 

evaporative condensers, and shower heads. Person-to-person spread has not been documented. 

3. The illness occurs seasonally (summer and fall) and has an incubation period of 2-10 days. 

4. Populations at risk 

a. Patients (particularly men) >50 years old 

b. Cigarette smokers 

c. Patients with a significant underlying disease (alcoholism, diabetes mellitus, COPD) 

d. lmmunosuppressed patients (especially those with transplants) 

e. Patients who live or work near construction or excavation sites 

f. Recent travel (especially to spas) or changes in plumbing 


1. General systemic manifestations (rigors, high fever, headache, malaise, myalgias, and weakness) 

2. Pulmonary symptoms 

a. An initially dry cough often becomes productive of purulent sputum and is occasionally accompanied by 

hemoptysis. 

b. Dyspnea 

c. Pleuritic chest pain (33%) 

d. Pontiac fever refers to a milder form of the infection resembling influenza. 

3. GI symptoms 

a. Watery diarrhea (50%) 

b. Nausea, vomiting, abdominal pain 

4. Neurologic signs 

a. Altered level of consciousness 

b. Gait disturbance 

c. Seizures 

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5. Clinical clues within the past history 

a. No response to ~-lactamase drugs (penicillin, cephalosporins) or aminoglycosides for a recent infection 

b. Onset of symptoms within 10 days of hospital discharge 


a. Toxic appearance 

b. Disorientation and confusion 

c. Diffuse inspiratory rales, progressing to signs of consolidation 

d. Relative bradycardia (50%) 


1. WBC count 10,000-20,000/mm 3 with a left shift 

2. Increased sedimentation rate 

3. Abnormal serum chemistries 

a. Increased liver function tests 

b. Hyponatremia (


3. Human-to-human transmission can occur by direct contact with infectious body fluids, including: 

a. Saliva 

b. Mucus 

C. Vomit 

d. Feces 

e. Tears 

f. Breast milk 

g. Urine 

h. Semen 

i. Respiratory droplets 

4. Transmission can occur when infected body fluids contact the eyes, nose, mouth, open wound, or abrasion of 

an uninfected person. 

5. First cases of hemorrhagic fever caused by Ebola occurred in Zaire in 1976. 

6. Sporadic isolated outbreaks have been documented between 1976 and 2014, usually in remote forested areas 

of central Africa. 

7. In 2014, a larger scale epidemic spread to urban areas of central Africa, including cities in Guinea, Sierra 

Leone, Liberia, and Nigeria. 

8. Several cases were imported from these areas to western nations, including the United States. 


1. Classic presenting symptoms 

a. Fever 

b. Excessive diarrhea 

C. Vomiting 

d. Abdominal pain 

e. Weakness 

f. Headache 

g. Malaise 

2. Early symptoms can be difficult to distinguish from influenza, malaria, and other more common infections. 

3. Distinguishing physical examination findings 

a. Conjunctiva! injection (early) 

b. Diffuse erythematous maculopapular rash (early) 

c. Bruising 

d. Petechiae 

e. Mucosal bleeding 

f. GI bleeding/hemorrhage 

g. Vaginal bleeding 


1. Laboratory abnormalities 

a. Increased BUN and creatinine 

b. Transaminitis 

c. Hypocalcemia 

d. Lymphopenia 

e. Leukocytosis 

f. Thrombocytopenia 

g. Disseminated intravascular coagulation 

2. Reverse transcriptase PCR is the fastest, most reliable test. 

3. False-negatives are possible within 3 days of symptom onset, so retesting may be required if high suspicion and 

early clinical presentation. 

4. Recommend concurrent testing for alternative diagnoses such as malaria. 

779


D. Infection control measures 

1. Standard, contact, and droplet precautions are advised with all suspected cases. 

2. Providers must don and doff personal protective equipment with a trained observer for optimal infection 

control. 

3. Suspected cases should be treated in single private treatment rooms, with a private bathroom or covered 

bedside commode and closable room door. 

E. Treatment 

1. Respiratory and intravascular supportive measures 

2. Early aggressive oral and/or IV hydration 

3. Correction of coagulopathies 

4. Electrolyte repletion 

5. Empiric antibiotics and antimalarial drugs should be considered initially to ensure coverage of sepsis and 

malaria for undifferentiated patients. 

780

SYSTEMIC INFECTIOUS DISORDERS: PRACTICE CLINICAL SCENARIOS 

SYSTEMIC INFECTIOUS DISORDERS: PRACTICE CLINICAL 

SCENARIOS 


Scenario A 

Presentation: An elderly, demented nursing-home patient presents with altered mental status from baseline 

(less communicative). The patient is febrile and tachycardic, with a borderline low blood pressure. 


Scenario B 

Presentation: An avid hiker presents to the emergency department unable to close one eye or drink water 

because of a unilateral facial paralysis. She recalls having a rash on her thigh about a month ago that 

resembled a bull's eye and was not painful or pruritic. 


Scenario C 

Presentation: A thin patient with temporal wasting and thrush with a history of IV drug abuse is brought in 

by concerned family for bizarre behavior. He has had a headache for weeks, and bright light bothers his 

eyes. Results of laboratory studies show a low absolute lymphocyte count and positive HIV serology. A CT 

of the brain with and without contrast excludes any intracranial ring-enhancing lesions. A lumbar puncture 

reveals a high opening pressure and is positive for cryptococcal antigen. 


Scenario D 

Presentation: A patient presents with a history of HIV and medication noncompliance. She recalls that she 

is supposed to take TMP-SMX once per day. She complains of shortness of breath and a nonproductive 

cough. Her pulse oximetry is in the mid 80s. 


781

SYSTEMIC INFECTIOUS DISORDERS: PRACTICE CLINICAL SCENARIOS 


Scenario A 

Diagnosis: severe sepsis 

Diagnostic evaluation: Chest radiographs are done, as well as blood and urine cultures, urinalysis, CBC, 

and lactate. 

Management: Treatment includes early and aggressive IV fluid resuscitation, broad-spectrum antibiotics, 

and admission. 

Scenario B 

Diagnosis: Lyme disease 

Diagnostic evaluation: Diagnostic evaluation involves confirming that there is Lyme disease in the area 

where the patient has been hiking. Serology should be sent at this stage of the disease. An ECG should be 

done to screen for cardiac involvement (AV nodal block). 

Management: Treatment for isolated facial palsy is doxycycline for 2 weeks. If there is cardiac 

involvement, IV ceftriaxone is given for up to 3 weeks. 

Scenario C 

Diagnosis: cryptococcal meningitis 

Management: The patient is admitted for IV antifungal therapy and infectious disease consult. 

Scenario D 

Diagnosis: Pneumocystis jiroveci pneumonia 

Diagnostic evaluation: Chest radiograph is unremarkable; results of laboratory studies include low WBC 

and absolute lymphocyte counts, and an increased lactate dehydrogenase level. 

Management: The patient is admitted to the hospital, and supplemental oxygen is administered. Steroids 

are started before TMP-SMX therapy in the emergency department. 

782

IMMUNE SYSTEM DISORDERS 


RHEUMATOLOGIC DISORDERS .............................................................................................................................. 786 

Raynaud Disease ....................................................................................................................................................... 786 

Reiter Syndrome ....................................................................................................................................................... 786 

Scleroderma .............................................................................................................................................................. 787 

Systemic Lupus Erythematosus .................................................................................................................................. 788 

ALLERGIC EMERGENCIES (REACTIONS AND ANAPHYLAXIS) ................................................................................ 789 

Types of Allergic (Hypersensitivity) Reactions ........................................................................................................... 789 

Immediate Reactions (Type 1) .............................................................................................................................. 789 

Cytotoxic Reactions (Type II) .............................................................................................................................. 789 

Immune Complex-Mediated Reactions (Type 111) ................................................................................................ 789 

Delayed Cell-Mediated Reactions (Type IV) ........................................................................................................ 789 

Clinical Manifestations of Allergic (Hypersensitivity) Reactions ................................................................................ 790 

Urticaria ............................................................................................................................................................. 790 

Angioedema ....................................................................................................................................................... 791 

Erythema Multiforme .......................................................................................................................................... 791 

Stevens-Johnson Syndrome ................................................................................................................................. 792 

Allergic Drug Reactions ...................................................................................................................................... 792 

Adverse Food Reactions ..................................................................................................................................... 794 

Anaphylaxis ....................................................................................................................................................... 795 

Anaphylactoid Reactions .................................................................................................................................... 796 

783

IMMUNE SYSTEM DISORDERS: SELF-ASSESSMENT QUESTIONS 

IMMUNE DISORDERS: SELF-ASSESSMENT QUESTIONS 

1. The type of reaction that occurs with blood transfusions is most accurately classified as a: 

(a) Type I allergic reaction 

(b) Type II allergic reaction 

(c) Type Ill allergic reaction 

(d) Type IV allergic reaction 

2. Type Ill allergic reactions are mediated by: 

(a) 

lgE complexes and platelet aggregates 

(b) lgG or lgM 

(c) lgM 


3. Which of the fol lowing statements regarding the skin lesions of erythema multiforme are true? 

(a) They are typically red, raised, purpura. 

(b) They may not associated with Stevens-Johnson syndrome. 

(c) They are generally very pruritic. 

(d) They are classically located on the palms and soles, dorsum of the hands and feet, and on extensor surfaces of 

the extremities. 

4. Which of the fol lowing statements regarding the Jarisch-Herxheimer reaction are true? 

(a) 

It is a febrile reaction to parasitic or bacterial antigens that are liberated when the organisms are destroyed. 

(b) It is most commonly seen in association with the treatment of encapsulated organism infections. 

(c) It generally starts several days after the start of antibiotic therapy. 

(d) It is frequently life threatening. 

5. Which of the following reactions does not require prior exposure? 

(a) 

Phototoxic reactions 

(b) Photoallergic reactions 

(c) Anaphylactic reactions 


6. All of the following agents have been associated with the development of photoallergic reactions except: 

(a) Musk ambrette 

(b) Thiazide diuretics 

(c) Para-aminobenzoic acid 

(d) Phenothiazines 

7. A patient who was stung by a bee approximately 30 minutes before arrival presents with acute respiratory distress 

and hypotension. On examination, her blood pressure is 70/30 mmHg, and she is wheezing and has perioral and 

periorbital swelling. Her skin is cold and clammy. The nurses have already placed her on a monitor, given her 

supplemental oxygen, and started a large-bore IV line. The initial drug therapy of choice is: 

(a) Epinephrine 0.01 ml/kg (up to 0.5 ml of a 1 :1,000 solution) SC 

(b) Benadryl 1-2 mg/kg IV push 

(c) Inhaled ~-adrenergic agent such as albuterol 

(d) Epinephrine 0.1 ml/kg (up to 5 ml of a 1:10,000 solution) slow IV push 

8. Which of the following agents have been associated with anaphylactoid reactions? 

(a) 

Radiographic contrast media 

(b) Thiazide diuretics 

(c) Acetaminophen 

(d) Penicillin 

784

IMMUNE SYSTEM DISORDERS: SELF-ASSESSMENT QUESTIONS 

9. A 40-year-old woman presents with a 5-day history of fever, arthralgias, red and irritated eyes, and rash that has 

a target appearance on her palms and soles of her feet. Over the last 24 hours, she has had increasing pain in her 

mouth and has been unable to eat or drink. Physical examination shows bullous lesions on the skin, target lesions 

on the palms and soles, purulent conjunctivitis, and oral mucosa lesions and desquamation. The most appropriate 

management is: 

(a) Antipyretics, anti-inflammatories, 7-day course of acyclovir, and outpatient ophthalmology consult 

(b) IV fluids, steroids, analgesics, and admission for observation 

(c) Antipyretics, analgesics, 10-day course of doxycycline, and outpatient follow up 

(d) IV Vancomycin, analgesics, gentamicin ophthalmic drops, and admission for observation 

10. Erythema multiforme is commonly induced by which of the following? 

(a) ACE inhibitors 

(b) Lyme disease 

(c) Oral hypoglycemics 

(d) Barbiturates 

11. Which of the fol lowing is part of the classic triad of systemic lupus erythematosus? 

(a) Fever 

(b) Joint pain 

(c) Rash in a female of childbearing age 


12. Which of the following is true about scleroderma? 

(a) It has no association with Raynaud phenomenon. 

(b) It has no relationship with Sjogren syndrome. 

(c) It is predominately a disease affecting the skin and rarely involves other organ systems. 

(d) Classic presentation includes skin tightness, induration, and pruritus. 

13. Which of the following is not true about Reiter syndrome? 

(a) Classic triad is conjunctivitis, urethritis, and arthritis. 

(b) Enteral involvement should not be treated with antibiotics. 

(c) It is associated with E coli and Clostridium difficile infections. 

(d) Fever, myalgias, and arthralgias can be safely treated with NSAIDs. 

14. An 18-year-old previously healthy woman presents with a complaint of pale and numb finger tips on her left hand 

after snow skiing for several hours. On physical examination, there is a well-demarcated area of pallor on the distal 

portion of the second, third, and fourth digits on her left hand. They are numb to the touch. The remainder of the 

hand is normal. The most appropriate management includes all of the following except: 

(a) Warm the local body part. 

(b) Evaluate the patient for arterial occlusion. 

(c) Educate on cessation of vasoconstricting agents such as nicotine. 

(d) Educate on avoiding precipitating factors. 

ANSWERS 

1. b 4. a 7. d 10. C 13. 

2. a 5. a 8. a 11 . d 14. 

3. d 6. b 9. b 12. d 



C 

b 

785


RHEUMATOLOGIC DISORDERS 

I. RAYNAUD DISEASE 

A. Recurrent artery or arteriole vasospasm most commonly in the fingers and toes, usually in response to 

stress or cold exposure 


1. Numbness and parethesias 

2. Pain in the affected area 

3. Affected areas show at least two color changes 

a. Pallor 

b. Cyanosis 

c. Hyperemia 

4. Transient lasting minutes to hours 

C. Management 

1. Warm local body part 

2. Discontinue vasoconstricting agents such as nicotine 

3. Avoid precipitating factors 

4. Calcium channel blockers 

II. REITER SYNDROME 

A. Reactive arthritis following enteric or venereal infections associated with human leukocyte antigen (HLA)-B27 

B. Associated bacteria 

1. Chlamydia (most common sexually transmitted infection) 

2. Campylobacter (most common enteric infection) 

3. Salmonella 

4. Shigella 

5. Yersinia 

6. Cyc!ospora 

7. Group A streptococci 

C. Clinical presentation-classic triad: "can't see, can't pee, can't dance with me" 

1. Conjunctivitis-"can't see" 

a. Erythema 

b. Burning 

C. Tearing 

d. Pain 

e. Photophobia 

2. Nongonococcal urethritis-"can't pee" 

a. Frequency 

b. Dysuria 

c. Urgency 

d. Urethral discharge 

3. Arthritis-"can't dance with me" 

a. Asymmetric arthralgia 

b. Joint stiffness 

c. Primarily involving the knees, ankles, and feet; worse with rest or inactivity 

4. May also have fever, myalgias, low back pain, mouth ulcers, and keratoderma blennorrhagica (patches of scaly 

skin on palms, soles, and scalp) 

786


D. Management 

1. NSAIDs 

2. Tetracycline for cases caused by Chlamydia 

3. Antibiotics are no benefit in cases with enteral causes. 

Ill. SCLERODERMA 

A. Systemic autoimmune disease characterized by skin induration and thickening accompanied by 

tissue fibrosis, chronic inflammatory infiltration of visceral organs, and cellular immune alterations 


1. Skin 

a. Tightness 

b. lnduration 

c. Pruritus 

d. CREST is the limited cutaneous sclerosis: .C.alcinosis, Raynaud, fsophageal dysmotility, .Sclerodactyly, 

Ielangiectasias 

2. Vascular 

a. 95% have associated Raynaud phenomenon 

3. GI 

b. Ulcers on fingertips 

c. Telangiectasis 

a. Gastroesophageal reflux disease 

b. Dyspepsia 

c. Constipation alternating with diarrhea 

4. Pulmonary 

a. Dry cough 

b. Dyspnea 

c. Pulmonary hypertension 

5. Musculoskeletal 

a. Arthralgia 

b. Myalgia 

c. Loss of joint range of motion and joint flexion contractures 

d. Muscle weakness 

6. Cardiovascular 

a. Pericardia! effusion 

b. CHF 

c. Myocardial fibrosis 

7. ENT 

a. Sicca/Sjogren syndrome with dry eyes and dry mouth (due to destruction of salivary and lacrimal glands) 

b. Poor dentition 

c. Hoarseness 

8. Renal 

a. Hypertension 

b. Renal insufficiency 

9. Neurologic 

a. Trigeminal neuralgia 

b. Paresthesias and weakness 

c. Headache 

787


C. Management 

1. Most treatment focused on complications of the disease 

2. Skin symptoms: phototherapy 

3. GI symptoms: antacids, H 2 

-blockers and proton-pump inhibitors 

4. Pulmonary symptoms: cyclophosphamides 

5. Renal symptoms: ACE inhibitors 

6. Muscle symptoms: low-dose steroids 

IV. SYSTEMIC LUPUS ERYTHEMATOSUS 

A. Chronic autoimmune disease that can affect almost any organ system, making its presentation and 

course highly variable 


1. Classic triad: fever, joint pain, and rash in a woman of childbearing age 

2. Constitutional: fatigue, fever, weight changes 

3. Musculoskeletal: arthralgia, arthropathy, myalgia, avascular necrosis 

4. Dermatologic: malar rash, photosensitivity, discoid lupus 

5. Renal: acute or chronic renal failure, acute nephritic disease 

6. Neuropsychiatric: seizure, psychosis, stroke 

7. Pulmonary: pleurisy, pleural effusion, pneumonitis, pulmonary hypertension, interstitial lung disease, 


8. GI: nausea, dyspepsia, abdominal pain 

9. Cardiac: pericarditis, myocarditis, acute Ml, tamponade 

10. Hematologic: leukopenia, lymphopenia, anemia, or thrombocytopenia 

C. Management 

1. Emergency department management often focuses on the complications of the disease (acute Ml, pulmonary 

embolism, etc). 

2. Antimalarials: hydroxychloroquine 

3. Corticosteroids 

4. NSAIDs 

5. Rheumatology consult 

788


ALLERGIC EMERGENCIES (REACTIONS AND 

ANAPHYLAXIS) 

I. TYPES OF ALLERGIC (HYPERSENSITIVITY} REACTIONS 

A. Immediate reactions (Type I) 

1. Sequence of events: initial exposure to antigen - activates T-helper lymphocyte itself or binding with protein 

(hapten-protein complex) - induces plasma cells to produce specific lgE antibody that binds to mast cells 

and basophils - subsequent reexposure to the antigen - antigen binding with lgE on cell surfaces - release 

of preformed chemical mediators (histamine, eosinophil chemotactic factor of anaphylaxis [ECF-A], high 

molecular weight neutrophil chemotactic factor [HMW-NCF], kallikreins) and spontaneously generated 

mediators (leukotrienes, prostaglandins, platelet-activating factor, thromboxane) 

2. These reactions are lgE- or lgG 4 

-mediated and are responsible for most anaphylactic reactions. 

3. Examples 

a. Drug-induced reactions: penicillin is the most common and the leading cause of fatal anaphylaxis (others 

include ASA, vancomycin, TMP-SMX, and NSAIDs) 

b. Hymenoptera venoms 

c. Foods (shellfish, nuts, egg white, soybeans, wheat, and peanuts [the most common cause of fatal food 

anaphylaxis]) 

d. Environmental reactions (dust, ragweed, etc) 

e. Radiologic contrast material 

f. Food additives (MSG, nitrates/nitrites, tartrazine dyes) 

B. Cytotoxic reactions (Type II) 

1. Sequence of events: target antigen (a cellular component or a substance that cross-reacts with a cellular 

component) - complement activation or direct injury to lymphocytes - release of cell mediators 

2. These reactions involve binding of lgG or lgM to a cell-bound antigen. 

3. Examples 

a. Blood transfusion reactions 

b. Immune hemolytic anemias 

c. Thrombocytopenia (idiopathic thrombocytopenic purpura) 

C. Immune complex-mediated reactions (Type Ill) 

1. Sequence of events: soluble antigen-antibody complex - activation of complement system and platelets - 

lgE complexes and platelet aggregates - release of cell mediators 

2. Examples 

a. Arthus reactions 

(1) lntradermal injection of an antigen to which the patient has been previously sensitized - edema and 

erythema at the injection site 

(2) Can occur after administration of tetanus toxoid in the patient who has received too-frequent doses 

of tetanus toxoid 

b. Serum sickness (fever, rash, arthralgia, and lymphadenopathy) 

D. Delayed cell-mediated reactions (Type IV) 

1. Sequence of events: antigen-specific T lymphocytes migrate to the site of the antigen injection - release of 

cell mediators 

2. These reactions do not involve antibodies or complement. 

3. Signs/symptoms do not develop for 24-72 hours after exposure. 

4. Examples: tuberculin skin test, contact dermatitis 

5. This classification is somewhat oversimplified in that many allergic reactions consist of more than one type 

of immune mechanism. Because Types 1-111 involve complement activation (which can result in varying 

degrees of anaphylaxis), some degree of overlap does occur. However, the most severe anaphylactic reactions 

are primarily Type I; Type II is generally less severe, and Type Ill is the least severe. Type IV does not involve 

complement activation and therefore does not cause any form of anaphylaxis. 

789


II. CLINICAL MANIFESTATIONS OF ALLERGIC (HYPERSENSITIVITY) 

REACTIONS 

A. Urticaria 

1. A vascular reaction involving the skin with transient, pruritic wheals and welts 


a. Edematous papules coalescing into plaques that can affect any area of the skin 

b. White, pink, or erythematous nonscaling lesions that range in size from 10 cm 

c. Wax and wane over 24-48 hours 

3. Causes 

a. Drug reaction (most common) 

(1) Penicillin (most commonly implicated) and sulfa 

(2) Local anesthetics 

(3) ASA (most commonly implicated) 

(4) Diuretics 

(5) Laxatives 

(6) NSAIDs 

(7) Morphine and codeine 

(8) Progesterone 

b. Infection 

(1) Infectious mononucleosis 

(2) Hepatitis B 

(3) Coxsackie virus 

(4) Parasitic infestations 

c. Environmental and physical factors 

(1) Heat or cold 

(2) Sun exposure 

(3) Exercise 

(4) Latex 

(5) Raw fish 

(6) Metals (eg, nickel) 

(7) Animal saliva 

d. Malignancies 

e. Hyperthyroidism 

f. Pregnancy 

g. Foods (fish, eggs, nuts, peanuts, strawberries, lobster) 

h. Mastocytosis (overproliferation of mast cells in tissues) 

4. Management 

a. Symptomatic in most cases; however, urticaria alone has been known to progress to full-blown anaphylaxis. 

b. Diphenhydramine (an H 1 

-blocker) is usually the drug of choice for these reactions. Other excellent choices 

include: 

(1) Hydroxyzine 

(2) Chlorpheniramine (pregnancy) 

(3) Cyproheptadine (cold urticaria) 

(4) Long-acting nonsedating antihistamine: fexofenadine, loratadine, cetirizine 

c. The addition of an H 2 

-blocker (eg, cimetidine) can provide additional benefit in 10%-15% patients who 

have an incomplete response to diphenhydramine alone. 

d. Epinephrine and/or steroid may be required in resistant cases. 

(1) Moderate to severe cases - methylprednisolone 125 mg IV 

(2) Severe, life-threatening cases - add IV epinephrine 0.1 mg/kg IV in a 1 :10,000 solution 

790


e. Patients who are discharged should be: 

B. Angioedema 

(1) Continued on oral antihistamines for 3 days 

(2) Continued on steroids if these drugs were required during emergency department treatment 

(3) Advised to avoid offending agent if known; if unknown, advised to follow up with a dermatologist to 

identify the offending agent 

1. Edema due to capillary dilation of the deeper layers of skin caused by a C1 esterase inhibitor deficiency or 

defect that results in decreased levels of C4 


a. Painless, nonpruritic, nonpitting edema of skin 

b. Most commonly affects tongue, lips, and face 

c. Hands and feet 

d. Scrotum and foreskin 

e. Can affect abdominal organs and upper airway in more severe cases 

3. Drug-induced angioedema 

a. ACE inhibitors (a common cause and can occur any time in course of use, even a year later); NSAIDs, 

aspirin, contrast media 

b. Management 

(1) Be ready to establish a definitive airway (fiberoptic intubation procedure of choice). 

(2) Symptomatic (similar to that for urticaria) in most cases, but progression to anaphylaxis can occur. 

(Angioedema is not lgE associated; antihistamines and steroids have not clearly been shown to be of 

benefit.) 

(3) Administration of fresh frozen plasma to replace C1 esterase inhibitor in severe cases 

(4) Administration of racemic epinephrine should be considered if there is evidence of impending upper 

airway obstruction. 

4. Hereditary angioedema 

a. Edema of the face, airway, or extremities and abdominal pain with nausea, vomiting, and diarrhea 

is characteristic; hereditary angioedema is caused by C1 esterase inhibitor deficiency and is usually 

precipitated by stress or trauma. 

b. Management 

(1) Frozen plasma (containing C1 esterase inhibitor) 

(2) High-dose epinephrine may also be effective. However, life-threatening acute attacks do not respond 

to standard doses of epinephrine or to antihistamines or steroids. 

(3) The attenuated androgens (danazol and stanozolol) may help for both acute and chronic hereditary 

angioedema. 

(4) There are also several new FDA-approved drugs for treatment of hereditary angioedema, including 

ecallantide, Cinryze®, and Berinert®, which have shown good efficacy in treating acute episodes. 

C. Erythema multiforme 

1. A more severe variant of an urticaria! reaction causing a limited hypersensitivity reaction in the skin 


a. Typical lesions are red, raised, and multishaped with clear centers (iris or target lesions) that may become 

bullous. These nonpruritic lesions have a symmetric distribution and are typically located on the: 

(1) Palms and soles (characteristic) 

(2) Dorsum of the hands/wrist (usual location of target lesions) and feet 

(3) Extensor surfaces of the extremities 

b. Often following a course offever, myalgias, headache, and malaise 

3. Etiology 

a. Drug induced is most common: mnemonic "SOAPS" for Sulfa, Oral hypoglycemic, Anticonvulsants, 

Penicillin, NSAIDs 

b. Infectious agents: herpes simplex virus, Mycoplasma, tuberculosis 

c. Malignancy: lymphoma 

791


4. Management 

a. Self-limited 

b. Treat the underlying condition and remove the offending agent. 

c. Acyclovir for cases involving herpes simplex virus 

D. Stevens-Johnson syndrome 

1. A severe, potentially fatal form of erythema multiforme characterized by bullae, mucous membrane lesions, 

and multisystem involvement 


a. Often preceded by a prodrome of malaise, fever, arthralgias, and myalgias 

b. Purulent conjunctivitis may be so severe that the eyes are swollen shut. 

c. Mucous membrane breakdown and systemic involvement 

3. Precipitating factors 

a. Long-acting sulfonamides (eg, TMP-SMX) 

b. Herpes simplex virus and Mycoplasma infection 

c. Drugs: typically antibiotics and anticonvulsants 

d. Malignancy 

4. Management 

a. Without systemic manifestation and mucous membrane involvement, it can be outpatient with steroid bursts. 

b. Patients with extensive disease need ICU management, fluids and electrolyte replacement, and 

management of infectious and thermoregulatory issues. 

E. Allergic drug reactions 

1. Cutaneous manifestations 

a. Urticaria with or without angioedema 

b. Erythema multiforme (or nodosum) 

C. Anaphylaxis 

d. Maculopapular eruptions 

e. Pruritus with or without a rash 

f. Contact dermatitis 

g. Photodermatitis 

h. Purpura 

I. Fixed drug eruption 

j. Exfoliative dermatitis 

k. Stevens-Johnson syndrome 

I. Toxic epidermal necrolysis 

2. Systemic manifestations 

a. Serum sickness 

b. Interstitial nephritis and glomerulonephritis 

C. Vasculitis 

d. Arthralgias and arthritis 

3. Drug reactions associated with cutaneous and systemic manifestations 

a. Serum sickness 


(a) 

Urticaria 

(b) Fever and lymphadenopathy 

(c) Arthralgia and arthritis 

(d) Glomerulonephritis 

(2) Drug etiology 

(a) 

Penicillin and sulfa 

(b) Barbiturates 

(c) Thiazide diuretics 

(3) Treatment 

(a) 

Remove offending agent. 

792


(b) Anti-inflammatories 

(c) Anithistamines 

b. Acute interstitial nephritis 


(a) Fever and skin rash 

(b) Proteinuria, hematuria, and leukocyturia 

(c) Eosinophilia and eosinophiluria 

(d) Azotemia and oliguria 


(a) 

Penicillins (especially methicillin) 

(b) Cephalosporins 

(c) NSAIDs (especially fenoprofen) 

(d) Cimetidine 

(e) Sulfonamides 

(f) 

Phenytoin 

(g) Thiazide diuretics 

(h) Vancomycin 

(i) 

(j) 

Diltiazem 

Omeprazole 

(k) Snake antivenin 

(I) 

Streptomycin 


(a) Supportive care measures with fluid and electrolyte maintenance 

(b) Symptomatic relief of fever and systemic symptoms 

(c) Avoid nephrotoxic drugs 

(d) Corticosteroid therapy 

c. Hypersensitivity vasculitis 


(a) Palpable purpura on lower extremities 

(b) Vasculitis involving the CNS, GI tract, lungs, and kidneys 


(a) Penicillin and sulfa 

(b) Phenytoin 

(c) Cephalosporins 

(d) Thiazide diuretics 

(e) Allopurinol 

(3) Associated infections (occur in some patients) 

(a) Chronic bacteremia 

(b) Hepatitis B and C 

(c) HIV 


(a) Remove offending agent. 

(b) Systemic corticosteroid therapy 

4. Other allergic drug reactions 

a. Jarisch-Herxheimer reaction 

(1) A febrile reaction to parasitic or bacterial antigens that are liberated when the organisms are 

destroyed by antibiotic therapy 

(2) Most commonly occurs in association with treatment of spirochete infections (syphilis, Lyme disease, 

relapsing tick-borne fever, and leptospirosis) 

(3) Generally occurs 2-12 hours after the start of antibiotic therapy (especially penicillin or a 

tetracycline) and lasts


b. Maculopapular eruptions 

(1) Can be caused by any drug, but ampicillin is an especially common offender 

(2) If the causative agent is not discontinued, erythroderma or exfoliative dermatitis may develop. 

c. Contact dermatitis 

(1) Application of any topical agent (including cosmetic creams and lotions) can cause a cell-mediated 

reaction (Type IV) characterized by redness, itching, maculopapular, or vesicular eruptions. 

(2) Treatment consists of topical steroids, antihistamines, and cold wet dressings soaked in Burrow solution. 

d. Fixed drug eruption 

(1) A rash that recurs at the same site each time the offending drug is used 

(2) Lesions are often pigmented (violaceous or dusky red), round or oval in shape, and can be quite pruritic. 

(3) Most common cause is phenolphthalein in OTC laxatives. Other offenders include: 

(a) Aspirin 

(b) Sulfa 

(c) Tetracycline 

(d) Barbiturates 

(e) 

NSAIDs (especially naproxen and tolmetin) 

(4) Management consists of discontinuing the offending agent, steroids, and antihistamines. 

e. Photosensitive reactions 

(1) Adverse reactions to a combination of a drug (systemic or topically applied) and ultraviolet light 

(2) Lesions are restricted to sun-exposed areas of the skin (face, nuchal area of the neck, dorsal aspects of 

the upper extremities). 

(3) Two types of photosensitive reactions: phototoxic (most common) and photoallergic 

(a) A photoallergic reaction is a delayed hypersensitivity reaction. Therefore, it occurs only in 

sensitized individuals. The eruption is generally intensely pruritic and resembles that seen with 

contact dermatitis. Topical agents are the most common sensitizers, especially those containing 

one of the following: 

i. Para-aminobenzoic acid 

ii. Musk ambrette (colognes and perfumes) 

iii. Halogenated salicylanilides (in soaps, cosmetics) 

iv. Phenothiazines 

(b) A phototoxic reaction does not involve immunologic mechanisms and can, therefore, occur on 

first exposure (drug and adequate sunlight). These reactions appear as exaggerated sunburns; 

associated pruritus is mild or absent. Commonly implicated drugs include: 

i. Tetracyclines (especially doxycycline) 

ii. Phenothiazines (especially chlorpromazine) 

iii. Sulfonamides and sulfonylureas 

iv. Thiazide diuretics 

v. Chlordiazepoxide 

vi. NSAIDs (especially piroxicam and naproxen) 

(4) Management consists of discontinuing the offending agent, avoiding sun exposure, and steroids. 

F. Adverse food reactions - direct histamine release 

1. "Chinese restaurant syndrome": the most common because the food contains most, if not all, of the potential 

causes (allergens, preservatives, color additives, flavor enhancers, and toxins) 

2. Su lfites (preservatives) 

a. Can cause flushing, bronchospasm, urticaria, and hypotension within minutes of ingestion; nausea, 

vomiting, diarrhea, and abdominal cramps can also occur. 

b. Foods containing sulfite: packaged salads, shrimp, dried fruit, gelatin, pickles, sausages, cheeses, wine, and 

fruit juices 

c. 5%-10% of the asthmatic population is sensitive to sulfites, which may produce anaphylactic reactions in 

these patients. 

3. Tartrazine dye (yellow dye #5, a food and drug color additive) and parabeus (a pharmaceutical additive) can 

cause urticaria, angioedema, acute bronchospasm, or anaphylaxis. 

794


4. Monosodium glutamate (flavor enhancer) can cause flushing, chest pain, wheezing, facial pressure and 

burning, a burning sensation at the back of the neck, dizziness, paresthesias, headache, palpitations, weakness, 

nausea, and vomiting. 

5. Scombroidosis (food toxins) is due to spoiled salt water fish and can cause flushing (resembles a sunburn), 

headache, urticaria, itching, abdominal cramping, and diarrhea; sometimes a metallic, bitter, or "peppery" taste 

is noted at the time of ingestion. 

G. Anaphylaxis 


a. A severe systemic allergic reaction to an antigen that is precipitated by the abrupt release of chemical 

mediators in a previously sensitized patient and involving two or more organ systems. Prior exposure to 

the antigen is necessary for anaphylactic shock to occur. 

b. Antigens that can cause anaphylaxis include foods, drugs, vaccines, blood products, pollens, and insect 

venoms; penicillin remains the leading cause of fatal anaphylaxis. 

c. Patients on ~-blockers may have a higher risk of anaphylaxis and of a more severe reaction due to 

interference with traditional therapies. 


a. Early signs of impending anaphylaxis 

(1) Nasal itching or stuffiness 

(2) A "lump" in the throat (laryngeal edema) or hoarseness 

(3) lightheadedness and syncope 

(4) Chest pain, shortness of breath, and tachypnea 

(5) Skin complaints: warmth and tingling of the face (especially the mouth), upper chest, and palms or 

soles are usually the first clinical manifestations of anaphylaxis. 

(6) GI complaints: nausea, vomiting, diarrhea with tenesmus or crampy abdominal pain 

(7) An "aura" of impending disaster (may occur in patients with a prior history of anaphylaxis) 

b. Ful I-blown anaphylaxis 

(1) Angioedema of the tongue, pharynx, and larynx that can lead quickly to upper airway obstruction 

(2) Hypotension, tachycardia (or other dysrhythmias), altered sensorium, dizziness, wheezing, and 

cyanosis that can lead quickly to cardiopulmonary failure. Coughing is an ominous sign that frequently 

heralds the onset of pulmonary edema. 

(3) The skin may or may not show the classic wheal-and-flare reaction. If the patient is severely 

hypotensive, a skin reaction may be difficult to see because of poor perfusion. 

3. Management 

a. Supportive measures 

(1) Supplemental high-flow oxygen and cardiac monitoring 

(2) Normal saline or lactated Ringer's IV (at least 2 l) for circulatory support 

(3) laryngospasm may necessitate oral intubation (the procedure of choice) or cricothyrotomy; racemic 

epinephrine (2.25% solution 5 ml in 2.5 ml normal saline) may be used as a temporizing measure 

while setting up for definitive airway management. Sedation and paralysis should be used with 

caution, because a distorted airway may preclude intubation after paralysis. 

b. Parenteral drug therapy 

(1) Epinephrine (drug of choice) 

(a) Mild anaphylaxis (urticaria, rhinitis, conjunctivitis, mild bronchospasm)-"" 0.3-0.5 ml 1 :1,000 

solution IM 

(b) Moderate anaphylaxis (generalized urticaria, angioedema, early laryngeal edema, hypotension 

[blood pressure >80 mmHg])-"" 0.3-0.5 ml 1 :1,000 solution IM. May repeat every 5-20 minutes 

to a total of 3 doses as needed. 

Studies have shown that IM administration in the lateral thigh achieves a rapid rise of serum 

levels of epinephrine, much faster than administration IM in the deltoid or SC in the arm. 

(c) Severe anaphylaxis (laryngeal edema, respiratory failure, shock)-"" 1-5 ml 1:10,000 solution IV 

over 10 minutes. If no improvement, start epinephrine drip as follows: mix 1 ml 1 :1,000 solution 

in 250 ml D5W (4 mcg/ml); run at 1-4 mcg/min. Patients on ~-blockers may be refractory to 

standard dosages of epinephrine; administration of IV glucagon may allow the epinephrine to 

work. 

795


(2) Diphenhydramine 

(a) Mild anaphylaxis: 25-50 mg orally or IM 

(b) Moderate anaphylaxis: 50-100 mg IM or IV 

(c) Severe anaphylaxis: 50-100 mg IV over 3 minutes, may be repeated every 4-6 hours as needed 

(3) Cimetidine or other H 2 

-blockers should be administered IV to those patients whose symptoms persist 

despite the above therapy. However, if the patient is on a r-blocker, cimetidine should be avoided 

because it may prolong the activity of the r-blocker. 

(4) Aerosolized albuterol 0.5 ml (of a 0.5% solution) in 2.5 ml normal saline every 20 minutes as needed 

should be used to treat persistent bronchospasm. Aerosolized ipratropium with albuterol is also 

effective; dosage is 0.5 mg in 2.5 ml normal saline every 20 minutes. 

(5) Corticosteroids 

(a) 

Potentiate the effects of epinephrine and decrease capillary permeability, but these effects are not 

immediate. 

(b) Initial dose of methylprednisolone is 125-250 mg IV; may be repeated every 6 hours. 

(6) Glucagon (I mg IV every 6 minutes as needed) may be beneficial for patients on a r-blocker who 

have persistent hypotension, as well as for other patients in whom IV epinephrine is relatively 

contraindicated (eg, pregnant patients, those >35 years old, and those with coronary artery disease) or 

who are epinephrine-resistant. 

(7) Heliox (helium oxygen) may be administered to patients with resistant upper airway obstruction or 

angioedema. 

c. Disposition 

(1) These patients should generally be admitted for observation and repeated doses of antihistamines and 

steroids; this includes all patients on r-blockers in whom "rebound" can occur once the therapeutic 

medication effects have dissipated, as well as all other patients whose symptoms were resistant to 

epinephrine and diphenhydramine therapy. 

(2) If discharged, these patients should be continued on oral antihistamines and steroids for 3 days and 

given a prescription for an epinephrine injection kit for initial self-treatment in the event of reexposure. 

(3) Recommended criteria for discharge 

H. Anaphylactoid reactions 

(a) Mild anaphylaxis (no hypotension or signs of upper airway obstruction) 

(b) Rapid and complete response to emergency department therapy 

(c) 6-hour observation without symptom recurrence 

(d) Safe discharge to the care of a responsible adult with instructions to return immediately if 

symptoms recur 

1. Anaphylactoid reactions resemble anaphylactic reactions but do not require prior exposure; they are not 

immunologically mediated. The final pathway is identical to that of anaphylaxis but does not require initial 

sensitizing to the antigen. 

2. Commonly implicated agents 

a. Radiographic contrast media (most common) 

b. Aspirin 

c. NSAIDs (especially the pyrazole derivatives) 

d. Codeine 

3. Treatment is the same as that for anaphylaxis. 

796

IMMUNE SYSTEM DISORDERS: PRACTICE CLINICAL SCENARIOS 

IMMUNE DISORDERS: PRACTICE CLINICAL SCENARIOS 


Scenario A 

Presentation: A patient presents several days after an uncomplicated illness on TMP-SMX. She has fever, 

arthralgias, red and irritated eyes, a rash that has a target appearance on her palms and soles of her feet, 

and oral pain and lesions. 


Scenario B 

Presentation: A patient presents with an abrupt onset of swelling of the upper lip and tongue. He denies 

any difficulty swallowing and shortness of breath. He has no fever, pain, or itching and no history of this in 

the past. He has a history of hypertension for which he takes a "blood pressure medication" but no other 

medical problems or allergies. 

Physical examination: Heart rate is 86 beats per minute, blood pressure is 124/84 mmHg, respiratory 

rate is 16 breaths per minute, oxygen saturation is 99%, and temperature is 98.6°F (3 7°(). Physical 

examination shows edema and swelling in the upper lip and tongue, which seems to be more notable on 

the left half of the tongue. The patient is swallowing without difficulties and has a normal neck and breath 

sounds. The remainder of the dermatologic examination is normal. 


Scenario C 

Presentation: A patient presents with a gradual onset of redness, burning, and pain in both eyes. On 

questioning, patient also notes that he has been suffering from a significant bout of diarrhea and significant 

pain on urination. He denies any chemical exposure to the eyes and does not recall any injuries. He does 

not wear contacts or glasses and denies any changes in his ability to see or read. 

Physical examination: Heart rate is 104 beats per minute, blood pressure is 118/78 mm Hg, respiratory 

rate is 16 breaths per minute, oxygen saturation is 99%, and temperature is 101 °F (38.3 °C). Both eyes are 

erythematous, tearing, and photophobic. Heart and lungs are normal, as is the abdominal examination. 

The patient seems to have diffuse joint discomfort with range of motion. The remainder of examination 

is normal. 


Scenario D 

Presentation: A patient presents after an abrupt onset of facial flushing, hives, itching, and wheezing while 

having dinner in "Chinatown." While in the emergency department, he also develops nausea, vomiting, 

and diffuse abdominal pain. 

Physical examination: Heart rate is 110 beats per minute, blood pressure is 90/50 mm Hg, respiratory rate 

is 18 breaths per minute, oxygen saturation is 99%, and temperature is 98.6°F (37°(). The patient's cheeks 

are flushed, and there is a diffuse urticaria! rash on his neck and trunk. Faint end expiratory wheezes are 

noted on chest auscultation, and the abdomen is soft without peritoneal signs. 


797


Scenario E 

Presentation: A 28-year-old woman presents with fatigue, dyspnea, chest pain, fever, and diffuse arthralgias 

that have become progressively worse over the last 2 months. 

Physical examination: The patient is febrile and has a malar rash. On chest auscultation, there is a cardiac 

friction rub and decreased breath sounds on the left side. Heart rate is 115 beats per minute, blood 

pressure is 110/65 mm Hg, respiratory rate is 22 breaths per minute, and oxygen saturation is 93%. 


Scenario F 

Presentation: The patient complains of numbness and parethesias in several of her fingertips. The affected 

areas become quite painful and seem to be associated with cold exposure. 

Physical examination: Several of her fingertips are blanched at the tips and well demarcated. The rest of 

the examination is normal 


Scenario G 

Presentation: The patient presents with dry mouth, irritated eyes, and skin feeling tight. He has 

occasionally had difficulties swallowing his food and reflux symptoms. He also notes that he had a recent 

diagnosis of trigeminal neuralgia. 

Physical examination: Vital signs are normal. Some ulcerations are noted on several fingertips. The oral 

mucosa is dry, and the patient's voice is hoarse. Eyes are injected and dry. Some diffuse arthralgias with 

joint movement are also noted. 


Scenario H 

Presentation: The patient presents with a rash several days after starting glipizide for diabetes. He notes no 

associated pain or pruritus with the rash. He has had associated fever, myalgias, and headache. 

Physical examination: Vital signs are normal. The skin shows red, raised patches with central clearing on 

his arms, hands, palms, and soles. The remainder of the examination is normal. 


Scenario I 

Presentation: The patient presents with a fever. He was seen at an urgent care center earlier today and was 

diagnosed with Lyme disease and started on tetracycline. He denies any other symptoms beyond the joint 

pain and rash that prompted him to go to the urgent care. He has not has any fever before this point. 

Physical examination: Heart rate is 95 beats per minute, blood pressure is 120/76 mmHg, oxygen 

saturation is 98%, respiratory rate is 16 breaths per minute, temperature is 101 °F. He has a classic 

erythema migrans rash and diffuse arthralgias consistent with his diagnosis of Lyme disease. The remainder 

of the examination is normal. 


798


ScenarioJ 

Presentation: An 18-year-old woman presents after being stung by a wasp at a family picnic. Very soon 

after the sting, she felt her skin itching and a lump in her throat, closely followed by facial flushing, 

shortness of breath, nausea, and vomiting. Her family brought her to the emergency department 

immediately and shortly after arriving at the triage area she has a syncopal episode. The family notes that 

she has been stung before last summer but never had any symptoms like this. 

Physical examination: Heart rate is 115 beats per minute, blood pressure is 80/42 mmHg, oxygen 

saturation is 98%, respiratory rate is 26 breaths per minute, and temperature is 98.6°F. The patient is in 

obvious respiratory distress with wheezing noted in all lung fields. She is diaphoretic and has a generalized 

swelling of the tongue and face. 


799



Scenario A 

Diagnosis: Stevens-Johnson syndrome 

Diagnostic evaluation: Physical examination findings are consistent with erythema multiforme (target 

lesions) and associated bullae, mucous membrane lesions and breakdown, and multisystem involvement. 

The patient may also have a history of herpes simplex virus or Mycoplasma infection. Diagnosis is based 

on physical examination with the consistent clinical presentation. 

Management: These patients should be admitted to the ICU for fluids and electrolyte therapy, and 

management of infectious and thermoregulatory issues. 

Scenario B 

Diagnosis: angioedema 

Key facts: The patient may also have a family history of such presentation, which would differentiate the 

drug-induced from the hereditary form of angioedema. The patient would not respond well to treatment 

with steroids and antihistamines and may develop significant airway issues. In severe cases, epinephrine 

and fresh frozen plasma may be required. 

Scenario C 

Diagnosis: Reiter syndrome 

Diagnostic evaluation: The patient may also have a history of urethral discharge, a recently treated 

sexually transmitted infection, or bloody diarrhea representing possible pathogens that may be causing this 

syndrome. This patient is presenting with the triad of conjunctivitis, urethritis, and arthritis. 

Management: In this particular case, an enteral bacterial cause is likely, and the patient would not benefit 

from antibiotic therapy. Treatment includes NSAIDs and other antipyretics. 

Scenario D 

Diagnosis: adverse food reaction 

Diagnostic evaluation: The patient may also have a history of recently consuming wine, cheese, or other 

foods that may contain high levels of sulfites. Other possibilities include heavy doses of food dyes, MSG, 

or fish that potentially could be spoiled. 

Management: This direct histamine release reaction due to ingestion of a particular food should be treated 

with antihistamines and other supportive measures. 

Scenario E 

Diagnosis: systemic lupus erythematosus 

Key facts: The patient could have numerous other presentations suggesting acute emergent complications 

of the disease involving almost any organ system. This scenario suggests potential pericarditis, pleural 

effusion, cardiac tamponade, pulmonary embolism, pneumonia, or sepsis. Diagnosis would likely not be 

formally made in the emergency department but focus on the acute management of the complications 

of the disease, followed by managing the disease itself with hydroxychloroquine, steroids, NSAIDs, and 

rheumatology consult. 

800


Scenario F 

Diagnosis: Raynaud disease 

Diagnostic evaluation: This patient is experiencing the recurrent artery or arteriole vasospasm of Raynaud 

disease, which occurs most commonly in the fingers and toes and usually in response to stress or cold 

exposure. The affected areas show at least two color changes (pallor, cyanosis, or hyperemia), and spasm is 

transient lasting minutes to hours. 

Management: Local body parts should be warmed and vasoconstricting agents (such as nicotine) 

discontinued. Precipitating factors should be avoided. Calcium channel blockers may be used in extreme 

cases. 

Scenario G 

Diagnosis: scleroderma 

Diagnostic evaluation: This patient is expressing some of the many symptoms associated with a systemic 

autoimmune disease characterized by skin induration and thickening accompanied by tissue fibrosis, 

chronic inflammatory infiltration of visceral organs and the salivary and lacrimal glands, and cellular 

immune alterations. 

Management: Treatment is focused on managing complications of the disease. 

Scenario H 

Diagnosis: erythema multiforme 

Diagnostic evaluation: This patient is experiencing a classic rash of erythema multiforme that is related 

to the glipizide he just started. Remember the mnemonic "SOAPS" (for Sulfa, Oral hypoglycemic, 

Anticonvulsants, Penicillin, NSAIDs). This is a more severe variant of an urticaria! reaction causing a 

limited hypersensitivity reaction in the skin. Attention should be given to examining the patient for signs of 

Stevens-Johnson syndrome, which this reaction can progress to. 

Management: This process is self-limiting, and management should focus on treating the underlying 

condition and removing the offending agent. Acyclovir is used in cases involving herpes simplex virus. 

Scenario I 

Diagnosis: Jarisch-Herxheimer reaction 

Diagnostic evaluation: This patient has been treated appropriately for a Borrelia infection. He is now 

experiencing a febrile reaction to the parasitic or bacterial antigens that are liberated when the organisms 

are destroyed by antibiotic therapy; this typically occurs 2-12 hours after antibiotic therapy has started. 

Management: Management consists of supportive care, antipyretics, and occasionally corticosteroids. 

ScenarioJ 

Diagnosis: anaphylaxis 

Diagnostic evaluation: This patient has a history of a previous exposure to insect venom, which is 

necessary for anaphylactic shock to occur. The severe systemic allergic reaction to an antigen is 

precipitated by the abrupt release of chemical mediators. In this patient, anaphylaxis is categorized as 

severe because of the presence of laryngeal edema, respiratory failure, and shock. 

Management: This patient is in severe anaphylaxis and needs epinephrine. She would likely also benefit 

from concurrent administration of diphenhydramine, cimetidine, and corticosteroids. Aerosolized albuterol 

would be beneficial because of the respiratory symptoms. 

801

802 

NOTES

RENAL AND UROLOGIC DISORDERS 


Acute Kidney Injury/Failure ...................................................................................................................................... 806 

Chronic Kidney Disease ............................................................................................................................................ 811 

Hemodialysis-Related Problems ................................................................................................................................ 812 

Complications Associated with Kidney Transplantation ............................................................................................ 813 

Urinary Tract Infections ............................................................................................................................................ 814 

Nephrolithiasis .......................................................................................................................................................... 816 

Male Genital Problems .............................................................................................................................................. 818 

Urethritis ............................................................................................................................................................ 818 

Orchitis .............................................................................................................................................................. 819 

Acute Bacterial Prostatitis ................................................................................................................................... 819 

Genital Ulcers .................................................................................................................................................... 819 

Fournier Gangrene ............................................................................................................................................. 821 

Balanoposthitis ................................................................................................................................................... 821 

Phimosis ............................................................................................................................................................. 821 

Paraphimosis ...................................................................................................................................................... 822 

Constriction Injuries to the Penis/Tourniquet Syndrome ...................................................................................... 822 

Fracture of the Penis ........................................................................................................................................... 822 

Peyronie Disease ................................................................................................................................................ 822 

Carcinoma ......................................................................................................................................................... 822 

Priapism ............................................................................................................................................................. 822 

Testicular Torsion ................................................................................................................................................ 823 

Torsion of Appendices Epididymis and Testis ...................................................................................................... 824 

Epididymitis ....................................................................................................................................................... 824 

Urethral Stricture ................................................................................................................................................ 825 

Urethral Foreign Bodies ...................................................................................................................................... 825 

Urinary Retention ............................................................................................................................................... 825 

803

RENAL AND UROLOGIC DISORDERS: SELF-ASSESSMENT QUESTIONS 


1. A patient presents with acute kidney injury. Urinalysis reveals a specific gravity of 1.025 and occasional hyaline 

casts but is otherwise normal. The urine sodium is


9. A healthy 28-year-old man presents with rectal itching and a discharge. When specifically asked, he states that his 

sexual preference is male and that he practices anal receptive intercourse. Examination reveals a purulent discharge 

and inflammation. The most appropriate initial therapy is: 

(a) Ceftriaxone 250 mg IM 

(b) Doxycycline 100 mg orally bid x 10 days 

(c) Ceftriaxone 250 mg IM plus doxycycline 100 mg orally bid x 7 days 

(d) Erythromycin base 500 mg orally qid x 7 days 

10. All of the following drug classes are typically associated with urinary retention except: 

(a) Sympatholytics 

(b) a-Adrenergic stimulants 

(c) Cyclic antidepressants 

(d) Antihistamines 

11. An elderly man from a nursing home is sent to the emergency department for evaluation of abdominal distention 

and discomfort. Examination reveals a markedly distended bladder. A Foley catheter is passed and returns 2,000 ml 

initially and 900 ml/hr over the next 3 hours. The most appropriate management is: 

(a) 

Discharge to the nursing home with the catheter in place 

(b) Removal of the catheter and discharge to the nursing home 

(c) Admission to the hospital for IV fluid resuscitation and correction of electrolyte imbalance 


ANSWERS 

1 . a 7. C 

2. C 8. d 

3. d 9. C 

4. C 10. a 

5. C 11. C 

6. b 



805


I. ACUTE KIDNEY INJURY /FAILURE 

A. Causes of acute kidney injury, defined as an abrupt decline in glomerular filtration rate (GFR) are primarily 

prerenal causes and acute tubular necrosis, accounting for 65%-75% of cases. All causes include: 

1. Prerenal 

a. Occurs when normal kidneys are hypoperfused 

(1) These patients are oliguric (urine volume


(3) Urethral obstruction 

3. Renal intrinsic 

(a) Strictures 

(b) Phimosis (uncommon cause of azotemia) 

(c) Meatal stenosis (uncommon cause of azotemia) 

(d) Posterior urethral valves (a common cause in children) 

a. Occurs when there is pathology of the kidney or renal tubule 

(1) Signs and symptoms (including urine flow) depend on the site and nature of the disorder. The urine 

sediment is abnormal; exact findings vary with the underlying cause of the renal failure. 

(a) Acute tubular necrosis: renal tubular casts and muddy brown granular casts 

(b) Acute interstitial nephritis: eosinophilia, granular and white cell casts 

(c) Acute glomerulonephritis: RBCs, RBC casts, and proteinuria 

(2) In these patients, the renal tubules lose their ability to concentrate and reabsorb sodium; therefore, the 

urine is dilute (specific gravity 1.010), and the urine sodium concentration is increased (>40 mEq/L). 

b. Etiology 

(1) Acute tubular necrosis: responsible for 90% of intrinsic cases and in general is a reversible injury to 

the renal tubule 

(a) 

lschemia (most common cause of acute tubular necrosis) 

i. Prolonged hypoperfusion 

ii. Hemorrhage 

iii. Sepsis 

(b) Nephrotoxins 

i. Aminoglycosides 

ii. Heavy metals 

iii. Contrast 

iv. IV immunoglobulins 

(c) Heme pigments 

(2) Vascular disease 

(a) Vasoconstrictive disease (malignant hypertension, thrombocytopenic purpura) 

(b) Vasculitis 

(3) Thrombosis (renal artery/vein) 

(4) Acute interstitial nephritis: interstitial inflammation most commonly due to medication 

(a) 

Drug-related (penicillin, cephalosporins, sulfonamides, NSAIDs, diuretics, allopurinol, cimetidine, 

anticoagulants); methicillin is the most commonly implicated drug. 

(b) Infection-related (bacterial, protozoan, fungal) 

(c) Immune-related (lupus, leukemia, lymphoma, sarcoidosis) 

(5) Glomerular disease: characterized by inflammation of the glomeruli; seen most commonly in children 

(a) Postinfectious: poststreptococcal (primary process) 

(b) Noninfectious: lupus, Goodpasture syndrome (secondary processes) 

(c) lgA nephropathy: most common cause of primary glomerulonephritis 

B. Diagnosis of acute kidney injury according to type 

1. The history and physical examination should suggest etiology. 

a. Hypoperfusion - prerenal 

b. Signs and symptoms of obstruction - postrenal 

c. History of a primary disorder that can cause renal disease or a history of exposure to a contrast material, 

drug, or heavy metal - intrinsic 

2. Laboratory studies, procedures, and other diagnostic measures help to identify the cause and site of obstruction 

due to postrenal causes. 

a. Postvoid residual urine measurement (by catheter or ultrasound bladder scan) 

b. Urinalysis 

c. Renal ultrasound (98% sensitivity in identifying upper-tract obstruction) 

807


3. Helpful laboratory studies in defining specific abnormalities related to intrinsic renal disease 

a. Microscopic examination of urine sediment (eosinophilia suggests a drug-related cause) 

b. Urine for myoglobin 

c. Urine and serum sodium and creatinine 

d. Urine osmolality (measures concentrating ability) 

4. In cases in which you are not sure of the (acute) type of failure (prerenal, postrenal, or renal), learn to calculate 

the renal indices. 

a. These tests are not useful in patients with chronic renal failure, on diuretics, or with a history of obstruction. 

There can be an overlap between categories, which emphasizes the importance of a good history and 

physical examination in determining etiology. 

b. Calculate the indices. 

FENa = fractional excretion of sodium 

FENa (%) = 

urine sodium/serum sodium 

urine creatinine/serum creatinine 

X 100 

RFI = renal failure index 

RFI (%) = 

urine sodium 

urine creatinine/serum creatinine 

X 100 

c. Interpret the indices. 

Table 49: Laboratory Findings in Acute Kidney Injury 

Prerenal 

Acute tubular Acute glomerular Acute interstitial 

necrosis nephritis nephritis 

Postrenal 

Serum BUN/ >20:1 20:1 20:1 

creatinine ratio 

UNa (mEq/L) 20


D. Complications of acute kidney injury 

1. Hyperkalemia (most immediate life-threatening complication; see also pages 606-607) 

a. A serum potassium and ECG are probably two of the most important laboratory studies to obtain in patients 

with acute renal failure. 

b. Hyperkalemia primarily manifests as cardiotoxicity (cardiac dysrhythmias and sudden death). 

c. Management: determined by the potassium level and the ECG findings and can involve a combination of 

the following modalities: 

(1) IV calcium 

(2) IV glucose and insulin 

(3) IV sodium bicarbonate 

(4) IV sodium chloride 3% (in severe hyperkalemia only) 

(5) Inhaled f:3-adrenergic agents 

(6) IV diuretics 

(7) Cation exchange resins: sodium polystyrene sulfonate and patiromer sorbitex calcium (Note: not for 

initial treatment of life-threatening hyperkalemia) 

(8) Dialysis 

2. Hypocalcemia (see also pages 607-608) 

a. Common in chronic renal failure but can occur in acute renal failure in which it is usually asymptomatic 

b. Treatment: IV calcium gluconate or calcium chloride in symptomatic patients 

3. Hypermagnesemia is common but rarely significant; magnesiumcontaining antacids and laxatives should be 

avoided in these patients. 

4. High anion gap metabolic acidosis is almost always present but is generally mild and rarely requires correction. 

5. Volume overload 

a. Common in oliguric patients 

b. Can lead to CHF and pulmonary edema 

c. IV diuretics and nitroglycerin as well as Bi PAP can be used as temporizing measures while arrangements 

for dialysis are being made. 

E. Antibiotics to avoid in the presence of kidney injury 

1. Tetracycline 

2. Nitrofurantoin 

3. Penicillin (most common offender) 

4. Cephalosporins and aminoglycosides 

5. Bacitracin IM (uncommonly used) 

F. Indications for dialysis in acute kidney injury 

1. Hyperkalemia (ECG or clinical manifestations are resistant to therapy) 

2. Fluid overload 

3. Significant acidosis 

4. Presence of certain toxins (ethylene glycol, methanol) 

5. Uremic symptoms (pericarditis, encephalopathy, bleeding complications) 

6. BUN >100 mg/dl, creatinine >10 mg/dl (relative indication) 

G. Heme pigment-induced kidney injury 

1. Pathophysiology: injury occurs three ways: 

a. Tubular obstruction 

b. Direct proximal tubular cell injury 

c. Vasoconstriction 

2. Rhabdomyolysis (see pages 331 and 404-405, crush injury) 

a. Trauma (especially crush injuries, burns, seizures, prolonged strenuous muscle contraction) -a> 

rhabdomyolysis (destruction of skeletal muscle cells) - release of myoglobin into the serum, which passes 

through the kidneys and has a direct toxic effect on the renal tubules -a> acute tubular necrosis -a> renal 

failure (t serum creatinine) 

b. Also can be from hemoglobin in hemolytic anemia 

809


3. Epidemiology: suspect in the clinical settings listed below: 

a. Major trauma 

b. Major burns 

c. Electrical injuries 

d. Intoxicated patients (especially alcohol and phencyclidine [PCP]) 

(1) In alcoholic patients, rhabdomyolysis is due to the direct toxic effect of ethanol on the skeletal muscle 

cell membrane in addition to pressure necrosis of muscle as a result of prolonged immobilization. 

(2) In phencyclidine (PCP) overdose, rhabdomyolysis is due to the excessive muscle activity and agitation 

that this drug induces. 

e. Voluntary/involuntary muscle activity (exertion/seizure) 

f. Infections (influenza A and B, coxsackie virus, Ebstein-Barr virus, HIV, Legione//a spp) 


a. Urinary findings 

(1) Color may be smoky (reddish brown) because of the presence of myoglobin (but do not wait for a 

color change before pursuing the diagnosis). 

(2) Positive for blood on dipstick examination, but no RBCs are seen on microscopic examination 

(indicates myoglobinuria). 

(3) Renal tubular casts and muddy brown granular casts may be present on microscopic examination. 

(4) Myoglobinuria may be present; however, it is not a reliable marker of rhabdomyolysis, because it is 

rapidly cleared from the urine and can be absent (despite the presence of significant rhabdomyolysis). 

b. Serum myoglobin may be positive but, like urine myoglobin, is rapidly cleared and is, therefore, not a 

reliable indicator of rhabdomyolysis. 

c. Serum creatine kinase 

(1) The most sensitive test for detecting rhabdomyolysis 

(2) Released immediately after muscle injury; clearance from serum is slow. 

d. Hypocalcemia (63%), hyperkalemia (


U. CHRONIC KIDNEY DISEASE 

A. Chronic kidney disease is a heterogenous group of disorders characterized by alterations in kidney structure 

and function. Defined as a presence of kidney damage or decreased kidney function for


Ill. HEMODIALYSIS-RELATED PROBLEMS 

A. Complications during hemodialysis 

1 . Hypotension 

2. Cramps 

3. Nausea and vomiting 

4. Headache 

5. Dyspnea 

6. Chest pain/arrhythmias 

7. Back pain 

8. Air embolism: rare because of detection filters 

9. Dysequilibrium syndrome 

a. Occurs during or immediately after dialysis (most frequently during a patient's first dialysis treatment) 

b. Caused by cerebral edema hypothesized to be due to reverse osmotic shift (reduction in urea causes 

transient osmotic gradient) or intracerebral acidosis 

c. Clinical presentation: symptoms range from headache, nausea, vomiting, and muscle cramps to altered 

mental status, grand mal seizures, and coma. 

d. Management: symptomatic treatment (rest, analgesics, antiemetics) is all that is needed for most patients; 

however, other causes of neurologic dysfunction (hypoglycemia, hypocalcemia, intracranial hemorrhage, 

etc) should be considered and excluded, particularly in patient whose symptoms persist or worsen over a 

period of observation. 

B. Complications associated with vascular access 

1 . Hemorrhage 

a. Minor bleeding associated with dialysis puncture or mild trauma 

(1) Apply nonocclusive pressure to the site. If this is unsuccessful, apply topical thrombin or neutralize 

excessive anticoagulation with vitamin Kor protamine sulfate. 

(2) Recheck access for presence of a thrill. 

(3) Evaluate extent of blood loss. 

(4) Observe in emergency department for rebleeding. 

b. Extensive bleeding from an aneurysm or pseudoaneurysm 

(1) Control bleeding with direct pressure. 

(2) Stabilize patient with IV fluids (normal saline or lactated Ringer's), oxygen, and cardiac monitoring. 

(3) Draw blood for laboratory studies (CBC, INR, type and cross). 

(4) Obtain stat vascular surgery consult. 

2. Thrombosis (signaled by loss of a thrill in the access) 

a. Obtain immediate vascular surgery consult to determine whether to remove the clot surgically or use a 

thrombolytic agent. 

b. Do not attempt to irrigate the access device, because this can result in clot embolization. 

3. Infection (usually due to Staphylococcus) 

a. More common in artificial than native grafts 

b. Can produce recurrent bacteremia and loss of access site 

c. Local signs (redness, warmth, tenderness, and induration of access site) may be absent; some patients 

present with only a fever or recurrent episodes of bacteremia. 

d. Management 

(1) Obtain blood cultures. 

(2) Administer IV antibiotics (usually vancomycin). 

812


IV. COMPLICATIONS ASSOCIATED WITH KIDNEY 

TRANSPLANTATION 

A. Kidney allograft dysfunction 

1. Principal causes are categorized 

a. Hyperacute rejection (rarest) occurs within a few minutes to a few hours after surgery and results in 

irreversible allograft destruction. 

b. Acute rejection (most common) generally occurs within 1-12 weeks after surgery; 90% may be successfully 

reversed if recognized and treated promptly. 

c. Chronic rejection is indolent and difficult to arrest. 


a. Tenderness over the allograft (located in the iliac fossa) 

b. Decreased urine output 

c. Fever (low-grade) 

d. Generalized discomfort 

e. Worsening hypertension 

f. Precipitous weight gain 

g. Peripheral edema 

3. Diagnostic evaluation should be directed toward excluding other causes of decreased renal function that occur 

in renal transplant patients (eg, volume contraction, drug-induced nephrotoxicity, infection, etc) and should 

include: 

a. Urinalysis 

b. BUN/creatinine 

c. Renal ultrasonography and bladder scan for residual urine 

d. Trough level of cyclosporine 

4. Management 

B. Infections 

a. High-dose steroids (IV or orally) for 3-4 days followed by: 

b. Allograft biopsy (to document the presence of ongoing rejection) in those patients who show little or no 

improvement, and 

c. Administration of an antibody preparation directed toward lymphocytes (such as OKT3, a monoclonal antihuman 

T cell antibody [lgG2]) to those patients with documented unremitting allograft rejection. 


a. Because of ongoing immunosuppression, infections (particularly opportunistic ones) are common in these 

patients. 

b. May present with a paucity of findings (fever and typical physical findings may be absent) 

2. Prevention 

a. In an attempt to prevent these infections, patients are given multiple vaccines and prophylactic 

medications. 

b. The regimen generally includes the following: 

(1) Pneumococcal vaccine 

(2) Hepatitis B vaccine 

(3) Nystatin 

(4) TMP-SMX (for prevention of Pneumocystis jiroveci pneumonia) 

3. Cytomegalovirus infection 

a. The most common life-threatening infection in these patients (as well as recipients of other solid organ 

transplants and bone marrow recipients) 

b. Generally occurs 1-6 months after transplantation surgery 

c. Manifestations range from daily fever and malaise to leukopenia, lymphadenopathy, t liver function tests, 

epigastric pain, diarrhea, and pneumonia. 

d. Evaluation should include a CBC, liver function tests, viral PCR, and chest radiograph. 

813


e. Management 

(1) Reducing immunosuppressive therapy and 

(2) IV ganciclovir (with or without immune globulin) if lung, GI, or liver involvement is present 

4. Urinary tract infections develop in 20% of patients in the first 4 months after kidney transplantation. 

V. URINARY TRACT INFECTIONS 

A. Definition: significant bacteriuria in a symptomatic patient 

B. Incidence 

1. Females have a steadily increasing incidence with age; peaks occur in infancy, preschool, and childbearing years. 

2. Males have approximately the same incidence as females during infancy, but then this rapidly declines and 

remains low until middle age when prostatism occurs. 

C. Etiology 

1. Uncomplicated urinary tract infections (UTls) 

a. Represents most UTls 

b. Occur in normal individuals in whom no anatomic defect in the urinary system can be found 

c. Usually caused by gram-negative aerobic bacilli from the gut; Escherichia coli is the predominant pathogen. 

Occasional other species of Enterobacteriaceae (such as Proteus mirabilis and Klebsiella pneumoniae) or 

other bacteria such as Staphylococcus saprophyticus. 

2. Complicated UTls 

a. Occur in patients with underlying structural, neurologic, or immunologic disease 

b. May be caused by unusual organisms (Pseudomonas, Serratia marcescens, etc); however, typical pathogens 

predominate. 

D. Normal host-defense mechanisms 

1. Acidity: pH


(a) 2-5 WBCs/high-power field on a centrifuged specimen is considered to be significant by most 

authors. 

(b) 1-2 WBCs/high-power field in men if bacteria are also present 

(2) Significant bacteriuria 

(a) 

Any bacteria seen on unspun urine is considered significant when viewed under high-powered field. 

(b) > 15/high-powered field (high dry) on spun sediment 

c. Diagnosis of a UTI based on a urinalysis is presumptive. 

(1) False-positives occur secondary to contamination with bacteria from the skin or from other causes of 

pyuria. 

(2) False-negatives occur secondary to diuresis or an infection that is due to a more virulent bacterium (in 

which case, few organisms are required to cause infection), and they may not be seen in significant 

numbers on microscopic examination. 

2. Definitive diagnosis is made by urine culture. 

a. A colony count> 10 2 /ml is considered significant in the symptomatic patient (much literature still suggests 

10 5 /ml). 

b. Cultures should be ordered on: 

(1) Extremes of age (infants, children, and the elderly) 

(2) Adult men 

(3) Pregnant women 

(4) Patients with any of the following: 

(a) 

Pyelonephritis 

(b) Prolonged symptoms (>6 days) 

(c) Underlying medical disease/immunocompromised (diabetes mellitus, sickle cell anemia, cancer) 

or history of kidney stones 

(d) Urologic abnormalities (structural or neurologic) 

(e) History of recent urologic instrumentation 

(f) 

G. Management 

Those who relapse, require hospitalization, or have a chronic indwelling catheter 

1. In females, look for and exclude cervicitis 1 

pelvic inflammatory disease, and vulvovaginitis. 

2. In males, look for and exclude urethritis. 

3. Outpatient antibiotic therapy for UTls 

a. Patients with uncomplicated UTls should be treated with an agent effective against community-acquired 

E coli. A 3-day course of antibiotics is optimal if there are no complicating factors; this regimen is 

inexpensive, associated with good compliance, has fewer adverse effects than a traditional 10-14 day 

regimen, and has a cure rate similar to that of 7-day therapy. 

(1) TMP-SMX or amoxicillin-clavulanate (first-line drugs only if local resistance patterns to f coli are 1 0% or 

(b) If the patient is male with urethritis not caused by a sexually transmitted disease (3-day therapy) or 

cystitis (7-10 day regimen) 

b. Pregnant patients: despite increasing resistance rates, ampicillin, amoxicillin, and cephalosporins remain 

first-line agents. 

(1) Optimal duration of treatment is not known (usually 3-7 days). 

(2) Nitrofurantoin is becoming a first-line agent because it is efficacious, inexpensive, and well-tolerated; 

because of its short half-life, it must be taken for at least 7 days. Do not give to patients with glucose 

6-phosphate dehydrogenase deficiency. Can be used in pregnancy but not at term because of concern 

for hemolytic anemia in infant related to glutathione instability. 

c. If Chlamydia trachomatis is the suspected pathogen (history of new sexual partner or the presence of pyuria 

without bacteriuria) 1 

culture for Chlamydia trachomatis and begin therapy with doxycycline, TMP-SMX, or 

a quinolone (levofloxacin or ofloxacin; ciprofloxacin does not have activity against Chlamydia). Therapy 

should be for 10-14 days. 

d. Complicated, resistant, or recurrent infections (but no pyelonephritis): start therapy with a quinolone (eg, 

ciprofloxacin), and adjust as needed based on culture and sensitivity; may require 1 0-14 days of therapy. 

815


e. Single-dose therapy is not appropriate for typical emergency department patients, many of whom have 

subclinical pyelonephritis and no identified medical doctor. 

(1) Single-dose therapy has not been uniformly accepted in spite of reported cure rates (80%-100%) with 

TMP-SMX. 

(2) Single-dose therapy should be reserved for the reliable patient with an uncomplicated UTI and an 

identified personal physician who can reassess the patient within 1 week. 

(3) Single-dose therapy should be avoided in infants and adult men. 

f. Consider offering a 2-day course of a bladder analgesic such as phenazopyridine to patients experiencing 

painful urination, and encourage frequent voiding. 

4. Outpatient antibiotic therapy for patients with mild to moderate uncomplicated pyelonephritis who tolerate 

oral intake 

a. Consider "sequential" treatment with a parenteral dose of gentamicin, ceftriaxone, or a fluoroquinolone 

before starting oral therapy. 

b. Discharge on a fluoroquinolone for 7-14 days with instructions for follow-up in 1 week. 

5. Indications for admission in patients with pyelonephritis 

a. Severely ill/uroseptic 

b. The very young or elderly; men >60 years old 

c. Diagnostic uncertainty 

d. Underlying anatomic urinary tract abnormality or medical problems (including renal failure) 

e. History of obstruction, stones, or instrumentation 

f. Progression of uncomplicated UTl/failed outpatient management 

g. Persistent vomiting or inability to tolerate oral antibiotics 

h. lmmunocompromised patient (diabetes, cancer, sickle cell disease, transplant recipient) 

1. Poor social situation/inadequate access to follow up 

j. Pregnancy 

6. Indications for urologic referral to search for an underlying anatomic abnormality 

a. All children and adult men with UTls 

b. Any adult with multiple recurrences of infection (>3/year) 

7. Patients with obstruction and a UTI (stones are the most common cause) have a potentially life-threatening 

condition; a genitourinary consult should be obtained immediately. 

VI. NEPHROLITHIASIS 

A. Etiology 

1. Most kidney stones (80%) contain calcium (oxalate or phosphate) and are radiopaque. 

2. The theory of calcium stone formation is that stones form in the medullary portion of the kidney or by 

hypersaturation of the urine in chronic hypercalcemic states such as: 

a. Hyperthyroidism 

b. Hyperparathyroidism 

c. Neoplasm 

d. Sarcoidosis 

e. Multiple myeloma 

f. Distal renal tubular acidosis 

2. Struvite stones (magnesium-ammonium-phosphate) are radiopaque and are caused by a chronic urinary tract 

infection associated with urea-splitting organisms (usually Proteus or Klebsiel/a). 

3. Uric acid stones are radiolucent and are seen in patients with: 

a. Gout 

b. Myeloproliferative disease or leukemia 

c. High-protein diet 

4. Cystine stones (1 %-3%) are radiopaque and associated with a rare, inherited defect of amino acid transport 

within the kidney. 

816



1. Increased in patients with enhanced enteric oxalate absorption (eg, gastric bypass, bariatric surgery, short 

bowel syndrome). 

2. Stone disease is 2-fold higher in patients with hypertension. This accounts for change in male to female ratio 

from 3:1 to 1.3-1.6:1. 

3. Other diseases, such as diabetes, gout, and obesity, increase the risk. Commonly have increased uric acid states 

or acidic urine. 

4. There is a familial and hereditary predisposition. 

5. Excessive physical exercise 

6. Prior history of nephrolithiasis. Recurrence can be as high as 50% at 10 years, and the risk increases with each 

additional stone episode. 


1. Unilateral colicky pain in the flank, back, or lower quadrant with radiation to the groin, labia, or testicles; 

distinguishing from an abdominal aortic aneurysm is essential. 

2. The pain is usually severe and often accompanied by dysuria, frequency, and hematuria. 

3. Nausea and vomiting occur as the pain increases in severity. 

4. If the stone passes into the bladder, the severity of pain diminishes markedly but may persist as a dull ache due 

to ureteral spasm. 


1. Definitive diagnosis of the type of stone requires stone analysis and is indicated for patients in whom stones 

recur. A 24-hour urine collection and analysis can provide definitive recommendations for prevention of 

stones; studies include urine volume and pH as well as stone identification (calcium, oxalate, citrate, or 

magnesium). 


a. CBC is not indicated but should be considered in the presentation that suggests anemia, infection, or 

abdominal aortic aneurysm. 

b. Urinalysis/urine human chorionic gonadotropin (in women of reproductive age) 

(1) Hematuria is typical of urolithiasis, but its absence does not exclude the diagnosis; 20% of patients 

will not have microscopic hematuria. Also, there does not appear to be any correlation between the 

degree of obstruction and the absence of hematuria. 

(2) If the urinary pH is >7.6, suspect the presence of urea-splitting organisms (Proteus); a pH


3. Facilitation of stone passage: alpha blocker therapy (eg, tamsulosin) and calcium channel blockers (eg, 

nifedipine) have been used; tamsulosin 0.4 mg/day is considered mainstay therapy for larger stones (5-10 mm). 

4. Patients who are discharged should: 

a. Be encouraged to drink two glasses of water every 2 hours (no studies prove that hydration facilitates 

stone passage) 

b. Strain their urine to collect the stone for analysis 

c. Be referred to urology for follow-up 

d. Be advised to return if problems develop (persistent vomiting, fever, chills, unremitting pain) 

5. Indications for admission 

a. Presence of an associated urinary tract infection (pyuria, bacteriuria, leukocytosis, fever) 

b. Uncontrolled pain requiring parenteral narcotics 

c. Intractable nausea and vomiting 

d. Hypercalcemic crisis 

e. Acute kidney injury or anuria 

f. Solitary kidney (relative) 

g. Intrinsic renal disease (relative) 

h. High-grade obstruction (relative) 

1. Stone >5 mm (relative); stone size is a determinant of spontaneous passage but not used solely to determine 

treatment. 

VII. MALE GENITAL PROBLEMS 

A. Urethritis 

1. Etiology 

a. Neisseria gonorrhoeae 

b. Chlamydia trachomatis is most common cause of non-gonococcal urethritis, followed by Mycoplasma 

genitalium. 

c. In almost half of cases of non-gonococcal urethritis, no cause is identified. 

d. Simultaneous infection (which may be asymptomatic) with both gonorrhea and Chlamydia occurs in 

30%-50% of cases; antibiotic therapy should target both of these organisms. 

2. Classic clinical scenario: the patient usually complains of dysuria and a urethral discharge but may be 

asymptomatic. 


a. Mucopurulent or purulent discharge 

b. Gram stain of the discharge reveals c::2 WBCs/high-power field (oil) and may demonstrate gram-negative 

intracellular diplococci with gonorrhea. 

c. Positive leukocyte esterase test on dipstick. 

4. Management 

a. Recommended regimens for gonorrhea and Chlamydia must also be prescribed. 

(1) Ceftriaxone 250 mg IM with azithromycin 1 g; doxycycline can be used as a substitute for 

azithromycin at 100 mg twice daily for 7 days. 

(2) Alternative regimens can be used if injectable cephalosporin is not available. Cefixime 400 mg po 

used in combination with the above other drugs can be used if microbiologic test of cure can be done 

1 week later. 

(3) For severe cephalosporin allergies, azithromycin 2 g with either gentamicin (240 mg IM, once) or 

gemifloxacin (320 mg) may be considered. 

b. If an associated epididymitis is suspected, 7-10 days of therapy are required. 

c. Infection with Trichomonas vagina/is, if present, should be treated with metronidazole 2 g orally. 

Trichomonal infection should be considered in those patients who present with persistent symptoms (in the 

absence of noncompliance and reexposure) despite adequate treatment for gonorrhea and Chlamydia. 

818


B. Orchitis (inflammation of the testicle) 

1. Isolated orchitis is rare. 

2. Most cases of orchitis are the result of direct extension of an epididymal infection and occur as a complication 

of a systemic illness, either bacterial or viral. 

3. Viral orchitis is most often caused by mumps. 

4. The patient presents with testicular pain and swelling (urinary and urethral symptoms are usually absent). In 

the case of mumps orchitis, symptoms usually evolve several days after the onset of parotitis, whereas bacterial 

orchitis can have a more acute presentation. 

5. An immediate urologic consult should be obtained to confirm the diagnosis, because orchitis is extremely 

uncommon; testicular torsion and tumor are far more common. 

C. Acute bacterial prostatitis 

1. Etiology 

a. Usually bacterial, primarily gram-negative organisms (80% are E coli, 20% are Klebsiella, Enterobacter, 

Proteus, or Pseudomonas) 

b. Mixed bacterial infections are uncommon. 

c. Tuberculosis is a possibility when renal tuberculosis is present. 


a. The patient presents acutely ill with dysuria, frequency, urgency, and occasionally urinary retention 

accompanied by pain in the perineum, pelvis, and low back; systemic signs of infection may also occur 

(chills, fever, myalgias, malaise). 

b. Examination reveals a tender, swollen prostate that is warm and firm to the touch. 

c. Prostatic massage should not be done in patients with acute infection, because it can precipitate 

bacteremia; urine culture is sufficient for diagnosis, because cystitis is also present in most cases. 

3. Management 

a. Antibiotics 

(1) Outpatient 

(a) TMP-SMX one double-strength tablet every 12 hours 

(b) Fluoroquinolones (eg, levofloxacin 500 mg/day orally or ciprofloxacin 500 mg bid) 

(c) Treatment is for 6 weeks. 

(2) Inpatient (sepsis, urinary retention): IV fluoroquinolone plus gentamicin 3-5 mg/kg/day 

b. Prompt urologic consultation is indicated for patients who present with acute urinary retention. 

c. Supportive measures 

D. Genital ulcers 

1. Etiology 

(1) Hydration 

(2) Bed rest 

(3) Analgesics (NSAIDs or narcotics as needed) 

(4) Fecal softeners/laxatives (especially if narcotics are prescribed) 

a. Herpes simplex virus (types I and II) 

b. Syphilis 

c. Chancroid (Haemophilus ducreyi) 

d. Granuloma inguinale (Klebsiella granulomatis [formerly Calymmatobacterium granulomatis]) 

e. Lymphogranuloma venereum (Chlamydia trachomatis) 

f. Behcet syndrome 

(1) Vasculitis of uncertain etiology but thought to be an autoimmune disorder 

(2) Clinical triad 

(a) Chronic oral ulcerations 

(b) Relapsing iridocyclitis 

(c) Genital ulcers 

(3) Can be comp I icated by polyarthritis and erythema nodosum 

(4) Lasts for many years with relapses and remissions but can be suppressed by corticosteroids. 

819



a. Serologic testing for syphilis: a VDRL or rapid plasma reagent (nontreponemal tests) should be done initially 

and, if positive, should be confirmed with an FTA-ABS or other treponemal test. A VDRL should also be 

repeated at 3, 6, and 12 months after treatment to monitor response; with successful treatment, VDRL titers 

should gradually decrease. 

b. Bacterial and viral cultures (especially for herpes simplex virus) of lesions 

c. Examination of material from base of ulcer can be done. 

(1) Tzanck smear (done with Wright or Giemsa stain) - multi nucleated giant cells or immunofluorescent 

staining (herpes) 

(2) Darkfield examination - spirochetes (syphilis) 

(3) Gram stain 

(a) Gram-negative rods in a linear or parallel arrangement (chancroid) 

(b) "Donovan bodies" (granuloma inguinale) 

(4) Lymphogranuloma venereum complement fixation test is positive or microimmunofluorescence. 

3. Management: empiric therapy recommended 

a. Herpes 

(1) Acyclovir 

(a) 

Primary infections are treated with 400 mg orally every 8 hours x 7-10 days or until clinical 

resolution. 

(b) Patients with recurrent episodes may benefit from acyclovir if therapy is started within 24 hours of 

the appearance of lesions. Dosage regimens are: 

i. 400 mg orally every 8 hours x 5 days or 

ii. 800 mg orally every 12 hours x 5 days 

(c) Daily suppressive therapy is useful for patients with >6 recurrences per year. The dosage is 400 mg 

orally bid. Alternative regimens include famciclovir 250 mg orally every 12 hours, valacyclovir 

500 mg/day orally, or valacyclovir 1 g!day orally. 

(d) Patients with severe disease or complications requiring hospitalization are treated with IV 

acyclovir. The dosage is 5-10 mg/kg IV every 8 hours x 5-7 days or until clinical resolution. 

(2) Other regimens that are equally efficacious 

b. Syphilis 

(a) Famciclovir 250 mg orally every 8 hours x 7-10 days or 

(b) Valacyclovir 1 g orally every 12 hours x 7-10 days 

(1) Primary, secondary, and early latent (1 year duration) and late syphilis (except neurosyphilis) 

(a) Benzathine penicillin G 2.4 million units IM weekly for 3 doses or 

(b) Doxycycline 100 mg orally every 12 hours x 4 weeks or 

(c) Tetracycline 500 mg orally every 6 hours x 4 weeks 

(3) Neurosyphilis 

(a) Aqueous crystalline penicillin G 2-4 million units IV every 4 hours x 10-14 days or 

(b) Procaine penicillin G 2.4 million units IM every day plus probenecid 500 mg orally every 6 hours 

for 1 0-14 days 

(c) Penicillin-allergic patients require desensitization followed by one of the above regimens. 

Pregnant patients allergic to penicillin should be desensitized and treated with the appropriate 

penicillin regimen; all patients with syphilis should be tested for HIV. 

c. Chancroid (high rate of HIV co-infection) 

(1) Azithromycin 1 g orally in a single dose or 

(2) Ceftriaxone 250 mg IM in a single dose or 

(3) Erythromycin base 500 mg orally three times a day x 7 days or 

(4) Ciprofloxacin 500 mg orally every 12 hours x 3 days 

820


d. Granuloma inguinale (all medications must be given for at least 3 weeks and until all lesions have 

completely healed) 

(1) Doxycycline 100 mg orally every 12 hours or 

(2) Alternative regimens 

(a) Azithromycin 1 g orally once per week 

(b) Ciprofloxacin 500 mg orally every 12 hours x 3 days 

(c) Erythromycin base 500 mg orally 3 times a day x 7 days 

(d) TMP-SMX one double-strength tablet (160 mg/800 mg) orally every 12 hours 

e. Lymphogranuloma venereum 

(1) Doxycycline 100 mg orally every 12 hours x 21 days or 

(2) Erythromycin 500 mg orally every 6 hours x 21 days 

E. Fournier gangrene (idiopathic scrotal gangrene) 


a. Painful, erythematous or necrotic scrotum, penis, or perineum 

b. Febrile and appears toxic 

c. Acute onset of pain and swelling 

d. Urinary tract symptoms 

e. The patient is usually older and immunocompromised in some way (diabetes, chronic steroids, chronic 

alcoholism). 

2. This is a potentially life-threatening disease. 

3. Etiology 

a. Usually due to infection originating from the perianal area 

b. Several organisms, both anaerobic and aerobic, are generally involved. Bacteroides fragilis is the 

predominant anaerobe and f coli is usually the predominant aerobe. Other agents include hemolytic 

Streptococcus, Staphylococcus, and C!ostridium spp. 

4. Management 

a. Early and aggressive surgical debridement 

b. Broad-spectrum parenteral antibiotics against anaerobes and gram-negative enteric organisms 

F. Balanoposthitis 

1. An inflammation of the glans penis (balanitis) and foreskin (posthitis) that is often caused by Candida, 

Cardnerella, anaerobes, herpes simplex virus, human papillomavirus. 

2. Noninfectious causes should be considered, eg, psoriasis, eczema, scabies. 

3. Recurrent balanoposthitis can be the sole presenting sign of diabetes. 


a. Retraction of the foreskin reveals foul, purulent material. 

b. The glans is red, swollen, and tender to palpation. 

5. Management 

G. Phimosis 

a. Good hygiene 

b. Consider circumcision 

c. Antifungal creams (nystatin or clotrimazole) 

d. Broad-spectrum antibiotics if secondary infection present (Streptococcus infection may be indistinguishable 

from nonspecific balanitis; cultures or empiric therapy should be considered.) 

e. Evaluation for diabetes (if infection recurrent) 

1. Definition 

a. Inability to retract the foreskin behind the glans 

b. Usually secondary to chronic infection of the foreskin associated with progressive scarring 

2. Management 

a. Emergency treatment with a dorsal slit of the foreskin is occasionally required in severe cases. 

b. Definitive therapy has traditionally been circumcision (after the infection has been controlled with broadspectrum 

antibiotics). Topical steroids (triamcinolone 0.025% every 12 hours or betamethasone 0.05% 

every day) have been shown to be 70%-90% effective in treating phimosis to allow for some degree of 

foreskin retraction and avert circumcision. 

821


H. Paraphimosis 

1. Definition: inability to pull retracted foreskin back over the glans 

2. Management 

a. Emergency treatment is indicated; vascular compromise can occur. 

b. Apply continuous, firm pressure to the glans penis for 5-10 minutes to reduce edema, and then pull the 

foreskin over the glans. 

c. If manual reduction is unsuccessful, infiltrate the constricting ring with a local anesthetic and make a 

superficial vertical incision dorsally in the midline (dorsal slit). 

d. Definitive treatment is circumcision (after inflammation subsides). 

I. Constriction injuries to the penis/tourniquet syndrome 

1. Must be treated immediately 

2. Rings, rubber bands, wire, hair, and other objects can transect the urethra and cause neurovascular 

compromise. 

J. Fracture of the penis 

1. Acute tear of the tunica albuginea (usually during erection) causes a swollen (or bent), painful penis. Occurs 

suddenly and "snap" may be heard. If Buck's fascia remains intact, swelling confined to penile shaft. If not, 

blood may dissect into scrotum, perineum, and suprapubic spaces. 


a. Retrograde urethrogram to exclude associated urethral injury 

b. Immediate urologic consult 

3. Treatment: surgical repair 

K. Peyronie disease 


a. Patients present with a history of dorsal penile curvature with painful erections (and may be associated with 

Dupuytren contracture of the hand). 

b. Examination reveals a thickened plaque involving the tunica albuginea of the corporal bodies. 

2. Management 

L. Carcinoma 

a. This is not an emergency. 

b. If the patient is bothered by it, urologic referral is in order. 


a. A nontender or warty growth is usually found on the glans of uncircumcised men >50-60 years old. 

b. On physical examination, always retract the foreskin to look for this. 

2. Management: immediate referral for this aggressive tumor 

M. Priapism 

1. Definition: a sustained erection unrelated to sexual stimulation; there are two forms: 

a. Low-flow (ischemic) priapism: painful 

(1) Pathophysiology: venous outflow-,, venous stasis and ischemia that involves the corpus cavernosae 

but spares the glans and corpus spongiosum-,, rigid, painful penile shaft and soft glans 

(2) Because the spongiosum is spared, the patient should be able to void. 

(3) A surgical emergency: irreversible damage occurs in 24-48 hours. 

(4) Etiology 

(a) Reversible (may respond to medical therapy) 

i. Sickle cell disease or trait (most common cause in children) 

ii. lntracavernosal injections of papaverine, phentolamine, alprostadil, and prostaglandin E1 for 

erectile dysfunction (most common cause in adults) 

iii. Leukemic infiltration 

(b) Irreversible (generally unresponsive to medical therapy) 

i. Medications (antihypertensives, anticoagulants, and antidepressents) 

ii. illegal substances (alcohol, marijuana, cocaine) 

iii. Idiopathic 

822


b. High-flow (nonischemic) priapism: rare and usually painless 

(1) Not a true emergent condition; long-term sequelae are rare. 

(2) Pathophysiology: t arterial blood flow to the corpus cavernosae - t venous blood flow - partially 

rigid, painless penile shaft and hard glans 

(3) Etiology 

2. Management 

(a) Groin or straddle injury - 

(b) High spinal cord injury/lesion 

a. Obtain immediate urologic consult. 

arterial-cavernosal shunt formation (most common cause) 

b. Manage ischemic priapism in a stepwise fashion to achieve resolution as quickly as possible: dry 

aspiration - aspiration with irrigation - intracavernosus injections of phenylephrine (dilute with normal 

saline to a concentration of 100-500 mcg/ml) 

(1) Repeated injections (1 ml every 3-5 minutes as needed up to 1 hour) should be performed before 

deciding that this treatment is unsuccessful and a surgical shunt is required. 

(2) Monitor for adverse effects during and after intracavernosus injection(s): 

(a) Abnormal vital signs (hypertension, tachycardia/bradycardia) 

(b) Cardiac dysrhythmias 

(c) Headache, palpitations 

(3) In patients with an underlying disorder (sickle cell disease, hematologic malignancy), systemic 

treatment of the disorder should be administered concurrently with the intracavernosus injection(s). 

c. Initial management of nonischemic priapism should be observation. Corporal aspiration should be 

performed only if the diagnosis is in question. Selective arterial embolization is recommended for patients 

who request treatment. 

N. Testicular torsion 

1. Incidence: may occur at any age but has bimodal peaks at the first few days of life and then between ages 12 

and 18. 


a. Acute onset of severe, unilateral testicular pain or lower abdominal pain is typical; there may be a recent 

history of strenuous physical activity or a past history of testicular pain with spontaneous relief. 

b. Swelling occurs within hours; examination (conducted with the patient in the standing position) reveals 

a swollen, firm, "high-riding" testicle with a transverse lie; the contralateral testicle may also have a 

transverse lie, because the underlying anatomic abnormality ("bell-clapper deformity"), which predisposes 

the patient to torsion, may be bilateral. 

c. An associated reactive hydrocele may be present; loss of the cremasteric reflex is an associated finding with 

high specificity, but it is not diagnostic and is not always present. 

d. Urinary symptoms, pyuria, leukocytosis, and fever are typically absent. 

e. The most common misdiagnosis is "epididymitis," because there is tenderness posteriorly where the 

epididymis is normally located. However, what you are actually feeling is a tender testicle, because when 

the testicle is "torsed" (twisted around), the epididymis is then located anteriorly. 


a. Never exclude the diagnosis of testicular torsion based on a single element of the history or physical 

examination finding. 

(1) A prior history of torsion and orchiopexy does not exclude the diagnosis (especially if absorbable 

sutures were used). 

(2) Up to 80% of patients report anorexia, nausea, and vomiting. 

(3) Of all the examination findings, presence of the cremasteric reflex is the most helpful in excluding the 

diagnosis of torsion. 

b. Ultrasound examination and technetium testicular scanning detect the amount of blood flow to the testicle 

(with the normal testicle serving as control); flow is decreased or absent on the affected side with torsion. 

Color Doppler ultrasound is more accurate than the traditional Doppler examination and is now the test of 

choice in most hospitals. Sensitivity ranges from 83% to 100%; however, sensitivity is decreased in younger 

age groups, especially neonates. 

c. Do not delay urologic consult to wait for a scan. 

d. Emergency surgical exploration of the scrotum is the definitive diagnostic test and is indicated if testicular 

torsion cannot be excluded with certainty. 

823


4. Management 

a. Obtain immediate urologic consult. 

b. Order a CBC and urinalysis (usually normal in torsion) and prepare patient for surgery. 

c. Radionuclide scanning or Doppler examination may be performed if either is immediately available and 

desired by the urologic consultant, but they should not delay definitive treatment. 

d. Surgery is indicated as soon as the diagnosis is made, because testicular viability decreases rapidly; salvage 

rate is 80%-100% up to 6 hours of ischemia, 20% after 1 0 hours, and approaches zero after 24 hours. 

e. Symptomatic therapy for patients awaiting surgery is most appropriate. 

0. Torsion of the appendices epididymis and testis 

1. These appendages are small pedunculated structures (without any known function) attached to the epididymis 

and testis that can torse and produce pain. 


a. Early on, pain is localized and a tender nodule is palpated. The "blue dot sign" on transillumination of the 

testis is pathognomonic. 

b. If seen late, pain is diffuse and swelling is present, making diagnosis more difficult. 

3. Management 

a. If the diagnosis is certain, surgery is not required because these structures calcify. 

b. If the diagnosis is uncertain, surgery is indicated to exclude testicular torsion. 

P. Epididymitis 


a. Inflammation of the epididymis is usually caused by bacterial infection and is more common in young 

adults than in preadolescent boys or older men. 

b. There is a gradual onset of unilateral pain and swelling (sudden onset is more common with torsion). 

c. Associated fever and dysuria are common. 

d. On examination, the epididymis is tender, swollen, and located in its normal posterior position. 

e. Elevation of the testicle is associated with relief of pain (Prehn sign), but this sign is unreliable; it cannot be 

used to distinguish epididymitis from torsion. 

2. Etiology is age dependent. 

a. Chlamydia trachomatis (usually sexually transmitted) is the most common pathogen (followed by Neisseria 

gonorrhoeae) in patients 35 years old. 

c. Fungal infection must be considered in homosexual men with epididymitis or epididymo-orchitis. 


a. Urinalysis: a few WBCs are common (but may also be seen with torsion). 

b. Urine culture 

c. CBC: a leukocytosis of 10,000-30,000/mm 3 is common. 

d. Urethral Gram stain 

e. Urethral culture for gonorrhea and Chlamydia 

4. Management 

a 

Supportive measures 

(1) Bed rest initially, followed by scrotal support 

(2) Ice packs 


(4) Fecal softeners 

b. Start antibiotics: antibiotic selection for acute epididymitis should be based on the patient's age, likelihood 

of gonorrhea and Chlamydia, and other presumed pathogens. 

(1) Homosexual (men who practice insertive anal sex) or sexually active men (coliforms) 

(a) 

Ceftriaxone 250 mg IM plus levofloxacin 500 mg orally every 12 hours or ofloxacin 200 mg orally 

every 12 hours x 10-14 days is the usual regimen. 

(b) If


(2) Heterosexual men 35 years old or bisexual men (usually coliforms, but gonorrhea and Chlamydia 

may contribute): levofloxacin 500 mg/day orally or ofloxacin 300 mg orally bid x 10 days 

c. Refer to urologist for follow-up in 5-7 days. 

d. Admission for IV antibiotics is indicated for: 

Q. Urethral stricture 

(1) Toxic-appearing patients (particularly those who are older and in whom a scrotal abscess is suspected) 

(2) lmmunosuppressed patients 

(3) Patients with severe bilateral epididymitis 

1. Etiology: trauma, urethral instrumentation, or a complication of chlamydia! or gonorrheal infection 


a. History of partial or complete retention 

b. If unable to pass a catheter, a retrograde urethrogram can determine the extent and location of the stricture. 

3. Management 

a. Catheterization 

b. If unable to pass a regular or Coude catheter after 2 or 3 careful attempts, obtain a urologic consult for 

catheterization using fi I iforms. 

R. Urethral foreign bodies 

1. Occur at any age 

2. Clinical presentation: hematuria or signs and symptoms of obstruction or infection 

3. Diagnosis: made by palpation and confirmed on plain radiograph, retrograde urethrogram, or cystoscopy 

4. Management: urologic consult for removal 

S. Urinary retention 

1. Etiology 

a. Benign prostatic hypertrophy with bladder neck obstruction (most common cause in men >50 years old) 

b. Strictures (history of a sexually transmitted infection or pelvic trauma) 

c. Drugs 

(1) Antihistamines 

(2) Anticholinergic agents 

(3) Antispasmodic agents 

(4) Cyclic antidepressants 

(5) a-adrenergic stimulants 

(6) Antipsychotic agents 

d. Meatal stenosis 

e. Bladder neck contracture 

f. Bladder cancer 

g. Cancer of the prostate 

h. Neurogenic 


a. The patient is in distress (unless he has a neurogenic bladder) and complains of hesitancy or poor stream 

followed by low abdominal pain and inability to void for 6-8 hours. 

b. On physical examination, the bladder is often visibly distended and easily palpable. 


a. Urinalysis to exclude co-infection 

b. BUN/creatinine to assess renal function 

825


4. Management 

a 

Pass a Foley catheter; this is both diagnostic and therapeutic. 

b. Observe patient with chronic urinary retention for 2-4 hours after relief of urinary retention for 

development of postobstructive diuresis. 

(1) Syndrome of massive urine output that can produce volume depletion, electrolyte imbalance, and 

hypotension 

(2) These patients require hospitalization and additional laboratory studies (serum and urine electrolytes). 

c. Most other patients can be discharged to home with the catheter in place and referred to a urologist 

for evaluation. 

d. Antibiotics (trimethoprim or TMP-SMX) should be prescribed if a concomitant urinary tract infection 

is present. 

e. Belladonna and opium suppositories should not be prescribed for these patients. Continued use will 

prevent a successful voiding trial when the catheter is removed. 

826

RENAL AND UROLOGIC DISORDERS: PRACTICE CLINICAL SCENARIOS 



Scenario A 

Presentation: A 7-year-old child presents with facial swelling and "dark urine." The child had a sore throat 

last week. 


Scenario B 

Presentation: A 60-year-old man on peritoneal dialysis presents with fever and abdominal pain. He states 

the dialysate fluid on return is "cloudy." 


Scenario C 

Presentation: A 57-year-old diabetic man has pain in his scrotum. 

Physical examination: There is evidence of ecchymosis with surrounding erythema. 


Scenario D 

Presentation: A 15-year-old male has pain on the right side of his flank and testicle. 

Physical examination: The testicle is swollen, firm, and high-riding with a transverse lie; the cremasteric 

reflex is absent. 


Scenario E 

Presentation: A pregnant woman presents with urinary tract symptoms of dysuria. Urinalysis shows 50 

WBC/high-power field on a centrifuged specimen. 


827



Scenario A 

Diagnosis: acute glomerulonephritis 

Diagnostic evaluation: Urine sediment shows RBCs, RBC casts, and proteinuria. 

Scenario B 

Diagnosis: spontaneous bacterial peritonitis 

Scenario C 

Diagnosis: Fournier gangrene 

Management: Management includes general supportive measures, cultures, and broad-spectrum parenteral 

antibiotics against anaerobes and gram-negative enteric organisms. Prompt urology consult should be 

obtained for surgical debridement. Hyperbaric oxygen has been used, but its efficacy is unknown and it is 

rarely necessary. 

Scenario D 

Diagnosis: testicular torsion 

Diagnostic evaluation: Never exclude the diagnosis of testicular torsion based on a single element of the 

history or physical examination finding. A prior history of torsion and orchiopexy does not exclude the 

diagnosis (especially if absorbable sutures were used). Up to 80% of patients report anorexia, nausea, 

and vomiting. Of all the examination findings, presence of the cremasteric reflex is the most helpful in 

excluding the diagnosis of torsion. 

Ultrasound examination and technetium testicular scanning detect the amount of blood flow to the testicle 

(with the normal testicle serving as control); flow is decreased or absent on the affected side with torsion. 

Color Doppler ultrasound is more accurate than the traditional Doppler examination and is now the test 

of choice in most hospitals. Sensitivity ranges from 83% to 100%; however, sensitivity is decreased in 

younger age groups, especially neonates. Do not delay urofogic consult to wait for a scan. 

Emergency surgical exploration of the scrotum is the definitive diagnostic test and is indicated if testicular 

torsion cannot be excluded with certainty. 

Scenario E 

Diagnosis: UT! 

Management: In pregnant patients, ampicillin, amoxicillin, and cephalosporins remain first-line agents 

despite increasing resistance rates. Duration of therapy of 3-7 days is recommended. Nitrofurantoin 

is becoming a first-line agent because it is efficacious, inexpensive, and well-tolerated; because of its 

short half-life, it must be taken for at least 7 days. Do not give to patients with glucose-6-phosphate 

dehydrogenase deficiency or who are at 38 weeks because of concern for hemolytic anemia in the infant. 

828

CUTANEOUS DISORDERS 


Introduction .............................................................................................................................................................. 832 

General Approach to the Patient Presenting with a Rash .......................................................................................... 832 

Toxicodendrons (Poison Ivy, Poison Oak, Poison Sumac) .......................................................................................... 832 

Diaper Dermatitis ..................................................................................................................................................... 833 

Eczema ...................................................................................................................................................................... 834 

Psoriasis .................................................................................................................................................................... 835 

Exfoliative Dermatitis/Exfoliative Erythroderma Syndrome ....................................................................................... 835 

Erythema Multiforme ................................................................................................................................................ 836 

Steven-Johnsons Syndrome and Toxic Epidermal Necrosis ........................................................................................ 838 

Erythema Nodosum ................................................................................................................................................... 839 

Pityriasis Rosea ......................................................................................................................................................... 840 

Cellulitis/Erysipelas ................................................................................................................................................... 840 

Impetigo .................................................................................................................................................................... 842 

Necrotizing Fasciitis .................................................................................................................................................. 844 

Cutaneous Abscess .................................................................................................................................................... 844 

Staphylococcal Scalded Skin Syndrome .................................................................................................................... 845 

Pemphigus Vulgaris ................................................................................................................................................... 846 

Bullous Pemphigoid ................................................................................................................................................... 846 

Herpes Simplex ......................................................................................................................................................... 847 

Herpes Zoster (Shingles) ........................................................................................................................................... 848 

Aphthous Ulcers ....................................................................................................................................................... 850 

Mulloscum Contagiosum ........................................................................................................................................... 850 

Fungal Disorders ....................................................................................................................................................... 850 

Pressure Ulcers (Decubitus Ulcers) ........................................................................................................................... 853 

Dermatologic Cancers .............................................................................................................................................. 853 

829

CUTANEOUS DISORDERS: SELF-ASSESSMENT QUESTIONS 


1. Which of the following is true regarding erythema multiforme? 

(a) 

Both erythema multiforme minor and major involve the mucous membranes. 

(b) The rash may be precipitated by trauma. 

(c) It is most commonly precipitated by a bacterial infection. 

(d) The rash will generally fade within 2 weeks. 

2. The presence of "target lesions" (erythematous plaques with dusky centers and bright red borders) on the palms and 

soles is classically associated with: 

(a) 

Erythema multiforme 

(b) Secondary syphilis 

(c) Disseminated gonococcal disease 

(d) Pityriasis rosea 

3. A positive Nikolsky sign is typical of skin lesions associated with: 

(a) Toxic shock syndrome 

(b) Herpes zoster 

(c) Toxic epidermal necrolysis 

(d) Contact dermatitis 

4. A Tzanck smear can be useful in making the diagnosis of all of the following except: 

(a) Herpes simplex (types 1 and 2) 

(b) Varicella (chickenpox) 

(c) Erythema multiforme 

(d) Herpes zoster (shingles) 

5. Which of the following statements regarding erysipelas is true? 

(a) It is caused by Staphylococcus aureus. 

(b) The rash is typically a tender, red plaque with sharply demarcated borders. 

(c) It is seen most commonly on the chest and upper back. 

(d) Supportive care is the mainstay of treatment. 

6. A pink to red maculopapular rash that starts on the face and rapidly spreads to the trunk and extremities and is associated 

with lymphadenopathy (especially postauricular, suboccipital, and posterior cervical) is most characteristic of: 

(a) 

Rubella 

(b) Roseola 

(c) Rubeola 

(d) Varicella 

7. All of the following statements about Koplik spots are true except: 

(a) They are found on the buccal mucosa. 

(b) They are pruritic. 

(c) They are described as white papules on an erythematous base. 

(d) They appear 1-3 days before the onset of the rash associated with measles. 

8. A herald patch is most closely associated with: 

(a) 

Psoriasis 

(b) Exfoliative dermatitis 

(c) Toxic shock syndrome 

(d) Pityriasis rosea 

9. In which of the fol lowing diseases are mucous membranes spared? 

(a) 

Stevens-Johnson syndrome 

(b) Erythema multiforme 

(c) Toxic epidermal necrolysis 

(d) Staphylococcal scalded skin syndrome 

830


10. Which of the fol lowing statements regarding oral acyclovir or valcyclovir in the treatment of herpes simplex is true? 

(a) It is recommended for the treatment of primary infections, especially urogenital infections. 

(b) It decreases viral shedding, accelerates healing, and shortens the duration of symptoms. 

(c) It may be used prophylactically in patients who have very frequent recurrences. 


11. Which of the fol lowing is a characteristic of toxic epidermal necrolysis but not of staphylococcal-induced scalded 

skin syndrome? 

(a) Mucous membrane involvement 

(b) A positive Nikolsky sign 

(c) Often follows an upper respiratory infection 

(d) The rash results from a toxin-mediated infection. 

12. All of the following conditions classically produce lesions involving the soles and palms except: 

(a) Erythema multiforme 

(b) Varicella 

(c) Secondary syphilis 

(d) Hand-foot-and-mouth disease 

13. An immunocompromised patient presents with a painful vesicular rash that has a dermatomal distribution. The most 

appropriate management for this patient is: 

(a) Oral acyclovir 

(b) Analgesics and drying compresses 

(c) Systemic corticosteroids 

(d) IV acyclovir and hospital admission 

14. Which of the fol lowing statements regarding disseminated gonococcal infection is true? 

(a) 

Rash is typically distributed over the periarticular regions of the distal extremities. 

(b) It occurs more commonly in men than women. 

(c) Sending urethral or cervical gonorrhea cultures is contraindicated. 

(d) The diagnosis is unlikely in the absence of genitourinary symptoms. 

15. Potential complications of impetigo contagiosa include: 

(a) Rheumatic fever 

(b) Myocarditis 

(c) Scarlet fever 

(d) Acute poststreptococcal glomerulonephritis 

16. Which of the following statements regarding herpes zoster is accurate? 

(a) The cervical dermatome is the most commonly involved. 

(b) It is not communicable. 

(c) Lesions at the tip of the nose indicate possible ocular involvement. 

(d) Post-herpetic neuralgia, a complication of this infection, is most commonly seen in patients >30 years old. 

17. The lesions of erythema nodosum are most commonly found on the: 

(a) Arms 

(b) Face 

(c) Legs 

(d) Trunk 

ANSWERS 

I. d 4. C 7. b 10. d 13. d 16. C 

2. a 5. b 8. d 11. a 14. a 17. c 

3. c 6. a 9. d 12. b 15. d 



831


I. INTRODUCTION 

Cutaneous disorders comprise a small portion (1 %) of the examination content. Pictorial identification is especially 

important. The lesions and rashes you are likely to be asked to identify are described in this chapter. You may also 

wish to consult a color dermatology atlas, such as Fitzpatrick's Color Atlas and Synopsis of Clinical Dermatology, 

Weston and Lane's Color Textbook of Pediatric Dermatology, or Knoop's The Atlas of Emergency Medicine. You 

should be familiar with all the color plates in the most recent edition ofTintinalli's textbook. 

II. GENERAL APPROACH TO THE PATIENT PRESENTING WITH 

A RASH 

A. Inquire about prodromal symptoms, time course, and antecedent events (eg, new medications). 

B. Note patient's age, immune status, past medical history, sexual history, medications, allergies, and 

presence/absence of toxicity. 

C. Examine the rash and determine its characteristics. 

1 . Appearance 

a. Macular - flat and ::cl cm 

b. Patchy - flat and > 1 cm 

c. Papular - raised and ::cl cm 

d. Plaque - raised and > 1 cm 

e. Maculopapular, nodular - dermal or subcutaneous solid lesion 1-2 cm 

f. Tumor - dermal or subcutaneous solid lesion >2 cm 

g. Vesicular - blister ::cl cm 

h. Bullous - blister >1 cm 

i. Pustules - small blister containing purulent material 

j. Scales or keratoses - built up epidermis 

k. Crusts, erosions - loss of part or all of epidermis 

I. Ulceration - loss of dermis or deeper 

2. Evolution: determine where it started and how it has spread. 

3. Distribution: note location of the rash, including involvement of mucous membranes, palms, and soles. 

4. Symptoms: determine if pruritic or painful; note any systemic symptoms (fever, odynophagia, malaise). 

5. Treatments: determine what, if anything, the patient has done to treat the rash (eg, applied topical steroids, 

zinc, or a neomycin-containing antibacterial ointment), because this might have changed the appearance of the 

rash or caused a secondary contact dermatitis. 

Ill. TOXICODENDRONS (POISON IVY, POISON OAK, POISON 

SUMAC} 

A. Overview 

1. Toxicodendron reactions are the most common cause of allergic contact dermatitis in North America. 

2. The development of a reaction requires prior sensitization (days or years earlier); these are type IV cellmediated, 

delayed hypersensitivity reactions. 

3. The antigen responsible for producing the skin reaction is urushiol, which is found in poison ivy, poison oak, 

poison sumac, and mangoes. 


1. The rash is characterized by erythema (frequently in a linear configuration), papules, and intense pruritus, 

typically in exposed areas. The rash can progress to vesicles, or bullae with edema. It might weep fluid. 

832



2. The rash usually appears 5 hours to 15 days after an exposure (most often between 24 and 48 hours). 

3. A widely held misconception is that rupture of the vesicles spreads the rash, but the blister fluid does not 

contain antigen and therefore cannot spread the rash. Of note, different areas of the skin can react at 

different times, furthering this misconception. 

C. Management 

1. Mild dermatitis: topical calamine lotion, colloidal oatmeal or baking soda baths, topical steroids (0.1 % 

triamcinolone or 0.1 % betamethasone applied bid or tid), cool compresses, and an oral antihistamine 

2. Moderate to severe dermatitis 

a. Wet-to-dry compresses with water or aluminum acetate, eg, Burow solution 

b. Oral antihistamines (eg, hydroxyzine, diphenhydramine) 

c. Systemic corticosteroids are indicated for severe reactions. They should be continued for 2-3 weeks, with 

a gradual taper to avoid rebound. Too short a duration can result in rebound flare. Typical starting dose is 

prednisone 1-2 mg/kg/day x 1 week. 

3. Avoid topical antihistamines and antibiotics. 

4. Without treatment, symptoms resolve in 3-6 weeks. 

D. Prophylaxis 

1. After an exposure, the area should be washed immediately with cold soapy water. Urushiol is absorbed in 

10-30 minutes, so the allergen must be removed quickly. 

2. This practice can prevent dermatitis from developing, or at least lessen its severity. 

IV. DIAPER DERMATITIS 

A. Overview 

1. This is not a specific entity but rather a nonspecific term referring to several dermatologic conditions that occur 

in the diaper area. Be able to distinguish irritant, contact dermatitis, and Candida diaper rashes. 

2. The most important inciting factor is constant moisture. Other factors are diaper detergents, disinfectants, an 

alkaline pH, fecal material, intestinal enzymes, and friction caused by the diaper. 

3. The effects of local irritants are amplified by infrequent diaper changes, inadequate skin cleansing, and 

occlusive diapers. 

4. Incidence is highest in babies 9-12 months old, rarely seen at age



2. The involved skin may become hyperpigmented after resolution. 

3. Diaper dermatitis can be a manifestation of the following conditions: 

a. Atopic or seborrheic dermatitis: a clue is the presence of concurrent facial lesions (atopic dermatitis) or 

scalp lesions (seborrheic dermatitis). 

b. Primary irritant contact dermatitis: from ammonia and bacterially produced putrefactive enzymes (the 

odors are characteristic and the skin folds are notably spared) or from a new soap, shampoo, or laundry 

detergent. 

c. Secondary infection with Candida a/bicans: a clue is the classic appearance of the rash (moist, beefyred 

plaques with wellmarked edges in association with satellite lesions and skin fold involvement) and a 

duration >3 days. 

C. Management 

1 . General measures 

a. Discontinue use of plastic or rubber occlusive diaper pants. 

b. Use super-absorbent disposable diapers or cloth diapers, and change them frequently. 

c. Avoid the use of harsh cleansing agents, even "baby wipes" and soaps (which remove protective skin oils); 

use tepid water, and pat dry. 

d. Leave diapers off for extended periods of time or dry diaper area with cool hairdryer. 

e. Protect the skin from maceration with a barrier cream such as commercial zinc oxide diaper rash creams or 

petrolatum ointment. Do not use baby powder with cornstarch, which is metabolized by bacteria. 

2. Additional specific measures 

a. For mild inflammation secondary to atopic, seborrheic, or contact dermatitis, use 1 % hydrocortisone cream 

with a barrier, such as zinc oxide ointment or petrolatum gel (to prevent it from washing off). 

b. If the rash is more severe or persists >3-4 days, or if the patient has overt signs of Candida infection, add 

nystatin, clotrimazole, or miconazole cream for 2-3 weeks. 

V. ECZEMA 

A. Overview 

1. A pruritic, chronic, relapsing atopic dermatitis: "the itch that rashes" 

2. 85% of cases appear by age 5 

3. Familial predominance 

4. Associated with food allergies and asthma 


1. Children: face, scalp, and torso are most commonly affected 

2. Adults: flexure aspects of the extremities 

3. Rash is papules and plaques that are intensely pruritic, scaly, and erythematous. 

4. Dark-skinned patients could have hypo- or hyperpigmented areas. 

834


C. Management 

1. Topical corticosteroids should be applied to the affected areas. 

2. Minimize showers; avoid bathing to help maintain skin hydration. 

3. Use antihistamines for pruritus. 

4. Topical emollients or petroleum jelly can be applied to damp skin to maintain moisture. 

VI. PSORIASIS 

A. Overview 

1. An intermittent, chronic inflammatory disease that can develop at any age 

2. Affects approximately 2% of the world's population 

3. Chronic plaque psoriasis can affect 1 %-90% of the body surface area. 

4. Inverse psoriasis is a variant that affects intertriginous or thin-skinned areas (eg, genitals, eyelids). 

5. Pustular psoriasis is a rare variant characterized by diffuse erythematous papules. 

6. Guttate psoriasis is seen in children/young adults with sores that are shaped like a water drop and are 

commonly triggered by a bacterial infection like a streptococcal pharyngitis. Scales tend to be less thick, and 

resolution is expectant but relapses can occur. 


1. Sharply demarcated thick, silver, scaly, mildly pruritic plaques generally affecting the scalp, elbow, and knees 

2. Can also affect the hands, feet, trunk, or nails 

3. Removing plaques causes pinpoint bleeding (Auspitz sign). 

C. Management 

1. High-potency topical corticosteroids (eg, fluocinonide applied every 12 hours) if disease is localized. Do not 

use on areas of thin skin or near the eyes. 

2. Tar-based shampoos for scalp lesions 

3. The use of systemic steroids can lead to severe exacerbations of the disease when therapy is discontinued and 

should therefore be avoided. 

4. Requires long-term management by a dermatologist or primary care physician. 

VII. EXFOLIATIVE DERMATITIS/EXFOLIATIVE ERYTHRODERMA 

SYNDROME 

A. Overview 

1. Widespread erythematous pruritic dermatitis 

2. Etiology 

a. Idiopathic is most common form. 

b. Drug-induced (>50 drugs have been implicated) 

c. Underlying malignancy (cutaneous lymphoma, leukemia, or other lymphoreticular malignancy) or 

immunosuppression (HIV) 

d. Preexisting dermatoses (eg, psoriasis, eczema, seborrhea) 

e. Allergic contact dermatitis 


1. Shiny, erythematous, pruritic rash with scaling; begins localized then spreads and generalizes; spares the palms 

and soles 

2. Classic clinical scenario: A 57-year-old man who has a past medical history of seizures and who is taking a 

new medication appears ill and complains of itching, a chilly sensation, and "tightness" of the skin. He has 

a low-grade fever and is hypotensive with tachycardia. On examination, a scaly, warm, erythematous rash is 

found to be covering >50% of his body surface area. There is no oral involvement, and the rash is not tender to 

the touch. Nikolsky sign is negative. 

835



3. Other findings can include fever or hypothermia, dehydration, lymphadenopathy, hepatosplenomegaly, lower 

extremity edema, or gynecomastia. 

4. Scratching can result in lichenification and erosions. 

5. Because of increased blood flow to the skin, the patient might have high output heart failure. 


1. Consider CBC, serum chemistries, liver function tests, erythrocyte sedimentation rate, urinalysis, and HIV 

testing in the search for systemic causes. 

2. Because this disorder is usually the result of an underlying cutaneous disease, a systemic disease, or a response 

to a drug or chemical, patients should be admitted for a diagnostic evaluation. The mortality rate is as high as 

30%. 

3. Obtain skin biopsy (lymph node biopsy if significant lymphadenopathy is present) 

D. Differential diagnosis 

1. Erythema multiforme 

2. Toxic epidermal necrolysis 

3. Toxic shock syndrome 

4. Staphylococcal scalded skin syndrome 

5. Kawasaki disease (children) 

E. Management 

1. Goal is to correct/eliminate the underlying cause while providing symptomatic relief and maintaining skin 

moisture. 

2. Stop new medications, if at all possible. 

3. Antihistamines 

4. Topical steroids covered with an occlusive dressing and continued for weeks or months. 

5. Warm water baths with bath oils and skin emollients are also helpful. 

6. Severe or resistant cases are treated with systemic corticosteroids. 

VIII. ERYTHEMA MULTIFORME (EM} 

A. Overview 

1. There has been controversy regarding the nomenclature of EM through the years, but it is now generally 

agreed that there are two forms: erythema multiforme minor and erythema multiforme major (or bullous EM) 

2. Occurs as a response to infection 

a. Most commonly HSV-1 or HSV-2 

b. Varicella, parapoxvirus, adenovirus, coxsackievirus, influenza, HIV, hepatitis, M pneumoniae, Salmonella, 

streptococci 


1. EM minor: target lesions or raised papules with acral distribution; no mucous membrane involvement 

836



2. EM major (or bullous EM):


IX. STEVEN-JOHNSONS SYNDROME AND TOXIC EPIDERMAL 

NECROLYSIS 

A. Overview 

1. A drug reaction that causes sloughing of skin and mucous membranes 

2. Previously thought to be a variant of erythema mu ltiforme 

3. Now the spectrum of Stevens-Johnson syndrome (SJS) __,. SJS/toxic epidermal necrolysis (SJS/TEN) overlap__,. 

TEN is recognized as its own entity. 

4. Death rate: SJS, 1 %-5%; SJS/TEN, 6%; TEN, 25%-35% 

5. Worse outcome with increased BSA involvement, advanced age, malignancy, tachycardia, BUN > 10 mEq/L, 

acidosis, and hyperglycemia. 

6. Common inciting agents are NSAIDs, antibiotics (sulfonamides, penicillins, cephalosporins), anticonvulsants, 

and allopurinol. 


1. SJS:



X. ERYTHEMA NODOSUM 

A. Overview 

1. An inflammatory/immunologic reaction of the panniculus (fat) that most commonly affects women 15-30 years old 

2. Streptococcal infection is the most common precipitant in children. 

3. Sarcoidosis, inflammatory bowel disease, malignancy, and drug reaction (particularly to birth control pills and 

sulfonamides) are the most common triggers in adults. 


1. Characterized by painful, deep-seated nodules (2-5 cm) on the lower extremities (bilateral but not symmetrical) 

2. Nodules are initially bright red and slightly elevated; then, over 1-2 weeks, they become violet or maroon and 

less raised. 

3. Nodules are typically located in the pre-tibial region but can also be seen on the arms and (rarely) the face. 

4. Arthralgias (particularly of the ankles) often precede the cutaneous eruption. 

5. Single lesions generally last about 2 weeks, but new lesions may continue to recur up to 3-6 weeks. 


839


C. Management 

1. Identify and treat the underlying cause; this condition is self-limited (3-6 weeks) if the cause can be eliminated. 

2. Symptomatic measures include bed rest and leg elevation, compressive dressings, NSAIDs, and colchicine. 

XI. PITYRIASIS ROSEA 

A. Overview 

1. A self-limited rash, typically lasting 4-8 weeks 

2. Unclear cause, presumed to be viral 

3. May be preceded by a flu-like prodrome 

4. Risk of premature birth if it occurs during pregnancy 


1. A single salmon-colored oval patch or plaque (the herald patch) appears first. 

2. Days to weeks later, salmon-colored circular or oval patches and plaque with scaling appear in a Christmas 

tree pattern. 

3. Rash may be asymptomatic or pruritic. 

Courtesy of Laura J. Bontempo, MD, MEd, FACEP 

C. Management 

1. Self-limited; no treatment required. 

2. Antihistamines, if needed, for pruritus. 

XII. CELLULITIS/ERYSIPELAS 

A. Overview 

1. Cellulitis is a local soft-tissue inflammatory reaction secondary to bacterial invasion of the skin. 

2. Although cellulitis is classically associated with comorbidities such as diabetes or peripheral vascular disease, 



2. Systemic involvement such as fever and bacteremia can occur and is most common in immunosuppressed 

patients. 

3. Erysipelas 

a. A specific type of cellulitis caused by group A streptococci, usually Streptococcus pyogenes 

b. Characterized by a bright red color, sharp margins, and tender plaques 

c. Commonly affects the face and lower extremities (especially in patients with venous insufficiency) 

d. Generally affects patients >60 years old and is associated with fever, chills, and malaise 



1. Blood cultures, tissue biopsies, and swabs are not routinely recommended. 

2. Blood cultures are recommended for patients with cellulitis who are immunocompromised, who suffered an 

immersion injury, and who were bitten by an animal. 

D. Management 

1. Elevate the affected area as much as possible. 

2. Cellulitis associated with penetrating trauma, MRSA infection, a history of MRSA, IV drug abuse, or systemic 

infection should be treated with vancomycin. 

3. Cellulitis in an immunocompromised host, in a patient with neutropenia, after an animal bite, or after an 

immersion injury should be treated with vancomycin plus either piperacillin/tazobactam, imipenem, or 

meropenem. 

4. Duration of treatment is usually 5 days but may be extended if infection is not improving. 

5. Outpatient treatment is acceptable for immunocompetent patients without systemic infection. 

841


6. Systemic corticosteroids can be considered as adjunctive treatment for erysipelas in nondiabetic adult 

patients. 

7. Erysipelas: treat with penicillin G or VK, dicloxacillin, or clindamycin (if the patient is allergic to penicillin. 

8. In cases of exposure to fresh, salt, or brackish water, treat with doxycycline, fluoroquinolones, or 

ceftazidime. 

9. Treat patients with cellulitis after a mammalian bite with amoxicillinclavulanate. If penicillin-allergic, treat 

with fluoroquinolone + clindamycin or TMP-SMX + metronidazole. 

XIII. IMPETIGO 

A. Overview 

1. Superficial gram-positive bacterial skin infection that can occur in any group but is most prevalent in children 



b. Lesions 

(1) The lesions are flaccid, thin-walled bullae (1-3 cm in diameter) that contain a purulent material. The 

bullae rupture, leaving shiny, rounded, erythematous erosions with peeling edges and crusting ( 11 coin 11 

lesions). 

(2) There is no surrounding erythema. 

(3) Associated regional lymphadenopathy is rare. 

(4) Nikolsky sign is negative. 

3. Ecthyma is a condition very close to impetigo that is usually caused by streptococci. The lesions are typically 

on the legs and begin as pustules that erode and then ulcerate. The infection is usually deeper than impetigo, is 

painful, and has a high rate of scarring. 

C. Diagnostics: not usually needed 

D. Management 

1. Wound care: remove crust with warm water or hydrogen peroxide. 

2. Antibiotics (oral or topical) 

a. Usually treated with a 7-day course of an oral antibiotic effective against both staphylococci and streptococci 

(1) 13-lactamase-resistant antibiotics are first-line treatment (dicloxacillin, cephalexin). 

(2) Doxycycline, clindamycin, or TMP-SMX for suspected MRSA 

(3) Clindamycin or azithromycin if patient is allergic to penicillin 

b. A topical antibiotic that can be used alone for localized infections. 

(1) Mupirocin 2% bid x 5 days 

(2) Retapamulin ointment bid 

3. Good hand washing and personal hygiene, and not sharing linens (eg, towels) limit spread of the infection 

to others. 

E. Complications (focal and systemic) 

1. Spread (both locally and to others); children should not return to school until after 24 hours of antibiotic 

treatment. 

2. Acute poststreptococcal glomerulonephritis (incidence


XIV. NECROTIZING FASCIITIS 

A. Overview 

1. A bacterial infection that tracks along the fascial planes; surface erythema often underrepresents the extent of 

infection. 

2. Classically caused by group A ~-hemolytic streptococci but may also be caused by 5 aureus, Vibrio vulnificus, 

Enterobacteriaceae, and Bacteroides. 

3. V vulnificus infections are related to exposure to seawater. 

4. Aeromonas hydrophila infections are associated with exposure to brackish water, soil, wood, and ditches. 

5. Risk factors include skin trauma, diabetes mellitus, malignancy, and alcoholism. 

6. The mortality rate is high. 

7. Fournier gangrene is necrotizing fasciitis of the groin, scrotum, and lower abdomen. 


1. Patients are ill appearing with systemic symptoms, including fever, tachycardia, lethargy, and possibly 

hypotension. 

2. Pain and tenderness extend beyond the area of erythema and can be severe. 

3. Skin may have erythema resembling cellulitis, edema, hemorrhagic bullae, or necrosis depending on the stage 

of the disease. 

4. Skin findings progress quickly. 


1. CT or MRI may show edema along fascial planes or gas in the tissue; however, a negative imaging study does 

not exclude the diagnosis. 

2. Blood cultures can be helpful for long-term management. 

3. Definitive diagnosis is made through direct tissue sampling. 

D. Management 

1. Surgical debridement of the necrotic tissue is the mainstay of treatment. 

2. Broad-spectrum antibiotics are needed. 

a. Piperacillin-tazobactam plus vancomycin 

b. Doxycycline plus ceftazidime if V fulnificus is suspected 

c. Doxycycline plus ciprofloxacin if A hydrophila is suspected 

3. Admit to ICU. 

XV. CUTANEOUS ABSCESS 

A. Overview 

1. A cutaneous abscess is a localized collection of pus with associated pain, fluctuant mass, and erythema. 

2. Most abscesses (95%) contain bacteria, most commonly S aureus and streptococci. 

3. While abscesses are usually localized, the presence of fever or other systemic symptoms suggests possible 

bacteremia. 

4. A furuncle is a localized abscess associated with hair follicles. A carbuncle results if several furuncles 

coalesce and interconnect by sinus tracts; it may develop in areas of thick skin such as the back of the neck. 


844



1. The development of cutaneous abscess depends on location. On extremities, the cause is usually minor 

trauma that damages the integrity of the epithelium. In intertriginous regions, abscesses are associated with 

obstructed apocrine sweat glands. 

2. Community-associated MRSA has emerged as the prevalent pathogen of skin and soft-tissue infections in 

urban areas. Furunculosis appears to be the strongest predictor of community-associated MRSA. 

C. Management 

1. Abscess size and depth can be evaluated by ultrasound. 

2. Incision and drainage are the mainstay of therapy. 

3. Consider antibiotics only if the patient is systemically ill, is immunosuppressed, has recurrent or multiple 

abscesses, or on follow-up evaluation is found to have not responded to incision and drainage alone. 

4. Packing of the abscess is not necessary. 

XVI. STAPHYLOCOCCAL SCALDED SKIN SYNDROME 

A. Overview 

1. A skin infection by exotoxin-producing S aureus of phage group 2 

2. Mainly affects children 60% and potentially higher if immunocompromised. 


1. Often follows an upper respiratory infection or purulent conjunctivitis 

2. Tender erythema of the face (perioral area is classic), neck, or axillae that generalizes over the body within 

48 hours. Flaccid bullae develop and, within 48 hours, skin sloughs. Desquamation duration is 5 days. 

3. Crusting around the mouth and eyes and lip fissuring are also frequently present. 

4. In newborns, the entire skin surface may be involved (Ritter disease). 


5. Mucous membranes are not involved, which helps differentiate this syndrome from toxic epidermal necrolysis. 

6. Tense pressure applied to the bullae can result in extension of the bullae because of an unstable epidermis; 

this is a positive Nikolsky sign. 

7. The cleavage plane is intraepidermal; therefore, only the superficial layers of the epidermis are shed, which 

also differentiates it from toxic epidermal necrolysis. 

8. Lesions usually resolve in 2 weeks without scarring. 

C. Management 

1. Antibiotics to treat 5 aureus: ~-lactamase/penicillinase-resistant penicillin such as IV oxacillin/nafcillin is the 

treatment of choice. Azithromycin IV is an alternative therapy. Vancomycin may be considered if MRSA is a 

concern. 

2. Steroids are contraindicated (they may exacerbate the illness). 

3. Hospitalization for hydration and skin care is indicated for most patients (especially infants). 

4. Treatment is similar to that for thermal burn patients; therefore, consider burn unit admission. 

845


XVII. PEMPHIGUS VULGARIS 

A. Overview 

1. An autoimmune bullous disease of skin and mucous membranes 

2. A pathologic lgG attacks the intercellular binding substance of epidermal keratinocytes, disrupting cell-cell 

adhesion and resulting in the formation of bullae 

3. Most commonly affects patients 40-60 years old; equal gender incidence 

4. Associated with the presence of other autoimmune diseases 

5. Mortality rate is currently 5%; however, before the use of corticosteroid therapy, this disease was almost 

uniformly fatal. 


1. Classic clinical scenario: A 55-year-old patient with a past medical history of myasthenia gravis presents with a 

multiple fluid-filled bullae and painful, crusted ulcers. She has a recent history of several months of oral lesions 

of unknown etiology. Physical examination is significant for a positive Nikolsky sign. 

2. Mucous membrane involvement (most commonly of the mouth) typically precedes development of cutaneous 

lesions by several months. 

3. The cutaneous lesions are flaccid vesicles and bullae that rupture easily, leaving behind superficial erosions 

and crusted ulcerations. They are painful and can be seen anywhere. 

4. Nikolsky sign is positive. 

5. Large areas of denuded skin increase the risk of secondary infection. 


1. Skin biopsy with Tzanck smear: a positive test (the presence of acantholytic epidermal cells with large nuclei in 

condensed cytoplasm) is suggestive but not specific. 

D. Management 

1. Dermatology consult 

2. High-dose oral steroids (prednisone 1 mg/kg daily) 

3. Concomitant immunosuppressive therapy (eg, azathioprine, mycophenolate) 

4. Antibiotics to treat secondary bacterial infection 

5. Local therapy (eg, topical steroids) 

6. Hospitalization for patients with extensive bullae and erosions 

7. Other treatments include dapsone, rituximab, IV immunoglobulin, and plasmaphoresis. 

XVIII. BULLOUS PEMPHIGOID 

A. Overview 

1. An lgG autoimmune, chronic disease of the elderly 

2. Associated with other autoimmune diseases 

3. Duration may be months to years 


1. Pruritic tense bullae on normal skin or an erythematous base 

2. Bullae filled with clear or blood-tinged fluid 

3. Most often seen on lower abdomen and flexure surfaces of the thighs and forearms 

4. Typically no mucosal involvement 

5. No Nikolsky sign (lesions do not erode or spread with light pressure) 

C. Management 

1. Localized disease: high-potency topical corticosteroids (eg, clobetasol) 

2. Extensive disease: prednisone, 1 mg/kg daily 

3. Dermatology might consider IVIG for resistant cases. 

846


XIX. HERPES SIMPLEX 

A. Overview 

See also herpetic whitlow, page 402; genital herpes, pages 448-449; and herpetic keratitis, pages 117-118. 

1. Two variants: type 1 (HSV-1) and type 2 (HSV-2) 

2. Most HSV-1 infections involve nongenital areas: the lips (herpes labialis), the eyes (herpes keratitis), and 

the fingers (herpetic whitlow). However, HSY-1 is responsible for 10%-30% of infections involving the 

urogenital area. 


3. Most HSV-2 infections involve the urogenital area: the vulva, vagina, cervix, and perineum in females and the 

penile shaft, glans penis, and anal area in males. 


4. Spread of infection occurs through direct contact of the vesicular fluid with mucous membranes or abraded 

skin, or through contact with body fluids during viral shedding. 

5. Incubation period for primary HSY infection is 2-20 days (average 6 days); resolution occurs within 2-6 weeks. 

6. Once a person is infected, the virus remains in the dorsal root ganglia. Symptoms occur with viral 

reactivation. Recurrent disease occurs in 30%-50% of oral and 95% of genital HSY infections. 


1. The skin lesions begin as groups of vesicles (uniform in size) on an erythematous base that later rupture and 

form a crusted ulcer. The lesions develop at the site of inoculation, have a nondermatomal distribution, and 

are exquisitely tender. 

2. Symptomatic primary HSY infections are usually more severe than recurrent infections and are often 

accompanied by systemic signs and symptoms such as fever, malaise, and regional adenopathy. Systemic 

symptoms are usually absent in recurrent episodes. 

3. Many primary HSY-1 infections are asymptomatic (but they can be severe). Herpetic gingivostomatitis 

presents with fever, malaise, painful gums, pain with eating, and possibly pharyngitis. 

4. Primary HSY-2 genital infection presents with headache, fever, malaise, pain, and dysuria. Genital herpes 

often has urethral involvement and may present with severe dysuria and urinary retention. 

5. In recurrent herpes (HSY-1 or HSY-2), a prodrome of local pain, burning, itching, and hyperesthesia usually 

precedes development of visible cutaneous lesions. 

847



1. Tzanck smear (look for multinucleated giant cells), viral culture (highest yield when lesions are vesicular), 

PCR, or a direct fluorescent antibody test can be used to confirm the diagnosis. 

D. Management 

1. Antiviral medications decrease viral shedding, accelerate healing, and shorten the duration of symptoms but 

do not eliminate the herpes infection or affect the frequency of recurrence. Options are listed below. 

a. Oral acyclovir 400 mg tid for 7-10 days 

b. Famciclovir 250 mg tid for 7-10 days 

c. Valacyclovir 1 g bid 7-10 days 

2. IV acyclovir is reserved for patients with severe disease or complications requiring hospitalization; dosage is 

5-10 mg/kg IV every 8 hours for 5-7 days or until clinical resolution. 

3. Episodic treatment (treatment with each outbreak) should be started at the onset of the initial prodromal 

symptoms or within 1-2 days after lesions appear. 

4. Continuous daily suppressive therapy with oral antivirals is occasionally recommended for patients with 

frequent recurrences (>6 per year); it decreases the recurrence rate by up to 80%. 

5. Analgesia is often needed, particularly for primary infections. Topical viscous lidocaine is very effective, but 

oral agents may also be required. 

6. Prompt ophthalmologic consult should be obtained for patients with ocular lesions. 

7. Advise patients to avoid skin-to-skin contact when lesions or prodromal symptoms are present. 


1. Disseminated HSV can occur in neonates and adults with AIDS, malignancy, immunosuppression, or 

dermatitis and may result in multisystem involvement. Disseminated infection can lead to pneumonitis. 

2. Patients with HSV are at risk of bacterial superinfection, radiculoneuropathy, Bell's palsy, encephalitis, and 

hepatitis. 

3. Eczema herpeticum refers to an acute infection of herpes simplex involving the skin lesions of atopic 

dermatitis. Lesions are typically vesicular but may umbilicate and ulcerate. Dissemination may occur. Most 

severe cases are in the very young or immunosuppressed and require hospitalization for IV antiviral therapy. 

XX. HERPES ZOSTER {SHINGLES) 

A. Overview 

1. Herpes zoster is caused by reactivation of latent varicella-zoster virus (present in the dorsal ganglia since the 

initial infection with chickenpox). 

2. The elderly and immunocompromised are most commonly affected. 


1. Classic clinical scenario: A 77-year-old woman has a history of 3 days of constant right-sided chest pain in a 

band-like distribution. She reports recent increased stress from the loss of a pet. Her past medical history is 

significant for having had varicella as a child. On examination, a vesicular rash in a dermatomal distribution 

is seen. 

2. Burning pain or paresthesia develops in a dermatomal distribution 3-5 days (range 1-21 days) before the 

skin eruption. 

3. Rash appears as herpetiform clusters of vesicles (which vary in size) on an erythematous, edematous base, 

with most of the vesicles concentrated on the proximal end of the dermatome. 

4. The lesions are almost always unilateral in distribution and limited to one or two contiguous dermatomes. 

The most commonly involved dermatomes are the thoracic (>50%), lumbosacral (10%-20%), and trigeminal 

(10%-20%). 

848



5. Disseminated disease is defined as >20 lesions outside the affected or immediately adjacent dermatome. It is 

primarily a disease of immunosuppressed patients. 

6. Hutchinson sign 

a. Lesions at the tip of the nose signal possible eye involvement (the virus travels along the nasociliary 

branch of the trigeminal nerve, which is the ophthalmic division). 

b. Antiviral therapy is necessary to prevent blindness. 

7. Ramsay Hunt syndrome 

a. Facial palsy (similar to Bell palsy) associated with vesicles in the ear canal and on the pinna, tympanic 

membrane, and/or the pharynx (often associated with involvement of cranial nerve VIII) 

b. Presents with vertigo, ipsilateral facial weakness, and ipsilateral deafness 


1. Tzanck smear (looking for multinucleated giant cells), PCR, or direct fluorescent antibody can confirm the 

diagnosis. 

D. Management 

1. Cover the affected area with drying compresses (aluminum acetate, potassium permanganate). 

2. Analgesics 

3. Oral antiviral therapy for immunocompetent patients if it can be administered within 72 hours after the 

eruption. 

a. Shortens the length and duration of symptoms and could decrease the incidence of post-herpetic 

neuralgia 

b. Acyclovir 800 mg 5 times a day for 7-10 days 

c. Valacyclovir 1,000 mg tid for 7 days 

d. Famciclovir 500 mg tid for 7 days 

4. IV antivirals for immunocompromised patients (including patients receiving steroids or chemotherapy), those 

with disseminated zoster, and those with eye involvement. 

a. Decreases the rate of dissemination as well as morbidity in these groups 

b. Acyclovir 1 0 mg/kg tid for 5-7 days 

c. Foscarnet 40 mg/kg IV tid for 10 days; used if patient is resistant to acyclovir 

5. Systemic corticosteroids may acute pain but have not been proved to prevent post-herpetic neuralgia. 

6. Immediate ophthalmologic consult is indicated if the ophthalmic branch of the trigeminal nerve is involved. 

(See also herpes zoster ophthalmicus and its management, page 118.) 

7. Herpes zoster is a communicable disease; nonimmune contacts can develop chickenpox (varicella). 

a. Patients with herpes zoster should be advised to avoid contact with people who have not had chickenpox 

(the nonimmune), pregnant women, and immunocompromised patients. 

b. Susceptible immunocompromised patients who are exposed should be given varicella-zoster immune 

globulin within 72 hours after exposure. 

849



1. Post-herpetic neuralgia (persistent pain in the affected dermatome): more common in the elderly, women, 

and those with greater rash severity; risk is >40% in patients >60 years old. 

2. Encephalitis due to herpes zoster: appears within 2 weeks after lesion onset. 

3. Bacterial superinfection 

4. Reactivation or recurrence (immunocompromised host) 

5. Cranial and peripheral nerve palsies 

6. Acute retinal necrosis (may cause blindness in HIV patients) 

XXI. APTHOUS ULCERS 

A. Overview 

1. An acute, recurrent, painful ulcerative disease of the mouth 

2. Commonly referred to as canker sores 

3. Highest incidence during second through fourth decades 

4. The cause is unclear but is believed to be noninfectious. 


1. Painful ulcers with a surrounding erythematous halo and a yellow pseudomembrane at their base 

2. Present on the inner lips and buccal surfaces of the mouth; not on the hard palate or gingiva 

3. Ulcers can vary in size from 0.1 to >1 cm; may present in batches 

C. Management 

1. Topical corticosteroid gel (eg, clobetasol, triamcinolone) 

2. Symptomatic treatments include topical anesthetics (lidocaine gel), anesthetic mouthwash, sucralfate, and pain 

medicines. 

XXII. MOLLUSCUM CONTAGIOSUM 

A. Overview 

1. A contagious rash caused by a DNA poxvirus 

2. Spread by sexual transmission or direct contact 

3. Host may autoinoculate, causing the rash to spread 

4. Usually self-limited, with duration of months to 2 years 


1. Smooth, firm, white or skin-colored papules with central umbilication 

2. Adults: lesions typically appear on the lower abdomen and perineum 

C. Management 

1. Self-limited disease 

2. Cryotherapy 

XXIII. FUNGAL DISORDERS 

A. Overview 

1. A group of fungal (including yeast) disorders that affect various parts of the body; disorders are generally 

named by the body area affected. 

2. Dermatophyte is the term used for three types of fungi that cause skin diseases. 

3. Fungal infections generally create an annular, erythematous, scaling plaque rash. 

4. Candida albicans is responsible for 80% of yeast infections. 

5. Infections are more prevalent in warmer environments. 

850



1. Tinea capitis 

a. A dermatophyte infection of the scalp characterized by areas of alopecia, broken hairs ("black dots"), 

and peripheral scaling 


b. Seen most commonly in children, with increased frequency among black Americans 

c. Uncommonly, an intense inflammatory response results in a boggy, tender, indurated plaque with 

pustules and alopecia referred to as a kerion. This lesion may result in permanent scarring and hair loss. 

2. Tinea corporis 

a. A dermatophyte of the skin, commonly referred to as ringworm 

b. Characterized by annular, erythematous, scaling plaques with central clearing; erythematous border may 

demonstrate papules and vesicles 

c. Can spread on its host through self-inoculation 

3. Tinea barbae 

a. A dermatophyte infection of the beard area characterized by areas of plaques and patches 

b. Can resemble bacterial folliculitis 

c. Most common in adult men 

4. Tinea pedis 

a. A dermatophyte infection of the feet seen most often in young adult men 

b. Three main types of infection: interdigital (most common), moccasin, and vesicular 

5. Tinea manuum 

a. A dermatophyte infection of the palmar surface of the hands 

b. Characterized by dry scales and minimal inflammation 

6. Tinea cruris 

a. A dermatophyte infection of the groin common in adult men 

b. Characterized by erythema with scaling borders of the inner thighs and buttocks, avoiding the scrotum 

and penis 

7. Tinea versicolor 

a. A superficial yeast infection caused by Malassezia globosa 

b. Characterized by superficial scaling patches of various colors 


851


8. Candida! intertrigo 

a. Infections that usually favor moist occluded areas such as skin folds and diaper areas 

b. Characterized by erythema and maceration as well as surrounding erythematous papules (satellites) 


c. Predisposing factors include previous antibiotic or corticosteroid use, as well as immunocompromised 

states and obesity. 

9. Oral or esophageal candidiasis (thrush) 

a. Can affect immunocompetent patients but is more common in immunocompromised patients 

b. Patients complain of burning soreness in their mouth. 

c. Curd-like white papules and plaques that wipe off are seen on the mucous membranes of the mouth. 

10. Sporotrichosis 

a. A mycotic infection, also known as Rose Gardener disease, caused by the fungus Sporothrix schenckii, 

which is common in soil and plants 

b. Result of traumatic inoculation that results in a local inflammatory response involving lymphatics; 

however, dissemination may occur and result in systemic illness. 

c. Characterized by painless nodules in lymphatic distribution, especially on upper extremities, which 

appear over weeks. 


1. Rash scrapings may be prepared with potassium hydroxide and viewed under a microscope; a positive 

examination reveals hyphae. Yeast such as Candida demonstrate pseudohyphae and spores. 

2. Wood's light examination is of less help, because many dermatophytes do not fluoresce. 

C. Management 

1. Topical imidazole antifungal agents (eg, clotrimazole 1 %) and allylamine antifungal agents (eg, naftifine 1 %) 

are indicated for most cutaneous fungal infections. Treatment should continue for an additional week after 

lesions have cleared. 

2. Tinea capitis 

a. Oral griseofulvin for 8 weeks 

b. A topical shampoo containing ketoconazole is used to reduce contagion. 

c. Kerion: oral prednisone is indicated as well as oral cephalexin for bacterial superinfection. 

3. Sporotrichosis 

a. Oral itraconazole for 3-6 months 

b. IV amphotericin B is reserved for disseminated cases. 

4. Tinea versicolor 

a. 2.5% selenium shampoo 

b. Recurrence rates are as high as 50%. 

5. Candida 

a. Clotrimazole troches 5 times a day or nystatin rinse 5 ml 4 times a day for thrush 

b. lntertrigo: nystatin or miconazole cream or powder 

6. All lesions should be kept clean and dry. Astringents such as 5% aluminum acetate aid in drying. 

7. Do not treat with topical steroids. 

852


XXIV. PRESSURE ULCERS (DECUBITUS ULCERS} 

A. Overview 

1. The pressure of the individual's weight against a hard surface causes tissue ischemia. 

2. The normal instinct to shift positions is impaired by mobility issues, sedation, contraction/spasticity, or sensory 

loss. 

3. Other contributors include malnutrition, anemia, comorbidities, and improper skin care. 

4. Patients at risk include the elderly, those who are hospitalized or in an extended-care facility, and those with 

neurologic impairments. 

5. The Braden scale is used to assess patients at risk of developing pressure ulcers. 


1. Classic clinical presentation: A 67-year-old woman from an extended-care facility has severe multiple sclerosis 

and a fever. On examination, a large, malodorous, necrotic decubitus ulcer is noted over her sacrum. On 

probing, the tract is found to extend to the sacrum. Results of laboratory studies include increased WBC count, 

erythrocyte sedimentation rate, and (-reactive protein. Radiographs reveal osteomyelitis. 


2. Occurs primarily over bony prominences on the hip/buttocks (70%) and lower extremities (25%) 

3. Muscle necrosis occurs before skin breakdown; a small breakdown of skin can herald a large underlying cavity. 

4. Stages of pressure ulcers 

a. Stage I: skin intact with nonblanching erythema 

b. Stage II: partial-thickness loss of skin; no necrotic tissue 

c. Stage Ill: full-thickness loss of skin extending into subcutaneous tissue with a crater-like appearance 

d. Stage IV: full-thickness loss of skin with extension to muscle, bone, tendon, joint, or other deep structure; 

may be associated with osteomyelitis 

C. Management 

1. Position patient to remove pressure from the affected area. 

2. Cleanse the wound with saline, and debride it. 

3. If the wound appears infected (odor, drainage, necrosis), then treat with broad-spectrum antibiotics. 

4. Wet-to-dry or occlusive dressings should be applied. 

5. Consult a wound care team. 

XXV. DERMATOLOGIC CANCERS 

A. Basal cell carcinoma 

1. Overview 

a. Basal cell carcinoma is the most common skin cancer. 

b. Most commonly found on the head, neck, face, and nose but can occur anywhere 

c. Risk factors include fair skin, chronic sun exposure, immunosuppression, and therapeutic radiation exposure. 

853



a. Dry, scaly, pink to red, flat papules or plaques with distinct borders; the border might be raised. 

b. Enlarge slowly 

3. Management 

B. Melanoma 

a. No emergent treatment 

b. Recognition and referral are key. 

1. Overview 

a. A malignancy of melanocytes (pigment producing cells) 

b. Metastases go to the lungs, liver, and brain. 

c. Risk factors include family history, prior severe sunburns, fair skin, older age, and multiple atypical nevi. 


a. Asymmetric macule with variegated pigmentation and ragged borders 

b. ABCDE assessment: Asymmetry, _Harders that are irregular and ragged, .Color that is variegated, _!2iameter 

>6 mm, and .Evolving (changing) appearance 

3. Management 

a. No emergent treatment 

b. Recognition and early referral are key. 

C. Squamous cell carcinoma 

1. Overview 

a. A malignancy that occurs in sun-exposed areas (commonly the face and dorsal surface of the hands) 

b. May occur in the oral mucosa and lips 

c. Risk factors include family history, fair skin, blue eyes, chronic sun exposure, immunosuppression, and 

radiation exposure. 


a. An erythematous, hyperkeratotic papule or nodule on sun-exposed areas of skin 

b. Lesion may ulcerate and become fixed to deeper structures. 

3. Management 

a. No emergency treatment 

b. Recognition and early referral are key. 

854


CUTANEOUS DISORDERS: QUICK REVIEW TIPS 

Differential diagnosis of genital ulcers 

• Chancre (primary syphilis) - Treponema pallidum 

• Genital herpes - herpes simplex 

• Chancroid _,, Haemophi/us ducreyi 

• Lymphogranuloma venereum - Chlamydia trachomatis 

• Granuloma inguinale (donovanosis) - Klebsiella granulomatis 

Wood's light 

The Wood's light is useful in detecting certain organisms and conditions (listed below) because they fluoresce. It 

can give false-positive results when certain substances that fluoresce (eg, exudates, tetracycline in sweat, make-up, 

deodorant, and soap) are also detected. Trichophyton tonsurans (the most common cause of tinea capitis) does not 

fluoresce. 

• Golden yellow (Tinea versicolor) 

• Pale green (Trichophyton schoenleim) 

• Bright yellow-green (Microsporum audouinii or M canis) 

• Aquagreen to blue (Pseudomonas aeruginosa) 

• Pink to pink-orange (porphyria cutanea tarda) 

• Ash-leaf-shaped spot (tuberous sclerosis) 

• Blue-white (leprosy) 

• Pale white (hypopigmentation) 

• Bright white or blue white (depigmentation, vitiligo) 

• Bright white (albinism) 

855

CUTANEOUS DISORDERS: PRACTICE CLINICAL SCENARIOS 



Scenario A 

Presentation: A patient presents with salmon-colored papules and plaques (sharply marginated) covered 

with silvery white scales. Lesions are also found on the scalp, presacral area, knees, elbows, gluteal cleft, 

palms, soles, and extensor surfaces of the arms and legs. There is nail involvement with "pitting" and "oil 

spots." 



Scenario B 

Presentation: A patient presents with erythematous papules and whitish "burrows" that are intensely 

pruritic and excoriated. Lesions are seen on the web spaces of the fingers, the flexion creases of the wrist 

and elbow, the penis, the buttocks, and the nipples. Pruritus intensifies at night. 



856


Scenario C 

Presentation: A patient has a painless, indurated ulcer with a smooth base and raised border on the 

genitals and another on the mucous membranes of the mouth (the site of inoculation). He also has a 

painless regional adenopathy. 



Scenario D 

Presentation: A patient presents with an erythematous or pink maculopapular or papulosquamous eruption 

with a symmetric distribution over the entire trunk and the extremities, including the palms and soles. 

Lesions are nonpruritic and accompanied by generalized lymphadenopathy and malaise. 



857


Scenario E 

Presentation: A patient presents with pedunculated, pale, cauliflower-like warts. The lesions are soft, moist, 

and painless. 



Scenario F 

Presentation: A young, sexually active woman presents with tender, erythematous (or hemorrhagic) 

macules or papules that are evolving into pustules and vesicles with a "red halo" and a gray necrotic 

center. Lesions are few in number and have a predilection for the periarticular regions of the distal 

extremities. The patient also has a low-grade fever, chills, and migratory polyarthralgias. 



858


Scenario G 

Presentation: A teenager presents with oval-shaped, salmon-colored papules or plaques that have erupted 

on the trunk and proximal extremities. The lesions have a marginal collarette of scales, are mildly pruritic, 

and are distributed along the lines of skin cleavage, with the long axis of the lesions parallel to the ribs, 

forming a "Christmas tree" pattern on the trunk. On further questioning, the patient describes a different 

larger patch-like lesion that occurred about a week ago. 



Scenario H 

Presentation: A patient presents with a pink/red maculopapular rash that first appeared on the face, but 

then rapidly spread to the neck, trunk, and extremities, and now on the third day is fading. 



859


Scenario I 

Presentation: An active well-appearing child had a high fever for 3-4 days followed by eruption of an 

evanescent, blanching, rose-colored macular to maculopapular rash that started on the trunk and spread 

rapidly to the neck and proximal extremities. Mucous membrane involvement is absent. His fever broke as 

the rash erupted. 



ScenarioJ 

Presentation: A patient presents with a vesicular skin eruption that started on the trunk and then spread 

to the face (including the mucous membranes of the mouth) and extremities. The palms and soles are 

spared. The vesicles (described as "dew drops on a rose petal") rapidly evolve into pustules that umbilicate 

and crust. Successive crops of lesions continue to erupt over several days, so that lesions in all stages of 

development are present. 



860


Scenario K 

Presentation: A patient presents with a tender vesicular rash that started on the oral mucosa and then 

spread a day later to involve the buttocks, hands, and feet (including the palms and soles). The vesicles are 

flat-topped and have an erythematous base. 

Courtesy of David Effron, lv!D, FACEP 


Scenario L 

Presentation: A patient presents after having had a bright-red malar rash ("slapped cheek" appearance) for 

2 days. It has now developed into an erythematous, maculopapular rash that has spread to the trunk and 

limbs (the palms and soles are spared). The rash is fading with central clearing, creating a reticulated or 

lacy pattern. 



861


Scenario M 

Presentation: A patient presents with red to purple skin and mucous membrane lesions that do not blanch 

with pressure. 



Scenario N 

Presentation: A patient reports mucous membrane hyperemia and a diffuse blanching, macular 

erythroderma (looked like a first-degree sunburn) that faded within 72 hours of its appearance. After 

another 1-2 weeks, there is now desquamation, particularly on the palms and soles. The patient has a fever 

(c':38.9°(), hypotension, and involvement of three or more organ systems. 



862


Scenario 0 

Presentation: A patient presents with a tender, shiny, erythematous plaque with raised and sharply 

demarcated borders on the face. 



Scenario P 

Presentation: A patient presents with erythematous macules that evolved quickly to bullae or pustules. The 

epidermis is sloughing, revealing an indurated, gunmetal gray, painless ulcer. 



863


ANSWERS TO CLINICAL PRACTICE SCENARIOS 

Scenario A 

Diagnosis: psoriasis 

Management: Treatment options include topical steroids, UV light, coal tar-based shampoos, and 

immunosuppressants for severe cases; refer to dermatology. 

Scenario B 

Diagnosis: scabies (Be able to recognize a picture of the mite that causes scabies.) 

Management: Treat with a scabicide (lindane or permethrin) and an antihistamine or topical steroid for 

pruritus. Treat household contacts and counsel the patient regarding the washing of linens. 

Scenario C 

Diagnosis: chancre of primary syphilis 

Management: 2.4 million units penicillin G (1 dose) IM. Note that the average incubation period is 21 days 

but ranges from 1 0 to 90 days. 

Scenario D 

Diagnosis: secondary syphilis 

Management: 2.4 million units penicillin G (1 dose) IM. Note that the rash usually erupts 2 weeks to 6 

months (average 9 weeks) after the primary chancre appears. 

Scenario E 

Diagnosis: condyloma lata (a highly contagious manifestation of secondary syphilis) 

Scenario F 

Diagnosis: disseminated gonococcal disease 

Management: Admit for treatment with IV ceftriaxone. Watch for complications, which include septic 

joint, meningitis, and endocarditis. 

Scenario G 

Diagnosis: pityriasis rosea 

Management: Treatment is not necessary in most cases. Children can return to school with this rash. 

864


Scenario H 

Diagnosis: German or three-day measles (rubella) 

Key facts: 

• Caused by a genus of the rubivirus 

• Incubation period of 14-21 days 

• Period of infectivity extends from 7 days before until 7 days after onset of the rash. 

• A prodrome of headache, malaise, sore throat, coryza, and low-grade fever is common in adults and 

adolescents 1-5 days before onset of the rash but is often absent or minimal in children. 

• Forchheimer sign (pinpoint petechiae on the soft palate) may be present during the prodrome. 

• Lymphadenopathy (suboccipital, postauricular, and posterior cervical) is characteristic. 

• Complications include arthritis in adults (especially women), encephalitis, thrombocytopenia, and 

the congenital rubella syndrome when exposure occurs during the first trimester of pregnancy. 

Scenario I 

Diagnosis: roseola infantum (exanthem subitum) 

Key facts: 

• Caused by human herpesvirus types 6 and 7 


• Most commonly affects children 6 months to 3 years old 

• Febrile seizures are a common complication. 

ScenarioJ 

Diagnosis: chickenpox (varicella) 

Key facts: 

• Caused by the varicella-zoster virus 


• Period of infectivity is from several days before onset of the rash until all the lesions have crusted over. 

• Prodrome of low-grade fever, malaise, and headache occurs in adults and adolescents 1 or 2 days 

before the rash appears. 

• Diagnosis is usually made clinically but can be confirmed by Tzanck smear (multi nucleated giant 

cells) or culture. 

• Common complications include bacterial superinfection of the skin lesions, pneumonia, and 

encephalitis. Maternal infection during the first trimester can result in the congenital varicella 

syndrome. Perinatal maternal infection (5 days before to 2 days after delivery) can result in 

disseminated herpes in the neonate. 

Scenario K 

Diagnosis: hand-foot-and-mouth disease 

Key facts: 

• Caused by an enterovirus (usually coxsackie A 16) 


• Brief prodrome (if any) of low-grade fever, malaise, and sore mouth 

• Infection during the first trimester of pregnancy may result in spontaneous abortion. 

865


Scenario L 

Diagnosis: fifth disease (erythema infectiosum) 

Key facts: 

• Caused by human parvovirus B 19 


• May be accompanied by fever, headache, malaise, and myalgia; in adults (particularly women), 

arthralgia and arthritis are also common. 

• May recur with various stimuli over several months 

• Once the rash appears, children are generally no longer contagious. 

• Complications are rare unless the infection occurs during pregnancy (which may cause hydrops 

fetal is or fetal death), or they may occur in patients with chronic hemolytic anemias (which may 

cause aplastic crisis). 

Scenario M 

Diagnosis: purpura 

Key facts: 

• Purpuric lesions 90% of menstrual-related and -60% 

of nonmenstrual-related) are caused by strains of S aureus that produce toxic shock syndrome toxin 1. 

• Although prevalent in the 1980s, the number of cases of menstrual-related toxic shock syndrome 

has declined sharply and currently represents only 50% of all toxic shock syndrome cases. 

• Treatment includes early antibiotics (clindamycin is preferred), removal of source, and aggressive 


866


Scenario 0 

Diagnosis: erysipelas 

Key facts: 

• This variety of cellulitis (caused by group A streptococci) involves only the upper dermis. Traditional 

cellulitis has a much less distinct border and involves the deep dermis and subcutaneous fat. 

• Incubation period of several days 

• Infants, young children, and the elderly are most commonly affected. 

• Associated signs and symptoms (high fever, chills, and anorexia) develop rapidly and may precede 

the appearance of the cellulitis by 1-2 days. 

• Appropriate antibiotics include penicillins, cephalosporins, and macrolides. 

Scenario P 

Diagnosis: ecthyma gangrenosum 

Management: Admit for IV antibiotics; choices include broad-spectrum penicillins such as piperacillin, 

third-generation cephalosporins such as cefepime, aminoglycosides, and fluoroquinolones. The most 

common cause is Pseudomonas aeruginosa. The mortality rate is >50% mortality when the condition is 

associated with bacteremia. 

867

868 

NOTES

EMERGENCY MEDICAL SERVICES 


Background Information ........................................................................................................................................... 872 

Definition ........................................................................................................................................................... 872 

Origin of the Current EMS System ...................................................................................................................... 872 

Models of EMS Service/System Design ............................................................................................................... 873 

Planning for EMS System Demands .................................................................................................................... 874 

Components of an Emergency Medical Services System ........................................................................................... 874 

Prevention .......................................................................................................................................................... 87 4 

Manpower .......................................................................................................................................................... 874 

Education and Training of EMS Providers ............................................................................................................ 874 

Communications ................................................................................................................................................ 875 

Hospital Emergency Department and Specialty Service Categorization Program ................................................. 875 

Medical Control ................................................................................................................................................. 875 

Transport ............................................................................................................................................................ 876 

Medical-Legal Issues .......................................................................................................................................... 876 

Occupational Issues for EMS Providers ............................................................................................................... 877 

Aeromedical Transport. ....................................................................................................................................... 877 

Disaster Planning and Operation .............................................................................................................................. 878 

869

EMERGENCY MEDICAL SERVICES: SELF-ASSESSMENT QUESTIONS 

EMERGENCY MEDICAL SYSTEMS: SELF-ASSESSMENT QUESTIONS 

1. You are a physician at a remotely located community hospital, and you determine that your patient is in need of 

specialized cardiac care. Your patient requires the services of a cardiac catheterization lab almost 60 miles away. 

Helicopter transport is not an option because of weather, and your local EMS crew is a basic life support (BLS)-only 

service. Your patient is hemodynamically stable, on a heparin drip, and still reports active chest pain. What is the 

best course of action for your patient? 

(a) 

Send the patient BLS and suspend the heparin infusion. 

(b) Stabilize the patient locally and wait until the helicopter is back in service. 

(c) Utilize the services of a regional ground critical care interfacility transport team. 

(d) Call 911 and request an advanced life support (ALS) ambulance. 

2. The major role of the hospital during a disaster operation is: 

(a) Triage, stabilization, and transportation 

(b) Providing scene-response medical teams 

(c) Assuring the safety of emergency personnel, victims, and bystanders 

(d) Medical care of disaster victims and the ongoing routine medical needs of the community 

3. The primary goal of triage during a disaster operation is to: 

(a) Treat victims as quickly as possible 

(b) Do everything medically possible for each disaster victim 

(c) Treat as many patients as possible with the given resources 

(d) Classify victims according to treatment priorities to do the most good for the greatest number of potential 

survivors 

4. During a disaster operation, patients who are unlikely to survive are classified by the triage color: 

(a) 

Red 

(b) Yellow 

(c) Green 

(d) Black 

5. In order to be in compliance with The Joint Commission, all hospitals must have a written disaster plan and conduct 

disaster drills: 

(a) One time per year 

(b) Two times per year 

(c) Three times per year 

(d) Disaster drills are recommended but are not required, because they disrupt normal hospital operations. 

6. An on-scene physician wants to assist advanced life support providers at the scene of an emergency call. The 

physician is recommending treatment that may differ from local EMS operational protocols. The EMS providers 

should take the following action: 

(a) Permit the on-scene physician to carry out interventions outside the scope of the provider's practice 

(b) Defer al I decisions about patient care to the on-scene physician 

(c) 

Refuse to relinquish care unless the physician provides verification of current licensure 

(d) Request that the physician accompany the patient and providers to the hospital and document all physicianperformed 

interventions 

7. Which of the following is true regarding aeromedical transport? 

(a) There is research to support use of rotary wing transport for all critically ill patients. 

(b) Ground transportation is a better option for travel up to 30 miles or 30 minutes. 

(c) Cost should not be considered in making the decision to use a specific transport method. 

(d) When used for medical transport, fixed-wing aircraft fly at lower than standard altitudes to avoid problems such 

as air embolism and hypoxemia. 

870

EMERGENCY MEDICAL SERVICES: SELF-ASSESSMENT QUESTIONS 

8. Which of the following EMS providers can give oxygen, transport a patient, and assist with administration of a 

patient's own prescribed medications? 

(a) 

Emergency Medical Technician 

(b) Advanced Emergency Medical Technician 

(c) 

Emergency Medical Responder 

(d) Emergency Medical Technician-Intermediate 

9. An ambulance transporting a critically ill trauma patient arrives unexpectedly at your emergency department 

without prior consultation with medical control. The patient requires rapid administration of blood products and 

placement of a chest tube. What are the most appropriate next steps? 

(a) 

Refuse to accept responsibility for the patient, because the providers failed to consult and your emergency 

department does not have sufficient resources. 

(b) Stabilize the patient to the best of your ability, and instruct the ambulance to proceed to the nearest trauma 

center. 

(c) Perform the necessary lifesaving and stabilizing interventions, and ensure that the ambulance that will 

transfer the patient to the accepting trauma center has personnel trained to assess and monitor for emergency 

interventions. 

(d) Have an emergency department nurse accompany the patient to the nearest trauma center. 

ANSWERS 

I. c 4. d 7. b 

2. d 5. b 8. a 

3. d 6. d 9. c 



871


I. BACKGROUND INFORMATION 

A. Definition 

1. The modern emergency medical services (EMS) system encompasses the delivery of comprehensive patient 

care outside of the hospital. EMS personnel interface with public health agencies, medical systems, and 

emergency departments to deliver time-sensitive and condition-appropriate care. 

2. The EMS system began in the 1960s as an extension of emergency medical care into the community. Today, 

there are three distinct phases within the spectrum of the EMS system. 

a. Prehospital care 

b. Emergency department care 

c. In-hospital care 

3. In 2010, EMS was recognized as a distinct medical subspecialty, and a number of post-residency fellowships 

accredited by the ACGME (Accreditation Council for Graduate Medical Education) are available for physicians 

seeking additional recognition or board certification. 

B. Origin of the current EMS system 

1. Highway Safety Act of 1966 

a. Established the Department ofTransportation and gave it legislative and financial authority to improve EMS, 

with each state required to develop regional EMS systems to handle their specific prehospital needs 

b. Emphasis was placed on developing highway safety programs, EMS standards, improvement of ambulance 

service, and provider training. 

c. Matching funds from state and local government targeted millions of dollars toward EMS research and 

development in the 1970s and 1980s. 

2. Emergency Medical Services Act: initiated in 1973 and provided funds for the development of local, state, and 

regional EMS systems; included development of guidelines for emergency medical care 

a. State EMS system 

(1) The central EMS authority with ultimate responsibility for planning, implementing, and operating the 

state EMS system. 

(2) May delegate authority to regional, county, and local authorities 

b. Established 15 essential components of an EMS system 

(1) Manpower 

(2) Training 

(3) Mutual aid 

(4) Disaster plan 

(5) Facilities 

(6) Transportation 

(7) Access to care 

(8) Communications 

(9) Critical care units 

(10) Public safety agencies 

(11) Consumer participation 

(12) Patient transfer 

(13) Public info/education 

(14) Review and evaluation 

(15) Coordinated patient record keeping 

3. Establishment of communication and ambulance standards 

a. The Department ofTransportation and White House Office ofTelecommunications advocated for national 

standard emergency access (911 ). 

b. The Federal Communications Commissions established rules and regulations for EMS communications and 

dedicated specific radio frequencies for emergency systems. 

c. The Department of Health, Education and Welfare delineated optimal ambulance design as well as 

essential equipment recommendations. 

d. The General Services Administration issued federal specifications for ambulance safety and design. 

872


4. Establishment of industrial and EMS-related standards developed by the National Highway Transportation 

Services Administration's Emergency Services Bureau include the following: 

a. EMS curriculum 

b. Medical aircraft (rotary and fixed-wing) 

c. EMS system organization 

5. Trauma Care Systems Planning and Development Act of 1990 encouraged further EMS development and set a 

standard for directing patients to an appropriate designated facility for time-sensitive treatment. 

6. The EMS Agenda for the Future, first published in 1996, developed by a multidisciplinary group, outlined 

the current state of EMS and posted future goals with emphasis on improving system efficiency, utilizing 

technology, developing healthcare networks that include EMS, and engaging in public health activities. 

a. An "Implementation Guide" set forth clear goals and objectives, along with interim steps to ensure their 

attainment. 

b. The EMS Education Agenda for the Future Uune 2000) revised the National Standard Curriculum. 

c. The most recent Agenda cal Is for an updated scope of practice model. The scope of practice model is 

consistent with training paradigms found in other allied health professions. Nationally recognized provider 

levels include: 

(1) Emergency Medical Responder (formerly "First Responder") 

(2) Emergency Medical Technician (formerly Emergency Medical Technician-Basic) 

(3) Advanced Emergency Medical Technician (formerly EMT-Intermediate) 

(4) Paramedic (formerly "EMT-Paramedic") 

d. The EMS functions at the federal level are overseen in the Department ofTransportation and National 

Highway Traffic Safety Administration office of EMS. 

Table 50: Comparison of Nationally Recognized Emergency Medical Services Providers 

Emergency 

Medical Emergency Medical Advanced Emergency 

Responder Technician Medical Technician Paramedic 

Focus Initiates life-saving Provides emergency Provides basic and Provides advanced level 

care care and limited advanced life care to critically i 11 and 

transportation support care injured; provides link 

from the scene to the 

emergency health care 

system 

Skill set Noninvasive Basic life support Limited medications, Full complement of 

airway skills, oxygen airway management, advanced cardiac life 

management, administration, patient IV fluids support medications, 

hemorrhage transport advanced airway 

control, use 

management, advanced 

of automated 

patient assessment 

defibri I la tor 

C. Models of EMS service/system design 

1. Fire service-based EMS model: Under this design, the fire department provides all EMS services. 

2. "Third service" model: In this model, the EMS delivery system is housed in a specially formed municipal 

department (separate from police and fire services) and provides basic life support (BLS) and advanced life 

support (ALS) services using municipal owned, operated and staffed ambulances. 

3. "Public utility" model: In this model, a community contracts with a private ambulance company to provide BLS 

and ALS ambulance services for all emergency calls in their community. 

4. Volunteer model: BLS, and in some systems, ALS ambulance service is provided by unpaid public service 

personnel. 

5. Combination models: This service model combines different first-response and transport agencies. 

873


D. Planning for EMS system demands 

1. EMS providers should anticipate 100 service requests for EMS annually per 1,000 population in the area they 

are serving. 

2. In service areas with a high volume of elderly or medically underserved, the call volume will be greater. 

3. The EMS Agenda for the Future encourages collaboration with emergency health care services and public 

health agencies to participate in disease surveillance and injury prevention. 

4. Currently, the Centers for Medicare and Medicaid Services (CMS) sets levels of reimbursement for patients 

transported by emergency medical services. Different rates apply for basic, advanced, and "specialty" care 

transportation. 

II. COMPONENTS OF AN EMERGENCY MEDICAL SERVICES SYSTEM 

A. Prevention (public education) 

1 . Safety and accident prevention 

2. Vehicle safety and protective equipment 

3. Poisoning prevention (including "childproof medications") 

4. Education in schools 

5. CPR, first aid, and automated defibrillator training 

B. Manpower 

1. 70%-80% of emergency medical technicians (EMTs) in the United States are volunteers. 

2. The percentage of volunteers is highest in rural areas. 

C. Education and training of EMS providers 

1. In previous years, an emergency medical responder's scope of practice was defined by the National Standard 

Curriculum. Future EMS certification examinations and provider designations will be based on the National 

Scope of Practice EMS provider level. Although classifications are similar, the Scope of Practice model attempts 

to standardize training requirements. 

2. Emergency Medical Responder (formerly "First Responder") 

a. Basic life support skills 

b. Hemorrhage control 

c. Scene safety and vehicle extrication techniques 

3. Emergency Medical Technician (formerly "Emergency Medical Technician-Basic") 

a. Includes skill set and knowledge base of the emergency medical responder 

b. Automated external defibrillation 

c. Patient-assisted medication delivery (nitroglycerin, albuterol) 

4. Advanced Emergency Medical Technician (formerly "Emergency Medical Technician-Intermediate") 

a. Includes EMT skills 

b. Supraglottic airway management 

c. Limited medications (epinephrine for anaphylaxis, narcotic antagonist) 

d. Patient-assisted medication administration 

5. Paramedic (formerly "Emergency Medical Technician-Paramedic") 

a. Includes Advanced EMT skills 

b. Training in differential diagnosis, medical decision making 

c. Invasive airway management 

d. Advanced patient assessment skills 

e. Licensure requirement includes graduation from nationally accredited certificate or associate's degree program 

6. States may designate specialty levels of emergency medical services providers according to regional needs. 

Other commonly encountered "specialty" providers include: 

a. Critical care paramedic: EMS professional trained to the "paramedic" level and credentialed to provide 

interventions outside the typical scope of practice. Critical care providers may be trained to manage 

ventilators, administer blood, or perform advanced skills 

b. Advanced practice or community paramedic: In some regions, paramedics function as physician extenders. 

Advanced practice paramedics may collaborate with local health departments to conduct follow-up visits 

and monitor medications. 

874


D. Communications 

1. The purpose of a communications system is to provide a means of accessing and coordinating the EMS system. 

2. Basic elements of a communications system 

a. Discovery and response 

(1) Recognition of the need for emergency notification 

(2) Best resuscitation outcome is possible when BLS is started within 4 minutes of arrest and ALS is started 

within 8 minutes of arrest. 

b. Access (the ability to activate the EMS system) 

(1) A single telephone number (911) to access police, fire, and EMS is preferred over multiple seven-digit 

phone numbers, which may be difficult to locate/recall in a crisis. 

(2) An enhanced/augmented 911 system (E-911) is a computerized system that automatically displays the 

address and phone number of the 911 cal l's origin to the emergency medical dispatcher. 

(3) New system elements are present for automatic location of cell phone calls, which now account for a 

large percentage of 911 calls. 

c. Receiving and dispatch 

(1) Some EMS systems have separate 911 access/receiving and dispatch functions. 

(2) The goal is to dispatch the most appropriate personnel and equipment to the location; initiating a 

maximal response (lights and sirens) for all requests is ineffective in terms of manpower (and financial 

resources) and can result in unnecessary harm to EMS providers and the public because of EMS 

vehicle accidents. 

(3) The emergency medical dispatcher is responsible for: 

(a) Taking and triaging the call 

1. Relevant information about the emergency is ascertained first (including verification of 

location, nature of the call, and number of people involved). 

ii. The dispatcher prioritizes the call as requiring a maximal or prompt response. 

(b) Alerting and dispatching the appropriate unit 

(c) Ensuring that prehospital personnel can find the address 

(d) Providing prearrival instructions on how to assist the victim until the ambulance arrives 

(e) Some systems have developed alternative call-management systems for 911. This allows lowpriority 

calls to be managed over the phone or by using nonemergency resources. Alternative callmanagement 

systems may include the use of registered nurses or other professionals to provide 

medical-related advice via telephone. 

d. Hospital notification and participation 

(1) EMT crews may communicate with medical control (on-line medical direction), which may or may not 

be the receiving hospital. 

(2) An advantage of hospital notification is that it allows time for emergency department personnel to 

mobilize the appropriate resources for patients' needs (particularly when an incident involves multiple 

casualties). 

E. Hospital emergency department and specialty service categorization program (developed by CMS) 

1. Type A: fully equipped and staffed emergency department with equipment and personnel available 24/7, either 

with a license or accepted by the public as able to treat patients emergently 

2. Type B: licensed by the state as an emergency department, held out to the public by posted signs, seeing at 

least one-third of visits on an urgent basis without appointment (Type B emergency departments are paid at a 

lower rate than Type A.) 

F. Medical control 

1. Physician input and surveillance assures medical competence of an EMS system. Medical control can be the 

responsibility of one physician, a group of physicians, or a hospital (referred to as the "resource hospital"). 

2. Components 

a. Off-line (indirect) medical control 

(1) Development of procedural/treatment protocols 

(2) Provision of standing orders when contact with medical control is not feasible in a timely fashion 

(3) Training and testing 

(4) Ongoing education and surveillance 

(5) Quality reviews and improvement 

875


G. Transport 

b. On-line (direct) medical control 

(1) Provision of direct medical orders to EMTs in the field 

(2) Direct in-field observation: the most effective method for assessing the quality of care provided by 

EMS personnel; provides the most complete data gathering as well as prompt feedback 

1. Vehicle standards (physical and medical) and standards for essential equipment are established jointly by 

government agencies and medical specialty groups. 

2. The cost of an EMS ambulance varies according to its function and design. For example, ambulances providing 

rescue services (extrication) in addition to patient care may cost in excess of $200,000. A basic life-support 

interfacility transport service may meet all patient care objectives through utilization of a smaller, van-type 

(Type II) chassis. 

3. The type of transport used is determined by the distance and time needed to reach the hospital, the patient's 

condition, the weather, and terrain. The following guidelines are helpful in determining the optimal use of 

each mode of transportation. The type of transport is best understood as a medical decision. Physicians should 

have a basic understanding of the capabilities and limitations of various ambulance crew configurations and 

transport modalities. 

a. Ground transportation: best choice for distance ranges up to 30 miles or a transport time 100 miles; use may be limited by weather 

conditions, runways of inappropriate length/condition, refueling requirements, and altitude problems 

(hypoxemia, air embolism, expansion of air within catheter or endotracheal balloons). 

H. Medical-legal issues 

1. Consent to care is same as described for the emergency department 

2. Refusal of care 

a. A potentially significant legal problem (>50% of litigation against EMS providers is related to the issue of 

failure or refusal to treat or transport a patient who requests treatment or transportation). 

b. A competent, conscious adult may make an informed decision to refuse treatment or transportation. 

(1) The decision whether the patient is competent may be made in conjunction with the on-line medical 

control physician. 

(2) The patient is informed of the risks involved in refusing care. 

(3) The refusal should be well documented, and a release of liability waiver completed. 

c. An incompetent patient (as determined by the EMS on-scene providers with or without EMS physician 

involvement) should not be allowed to refuse care. (Appropriate treatment and transportation should be 

provided, even if the patient physically resists it. Police may need to be called to the scene to help manage 

such patients.) 

3. On-scene physician 

a. An on-scene physician who is unknown to EMS providers must be able to provide proof of identity and 

medical licensure before being allowed to provide patient care guidance. 

b. An on-scene physician may assist with treatment that is in line with EMS protocols without assuming 

responsibility and being required to accompany the patient to the hospital. 

c. No physician, including the on-scene physician, can direct EMS providers to administer emergency care 

and treatment that is beyond the EMS providers' training and state regulations. 

d. The on-line medical control physician may relinquish responsibility for guiding medical care of a patient to 

the on-scene physician; if the on-scene physician wishes to assume medical control, he or she must accept 

full medicolegal responsibility for all patient care and should accompany the patient to the hospital. 

4. lnterfacility transport pearls 

a. A "sending" emergency physician is responsible for ensuring that a patient in need of transfer receives 

appropriate care en route. Simply stated, the training and capabilities of the interfacility transport crew 

must be matched with patient needs. For example, a registered nurse might be needed for patients 

receiving certain vasoactive medications or specialized medication infusions. 

876


b. In specific circumstances, it may be appropriate to consider the transfer of "unstable" patients. Patients 

in need of definitive care (such as a cardiac catheterization or a specialized trauma intensive care unit) 

may be better served by transport to a specialized care facility. The sending physician is responsible for 

assuring that the transfer is made with appropriate equipment and qualified medical personnel. 

I. Occupational issues for EMS providers 

1 Infectious disease risk 

a. EMS personnel should observe universal precautions with every patient encounter because of risk of 

exposure to blood-borne pathogens. 

b. EMS personnel should also observe appropriate precautions for disease-specific risks (eg, meningitis, HIV, 

tuberculosis, etc) 

2. Occupational risks 

a. Slips, falls 

b. Lifting injuries 

c. Assault 

3. Legal risk 

a. Malpractice risk: 1 claim/24,000 EMS calls 

b. Operational risk: areas of liability include vehicle accidents, patient injury, medication errors, etc. 

J. Aeromedical transport 

1. lnterfacility transports account for a larger percentage of all hospital-based transport flights versus scene 

responses. 

2. Aeromedical transport of severely injured victims from a trauma scene has been shown to reduce mortality. Its 

effectiveness in reducing the morbidity and mortality of nontrauma patients, however, has not yet been clearly 

established. 

3. The Federal Aviation Administration (FAA) regulates the aviation component (aircraft, flight crews, 

maintenance) of air medical services; specific FAA regulations apply only to EMS aircraft (not to in-flight patient 

care). Because of multiple aircraft crashes and fatalities, the FAA is increasing industry regulation. 

4. The Commission on Accreditation of Air Medical Services, established in 1990, was developed to create 

a national voluntary accreditation process for air medical services. In 1997, it changed its name to the 

Commission on Accreditation of Medical Transport Systems (CAMTS). Accreditation standards were extended to 

address critical-care ground transport teams. While there are no regulatory implications, several managed care 

companies, state EMS agencies, and federal organizations are using CAMTS standards for benchmarking quality 

services as a prerequisite for contractural relationships and a requirement for state licensure. 

5. Helicopter (rotary-wing) transport programs 

a. Many rotary-wing programs permit flight only under visual flight rule conditions (clear weather). Many 

programs mandate that all aeromedical aircraft be equipped for instrument flight rule conditions to allow 

safe landing should poor weather develop en route. 

b. Recent increases in the rate of fatal helicopter accidents have motivated discussions about rotary-wing 

safety. A decision to use helicopter transport should be predicated on: 

(1) A thorough understanding of the patient's condition 

(2) Associated hazards, including weather and risk to personnel 

c. Helicopter emergency medical services have significant costs associated with operation and transport. 

Costs to the patient for an aeromedical evaluation can exceed $6,000. 

6. Airplane (fixed-wing) transport 

a. Fixed-wing aircraft have a better safety record than helicopters; they are able to fly under a wider range of 

weather conditions and are generally less expensive to operate. 

b. The cost for transport by fixed-wing aircraft ranges in the thousands, depending on the aircraft used and the 

distance flown. 

c. Airplanes also provide an increased mile range; greater speed; and increased patient, crew, and equipment 

capacity. However, they are limited to areas with airports. 

877


Ill. DISASTER PLANNING AND OPERATION 

A. Definition of a medical disaster 

1. An incident that results in multiple casualties, overwhelming numbers, or occurring at a rate that cannot be 

handled by the community resources 

a. Natural disasters (hurricanes, floods, earthquakes, etc) 

b. Human disasters (crashes lair, train, water], explosions, fires, environmental contamination, riots, terrorism, etc) 

2. The key issue is not the absolute number of victims but the relationship between the needs of the victims and 

the ability of the health care system to meet those needs using normal operating procedures. 

B. Disaster classification: disasters are most often classified according to the ability of the community, region, 

or state to meet the needs of the disaster response. Federally recognized disasters are usually those that 

cross jurisdictional boundaries and overwhelm the capabilities of local government. 

1. Level I disaster: local medical resources are adequate and quickly mobilized; declared by local officials. 

2. Level II disaster: requires medical resources from adjacent communities and regions (mutual aid); mobilization 

of such additional resources may take several hours to a day. 

3. Level Ill disaster: requires state or federal resources; requested by a local official, but actually declared by the 

governor or president; mobilization of these resources may take 2-3 days. 

C. Creating a disaster plan 

1. Characteristics of a disaster plan 

a. Must comply with the National Response Framework (NRF); the NRF document, distributed by the Federal 

Emergency Management Agency, outlines guiding principles to fol low in the event of a disaster. The goal 

of the NRF is for agencies involved in emergency preparedness to follow uniform disaster management 

strategies. 

b. Must be simple but flexible enough to accommodate the type and size of the disaster 

c. Must be as closely aligned with normal daily operating procedures as possible 

d. Must be coordinated with adjacent geopolitical areas (mutual aid agreements) 

e. Must include input and roles of local emergency management agencies, law enforcement, fire, public 

health departments, ambulance services, EMS council, hospitals, and the local medical community 

f. Must be organized with a structure including the Incident Command System (JCS) and the National 

Incident Management System (NIMS) 

(1) Incident command functions are unified under a designated "Incident Commander." 

(2) The ICS is a standardized, yet flexible template for local disaster operations. 

(3) The ICS is further subdivided into four major "sections." Each section has specific responsibilities. 

Table 51: Key Components of the Incident Command System (ICS) 

Operations Planning logistics Finance 

Search and rescue Collect and manage Provide necessary Manage financial 

activities incident-related data support for incident aspects of operation 

Tactical operations Formulate incident operations Track responder time 

Treat and transport action plans Facilities and pay 

injured Conduct required Transport of supplies Ensure ongoing financial 

Triage of injured meetings Equipment maintenance support and distribution 

Ensure adequate and and fueling of funding to branches/ 

transparent flow of 

sections 

Food and medical 

information between services for responders 

sections 

g. Courses on incident management free of charge to health care providers are available on the Federal 

Emergency Management Agency website (http://www.fema.gov/incident-command-system#item7). 

h. Must include a joint public information operation 

2. Essential phases of a disaster plan 

a. Activation 

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(1) Notification and initial response: The initial EMS personnel arriving on the scene report on the nature 

of the incident, extent of damage, the estimated numbers and types of injuries, hazards for the victims 

and rescuers, and the best access to the scene or routes that are known to be blocked. Activation is 

rapid (within minutes). 

(2) Organization of an incident command post by senior fire/emergency response officials. A more indepth 

assessment of the scene and associated hazards takes place after command post set-up. 

b. Implementation 

(1) Search and rescue (fire/rescue operation of identifying victims) 

(2) Triage, stabilization, and transport (medical providers) 

(3) Definitive management of scene hazards (firefighters) and victims (medical providers) 

(4) Hospital activities during field operations 

c. Recovery 

(a) Alert all area hospitals 

(b) Define levels of care needed 

(c) Monitor the status of the scene 

(1) Scene withdrawal (includes a systematic recheck for any missed victims) 

(2) Return to normal operations (includes restocking) 

(3) Debriefing 

D. The disaster operation 

(a) Evaluation of the disaster response 

(b) Identification of psychological difficulties experienced by the rescuers 

1. The most important prerequisite for good disaster management is that the EMS system must be functioning well 

on a routine basis. The most important first step is to assess the extent of the disaster and mobilize resources. 

2. Prehospital phase 

a. First responders 

(1) The major role of law enforcement is to secure the area and assure the safety of emergency workers, 

victims, and bystanders; in addition, they often establish initial communications. 

(2) The fire department plays an important role in life safety, rescue and hazard containment, and 

removing victims from hazardous areas. 

b. Triage 

(1) Definition: an ongoing process of sorting and classifying victims according to treatment priorities; 

field triage is usually performed by EMS personnel, because physicians and nurses are most useful 

in hospital settings. Triage should be incorporated into daily practice to facilitate its use during 

more chaotic, mass casualty situations. Most hospital systems adopt a codified system of triage that 

incorporates the use of pre-printed tags for victim identification and classification. 

(a) Primary triage: initial field triage in which classification (usually with a color-coding system) is 

begun. 

(b) Secondary triage: reexamination, re-triage, and further stabilization occurs at the casualty 

collection area. 

(c) Tertiary triage: reexamination, re-triage, and definitive care occurs at the appropriate receiving 

hospital. 

(2) Categories 

(a) Hopelessly injured (unsalvageable or dead): in the disaster setting, resuscitative efforts and 

resources should not be expended on any patient in cardiorespiratory arrest or those with 

injuries deemed unsalvageable. 

(b) Severe (first priority): seriously injured but salvageable patients that require immediate 

treatment 

(c) Moderate (second priority): seriously injured patients in whom treatment can be delayed 

without loss of life or limb 

(d) Mild (walking wounded): patients with minor injuries 

(3) Marking triage categories using four colors is the most commonly used system and is based on injury 

severity and prognosis: 

(a) Black: unsalvageable or dead 

(b) Red: first priority 

879


(c) Yellow: second priority 

(d) Green: walking wounded 

(4) Triage team: usually consists of experienced EMS personnel. Staff may be drawn from local hospitals, 

but they must be trained (or experienced) in disaster operations. Triage personnel are under the 

command of the medical triage officer. 

c. Scene control 

(1) Overall scene control by fire and rescue personnel to receive and collate information regarding 

efforts at the scene 

(2) Incident command system established. A command post should be established by the fire personnel 

at the disaster site (usually uphill and upwind of any hazard). 

d. Communications (the most common problem in a disaster) 

(1) The disaster plan should provide for a variety of communication systems capable of reaching all 

responding agencies. 

(2) Preplanning is required to determine the modes of communication that will be used (landline, cell 

phone, radio) and to develop protocols for their use. 

(3) Use of standard language that avoids jargon and "10-codes" facilitates ease of understanding and is 

mandated under the National Incident Management System. 

(4) Hospitals should be surveyed to update the availability of critical care and surgical beds. 

e. Miscellaneous considerations 

(1) A support system should be provided for disaster victims and workers to deal with the psychological 

effects of the disaster. 

(2) A mechanism for storing the dead must be established. 

3. Hospital phase 

a. The Joint Commission requires all hospitals to have a written disaster plan. Disaster drills are required 

twice yearly. 

b. Hospitals develop preparedness plans based on a hazard vulnerability analysis. Each hospital has elements 

of the items below, arranged according to specific risks and needs. 

c. Emergency Operations Center or hospital command center: An in-house control center that is near but not 

in the emergency department should be established to monitor the activities of participating hospitals. 

d. Plan activation: A system of rapid activation must be established that includes a clear delineation of each 

participant's responsibilities. Additional requirements are the following: 

(1) A system for calling in necessary personnel 

(2) Rapid clearing of patients that are currently in the emergency department (and in-house) to make room 

for the incoming casualties; these patients should be admitted or discharged as appropriate. 

(3) Establishing a temporary morgue may be necessary. 

e. Treatment areas 

(1) Receiving and triage area: Established near the emergency entrance, tertiary triage is conducted here 

(primary and secondary triage are generally conducted in the prehospital phase). 

(2) Critical treatment area: for patients who require the most intensive care; patients stabilized in this area 

should be placed in an intermediate care area to await surgery or admission. 

(3) Intermediate treatment area: for patients who are seriously injured but stable 

(4) Delayed treatment area: for patients whose treatment can be delayed without adverse effect (eg, the 

walking wounded) 

(5) Palliative care area: for unsalvageable patients 

f. Documentation 

(1) Patient charts 

(a) 

Information should be limited to critical findings and treatments; ideally, the chart should be kept 

with the patient at all times. 

(b) Prelabeled kits are preferable to the standard chart system when dealing with unidentified 

critically ill or injured patients, because the registration process is cumbersome in this situation. 

All of the contents are prelabeled with a disaster number. These numbers are acceptable 

to medical records and laboratory computers and become the patient's "identity" until full 

registration is possible. Contents of the kit include: 

880


1. The emergency department record 

11. Radiology requests 

iii. Laboratory slips and tubes 

iv. Wrist bands 

(2) A separate casualty list should be kept to account for and identify all deceased victims. 

g. Security: Additional security is needed early during the mitigation of any incident. Security personnel are 

essential to the integrity of entrance points and the maintenance of order. 

h. Waiting areas 

(1) There should be designated waiting areas away from the treatment areas; media will need an 

appropriate area, but a separate area must be available for family members only. 

(2) A hospital public relations officer should act as the public information officer with emergency 

department personnel, law enforcement, media, and families to provide accurate information to those 

in the waiting areas. 

(3) Each waiting area should have adequate telephone access. 

4. The National Disaster Medical System (NDMS), created in 1984, is an organization of civilian resources that 

handles large-scale military or civilian disasters. 

a. Components of the NDMS 

(1) Organization of the participating civilian hospitals and health care providers of designated NDMS 

metropolitan areas. 

(2) Development of disaster medical assistance teams 

b. The NDMS is not designated to replace local, state, or regional disaster plans; it is a federal resource 

available after about 72 hours and is used only in the event of a massive disaster. 

881

EMERGENCY MEDICAL SERVICES: PRACTICE CLINICAL SCENARIOS 

EMERGENCY MEDICAL SERVICES: QUICK REVIEW TIPS 

Basic Disaster Medical Operations: Triage 

Triage is the process of sorting patients according to the severity of injury and the availability of medical resources. In a 

disaster of mass casualty incident, it is imperative to distinguish between the critically ill and the walking wounded. The 

first round of triage is usually dedicated to sorting patients into predetermined categories. 

Triage tips 

• Moribund patients or those in respiratory/cardiac arrest: Patients without spontaneous respirations or without a 

pulse are generally categorized as "black" or unsalvageable. Triaging patients into this category does not preclude 

palliative treatments such as oxygen or morphine for pain. 

• Ambulatory patients: Patients able to follow commands and ambulate without assistance may be tagged as 

"green" or minor. Patients in this category have sustained minor injuries such as lacerations, abrasions, or sprains. 

Reverse triage: Multiple injuries resulting from a lightning strike may benefit from reverse triage. Patients in 

cardiopulmonary arrest from a lightning strike may benefit from cardiac compressions and resuscitation. This is a reversal 

of the usual triage process in that a significant amount of resources are dedicated to patients without initial vital signs. 

Compliance with the Emergency Medical Treatment and Active Labor Act (EMTALA) 

Patients presenting to the emergency department via EMS are essentially requesting a medical screening examination, 

performed to identify life-threatening conditions and prompt initial stabilizing interventions. Patients transported 

by EMS have "arrived at the hospital" as soon as the ambulance arrives on hospital property. The lack of prior radio 

contact or a delay in an orderly transfer of care from EMS to hospital providers does not release the hospital from 

responsibility under EMTALA. If an emergency department cannot provide services required to stabilize or treat an 

identified emergency medical condition, then the emergency department is obligated to transfer patients for definitive 

care. The transfer must take place with resources and personnel sufficient enough to prevent deterioration of the 

patient's condition en route. If a hospital emergency department is experiencing an internal disaster (eg, flooding, 

loss of power) or other catastrophic operational condition, it should officially declare "diversion" or "reroute" 

status so that incoming ambulances are aware of the emergency department's inability to perform medical screening 

examinations. 

882

PROCEDURES AND SKILLS 

PROCEDURES AND SKILLS INTEGRAL TO THE 

PRACTICE OF EMERGENCY MEDICINE 

Adult Cardiopulmonary Resuscitation ....................................................................................................................... 886 

Universal Algorithm ........................................................................................................................................... 886 

Bystander CPR .................................................................................................................................................... 886 

Healthcare Provider CPR .................................................................................................................................... 886 

Synchronized Cardioversion ............................................................................................................................... 887 

Pacing ................................................................................................................................................................ 887 

Postresuscitation Care ......................................................................................................................................... 887 

Resuscitation Procedures .......................................................................................................................................... 889 

Noninvasive Positive-Pressure Ventilation ........................................................................................................... 889 

Tracheal Intubation ............................................................................................................................................. 890 

Rapid Sequence Intubation ................................................................................................................................. 890 

Surgical Airway Management ............................................................................................................................. 894 

Venous and lntraosseous Access in Adults .......................................................................................................... 896 

lntraosseous and Central Venous Access in Children and Neonates .................................................................... 901 

Arterial Catheter Insertion ................................................................................................................................... 902 

Tube Thoracostomy ............................................................................................................................................ 903 

Emergency Department Thoracotomy ................................................................................................................. 904 

Pericardiocentesis ............................................................................................................................................... 907 

Peri mortem Cesarean Section ............................................................................................................................. 908 

Diagnostic Procedures .............................................................................................................................................. 908 

Lumbar Puncture ................................................................................................................................................ 908 

Paracentesis ........................................................................................................................................................ 909 

Thoracentesis ..................................................................................................................................................... 910 

Arthrocentesis .................................................................................................................................................... 911 

Pain Management ...................................................................................................................................................... 911 

Acute Pain Management in Adults ...................................................................................................................... 911 

Pain Management in Children and Neonates ...................................................................................................... 913 

Procedural Sedation and Analgesia ..................................................................................................................... 915 

Cutaneous Diagnostic and Therapeutic Procedures .................................................................................................. 917 

Wound Management .......................................................................................................................................... 917 

Wound Closure Techniques ................................................................................................................................ 920 

Incision and Drainage ........................................................................................................................................ 923 

Nail Trephination ............................................................................................................................................... 924 

Escharotomy ....................................................................................................................................................... 925 

Ultrasound ................................................................................................................................................................ 926 

Bedside Ultrasound ............................................................................................................................................ 926 

Trauma eFAST .................................................................................................................................................... 92 7 

Aortic Ultrasound ............................................................................................................................................... 930 

Pelvic Ultrasound ............................................................................................................................................... 931 

Cardiac Ultrasound ............................................................................................................................................ 932 

Biliary Ultrasound .............................................................................................................................................. 934 

Renal Ultrasound ............................................................................................................................................... 936 

Deep-Vein Thrombosis Ultrasound ..................................................................................................................... 937 

Procedural Ultrasound Uses ............................................................................................................................... 938 

883

PROCEDURES AND SKILLS: SELF-ASSSESSMENT QUESTIONS 

PROCEDURES AND SKILLS: SELF-ASSESSMENT QUESTIONS 

1. A 60-year-old man collapses at work. Optimal citizen's CPR for this patient is: 

(a) 

No CPR, just defibrillation with an automatic external defibrillator 

(b) CPR with a compression/ventilation ratio of 30:2 

(c) Chest compression only CPR 

(d) CPR with a compression/ventilation ration of 15:1 

2. Which of the following is true regarding targeted temperature management for the post-arrest patient? 

(a) 

It can be used for patients who experience traumatic arrest. 

(b) It decreases ischemic-reperfusion injury. 

(c) The goal is to maintain a temperature

PROCEDURES AND SKILLS: SELF-ASSSESSMENT QUESTIONS 

10. Nonabsorbable sutures retain tensile strength for: 

(a) At least 60 days 

(b) At least 30 days 

(c) At least 120 days 

(d) At least 7 days 

11. Which of the following is not true regarding hair removal before suturing? 

(a) It reduces the risk of infection. 

(b) It can hinder suture removal. 

(c) Shaving increases the risk of infection 3-9 times compared with clipping. 

(d) Hair near hairlines and in eyebrows should not be removed. 

12. Which of the following is true regarding OB ultrasound? 

(a) The patient definitely does not have an ectopic pregnancy with a serum HCC


I. ADULT CARDIOPULMONARY RESUSCITATION 

A. Universal algorithm 

1 . Check for responsiveness. 

2. Activate emergency response system (911, code team, call for help, etc). 

3. Cal I for defibri I la tor. 

B. Bystander CPR 

1. Assess responsiveness, no check for breathing, no pulse check. 

2. Compression-only CPR at a rate of 100-120/minute has been shown to improve survival when compared with 

conventional CPR by lay rescuers. 

3. For lay rescuers who are appropriately trained, consider administration of naloxone for known or suspected 

opiate overdose. 

C. Healthcare provider CPR 

1. CABD: if no response, start CPR 

a . .Circulation: check pulse, start CPR within 10 sec 

b. Airway: open airway 

c. .B.reathing: look, listen, feel 

d. Qefibrillator: attach monitor/defibrillator (consider earlier defibrillation when available) 

2. Analyze rhythm: shock if ventricular fibrillation/pulseless ventricular tachycardia 

3. CPR for 2 minutes at a rate of at least 100-120/minute; 30 compressions/2 breaths until definitive airway 

established, minimize interruptions 

4. Secondary ABCD 

a. Airway: secure airway 

b. Breathing: confirm placement and adequacy of ventilation 

c. Circulation: intravenous/intraosseous access, medications, monitor and determine rhythm 

d. Differential diagnosis and treat reversible causes (Table 52) 

Table 52: Potentially Reversible Causes and Treatment of Cardiac Arrest 

Hypovolemia/hemorrhage (IV fluids, blood) 

Hypoxia (0 2 

, ventilate) 

Hydrogen/acidosis (ventilate, possibly HCO 3 

) 

Hyperkalemia (Ca 2 +, insulin/D50 vs KCI) 

Toxins/Tablets/Trauma - overdose (naloxone, 

possibly HCO 3 

) 

Tamponade (pericardiocentesis) 

Tension pneumothorax (needle decompress) 

Thrombosis - acute coronary syndrome or 

pulmonary embolism (PCI vs tPA) 

Hypothermia (warm) 

Note: tPA = tissue plasminogen activator; PCI = percutaneous coronary intervention 

5. Continue CPR, check pulse every 2 minutes. 

6. If ventricular fibrillation/ventricular tachycardia 

a. Pads preferred over paddles (improved contact and safety) 

b. Biphasic (preferred): follow manufacturer's recommendation; usually 150 joules for first shock, then 200 joules 

c. Monophasic defibrillator: 360 joules for all shocks 

d. 2 minutes of CPR between shocks 

7. Medications: introduce after first 2 minutes of CPR 

a. Vasopressors 

(1) Epinephrine 1 mg every 3-5 minutes 

b. Antiarrhythmics 

(1) Amiodarone 300 mg once, may repeat 150 mg 

(2) Lidocaine 1-1.5 mg/kg, then 0.5 mg/kg every 5 minutes (maximum 3 mg/kg) 

(3) Magnesium 1-2 g IV push (consider if concern for torsades de pointes) 

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c. Calcium chloride 1 ampule (consider if concern for hyperkalemia or hypermagnesemia) 

d. Bicarbonate (consider in toxic overdose, prolonged arrest) 

e. Atropine 1 mg every 5 minutes up to 3 mg for symptomatic bradycardia (routine use in asystole/pulseless 

electrical activity unlikely to provide benefit) 

8. Return of spontaneous circulation (ROSC) 

a. Avoid postarrest hypotension (mean arterial pressure


(4) Electrolyte imbalance 

(5) Disseminated intravascular coagulation 

(6) Bacteria translocation from intestines to blood 

2. Postresuscitation care goals 

a. Goal-directed restoration of circulation, oxygenation, and ventilation 

(1) Secure airway 

(a) Maintain SpO 2 

>94%, avoid PaO 2 

>300 mmHg 

(b) Maintain PaCO 2 

40-45 mmHg (prevents hypocapnia-induced cerebral vasoconstriction) 

(2) Establish central venous access 

(3) Volume resuscitation 

(a) Crystal loid infusion to maintain central venous pressure 10-15 mm Hg 

(b) Blood transfusion to maintain hemoglobin> 10 mg/dL 

(4) Hemodynamic support 

(a) Vasopressors to maintain mean arterial pressure >65 mmHg 

i. Norepinephrine is preferred agent 0.01-1 mcg!kg/min. 

ii. Consider dobutamine 2-15 mcg/kg/min in cardiogenic shock. 

(b) Establish arterial line to monitor blood pressure. 

(c) Antiarrhythmic medications for recurrent or unstable arrhythmias 

i. Treat the underlying etiology of arrhythmia. 

ii. There are no data to recommend prophylactic use of antiarrhythmic medications. 

(d) Consider intra-aortic balloon pump for persistent hypotension. 

b. Identify and treat cause of arrest. 

(1) ECG: evaluate for STEM! 

Some authors advocate PCI for all patients with ROSC and suspected cardiac etiology of arrest. 

(2) Bedside ultrasound: evaluate for pericardia! effusion, right ventricular strain, global or focal wall 

motion abnormalities, inferior vena cava diameter 

(3) Chest radiography 

(4) Laboratory assessment 

(a) Hematocrit/hemoglobin 

(b) Electrolytes 

(c) Lactate: monitor for persistent ischemia 

(d) Serial troponin: consider PCI if rising troponin 

(e) Blood gas analysis 

c. Minimize ischemic brain injury: targeted temperature management (therapeutic hypothermia) 

(1) Evidence 

(a) Two studies demonstrated improved outcomes in patients after ventricular fibrillation arrest who 

were cooled to 32°-34°C and maintained for 12-24 hours after ROSC. 

(b) Further studies demonstrated benefit in other arrest situations, providing ROSC was attained in 



(a) Advance directives, indicating do-not-resuscitate 

(b) Traumatic arrest 

(c) Pregnancy 

(d) Active bleeding 

(e) Sepsis 

(5) Cooling technique: goal is 33°-36°C (based on institutional preference; evidence is insufficient to 

suggest particular temperature goal) 

(a) External cooling: ice packs in axillae and groin 

(b) Cold IV fluids (lactated Ringer's) x 2 L 

(c) Cutaneous commercial cooling device 

(d) lntravascular cooling device 

(6) Monitoring 

(a) Core temperature monitor (eg, bladder or esophageal temperature probe) 

(b) Cardiac monitor: monitor for dysrhythmias 

(7) Medications 

(a) Sedation/seizure prevention: fentanyl or midazolam 

(b) Prevention of shivering: paralysis with vecuronium 

d. Manage cardiovascular dysfunction 

(1) Hemodynamic support (see above) 

(2) ASA per rectum if no contraindications for myocardial infarction 

e. Manage complications of global ischemia and reperfusion injury 

(1) EEG 

(2) Goal-directed resuscitation 

(3) Treat blood glucose> 150 mg/dL with regular insulin IV 

II. RESUSCITATION PROCEDURES 

A. Noninvasive positive-pressure ventilation 

1. Indicated for respiratory distress due to COPD and cardiogenic pulmonary edema. 

2. Both continuous positive-airway pressure (CPAP) and bi-level positive-airway pressure (BPAP) are effective in 

reducing rates of intubation/intubation complications. 

3. Contraindications: cardiopulmonary arrest, altered mental status, vomiting or excessive secretions, recent upper 

airway or upper GI surgery, inability to wear/tolerate mask 

4. Cautions: abdominal distention, oral secretions, autopositive end-expiratory pressure (PEEP) in COPD, reassess 

frequently, intubate if not improved 

5. Prehospital CPAP: decreases emergency department intubations and overall mortality 

6. CHF in emergency department 

a. No advantage of BPAP over CPAP 

b. Improves heart rate, blood pressure, 0 2 

saturation, Pa0 2 

, A-a gradient 

c. Reduces intubation rate, mortality 

7. COPD in emergency department 

a. Only advantageous in severe distress 

b. Decreases hypoxia, acidosis, hypercapnia within 1 hour 

c. Reduces length of stay, intubation rate, mortality 

8. Settings 

a. May use full mask or nasal pillows 

b. CPAP: 5 cm H 2 

0 1 titrate up by 1-2 cm H 2 

0 

c. BPAP inspiratory positive-airway pressure (IPAP) 8-10, expiratory positive-airway pressure (EPAP) 4-5 

(1) Most studies show effective range IPAP 14-20 1 

EPAP 5-8 

(2) Increase EPAP/IPAP by 1-2, maintain IPAP:EPAP ratio of about 2.5:1 

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(3) Consider increasing IPAP:EPAP ratio for hypercarbia 

(4) Avoid !PAP >20 cm H 2 

0 to prevent gastric insufflation 

d. Oxygen bleed-in/Fi0 2 

to maintain 0 2 

saturation 86%-92% 

B. Tracheal intubation 

1. Indications 

a. Inability to protect airway 

b. Hypoxia not corrected with oxygen or noninvasive positive-pressure ventilation 

c. Hypercarbia 

d. Hypoventi lation 

e. Respiratory failure or impending failure 

2. Routes 

a. Orotracheal 

(1) Standard direct laryngoscopy versus video-assisted 

(2) Tube size: 7.5-9.0 mm for men, 7.0-8.0 mm for women, (age/4) + 4 mm uncuffed for children, 

decrease size by 0.5 for cuffed tubes 

b. Nasotracheal 

(1) Infrequently used because more morbidity and technically more difficult than endotracheal intubation 

(2) Benefit for spontaneously breathing patients with angioedema of tongue, clenched teeth, oral trauma, 

inability to move neck 

(3) Contraindications: nasal/midface trauma, basilar skull fracture, caution with patients receiving tPA or 

anticoagu I ants 

(4) Special nasal intubation that allows flexion of the tip highly recommended. 

(5) Insert lubricated tube (no stylet) through largest nare that has been prepared with topical 

vasoconstrictor. 

(6) Orient bevel toward septum, pass tube toward occiput, gently rotate tube to facilitate passage, listen for 

breath through tube, advance tube during initiation of inspiration using breath sounds to guide tube. 

(7) Advance to 28 cm at nare for men, 26 cm for women. 

(8) May be used in conjunction with fiberoptic scope for patients at high risk of failed airway 

C. Rapid sequence intubation (RSI) 

1. Overview 

a. Simultaneous administration of induction agent and paralytic agent 

b. Method of choice in emergency department intubations: highest success rates, fewest complications 

c. Exceptions 

(1) Cardiac/respiratory arrest, patient with no gag reflex 

(2) Spontaneously breathing patient with high risk of inability to ventilate or intubate (see below) 

2. Airway evaluation 

a. Predict difficulty with bag-valve-mask ventilation and/or intubation (Table 53) 

b. Indicated except in cases of crash airway (respiratory arrest) 

c. Predictors of difficulty with ventilation: presence of c::2 factors predictive of inability to ventilate effectively 

(1) Obesity (also pregnancy): difficult to achieve adequate tidal volume 

(2) Beard: difficult seal 

(3) Elderly (>55 years old) 

(4) Snorers: airway obstruction 

(5) Edentulous: difficult seal 

890


Table 53: LEMON Rule for Prediction of Difficult Intubation 

Predictor of Difficult Intubation 

look externally 

_!;valuate 3-3-2 rule 

Mallampati Score 

Qbstruction/obesity 

l's.eek mobility 

Sunken cheeks, edentulous, protruding incisors, micrognathia, facial/ 

cervical trauma 

Mouth opening


Table 54: Sedative Agents 

Agent 

Dosage 

Onset 

(sec) 

Duration of 

Action (min) 

Benefits 

Cautions 

Etomidate 0.3 mg/kg IV 10-15 4-10 Little hemodynamic effect Causes myoclonus 

(total body Decreases ICP No analgesia 

weight) 

Decreased cortisol 

release* 

Propofol 1.5-3 mg/kg 15-45 5-10 Bronchodilation Can cause hypotension 

IV (total body Decreases ICP Avoid in patients with 

weight) 

Anticonvu lsant 

low ejection fraction 

Avoid with egg allergy 

No analgesia 

Ketamine 1-2 mg/kg IV 60-90 10-20 Increases blood pressure Use in increased ICP 

(ideal body Bronchodilation controversial** 

weight) 

Provides analgesia 

Can cause hypotension 

in low ejection fraction 

or catecholaminedepleted 

patients 

May experience 

emergence reaction 

Midazolam 0.2-0.3 mg/kg 60-90 15-30 Anticonvu lsant Hypotension 

IV (total body Potent amnestic Slow onset 

weight) 

Frequently underdosed 

* Etomidate is associated with transient suppression of adrenal function but no clear change in mortality; no study to date powered to detect 

effects on hospital or ICU length of stay, ventilator days, or mortality. 

** 

Historic teaching about ketamine has recommended this agent be avoided in patients with suspected increased ICP. However, recent data 

has shown that use of ketamine is safe in patients with increased ICP. 

(3) Neuromuscular blocking agents decrease complications and improve intubating conditions 

(a) Muscle paralysis through noncompetitive (Table 55) or competitive (Table 55) binding to 

acetylcholine receptors 

892


Table 55: Neuromuscular Blocking Agents 

Agent 

Dosage 

Noncompetitive depolarizing agent 

Succinylcholine 

1.5 mg/kg IV 

(total body 

weight) 

Competitive nondepolarizing agents 

Rocuronium 

Vecuronium 

0.6-1 .2 mg/kg 

IV (ideal body 

weight) 

0.1 mg/kg IV 

(ideal body 

weight) 

Onset 

(sec) 

45-60 sec 

1-4 min 

2-4 min 

Duration of 

Action (min) 

5-9 

30-45 

45-60 

Benefits 

Drug of choice for 

RSI due to onset and 

duration of action 

First choice alternative to 

succinylcholine 

Least ideal agent for RSI 

Cautions 

Hyperkalemia* 

Fasciculations 

Masseter spasm 

Malignant hyperthermia 

Bradycardia 

Increased intraocular 

pressure** 

Paralysis time longer 

than induction agent 

Slow onset 

Prolonged paralysis 

(duration may 

be prolonged in 

hepatorenal failure) 

* Patients at risk include those with known hyperkalemia, burns >5 days old, denervation/severe crush injury >5 days old, severe infection 

>5 days old, preexisting myopathy, or neuromuscular disease. 

** May increase intraocular pressure and ICP, although this is refuted by recent studies. 

f. Placement with confirmation 

(1) Placement: goal is to identify vocal cords and pass tube 

(a) 

Direct laryngoscopy 

i. Place blade in right side of mouth, sweep tongue to the left. 

ii. Identify epiglottis. 

iii. Straight (Miller) blade: lift epiglottis. 

iv. Curved (Macintosh) blade: insert into vallecula and lift up and away. 

v. Lift up on jaw to expose vocal cords; do not rock laryngoscope back on patient's teeth. 

(b) Video-guided laryngoscopy 

i. Insert blade in midline of tongue, advance along midline until vocal cords are visualized. 

ii. Special stylet may be required. 

iii. Limited by secretions or blood in airway 

iv. Improves visualization of cords with minimal neck movement 

(c) Visualization improved with tracheal manipulation as needed by intubator with position, then 

maintained by assistant. 

(d) Routine cricoid pressure is no longer recommended. 

(e) If unable to visualize larynx, withdraw and try secondary method. 

(f) 

Insert endotracheal tube on right side of mouth, rotate through cords. 

(g) Difficulties with passing tube usually due to too large tube size, cricoid pressure, improper stylet 

bend (35° optimal) 

(h) Advance tube 3-4 cm after cuff is beyond vocal cords. 

(i) 

(2) Confirmation 

Withdraw blade, inflate cuff


(d) Colorimetric end-tidal CO 2 

i. Give six breaths to ensure not false positive 

ii. May produce false negative in low-flow states 

(e) Air aspiration 

(f) 

g. Postintubation care 

i. 30-ml syringe attached to endotracheal tube, withdraw. 

ii. If in trachea, air is easily withdrawn. 

Chest radiograph to confirm absence of right main-stem bronchus intubation but not a reliable 

means to confirm endotracheal placement 

(1) Secure tube in place without decreasing venous return. 

(2) Place orogastric or nasogastric tube. 

(3) Maintain adequate sedation/analgesia to prevent agitation/extubation. 

(4) Usual initial ventilator settings 

(a) Mode: assist control (NC) 

(b) Fi 0 2 

: 100%, decrease to maintain PO 2 

60-90 mm Hg 

(c) Tidal volume 6-8 ml/kg (use ideal body weight in obese patients) 

(d) Respiratory rate: 10-14 breaths per minute, increase in acidosis 

(e) 

(f) 

4. Troubleshooting 

lnspiration:expiration ratio 1 :2; increase expiratory duration for obstructive lung disease 

PEEP: start 5 cm H 2 

0, gradually increase in hypoxia 

a. Disconnect from ventilator and use bag-valve-mask. 

b. Evaluate for malfunctions ("DOPE" mnemonic). 

(1) Q.isplacement: evaluate for tube displacement 

(2) Qbstruction: suction tube and deep airways 

(3) fneumothorax/autoPEEP: evaluate for pneumothorax or stacked breaths 

(4) J;quipment: reevaluate ventilator settings 

5. Difficult airway tools 

a. Gum elastic bougie 

(1) Flexible, plastic rod with angled tip 

(2) Used with direct laryngoscopy when only arytenoid cartilage visible 

(a) 

Insert bougie into trachea using direct laryngoscopy. 

(b) Confirm placement by advancing bougie to carina and feeling firm tracheal rings when advancing, 

retracting bougie. 

(c) Thread endotracheal tube over bougie. 

b. Video-assisted intubation (see above) 

c. Fiberoptic 

(1) Requires training/practice, set up time, and compliant, spontaneously breathing patient 

(2) Nasal preferred to oral route: topical anesthetic and vasoconstrictor keys to success 

(3) Requires :::7.5 mm endotracheal tube 

(4) Thread tube over fiberoptic scope (adapter removed) 

(5) Pass fiberoptic scope through cords and advance tube 

D. Surgical airway management 

1. Surgical cricothyrotomy 

a. Indication: failed airway (ie, can't intubate, can't ventilate) 

b. Contraindications 

(1) Age :S:8 years: cricothyroid membrane too smal I and risk of injuring surrounding structures 

(2) Partial or complete tracheal transection 

(3) Obstruction deep to the cricothyroid membrane 

c. Minimum equipment required 

(1) Scalpel (#10 or 11 blade) 

(2) 6.0 or smaller endotracheal or tracheostomy tube 

894

OTHER COMPONENTS 

5. Watch endorsements, and make sure your identity is clear to avoid violation of the Federal Trade Commission's 

Guides Concerning the Use ofTestimonials and Endorsements. 

6. Make sure you are familiar with your employer's and hospital system's social media and electronic 

communication policies. 

V. LEADERSHIP AND MANAGEMENT PRINCIPLES 

A. Many guides on how to be a good leader involve switching focus from "I" to "we" or "team:' 

B. Leadership roles 

1. Traditional leadership roles focused on a top-down approach. 

2. Modern leadership roles focus on a collaborative approach with a partnership model. A leader seeks to 

empower and motivate others rather than demand performance. 

VI. WELL-BEING 

A. Rights of emergency physicians: ACEP Policy 

1. Autonomy in clinical decision making shall be respected. 

2. Physicians have the right to expect adequate staffing and equipment. 

3. Physicians will be compensated for services and not be required to pay for privileges or referrals, nor shall they 

receive anything of value for referrals to others. 

4. Autonomy should not be restricted by cost-saving protocols. 

B. Fatigue and impairment 

1. Fatigue can be an impairment (see also ethical principles, page 967). Every physician should be mindful of his 

or her limits. 

2. Residents have work hour restrictions that teaching attending should be aware of. 

3. Schedules for emergency physicians should be created keeping in mind patient volume and the need for sleep 

between busy shifts. Strategies may vary by group (eg, 10 hours minimum between busy shifts, 24 hours off 

between 24-hour shifts, etc). 

C. Time management, life balance, and organizational skills 

1. Physicians are often busy and overstretched. Learning how to prioritize and organize can help with job and 

personal life satisfaction. Each person needs to decide which clinical, professional, and social activities are 

worth pursuing. 

2. Learning how to say "no" without feeling guilty may have to be learned and practiced. Seminars, lectures, and 

books are available and can help. A mentor or life coach might also be beneficial. 

D. Work dysphoria (burnout) 

1. In the United States, 30%-40% of physicians experience some degree of burnout. 

2. Work-related stress causes burnout. 

3. Increasing paperwork burden, decreasing autonomy, decreasing reimbursement, lack of tort reform, problems 

with work/life balance, and physician shortages may all contribute to burnout. 

4. Medical schools, medical societies, hospitals, and residency programs should have policies to promote 

physician well-being and patient safety. 

969

OTHER COMPONENTS: PRACTICE CLINICAL SCENARIOS 

OTHER COMPONENTS OF THE PRACTICE OF EMERGENCY 

MEDICINE: PRACTICE CLINICAL SCENARIOS 


Scenario A 

Presentation: A patient presents to your hospital in labor, but her insurance does not cover admissions. 

What law requires that your hospital handle the delivery of the fetus and placenta before she and the baby 

can be transferred? 

Scenario B 

Presentation: A patient is brought in by police for calling 911 to express suicidal ideation. The patient has 

ongoing suicidal thoughts and auditory hallucinations. The patient states he is going to kill his brother and 

gives his name. The patient requests discharge. 

What is the management? 

Scenario C 

Presentation: An elderly patient presents from home via ambulance with a chief complaint of fever. 

Examination reveals infected bedsores, soiled clothes, and unkempt appearance. The patient tells you she 

lives with her son, who feeds her once a day and uses her social security check to buy his cigarettes. She is 

bedbound from a previous stroke. 


ScenarioD 

Presentation: A patient is brought in by EMS for a fall. She had fallen the day before and neighbor found 

her on the floor when he came to check on her. She lives alone with her cat. EMS noted little human 

food in the house, cat food tins piled up around the living room and multiple medications from different 

providers with duplications. Patient appears frail and unkempt. Her nails are long and dirty and her clothes 

are unwashed. The patient is delirious and has multiple bruises in various states of healing 


Scenario E 

Presentation: Dr. Smith notices that her coworker, Dr. Jones, seems anxious and annoyed over the busy 

pace in the emergency department. He is easily frustrated and expresses anger at nurses. A nurse comes 

to Dr. Smith and expresses concern that Dr. Jones did not examine a patient with hypotension and put the 

chart up for discharge. Dr. Smith asks Dr. Jones about it, and he states he knows what he is doing and to 

leave him alone. Dr. Smith notices that Dr. Jones is sweating and seems shaky. 


970


Scenario F 

Presentation: A 16-year-old arrives by herself for evaluation. She refuses to have her parents called for 

consent to treat. When she is interviewed by the emergency physician, she indicates that she is concerned 

she is pregnant. A medical screening examination is performed, and a urine pregnancy test is positive. 

Ultrasound shows a 6-week intrauterine pregnancy. She has no signs of illness and denies pain or 

bleeding. She is given a prescription for prenatal vitamins, and a follow-up appointment is scheduled with 

the hospital obstetrics clinic. She is urged to tell her family about the pregnancy, because she will need 

support. She is discharged without her parents having been contacted. 

What type of situation is being described? 

Scenario G 

Presentation: A 70-year-old male retired factory worker presents with hypotension and a lower GI bleed. 

He refuses a blood transfusion on religious grounds. He is urged to change his mind given his hypotension 

despite treatment with IV fluids. Laboratory tests show severe anemia. A surgeon has been called in to try 

to stop the bleeding but has not arrived yet. The patient states he understands that he might die without a 

blood transfusion, but he still refuses to undergo the procedure. 

What type of situation is being described? 

Scenario H 

Presentation: A celebrity presents to the emergency department with a gunshot wound to the leg. He asks 

that this not be reported, because he does not want the publicity and it was an accident. He would like to 

be treated and discharged without having to talk to the police. 

What is the management? 

971



Scenario A 

EMTALA 

Key facts: Under EMT ALA, the patient and her infant can be transferred once medically stable. If the infant 

is unstable, all attempts to stabilize him or her must be made. If there is no inpatient neonatal unit, the 

infant can be transported even if he or she remains unstable if: 

• You as the treating physician certify that the medical benefits outweigh the risks. 

• You send copies of the medical records. 

• The receiving hospital has the space and personnel to treat. 

• The receiving hospital has agreed to accept the transfer, and 

• The transfer will be performed by qualified personnel with appropriate equipment. 

Scenario B 

Diagnosis: mental health 

Management: The physician has the duty to treat the patient and to warn the patient's brother. The 

physician cannot discharge the patient despite the patient's request because of the potential harm to 

the patient and the brother. The patient can be committed against his will for a fixed period of time. The 

physician should attempt to contact the brother and the police about the patient's homicidal thoughts. 

Scenario C 

Diagnosis: elder maltreatment 

Management: You check your state laws and you have mandatory reporting of elder abuse. You contact the 

appropriate agency that will investigate. You admit the patient for treatment of her infected bedsores and 

initiate a social work consult. 

Scenario D 

Diagnosis: elder self-neglect 

Laboratory evaluation: Laboratory tests show dehydration, infection, and low albumin. 

Management: The patient should be admitted for treatment and social work evaluation. 

Scenario E 

Diagnosis: physician impairment 

Management: Dr. Smith, concerned that Dr. Jones is impaired, needs to take immediate action to prevent 

harm to patients. Fatigue, drug and alcohol abuse or withdrawal, or mental illness may cause a physician 

to become impaired. Hospital and state policies guide the removal of a physician from duty, but no delay 

should occur when a patient is at risk. 

972


Scenario F 

Diagnosis: minor seeking treatment without consent of parent or guardian 

Management: Minors are allowed to be treated without parental consent for mental illness, pregnancy, 

drug abuse, and in some cases pregnancy prevention. If the pregnancy is the result of sexual abuse or 

statutory rape, then the physician is obligated to report to children's services and should detain the patient 

for the investigation. 

ScenarioG 

Diagnosis: refusal of care 

Management: Adult patients who are conscious have the right to refuse all medical care, including that 

for life-threatening conditions. The treating physician should assess the patient's decision-making capacity 

and should have the treatment discussion witnessed by another health care provider and if possible the 

patient's family. 

Scenario H 

Diagnosis: mandatory reporting 

Management: In all states, gunshot wounds or suspected gunshot wounds must be reported, even if 

accidental. The reporting should be done per the local law and hospital policy without any unnecessary 

release of protected health information. Physicians should defer all questions from the media, should they 

occur, to the hospital public relations personnel. 

973

974 

NOTES

MECHANICS OF THE WRITTEN BOARD EXAM 


The written board exam in emergency medicine tests your knowledge base relative to predetermined criteria of clinical 

competency. Consequently, there are two critical aspects of this test: 

1. What is the written exam actually testing? 

2. How are you being evaluated? 

In addition, multiple-choice exams usually assess the goals of learning, which include: 

• Knowledge of terminology or specific facts 

• Knowledge and application of methods and procedures 

• Ability to apply facts and principles in a given situation 

• Ability to interpret cause and effect relationships 

The written board exam tests both the outcomes of learning as well as the goals of learning. This text was designed and 

written with this in mind, which is why it is a teaching text (not just a reference text). In addition to providing facts, 

special attention has been given to the reader's need to understand concepts and to think critically, thus improving the 

ability to analyze, apply, synthesize, and interpret information. This is essential to effective learning, which is what this 

exam is really testing. 

The second critical aspect of the written board exam is understanding how you are being evaluated. Some written exams 

discriminate among individuals, ranking them on relative levels of learning. These exams are "norm referenced" and 

are designed to discriminate in a way so that a certain percentage of candidates will not pass. The written board exam 

in emergency medicine does not discriminate; it is "criterion referenced," which means that there is no ranking, ie, 

100% of candidates can pass. It describes what an individual can or cannot perform, with the difficulty of the test item 

matching the difficulty of the task. 

Examination Format 

The Written Board Exam in emergency medicine may be administered by the American Board of Emergency Medicine 

(ABEM), the American Osteopathic Board of Emergency Medicine (AOBEM), or the American Board of Physician 

Specialties (ASPS). For the most recent information on the examination format for ABEM, visit www.abem.org. For the 

most recent information on the examination format for AOBEM, visit www.aobem.org. For the most recent information 

on the examination format for ASPS, visit www.abpsus.org. At each of these individual websites, candidates may be able 

to access exam specifics, including logistical and procedural information as well as mechanics of each individual exam. 

Helpful resources such as sample questions, content specifications, candidate booklets, and scoring information may 

also be posted on these websites. 

ABEM Written Examination 

The American Board of Emergency Medicine (ABEM) is recognized by the American Board of Medical Specialties. 

ABEM certifies emergency physicians who meet its educational, professional standing, and examination standards. The 

Model of the Clinical Practice of Emergency Medicine (EM Model) forms the basis of each of ABEM's multiple-choice 

examination questions and describes the relative weight on the ABEM exam. The content of the ABEM's written board 

exams is based on a national (not regional) standard of care. Regardless of where you practice or the patient volume you 

encounter, you will be tested on a "national norm," which we have adhered to in this text. The initial ABEM written exam 

is called the Qualifying Exam. ABEM-certified physicians must then pass the written ConCertTM Examination during years 

6-10 of their certification. A score of 75% or greater is required to pass the ABEM examination. Additional information 

can be found at www.abem.org. 

AOBEM Written Examination 

The American Osteopathic Board of Emergency Medicine (AOBEM) is the certifying body of the American Osteopathic 

Association. The AOBEM Table of Specificity forms the basis of each of AOBEM's multiple-choice examination questions 

and ranks the Core Content Categories into high, medium, and low relative weights. The initial written AOBEM exam 

is called the Certification Examination. The Formal Recertification Examination includes a computer-based exam. It 

is offered once a year, and AOBEM has established a predetermined pass rate. The scores are not curved in any way. 

Additional information can be found at www.aobem.org. 

ABPS Written Examination 

The American Board of Physician Specialties (ASPS), the official certifying body of the American Association of Physician 

Specialists, Inc. (AAPS), administers a written certification examination for the Board of Certification in Emergency 

Medicine (BCEM). The Domain Table forms the basis of each of ASPS' multiple-choice examination questions and lists 

the number of questions in each of the domain categories. The exam is offered twice a year. Currently the minimum 

score for passing, depending on the form of the examination, ranges from approximately 75% to 82%. Additional 

information can be found at www.abpsus.org. 

975


How To Take a Multiple-Choice Exam 

Your skill in taking a multiple-choice exam is as important as adequate preparation. A common misconception is that 

all candidates who fail this type of exam do so because they have failed to master the subject matter. In truth, some 

test-takers have not learned how to apply their knowledge to a multiple-choice exam. Did you know that changing the 

sentence structure, either in the question or the answers, can dramatically affect performance (whether one gets that 

question right or wrong) on that question? A good test taker will get it right with either structure, while the less well able 

(trained) test taker will not. For those of you who have previously encountered some difficulty with this type of exam, 

included are some general recommendations as well as specific test-taking strategies. 

Remember 

1. The exam is testing basic knowledge, not sophisticated, new age issues, not nuances, not areas of controversy (eg, 

if two sources disagree, this will not be on the exam). It is based on national standards, not what is going on in your 

hospital. Know the basics. Know the standard of care. 

2. Field questions are part of the exam. Field questions do not count either for you or against you. So if you do not 

know the answer to any particular question, tell yourself, convince yourself, "this was a field question and will not 

count anyway." 

3. This is an exam for emergency physicians. It is an action-oriented exam; you are expected to do something. 

4. Absolute contraindications are more important to know than relative contraindications. 

5. This is a time-sensitive exam. You have approximately 1 minute per question. 

6. Read the question and all the answers carefully. If part of the answer is wrong, and part of the answer is right, 

it is the wrong answer. 

7. Associations are important on board exams. Learn them! You cannot ask for any additional information when 

taking the exam-no new laboratory studies, no new imaging studies, etc. The exam question writer must give you 

information that can help you associate what is in the question to the right answer. Here are some examples of 

associations: 

a. The most common cause of osteomyelitis caused by a rusty nail through a running shoe is Pseudomonas 

aeruginosa. However, the most common cause of soft-tissue infection caused by that same rusty nail through a 

running shoe is Staphylococcus or Streptococcus. 

b. In a patient with a recent past history of Guillain-Barre syndrome who now has diarrhea, the cause of the 

diarrhea is most likely Campylobacter. 

c. Humeral shaft fracture is associated with wrist drop due to radial nerve injury. 

d. Ring-enhancing lesions on CT brain are associated with toxoplasmosis, neurocysticercosis, or brain abscess. 

These are just a few examples of many. But be assured that ABEM loves associations. 

8. Acuity frames in terms of percentage on the ABEM exam 

a. Critical 30% 

b. Emergent 40% 

c. Lower acuity 21 % 

d. None 9% 

9. Modifying factors for age on the ABEM exam 

a. Pediatrics 8% 

b. Geriatrics 6% 

10. Spend your time on what is important. 

a. Most common 

b. Triads, pentads 

c. Diagnosis 

d. Deadly causes 

e. Indications, contraindications 

f. Complications 

g. Associations 

h. Worst-case scenario for a given presentation 

i. Things we do that may kill 

j. Things that if we do not do, may kill 

k. Things we get sued for 

I. ACLS, ATLS, PALS 

976


11. Red flags: abnormal vital signs, missing vital signs 

12. Missing information is common on the exam. If you were given al I the information in a particular question, 

the answer would jump out at you and the question would be too easy. 

13. Be careful of similarities, which can fool you. 

a. Erythema migrans (Lyme disease) vs erythema marginatum (Jones' criteria/rheumatic fever) 

b. Erlichiosis (tickborne bacterial infection) vs erysipelas (Streptococcus/St Anthony's fire) 

c. Condylomata acuminate (human papillomavirus) vs condylomata lata (syphilis) 

d. Using nimodipine for spontaneous subarachnoid hemorrhage, not nifedipine 

14. Keycepts to types of questions 

a. Knowledge questions 

(1) If in your knowledge base, do notfal I for the sucker punch, which is the answer most people will 

be drawn to at first glance and it usually placed before the right answer. 

(2) If not in your knowledge base, guess smart. 

b. Concept questions: time awareness (one minute per question overall exam) 

c. Math questions: math will be simple (this is not a mathematics exam). 

d. Dosages of medications: know the ones used every day in the emergency department. You will be given 

the dosage of medications used less frequently. 

General Recommendations 

1. Learn how to relax during the written exam. If you feel tense before the exam actually begins, take a few seconds to 

induce a sense of positive self-expectancy. Say to yourself, "I will do well because I expect to do well." Believe it or 

not, psychological studies have shown that if you expect to do well, the odds are better that you will. 

After you have induced a sense of positive self-expectancy, close your eyes, take a deep breath, and command 

yourself to relax. As you begin taking the exam, some of the tension will dissipate spontaneously simply because the 

conscious mind cannot do two things at once; you cannot think about being tense while thinking about the answer 

to a question. To stay relaxed during the exam, work rapidly but carefully. If you are not sure of an answer, skip 

that one and come back to it later. This is very important psychologically. Answer all the questions you know first 

and then go back later to work on those you don't know. You can tag questions you want to go back to later on the 

computer during the test. 

2. Avoid fatigue. Have a good night's sleep before your exam day. Because the exam is a long one, give yourself a rest 

period every hour or so during the exam, even if it is a very short one. Relax in your seat, and close your eyes for a 

minute or two. These rest periods will help maintain your mental capacity/efficiency at a high level. 

Specific Test-Taking Strategies 

Guessing is part of any multiple-choice exam. Although guessing will probably not significantly improve your score, it 

will not lower it either. Guessing smart is the key to guessing. Here are some guidelines that can help you select the best 

answer when the answer is not coming to you. 

The first thing you have to determine is whether you understand the question but don't know the answer or you not sure 

what the question is asking. 

Let's begin with questions you understand but are unsure of the correct (best) answer: 

1. Eliminate obviously incorrect answers. Then concentrate on the remaining answers. 

a. An answer that "doesn't fit" with the other answers is probably wrong. 

b. A wordy answer that is unclear or does not read well is probably wrong. 

c. An answer with the words "always" or "never" is probably wrong (but these are rarely found in tests today 

because they were recognized as "give aways"). 

d. An answer that does not correlate grammatically with the question is probably wrong. 

2. If you have eliminated obvious and probable incorrect answers and you still have more than one answer remaining, 

try looking at the question and completing it mentally before looking at the answers. 

a. A spontaneous completion that corresponds to one of the answers is usually correct. 

b. A spontaneous completion that is similar to two answers suggests that one of them is correct. Determine which 

one best completes the statement. 

c. A spontaneous completion that is opposite to one of the remaining answers eliminates that choice. 

3. Look at adjectives and adverbs in the question. Descriptive (key) words are frequently clues to the correct answer. 

Words like "acute" or "classic" or "routinely" are examples. This is a particularly valuable strategy if you are dealing 

with a question that seems to have two possible answers (the key word will fit one answer better than the other). 

977


Another example is "definitive" treatment versus "initial" (the ABCs) treatment, and classic (original description) vs 

most common. Exact terms in the answer, such as all, always, never, none, must necessarily, are usually part of a 

wrong answer. 

4. If you encounter a question containing a clinical presentation and you are asked to make a diagnosis based on an 

image (ECG, radiograph, ultrasound, photo of a skin lesion, etc), answer the question before looking at the picture. 

Then, look at the picture to confirm your answer was right. If the picture is required to answer the question and 

you are not sure what the image shows, try to answer the question again, now considering the picture. The correct 

answer should "match" the clinical presentation. 

5. If a question covers a subject you know little or nothing about, see if there are other questions within the 

examination that include the same material. You can sometimes find useful information contained in other questions 

that can help you answer this question. 

Points to Consider About Answers 

1. If there are numbers contained in the answers and two answers have similar numbers, one of them is usually the 

correct one. 

2. If one of the answers is "all of the above," look for two correct answers. If you find them, "all of the above" is the 

correct answer. 

3. If one of the answers is "none of the above," look for one correct answer. This excludes "none of the above." 

All of these techniques can be used to answer questions you understand. 

Now let's deal with questions you don't understand. 

Some questions are designed to test your ability to think critically or analytically. The answers to these questions are not 

obvious-they are inferred. Here's an example: 

"What is the best pharmacologic choice for the patient with supraventricular tachycardia and hypertension?" 

(a) Adenosine 

(b) Digoxin 

(c) Methoxamine 

(d) Edrophonium 

If you look in standard emergency medicine textbooks, you will not find a drug listed for the treatment of 

supraventricular tachycardia with hypertension. You will find, however, several drugs listed that should not be given 

to patients with hypertension: all the vasopressors (methoxamine, norepinephrine, metaraminol, phenylephrine, etc), 

digitalis preparations, and edrophonium chloride. Therefore, the question does not ask you to directly identify the 

treatment of choice. Instead, the question asks you to infer the treatment of choice by eliminating the agents you should 

not use; the agent remaining will be the correct answer (adenosine). 

Here is another example of an "inferred" answer: 

"What drug should be used in the patient with CHF who also has signs of digitalis toxicity?" 

(a) Furosemide (Remember, the question is about digitalis toxicity, not CHF.) 

(b) Quinidine 

(c) Nitroprusside 

(d) Propranolol 

Again, there is no "drug of choice" for patients with CHF who are digitalis toxic. There are, however, drugs that should 

not be used in the presence of digitalis toxicity. Quinidine and calcium channel blockers (nifedipine, verapamil, and 

diltiazem) decrease digitalis clearance, so they should not be used. Furosemide tends to induce hypokalemia, which 

increases the risk of digitalis toxicity, so this is not a good choice. ~-blockers (propranolol, nadolol, metaprolol, atenolol, 

timolol) are contraindicated in patients with severe CHF and should not be used. On the other hand, vasodilators 

(nitroglycerin, nitroprusside, prazosin, and hydralazine) lower systemic vascular resistance and improve cardiac output. 

The correct answer, therefore, is nitroprusside. 

Practice, Practice, Practice Makes Perfect 

In developing any skill, practice is important. Practice answering multiple-choice questions on a regular basis. It is not 

only a good way to assess your knowledge base, but it is also a training mechanism for developing test-taking skills. As 

you go through the current PEER products, apply the techniques you have learned here when confronted with problem 

questions. With practice, this skill will improve, and you will feel more confident about your ability to use it effectively. 

On any given exam, test-taking strategies can be successfully applied to 5%-15% of the questions. Some candidates fail 

this exam by only one or two points, so using these techniques might be just enough to help you pass. 

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ADDITIONAL TIPS FOR GOOD PERFORMANCE 


Preparing for the written board exam is an arduous task, one that requires intense review and study. In some respects, 

the final phase of preparation is more difficult than the earlier ones. For one thing, you are tired. In addition to studying, 

most of you are working full time. Another problem is that your anxiety level is likely to peak as the exam date draws 

near. Finally, your self-study plan/preparation may leave you with a feeling of being overwhelmed by the amount of 

academic information you have been learning and relearning. 

In this section are some guidelines to follow in the time remaining before the exam. It is recommended that you map out 

a program that will reduce your fatigue, lessen your anxiety, and allow you to focus your attention on the most important 

academic information you need to know. 

Self-Care 

Good health habits are important. If you have unhealthy habits, it will become increasingly harder to study and you 

will retain less. 

1. Get plenty of sleep. 

2. Eat more fiber-containing foods and less sugar and fat. You are more likely to be alert when you study as well as 

have greater endurance. 

3. Engage in some form of mild exercise. Walking is excellent if you are not a runner; aerobics and swimming 

are also helpful. 

Positive Self-Expectancy 

A positive attitude is also important. Your attitude, both before and during the exam, can affect your exam score. A 

negative attitude will foster procrastination before the exam and will interfere with your performance during the exam. 

On the other hand, a positive attitude will facilitate your preparatory efforts and enhance your performance during the 

exam. 

A technique that can help you build and maintain a positive attitude for the written board exam is called "mental 

rehearsal," and it can be very effective in reaching a goal and achieving success. 

Mental rehearsal consists of previewing an upcoming event in a positive frame of mind. This should be done during the 

weeks before the exam. The purpose is twofold: to allow you to prepare for the exam as completely and thoroughly as 

you can in the allotted time, and to maximize the probability of a good performance on the exam day. 

The art of positive self-expectancy is one that is practiced by many professionals before a major event. Essentially it 

consists of mentally rehearsing a perfect performance during the days, and even weeks, before the actual event. To use 

this technique, set aside time each day when you are completely alone and relaxed and imagine yourself taking the 

exam in a calm, confident manner with the expectation of doing well. 

When you use the mental rehearsal technique, concentrate on what you know rather than on what you don't know. 

Do not worry about subjects or areas that you didn't have time to study. Rather, focus on what you have studied and 

then make some affirmations about your ability to do well on exam day: "I will do well on the exam. I have studied 

and worked hard to get where I am today and now, I'm going to go further still. I can do it." Positive affirmations have a 

powerful effect on the subconscious mind because they foster our belief in ourselves, which translates into confidence in 

our ability. 

Don't put yourself into a position to be discouraged when you start rehearsing. Just do your best. Within a short time, the 

result of this technique will speak for itself, providing you with all the justification you need. 

Written Board Courses 

Many state ACEP chapters (and other organizations) conduct courses for emergency physicians taking the written board 

exam. These are intensive programs (4-7 days) that provide a comprehensive review of emergency medicine. They 

are usually given about a month before the exam. The utility of these courses varies from one course to another and 

from one physician to another. Not everyone needs or benefits from a written board review course. Many emergency 

physicians have passed the exam without it. 

Ohio ACEP offers a 5-day comprehensive academic review of emergency medicine, as well as a 3-day course that 

focuses on key facts and pearls of each emergency medicine topic. 

The ACEP master calendar (www.acep.org) can provide information on a course that suits your schedule and location 

needs. Also, EMRA puts out a periodic review of board review courses; refer to them as a reliable, independent resource 

to select a course. 

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How to Use an Emergency Medicine Written Board Course 

If you attend a written board course without any prior preparation, the program can be overwhelming. A lot of material is 

delivered very fast. If you have been reading this text before the course, your task will be a lot easier. 

Read as much of this text as possible before the course. Remember to highlight key concepts and important facts. Take 

this book with you to the course; this is your base on which to build. Use the book as your guide during the course. 

If you are attending an ACEP course, take the daily pretests and grade yourself; participate in evening review sessions, 

which cover hundreds of board-type questions. If you missed any questions, determine whether you didn't know the 

material or you did know the material but misread (misinterpreted) the question. Pay attention to pretest scores that are 

lower than 75% or several questions you did not know on certain topics. These are weak areas. 

For those of you who have been studying for more than 3 months, listen to your speakers very selectively. Listen for 

information that is new to you. If you have been studying with some regularity the last few months or so, your database 

is fairly strong. The course will not only be a review for you but will also fill gaps in your knowledge base. Use this text 

to write in new information that seems important. 

For those of you who have been studying less than 3 months, a different approach may be helpful. If at all possible, 

review the syllabus material before each lecture. While you are listening to the lecture, take notes and mark your 

syllabus (underline) important information. Later, insert the syllabus material in this text. 

For all of you: From the time you finish the course until a couple of days before the exam, review only the highlights of 

the study materials you have been using; it should all be in this text now. 

1. Review any material that is likely to be on the exam, ie, any information that your speakers pointed out as "must 

know for the exam. 11 You don't want to miss questions that you expect to see on the exam. 

2. Review any information you learned in this text or during the course that clarifies your understanding of a particular 

subject. This is important because if you encounter questions on this topic and you are not sure of the answer, you 

will be able to figure it out. 

3. Review any area where you are weak. Do not pick more than three because you do not want to 11 cram 11 at this stage 

of your preparation. Select the most important topics (those that are most heavily covered on the exam), and let the 

rest go. 

Practice the Exam Process 

Set aside some time shortly before the exam to run through multiple-choice questions and answers (as many as you can). 

If you haven't taken this type of exam for a while, you need to retrain your mind in this type of test-taking. 

In addition to answering the multiple-choice questions throughout this text, go through a self-assessment or mock exam 

product. Most written board courses have pretests (and post-tests) that amount to a couple of hundred or more multiplechoice 

questions. 

Go through the questions as if you were actually taking the exam. Answer all the questions you know first. Go back later 

to work on the questions you didn't know or were unsure of. There is a reason for this based on test-taking psychology: 

answering questions you are sure of first increases your confidence in answering questions you are unsure of later. If you 

are still unsure of some questions when you return to them, try using the techniques described in the section "How to 

Take a Multiple-Choice Exam. 11 

At the Exam 

1. Set your watch. 

2. Concentrate. 

3. Read the question and all answers carefully. 

4. Recognize key terms. 

5. Psych yourself up for a good game. 

A Few Points about Studying 

First remember this reality: You must read things five times to store them in your long-term memory. 

1. When do you study best? Early morning, late evening, other? Use that time to study. 

2. How do you learn best? Reading, listening, watching, computer-generated learning? Use that technique the most. 

3. No matter how or when you learn best, practice multiple choice questions over and over and over again. 

4. Identify areas of weakness and focus on these areas. Focus first on the topics with the most questions on the exam 

(eg, trauma, cardiovascular, etc). 

5. When you are freshest, do the things you find difficult. 

6. When you are less fresh, do pictures, ECGs, radiographs, ultrasound, CT scans, MRls, VQ scan, etc. 

980


7. When you are least fresh, do some multiple choice questions. 

8. Improve retention by doing the following: 

a. Study in cycles 

(1) Study for 30 minutes; concentrate hard. 

(2) Take a 5-minute break. 

(3) Go back and do another 30 minutes study time. 

(4) Take a 5-minute break. 

(5) Go back and do another 30 minutes study time. 

(6) This is the end of the cycle. 

b. You can do 3 of these cycles per day (no more). 

9. Foil analysis: When you answer questions, analyze the foils, looking at which ones were wrong and why were they 

wrong. And if you answered the question wrong, ask yourself, "why did I miss that question?" 

10. Use review cards for everything except for those topics in which you are strong. 

11. Do: 

a. Get plenty of rest 

b. Exercise 

c. Meditate 

12. Do not: 

a. Use sleeping aids before the exam. 

b. Use alcohol. 

c. Drink too much coffee. 

Do not study intently the last day or two before the exam. Your ability to answer questions correctly will be greater 

because your analytical ability will be high and not overridden by specific recall from the last day's cramming. 

981

CarolRivers-combined

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