Streptococcus bovis - Gundersen Lutheran Health System

Th e 

Gundersen 

Lu T h e r a n 

M e d i C A L J o u r n A L 

Volume 6, number 1 

June 2009 

oriGinAL reSeArCh ArtiCLeS 

Placebo Effects on Exercise Performance 

Outcomes from a Screening Procedure for Oropharyngeal Dysphagia 

Following Acute Stroke 

CASe reportS 

Colonoscopic Diagnosis of Appendicitis in a Patient with Ulcerative 

Colitis: A Case Report and Review of the Literature 

Intracranial Mycotic Aneurysm Due to Streptococcus bovis 

Endocarditis 

Giant-Cell Reaction to a Bioabsorbable Implant 

Post–Cesarean Delivery Septic Ovarian Vein Thrombosis 

hiStory of MediCine 

Historical Notes on Amputation and Phantom Limb Pain: 

“All Quiet on the Western Front?” 

The History of Cardiac Rehabilitation at the University of 

Wisconsin–La Crosse

1 

3 

8 

14 

18 

21 

24 

26 

30 

Th e 

Gu n d e r s e n 

Lu T h e r a n 

M e d i C A L J o u r n A L 

Contents 

Editor’s Message 

David E. Hartman, PhD, BC-ANCDS(A) 

oriGinAL reSeArCh ArtiCLeS 


Glenn Wright, PhD; John P. Porcari, PhD, RCEP; Carl C. Foster, PhD; Heidi Felker, MS; Ashley Kosholek, MS; 

Jennifer Otto, MS; Erik M. Sorenson, MS; Brian E. Udermann, PhD, ATC, FACSM 

Outcomes from a Screening Procedure for Oropharyngeal Dysphagia Following Acute Stroke 

David E. Hartman, PhD, BC-ANCDS(A); Melissa Hunter; Richard D. Hutter, MD; Claudia Schneller, RN; 

Jake Gundrum, MS 

CASe reportS 

Colonoscopic Diagnosis of Appendicitis in a Patient with Ulcerative Colitis: A Case Report and Review of the 

Literature 

Alexander D. Wade, MD; Frank J. Aberger, MD 

Intracranial Mycotic Aneurysm Due to Streptococcus bovis Endocarditis 

Abhishek Tandon, MD; Steven B. Pearson, MD; Todd J. Kowalski, MD 


Robert E. Ryan, MA, ATC; Troy E. Ward, MA, ATC; Steven R. Murray, DA; Mitchell T. Copeland, DO; Brian E. 

Udermann, PhD, ATC, FACSM; Robert W. Pettitt, PhD, ATC 

Post–Cesarean Delivery Septic Ovarian Vein Thrombosis 

Meghana Raghavendra, MB, BS; William A. Agger, MD 

hiStory of MediCine 

Historical Notes on Amputation and Phantom Limb Pain: “All Quiet on the Western Front?” 

Ines H. Berger, MD, PhD; Douglas R. Bacon, MD, MA 

The History of Cardiac Rehabilitation at the University of Wisconsin–La Crosse 

Brian E. Udermann, PhD, ATC, FACSM; John P. Porcari, PhD, RCEP; Carl C. Foster, PhD

editor 


Department of Neurology 

Speech Pathology 

MAnAGinG editor 

Cathy Mikkelson Fischer, MA 

Gundersen Lutheran Medical Foundation 

editoriAL boArd MeMberS 

William A. Agger, MD, FACP 

Department of Internal Medicine 

Section of Infectious Disease 

Director of Research 


Robert H. Caplan, MD, FACP, FACE 


Section of Endocrinology 

David H. Chestnut, MD 

Department of Anesthesiology 

Director of Medical Education 


As sociate Dean for the Western Academic 

Campus 

University of Wisconsin School of Medicine 

and Public Health 

Ronald S. Go, MD 

Department of Hematology 

Steven B. Pearson, MD, FACP 


Internal Medicine Residency Program Director 

Jeffrey S. Sartin, MD 



Mark L. Saxton, MD, FACS 

Department of Surgery 

Pediatric Surgery 

Brian E. Udermann, PhD, ATC, FACSM 

Department of Exercise and Sport Science 

University of Wisconsin–La Crosse 

Support StAff 

Deborah Brostrom 

Research Manager 


Pamela Maas 

Chief Officer 

Business Development & Marketing 

Sarah J. Fillbach 

Marketing & Communication Specialist 


Barbara K. Beeson 

Graphic Designer 


Beth A. Frechette 

Marketing & Communication Specialist 


Gundersen Lutheran Medical Journal publishes material related to the life sciences. We welcome submission of original research, reviews, case reports, 

commentaries, and letters. Please consult our “Instructions for Authors,” provided on our Website, for submission and manuscript preparation 

guidelines. Direct questions or submit manuscripts for consideration to 

Gundersen Lutheran Medical Journal 


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Email: glmjeditor@gundluth.org 

Website: http://www.gundluth.org/journal 

Ad hoC reVieWerS 

Gundersen Lutheran Medical Journal is a peer-reviewed journal published by Gundersen Lutheran Medical Foundation, 

1836 South Avenue, La Crosse, WI 54601. Copyright 2009 by Gundersen Lutheran Medical Foundation. All rights reserved. 

Joseph B. Binegar, MD 

Christopher P. Born, MD 

Heather J. Chial, MD 

Mark E. Domroese MD, PhD 

A. Erik Gundersen, MD 

Michael J. Henry, MD 

Richard D. Hutter, MD 

Todd J. Kowalski, MD 

John D. Larson, MD 

Kenneth W. Merkitch, MD 

Jerry J. Miller, MD 

Kurt K. Mueller, MD 

Edward R. Winga, MD 

Individuals may photocopy parts of the Journal for educational purposes. The Journal is archived on the Gundersen Lutheran Medical Journal Website. 

Permission for use of the Journal for other purposes must be obtained in writing from the Editor. Gundersen Lutheran Medical Journal accepts no 

responsibility for statements made by contributors.

editor’S MeSSAGe 

Welcome to the Summer issue of the GLMJ ! Thanks to our authors for their 

contributions, and to the reviewers for taking time out of their busy schedules to review 

and comment on the submissions. 

The Journal’s Editorial Board is exploring ways in which it can contribute to Gundersen 

Lutheran’s mission: “We distinguish ourselves through excellence in patient care, 

education, research, and through improved health in the communities we serve.” In 

order to increase awareness of the depth and breadth of our collective scholarly and 

research interests, each year we will publish abstracts of professional oral and poster 

presentations and of published journal articles. We will note publication of books 

and book chapters, as well. The Board is also developing a timeline for implementing 

the steps necessary to make successful application to have the Journal indexed in 

MEDLINE. Among these steps are expanding distribution of the Journal, increasing 

the number and quality of submissions, and recruiting more authors and reviewers from 

outside our organization. 

In the Original Research section of this issue, Dr Wright and colleagues from the 

University of Wisconsin–La Crossse apply the concept of the placebo effect to exercise. 

They tested whether groups who believed they were receiving a nutritional ergogenic aid 

(in fact, a placebo) experienced improvement in their exercise performance. 

My colleagues and I reviewed the efficacy and outcomes for a screening measure for 

dysphagia implemented for acute stroke patients for a consecutive 8-year period. Coauthor 

Melissa Hunter was my summer fellow in 2007 through the Gundersen Lutheran 

Medical Foundation. Her diligent work and assistance saw this project through to 

fruition. 

This issue’s Case Reports section features several unusual cases. Drs Wade and Aberger 

present a case of colonoscopically diagnosed appendicitis in a patient with known 

ulcerative colitis, possibly the first such case reported in the literature. 

Dr Tandon and colleagues discuss the history and course for a patient with infective 

endocarditis who developed neurologic signs and radiographic evidence for multiple 

intracranial mycotic aneurysms. Mycotic aneurysms are usually fatal if not diagnosed 

and treated in a timely manner. 

Mr Ryan and colleagues, representing institutions in Colorado, Minnesota, and 

Wisconsin, discuss a case of a giant-cell reaction to a bioabsorbable implant used to 

repair a torn supraspinatus muscle in a patient with impingement syndrome. 

Drs Raghavendra and Agger offer insights into diagnosis and treatment of postpartum 

ovarian vein thrombosis. 

Finally, in the History of Medicine section, Drs Berger and Bacon provide an interesting 

and detailed history of phantom limb syndrome, while Dr Udermann and colleagues 

from the University of Wisconsin–La Crossse provide a comprehensive story of cardiac 

rehabilitation in La Crosse since its inception in 1970. 

Along with the Editorial Board, I hope that you enjoy this issue of the GLMJ. Your 

contributions and suggestions for the Journal are welcomed and encouraged. We 

encourage Gundersen Lutheran staff to document their presentations and publications 

1

through our online Scholarly Activity Report as they are completed. We’d hate to miss including 

your abstract in our winter issue. Please feel free to contact me or Cathy L. Fischer, Managing 

Editor, with your submissions, comments, or concerns. 


Editor 


2 Gundersen Lutheran Medical Journal • Volume 6, Number 1, June 2009

Authors: 

Glenn Wright, PhD 

John P. Porcari, PhD, RCEP 

Carl C. Foster, PhD 

Heidi Felker, MS 

Ashley Kosholek, MS 

Jennifer Otto, MS 

Erik M. Sorenson, MS 

Brian E. Udermann, PhD, ATC, 

FACSM 

Department of Exercise and 

Sport Science 

University of Wisconsin–La Crossse 

Address for correspondence: 

Glenn Wright, PhD 


Sport Science 


1725 State Street 


email: wright.glen@uwlax.edu 


AbStrACt 

The concept of controlling for placebo effects during 

experimental and clinical intervention studies is well 

established. The power of the placebo effect has been recognized 

in the literature, with the general expectation that about 33% of 

experimental subjects or patients will respond solely on the basis of 

the placebo effect. 1 Well-documented effects related to subjective 

outcome measures, 2 depression, 3 pain relief, 4 symptom relief, 5,6 

blood pressure reduction, 7 and asthma relief 8 have been reported. 

Although virtually all exercise intervention studies include control 

groups to account for the placebo effect, data documenting the 

magnitude of the placebo effect during exercise are limited. 

Accordingly, the purpose of this study was to assess the magnitude 

of the placebo effect during exercise, with particular reference to 

the type of exercise (aerobic vs anaerobic) and exerciser (athletes, 

healthy nonathletes, patients). 

MethodS 

Approach to the Problem 

This study was designed to test the hypothesis that there would 

be a significant placebo effect during exercise in different types of 

exercise and in different types of exercisers. It was conducted in 3 

distinct parts. In all parts of the study, subjects provided written 

informed consent, and the study protocols had been approved by 

the university Institutional Review Board. In all parts of the study, 

the subjects had performed a practice trial of the criterion task to 

ensure that they were fully task habituated. Placebo and control 

studies were performed in random order with ≥ 48 hours without 

heavy exercise prior to each trial. 

Despite the routine use of placebo control in exercise intervention studies, there is inadequate 

information about the magnitude of the placebo effect and how it might respond during 

different types of exercise. This study was designed to evaluate the placebo effect in different 

populations and in different types of exercise. In a 3-part study the effect of purported 

nutritional ergogenic aids was measured in: (A) trained runners in a 5-km time trial, (B) physical 

education students during a high-intensity cycle sprint test, and (C) in clinically stable patients 

during a 6-minute walk test. In A, performance was improved by 83 seconds (6.5%), with a 

larger placebo effect in the slower runners. In B, there was no significant effect on peak or mean 

power output, or on the pattern of fatigue. In C, although there was no significant difference 

in the distance completed in the 6-minute walk test, there was a significant trend (P = .08) for 

patients to walk faster during the first minute of the test. The results suggest that the placebo 

effect may be of significant magnitude, particularly during more prolonged tasks, and may 

influence both athletes and patients. 

9 -14 

SubJeCtS 

In Part A, healthy, well-trained competitive runners ranging 

from university to recreational class (23 men, mean [SD] age 28 

[13] years; 9 women, mean [SD] age 30 [13] years) were studied 

during 5-km running time trials. In Part B, healthy physical 

education students (8 men, mean [SD] age 20 [1] years; 10 

women, mean [SD] age 21 [1] years) were studied during highintensity 

sprint cycling (Wingate Test). In Part C, patients with 

stable cardiovascular disease who were participants for longer than 

1 year in a community-based exercise program (6 men, mean [SD] 

age 62 [10] years; 4 women, mean [SD] age 64 [8] years) were 

studied while performing the 6-minute walk test. 

proCedureS 

In all 3 parts of the study, subjects were intentionally 

misinformed of the purported beneficial effects of the placebo agent 

by having them view a video (Part A = super-oxygenated water), by 

having them attend a graduate class on ergogenic aids (Part B = fastacting 

creatine monohydrate), or by having them read a brochure 

purporting to report results of previous studies (Part C = Peligrino 

Spa water). In all cases, subjects were given an inactive agent (tap 

water) in both the placebo and control conditions. We deliberately 

let the subjects know when they were receiving the “active” agent, 

so that they would be expecting an ergogenic benefit. Polling of the 

subjects indicated that they generally felt that the “active” agent (ie, 

placebo) was likely to help their performance. 

In Part A, the subjects ran two 5-km time trials (running 

without the benefit of other competitors) on an indoor 200-m 

track. The warm-up before each run was based on the normal pre- 

Gundersen Lutheran Medical Journal • Volume 6, Number 1, June 2009 3

competition practice of each subject, and was consistent between 

trials within each subject. During the trial, the time for each lap 

was called to the subject to facilitate pacing, which is a common 

practice during competitions. Prior to the warm-up (~30 minutes 

prior to the beginning of the time trial) each subject consumed 

300 ml of tap water. In the placebo trial, the water was labeled 

“super-oxygenated water” in order to create the impression that 

subjects were consuming an ergogenic aid. In the control trial, 

the water was correctly labeled as “water.” During the time 

trials, running time was recorded for each of the 25 laps, and 

heart rate was recorded using radio telemetry (Polar Electro OY, 

Finland). Within 60 seconds of completing the trial, blood lactate 

concentration was measured in capillary blood using an enzyme 

electrode system (YSI Sport, Yellow Springs, OH), and the rating 

of perceived exertion (RPE) was measured using the Borg category 

ratio scale (CR10 Scale). 15 

In Part B the subjects performed 2 Wingate anaerobic tests 16 

on an electronically braked cycle ergometer (LODE Excalibur, 

Netherlands), with the resistance set at 75 g.kg -1 body weight. 

These tests were performed at least 3 days apart. The warm-up 

was standardized for each subject and consisted of continuous 

cycling at 75 watts (W) for 10 minutes. During the last 5 minutes 

of the warm-up, the subjects accelerated to maximal power output 

for ~5 seconds on 2 occasions in order to ensure that the subject 

had a sense of the feeling of the power output required during the 

test. Following the warm-up the subjects recovered by pedaling at 

25 W for 5 minutes. The protocol of the test was controlled by 

software in the cycle, with a 30-second countdown prior to the test 

initiation. The subjects began maximal acceleration of the pedals at 

-3 seconds, and rapid adjustment of the resistance was performed 

by the ergometer software, such that the required resistance was 

achieved at the start of the 30-second Wingate test protocol. 

Subjects were verbally encouraged to pedal at maximal pedal 

revolutions (ie, the highest possible power output) throughout the 

test. The ergometer recorded the power output during each second 

of the test. In order to create the impression that they were taking 

an ergogenic aid, subjects in the placebo group were instructed 

to report to the laboratory to mix and consume 300 ml of water 

with 5 g of white powder labeled “alpha-hydroxycreatine” (placebo 

as maltodextrin) approximately 24 hours prior to the test, while 

the control group subjects consumed 300 ml of known water. An 

Lap Velocity, m.s -1 

5 

4.5 

4 

3.5 

C ontrol 

Placebo 

Lap Velocity 

0 1000 2000 3000 4000 5000 

Distance, m 

additional dose of the placebo or control beverage was consumed 

prior to the warm-up of the respective trial approximately 

30 minutes prior to the test. 

In Part C the subjects performed two 6-minute walk tests in a 

36-m hallway. An investigator positioned at the midpoint of the 

hall timed the subjects each time they touched the wall or passed 

the midpoint of the hallway, allowing velocity to be calculated 

over every 18 m. This was later converted to average velocity over 

every 30 seconds of the test. Heart rate was determined using radio 

telemetry. RPE was measured using the Category Ratio RPE scale. 

Prior to performing the test, subjects had walked for 10 minutes 

at their normal exercise training pace and had rested for 5 minutes 

immediately prior to beginning the test. In order to create the 

impression that they were taking an ergogenic aid, subjects in 

the placebo group were instructed to consume 300 ml of a liquid 

labelled “Pelegrino Spa Water” approximately 30 minutes before 

the warm-up, while the control group consumed 300 ml of a 

liquid labelled “water.” 

StAtiStiCAL AnALySiS 

For all parts of the study, outcome measures were analyzed 

using repeated measures analysis of variance (ANOVA) for an 

intervention by serial measurement design. Post hoc analyses 

were performed using the Tukey test when justified by ANOVA. 

Statistical significance was accepted when P < .05. 

reSuLtS 

All tests were completed without complication by all subjects. 

Questioning of the subjects indicated that the procedures used to 

create the expectation that the intervention beverage would confer 

an ergogenic effect were effective. 

pArt A 

On average, subjects ran the placebo trial significantly faster 

(83 seconds faster, 6.5%) than they ran the control trial (mean 

[SD] 19:41 [2:32] minutes vs 21:04 [3:34] minutes). Average 

running velocity, distributed fairly evenly within the trial, was 

0.23 m.s -1 faster during the placebo trial (Figure 1 left). Heart rate 

(HR) (mean [SD] 179 [13] beats.min -1 vs 179 [11] beats.min -1 ), 

figure 1. (Left) Running velocity per lap during 5-km time trials in the control (solid circles) and placebo (open circles) conditions. (Right) 

Comparison of total running time for 5 km during the placebo and control trials. There was a significant overall effect (83 seconds) attributable 

to the placebo, but a proportionally larger placebo effect in the slower (> 1200 seconds) runners compared with the faster runners (2:22 ± 1:02 

vs 0:28 ± 1:08). 

4 Gundersen Lutheran Medical Journal • Volume 6, Number 1, June 2009 

Placebo Time, s 

1800 

1700 

1600 

1500 

1400 

1300 

1200 

1100 

1000 

900 

Control vs Placebo Time 

900 1000 1100 1200 1300 1400 1500 1600 1700 1800 

Control Time, s

RPE (0-10 scale) (mean [SD] 7.7 [1.2] vs 7.7 [1.4]), and blood 

lactate concentration (mean [SD] 10.2 [3.7] mmol.l -1 vs 9.8 [3.9] 

mmol.l -1 ) were not different between placebo and control trials, 

respectively. Using a 1.5% difference as a meaningful difference in 

performance, 17 75% of the subjects ran faster during the placebo 

trial, and 9% ran faster during the control trial. A direct comparison 

of performance during placebo and control trials suggested that the 

relatively slower subjects (control trial >1200 seconds) had a larger 

mean improvement in performance (mean [SD] 2:22 [1:02]) than 

the relatively faster subjects (control trial

effect. These data suggest that the placebo effect is more likely to 

be present during exercise that may need to be sustained for some 

moments and is more likely in individuals least likely to adequately 

monitor their physical response to exercise. The magnitude of 

effect supports the concept that something in excess of one-third 

of individuals will be responsive to the placebo effect. 1 

The results can be understood in terms of the anticipatoryperceived 

exertion feedback model, recently proposed by Tucker 

and Noakes. 18 According to this model, the pattern of energy 

output during a task is defined by a template based on individual 

expectations regarding the appropriate effort distribution and 

experience with the task. In the presence of a placebo, some 

individuals may revise their pre-exercise template and start exercise 

at a higher intensity. In most individuals (eg, the patients during 

the 6-minute walk test and the more accomplished runners) 

feedback from homeostatic disturbances during exercise causes a 

reduction of an overly ambitious pace to a more appropriate pace. 

This concept is supported by recent work in our laboratory 19 that 

has shown that the relative growth of effort sense (ie, RPE) during 

exercise is remarkably stable despite differences in task duration 

and/or the blinded administration of a hypoxic gas mixture. 

Similar findings have been reported in relation to running 

distance 20 and during both hypoxia and hyperoxia. 21-23 Morgan 24 

has demonstrated that less accomplished competitive runners do 

not adequately attend to the growth of fatigue during marathon 

running, preferring to dissociate from the sensations of running. 

This observation may explain the frequency of “hitting the wall” 

in less accomplished runners. It may also explain the persistence of 

a higher running pace in the less accomplished runners during the 

placebo trial, many of whom may not have raced enough to fully 

use their physiological capacity during competitions. 

Past experience with the criterion task may also affect the 

way energy is expended. Previous work from our laboratory 25 has 

demonstrated that performance often changes over the first several 

trials of a new task, primarily attributable to the subject being 

willing to begin at a faster pace. Given the failure to slow as much 

after the first laps of the 5 km (Part A) and the trend toward a faster 

start in the 6-minute walk (Part C), it seems reasonable to suggest 

that one of the ways in which the placebo works is to encourage a 

faster start. Similar results have been demonstrated with the clinical 

use of the 6-minute walk test, 26 where patients typically take 2 to 3 

trials to achieve a stable performance. It likewise seems reasonable 

to suggest that experience with performing a task and the placebo 

effect would influence performance in the same way. 

The failure to observe a significant placebo effect during the 

high-intensity exercise bout can be attributed to both the protocol 

employed and the nature of the task. In the Wingate Test it is 

ordinary to allow the subject to increase the pedaling rate of the 

cycle ergometer prior to loading the flywheel. 16 However, this may 

spuriously elevate the measured power output during the first 

seconds of the test. Although this pre-load spinning is a normal 

way of conducting this test, Havenetidis 27 and Reiser 28 have 

discussed the limitations of this approach. Mendez-Villaneuva 29 

has demonstrated in a repeated sprint protocol that losses in power 

output are attributable to an inherent loss of motor unit recruitment 

rather than to reductions of effort. Thus, both the nature of the 

experimental approach (peak power) and the way that power is 

reduced in sprint exercise (mean power), the Wingate Test would 

be somewhat resistant to demonstrating a placebo effect. 

In conclusion, the results of this study demonstrate that the 

placebo effect is of sufficient magnitude to justify the normal 

practice of including control groups for intervention studies 

involving exercise capacity as an outcome from exercise training 30 

or pharmacologic interventions. 31 Although the specific results 

of this study (Part B) did not demonstrate an effect on sprint 

performance, the results of the other portions of the study suggest 

that the general practice of using a control group is well-justified. 

referenCeS 

1. Beecher HK. The powerful placebo. J Am Med Assoc. 1955;159(17):1602-1606. 

2. Turner JA, Deyo RA, Loeser JD, Von Korff M, Fordyce WE. The importance of 

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3. Kirsch IPD, Sapirstein GPD. Listening to Prozac but hearing placebo: a metaanalysis 

of antidepressant medication. Prevention & Treatment. 1998;1(2). 

4. Benson H, McCallie DP Jr. Angina pectoris and the placebo effect. N Engl J Med. 

1979;300(25):1424-1429. 

5. Hashish I, Harvey W, Harris M. Anti-inflammatory effects of ultrasound therapy: 

evidence for a major placebo effect. Br J Rheumatol. 1986;25(1):77-81. 

6. Moseley JB, O’Malley K, Petersen NJ, et al. A controlled trial of arthroscopic 

surgery for osteoarthritis of the knee. N Engl J Med. 2002;347(2):81-88. 

7. Preston RA, Materson BJ, Reda DJ, Williams DW. Placebo-associated blood 

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8. Godfrey S, Silverman M. Demonstration by placebo response in asthma by means 

of exercise testing. J Psychosom Res. 1973;17(4):293-297. 

9. Ariel G, Saville W. Anabolic steroids: the physiological effects of placebos. Med Sci 

Sports Exerc. 1972;4:124-126. 

10. Clark VR, Hopkins WG, Hawley JA, Burke LM. Placebo effect of carbohydrate 

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1647. 

11. Maganaris CN, Collins DJ, Sharp M. Expectancy effects and strength training: 

do steroids make a difference? Sport Psychologist. 2000;14:272-278. 

12. Sonetti DA, Wetter TJ, Pegelow DF, Dempsey JA. Effects of respiratory muscle 

training versus placebo on endurance exercise performance. Respir Physiol. 

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13. Beedie CJ, Stuart EM, Coleman DA, Foad AJ. Placebo effects of caffeine on 

cycling performance. Med Sci Sports Exerc. 2006;38(12):2159-2164. 

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Kinetics; 1998:104. 

16. Maud PJ, Berning JM, Foster C, et al. Testing for anaerobic ability. In: Maud PJ, 

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Human Kinetics; 2006:77-92. 

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February 17, 2009]. Br J Sports Med. doi:10.1136/bjsm.2008.050799. 


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20. Faulkner J, Parfitt G, Eston R. The rating of perceived exertion during competitive 

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21. Amann M, Eldridge MW, Lovering AT, Stickland MK, Pegelow DF, Dempsey JA. 

Arterial oxygenation influences central motor output and exercise performance 

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22. Peltonen JE, Rantamaki J, Niittymaki SP, Sweins K, Viitasalo JT, Rusko HK. 

Effects of oxygen fraction in inspired air on rowing performance. Med Sci Sports 

Exerc. 1995;27(4):573-579. 

23. Tucker R, Kayser B, Rae E, Raunch L, Bosch A, Noakes T. Hyperoxia improves 

20 km cycling time trial performance by increasing muscle activation levels while 

perceived exertion stays the same. Eur J Appl Physiol. 2007;101(6):771-781. 

24. Morgan WP, Pollock ML. Psychologic characterization of the elite distance 

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25. Foster C, Hendrickson K, Peyer K, et al. Pattern of developing the performance 

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pLACebo effeCtS on exerCiSe perforMAnCe 

26. Guyatt GH, Pugsley SO, Sullivan MJ, et al. Effect of encouragement on walking 

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27. Havenetidis K, Cooke CB, Butterly R, King RF. Incorrect calculation of power 

outputs masks the ergogenic capacity of creatine supplementation. Appl Physiol 

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28. Reiser RF 2nd, Broker JP, Peterson ML. Inertial effects on mechanically braked 

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29. Mendez-Villanueva A, Hamer P, Bishop D. Fatigue in repeated-sprint exercise is 

related to muscle power factors and reduced neuromuscular activity. Eur J Appl 

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30. Foster C, Pollock ML, Anholm JD, et al. Work capacity and left ventricular 

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Zebra Family Jeff Hillesland 

Trauma & Emergency Center 


Authors: 

David E. Hartman, PhD, 

BC-ANCDS(A) 

Speech Pathology, Department of 

Neurology 

Gundersen Lutheran Health System 

Melissa Hunter 

Department of Research 

Gundersen Lutheran Medical 

Foundation 

Richard D. Hutter, MD 

Department of Neurology 


Claudia Schneller, RN 

Department of Nursing 


Jake Gundrum, MS 

Department of Research 


Foundation 


David E. Hartman, PhD, 

BC-ANCDS(A) 

Mail Stop EB3-005 




Telephone: (608) 782-7300 

Facsimile: (608) 791-6358 

email: dehartma@gundluth.org 

Outcomes from a Screening Procedure for 

Oropharyngeal Dysphagia Following Acute Stroke 

AbStrACt 

Stroke is the third leading cause of death and number one 

cause of adult disability in the United States, affecting more 

than 700 000 Americans each year, including 160 000 deaths from 

stroke-related causes. 1 It is estimated that over 3 million Americans 

are permanently disabled from stroke. 2 In 1999, stroke cost the 

United States approximately 30 billion dollars in healthcare 

costs and lost productivity. 1 Given inflation, more sophisticated 

technology for evaluation and treatment, and the overall rise in the 

cost of healthcare, this figure has steadily increased over the years. 

Stroke is the most common etiology for dysphagia, with 

30% or more of patients showing signs of aspiration by clinical 

examination or videofluorographic study of swallow (VFSS). 3-8 The 

likelihood of developing pneumonia is 7 times greater in stroke 

patients who aspirate than in those who do not, even though the 

typical course for dysphagia after stroke is gradual improvement 

over a 6-month period. 3,6,9,10 Untreated or undiagnosed dysphagia 

can lead to malnutrition, while pneumonia increases the chance of 

mortality 3-fold, particularly in those institutions that do not have 

a screening protocol for dysphagia. 11,12 

It has been the general consensus that in acute stroke, a 

bedside examination, even if supplemented by available dysphagia 

Oropharyngeal dysphagia and aspiration pneumonia are common sequelae to stroke. The 

purpose of the current investigation was to assess the effectiveness of a screening procedure 

for dysphagia and aspiration following acute stroke. Medical records of 753 patients who 

were seen through an acute stroke care pathway and screened for dysphagia and aspiration 

using the Gundersen Lutheran Acute Dysphagia Screen (GLADS) between 1998 and 2006 

were reviewed. Dysphagia, pneumonia, nutritional outcomes, and neurologic characteristics 

of patients who passed GLADS were compared with those of patients who failed. Five hundred 

seventy-eight patients passed GLADS. Of these, 524 (91%) remained stable on an oral diet and 

free of pneumonia during their hospitalization; 18 (3%) developed pneumonia during the study. 

One hundred seventy-five patients failed GLADS and had further evaluation and treatment. 

Eighty-two of these patients (47%) remained stable on an oral diet and free of pneumonia 

during their hospitalization; 16 (9%) developed pneumonia during the study. Patients who 

passed GLADS had significantly lower rates of pneumonia than those who failed. Length of 

hospital stay and cost of hospitalization were considerably greater for patients failing GLADS. 

Premorbid stroke and dysphagia were not good predictors of a patient’s ability to maintain 

a safe oral diet. No significant association was found between site of lesion, communicative 

or cognitive deficits, and pneumonia. Communicative or cognitive deficits were not good 

predictors of a patient’s ability to maintain a safe oral diet after stroke. GLADS appears to be an 

effective screening tool for dysphagia and preventing pneumonia following acute stroke. 

screening tools, is inadequate for assessing deglutitory function 

and for predicting dysphagia or its ramifications, including 

aspiration, pneumonia, or malnutrition. 7,8,13-19 Recently, however, 

Trapl and colleagues 20 described a bedside screening protocol used 

for 50 acute-stroke patients that, with further investigation, may 

allow for institution of a safe oral diet without the need for further 

evaluation of swallowing function. 

Martino and colleagues 21 and Perry and Love 22 conducted 

comprehensive literature reviews that identified several articles that 

met strict research criteria for dysphagia screening following acute 

stroke. Their combined results indicated a need for both creation 

and validation of efficacious screening procedures for dysphagia 

after stroke. This issue was also stressed in the 1999 Agency for 

Health Care Policy and Research report for dysphagia, 23 and by 

the Joint Commission, 24 Smith and colleagues, 25 Teramoto and 

Fukuchi, 26 Mosheim, 27 and Swigert, 11 particularly as bedside 

screening procedures are used to detect aspiration. 

In 1997, professional staff at our institution representing 

neurology, speech-language pathology, physical medicine and 

rehabilitation, internal medicine, neurosurgery, and nursing 

developed a comprehensive care pathway—Acute Stroke Care 


outCoMeS froM A SCreeninG proCedure for orophArynGeAL dySphAGiA 

Pathway (ASCP)—for evaluating and treating acute stroke patients 

admitted to our medical center. Various stroke pathways have been 

described elsewhere 12,28 and have been found to be efficacious for 

caring for acute stroke patients. 

In conjunction with the ASCP and based upon previous literature 

concerning bedside screening examinations for oropharyngeal 

dysphagia, 3,5,13-15,18,19,21,22,28-42 3 of the authors developed a screening 

tool, Gundersen Lutheran Acute Dysphagia Screen (GLADS), for 

use by nurses. In brief, GLADS used a checklist that incorporated 

several observable risk factors (ie, Critical Criteria) relevant for 

both dysphagia and aspiration, and assessment tools for secretions, 

swallowing frequency, and water swallows. 26,31,33,40,41 Prior to using 

it with stroke patients, a select cadre of 20 registered nurses was 

trained by the 3 authors to administer GLADS. 

Through the ASCP, medically stable and adequately alert 

patients were screened a minimum of 3 times following admission 

and up to 48 hours prior to a consultation being generated for more 

comprehensive evaluation of swallowing function. Observations 

of (1) 1 or more critical criteria, (2) continuous intermittent 

coughing on secretions, (3) coughing with water swallow trials, 32,33 

or (4) swallowing frequency fewer than 1 per minute or 4 per 

5 minutes 40,41 denoted failure on GLADS, prompted a nothing 

by mouth order, and generated referral for further evaluation. 

If available in liquid form, necessary medications were given 

intravenously or intramuscularly. 

Results from a pilot study using GLADS for 118 acute 

stroke patients showed that none developed either pneumonia 

or malnutrition during hospitalization or at 3-month followup 

and suggested that trained nurses could effectively implement 

a screening procedure for dysphagia following stroke. 43,44 The 

purpose of the current retrospective investigation was to (1) 

determine the outcomes for pneumonia and nutrition for patients 

admitted through the ASCP between 1998 and 2006 and 

undergoing GLADS as part of the stroke protocol, (2) determine 

the effectiveness of GLADS as a screening procedure for dysphagia 

and aspiration, and (3) compare the neurological characteristics of 

patients who passed GLADS with those of patients who failed. 

MethodS 

Approval for retrospective review of patient medical records 

was obtained from Gundersen Lutheran Health System’s 

Research Committee and Institutional Review Board. All 

patients admitted through the ASCP between January 1998 and 

December 2006 were identified by service code and their medical 

records reviewed by the authors. Of these, the records of those 

patients who underwent screening using GLADS were reviewed 

for outcomes during hospitalization and at 35 days following 

discharge from hospital. A determination of pneumonia was made 

by reviewing the comments and diagnoses made by the primary 

service (typically internal medicine or neurology) or pulmonary 

medicine and the findings from chest radiographs. Nutritional 

status was determined by reviewing the nutritional assessment 

recommendations made by registered dieticians or the metabolic 

support team. General statistical associations and proportion 

comparisons with categorical variables were assessed with the χ 2 

test. The Fisher exact test was used in place of the χ 2 test when at 

least 25% of the cells had counts less than 5. Univariate logistical 

models were used when predictive ability was tested. The cost and 

length-of-stay comparisons between groups were done with the 

Wilcoxon rank sum test of equal distributions. Exact confidence 

limits were calculated for the reported odds ratio. A P value < .05 

was considered significant. 

Gundersen Lutheran Acute Dysphagia Screen 

(GLADS) 

reSuLtS 

Seven hundred fifty-three stroke patients, average age 74 years, 

had GLADS administered in conjunction with the ASCP between 

January 1998 and December 2006. Five hundred seventy-eight 

patients (77%) passed GLADS. Of these, 571 did not undergo 

further assessment for dysphagia prior to implementation of an 

oral diet; the remaining 7 patients had normal VFSS test results 

and were started on an oral diet subsequent to study. However, 4 

of these patients had inadequate oral intake and were given enteral 

feedings, as well. One hundred seventy-five patients (23%) failed 

GLADS and went on for further evaluation (ie,VFSS, fiberoptic 

study of swallow, 29,45 or both) and treatment. 

Of the patients passing GLADS, 287 were men and 291 were 

women. By report, 10 patients had premorbid dysphagia, although 

its nature was unclear. Although 1 patient was described as having 

aspiration premorbidly, no patients were diagnosed with pneumonia 

at the point of admission through the ASCP. Five hundred twentyfour 

patients (91%) maintained an oral diet and were free from 

pneumonia during their hospitalization and within 35 days of 

Gundersen Lutheran Medical Journal • Volume 6, Number 1, June 2009 9 

ID Stamp: 

Reason for Admission/Primary Diagnosis:____________________________________________ 

Date of Admission:_____________ Attending Staff:__________________________________ 

House Staff:___________________________ RN Completing Index:_____________________ 

Dates:________________________________________________________________________ 

Trials 

Critical Criteria* Check if Present Check if Present Check if Present 

Decreased volitional cough _____ _____ _____ 

Wet hoarseness _____ _____ _____ 

Audible oropharyngeal pooling 

of secretions _____ _____ _____ 

Decreased mental status _____ _____ _____ 

Tracheostomy _____ _____ _____ 

Tube feedings, NG or gastrostomy _____ _____ _____ 

Assessment* 

Coughs on secretions _____ _____ _____ 

Coughs on 3-ounce H2O trials _____ _____ _____ 

Swallowing frequency (4 or < in 5’) _____ _____ _____ 

This screen should be administered a minimum of three times within 24-48 hours of admission. 

If patient demonstrates one or more of the critical criteria, coughs on secretions, has failed H2O 

swallowing trials, or swallows four times or less in a five minute time period, then status should 

be NPO including medications unless they can only be given orally) until the screen is passed or 

formal evaluation of deglutitory function has been completed.

discharge. Twelve patients (2%) developed pneumonia during 

their hospitalization, 6 of whom were diagnosed with aspiration 

pneumonia by clinical examination and chest radiograph. Neither 

prior stroke nor premorbid dysphagia were good predictors of a 

patient’s ability to maintain a safe oral diet (P = .34; P = .26). Six 

patients (1%) developed pneumonia after discharge from hospital 

and subsequent placement in an extended care facility. Thirty-two 

patients (6%) died during the course of the study, 3 of whom had 

pneumonia, although it was not determined if pneumonia was the 

cause of death. Three patients were lost to followup. 

Of the 578 patients who passed GLADS, 222 experienced a 

left cerebral hemisphere stroke, 190 had a right hemisphere stroke, 

25 had a brainstem stroke, and 21 had bihemispheric cerebral 

strokes, based upon clinical examination, radiographic study, or 

table 1. Demographic and Clinical Characteristics of 578 Patients 

Passing GLADS 

Characteristic n (%) 

Sex 

Men 

Women 

Prior stroke 

Yes 

No 

Premorbid conditions 

Dysphagia 

Pneumonia 

Aspiration 

Nutritional / pneumonia outcomes 

Adequate oral diet, no pneumonia 

Pneumonia during hospital stay 

Aspiration pneumonia 

Pneumonia after discharge 

Total pneumonias 

Supplemental nutrition 

Deaths 

Deaths with concurrent pneumonia 

Lost to follow-up 

Stroke location 

Left cerebral hemisphere 

Right cerebral hemisphere 

Brainstem 

Bihemispheric 

Undetermined 

Stroke type 

Ischemic 

Hemorrhagic 

Ischemic / hemorrhagic 

Undetermined 

Communicative / cognitive deficit 

Dysarthria / dyspraxia 

Aphasia 

Dementia 

None 

287 

291 

201 

377 

10 

0 

1 

524 

12 

6 

6 

18 

4 

32 

3 

3 

222 

190 

25 

21 

120 

334 

12 

4 

228 

124 

82 

99 

273 

(50) 

(50) 

(35) 

(65) 

(2) 

(0) 

(0) 

(91) 

(2) 

(50) 

(1) 

(3) 

(1) 

(6) 

(9) 

(1) 

(38) 

(33) 

(4) 

(4) 

(21) 

(58) 

(2) 

(1) 

(39) 

(21) 

(14) 

(17) 

(47) 

both. Site of lesion could not be determined from neuroimaging 

for the remaining 120 patients. We found no significant association 

between site of lesion and pneumonia (P = .24). 

Three hundred thirty-four patients (58%) experienced an 

ischemic stroke with the current admission, 12 hemorrhagic, and 

4 with features of both ischemic and hemorrhagic stroke. For 

228 (39%) patients, medical records failed to indicate if stroke 

was ischemic or hemorrhagic. However, all patients had at least 

1 neuroimaging study, so a hemorrhagic lesion, if present, likely 

would have been identified. Thus, it could be argued that these 

strokes were ischemic. Two hundred seventy-three patients (47%) 

had normal or minimally affected speech, language, and/or 

cognition. One hundred twenty-four patients had distinct focal 

speech deficits, that is, dysarthria or dyspraxia of speech. Eightytwo 

patients had aphasia, and 99 patients had findings consistent 

with dementia. There was no significant association between these 

findings and pneumonia (P = .15). Moreover, having either a 

communicative or cognitive deficit was not a good predictor of a 

patient’s ability to maintain a safe oral diet after stroke (P = .89). 

The median length of stay for patients passing GLADS was 3 days 

(range 1-38 days), and the median cost of hospitalization was 

$7,967. For the 12 patients who passed GLADS but developed 

pneumonia during hospitalization, the median length of stay was 

6.5 days, and the median cost was $20,099. Table 1 summarizes 

the findings for the 578 patients passing GLADS. 

Of the 175 patients failing GLADS, 88 were men and 87 

were women. Sixty-nine patients (39%) had a history of prior 

stroke. Thirteen patients reportedly had pre-existing dysphagia, 

the nature of which was unclear. Neither prior stroke nor preexisting 

dysphagia was a good predictor of a patient’s ability to 

safely tolerate an oral diet (P = .92, P = .28). 

With behavioral therapy for their dysphagia, 84 patients (48%) 

maintained an oral diet and 82 remained free from pneumonia 

within the study period. Fourteen patients developed pneumonia 

during their hospitalization—7 presumably due to aspiration—and 

2 developed pneumonia after discharge, for an overall pneumonia 

rate of 9%, a rate significantly higher than that of the patients who 

passed GLADS, both during hospitalization and after discharge 

(P = .0002; P = .0008). 

Thirty-two patients (18%) required enteral nutritional 

support in conjunction with their dysphagia therapy. Fifty-five 

patients (31%) died during the study period, 11 possibly due 

to pneumonia. Three patients were placed on comfort care, and 

1 patient was lost to follow-up. The death rate was significantly 

higher for patients who failed GLADS than for those who passed 

(31% vs 5.5%, odds ratio 7.8; range 4.9-12.6; P < .0001). Sixtyfive 

patients experienced a left hemispheric and 68 patients a right 

hemispheric stroke. Fourteen patients had brainstem and 4 patients 

had bihemispheric stroke, while site of lesion was undetermined 

from neuroimaging for 24 patients. Like those who passed, patients 

who failed GLADS exhibited no significant association between 

the site of lesion and pneumonia (P = .75). 

Like those patients who passed GLADS, most patients who 

failed had experienced an ischemic stroke (106 patients, 61%). 

Seven patients had experienced a hemorrhagic stroke, while for 62 

patients (35%), medical records failed to indicate if the stroke was 

ischemic or hemorrhagic. However, as previously posited for those 



patients who passed GLADS, these patients’ strokes were likely 

ischemic. Like those patients passing GLADS, those who failed 

had normal or minimally impaired speech, language, or cognitive 

function (78 patients, 45%). For those patients with impairment, a 

motor speech disorder was most common (44 patients, 25%), and 

a focal language disorder (aphasia) was least common (19 patients, 

11%). Thirty-four patients had dementia. We found no significant 

association between these deficits and pneumonia (P = .61), nor, as 

for those patients passing GLADS, were they good predictors of a 

patient’s ability to maintain a safe oral diet after stroke (P = .89). 

Median length of stay for patients failing GLADS was 5 days 

(range 1-62 days), significantly higher than for those patients who 

passed (3 days, P < .0001). Median cost of hospitalization for these 

patients was $11,703, which was also significantly higher than 

for those who passed (P < .0001). For the 14 patients who failed 

GLADS and developed pneumonia during hospitalization, the 

median length of stay was 7 days, and the median cost $19,933. 

Moreover, if odds ratios are considered, the 175 patients failing 

GLADS were 4 times more likely to develop pneumonia during 

hospitalization than were the 578 who passed (95% CI, 1.86- 

9.04). Table 2 summarizes the findings for the 175 patients failing 

GLADS. 

diSCuSSion 

Results of the current investigation suggest that GLADS is an 

effective screening measure for oropharyngeal dysphagia following 

acute stroke when administered by carefully trained nurses in 

conjunction with an ASCP. Barring unrelated stroke complications, 

over 90% of patients passing GLADS were able to maintain a safe 

and nutritionally sound oral diet without pneumonia or further 

comprehensive evaluation for dysphagia during hospitalization. 

They were also less likely than patients who failed GLADS to 

develop pneumonia during their hospitalization or after discharge. 

We found that neither site of lesion nor communicative or cognitive 

deficits was a predictor of who would develop pneumonia. We 

also found that prior stroke—even with related comorbidities 

including dysphagia or speech or cognitive deficits—was not a 

good predictor of a patient’s ability to maintain a safe oral diet 

following a new stroke. Not surprisingly, cost of hospitalization 

and length of stay were reduced when stroke was not complicated 

by pneumonia. 

One might argue that the 175 patients who failed GLADS 

had more devastating strokes that resulted in a complicated course 

with protracted hospitalization, increased expense, and a higher 

death rate than those who passed GLADS. Interestingly, however, 

with time and dysphagia therapy, almost half of these patients 

went on to become functional and safe oral feeders during their 

hospitalization. This finding could also represent the influence of 

the comprehensiveness and intensity of the ASCP itself. 

The importance of a swallowing screen as a component of an 

ASCP has been stressed by others. 42 Using a speech pathologist or 

certified nurse to screen for dysphagia, they found that 48 of 124 

patients (39%) failed the initial screen and required dietary texture 

change, as well as direct dysphagia therapy. Whereas in our study 

patients who failed GLADS were referred for further evaluation 

prior to initiation of an oral diet, their patients apparently did 

not undergo further workup for dysphagia or aspiration prior 

table 2. Demographic and Clinical Characteristics of 175 Patients 

Failing GLADS 

Characteristic n (%) 

Sex 

Men 

Women 

Prior stroke 

Yes 

No 

Premorbid conditions 

Dysphagia 

Pneumonia 

Aspiration 

Nutritional / pneumonia outcomes 

Adequate oral diet, no pneumonia 

Pneumonia during hospital stay 

Aspiration pneumonia 

Pneumonia after discharge 

Total pneumonias 

Supplemental nutrition 

Deaths 

Deaths with concurrent pneumonia 

Comfort measures 

Lost to follow-up 

Stroke location 

Left cerebral hemisphere 

Right cerebral hemisphere 

Brainstem 

Bihemispheric 

Undetermined 

Stroke type 

Ischemic 

Hemorrhagic 

Undetermined 

Communicative / cognitive deficit 

Dysarthria / dyspraxia 

Aphasia 

Dementia 

None 

to initiating an oral diet. However, none of their patients were 

reported to have developed aspiration pneumonia. Using a water 

swallow screening test for 100 consecutive acute stroke patients, 

Nilsson et all have reported a pneumonia rate of 14% (2 of 14 

dysphagic patients). 46 Apparently neither of the patients who 

developed pneumonia received direct swallowing therapy. In our 

study, 14 of 175 patients failing GLADS developed pneumonia 

during hospitalization, which—if odds ratios are considered—is 4 

times the likelihood of the 578 patients who passed. 

Aspiration pneumonia following stroke has a reported 

incidence rate of 13%. 47 Moreover, the incidence of pneumonia 

increases with age, particularly over 65 years. 48 Hinchey et al 12 

found from a prospective multicenter study that institutions that 

had formal dysphagia screening protocols for acute stroke had 

Gundersen Lutheran Medical Journal • Volume 6, Number 1, June 2009 11 

88 

87 

69 

106 

13 

0 

0 

82 

14 

7 

2 

16 

32 

55 

11 

3 

1 

65 

68 

14 

4 

24 

106 

7 

62 

44 

19 

34 

78 

(50) 

(50) 

(39) 

(61) 

(7) 

(0) 

(0) 

(47) 

(8) 

(50) 

(1) 

(9) 

(18) 

(31) 

(34) 

(2) 

(.5) 

(37) 

(39) 

(8) 

(2) 

(14) 

(61) 

(4) 

(35) 

(25) 

(11) 

(19) 

(45)

pneumonia rates of 2.4%, versus 5.4% for those that did not. 

Although the specific nature of the protocols was not fully 

described, and randomization was an issue, their results led 

them to conclude that “A formal dysphagia screen prevented 

pneumonia even after adjusting for stroke severity.” 12(p1973) 

Outcomes from the current and previous studies 

incorporating a screening procedure for dysphagia 

in acute stroke in conjunction with an acute care 

pathway 12,42 may be a reflection of the propensity of 

dysphagia following stroke to improve or resolve within 

6 months of onset, 3,9 the nature of acute stroke pathways, which 

are inherently designed to provide the most comprehensive 

and efficacious treatment for the patient and to prevent 

complications from acute stroke, or a combination of these 

factors. Other than diet modification and regular observation 

by the medical and nursing team for signs of change in status 

related to oral feedings, none of the 578 patients who passed 

GLADS received formal dysphagia therapy. Thus, it could be 

concluded that their dysphagia, if present, was mild and not 

disabling. 

Median length of hospital stay and cost of hospitalization 

were lower for those patients whose stroke was not 

complicated by pneumonia. Similar trends have been noted 

previously. 12,28,49 

Like others, 13 we believe that screening procedures like 

GLADS do not delineate the specific nature of dysphagia, 

only whether the patient is having or may be at risk for 

swallowing difficulties. Nonetheless, based upon the results 

of the current investigation as well as the work of others, 42 

we conclude that nursing staff can be trained to administer 

a screening tool for dysphagia following acute stroke that 

will allow implementation of oral feedings with minimal or 

no complications, even though the nature of the swallowing 

disorder may not have been fully delineated. 

We believe GLADS was effective not only because it was 

administered by trained nursing staff, but also because of 

elements included in the screening tool itself and how they 

were used, rather than individual screening measures that 

have been used previously for dysphagia, for example, the 3-oz 

water swallow test, 32,33 swallowing frequency, or a timed test 

of swallowing. 40,41 The importance of co-occuring risk factors 

(Critical Criteria) has been stressed by others as well. 5,7,18,34,50 

If a screening tool alone, such as GLADS, is effective 

for implementing an uncomplicated oral feeding regimen 

following acute stroke, what, then, is the role of VFSS and 

videoendoscopic swallowing evaluation? We propose, as 

implemented at our institution and suggested elsewhere, 23 

that these procedures be reserved for patients who fail a 

comprehensive screening procedure or who have inconclusive 

screening results, who have unstable medical conditions that 

can potentially affect deglutitory function and subsequent 

respiration, or who require radiographic or photographic 

documentation of swallowing function prior to and following 

an invasive or surgical procedure. 

Finally, we believe that we have taken a step in meeting 

1 of the recommendations concerning the need for further 

development of efficacious screening procedures and best 

practice strategies for dysphagia. 21-23 Although it proved 

difficult logistically to incorporate into this retrospective study, 

a measure of interrater reliability for nurses administering 

GLADS should be included in future prospective investigations. 

Given today’s healthcare environment, more research is both 

needed and recommended to develop safe, reliable, and costeffective 

screening tools for dysphagia following stroke. 

ACknoWLedGMentS 

The authors thank Gundersen Lutheran Medical 

Foundation for sponsoring Melissa Hunter’s summer research 

fellowship. We also wish to thank Cathy Lazarus, PhD, 

BRS-S, New York University School of Medicine, for her 

insightful and critical comments, and Gundersen Lutheran 

Health System and Gundersen Lutheran Medical Foundation 

for their ongoing support for research. 

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36. Addington WR, Stephens RE, Gilliland KA. Assessing the laryngeal cough reflex 

and the risk of developing pneumonia after stroke: an interhospital comparison. 

Stroke. 1999;30(6):1203-1207. 

37. Warms T, Richards J. “Wet voice” as a predictor of penetration and aspiration in 

oropharyngeal dysphagia. Dysphagia. 2000;15(2):84-88. 

38. Linden P, Kuhlemeier KV, Patterson C. The probability of correctly predicting 

subglottic penetration from clinical observations. Dysphagia. 1993;8(3):170-179. 

39. Mari F, Matei M, Ceravolo MG, Pisani A, Montesi A, Provinciali L. Predictive 

value of clinical indices in detecting aspiration in patients with neurological 

disorders. J Neurol Neurosurg Psychiatry. 1997;63(4):456-460. 

40. Murray J, Langmore SE, Ginsberg S, Dostie A. The significance of accumulated 

oropharyngeal secretions and swallowing frequency in predicting aspiration. 

Dysphagia. 1996;11(2):99-103. 

41. Nathadwarawala KM, Nicklin J, Wiles CM. A timed test of swallowing capacity 

for neurological patients. J Neurol Neurosurg Psychiatry. 1992;55(9):822-825. 

42. Odderson IR, Keaton JC, McKenna BS. Swallow management in patients 

on an acute stroke pathway: quality is cost effective. Arch Phys Med Rehabil. 

1995;76(12):1130-1133. 

43. Hartman DE, Havlik P, Hutter RD, Schneller C. Screening for oropharyngeal 

dysphagia in acute stroke. Paper presented at: Annual Meeting of the American 

Speech-Language-Hearing Association; November 2001; New Orleans, LA. 

44. Hartman DE, Hutter RD, Schneller C, Havlik P. A screening procedure for 

oropharyngeal dysphagia in an acute stroke care pathway. Paper presented at: 

Annual Meeting of the Wisconsin Speech-Language-Hearing Association; 

February 2002; Milwaukee, WI. 

45. Langmore SE, Schatz K, Olsen N. Fiberoptic endoscopic examination of 

swallowing safety: a new procedure. Dysphagia. 1988;2(4):216-219. 

46. Nilsson H, Ekberg O, Olsson R, Hindfelt B. Dysphagia in stroke: a prospective 

study of quantitative aspects of swallowing in dysphagic patients. Dysphagia. 

1998;13(1):32-38. 

47. Young EC, Durant-Jones L. Developing a dysphagia program in an acute care 

hospital: a needs assessment. Dysphagia. 1990;5(3):159-165. 

48. Houston MS, Silverstein MD, Suman VJ. Community-acquired lower 

respiratory tract infection in the elderly: a community-based study of incidence 

and outcome. J Am Board Fam Pract. 1995;8(5):347-356. 

49. Katzan IL, Dawson NV, Thomas CL, Votruba ME, Cebul RD. The cost of 

pneumonia after acute stroke. Neurology. 2007;68(22):1938-1943. 

50. Langmore SE, Terpenning MS, Schork A, et al. Predictors of aspiration 

pneumonia: how important is dysphagia? Dysphagia. 1998;13(2):69-81. 


Authors: 

Alexander D. Wade, MD 

Department of Medical Education 


Foundation 

Frank J. Aberger, MD 

Department of Gastroenterology 



Frank J. Aberger, MD 

Mail Stop H05-007 




Telephone: (608) 775-2702 

Facsimile: (608) 775-6395 

email: fjaberge@gundluth.org 

A 

Colonoscopic Diagnosis of Appendicitis in a 

Patient with Ulcerative Colitis: 

A Case Report and Review of the Literature 

AbStrACt 

ppendicitis is a common cause of acute abdominal pain. 

Over the past 2 decades, a number of cases of appendicitis 

due to colonoscopy have been reported, 1-8 as well as cases of 

appendicitis diagnosed by colonoscopy, 9-18 often when other 

diagnostic modalities have failed to diagnose appendicitis or have 

suggested other diagnoses. Unusual presentations of appendicitis, 

particularly in patients with abdominal comorbidities, sometimes 

lead to colonoscopy, which is almost never used as a first line of 

investigation because of the risk of complications such as bleeding or 

perforation, and because noninvasive tests such as ultrasonography 

and computed tomography (CT) are highly sensitive. 19 

CASe report 

A 17-year-old boy came to our urgent care clinic with a 2-week 

complaint of increasing periumbilical and right lower quadrant 

abdominal pain and recent rectal bleeding. He was known to have 

ulcerative colitis, diagnosed in 2001 by colonoscopy with biopsies. 

He had been hospitalized in 2005 for ulcerative colitis, at which time 

CT scan documented a 6- to 7-mm appendix but no inflammation. 

He was compliant with his medication (sulfasalazine 1000 mg by 

mouth twice a day), and his ulcerative colitis had been quiescent. 

His temperature was normal, his white blood cell (WBC) count was 

14 000/µL (75.2% neutrophils, 26% of which were bands), and 

his erythrocyte sedimentation rate (ESR) (105 mm/h, reference 

range = 0-15) and C-reactive protein (CRP) concentration (13.1 

mg/L, reference range = 0.08-3.1) were elevated. Results of an 

abdominal CT scan were normal (Figure 1). 

The patient’s gastroenterologist was notified and scheduled 

the patient for flexible sigmoidoscopy the following day, which 

documented normal rectal mucosa, decreasing the likelihood 

that the patient’s symptoms were attributable to ulcerative colitis. 

With his pain, rectal bleeding, and normal flexible sigmoidoscopy 

findings, Crohn disease was believed to be a possible diagnosis. 

A 17-year-old boy with a known history of ulcerative colitis came to urgent care with a 2-week 

history of periumbilical pain and an episode of rectal bleeding. His evaluation included a 

computed tomographic (CT) scan, gastroenterology consultation, flexible sigmoidoscopy, CT 

enterography, abdominal ultrasonography, double-contrast upper gastrointestinal study, 

esophagogastroduodenoscopy, and, ultimately, a complete colonoscopic examination 

that revealed pus exuding from the appendiceal orifice. Repeat CT scan, with knowledge 

of the colonoscopy results, was interpreted as normal. Laparoscopic appendectomy was 

performed and confirmed the diagnosis of suppurative appendicitis. The patient had a benign 

postoperative course, and his symptoms have not recurred. We review the English-language 

literature regarding colonoscopically diagnosed appendicitis. To our knowledge, this is the first 

report in the literature of a case of colonoscopically diagnosed appendicitis in a patient with 

ulcerative colitis. 

CT enterography demonstrated normal small bowel caliber and 

wall thickness. 

The patient’s pain persisted. He was scheduled for 

ultrasonographic examination of the abdomen, as well as a doublecontrast 

upper gastrointestinal (GI) series. The gastroenterologist 

suggested a complete colonoscopic examination to look for possible 

Crohn disease if these studies failed to diagnose the etiology of 

the pain. 

Two days later, because of persisting pain, the patient underwent 

abdominal ultrasonography. A single loop of slightly thick-walled 

small bowel (4.7 mm) was identified as the only abnormality. This 

was followed by a double-contrast upper GI series and small bowel 

follow-through that revealed a normal esophagus and stomach, and 

no evidence of hiatal hernia or gastroesophageal reflux. Transit time 

through the small bowel into the colon was approximately 2 hours. 

The small bowel loops, including the terminal ileum, appeared 

normal. By this time, the patient’s leukocytosis had normalized, 

although his ESR (78 mm/hr) and CRP concentration (2.8 mg/L) 

remained elevated. 

Almost 2 weeks after his initial visit, the patient was again seen 

by his gastroenterologist. He remained symptomatic, complaining 

of diarrhea and abdominal pain. Laboratory studies revealed a 

WBC count within reference range, with neutrophilia (77.9%, 

reference range = 34%-67%) and a persistently elevated ESR 

(46 mm/hr). Mild anemia was also detected (hemoglobin 

concentration 11.9 g/dL). His CRP concentration was within 

normal range. Findings from an upper endoscopic examination 

were unremarkable. 

He underwent a colonoscopy, the results of which proved 

negative for colitis. The rectum appeared normal, indicating that 

the symptoms were not related to his ulcerative colitis. The cecum 

and the distal ileum were examined and appeared normal, thus 

reducing the likelihood of Crohn disease as the etiology for the 

symptoms. A small amount of mucin or pus was seen to emanate 


figure 1. Axial reformatted computed tomographic scan of the 

abdomen and pelvis performed on the day of presentation. The 

appendix appears normal, and no other pathology is present to 

explain the patient’s pain. 

from the appendiceal orifice (Figure 2). This was aspirated and sent 

to the laboratory, where analysis detected a large number of white 

blood cells, gram-negative rods, and gram-positive cocci. Results of 

the biopsy of the mucosa at the base of the appendix demonstrated 

mild nonspecific chronic and focal acute inflammation. 

The general surgeon on call was notified and observed the 

appendiceal findings at colonoscopy. The patient’s generally 

benign condition and the duration of the symptoms were 

taken into consideration, as was the interesting finding of freely 

flowing pus from the appendiceal orifice. The surgeon elected to 

observe the patient over the weekend and repeat a CT scan if his 

symptoms persisted. 

The patient remained symptomatic and underwent a repeat CT 

scan. The radiologist noted that this scan was similar in appearance 

to the patient’s previous studies and that the appendix was fluidfilled, 

although the walls were not thickened and there were no 

inflammatory changes. The remainder of the abdomen and pelvis 

appeared normal. 

The following day, the patient underwent laparoscopic 

appendectomy. Intraoperative findings included an enlarged, 

inflamed appendix and mild mesenteric scarring around the 

CoLonoSCopiC diAGnoSiS of AppendiCitiS 

terminal ileum. No signs of active Crohn disease or ulcerative colitis 

were identified. No signs of a Meckel diverticulum were present. 

Routine pathologic evaluation of the appendix later confirmed the 

diagnosis of acute suppurative appendicitis with benign lymphoid 

hyperplasia. The patient was discharged home after a brief and 

benign recovery. 

Just over a month later, the patient was seen in the emergency 

department for recurrent abdominal pain, which quickly resolved 

without intervention. His postoperative course had been benign 

until that point, with the exception of a knee joint effusion, possibly 

related to trauma from playing basketball. Since that episode 24 

months ago, the patient has reported no abdominal pain. 

To our knowledge, this is the first report of colonoscopic 

diagnosis of appendicitis in a patient with known ulcerative colitis 

and possible Crohn disease, which significantly confounded the 

evaluation. 

diSCuSSion 

In 1994, Said et al reported a case of atypical appendicitis that 

was diagnosed by colonoscopy. The patient had experienced 

abdominal pain and fever for 2 weeks and was hospitalized and 

treated nonoperatively. The results of laboratory studies were 

consistent with inflammation. Workup included ultrasonography 

and upper endoscopy. On the third day after admission, 

colonoscopy was performed, pus was aspirated from the 

appendiceal orifice, and the patient’s symptoms resolved within 

a day. Interval appendectomy was performed 5 months later and 

confirmed a previous diagnosis of appendicitis. 14 

figure 2. Colonoscopy demonstrates pus from the appendiceal os, 

slight inflammation near the base of the appendix. 


Since that report, other authors have reported colonoscopic 

diagnosis of appendicitis in a patient with symptoms suggestive of 

inflammatory bowel disease, 15 a patient with symptoms suggestive 

of cecal cancer, 15 a cystic fibrosis patient with chronic abdominal 

pain and possible inflammatory bowel disease, 17 and a patient with 

intermittent abdominal pain seen for polyp surveillance. 16 A case of 

appendiceal intussusception in chronic appendicitis diagnosed by 

colonoscopy was noted in a patient with symptoms of 8 months’ 

duration. 13 An asymptomatic 67-year-old patient undergoing 

surveillance colonoscopy had acute appendicitis, and emergency 

surgery was performed and confirmed the diagnosis. 12 

This case demonstrates a fact well known among experienced 

surgeons but often poorly understood by referring caregivers: 

Appendicitis is often difficult to diagnose, as alluded to at a 

personal injury attorney’s Website: 

Appendicitis is one of the most commonly misdiagnosed 

conditions because its symptoms can masquerade as many 

other types of problems. The most common symptoms of 

appendicitis are generalized or acute pain in the abdomen and 

nausea, vomiting and fever. When presented with symptoms 

of likely appendicitis, the standard of care requires doctors to 

operate immediately. If a physician fails to perform a proper 

physical examination, including manual manipulation of the 

abdomen, or impress upon a patient the importance of coming 

in immediately should symptoms continue or worsen, he or 

she could be liable for medical malpractice. 20 

The experienced medical practitioner knows that a proper 

physical examination, along with an adequate history, is only the 

beginning of an evaluation for possible appendicitis. Even with 

“manual manipulation of the abdomen,” appendicitis can go 

unrecognized. 

Our patient had undergone extensive evaluation by experienced 

physicians who took into account his history of ulcerative colitis 

and the chronic, indolent nature of the complaint. Crohn disease 

was strongly considered in the differential diagnosis. This case, 

however, is unusual in that the patient’s appendix was unruptured 

after 2 to 6 weeks of inflammation without antibiotic treatment. 

Before CT scan imaging was widely available to evaluate patients 

with abdominal pain, the rate of appendectomy performed in 

the absence of clear signs and symptoms of appendicitis was much 

higher. This higher rate was justified in order to prevent a missed 

appendicitis. This, however, carries unacceptably high risks of 

morbidity and mortality. The increased use of CT for the evaluation 

of abdominal pain, and thus the diagnosis of appendicitis, has 

reduced the likelihood of inappropriate appendectomy from 15% 

or 20% to closer to 2%. The sensitivity of CT scan for appendicitis 

is high— according to 1 study, 94% (95% CI, 92%-97%) in 

children and 95% (95% CI, 94%-96%) in adults. 19 Unfortunately, 

our patient was among the 5% of patients who have false-negative 

CT findings. According to 1 study, 21 the specificity of CT scan 

for possible appendicitis is 88.3%, meaning that approximately 

8 in 9 patients without appendicitis will have a CT scan negative 

for appendicitis. 

It is impossible to determine unequivocally the true etiology of 

this patient’s early abdominal pain. Interestingly, the appendicitis 

occurred coincidentally during the workup for the as-yet- 

figure 3. Axial reformatted computed tomographic scan obtained 

after the colonoscopically diagnosed appendicitis continues to 

demonstrate a paucity of findings indicative of inflammation or 

infection of the appendix. 

unexplained chronic abdominal pain. Most surgeons would be 

reluctant to accept acute appendicitis as the explanation for the 

6 weeks of pain, knowing that the natural history of untreated 

appendicitis does not commonly involve such a benign course. It 

is possible that the diagnosis of acute appendicitis was ultimately 

incorrect—that a diagnosis of recurrent or chronic appendicitis 

was more accurate. Although this could explain the diagnostic 

conundrum, it is not universally accepted that chronic or recurrent 

appendicitis even exists. Conversely, since his appendectomy, this 

patient has had only 1 episode of abdominal pain, which quickly 

resolved, suggesting that the appendix was directly related to the 

symptoms. 

In summary, the diagnosis of appendicitis is rarely made 

by colonoscopy. This is the first case we know of in which a 

colonoscopic diagnosis of appendicitis was made in a patient with 

ulcerative colitis. We do not, however, suggest that colonoscopy 

be used as the tool for diagnosis in patients with suspected 

appendicitis. For our patient, who had no clear diagnosis for 

abdominal pain and a very low suspicion for appendicitis, the 

endoscopic findings are of interest and should be considered by 

other clinicians who encounter patients with similar unexplained 

abdominal discomfort. 


eferenCeS 

1. Houghton A, Aston N. Appendicitis complicating colonoscopy. Gastrointest 

Endosc. 1988;34:489. 

2. Vender R, Larson J, Garcia J, Topazian M, Ephraim P. Appendicitis as a 

complication of colonoscopy. Gastrointest Endosc. 1995;41:514-516. 

3. Hirata K, Noguchi J, Yoshikawa I, et al. Acute appendicitis immediately after 

colonoscopy. Am J Gastroenterol. 1996;91:2239-2240. 

4. Lipton S, Estrin J. Postcolonoscopy appendicitis: a case report. J Clin Gastroenterol. 

1999;28:255-256. 

5. Srivastava V, Pink J, Swarnkar K, Feroz A, Stephenson BM. Colonoscopically 

induced appendicitis. Colorectal Dis. 2004;6:124-125. 

6. Izzedine H, Thauvin H, Maisel A, Bourry E, Deschamps A. Post-colonoscopy 

appendicitis: case report and review of the literature. Am J Gastroenterol. 

2005;100:2815-2817. 

7. Rosen MJ, Sands BE. Acute appendicitis following colonoscopy. J Clin 

Gastroenterol. 2005;39:78. 

8. Volchok J, Cohn M. Rare complications following colonoscopy: case reports of 

splenic rupture and appendicitis. JSLS. 2006;10:114-116. 

9. Petro M, Minocha A. Asymptomatic early acute appendicitis initiated and 

diagnosed during colonoscopy: a case report. World J Gastroenterol. 2005;11: 

5398-5400. 

10. Chang HS, Yang SK, Myung SJ, et al. The role of colonoscopy in the diagnosis 

of appendicitis in patients with atypical presentations. Gastrointest Endosc. 

2002;56:343-348. 

11. Johnson TR, DeCosse JJ. Colonoscopic diagnosis of grumbling appendicitis. 

Lancet. 1998;351:495. 

CoLonoSCopiC diAGnoSiS of AppendiCitiS 

12. Uehara A, Ohta H, Nagamine M, Kawashima T, Kuribayashi H, KohgoY. 

Colonoscopic diagnosis of asymptomatic acute appendicitis. Am J Gastroenterol. 

2000;95:3010-3011. 

13. Nyam DC, Davendran K, Seow-Choen F. An endoscopic diagnosis of appendicular 

intussusception in chronic appendicitis. Singapore Med J. 1997;38:131. 

14. Said M, Ledochowski M, Dietze O, Simader H. Colonoscopic diagnosis and 

treatment of acute appendicitis. Eur J Gastroenterol Hepatol. 1995;7:569-571. 

15. Chen YY, Soon MS, Yen HH. Images of interest. Gastrointestinal: colonoscopic 

features of acute appendicitis. J Gastroenterol Hepatol. 2005;20:1940. 

16. Courtney ED, Melville D, Leicester RJ. Chronic appendicitis diagnosed 

incidentally by colonoscopy. Hosp Med. 2003;64:434-435. 

17. Theilmann L, Bachmann K, Kuhl PG. An unusual presentation of chronic 

appendicitis. Endoscopy. 2003;35:377. 

18. Johnson EA, Spier BJ, Mozena MG, Pfau PR. Colonoscopic clues cinch the 

diagnosis. Am J Med. 2007;120:942-944. 

19. Doria AS, Moineddin R, Kellenberger CJ, et al. US or CT for diagnosis of 

appendicitis in children and adults? A meta-analysis. Radiology. 2006;241: 

83-94. 

20. Digestive Disorders & Injuries. Illinois Personal Injury Legal Resource Web site. 

//www.il-injury.com/html/digestive-disorders-injuries.html. Accessed March 24, 

2008. 

21. Flum DR, McClure TD, Morris A, Koepsell T. Misdiagnosis of appendicitis and 

the use of diagnostic imaging. J Am Coll Surg. 2005;201:933-939. 

River Fog at Dawn Daniel Schraith 

Pathology 


Authors: 

Abhishek Tandon, MD 



Foundation 

Steven B. Pearson, MD 








Mail Stop C02-007 




Telephone: (608) 775-6882 

Facsimile: (608) 775-5542 

email: tjkowals@gundluth.org 

W 

Intracranial Mycotic Aneurysm Due to 

Streptococcus bovis Endocarditis 

AbStrACt 

illiam Osler first used the term mycotic aneurysm in his 

1885 Gulstonian Lecture series1 to refer to an aneurysm 

resulting from an infectious process of the arterial wall, although 

a more accurate term might have been endovascular infection or 

infective vasculitis, because mycotic aneurysms are not due to 

a fungal organism. Intracranial mycotic aneurysms (ICMAs) 

complicate about 2% to 3% of infective endocarditis (IE) cases, 

although as many as 15% to 29% of patients with IE have 

neurologic symptoms. 2-4 Of all intracerebral aneurysms, only 2% 

to 6% have an infectious etiology. Signs and symptoms of mycotic 

aneurysms may be misleading during the early stages, resulting in 

misdiagnosis and delays in treatment. 5 Early diagnosis of ICMA is 

the cornerstone of effective treatment. 

CASe report 

A 63-year-old man had a 2-month history of headaches, 

malaise, decreased appetite, night sweats, low-grade intermittent 

fevers, and unintentional 10-pound weight loss. His headaches 

were spasmodic and intense, and would partially remit with 

acetaminophen. He reported no history of trauma, new neurological 

deficits, visual changes, sensory or visual aura, radiation to the 

neck, or positional variation. He denied use of tobacco, alcohol, 

and illicit drugs. 

The patient had an extensive medical history, including 

a remote history of hemorrhagic stroke, subacute bacterial 

endocarditis, sigmoid colon cancer with successful resection, and 

ischemic stroke. Post-stroke deficits included moderate weakness 

in his left arm and left leg, and moderate vocal cord impairment. 

Family history was significant for stomach cancer. 

The patient was in no acute distress. His vital signs were: 

temperature, 36.6°C; blood pressure, 140/100 mm Hg; respiratory 

Mycotic aneurysm usually appears as a painful, pulsatile, and often enlarging mass in a patient 

with associated systemic features of infection. This condition is usually fatal without treatment. 

We report the case of a patient with infective endocarditis who exhibited neurological signs 

and symptoms and was subsequently found to have multiple intracranial mycotic aneurysms. 

We also review the recent literature on the diagnosis and treatment of intracranial mycotic 

aneurysms. 

rate, 18 breaths/min; heart rate, 76 beats/min; and oxygen 

saturation, 100% on room air. He had a 2/6 systolic ejection 

murmur over the mitral area on cardiac examination. Pulses were 

equal bilaterally, and no pedal edema was noted. He had residual 

left-sided weakness and decreased sensation in his left arm and 

left leg. No meningeal or cerebellar signs were noted, and findings 

from examination of the cranial nerve were normal. 

Laboratory studies revealed hematuria, an elevated erythrocyte 

sedimentation rate (49 mm/hr), and an elevated white blood cell 

count (15 400/µL). Computed tomographic (CT) scan of the head 

revealed an acute right hemispheric hemorrhagic stroke with right 

basil ganglion hemorrhage. Computed tomographic angiography 

(CTA) was recommended by neurosurgery to evaluate for vasculitis 

or arteriovenous malformation, and revealed multiple cerebral 

aneurysms. When compared with old imaging studies, CTA 

showed a new, large aneurysm that, based upon its appearance, was 

believed to be mycotic. A new, lobulated, irregular aneurysm of the 

distal right internal carotid artery, a left internal maxillary artery 

aneurysm, and a left external carotid pseudoaneurysm—versus 

mycotic aneurysm—were noted. Blood cultures subsequently grew 

Streptococcus bovis in all bottles. Echocardiogram demonstrated 

bileaflet mitral valve prolapse with posterior leaflet rupture and 

vegetations on the mitral valve consistent with endocarditis. 

Neurosurgical consultation was obtained, and nonoperative 

management of the aneurysms was recommended due to their 

location and number. Thus, with this recommendation and 

the infectious nature of the disease, ceftriaxone was initiated. 

Unfortunately, the patient developed worsening hemodynamic 

parameters, specifically hypotension, and was transferred to the 

intensive care unit. Despite vigorous medical management, over the 

next several days he experienced 2 grand mal seizures and became 

unresponsive. A repeat CT scan of the head demonstrated extensive, 


intrACrAniAL MyCotiC AneurySM due to StreptococcuS boviS endoCArditiS 

Large lobulated mycotic aneurysm arising from the internal carotid 

artery is indicated by the white arrow. 

new, right basal ganglia and right frontal lobe intraparenchymal 

hemorrhages consistent with rupture of the mycotic aneurysm. 

The patient’s family opted for comfort care measures, and the 

patient died shortly thereafter. An autopsy was not performed. 

diSCuSSion 

Mycotic aneurysms can be divided into 4 types: (1) embolic, 

secondary to bacterial endocarditis (embolomycotic aneurysms); 

(2) extravascular, secondary to extension of contiguous infection 

from a septic focus neighboring an artery; (3) cryptogenic or primary 

bacteremic; and (4) direct contamination following arterial wall 

trauma, which may be postprocedural. 6 Aneurysms can occur in 

the cerebral circulation, usually at points of vessel bifurcation, or 

in the systemic circulation. 7 In IE-associated mycotic aneurysms, 

septic emboli are released from infected cardiac vegetations. These 

tiny septic emboli occlude the vasa vasorum or entire arterial lumen, 

which leads to damage to the muscular layer of the vessel. ICMA 

tend to occur in the more distal portions of the middle cerebral 

artery, near the surface of the brain, involving the secondary and 

tertiary branches. In contrast, berry aneurysms occur at proximal 

branch points in or near the circle of Willis. 4 The outcome depends 

upon the anatomical location of the embolus, the causative 

bacteria and associated virulence of the organism, underlying host 

defenses, and appropriate antibiotic therapy. Mycotic aneurysms 

can decrease, increase, remain the same in size, or even disappear 

during treatment for endocarditis. 8 

Patients with bacterial intracranial aneurysms have 

variable neurological symptoms, and early symptoms of 

infection may be subtle. In ICMA, patients may have 

symptoms ranging from nonspecific, general complaints, 

including fever or headache, to neurological deficits or 

catastrophic intracranial hemorrhage. Laboratory results are 

typically suggestive of an underlying inflammatory process and 

may include leukocytosis, elevated erythrocyte sedimentation 

rate and/or C-reactive protein concentration, and anemia. Blood 

cultures are almost universally positive for microbial growth. 

Computed tomographic angiography, magnetic resonance 

angiography (MRA), and catheter angiography are used to study 

the size, location, and morphology of intracranial aneurysms. 

Aneurysms 5 mm in diameter or larger can be detected by CTA and 

MRA. Smaller aneurysms are detected less reliably or detected in 

retrospect after comparison with cerebral angiography. 9-11 Cerebral 

angiography is the gold standard and is often used in preoperative 

assessment and in determining prognosis 12 ; however, it is not 

routinely recommended due to risk of complications associated 

with it. The size of the aneurysm during therapy can be safely and 

accurately monitored using CTA and MRA. In our patient, CTA 

was selected as the diagnostic tool. 

Treatment of ICMA is controversial, in that the appropriate 

patients for surgical intervention, need for follow-up imaging, 

and most efficacious treatment are not well delineated in the 

medical literature. The appropriate treatment always involves 

medical and sometimes surgical therapies. 13 Moreover, there is no 

single uniformly accepted approach to the treatment of ICMA 

in IE. The aim of therapy is to cure the underlying infection 

and avoid complications from the aneurysm. Some lesions will 

resolve with antibiotic therapy alone. The decision to pursue 

surgical management is complex and involves a number of factors, 

including the number, site, and anatomy of the aneurysm(s) and 

the comorbidities of the patient. Treatment options for unruptured 

aneurysms include observation or surgical approaches, such as 

craniotomy and clipping or endovascular coiling. 14,15 The surgical 

choice of treatment for ICMA is controversial, patient-specific, and 

is generally beyond the scope of this article. Four- to 6-week courses 

of pathogen-specific intravenous antibiotic are recommended. 

In addition, medical therapy should include control of 

hypertension and seizures. Therapy should be monitored with 

serial CTA or MRA, and surgical intervention is generally 

recommended for enlarging aneurysms in accessible locations. 

Ruptured aneurysms are treated emergently with surgery to 

prevent rebleeding if possible. 

Staphylococcus aureus (~30%), Salmonella species (~15%), 

and less commonly viridans group streptococci are some of 

the causitive organisms of mycotic aneurysms in the 

postantibiotic era. 16 Recent reports suggest Streptococcus 

pneumoniae, including penicillin-resistant strains, are re-emerging 

as a cause of mycotic aneurysms. 17 Our patient was infected 

with Streptococcus bovis, a gram-positive cocci classified as group 

D streptococci. Endocarditis is the most significant clinical 

infection associated with S bovis, but bacteremia from enteric 

origins also occurs. S bovis accounts for 2% to 6% of streptococcal 

bloodstream isolates from hospitalized patients and for 2.4% to 

25% of organisms associated with IE. 18-22 S bovis is a rare cause of 

ICMA, however. Interestingly, S bovis endocarditis or bacteremia 

is associated with concomitant undiagnosed gastrointestinal (GI) 

tumors in up to 56 % of patients. 23 GI diseases associated with S 

bovis endocarditis include colonic cancers, gastric ulcers, gastric 


cancer, duodenal ulcers, inflammatory bowel disease, colonic 

diverticula, angiodysplasia, and liver cirrhosis. 18,24-26 Thus, any 

patient with S bovis bacteremia should undergo screening for occult 

GI malignancy. Although our patient died before such screening 

could be completed, he did have a family history of gastric cancer 

and a personal history of colon cancer. 

ConCLuSion 

S bovis bacteremia should prompt consideration of IE and 

occult GI malignancy. Our patient had multiple ICMAs secondary 

to S bovis, which ultimately led to his death. This case illustrates 

3 key take-home points for clinicians: (1) Subacute bacterial 

endocarditis often has vague, nonspecific symptoms that do 

not overtly suggest infection, but blood cultures are almost 

always diagnostic; (2) If a patient with IE has neurological 

complications or symptoms, ICMA should be considered; 

and (3) Patients with S bovis bacteremia should be screened for 

GI malignancy. 

referenCeS 

1. Osler W. Malignant endocarditis (Gulstonian Lecture I). Lancet. 1885;1:415-418. 

2. Chan FY, Crawford ES, Coselli JS, Safi HJ, Williams TW Jr. In situ prosthetic 

graft replacement for mycotic aneurysm of the aorta. Ann Thorac Surg. 1989;47(2): 

193-203. 

3. Bohmfalk GL, Story JL, Wissinger JP, Brown WE Jr. Bacterial intracranial 

aneurysm. J Neurosurg. 1978;48(3):369-382. 

4. Jones HR Jr, Siekert RG. Neurological manifestations of infective endocarditis. 

Review of clinical and therapeutic challenges. Brain. 1989;112(Pt 5):1295-1213. 

5. Leo PJ, Pearl J, Tsang W. Mycotic aneurysm: a diagnostic challenge. Am J Emerg 

Med. 1996;14(1):70-73. 

6. Cloft HJ, Kallmes DF, Jensen ME, Lanzino G, Dion JE. Endovascular treatment 

of ruptured, peripheral cerebral aneurysms: parent artery occlusion with short 

guglielmi detachable coils. AJNR Am J Neuroradiol. 1999;20(2):308-310. 

7. Shaikholeslami R, Tomlinson CW, Teoh KH, Molot MJ, Duke RJ. 

Mycotic aneurysm complicating staphylococcal endocarditis. Can J Cardiol. 

1999;15(2):217-222. 

8. Ziment I. Nervous system complications in bacterial endocarditis. Am J Med. 

1969;47(4):593-607. 

9. Walsh DW, Ho VB, Haggerty MF. Mycotic aneurysm of the aorta: MRI and MRA 

features. J Magn Reson Imaging. 1997;7(2):312-315. 

10. Huston J 3rd, Nichols DA, Luetmer PH, et al. Blinded prospective evaluation of 

sensitivity of MR angiography to known intracranial aneurysms: importance of 

aneurysm size. AJNR Am J Neuroradiol. 1994;15(9):1607-1614. 

11. Schwartz RB, Tice HM, Hooten SM, Hsu L, Stieg PE. Evaluation of cerebral 

aneurysms with helical CT: correlation with conventional angiography and MR 

angiography. Radiology. 1994;192(3):717-722. 

12. Benjamin ME, Cohn EJ Jr, Purtill WA, Hanna DJ, Lilly MP, Flinn WR. Arterial 

reconstruction with deep leg veins for the treatment of mycotic aneurysms. J Vasc 

Surg. 1999;30(6):1004-1015. 

13. Johnston SC, Wilson CB, Halbach VV, et al. Endovascular and surgical 

treatment of unruptured cerebral aneurysms: comparison of risks. Ann Neurol. 

2000;48(1):11-19. 

14. Bederson JB, Awad IA, Wiebers DO, et al. Recommendations for the management 

of patients with unruptured intracranial aneurysms: a statement for healthcare 

professionals from the Stroke Council of the American Heart Association. Stroke. 

2000;31(11):2742-2750. 

15. Johnston SC, Zhao S, Dudley RA, Berman MF, Gress DR. Treatment of 

unruptured cerebral aneurysms in California. Stroke. 2001;32(3):597-605. 

16. Brown SL, Busuttil RW, Baker JD, Machleder HI, Moore WS, Barker WF. 

Bacteriologic and surgical determinants of survival in patients with mycotic 

aneurysms. J Vasc Surg. 1984;1(4):541-547. 

17. Brouwer RE, van Bockel JH, van Dissel JT. Streptococcus pneumoniae, an emerging 

pathogen in mycotic aneurysms? Neth J Med. 1998;52(1):16-21. 

18. Ballet M, Gevigney G, Gare JP, Delahaye F, Etienne J, Delahaye JP. Infective 

endocarditis due to Streptococcus bovis. A report of 53 cases. Eur Heart J. 

1995;16(12):1975-1980. 

19. Murray HW, Roberts RB. Streptococcus bovis bacteremia and underlying 

gastrointestinal disease. Arch Intern Med. 1978;138(7):1097-1099. 

20. Selton-Suty C, Hoen B, Delahaye F, et al. Comparison of infective endocarditis 

in patients with and without previously recognized heart disease. Am J Cardiol. 

1996;77(12):1134-1137. 

21. Cabell CH, Jollis JG, Peterson GE, et al. Changing patient characteristics and the 

effect on mortality in endocarditis. Arch Intern Med. 2002;162(1):90-94. 

22. Roberts RB. Streptococcal endocarditis: the viridans and beta hemolytic 

streptococci. In: Kaye D, ed. Infective Endocarditis. 2nd ed. New York: Raven 

Press; 1992:191. 

23. Hoen B, Briancon S, Delahaye F, et al. Tumors of the colon increase the risk of 

developing Streptococcus bovis endocarditis: case-control study. Clin Infect Dis. 

1994;19(2):361-362. 

24. Zarkin BA, Lillemoe KD, Cameron JL, Effron PN, Magnuson TH, Pitt HA. The 

triad of Streptococcus bovis bacteremia, colonic pathology, and liver disease. Ann 

Surg. 1990;211(6):786-791. 

25. Kupferwasser I, Darius H, Muller AM, et al. Clinical and morphological 

characteristics in Streptococcus bovis endocarditis: a comparison with other 

causative microorganisms in 177 cases. Heart. 1998;80(3):276-280. 

26. Friedrich IA, Wormser GP, Gottfried EB. The association of remote Streptococcus 

bovis bacteremia with colonic neoplasia. Am J Gastroenterol. 1982;77(2):82-84. 


Authors: 

Robert E. Ryan, MA, ATC 

Troy E. Ward, MA, ATC 

Steven R. Murray, DA 

Mesa State College 

Grand Junction, Colorado 

Mitchell T. Copeland, DO 

Western Orthopedics and 

Sports Medicine 

Grand Junction, Colorado 


FACSM 


La Crosse, Wisconsin 

Robert W. Pettitt, PhD, ATC 

Minnesota State University –Mankato 

Mankato, Minnesota 



FACSM 

149 Mitchell Hall 




Telephone: (608) 785-8181 

email: udermann.bria@uwlax.edu 

I 

n a d 175, the ancient Greek physician Galen used a 

resorbable gut suture—the first recorded use of a 

bioabsorbable implant. 1 In the mid 1960s, bioabsorbable 

technology was introduced for clinical applications, since which 

time its use has increased dramatically. 2 Today some 40 different 

bioabsorbable polymers are being used for surgical procedures. 1,3 

Advantages have been noted for the use of bioabsorbable 

implants in orthopedics. First, they are readily absorbed by the 

body, thus reducing the need for surgical revisions and the overall 

cost of treatment. 4 Second, they prevent radiographic obscurities 

typically found with metallic implants. 4 Third, in that they soften 

over time, bioabsorbable implants provide an incremental transfer 

of stress to the affected bone, thus providing a load-sharing effect 

that enhances healing. 1 

While they have notable advantages, bioabsorbable implants 

have drawbacks, as well. Compared with their metallic counterparts, 

bioabsorbable implants are weaker and less stiff, have limited shelflife, 

and are initially more costly. 1 They also can cause exaggerated 

inflammatory reactions, such as synovitis, osteolysis, and, more 

rarely, giant-cell reactions. 5,6 

We report a case of a foreign-body giant-cell reaction to 

a bioabsorbable implant. This case exemplifies an iatrogenic 

etiology that should be considered when treating patients who are 

unresponsive to rehabilitative exercise for surgical repair. 


AbStrACt 

A 51-year-old woman had shoulder pain and dysfunction 14 months following the surgical 

repair of her supraspinatus muscle via a bioabsorbable implant. Diagnostic testing revealed 

a giant-cell reaction at the location of the implant. The patient underwent a second surgery 

to burr, irrigate, and fill the lytic lesion that resulted from the giant-cell reaction, and the 

supraspinatus muscle was sutured to the greater tuberosity of the humerus. The patient 

completed a standard rehabilitation protocol for 8 weeks, and at 6 months she had no further 

complications with normal daily activities. 

CASe report 

A 51-year-old woman had pain in her right shoulder. 

Examination of the shoulder revealed an impingement syndrome, 

acromioclavicular arthrosis, and a tear in the supraspinatus 

muscle. Initial conservative treatment with range-of-motion and 

strengthening exercises and subacromial injections of steroids 

(ie, 3 mg of betamethasone and 6 mg of 0.25% bupivicaine) was 

ineffective. The patient was counseled and scheduled for surgery. 

Surgery included a 2-step acromioplasty and an 8-mm resection 

of the distal clavicle. The supraspinatus muscle was repaired using 

a bioabsorbable implant (Arthrex Bio-Corkscrew), with 4 sutures 

placed in a figure-of-8 fashion through the greater tuberosity of 

the of the humerus. The patient progressed without complications 

for 12 weeks until marked pain returned to the shoulder area. 

Conservative treatment, including modest range-of-motion and 

strengthening exercises, ensued resulting in a return to normal 

daily activities, Fourteen months after surgery, a palpable lesion 

deficit was found in the area of the of the implant. Radiographs 

revealed a 4- to 6-mm circular lytic lesion consistent with the 

site of placement of the bioabsorbable implant in the greater 

tuberosity (Figure 1). Given the findings and the patient’s course 

postoperatively, she was scheduled for shoulder arthroscopy with 

possible supraspinatus muscle repair and placement of a bone graft 

in the area of erosion. 


figure 1. Radiograph depicting a 4- to 6-mm lytic lesion consistent 

with the placement of the bioabsorbable implant. 

During the second surgery, no sign of a re-tear of the 

supraspinatus muscle was present. Pathological findings suggested 

that the lytic lesion was caused by a giant-cell reaction to the 

bioabsorbable implant used in the first repair of the supraspinatus 

muscle (Figure 2). The lesion was burred, irrigated, and filled 

with 0.75 cc of Allomatrix. To avoid any further reaction, the 

supraspinatus muscle was sutured using #2 FiberWire through 

holes in the greater tuberosity. 

Two weeks after surgery the patient had less pain and was 

improving with passive range-of-motion exercises. Four weeks 

after surgery she was instructed to begin active-assisted exercise. 

Eight weeks after surgery, the patient was neurovascularly stable, 

had improved range of motion, and had no signs of impingement. 

The patient was instructed to continue range-of-motion exercises 

for another 4 weeks and at 3 months to begin strengthening 

exercises. At 6 months the patient had no further complaints 

regarding shoulder discomfort on the right side and returned to 

normal daily activities. 

diSCuSSion 

Our case is an example of an exaggerated inflammatory 

reaction to a bioabsorbable implant, stressing the need for both 

awareness and precaution when using implants for pain. Our 

patient developed a giant-cell reaction to a bioabsorbable screw 

that was used as an anchor for the sutures in a supraspinatus 

muscle repair. A giant-cell reaction is manifested by individual 

macrophages adhering to form a large, multinucleated cell that 

engulfs the foreign body. The presence of giant cells interferes 

with healing at the surgical site of the implant and can lead to a 

breakdown of healthy tissue in the surrounding area. 7 As in our 

case, this often necessitates a second surgery to correct the defect. 

The initial phase of implant degradation is hydrolysis. As the 

implant absorbs water, it begins to degrade. The more porous 

the implant, the more quickly it absorbs water. 8 Any remaining 

fragments are removed by normal phagocytic response; however, 

the rapid degradation of these implants, 4 coupled with excessive 

stress being placed on the implant, 9 has been postulated to be the 

cause of marked foreign-body reaction, as occurred in our patient. 

Various factors, including the metabolic activity of the living cells, 

figure 2. Multinucleated giant-cell reaction (hematoxalin and eosin 

stain under 25X magnification with partial polarized light showing 

biorefringent particulate material). 


type of implant, method of sterilization, site of implementation, 

and the stress placed on the implant, 1,10 affect the degradation of 

biodegradeable implants, often making it difficult to pinpoint 

the cause of the an exaggerated inflammatory response. Risk 

factors purported to be responsible for adverse tissue responses 

are “the presence of quinine dye, an implant with a large surface 

area such as a screw, and implant sites with low vascularity.” 11 

Our patient had 2 of the aforementioned risk factors: a screw 

was employed during the surgery, and repeated physical stress 

placed on the anchor-bone interface through the superspinatus 

tendon, affirming that these risk factors are potentially valid. 

Although bioabsorbable implants are absorbed readily by the 

body, thus eliminating the need for a follow-up surgery. They 

prevent radiographic obscurities, and they provide incremental 

stress transfer as they degrade, which promotes healing. However, 

clinicians need to be aware of the drawbacks of bioabsorbable 

implants. Compared with metallic implants, they are less strong 

and less stiff, have a limited shelf-life, cost more initially, and 

have a tendency for an exaggerated inflammatory reaction. The 

advantages do, however, appear to outweigh the disadvantages. 10 

As shown in the case reported here, the risk of an exaggerated 

inflammatory response to bioabsorbable implants increases when 

the implant has a large surface area, such as a screw, and when it is 

subjected to repeated stress. These risk factors should be considered 

in the development of treatment options. 

GiAnt CeLL reACtion to A bioAbSorbAbLe iMpLAnt 

referenCeS 

1. Bollom T, Meister K. Surgical principles: biodegradable materials in sports 

medicine. In: DeLee JC, Drez DJ, Miller MD, eds. DeLee & Drez’s Orthopaedic 

Sports Medicine: Principles and Practice. 2nd ed. Philadelphia, PA: Saunders; 

2003. 

2. Kulkarni RK, Pani KC, Neuman C, Leonard F. Polylactic acid for surgical implants. 

Arch Surg. 1966;93(5):839-843. 

3. Claes LE. Mechanical characterization of biodegradable implants. Clin Mater. 

1992;10(1-2):41-46. 

4. Ciccone WJ,2nd, Motz C, Bentley C, Tasto JP. Bioabsorbable implants in 

orthopaedics: new developments and clinical applications. J Am Acad Orthop Surg. 

2001;9(5):280-288. 

5. Simon JA, Di Cesare PE, Koval KJ. Bioresorbable materials in orthopaedics. Bull 

Hosp Jt Dis. 2000;59(4):232-240. 

6. Weiler A, Hoffmann RF, Stahelin AC, Helling HJ, Sudkamp NP. Biodegradable 

implants in sports medicine: the biological base. Arthroscopy. 2000;16(3): 

305-321. 

7. Anderson JM, Rodriguez A, Chang DT. Foreign body reaction to biomaterials. 

Semin Immunol. 2008;20(2):86-100. 

8. Athanasiou KA, Schmitz JP, Agrawal CM. The effects of porosity on in vitro 

degradation of polylactic acid-polyglycolic acid implants used in repair of articular 

cartilage. Tissue Eng. 1998;4(1):53-63. 

9. Glueck D, Wilson TC, Johnson DL. Extensive osteolysis after rotator cuff repair 

with a bioabsorbable suture anchor: a case report. Am J Sports Med. 2005;33(5): 

742-744. 

10. Ambrose CG, Clanton TO. Bioabsorbable implants: review of clinical experience 

in orthopedic surgery. Ann Biomed Eng. 2004;32(1):171-177. 

11. Bostman OM, Pihlajamaki HK. Adverse tissue reactions to bioabsorbable fixation 

devices. Clin Orthop Relat Res. 2000;(371)(371):216-227. 

Graceful John Larson 

Optometry 


Authors: 

Meghana Raghavendra, MB, BS 



Foundation 

Dr. Raghevendra now practices with 

IU Medical Group, Indianapolis, 

Indiana 

William A. Agger, MD 





William A. Agger, MD 

Mail Stop C04-007 




Telephone: (608) 775-2140 

Facsimile: (608) 775-5542 

email: waagger@gundluth.org 

Post–Cesarean Delivery Septic Ovarian Vein 

Thrombosis 

AbStrACt 

CASe 

A 32-year-old pregnant woman at 40 weeks gestation 

underwent a cesarean delivery due to failure to advance after 

prolonged rupture of membranes followed by chorioamnionitis. 

She was discharged 3 days after delivery but required readmission 

8 days later for fever, left lower abdominal pain, and fullness in her 

left lower abdomen. Her white blood cell count was 22.9 x 10 9 /L 

with 24% bands, and her erythrocyte sedimentation rate was 

96 mm/h. Urinalysis results were within normal limits. Cultures of 

blood drawn on admission remained negative for growth. 

Transvaginal ultrasonography revealed a mixed echogenic 

mass in the left adnexal area measuring 5.0 x 7.0 x 5.0 cm that 

appeared to be a mixture of small abscesses and phlegmon. Despite 

48 hours of intravenous treatment with a broad-spectrum antibiotic 

(ertapenam), she continued to have fevers as high as 39°C. 

A computed tomographic (CT) scan of abdomen and pelvis with 

contrast was obtained and revealed left ovarian vein thrombosis 

and a complex tubo-ovarian abscess (Figures 1 and 2). Enoxaparin 

was begun, and fever resolution occurred within 24 hours. The 

patient was discharged home on oral amoxicillin/clavulanate and 

warfarin. Her oral anticoagulation was stopped at 5 days due to 

uterine bleeding, and she has remained well for the last 6 months. 

diSCuSSion 

Postpartum ovarian vein thrombosis (OVT) occurs after 

0.003% to 0.18% of deliveries, 1,2 after 0.005% of febrile abortions, 3 

and occasionally after other inflammatory pelvic pathologies. 

Many consider OVT to be an extension of a more controversial 

diagnosis, pelvic thrombophlebitis. 2,4,5 OVT should be considered 

in women who have lower abdominal pain, lower quadrant mass, 

fever, and/or neutrophilia after childbirth or after pelvic surgery. 1,6 

Postpartum women with OVT usually develop fever within 48 to 

Eleven days after cesarean delivery, a 32-year-old woman was readmitted to hospital 

with fever and pain in her lower left abdomen. Her white blood cell count and 

erythrocyte sedimentation rate were elevated. Transvaginal ultrasonography revealed 

a mixed echogenic mass in the left adnexal area that appeared to be a mixture of 

small abscesses and phlegmon. She was started on an intravenous broad-spectrum 

antibiotic, but 48 hours later, her fever persisted. A computed tomographic scan 

of abdomen and pelvis with contrast was obtained and revealed left ovarian vein 

thrombosis and a complex tubo-ovarian abscess. Enoxaparin was begun, and the 

patient’s fever resolved within 24 hours. Postpartum pelvic infection with ovarian 

thrombosis and its therapy are reviewed. 

96 hours after delivery. 1,6 Lower abdominal pain and/or a cord-like, 

tender, lower abdominal fullness may be found in 50% to 67% 

of patients. 1,6 Nausea, ileus, and other gastrointestinal complaints 

may also occur. The differential diagnosis includes appendicitis, 

pyelonephritis, tubo-ovarian abscess, and endometritis with or 

without retained products of conception. 

figure 1. Computed tomographic scan with contrast illustrating left 

ovarian vein thrombus (white arrow). 


figure 2. Computed tomographic scan with contrast illustrating 

complex tubo-ovarian abscess (white arrow). 

While our patient had left-sided OVT, a right-sided 

predominance has been reported, probably attributable to the 

immediate postpartum retrograde flow of venous blood down 

the left ovarian vein, through the pelvis, and up the right ovarian 

vein. 6,7 With thrombosis, the clotted vein can be imaged along the 

psoas muscle to the vena cava on the right or left renal vein, as in 

our case. The clot may extend into the vena cava, and pulmonary 

embolus may ensue. Imaging studies reveal sensitivities of 100%, 

92%, and 50% for CT scans, magnetic resonance imaging scans, 

and ultrasonograms, respectively. 8 

Blood cultures usually remain negative for pathogens, with 

positive cultures seen in only about 3% of patients.1 The bacteria 

most commonly associated with OVT reflect the vaginal origin of 

these infections: enteric gram-negative rods, including Escherichia 

coli, Enterobacter and Klebsiella species, along with microaerophilic 

streptococci, and anaerobic bacteria such as Peptostreptococcus, 

Bacteroides, and Prevotella species. 1,3 Antimicrobial treatment of 

OVT should be directed against these gastrointestinal/genitourinary 

facultative and anaerobic flora. 

A genetic hypercoaguable state in has been found in 50% 

of women with OVT. 9 Our patient had no family history of 

thromboembolic disease, thus genetic causes for a hypercoagulable 

state were not evaluated. Literature approximately 40 years ago 

indicated that anticoagulation had replaced the surgical ligation of 

the vena cava or ovarian veins to prevent pulmonary emboli. 3 

More recent literature has shown that resolution of fever and 

length of hospitalization were not significantly different in women 

treated with antibiotics alone versus those treated with antibiotics 

and anticoagulation, probably due to a spectrum bias of earlier 

detection and, therefore, milder cases. 10 

poSt–CeSAreAn deLiVery SeptiC oVAriAn Vein throMboSiS 

Despite these recent reports, a short course of anticoagulation 

is often given due to concerns of vena cava thrombosis or 

pulmonary emboli seen in approximately 13% of OVT, 6 although 

the type and duration of anticoagulation for OVT remains 

controversial. 7,11,12 Until better evidence is available, the authors 

believe anticoagulation should be considered until the patient is 

ambulating and asymptomatic, and for 3 to 6 months in cases 

complicated by pulmonary emboli. If warfarin is given to a woman 

who breast feeds, Vitamin K supplement and coagulation testing 

of her infant is considered prudent. 

referenCeS 

1. Brown TK, Munsick RA. Puerperal ovarian vein thrombophlebitis: a syndrome. 

Am J Obstet Gynecol. 1971;109(2):263-273. 

2. Dunnihoo DR, Gallaspy JW, Wise RB, Otterson WN. Postpartum ovarian vein 

thrombophlebitis: a review. Obstet Gynecol Surv. 1991;46(7):415-427. 

3. Josey WE, Staggers SR,Jr. Heparin therapy in septic pelvic thrombophlebitis: a 

study of 46 cases. Am J Obstet Gynecol. 1974;120(2):228-233. 

4. Garcia J, Aboujaoude R, Apuzzio J, Alvarez JR. Septic pelvic thrombophlebitis: 

diagnosis and management. Infect Dis Obstet Gynecol. doi:10.1155/ 

IDOG/2006/15614. 

5. Witlin AG, Mercer BM, Sibai BM. Septic pelvic thrombophlebitis or refractory 

postpartum fever of undetermined etiology. J Matern Fetal Med. 1996;5(6): 

355-358. 

6. Munsick RA, Gillanders LA. A review of the syndrome of puerperal ovarian vein 

thrombophlebitis. Obstet Gynecol Surv. 1981;36(2):57-66. 

7. Kominiarek MA, Hibbard JU. Postpartum ovarian vein thrombosis: an update. 

Obstet Gynecol Surv. 2006;61(5):337-342. 

8. Twickler DM, Setiawan AT, Evans RS, et al. Imaging of puerperal septic 

thrombophlebitis: prospective comparison of MR imaging, CT, and sonography. 

AJR Am J Roentgenol. 1997;169(4):1039-1043. 

9. Salomon O, Apter S, Shaham D, et al. Risk factors associated with postpartum 

ovarian vein thrombosis. Thromb Haemost. 1999;82(3):1015-1019. 

10. Brown CE, Stettler RW, Twickler D, Cunningham FG. Puerperal septic pelvic 

thrombophlebitis: incidence and response to heparin therapy. Am J Obstet 

Gynecol. 1999;181(1):143-148. 

11. Beigi RH, Wiensenfeld HC. Enoxaparin for postpartum ovarian vein thrombosis. 

A case report. J Reprod Med. 2004;49(1):55-57. 

12. Ortin X, Ugarriza A, Espax RM, et al. Postpartum ovarian vein thrombosis. 

Thromb Haemost. 2005;93(5):1004-1005. 


Authors: 

Ines H. Berger, MD, PhD 

Department of Pain Medicine 


Douglas R. Bacon, MD, MA 

Department of Anesthesiology 

Mayo Clinic Foundation 

Rochester, Minnesota 


Ines H. Berger, MD, PhD 

Mail Stop EB3-001 




Telephone: (608) 775-9000 

Facsimile: (608) 775-1018 

email: ihberger@gundluth.org 

A 

Historical Notes on Amputation and Phantom 

Limb Pain: “All Quiet on the Western Front?” 

AbStrACt 

mputations have been performed since antiquity for 

punitive, therapeutic, and ritualistic purposes. 1 Hippocrates 

practiced amputation of gangrenous limbs, preferring transection 

through the gangrenous portion because it was less painful. Celsus, 

in contrast, stressed the necessity to sever between the healthy and 

the diseased body part. Since the 16th century, especially in France 

and in Germany, barber surgeons have attempted to perfect the 

techniques of amputation. Until the advent of adequate general 

and regional anesthesia techniques, an amputation was probably 

the most challenging operation a surgeon could perform. Although 

opium had been known for a long time, it did not find its use 

in amputations. With the lack of perioperative analgesia, the 

operation had to be short. It took an experienced barber surgeon 

3 to 4 minutes to amputate a leg and was performed as a circular 

cut—a single cut for skin, muscles, bone and tendon (Figure 1). A 

limb amputation was associated with an extremely high morbidity 

and mortality (50%-80%) prior to the introduction of antisepsis 

in the late 19th century. 

The invention of cannon balls and gunpowder worsened 

the injuries sustained in battle. Many famous surgeons, such 

as Ambroise Paré (Figure 2) and Baron Larrey, who reportedly 

amputated 200 limbs in a day, 2 have been associated with battle 

surgery. Important progress was made with the introduction of 

vessel ligature. Previously, hemostasis had to be achieved by 

immersing the stump in substances such as hot oil or vitriol, or 

cauterizing with a hot iron. Ambroise Paré described an arterial 

forceps for the use of vessel ligation in 1590, thereby significantly 

reducing blood loss. 3 

Amputations in the 16th and 17th centuries were primarily 

accomplished in a single cut through the soft tissue, thereby 

necessitating an assistant holding the limb. This was consequently 

modified into 2- and 3-stage circular cuts to reduce the tension 

on sutures. Lowdham (1679), Verduyn (1696), and Langenbeck 

(1810) changed the operative technique with the creation of a 

soft tissue flap to cover the stump without tension. Despite these 

advances, mortality was high and amputation remained the best 

option possible. William Keen, an American Civil War surgeon, 

The first detailed description of phantom limb pain is credited to the French barber surgeon 

Ambroise Paré (ad 1552) in his tract on “harquebusses and other guns.” He differentiated 

phantom limb pain from stump pain and phantom sensations. Paré speculated on peripheral 

and central nervous system involvement, as well as psychological factors in the algogenesis of 

this pain. Although classically described as occurring after limb amputation, the sensation can 

occur after a spinal cord injury, nerve avulsion, mastectomy, or removal or deafferentation of 

many other organs or body parts. Almost 450 years later, the incidence of phantom limb pain 

has remained high (up to 80% in some studies). Paré’s observation and theories are still the 

basis of our current treatment strategies, including aggressive postoperative analgesia, nerve 

blocks, centrally acting medications, physiotherapy and behavioral/psychological interventions. 

figure 1. Plate illustrating amputation at the thigh. Courtesy of the 

National Library of Medicine. 

wrote: “The popular opinion that the surgeons did a large amount 

of unnecessary amputating may have been justified in a few cases, 

but, taking the army as a whole, I have no hesitation in saying 

that far more lives were lost from refusal to amputate than by 


amputation.” 4 Given that a lot of these procedures were performed 

in fields or stables, it comes as no surprise to find gangrene, sepsis, 

hemorrhage, and tetanus as constantly dreaded complications 

associated with these operations. 4,5 

Postamputation pain 

Along with the lack of pain control during the amputation, 

the phenomenon of postamputation pain has been recognized 

for many centuries. Admiral Lord Nelson lost his right arm at an 

attack on Santa Cruz de Tenerife. 6 Not only was the amputation 

in itself quite challenging, but imagine the difficulty of performing 

this under a most compromised situation, namely, on a moving 

battleship, with little space, in the semi-darkness of the ship’s 

interior. Admiral Nelson, who barely survived hypothermia and 

considerable blood loss, found himself in tremendous pain after he 

survived the amputation of his arm—in the amputated arm! He 

found the emergence of painful phantom sensations to be proof of 

the existence of the soul, given that an extremity that was no longer 

there could hurt so much. Fortunately, a second operation, which 

likely relieved an inadvertently placed suture on the median nerve, 

relieved most of his pain and restored him to function. However, 

through the ages, a significant percentage of amputees could not 

be delivered from their torturous pain. 7,8 

S. Weir Mitchell, who is considered the Father of American 

Neurology, wrote a short story, “The Case of George Dedlow,” 

in 1886. 9 The central character, George Dedlow, progressively 

loses all 4 extremities and is befallen by phantom limb pain: “I 

was suddenly aware of a sharp cramp in my leg. I tried to get at it 

to rub it with my single arm, but finding myself too weak, hailed 

an attendant: ‘Just rub my left calf,’ said I, ‘if you please.’ ‘Calf?’ 

said he. ‘You ain’t none, pardner. It’s took off.’ ‘I know better,’ said 

I. ‘I have pain in both legs.’ ‘Wall, I never!’ said he. ‘You ain’t got 

nary leg.’” In this story, George Dedlow becomes the symbol for 

the cost of the Civil War, which left 500 000 soldiers disfigured, 

disabled, and in chronic pain. 10 

Erich Maria Remarque described in his classic novel All Quiet on 

the Western Front the sufferings endured by the generation involved 

in the atrocities of trench warfare in World War I. 11 Standing at 

the bedside of his severely injured friend, Franz Kemmerich, 

Albert Kropp asks, “How goes it Franz?” “Not so bad…but I have 

such a damned pain in my foot.” The leg has been amputated. 

With more than one meaning, Kropp commends, “Now you will 

soon be going home.” During the next visit, Franz is dying from 

complications of the amputation. He gives his “good army boots” 

to his friend Müller, also giving hope to go on fighting not only a 

war, but also the adversities in life. 

Ambroise Paré (1510-1590) described phantom pain in 

a surprisingly comprehensive fashion. 12 He differentiated 

preamputation pain from postamputation symptoms, and stump 

pain from phantom sensations and phantom limb pain. Paré 

recognized a psychological component in pain perception, as well 

as pain-alleviating and pain-modulating modalities. 

Paré’s tract was geared toward his surgical colleagues who were 

familiar with the challenges of treating postamputation pain. 

Paré rejected the use of multiple limb-shortening procedures for 

persistent pain and advocated for early amputation of necrotic 

limbs and nonsurgical treatment of phantom pain as a combination 

hiStoriCAL noteS on AMputAtion And phAntoM LiMb pAin 

figure 2. Ambroise Paré (1510-1590), French barber surgeon 

credited with the first detailed description of phantom limb pain. 

Courtesy of the National Library of Medicine. 

of massage therapy for the stump and neck and the use of an 

antispasmodic ointment. Paré used 2 neurological models to 

explain phantom sensation/pain: (1) A peripheral model focused 

on contractures of muscles, nerves, and tendons; contractures 

postinjury were commonplace in his era and, therefore, widely 

recognized; and (2) A central nervous system model that identified 

“pain memory” as the cause of pain without contractures. 

Silas Weir Mitchell, a 19th-century neurologist, is credited 

with coining the term phantom limb and the first concise description 

of the phantom pain phenomena, 13-15 though Charles Bell, a 

British physician, had also described phantom limb sensations in 

1830 in his monograph The Nervous System of the Human Body. 16,17 

Guéniot 18 described in an 1861 tract About Hallucination of 

Feeling in Certain Amputees, the phenomenon of regressive 

deformation, also known as telescoping. Telescoping refers to 

the process of shrinking of the phantom sensation as the digits 

become approximated to the stump, a phenomenon that seems 

more likely to occur in the arm than in the leg. It is a gradual 

process that occurs in 25% to 75% of amputees and is usually 

complete after the first year. Pain, recurrent trauma, and other 

similar events can reverse this process. 

Since these original descriptions, phantom limb phenomena 

have also been described with multiple other organ extirpations, 

such as the tongue, penis, testicle, breast, bladder, gallbladder, and 

teeth, as well as with spinal cord and nerve avulsion injuries. Bors 

described in 1951 phantom pain associated with spinal cord injury 


and nerve root avulsion. Simmel, in 1956, described phantom 

phenomena associated with thalamic lesions. Despite the 

many discoveries and blessings of modern-day medicine, the 

incidence of phantom limb pain has remained high, with 

estimates varying widely up to 79%. 19 Wartan describes an 

incidence of 55% in British war veterans after 50 years. 8 The 

pain from preamputation to postamputation state remains 

strikingly similar in quality and location, 19 and preamputation 

and acute pain are the best predictors of persistent chronic 

pain after the amputation. 20 

Although phantom limb pain has been recognized for 

several centuries, some people do not accept the phenomenon 

and believe the pain is imagined. Those who experience 

phantom pain and/or sensations make the point that their 

experience is real and that the missing or deafferented body 

part is the phantom. “Even 50 years after loosing my leg in 

World War II, the burning still comes. I don’t talk about it 

much: the doctor told me that it was all in my head. I just… 

try to get through the pain.” 7 

How do we understand and treat phantom limb 

pain today? 

Saints Cosmas and Damian, the twin physicians, are 

credited with the first attempt to cure phantom limb pain by 

transplantation of a new limb. This heroic attempt failed even 

in these “holy hands” and probably contributed to the fact 

that the physicians were also known as the “silver-less ones.” 

However, the fact that even saint physicians could not heal 

this deafferentation pain state illustrates the challenge that we 

encounter to this day: phantom limb pain continues to be 

exceedingly difficult to treat. 

The assumption of a psychogenic origin of this type of 

pain has not been supported in the recent literature. 21 

The aggravating effects of stress, anxiety, exhaustion, and 

depression on chronic pain, however, are well accepted. 22 

Peripheral mechanisms have been implicated in modulating 

phantom sensations via alterations in blood flow and stump 

manipulations. Spinal mechanisms are recognized 

in disinhibition of the dorsal horn neurons, thereby 

facilitating transmission of phantom pain. 23 Melzack 

proposed a central origin of phantom pain with the 

concept of a neuromatrix, with a somatosensory memory 

of the pain experienced. 24 The topographic representation 

of the body in the thalamus and cerebral cortex can be 

significantly altered by amputation. Thalamic mapping has 

supported the hypothesis that the thalamic representation 

of the limb or organ remains functional or even increases 

after amputation. Thalamic microstimulation of this area 

has been shown to reproduce phantom pain. 25 Somatotopic 

mapping using magnetoencephalography has revealed 

significant reorganization in cortical topography following 

deafferentation. 26 Recently, linking of cortical topography 

with perceptual experiences has also received tremendous 

impetus. 27 Harris recently hypothesized that disorganized or 

inappropriate cortical representation of proprioception may 

falsely signal incongruence between motor intention and 

movement, which results in pathological pain. 28 

Meticulous care of the amputation stump and wellfitted 

prosthesis are the prerequisites to stump and pain 

management. 22 In addition to traditional opioids and 

nonsteroidal antiinflammatories, antidepressants, and 

anticonvulsants, highly invasive techniques, such as deep brain 

stimulation and primary motor cortex stimulation, have added 

to the arsenal of possible treatment options. 29-31 Preemptive 

analgesia methods aim to minimize or prevent central 

neuroplastic changes from occurring in response to tissue 

injury and pain. Effective multimodal perioperative analgesia 

techniques, including regional anesthesia, nonsteroidal antiinflammatory 

drugs, local anesthetics, α 2 agonists, ketamine, 

α 2 δ ligands, and opioids have been successfully implemented 

to improve pain control in phantom pain. 32-35 

The functional relationship between cortical and 

subcortical reorganization and phantom limb pain suggests 

that neuromodulatory treatments aimed at modifying 

cortical reorganization and restoring the integrity of cortical 

information processing offer intriguing possibilities in treating 

the devastating symptoms of chronic pain after suffering the 

loss of bodily integrity. Ironically, after countless suggestions 

that amputees’ phantom limb pain is “all in their head,” it 

might truly be—albeit not in the original sense of the phrase. 

We need to shift our conceptualization of chronic pain away 

from Descartes’ notion of pain pathways that can be severed 

to treat pain 36 toward that of a complex neuromodulatory 

process that integrates physiological as well as psychological 

components. Doing so will affect not only our approach to 

the patient suffering from phantom pain, but also open a 

new dimension to our understanding and treatment of other 

neuropathic and centralized pain states. 

Paré’s observations led him to propose peripheral, spinal, 

and central mechanisms as causes for phantom limb pain. 

Today we are using the same peripheral, spinal, and central 

targets for our treatment strategies. 

After almost 450 years, there is new hope for relief from 

a syndrome that Paré described so well, even with the limited 

methodology of his time. We shall take the “good boots” of 

comrade Kemperich to accelerate our knowledge and give 

hope to those who suffer from unrelenting pain, knowing that 

Saints Cosmas and Damian, the patron saints of healers, are 

still a step ahead of us. 

referenCeS 

1. Magee R. Amputation through the ages: the oldest major surgical operation. 

Aust N Z J Surg. 1998;68(9):675-678. 

2. Larrey DJ. Mémoires De Chirurgie Militaire Et Campagnes. Paris: J Smith; 

1812:Vol IV, 57. 

3. Paré A. Les Oeuvres d’Ambroise Paré, Conseiller Et Premier Chirurgien Du 

Roy. Divisées En Vingt-Huit Livres, Avec Les Figures Et Portraits, Tant De 

l’Anatomie, Que Des Instruments De Chirurgie, & De Plusieurs Montres. 

Revues & Augmentées Par l’Auteur. Quatrième ed. FR; Paris: G. Buon; 

1585:387-388. 

4. Keen WW. Surgical reminiscences of the Civil War. Transactions and Studies 

of the College of Physicians of Philadelphia, Third Series. 1905;27:95-114. 


5. Sachs M, Bojunga J, Encke A. Historical evolution of limb amputation. World J 

Surg. 1999;23(10):1088-1093. 

6. Rüttimann B. Nelsons Oberarm-Amputation. Z Orthop Ihre Grenzgeb. 

1982;120(1):86-88. 

7. Machin P, de C Williams AC. Stiff upper lip: coping strategies of World War II 

veterans with phantom limb pain. Clin J Pain. 1998;14(4):290-294. 

8. Wartan SW, Hamann W, Wedley JR, McColl I. Phantom pain and sensation 

among British veteran amputees. Br J Anaesth. 1997;78(6):652-659. 

9. Mitchell SW. The Autobiography of a Quack: And, the Case of George Dedlow. New 

York: The Century Co.; 1900:115-149. 

10. Figg L, Farrell-Beck J. Amputation in the Civil War: physical and social 

dimensions. J Hist Med Allied Sci. 1993;48(4):454-475. 

11. Remarque EM. All Quiet on the Western Front. Boston: Little, Brown, and 

Company; 1983. 

12. Keil G. Sogenannte Erstbeschreibung des Phantomschmerzes von Ambroise 

Paré. Fortschr Med. 1990;108(4):62-66. 

13. Nathanson M. Phantom limbs as reported by S. Weir Mitchell. Neurology. 

1988;38(3):504-505. 

14. Mitchell SW. Phantom limbs. Lippincott’s Magazine of Popular Literature & 

Science. 1871;8:563-569. 

15. Mitchell SW. Neural maladies of stumps. In: Mitchell SW, ed. Injuries 

of Nerves and Their Consequences. Philadelphia: J.B. Lippincott; 1872: 

342-368. 

16. Furukawa T. Charles Bell’s description of the phantom phenomenon in 1830. 

Neurology. 1990;40(12):1830. 

17. Bell C. The Nervous System of the Human Body: Embracing the Papers Delivered 

to the Royal Society on the Subject of the Nerves. London: Longman, Rees, Orme, 

Brown, and Green; 1830:238, clxxvi. 

18. Guéniot M. D’une hallucination du toucher (ou hétéroptopie subjective des 

extrémités) particulière à certains amputés. Journal de la Physiologie de l’Homme 

et des Animaux. 1861;4:416-430. 

19. Katz J, Melzack R. Pain ‘memories’ in phantom limbs: review and clinical 

observations. Pain. 1990;43(3):319-336. 

20. Hanley MA, Jensen MP, Smith DG, Ehde DM, Edwards WT, Robinson LR. 

Preamputation pain and acute pain predict chronic pain after lower extremity 

amputation. J Pain. 2007;8(2):102-109. 

21. Sherman RA, Sherman CJ, Bruno GM. Psychological factors influencing 

chronic phantom limb pain: an analysis of the literature. Pain. 1987;28 

(3):285-295. 

hiStoriCAL noteS on AMputAtion And phAntoM LiMb pAin 

22. Sherman RA, Sherman CJ, Gall NG. A survey of current phantom limb pain 

treatment in the United States. Pain. 1980;8(1):85-99. 

23. Mackenzie N. Phantom limb pain during spinal anaesthesia. Recurrence in 

amputees. Anaesthesia. 1983;38(9):886-887. 

24. Melzack R. Phantom limbs and the concept of a neuromatrix. Trends Neurosci. 

1990;13(3):88-92. 

25. Davis KD, Kiss ZH, Luo L, Tasker RR, Lozano AM, Dostrovsky JO. Phantom 

sensations generated by thalamic microstimulation. Nature. 1998;391(6665):385- 

387. 

26. Birbaumer N, Lutzenberger W, Montoya P, et al. Effects of regional anesthesia on 

phantom limb pain are mirrored in changes in cortical reorganization. J Neurosci. 

1997;17(14):5503-5508. 

27. Ramachandran VS, Rogers-Ramachandran D. Phantom limbs and neural 

plasticity. Arch Neurol. 2000;57(3):317-320. 

28. Harris AJ. Cortical origin of pathological pain. Lancet. 1999;354(9188): 

1464-1466. 

29. Owen SL, Green AL, Nandi DD, Bittar RG, Wang S, Aziz TZ. Deep 

brain stimulation for neuropathic pain. Acta Neurochir Suppl. 2007;97 

(Pt 2):111-116. 

30. Saitoh Y, Yoshimine T. Stimulation of primary motor cortex for intractable 

deafferentation pain. Acta Neurochir Suppl. 2007;97(Pt 2):51-56. 

31. Wesolowski JA, Lema MJ. Phantom limb pain. Reg Anesth. 1993;18 

(2):121-127. 

32. Pinzur MS, Garla PG, Pluth T, Vrbos L. Continuous postoperative infusion of 

a regional anesthetic after an amputation of the lower extremity. A randomized 

clinical trial. J Bone Joint Surg Am. 1996;78(10):1501-1505. 

33. Madabhushi L, Reuben SS, Steinberg RB, Adesioye J. The efficacy of 

postoperative perineural infusion of bupivacaine and clonidine after lower 

extremity amputation in preventing phantom limb and stump pain. J Clin 

Anesth. 2007;19(3):226-229. 

34. Bach S, Noreng MF, Tjellden NU. Phantom limb pain in amputees during the 

first 12 months following limb amputation, after preoperative lumbar epidural 

blockade. Pain. 1988;33(3):297-301. 

35. Reuben SS, Buvanendran A. Preventing the development of chronic pain after 

orthopaedic surgery with preventive multimodal analgesic techniques. J Bone 

Joint Surg Am. 2007;89(6):1343-1358. 

36. Benini A, DeLeo JA. Rene Descartes’ physiology of pain. Spine. 1999;24(20): 

2115-2119. 


Authors: 


FACSM 

John P. Porcari, PhD, RCEP 

Carl C. Foster, PhD 


Sport Science 




FACSM 

149 Mitchell Hall 




Telephone: (608) 785-8181 

Facsimilie: (608) 785-8172 

email: udermann.bria@ulax.edu 

The La Crosse Exercise and Health Program (LEHP) has 

been serving the Seven Rivers Region since 1971. Since 

its inception, the program has gone through a number of name 

changes. In 1971 the program was known as the La Crosse Cardiac 

Rehabilitation Program. In 1976 the name was changed to the 

La Crosse Exercise Program, and in 1985 the current program 

name (LEHP) was adopted. To avoid confusion, LEHP will 

be used throughout this article. Also, in 1971 the Wisconsin 

State University of La Crosse underwent a name change to the 

University of Wisconsin–La Crossse (UW–L); we will use UW–L 

when referring to the university. 

The idea of using physical activity to help prevent and treat 

illness and disease dates back to nearly 500 b c. 1 Isolated reports 

document that some physicians were recommending physical 

activity for individuals with heart ailments in the 16th and 17th 

centuries, 2,3 but it wasn’t until the 1940s and 1950s that physicians 

and researchers started critically analyzing the standard treatment 

of coronary patients (eg, bed rest) and began investigating the role 

that prescribed physical activity could play in the rehabilitative 

process. 4,5 The amount of research and scientific inquiry on 

the topic continued to expand through the 1960s, resulting in 

unprecedented growth in the area of cardiac rehabilitation. 6-11 

In 1970, due in part to a greater acceptance of using exercise 

to help treat cardiac patients, a task force was formed in La Crosse 

to investigate the feasibility of creating an exercise program for 

cardiac patients. Two additional factors precipitated the creation 

of this task force. First, UW–L faculty wanted to focus more on 

laboratory-based exercise physiology (see Figure 1 for an early 

photograph taken in the Human Performance Laboratory at 

UW–L). Second, physicians in the Department of Cardiology at 

Lutheran Hospital were interested in offering expanded services. 

The task force consisted of Dr Allen Brailey (cardiologist 

and president of the La Crosse County Medical Society), 

Mr Jack Forbes (field representative, Wisconsin Heart Association), 

Dr Robert Green (cardiologist and consulting physician, La Crosse 

County Heart Unit), Dr Robert McMahon (internist and former 

director of health services at UW–L), and Dr Philip Wilson 

The History of Cardiac Rehabilitation at the 


figure 1. Exercise test in the UW–L Human Performance Laboratory. 

(associate professor in the College of Health, Physical Education, 

and Recreation at UW–L). 12 As the task force began the work 

of investigating the feasibility of creating a cardiac rehabilitation 

program at UW–L, it soon became apparent that the political 

climate within the medical community in the area would present a 

significant challenge to the idea. La Crosse was home to 2 competing 

hospitals: Lutheran Hospital, supported by Gundersen Clinic; and 

St. Francis Hospital, supported by Skemp Grandview Clinic and 

La Crosse Clinics. 12 The rivalry between these 2 healthcare facilities 

threatened to jeopardize the creation of a collaborative cardiac 

rehabilitation program. Dr Robert McMahon, who at different 

points in his career was employed by Gundersen Clinic, Skemp 

Clinic, and UW–L, was instrumental in facilitating discussion and 

developing rapport among representatives from the 3 institutions. 

As the task force was nearing the completion of its work, it 

was decided that 2 representatives (Drs McMahon and Wilson) 


the hiStory of CArdiAC rehAbiLitAtion At the uniVerSity of WiSConSin–LA CroSSSe 

would visit a number of existing cardiac rehabilitation programs 

around the country. The pair traveled to and observed programs 

at San Diego State College, the University of San Francisco, the 

University of Wisconsin–Madison, and the Cleveland Jewish 

Community Center. Shortly after the visits, the task force 

drafted a policies and procedures document for the LEHP. In the 

spring of 1971, an LEHP executive board was created and held 

its first meeting. The board consisted of Drs Robert Batchelder, 

Donovan Riley, and Philip Wilson (UW–L); Drs Allen Brailey, 

Robert Green, Robert McMahon, and Edward Winga (Gundersen 

Clinic); Dr Charles Link (Skemp Clinic); and Cal Jahn (consumer 

representative). The executive board was responsible for developing 

and monitoring the policies and procedures of the LEHP. 

Even though the LEHP was incorporated as an operational body 

of UW–L, the creation of the program truly was a collaborative 

effort between the University, the Wisconsin Heart Association, 

the La Crosse County Medical Society, and La Crosse Lutheran 

and St. Francis hospitals. The initial cost of LEHP was shared 

across institutions, and it was agreed that the program would be 

offered for a 1-year pilot period and then evaluated for possible 

continuance. 

On June 6, 1971, the first exercise session of the newly created 

LEHP was offered. Six cardiac rehabilitation patients completed 

an exercise class under the supervision of exercise physiologists and 

physicians. Program personnel made a strong effort to promote 

and market the LEHP, and after the first year the enrollment had 

grown from 6 to 31 participants. Area physicians appeared to be 

supportive of the program as well, with 14 physicians volunteering 

to help supervise LEHP activities. 

Over the next few years the program continued to grow in 

enrollment, and new policies and procedures were developed. 

Program personnel sought grants from the Grandview Foundation, 

the National Institutes of Health, the Wisconsin Heart Association, 

and the United Fund to help offset program costs, and a new cardiac 

rehabilitation internship program was created. It was decided 

that all cardiac rehabilitation participants would receive a graded 

exercise stress test prior to admittance into the program, and again 

after 3 and 6 months of participation. It was also decided that 

LEHP participants would be divided into cardiac-prone (1 or more 

cardiovascular risk factors) and advanced cardiac (known disease) 

groups and would exercise on different days of the week. 

In 1974, the American College of Cardiology selected UW-L 

(with support from Gundersen Clinic) as a training center for 

physicians interested in cardiac rehabilitation and exercise testing. 

It was also about this time that the LEHP sponsored a cardiac 

exercise technician workshop. Since the early 1970s, the LEHP has 

sponsored and conducted hundreds of educational programs on 

topics including cardiac rehabilitation, electrocardiogram (ECG) 

interpretation, weight management, industrial fitness, pulmonary 

rehabilitation, and exercise testing. One of the more successful 

workshops, a sports sciences symposium, was offered in 1984 and 

brought more than 600 medical personnel from the United States 

and around the world to La Crosse. It is estimated that over the 

past 35 years, over 10 000 participants, from all 50 states and 43 

countries, have attended LEHP workshops and symposia. 

In the fall of 1975 the LEHP began publishing Cardio-Gram, 

a bi-monthly newspaper that contained articles of interest to both 

LEHP participants and medical personnel working in the field of 

cardiac rehabilitation. Over the next few years the paper became 

more popular and grew to a circulation of over 3500 subscribers. 

In the early 1980s, LEHP staff secured a sponsorship for Cardio- 

Gram through Pfizer Laboratories (New York), which resulted in the 

paper being circulated to roughly 25 000 healthcare professionals. 

The paper was eventually replaced by a program newsletter. The 

Sun Rise Express, The Beat Goes On, and The Pacesetter are all titles 

the newsletter has had over the past 25 years. The program still 

publishes a popular monthly newsletter, The La Crosse Exercise and 

Health Program Newsletter. 

The mid 1970s was also a time when LEHP staff began 

offering educational programming to participants. Topics 

included nutrition, benefits of exercise, behavior modification, 

and risk factors for cardiovascular disease. Offering educational 

opportunities to both participants and community members 

has been a hallmark of the program for the past 30 years. Some 

current examples include 10-minute tidbits—short educational 

programs presented to participants every 2 weeks—and the LEHP 

Health Lecture Series, a new series of talks that will be offered 

every February to help recognize the American Heart Association’s 

Heart Health Month. 

Throughout the early and mid 1970s, the LEHP offered exercise 

programming for individuals in need of cardiac rehabilitation. 

However, in January of 1977, the program expanded services to 

nonclinical populations and created an adult fitness unit. The 

adult fitness unit was to serve apparently healthy individuals with 

the goal of helping participants prevent disease and maintain or 

increase fitness levels. Also in 1977, the Board of Regents of the 

University of Wisconsin System approved a master’s degree in 

Adult Fitness and Cardiac Rehabilitation at UW–L. This was an 

exciting time for the university because this was the first program 

of its kind in the country, and because until this program was 

approved, the only UW system school that offered medically 

related degree programs was UW–Madison. A number of other 

colleges and universities adopted the university-based cardiac 

rehabilitation model created at UW–L. In 2004, the Adult Fitness 

and Cardiac Rehabilitation Program was renamed and is now 

the Clinical Exercise Physiology program. In the past 30 years, 

roughly 500 students have graduated from this program and are 

employed in cardiac and pulmonary rehabilitation programs in 

nearly every state in the country, as well as a number of countries 

around the world. 

Over the years, LEHP staff has employed a variety of incentivebased 

initiatives to help motivate participants. One of the first, 

implemented in 1977, was a program in which participants who 

attended 3 exercise sessions a week for 6 months were rewarded 

with a t-shirt. The LEHP still uses a variety of incentive programs 

to help motivate participants to achieve their health- and fitnessrelated 

goals. Longtime LEHP member Don Kirby recently posed 

for a photograph wearing a 1000 Mile Club shirt he received in the 

late 1970s (Figure 2). 

In the early to mid 1980s, the LEHP continued to expand the 

services offered to the community. A collaborative diabetic services 

program was created and implemented with cooperation from 

the Gundersen and Skemp-Grandview clinics. The program also 

began offering services related to pulmonary rehabilitation and 


figure 2. Longtime LEHP member Don Kirby wearing an incentive 

t-shirt he received in the late 1970s. 

continued to expand its health promotion (eg, stress management, 

weight management, nutritional counceling, tobacco cessation) 

and exercise (eg, low-impact aerobics) programming. In addition, 

a program called Nutri Exercise was developed by Jean Storlie, 

MS, RD, and offered to area residents. 

Phil Wilson, the first executive director of the LEHP retired 

in July of 1987. Drs Patricia Hutchenson and Sandra Price each 

served as interim executive directors of the LEHP until 1989, 

when Dr John Porcari was appointed to the position. 

The leadership and staff of the LEHP have been influential in 

advancing the disciplines of cardiac and pulmonary rehabilitation. 

The American Association of Cardiovascular and Pulmonary 

Rehabilitation was formed in 1985, and since that time, 7 of 

the individuals who have served as president of that organization 

have worked with the LEHP: Philip Wilson, Linda Hall, Martha 

Livingston, Mark Williams, Jeanne Ruff, John Porcari, and Karen 

Lui, and 3 of these have received its Award of Excellence: Wilson, 

Hall, and Williams. 

Changes in the last decade have focused mainly on 

programmatic offerings. Research documenting the benefits of 

resistance training has resulted in approximately 75% of program 

participants participating in some sort of strength training, either in 

the weight room or in chair weight classes. A very popular offering 

is the nightly Rockin’ Rehab low-impact aerobic dance class. 

These classes were originally part of student Elaine Gotro’s 1998 

master’s project, and they continue to thrive. In fact, they became 

so popular that an instructional video tape and DVD have been 

produced and are available for participants to purchase. A fairly 

recent addition to the program has been stability ball and balance 

classes. As individuals get older and recognize the importance of 

strength, balance, and flexibility to maintain their independence, 

these classes are also increasing in popularity. Enrollment in the 

program has been stable over the past 5 to 10 years and is currently 

at 262 members—188 adult fitness members and 74 cardiac 

rehabilitation members. 

Another change to the program is that physicians no longer 

supervise the afternoon exercise sessions. The availability of an 

automated external defibrillator (AED) and the fact that all staff 

are certified in Advanced Cardiac Life Support (ACLS) has resulted 

in a change in philosophy regarding program supervision. 

Despite the fact that physicians no longer directly supervise 

the afternoon exercise sessions, the LEHP continues to work very 

closely with both area medical facilities. Students in the Clinical 

Exercise Physiology graduate program complete an equal number 

of rotations through the Phase I and II cardiac rehabilitation 

programs at each facility and rotate through the graded exercise 

testing laboratories at each hospital clinic. Physicians routinely 

give lectures to students on various topics related to cardiology 

and cardiac rehabilitation. The LEHP has a contract with each 

facility to provide a half-time exercise physiologist to work in their 

exercise physiology departments and to serve as a link between 

the University and their respective programs. The University and 

the hospitals jointly sponsor the previously mentioned continuing 

education workshops in cardiac and pulmonary rehabilitation that 

are attended by people from all over the world. 

referenCeS 

1. Balke B. Historical viewpoints: exercise and health. J Cardiopulm Rehabil. 

1990;10:447-454. 

2. Heberden W. Some account of a disorder of the breast. Medical Transactions. 

1772;2:59-67. 

3. Stokes W. The Diseases of the Heart and the Aorta. Dublin: Hodges & Smith; 1854. 

4. Harrison TR. Abuse of rest as a therapeutic measure for patients with cardiovascular 

disease. JAMA. 1944;125:1075-1077. 

5. Levine SA, Lown B. “Armchair” treatment of acute coronary thrombosis. JAMA. 

1952;148(16):1365-1369. 

6. Cain HD, Frasher WG, Jr., Stivelman R. Graded activity program for safe return 

to self-care after myocardial infarction. JAMA. 1961;177:111-115. 

7. Naughton J, Balke B, Nagle F. Refinements in method of evaluation and physical 

conditioning before and after myocardial infarction. Am J Cardiol. 1964;14: 

837-843. 

8. Torkelson LO. Rehabilitation of the patient with acute myocardial infarction. 

J Chronic Dis. 1964;17(8):685-704. 

9. Gottheiner V. Long-range strenuous sports training for cardiac reconditioning and 

rehabilitation. Am J Cardiol. 1968;22(3):426-435. 

10. Hellerstein HK. Techniques of exercise prescription and evaluation. J S C Med 

Assoc. 1969;65(12):46-56. 

11. Wenger NK, Gilbert CA, Siegel W. Symposium: The use of physical activity 

in the rehabilitation of patients after myocardial infarction. South Med J. 

1970;63(8):891-897. 

12. Vik CE. Twenty-year History of the La Crosse Exercise and Health Program, 

1971-1991. [MS]. University of Wisconsin–La Crossse; 1993. 


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La Crosse, Wisconsin 54601 

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C03-006B 


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