September 2011 - Osteopathic Physicians' Guide: COPD - American ...

Osteopathic Physicians’ Guide 

This guide is supported by Boehringer Ingelheim Pharmaceuticals, Inc.

TABLE OF 

CONTENTS 

Editors’ Message.............................................................................3 

Improving Outcomes in Patients With COPD 

Brian H. Foresman, DO 

Fredric Jaffe, DO 

Diagnostic Considerations 

in Chronic Obstructive Pulmonary Disease..................................5 

Rupen Amin, MD 

Interventions for Patients 

With Chronic Obstructive Pulmonary Disease...........................11 

Thomas F. Morley, DO 

Amita Pravinkumar Vasoya, DO 

Comorbidities and Systemic Effects 

in Chronic Obstructive Pulmonary Disease.................................18 

Kartik Shenoy, MD 

Fredric Jaffe, DO 

Osteopathic Principles and Practice 

in Chronic Obstructive Pulmonary Disease................................23 

Stephen J. Miller, DO, MPH 

Osteopathic Physicians’ Guide 

Cover Credits 

Nancy Horvat, AOA creative director. 

Acknowledgment 

With gratitude to the Galter Health Sciences Library of the Northwestern 

University Feinberg School of Medicine in Chicago, Illinois. 

This guide is available online at http://www.osteopathic.org/copd-guide. 

Statements and opinions expressed in this guide are those of the 

authors and not necessarily those of the American Osteopathic 

Association or the institutions with which the authors are affiliated, 

unless otherwise stated. 

©2011 by the American Osteopathic Association. No part of this 

guide may be reprinted or reproduced in any form without written 

permission of the publisher. 

Printed in the USA.

Editors’ Message 

Improving Outcomes in Patients 

With COPD 

Brian H. Foresman, DO | Fredric Jaffe, DO 

Chronic obstructive pulmonary disease (COPD) is a primary cause of more than 

120,000 deaths annually. 1 It is now the fourth leading cause of death in the United 

States. 2 Clinicians cannot cure this disease but can alleviate the debilitating 

effects of this disease with early diagnosis and stepwise intervention. A majority 

of COPD cases can be attributed to firsthand or secondhand tobacco smoke 

exposure. Remaining cases can be a result of genetic susceptibility followed by 

recurrent lung damage. This damage can come from infections or toxic exposure 

to lung-injuring particles. Smoking cessation and avoidance of secondhand smoke 

can arrest the acceleration of loss of lung function. However, although most COPD 

interventions can improve patients’ quality of life, such interventions do not 

reverse the progression of disease. 

The present guide provides physicians with a concise review of the latest 

research on assessing risk factors for COPD, diagnosing the disease, determining 

the best treatment plan, and recognizing and addressing comorbidities that are not 

recognized in patients with COPD. 

In the first article, “Diagnostic Considerations in Chronic Obstructive Pulmonary 

Disease,” 3 Rupen P. Amin, MD, analyzes COPD risk factors and symptoms 

and assesses diagnostic approaches and tools. Dr Amin emphasizes the importance 

of using simple spirometry in diagnosing COPD. This simple screening tool can 

help measure the severity of the disease and therefore determine the best course of 

treatment. 

The second article, written by Thomas F. Morley, DO, and Amita P. Vasoya, DO, 

and titled “Interventions for Chronic Obstructive Pulmonary Disease,” 4 outlines 

an incremental approach to treating patients with COPD. Paramount to the 

From the Roudebush VA Medical Center in Indianapolis, Indiana (Dr Foresman), and from the 

Division of Pulmonary and Critical Care Medicine at Temple University School of Medicine in Philadelphia, 

Pennsylvania (Dr Jaffe). 

Financial Disclosures: None reported. 

E-mail: fredric.jaffe@tuhs.temple.edu 

3

Osteopathic Physicians’ Guide: COPD 

management of COPD is smoking cessation in all who continue to smoke. As the 

disease becomes more severe, physicians may progress to treating patients with 

bronchodilators and inhaled corticosteroids. Long-term oxygen therapy, oral 

steroids, and surgical treatments may be indicated for very severe disease. Citing 

the recommendations of the Global Initiative for Chronic Obstructive Lung Disease 

(known as GOLD), Dr Morley and Dr Vasoya explain how this stepwise approach 

improves the efficacy of interventions, minimizes complications, and reduces costs. 

The authors provide a review of the various pharmacologic and nonpharmacologic 

treatment options for patients with COPD. 

Many physicians assume that COPD is a disease of only the lungs, but evidence 

suggests that the disease has more far-reaching effects. There are many systemic 

manifestations, including an increase in comorbidities such as cardiovascular disease, 

osteoporosis, and diabetes mellitus. All these comorbid conditions can affect 

quality of life and ultimately morbidity and mortality. In the third article, “Comorbidities 

and Systemic Effects in Chronic Obstructive Pulmonary Disease,” 5 Kartik 

Shenoy, MD, and Fredric Jaffe, DO, discuss the interrelationship of comorbid conditions 

and COPD and the management of patients with COPD who experience 

these diseases. 

In the final article, “Osteopathic Manipulative Medicine in Chronic Obstructive 

Pulmonary Disease,” 6 Stephen J. Miller, DO, MPH, reports that osteopathic 

manipulative treatment (OMT) has yet to be proven to be of much benefit in treating 

patients for COPD. Research indicates that OMT may improve patients’ quality 

of life and work capacity, but studies show that OMT may paradoxically worsen 

COPD patients’ lung function. Dr Miller emphasizes that more research is needed 

to fully assess the impact of OMT on patients with COPD. He suggests that research 

be conducted to investigate the effects of osteopathic medicine’s whole-patient philosophy 

on treating patients with COPD. 

Chronic obstructive pulmonary disease is a disease that all too often is undiagnosed 

until clinical symptoms become apparent. It is important for every physician 

to realize that early detection of the disease, along with systematic intervention as 

well as the recognition of comorbidities, can improve the quality of life and ultimately 

the survival rate of your COPD patients. We hope this publication will 

help guide your clinical decision-making and raise awareness of the ravages of the 

disease. We remain optimistic about the ability to intervene and to help increase 

quality of life in our COPD patients. 

References 

1. National Heart, Lung, and Blood Institute. Morbidity & Mortality: 2009 Chart Book on Cardiovascular, 

Lung, and Blood Diseases. Bethesda, MD: National Institutes of Health; 2009:59-68. http://www.nhlbi.nih. 

gov/resources/docs/2009_ChartBook.pdf. Accessed May 27, 2011. 

2. Jemal A, Ward E, Hao Y, Thun M. Trends in the leading causes of death in the United States, 1970- 

2002. JAMA. 2005;294(10):1255-1259. 

3. Amin R. Diagnostic considerations in chronic obstructive pulmonary disease. In: Foresman BH, Jaffe 

F, eds. Osteopathic Physicians’ Guide: COPD. Chicago, IL: American Osteopathic Association; 2011:5-10. 

4. Morley TF, Vasoya AP. Interventions for patients with chronic obstructive pulmonary disease. In: 

Foresman BH, Jaffe F, eds. Osteopathic Physicians’ Guide: COPD. Chicago, IL: American Osteopathic 

Association; 2011:11-17. 

5. Shenoy K, Jaffe F. Comorbidities and systemic effects in chronic obstructive pulmonary disease. In: 

Foresman BH, Jaffe F, eds. Osteopathic Physicians’ Guide: COPD. Chicago, IL: American Osteopathic 

Association; 2011:18-22. 

6. Miller SJ. Osteopathic principles and practice in chronic obstructive pulmonary disease. In: Foresman 

BH, Jaffe F, eds. Osteopathic Physicians’ Guide: COPD. Chicago, IL: American Osteopathic Association; 

2011:23-27. 

4


DIAGNOSTIC CONSIDERATIONS 

in Chronic Obstructive 

Pulmonary Disease 

Rupen Amin, MD 

Chronic obstructive pulmonary disease (COPD) is the fourth leading cause of death 

in the United States. Frequently, the diagnosis of COPD is not considered until 

patients experience symptomatic disease, at which point the disorder is usually 

more advanced. Furthermore, other disease entities that mimic COPD symptoms 

are known to occur and have specific treatments that can confound disease 

progress. In all circumstances, modifying the disease progression associated with 

COPD remains most effective when the condition is identified early. The present 

article reviews risk factors for development of COPD and key elements of medical 

history and physical examination associated with COPD. The article also provides 

an overview of testing used to obtain a diagnosis of COPD. 

Even with recent advances in treatment, 

chronic obstructive pulmonary 

disease (COPD) remains a severely debilitating 

condition. As the fourth leading 

cause of death in the United States, 

COPD claims more than 120,000 lives 

annually in this country. 1 Frequent 

office visits and hospitalizations and 

lengthy treatment periods lead to high 

financial costs for COPD, estimated at 

nearly $29 billion per year. 1 Less than 

half of this cost can be attributed to 

hospitalizations for COPD exacerbations, 

suggesting that earlier identification 

and improvements in outpatient 

therapy could substantially reduce 

the economic impact of this disorder. 

Moreover, smoking cessation and prevention 

of exposure to inciting agents 

remain paramount issues at all stages of 

COPD—independent of specific etiologic 

factors. 

Prevalence of “mild” cases of 

COPD in individuals between the ages 

of 25 and 75 years is estimated at 6.9%, 

whereas prevalence of “moderate” 

cases of COPD (indicating increased 

severity of airflow obstruction) in this 

age group is estimated at 6.6%. 2 Unfortunately, 

the prevalence of COPD 

is underestimated, because many cases 

of the disease remain undiagnosed until 

symptoms become grossly apparent 

and after irreversible pathophysiologic 

changes are established. Although 

COPD remains most prevalent in men 

worldwide, recent data have revealed 

alarming increases in COPD incidence, 

mortality, and morbidity among women. 

3 Much of these changes are attributable 

to the increased rate in smoking 

among women, though additional, 

poorly quantified factors appear to be 

present. 3 

From the Division of Pulmonary, Allergy, Critical Care, and Occupational Medicine in the Department of 

Medicine at Indiana University School of Medicine in Indianapolis. 


Address correspondence to Rupen Amin, MD, 301 W Michigan St, Apt 133, Indianapolis, IN 46202-3223. 

E-mail: ramin@iupui.edu 

Risk Factors 

Smoking 

Tobacco exposure, including both firsthand 

and second-hand exposure, is the 

single most important risk factor for 

the development of COPD. 1 Indeed, 

roughly 73% of mortality from COPD 

can be attributed to smoking. 4 Despite 

this high mortality rate, COPD will not 

develop in all smokers. Observations 

among individuals in Sweden revealed 

upwards of 25% of smokers having 

clinically significant COPD. 5 This finding 

would argue that while the great 

majority of COPD cases are attributable 

to the use of tobacco products, the 

remaining cases may have other contributing 

factors. Well-known genetic 

predispositions result in the development 

of COPD, as do environmental 

factors and recurrent pulmonary damage 

(eg, infection). 4,6 

The cumulative-dose exposure of 

smoking has been shown to correlate 

with the severity of disease. According 

to data derived in 1984 from a National 

Health and Nutrition Examination 

5


o Aerosolized oils 

o Coal 

o Cotton dust 

o Engine exhaust 

o Fire smoke 

o Grain dust 

o Osmium 

o Portland cement 

o Silica 

o Synthetic fibers 

Figure 1. Occupational environmental substances known to serve as risk factors for the 

development of chronic obstructive pulmonary disease (COPD), primarily by acting as irritants in 

the airways and leading to chronic inflammation. 21 

Survey in which 14,000 individuals were 

examined, 8.8% of the individuals were 

nonsmokers or former light smokers 

(ie, with a history of


Medical History 

The most common symptoms for patients 

with established COPD include 

chronic cough, dyspnea at rest or with 

exertion, and chronic sputum production. 

Any of these symptoms should 

prompt the consideration of COPD 

in the differential diagnosis. In many 

cases, chronic productive cough (>3 

tablespoons/d for >3 months) is 1 of 

the earliest presenting symptoms of 

COPD and is typically indicative of 

chronic bronchitis. However, by the 

time that patients with COPD present 

with these symptoms, they already have 

well-established disease. By contrast, 

many patients with mild COPD are 

asymptomatic or simply have a mild 

but chronic cough. 18 

A detailed history of tobacco exposure 

and environmental and occupational 

exposures (Figure 1) should be 

elicited from the patient. Cigarette or 

cigar smoke exposure should be quantified 

and defined as to whether it is 

first-hand or second-hand exposure. 

For cigarette smoking, the most common 

method of obtaining the patient’s 

history is to assess the pack-years of 

exposure (ie, the number of packs per 

day multiplied by the number of years). 

An increasing cumulative dose (ie, exposure) 

to tobacco smoke increases the 

likelihood of development of airway 

obstruction. 7 

Recurrent pulmonary infections 

can be indicative of a potential cause 

of COPD, or they may occur as a result 

of established COPD. Thus, a thorough 

history of respiratory infections 

dating to childhood should be elicited 

from the patient. A pattern of early, severe 

infections could indicate that the 

pulmonary damage initially occurred 

when the patient was a child. Later 

development of recurrent infections 

should be correlated with a smoking or 

environmental exposure history. Other 

confounding disorders that can be associated 

with such a history include 

uncontrolled asthma, cystic fibrosis, or 

immunodeficiency syndromes (eg, immunoglobulin 

A deficiency). 2 

A family history is useful for disclosing 

early cigarette smoke exposure, 

potential environmental exposures, 

and patterns of COPD development 

that might occur with genetic disorders. 

Any nonspecific—possibly genetic—associations 

that exist among 

first-degree relatives with COPD may 

increase suspicion of COPD as a clinical 

diagnosis. Environmental associations, 

as noted in Figure 1, can be 

identified by obtaining an occupational 

history of the patient’s parents. 

Age at symptom onset offers clues 

to the etiologic mechanisms and future 

progression of COPD. Respiratory 

manifestations of cystic fibrosis typically 

present in the first 3 decades of life. 

Premature emphysema resulting from 

A1AT deficiency typically manifests 

in the fourth, fifth, and sixth decades 

of life. Emphysema and severe COPD 

most commonly present in the sixth 

and seventh decades of life, though 

they may occur earlier in individuals 

with heavier smoking burdens. 22 

Review of Systems 

In asymptomatic patients, an increasingly 

sedentary lifestyle may point to 

early stages of COPD, because exercise 

tolerance decreases with the onset of 

airway obstruction. At the other extreme, 

patients presenting with unexplained 

weight loss or anorexia may 

have severe COPD, because the high 

metabolic requirements of advanced 

COPD may contribute to weight 

loss. Unexplained disorders of the 

liver or pancreas may suggest A1AT 

deficiency. 23 

Physical Examination—Early in 

the disease process, physical examination 

has relatively little sensitivity from 

a diagnostic standpoint, except for 

disorders with multisystem manifestations. 

As the disease process becomes 

more advanced, physical examination 

yields greater diagnostic value. One of 

the major reasons for a thorough physical 

examination lies in detecting disorders 

that mimic or confound COPD. 

COPD Severity 

100% 

70% 

60% 

50% 

35% 

MILD 

MODERATE 

MODERATELY SEVERE 

SEVERE 

VERY SEVERE 

FEV 1 

, % Predicted* 

Figure 2. Spirometric indices used to grade 

the physiologic severity of chronic obstructive 

pulmonary disease (COPD), according to the 

American Thoracic Society. 36 Lung function is 

measured with the forced expiratory volume in 1 

second (FEV 1 

) test. *FEV 1 

% predicted is the test 

result for the patient as a percent of the predicted 

values for healthy individuals with similar 

characteristics (eg, age, height, race, sex, weight). 

Yellowing teeth and fingernails 

are often an indication of substantial 

cigarette smoke exposure. A cyanotic 

hue to the lips or fingernails may suggest 

the presence of severe COPD associated 

with hypoxia. Clubbing of the 

fingernails—often as a result of chronic 

oxygen deficiency—may be present in 

individuals with advanced COPD, but 

it may also indicate other disorders. 

Pursed-lip breathing typically occurs 

spontaneously in patients with expiratory 

flow obstruction as a way to ease 

dyspnea. 24,25 

Evaluation of the thoracic cavity 

may reveal an increased anteroposterior 

diameter, also known as “barrel 

chest.” This appearance results from 

air trapping, which in turn results in 

chronic hyperinflation of the thoracic 

cavity. Individuals with more severe 

disease and those in acute respiratory 

distress may have intercostal or subcostal 

retractions, leading them to make 

routine use of accessory respiratory 

muscles. The use of these muscles is 

usually a sign of increased work during 

breathing or respiratory muscle fatigue. 

7


Palpation and percussion have little 

diagnostic value in detection of COPD 

in its early stages. However, in the later 

stages of COPD, an examiner may note 

the presence of decreased tactile fremitus 

and hyperresonance to percussion. 

Both findings are the result of hyperinflation 

of the lungs caused by airway 

obstruction. 

Auscultation should be performed 

for all lung fields in a systematic manner. 

Such a systematic progression allows 

for the differentiation of focal 

findings from global findings. In addition, 

detection of normal breath sounds 

in abnormal locations should lead to 

closer inspection and may suggest the 

need for additional testing. Classic respiratory 

signs of COPD include a prolonged 

expiratory phase, wheezing on 

forced exhalation, and decreased breath 

sounds. 26 With the variety of physical 

manifestations of COPD, many of the 

aforementioned findings may or may 

not be present. It should be noted, however, 

that the presence of diminished 

breath sounds in combination with a 

suggestive history is the most consistent 

physical finding in individuals with 

moderate COPD. 26 

A somewhat simple test that can be 

used in the office setting is to time how 

long the patient can forcibly exhale. 

Typically, a forced exhale time of greater 

than 5 seconds may indicate some 

form of airway obstruction. 27 Similarly, 

the inability of a patient to blow out a 

candle at a distance of 12 inches can be 

a useful indication of severe airway obstruction 

in some bedside settings. 

Cardiac examination may reveal 

evidence of right ventricular strain or 

failure, particularly in patients with advanced 

COPD. Sustained point of maximal 

impulse, if present, may suggest 

right ventricular dilatation or hypertrophy. 

Cardiac auscultation will often 

reveal distant heart sounds, secondary 

to lung hyperinflation. A right ventricular 

gallop, increased intensity of P2 

(ie, pulmonic second heart sound), and 

murmurs of pulmonary or tricuspid insufficiency 

are suggestive of right heart 

failure, possibly resulting from severe, 

chronic COPD. With the onset of right 

Celli BR, MacNee W; ATS/ERS Task Force. Standards for the diagnosis and treatment of patients with COPD: 

a summary of the ATS/ERS position paper. Eur Respir J. 2004;23(6):932-946. 

Guidelines: Executive summary: global strategy for diagnosis, management, and prevention of COPD. Global 

Initiative for Chronic Obstructive Lung Disease Web site; December 2009. 

US Preventive Services Task Force. Screening for chronic obstructive pulmonary disease using spirometry: 

US Preventive Services Task Force recommendation statement [published online ahead of print March 3, 

2008]. Ann Intern Med. 2008;148(7):529-534. 

Ferguson GT, Enright PL, Buist AS, Higgins MW. Office spirometry for lung health assessment in adults: a 

consensus statement from the National Lung Health Education Program. Chest. 2000;117(4):1146-1161. 

Figure 3. Recommended reading list for chronic obstructive pulmonary disease. 

heart failure, increased jugular venous 

distention and lower-extremity edema 

may also be observed—findings that 

are indicative of pulmonary hypertension 

or cor pulmonale. 25,26 

Imaging—Like the physical examination, 

most chest imaging techniques 

have relatively poor sensitivity 

for detecting mild to moderate COPD. 

Plain chest radiographs have a sensitivity 

of approximately 50% for diagnosing 

moderate COPD. 28 Radiograph 

findings may include flattening of the 

hemidiaphragms, bullae, increased anteroposterior 

diameter on lateral films, 

and narrowing of the cardiac silhouette. 

Localized or regional emphysema can 

be identified via radiographs in certain 

cases. A finding of basilar emphysema 

may suggest A1AT deficiency, especially 

in younger individuals. Such a finding 

results from a relative increase in blood 

flow, contrasting with the usual finding 

of apical emphysema in smokers. 29 

Computerized tomography (CT) 

scans are useful in identifying bullous 

lung disease and regional emphysema. 

Techniques to assess lung volumes using 

CT scans are available but are not 

routinely used. 

Spirometry—As previously noted, 

spirometry is essential in making a diagnosis 

of COPD and in grading the 

severity of the disease. Standard flowvolume 

loop assessments can often be 

performed in the office with good reliability. 

The objective of these assessments 

is to determine a gross estimation 

of effective lung volume (ie, forced 

vital capacity [FVC]), the effect on airflow 

(ie, the ratio of FEV 1 /FVC), and 

whether there is any reversibility. Reversibility 

is defined as a significant improvement 

in the FVC, FEV 1 , or FEV 1 / 

FVC after the administration of a bronchodilator 

(ie, >200 mL improvement 

in FVC or FEV 1 or 12% increase from 

prebronchodilator measurements). 30 

Physiologic severity of COPD may 

be graded by using the spirometric 

indices shown in Figure 2. 2 Symptomatic 

grading is often more useful from a 

clinical standpoint. 

Indications for performing spirometry 

include the following: chest tightness, 

coughing, dyspnea, occupational 

exposure to dust or chemicals, smokers 

older than 45 years, assessment of bronchodilator 

function, wheezing, and the 

presence of other lung disorders. 

A diagnosis of airflow obstruction 

is typically based on a reduction in the 

FEV 1 /FVC ratio. For practical purposes, 

a ratio value less than 0.7 confirms 

the presence of airflow obstruction. A 

lack of reversibility or an incomplete reversibility 

of the obstruction after bronchodilator 

use secures the diagnosis 

of COPD. Furthermore, the degree to 

which FEV 1 is decreased correlates with 

the severity of COPD (Figure 2). 

It should be noted that spirometric 

severity of disease does not necessarily 

correlate with functional debilitation. 

To assess functional limitations, exercise 

testing is typically necessary. 

Office-based spirometry has been 

validated for use in the diagnosis of 

COPD. 31 However, despite recommendations 

in national COPD guidelines, 

recent data suggest that spirometry in 

the office remains underutilized. 31,32 

Equipment maintenance and quality 

control requirements, practitioner attitudes, 

and inability to interpret results 

are the major speculative reasons for its 

underutilization. 33 Further information 

8


on the use of office-based spirometry 

is available through the National Lung 

Health Education Program (noted in 

the recommended reading in Figure 3). 

Differential Diagnoses 

Many other conditions can have similar 

clinical presentations as COPD. These 

conditions may at times be difficult to 

differentiate from COPD. 

Of special note, asthma and COPD 

can be difficult to differentiate. Both 

diseases have a primary presentation of 

airway obstruction and are associated 

with environmental exposures. However, 

the single most definitive means of 

differentiation between these 2 entities 

concerns the identification of reversibility 

of airway obstruction. Chronic 

obstructive pulmonary disease has 

classically been defined as airway obstruction 

that is not reversible or that 

is only partially reversible with use of 

bronchodilators. Asthma, by contrast, 

is a disease in which nearly complete 

airway reversibility can be achieved. As 

CONDITION 

Asthma 

Bronchiectasis 

Bronchiolitis Obliterans 

Congestive Heart Failure 

Diffuse Panbronchiolitis 

Tuberculosis 

such, airway obstruction that is fully 

reversible with administration of bronchodilators 

is considered to be asthma 

— not COPD. Patients with airway 

obstruction that is not fully reversible 

with administration of bronchodilators 

are considered to have COPD. 34 

These 2 conditions may coexist 

in the sense that an individual with 

asthma as a child may have COPD as 

an adult. Unfortunately, the overlap of 

asthma and COPD, which occurs occasionally, 

creates some difficulty for 

practitioners in regard to diagnosis and 

treatment. 35 For practical purposes, 

however, irreversibility in airway obstruction 

should lead to a diagnosis 

of COPD. Differential diagnosis criteria 

for COPD, based on the American 

Thoracic Society Task Force report, 36 

are shown in Figure 4. 

Conclusion 

Without question, every healthcare 

practitioner will encounter patients 

with COPD, either as a primary 

DIAGNOSTIC CONSIDERATIONS 

Hypersensitivity symptoms may be present 

Nocturnal symptoms may predominate 

Significant reversibility of airway obstruction is possible 

Copious sputum production 

Recurrent infections 

Coarse crackles on auscultation 

Chest computed tomography reveals bronchial dilation and 

bronchial wall thickening 

Patient may have rheumatoid arthritis or fume exposures 

Ground glass opacities seen on chest computed tomography 

Fine basilar crackles 

Radiograph reveals pulmonary edema, cardiomegaly 

No obstruction on spirometry, though restriction may be seen 

Predominant in men, nonsmokers 

Chronic sinusitis present 

Imaging may reveal centrilobular nodular opacities and 

hyperinflation 

Historical cues and risk factors (eg, exposure to endemic region, 

history of incarceration, unexplained weight loss, hemoptysis) 

Positive results to purified protein derivative test, sputum for acid 

fast stain, interferon-γ gold assay 

Figure 4. Differential diagnosis criteria for chronic obstructive pulmonary disease (COPD), based 

on a report by the American Thoracic Society Task Force. 36 

condition or as a confounding illness 

contributing to another medical condition. 

Earlier diagnosis of COPD can 

be achieved by keeping the disorder 

in mind when patients present with 

known risk factors, dyspnea, chronic 

cough, and/or chronic sputum production. 

Furthermore, additional cues derived 

from the patient’s family history, 

tobacco history, age at onset of symptoms, 

and environmental exposures 

provide insights that may lead the practitioner 

to suspect COPD as the culprit. 

Spirometry is considered the diagnostic 

tool of choice for determining 

the presence or absence of obstructive 

airway disease, as well as for grading 

the severity of any obstruction. Furthermore, 

office-based spirometry 

used by properly trained technicians 

and practitioners appropriately trained 

in its interpretation is a recognized 

and effective means of evaluating and 

tracking patients with COPD. 

Take-Home Points 

• COPD should be considered in any 

patient presenting with chronic 

cough, dyspnea, or chronic sputum 

production. 

• Information on family history, tobacco 

use, and potential occupational 

exposures should be elicited 

to discern a patient’s risk for having 

COPD. 

• Spirometry remains the gold standard 

for COPD diagnosis, whether 

performed in a full pulmonary-function 

laboratory or in an appropriately 

staffed office-based practice. 

• Consider α-1-antitrypsin deficiency 

and cystic fibrosis in patients younger 

than 40 years who present with a 

diagnosis of COPD. 

Acknowledgments 

I thank Brian Foresman, DO, for his 

guidance and support in the preparation 

of this article. 

continued… 

9


References 

1. National Heart, Lung, and Blood Institute. 

Morbidity & Mortality: 2009 Chart Book on Cardiovascular, 

Lung, and Blood Diseases. Bethesda, 

MD: National Institutes of Health; 2009:59- 

68. http://www.nhlbi.nih.gov/resources/docs/ 

2009_ChartBook.pdf. Accessed May 27, 2011. 

2. Celli BR, MacNee W; ATS/ERS Task Force. 

Standards for the diagnosis and treatment of patients 

with COPD: a summary of the ATS/ERS 

position paper. Eur Respir J. 2004;23(6):932-946. 

3. Kirkpatrick P, Dransfield M. Racial and sex 

differences in chronic obstructive pulmonary 

disease susceptibility, diagnosis, and treatment. 

Curr Opin Pulm Med. 2009;15(2):100-104. 

4. Mannino DM, Buist AS. Global burden of 

COPD: risk factors, prevalence, and future trends 

[review]. Lancet. 2007;370(9589):765-773. 

5. Lundback B, Lindberg A, Lindstrom M, et al; 

Obstructive Lung Disease in Northern Sweden 

Studies. Not 15 but 50% of smokers develop 

COPD?—Report from the Obstructive Lung 

Disease in Northern Sweden Studies. Respir Med. 

2003;97(2):115-122. 

6. Mannino DM. COPD: epidemiology, prevalence, 

morbidity and mortality, and disease heterogeneity. 

Chest. 2002;121(5 suppl):121S-126S. 

7. US Department of Health and Human Services. 

The Health Consequences of Smoking: Chronic 

Obstructive Lung Disease. A Report of the Surgeon 

General. Washington, DC: US Government 

Printing Office; 1984:32-39. http://profiles.nlm. 

nih.gov/ps/access/NNBCCS.pdf. Accessed May 

27, 2011. 

8. Lange P, Nyboe J, Appleyard M, Jensen G, 

Schnohr P. Relationship of the type of tobacco 

and inhalation pattern to pulmonary and total 

mortality. Eur Respir J. 1992;5(9):1111-1117. 

9. Beck GJ, Doyle CA, Schachter EN. Smoking 

and lung function. Am Rev Respir Dis. 

1981;123(2):149-155. 

10. Withey CH, Papacosta AO, Swan AV, et al. 

Respiratory effects of lowering tar and nicotine 

levels of cigarettes smoked by young male 

middle tar smokers. II. Results of a randomised 

controlled trial. J Epidemiol Community Health. 

1992;46(3):281-285. 

11. Lange P, Groth S, Nyboe J, et al. Decline of 

the lung function related to the type of tobacco 

smoked and inhalation [published correction 

appears in Thorax. 1990;45(3):240]. Thorax. 

1990;45(1):22-26. 

12. Burrows B, Knudson RJ, Cline MG, Lebowitz 

MD. Quantitative relationships between cigarette 

smoking and ventilatory function. Am Rev Respir 

Dis. 1977;115(2):395-205. 

13. Scanlon PD, Connett JE, Waller LA, Altose 

MD, Bailey WC, Buist AS. Smoking cessation 

and lung function in mild-to-moderate chronic 

obstructive pulmonary disease. The Lung Health 

Study. Am J Respir Crit Care Med. 2000;161(2 pt 

1):381-390. 

14. Chronic bronchitis diagnosis. Physicians’ 

Desk Reference Web site. http://www.pdrhealth. 

com/diseases/chronic-bronchitis/diagnosis. Accessed 

June 20, 2011. 

15. Viegi G, Pedreschi M, Pistelli F, et al. Prevalence 

of airways obstruction in a general population: 

European Respiratory Society vs American 

Thoracic Society definition. Chest. 2000;117(5 

suppl 2):339S-345S. 

16. Silverman EK, Chapman HA, Drazen JM, et 

al. Genetic epidemiology of severe, early-onset 

chronic obstructive pulmonary disease. Risk 

to relatives for airflow obstruction and chronic 

bronchitis. Am J Respir Crit Care Med. 1998;157(6 

pt 1):1770-1778. 

17. Webster PM, Lorimer EG, Man SF, Woolf CR, 

Zamel N. Pulmonary function in identical twins: 

comparison of nonsmokers and smokers. Am Rev 

Respir Dis. 1979;119(2):223-238. 

18. Stockley RA. Proteases/antiproteases: pathogenesis 

and role in therapy. Clin Pulm Med. 

1998;5:203-210. 

19. Davis PB. Pathophysiology of the lung disease 

in cystic fibrosis. In: Davis PB, ed. Cystic Fibrosis. 

New York, NY: Marcel Dekker; 1993:193. 

20. Fletcher C, Peto R. The natural history 

of chronic airflow obstruction. Br Med J. 

1977;1(6077):1645-1648. 

21. Becklake MR. Occupational exposures: evidence 

for a causal association with chronic obstructive 

pulmonary disease. Am Rev Respir Dis. 

1989;140(3 pt 2):S85-S91. 

22. A registry of patients with severe deficiency 

of alpha 1-antitrypsin. Design and methods. The 

Alpha 1-Antitrypsin Deficiency Registry Study 

Group. Chest. 1994;106(4):1223-1232. 

23. Hogarth DK, Rachelefsky G. Screening and 

familial testing of patients for α1-antitrypsin deficiency. 

Chest. 2008;133(4):981-988. 

24. Spahija J, de Marchie M, Grassino A. Effects 

of imposed pursed-lips breathing on respiratory 

mechanics and dyspnea at rest and during exercise 

in COPD. Chest. 2005;128(2):640-650. 

25. Currie GP, Legge JS. ABC of chronic obstructive 

pulmonary disease [review]. Diagnosis. BMJ. 

2006;332(7552):1261-1263. 

26. Badgett RG, Tanaka DJ, Hunt DK, et al. Can 

moderate chronic obstructive pulmonary disease 

be diagnosed by historical and physical findings 

alone? Am J Med. 1993;94(2):188-196. 

27. Siafakas NM, Vermeire P, Pride NB, et al. Optimal 

assessment and management of chronic obstructive 

pulmonary disease (COPD). The European 

Respiratory Society Task Force. Eur Respir J. 

1995;8(8):1398-1420. 

28. Wallace GM, Winter JH, Winter JE, Taylor A, 

Taylor TW, Cameron RC. Chest X-rays in COPD 

screening: Are they worthwhile [published online 

ahead of print July 24, 2009]? Respir Med. 

2009;103(12):1862-1865. 

29. Tobin MJ, Hutchison DC. An overview of the 

pulmonary features of alpha 1-antitrypsin deficiency. 

Arch Intern Med. 1982;142(7):1342-1348. 

30. Pellegrino R, Viegi G, Brusasco V, et al. Interpretative 

strategies for lung function tests. Eur 

Respir J. 2005;26(5):948-968. 

31. Han MK, Kim MG, Mardon R, et al. Spirometry 

utilization for COPD: how do we measure up 

[published online ahead of print June 5, 2007]? 

Chest. 2007;132(2):403-409. 

32. Lee TA, Bartle B, Weiss KB. Spirometry use 

in clinical practice following diagnosis of COPD. 

Chest. 2006;129(6):1509. 

33. Lin K, Watkins B, Johnson T, Rodriguez JA, 

Barton MB, US Preventive Services Task Force. 

Screening for chronic obstructive pulmonary 

disease using spirometry: summary of the evidence 

for the US Preventive Services Task Force. 

Ann Intern Med. 2008;148(7):535. 

34. Goedhart DM, Zanen P, Lammers JW. Relevant 

and redundant lung function parameters 

in discriminating asthma from COPD. COPD. 

2006;3(1):33-39. 

35. Yawn BP. Differential assessment and management 

of asthma vs chronic obstructive 

pulmonary disease [published online ahead 

of print January 21, 2009]. Medscape J Med. 

2009;11(1):20. 

36. Standards for the diagnosis and care of patients 

with chronic obstructive pulmonary disease. 

American Thoracic Society. Am J Respir Crit 

Care Med. 1995;152(5 pt 2):S77-S121. 

This guide is supported by Boehringer Ingelheim 

Pharmaceuticals, Inc. 

10


INTERVENTIONS 

for Patients With Chronic Obstructive 


Thomas F. Morley, DO | Amita Pravinkumar Vasoya, DO 

As the prevalence of chronic obstructive pulmonary disease grows, it is important 

for physicians—especially primary care physicians—to understand the prevention 

and treatment options available to patients. From smoking cessation to pulmonary 

rehabilitation and the various pharmacologic and nonpharmacologic options in 

between, the authors review interventions for patients at any disease stage. 

Chronic obstructive pulmonary 

disease (COPD) is a preventable and 

treatable disease with substantial 

extrapulmonary effects that may contribute 

to disease severity in some 

patients. 1 The current emphasis from 

researchers and physicians on prevention 

and management of COPD, even 

with established disease, represents an 

extension of our prior understanding 

of this condition. Various interventions 

can modify the course of COPD 

and survival, as found in a 2008 review 

by Celli. 2 These interventions include 

smoking cessation, 3 long-term oxygen 

therapy in hypoxemic patients, 4,5 

noninvasive ventilation in selected patients, 

6-8 and lung volume reduction 

surgery (LVRS) in patients with upper 

lobe predominant emphysema and 

poor exercise capacity. 9 

The cornerstone of interventions 

at all stages of COPD remains focused 

on prevention and smoking cessation. 

3 The Lung Health Study 12 clearly 

demonstrated that smoking cessation 

decreased the rate of decline in lung 

function and reduced the rate of death 

for all-cause mortality. 3,12 Similarly, the 

use of vaccines has proven effective for 

avoiding and reducing the severity of 

several infectious diseases. Vaccination 

is especially valuable in patients with 

more severe stages of COPD in which 

acute illnesses can lead to muscle loss 

and permanent declines in lung performance. 

In 1998, the Global Initiative for 

Chronic Obstructive Lung Disease 

(GOLD) was formed by experts from 

the World Health Organization and the 

US National Heart, Lung, and Blood 

Institute. The major goals of the group 

were to promote greater awareness of 

COPD, publish evidence-based recommendations 

regarding the prevention 

and management of COPD, and promote 

clinical research. The evidencebased 

guidelines from these initiatives 

were made available on the Internet 

and have been recently updated in the 

report The Global Initiative for Chronic 

Lung Disease: Global Strategy for the 

Diagnosis, Management, and Prevention 

of Chronic Obstructive Pulmonary 

Disease. 1 Similar recommendations for 

Dr Morley is a professor of medicine and Dr Vasoya is an assistant professor of medicine in the Division of 

Pulmonary, Critical Care, and Sleep Medicine at the University of Medicine and Dentistry of New Jersey- 

School of Osteopathic Medicine in Stratford. 


Address correspondence to Thomas F. Morley, DO, 42 E Laurel Rd, Suite 3100, 

Stratford, NJ 08084-1501. E-mail: tmorley@comcast.net 

patients with COPD have also been 

published by the American Thoracic 

Society and European Thoracic Society 

10 and the American College of Physicians. 

11 

Overall, the current approach to 

COPD interventions is based on the 

severity of disease as determined by 

spirometry readings and clinical symptoms 

defined by GOLD (Figure 1). 

Based on a patient’s disease severity, 

the physician adds interventions in an 

incremental or step-wise manner, starting 

with smoking avoidance and cessation. 

This approach improves the overall 

efficacy of interventions, reduces 

cost by avoiding unnecessary interventions, 

and minimizes complications. 

While relatively simple, the GOLD 

panel treatment recommendations 

are applicable to patients with stable 

COPD and those with acute exacerbations. 

The recommendations also provide 

a good foundation for physicians 

who treat patients with COPD. 

Medical interventions for patients 

with COPD can be divided into 2 

interventions: (1) those that are directed 

at symptomatic relief but typically 

have little or no survival benefit and 

(2) those that have limited short-term 

symptomatic benefit but may impart 

survival benefit or disease avoidance. 

11


I: Mild 

FEV 1 

/FVC < 0.70 

FEV 1 

> 80% predicted 

II: Moderate 

FEV 1 

/FVC < 0.70 

50%< FEV 1 

< 80% 

predicted 

Active reduction of risk factor(s): influenza vaccination 

Add short-acting bronchodilator (when needed) 

With 1 possible exception, 13 neither 

inhaled corticosteroids nor long-acting 

β 2 -adrenergic agonists have been 

shown to reduce the rate of decline in 

lung function in COPD patients. In 

the TORCH study, 13 an inhaled steroid 

alone or in combination with a longacting 

β 2 -adrenergic agonist decreased 

the rate of lung function decline, but 

this finding did not translate into significant 

survival benefit. Ultimately, 

the goal of medical therapy for COPD 

is to reduce symptoms, avoid adverse 

effects and complications, and reduce 

exacerbations. In the present article, 

we review the currently used treatment 

options (Figure 2) for patients with 

COPD. 

Pharmacologic Options 

Delivery Mechanisms 

Commonly used formulations of medications 

for patients with COPD are presented 

in the Table. When medications 

are administered by inhalation, careful 

attention must be given to the choice of 

agent. For most patients, metered dose 

III: Severe 

FEV 1 

/FVC < 0.70 

30% < FEV 1 

< 50% 

predicted 

IV: Very Severe 

FEV 1 

/FVC < 0.70 

FEV 1 

< 30% 

predicted or 

FEV 1 

< 50% predicted 

plus chronic respiratory 

failure 

Add regular treatment with one or more long-acting bronchodilators 

(when needed) 

Add rehabilitation 

Add inhaled glucocorticosteroids if repeated 

exacerbations 

Add long-term oxygen 

if chronic respiratory 

failure 

Consider surgical 

treatments 

Figure 1. Therapy at each stage of chronic obstructive pulmonary disease (COPD). Postbronchodilator 

FEV 1 is recommended for the diagnosis and assessment of severity of COPD. Chronic respiratory 

failure defined as arterial partial pressure of oxygen (PaO 2 ) less than 8 kPa (60 mm Hg) with or without 

arterial partial pressure of carbon dioxide (PaCO 2 ) greater than 6.7 kPa (50 mm Hg) while breathing 

air at sea level. Reprinted with permission from U.S. Health Network. 1 Abbreviations: FEV 1 , forced 

expiratory volume in 1 second; FVC, forced vital capacity. 

inhalers are as effective as other inhaled 

preparations and are substantially less 

costly. For metered dose inhalers, patients 

must be instructed on the proper 

technique for inhalation. Proper use remains 

a challenge for many patients attempting 

to coordinate the inhaler with 

the actuator. Under most circumstances, 

the use of a chamber or spacer for 

the delivery of inhaled medications will 

improve delivery and efficacy. Powder 

formulations of medications are typically 

designed to avoid the need for a 

chamber and may be technically easier 

for some patients. Patients with severe 

COPD (ie, forced expiratory volume 

in 1 second [FEV 1 ],


o BRONCHODILATORS 

• β 2 

-adrenergic agonists 

• Anticholinergic medications 

> Combined short-acting β 2 

-agonist 

with short-acting anticholinergic 

> Combined long-acting β 2 

-agonist 

with long-acting anticholinergic 

• Methylxanthine agents 

o ANTI-INFLAMMATORY AGENTS 

• Corticosteroids 

> Combined long-acting β 2 

-agonists 

with inhaled corticosteroids 

o ANTIBIOTICS 

o MUCOLYTIC AGENTS 

o VACCINES 

o ANTITUSSIVES 

o NONPHARMACOLOGIC OPTIONS 

• Oxygen 

• Pulmonary rehabilitation 

• Noninvasive ventilation 

o SURGICAL TREATMENTS 

• Lung volume reduction surgery 

• Lung transplantation 

• Bullectomy 

Figure 2. Treatment options for patients with 

chronic obstructive pulmonary disease. 

halation, became more widely available 

in the early 1990s. Working through 

a cholinergic blockade mechanism, 

these agents provided a bronchodilator 

effect through a different pathway 

than β 2 -adrenergic agonists. In COPD, 

as compared to asthma, the relative 

bronchodilatory effect of anticholinergics 

was often greater than that of the 

β 2 -adrenergic agonists. Adverse effects 

were common until the first of the new 

generation agents, ipratropium bromide, 

was released. The duration of 

action was about 6 hours. Newer and 

longer-acting agents are now available 

and have improved the management 

of COPD symptoms. For example, 

the long-acting anticholinergic agent, 

tiotropium, is efficacious for at least 

24 hours. Adverse effects associated 

with the newer anticholinergic medications 

are usually mild but may include 

dry mouth, urinary retention, narrow 

angle glaucoma, and hypersensitivity 

reactions. 

The combination of short-acting 

anticholinergic and short-acting 

β 2 -adrenergic agonists has been examined 

in patients with moderately 

severe, stable COPD. A 12-week prospective, 

double-blind trial compared 

the combination of albuterol and ipratropium 

with each agent alone to 

determine the degree of spirometric 

improvement during the first 4 hours 

after administration. 28 The agents were 

administered by metered-dose inhaler. 

Results from the study 28 indicated that 

combination therapy was more effective 

than either agent alone in terms of 

spirometric improvement. Symptom 

scores did not change over time and 

did not differ among treatment groups. 

Similar findings have been noted when 

a nebulized combination product containing 

both albuterol and ipratropium 

was compared to single agent therapy. 29 

Methylxanthine Agents—Methylxanthine 

agents are older and less used 

today because of their greater adverse 

effects, lesser efficacy, and need for serum 

monitoring. However, these medications 

offer some selected patients 

benefit through improved diaphragmatic 

function and effects on mucociliary 

function. Theophylline, the primary 

agent in this class, is a less potent 

bronchodilator than β 2 -adrenergic or 

anticholinergic agents. Theophylline 

is given either intravenously or orally. 

Serum levels should be monitored and 

plasma levels should generally not exceed 

12 μg/mL because higher levels 

are associated with greater toxicity in 

older patients. 27 Dosing may also be affected 

by food, drug interactions, and 

slowed metabolism in some patient 

populations (eg, elderly patients, cirrhotic 

patients). Theophylline is most 

beneficial for patients with severe 

COPD in whom other therapies failed 

and particularly patients with carbon 

dioxide retention. 

Corticosteroids 

Corticosteroids, which are not approved 

for use as monotherapy, are 

available in inhalation, oral, and intravenous 

forms. Regular treatment 

with inhaled corticosteroids has been 

shown to reduce the frequency of acute 

exacerbations, improve health status, 

improve lung function, and reduce use 

of rescue medication. 30-36 Most studies 

37-39 of inhaled corticosteroids have 

not demonstrated any improvement 

in the rate of decline in lung function. 

However, the TORCH study group 13 

was able to demonstrate a slower rate 

of decline of lung function in patients 

treated with either fluticasone propionate 

alone or the combination of 

fluticasone propionate and salmeterol. 

This trial 13 was a large, randomized, 

double-blind, placebo-controlled study 

that followed patients with moderate to 

severe COPD for 3 years. When compared 

to placebo, the differences in the 

primary end point of all-cause mortality 

was not statistically significant for 

any treatment group. 26 

The adverse effects of inhaled corticosteroids 

are usually minor, including 

upper airway thrush and dysphonia. 

However, an increased potential for 

pneumonia has been reported with the 

use of inhaled corticosteroids, 26,40 and 

withdrawal of inhaled corticosteroids 

may also be associated with acute exacerbations 

in certain patients. 36 

The use of oral maintenance corticosteroids 

is not recommended for 

patients with stable COPD because the 

systemic adverse effects of corticosteroids 

outweigh their potential benefits. 

However, oral corticosteroids are indicated 

as outpatient therapy for patients 

with acute COPD exacerbations. 41 

Intravenous corticosteroids may be 

used for inpatient acute exacerbations, 

although oral steroids are probably 

equally efficacious. 

Combined Bronchodilators 

and Corticosteroids 

Multiple studies 26,31,33,34,42-44 have demonstrated 

that an inhaled corticosteroid 

combined with a long-acting 

β 2 -adrenergic agonist is more effective 

than either component alone in improving 

lung function and health status 

and reducing exacerbations. However, 

such combined therapy may increase 

the risk of pneumonia. 26 Survival benefit 

of these combined agents remains 

uncertain. As noted previously, a large 

prospective trial was unable to demonstrate 

a survival benefit from combined 

therapy. 26 To our knowledge, only 1 

13


14 

DRUG 

β 2-agonists 

INHALER, μg 

SOLUTION for 

NEBULIZER, 

mg/mL 

ORAL 

VIALS for 

INJECTION, 

mg 

Short-acting 

Fenoterol 100-200 (MDI) 1 0.05% (syrup) 4-6 

Levabuterol 45-90 (MDI) 0.21, 0.42 6-8 

Salbutamol 

(albuterol) 

100, 200 (MDI, 

DPI) 

5 5 mg (pill), 

0.024% (syrup) 

0.1, 0.5 4-6 

DURATION of 

ACTION, hr 

Terbutaline 400, 500 (DPI) 2.5, 5 (pill) 0.2, 0.25 4-6 

Long-acting 

Formoterol 4.5-12 (MDI, DPI) 0.01* 12+ 

Arformoterol 0.0075 12+ 

Salmeterol 25-50 (MDI, DPI) 12+ 

Anticholinergics 

Short-acting 

Ipratropium 20, 40 (MDI) 0.25-0.5 6-8 

bromide 

Oxitropium bromide 100 (MDI) 1.5 7-9 

Long-acting 

Tiotropium 18(DPI), 5 (SMI) 24+ 

Combination short-acting β 2 

-agonists plus anticholinergic in 1 inhaler 

Fenoterol/ 

200/80 (MDI) 1.25/0.5 6-8 

Ipratropium 

Salbutamol/ 75-15 (MDI) 0.75/4.5 6-8 

Ipratropium 

Methylxanthines 

Aminophylline 

200-600 mg 

(pill) 

240 Variable, up 

to 24 

Theophylline (SR) 

Inhaled glucocorticosteroids 

Beclomethasone 50-400 

(MDI, DPI) 

Budesonide 100, 200, 400 

(DPI) 

Fluticasone 

50-500 (MDI, DPI) 

0.2-0.4 

0.20, 0.25, 0.5 

100-600 mg 

(pill) 

Triamcinolone 100 (MDI) 40 40 

Combination long-acting β 2 

-agonists plus glucocorticosteroids in 1 inhaler 

Formoterol/ 

budesonide 

Salmeterol/ 

fluticasone 

4.5/160, 9/320 

(DPI) 

50/100, 250, 500 

(DPI) 

25/50, 125, 250 

(MDI) 

Systemic glucocorticosteroids 

Prednisone 

Methylprednisolone 

5-60 mg (pill) 

4, 8, 16 mg (pill) 

* Formoterol nebulized solution is based on the unit dose vial containing 20 μg in a volume of 2.0 mL. 

Abbreviations: DPI, dry powder inhaler; MDI, metered dose inhaler; SMI, soft mist inhaler. 

Source: Reprinted with permission from U.S. Health Network. 

Variable, up 

to 24 

Table. Commonly Used Formulations of Drugs Used in Chronic Obstructive Pulmonary Disease 

study 13 to date has shown that inhaled 

salmeterol, fluticasone, or both salmeterol 

and fluticasone reduced the rate 

of FEV 1 decline in COPD patients with 

moderate or severe disease. A 6-week, 

multicenter, randomized, double-blind 

trial of patients with moderate COPD 

demonstrated superiority in lung function 

of the combination of inhaled 

tiotropium plus formoterol compared 

with the combination of salmeterol and 

fluticasone. 45 These data suggest that 

some disease modification might occur 

with combination bronchodilators and 

corticosteroids; however, confirmation 

of this effect awaits the completion of 

long-term studies. 

Nonpharmacologic 

Therapy 

Oxygen 

Oxygen therapy has a positive impact 

on hemodynamics, hematologic features, 

exercise capacity, lung mechanics, 

and mental state. 46 Long-term oxygen 

given for longer than 12 hours per 

day by nasal cannula has been shown to 

improve survival in chronically hypoxemic 

COPD patients. 4,5 Further benefit 

is derived when used 24 hours per day. 

Patients should be evaluated for the 

need of oxygen therapy using arterial 

blood gas or an assessment of oxygen 

saturation when they are clinically 

stable breathing room air. In most instances, 

an exercise evaluation may also 

be helpful. If the arterial oxygen saturation 

is less than or equal to 88%, or 

the arterial oxygen tension is less than 

or equal to 55 mm Hg, then the patient 

qualifies for supplemental oxygen. In 

circumstances where the arterial oxygen 

tension is 56 to 59 mm Hg or the 

saturation is 89%, the patient qualifies 

for supplemental oxygen if they have 

dependent edema suggesting congestive 

heart failure, pulmonary hypertension, 

cor pulmonale, or a hematocrit 

greater than 56%. 

Lung Volume Reduction Surgery 

During LVRS, severely emphysematous 

tissue is removed from both upper 

lung lobes. This operation allows 

the remaining lung to expand and the


diaphragm to assume a more normal 

position. A randomized trial of LVRS 

vs medical therapy for patients with 

severe COPD did not demonstrate a 

reduction in mortality for the LVRS 

patients. 9,47 However, improvement in 

lung function, exercise capacity, and respiratory 

quality of life was statistically 

significant. In a subgroup of patients 

with mostly upper lobe emphysema 

and low baseline exercise capacity, reduction 

of mortality was statistically 

significant. However, for patients with 

non-upper lobe predominant emphysema 

and higher baseline exercise 

capacity mortality was higher in the 

LVRS group than the medical therapy 

group. Patients with a FEV 1 

of no more 

than 20% predicted and either homogeneous 

emphysema or a carbon monoxide 

diffusing capacity of no more 

than 20% had a higher mortality. 47 

Lung Transplantation 

In patients with severe pulmonary emphysema, 

lung transplantation can normalize 

pulmonary function, improve 

exercise capacity, and restore quality 

of life. 48-51 The effect of lung transplantation 

on survival is unclear. 2 Median 

survival for lung transplantation is 

about 5 years and is significantly lower 

than for other solid organs. 27 When 

selecting candidates for lung transplantation 

functional status, projected 

survival without transplant, comorbidities, 

and patient preferences should be 

considered. Generally, patients should 

be younger than 65 years and without 

medical or psychiatric conditions that 

could worsen predicted survival. 2 A 

high BODE index, a multidimensional 

index for COPD survival, can help 

select patients for lung transplantation. 

52 Criteria that may help primary 

care physicians identify potential lung 

transplantation candidates include a 

FEV 1 of less than 35% predicted, PaO 2 

less than 55 to 60 mm Hg, PaCO 2 greater 

than 50 mm Hg, and secondary pulmonary 

hypertension. 53,54 

Pulmonary Rehabilitation 

Pulmonary rehabilitation is a multidisciplinary 

program designed to 

maximize lung function, improve gas 

exchange, optimize conditioning, and 

address nutritional issues. Typically, 

pulmonary rehabilitation programs are 

outpatient based. Patients in pulmonary 

rehabilitation are usually GOLD 

stage 2 or 3 (Figure 1) in terms of disease 

severity, but patients with more 

or less severe disease may also benefit. 

Patients who cannot ambulate, have 

unstable cardiac disease, or have neurologic 

problems or cognitive dysfunction 

may not be appropriate candidates 

for rehabilitation. 

Pulmonary rehabilitation does not 

directly improve lung mechanics or 

gas exchange. 55 Rather, it optimizes 

the function of other body systems to 

reduce the impact of lung dysfunction. 

56 These effects are derived from 

improved muscle function, reduction 

in dynamic hyperinflation, and desensitization 

to dyspnea. 57 Improvements 

in depression and social interactions 

may also contribute to the benefits of 

pulmonary rehabilitation. 57 

The major element of a pulmonary 

rehabilitation program is exercise. 

Generally, exercise of the legs is emphasized 

with walking (eg, on a treadmill) 

or cycling. High-intensity (target, 60% 

of maximal endurance) or lower-intensity 

regimens are determined based 

on patient tolerance. Upper extremity 

training can improve patients’ ability to 

perform their activities of daily living. 

Respiratory muscle training is no longer 

commonly used because it does not 

lead to increased functional capacity. 58 

Ancillary treatments, including optimal 

bronchodilation during rehabilitation 

session and use of supplemental 

oxygen, are also helpful. 57 

Cachexia in patients with COPD 

causes a depletion of lean body mass 

and is associated with a poor prognosis. 

Nutritional evaluation identified 

the patients with cachexia so that 

nutritional support can be provided; 

therefore, nutritional evaluations are a 

routine part of pulmonary rehabilitation. 

Unfortunately, nutritional interventions 

have not been uniformly effective 

in clinical trials for a variety of 

reasons. 59 Patients with COPD who are 

overweight have a greater degree of exercise 

limitation because of the effects 

of obesity on lung function. Weight loss 

is uniformly prescribed for these patients, 

but data on efficacy are lacking. 

Studies 60-62 have shown a positive 

effect for pulmonary rehabilitation regarding 

reductions in hospitalizations 

and other measures of healthcare utilization, 

as well as improvements in 

cost-effectiveness. Although pulmonary 

rehabilitation has not been shown 

to improve survival in COPD patients, 

the randomized trials that have investigated 

survival were inadequately powered 

to detect this effect. 58 

Conclusion 

Treatment of patients with COPD warrants 

an aggressive approach beginning 

with smoking cessation at the earliest 

15


possible stage. A variety of pharmacologic 

and nonpharmacologic therapies 

are available for COPD patients, who 

can improve their function and quality 

of life. Recent evidence suggests that 

acute exacerbations of COPD play an 

important part in disease progression 

and, therefore, a focus on prevention 

should be a part of any therapeutic consideration. 

63 Myriad medications have 

been found to reduce the frequency 

of exacerbations, and some medications 

or combinations of medications 

may slow disease progression in these 

patients. Together with smoking cessation, 

all of these therapies offer hope for 

a population of patients becoming ever 

more prevalent worldwide. 

References 

1. The Global Initiative for Chronic Obstructive 

Lung Disease: Global Strategy for the Diagnosis, 

Management, and Prevention of Chronic Obstructive 

Pulmonary Disease. Gig Harbor, WA: Medical 

Communications Resources, Inc; 2009. 

2. Celli BR. Update on the management of 

COPD. Chest. 2008;133(6):1451-1462. 

3. Anthonisen NR, Skeans MA, Wise RA, Manfreda 

J, Kanner RE, Connett JE. The effects of 

a smoking cessation intervention on 14.5-year 

mortality. Ann Intern Med. 2005;142(4):233-239. 

4. Nocturnal Oxygen Therapy Trial Group. Continuous 

or nocturnal oxygen therapy in hypoxemic 

chronic obstructive lung disease: a clinical 

trial. Ann Intern Med. 1980;93(3):391-398. 

5. Report of the Medical Research Council Working 

Party. Long term domiciliary oxygen therapy 

in chronic hypoxic cor pulmonale complicating 

chronic bronchitis and emphysema. Lancet. 

1981;1(8222):681-686. 

6. Brochard L, Mancebo J, Wysocki M, et al. 

Noninvasive ventilation for acute exacerbation 

of chronic obstructive pulmonary disease 

[published correction appears in N Engl 

J Med. 1996;334(11):743]. N Engl J Med. 

1995;333(13):817-822. 

7. Kramer N, Meyer TJ, Meharg J, Cece RD, 

Hill NS. Randomized, prospective trial of noninvasive 

positive pressure ventilation in acute 

respiratory failure. Am J Respir Crit Care Med. 

1995;151(6):1799-1806. 

8. Bott J, Carroll MP, Conway JH, et al. 

Randomised controlled trial of nasal ventilation 

in acute ventilatory failure due to 

chronic obstructive airways disease. Lancet. 

1993;341(8860):1555-1557. 

9. Fishman A, Martinez F, Naunheim K, et 

al; National Emphysema Treatment Trial Research 

Group. A randomized trial comparing 

lung-volume-reduction surgery with medical 

therapy for severe emphysema. N Engl J Med. 

2003;348(21):2059-2073. 

16 

10. Celli BR, MacNee W; ATS/ERS Task Force. 

Standards for the diagnosis and treatment of patients 

with COPD: a summary of the ATS/ERS 

position paper [published correction appears 

in Euro Respir J. 2006;27(1):242]. Euro Respir J. 

2004;23(6):932-946. 

11. Qaseem A, Snow V, Shekelle P; for the Clinical 

Efficacy Assessment Subcommittee of the 

American College of Physicians. Diagnosis and 

management of stable chronic obstructive pulmonary 

disease: a clinical practice guideline 

from the American College of Physicians. Ann 

Intern Med. 2007;147(9):633-638. 

12. Anthonisen NR, Connett JE, Kiley JP, et al. 

Effects of smoking intervention and the use of 

an inhaled anticholinergic bronchodilator on the 

rate of decline of FEV 1 : the Lung Health Study. 

JAMA. 1994;272(19):1497-1505. 

13. Celli BR, Thomas NE, Anderson JA, et al. 

Effect of pharmacotherapy on rate of decline of 

lung function in chronic obstructive pulmonary 

disease: results from the TORCH study. Am J 

Respir Crit Care Med. 2008;178(4):332-338. 

14. Vanthenen AS, Britton JR, Ebden P, Cookson 

JB, Wharrad HJ, Tattersfield AE. High-dose inhaled 

albuterol in severe chronic airflow limitation. 

Am J Respir Dis. 1988;138(4):850-855. 

15. Gross NJ, Petty TL, Friedman M, Skorodin 

MS, Silvers GW, Donohue JF. Dose response 

to ipratropium as a nebulized solution in patients 

with chronic obstructive pulmonary disease: 

a three-center study. Am Rev Respir Dis. 

1989;139(5):1188-1191. 

16. Chrystyn H, Mulley BA, Peake MD. Dose 

response relation to oral theophylline in severe 

chronic obstructive airways disease. BMJ. 

1988;297(6662):1506-1510. 

17. Higgins BG, Powell RM, Cooper S, Tattersfield 

AE. Effect of salbutamol and ipratropium 

bromide on airway calibre and bronchial reactivity 

in asthma and chronic bronchitis. Eur Respir J. 

1991;4(4):415-420. 

18. Ikeda A, Nishimura K, Koyama H, Izumi T. 

Bronchodilating effects of combined therapy 

with clinical dosages of ipratropium bromide 

and salbutamol for stable COPD: comparison 

with ipratropium bromide alone. Chest. 

1995;107(2):401-405. 

19. Guyatt GH, Townsend M, Pugsley SO, et 

al. Bronchodilators in chronic air-flow limitation. 

Effects on airway function, exercise capacity, 

and quality of life. Am Rev Respir Dis. 

1987;135(5):1069-1074. 

20. Man WD, Mustfa N, Nikoletou D, et al. Effect 

of salmeterol on respiratory muscle activity during 

exercise in poorly reversible COPD. Thorax. 

2004;59(6):471-476. 

21. O’Donnell DE, Flüge T, Gerken F, et al. Effects 

of tiotropium on lung hyperinflation, dyspnea, 

and exercise tolerance in COPD. Euro Respir J. 

2004;23(6):832-840. 

22. Vincken W, van Noord JA, Greefhorst APM, 

et al; Dutch/Belgian Tiotropium Study Group. 

Improved health outcomes in patients with 

COPD during 1 yr’s treatment with tiotropium. 

Eur Respir J. 2002;19(2):209-216. 

23. Mahler DA, Donohue JF, Barbee RA, et al. Efficacy 

of salmeterol xinafoate in the treatment of 

COPD. Chest. 1999;115(4):957-965. 

24. Tashkin DP, Celli B, Senn S, et al; UPLIFT 

Study Investigators. A 4-year trial of tiotropium 

in chronic obstructive pulmonary disease [published 

online ahead of print October 5, 2008]. N 

Engl J Med. 2008;359(15):1543-1554. 

25. Sin DD, McAlister FA, Man SFP, Anthonisen 

NR. Contemporary management of chronic obstructive 

pulmonary disease: scientific review. 

JAMA. 2003;290(17):2301-2312.


26. Calverley PMA, Anderson JA, Celli B, et al; 

TORCH Investigators. Salmeterol and fluticasone 

propionate and survival in chronic obstructive 

pulmonary disease. N Engl J Med. 

2007;356(8):775-789. 

27. Niewoehner DE. Outpatient management of 

severe COPD [clinical practice]. N Engl J Med. 

2010;362(15):1407-1416. 

28. COMBIVENT Inhalation Aerosol Study 

Group. In chronic obstructive pulmonary disease, 

a combination of ipratropium and albuterol 

is more effective than either agent alone: an 85- 

day multicenter trial. Chest. 1994;105(5):1411- 

1419. 

29. Gross N, Tashkin D, Miller R, Oren J, Coleman 

W, Linberg S; Dey Combination Solution 

Study Group. Inhalation by nebulization of albuterol-ipratropium 

combination (Dey combination) 

is superior to either agent alone in the treatment 

of chronic obstructive pulmonary disease. 

Respiration. 1998;65(5):354-362. 

30. Lung Health Study Research Group. Effect of 

inhaled triamcinolone on the decline in pulmonary 

function in chronic obstructive pulmonary 

disease. N Engl J Med. 2000;343(26):1902-1909. 

31. Mahler DA, Wire P, Horstman D, et al. Effectiveness 

of fluticasone propionate and salmeterol 

combination delivered via the Diskus 

device in the treatment of chronic obstructive 

pulmonary disease. Am J Respir Crit Care Med. 

2002;166(8):1084-1091. 

32. Jones PW, Willits LR, Burge PS, Calverley PM; 

Inhaled Steroids in Obstructive Lung Disease in 

Europe study investigators. Disease severity and 

the effect of fluticasone propionate on chronic 

obstructive pulmonary disease exacerbations. 

Eur Respir J. 2003;21(1):68-73. 

33. Calverley P, Pauwels R, Vestbo J, et al; for 

the TRISTAN (TRial of Inhaled STeroids ANd 

long-acting β 2 agonists) study group. Combined 

salmeterol and fluticasone in the treatment of 

chronic obstructive pulmonary disease: a randomised 

controlled trial [published correction 

appears in Lancet. 2003;361(9369):1660]. Lancet. 

2003;361(9356):449-456. 

34. Szafranski W, Cukier A, Ramirez A, et al. Efficacy 

and safety of budesonide/formoterol in the 

management of chronic obstructive pulmonary 

disease. Eur Respir J. 2003;21(1):74-81. 

35. Spencer S, Calverley PMA, Burge PS, Jones 

PW. Impact of preventing exacerbations on deterioration 

of health status in COPD. Eur Respir J. 

2004;23(5):698-702. 

36. van der Valk P, Monninkhof E, van der Palen 

J, Zielhuis G, van Herwaarden C. Effect of discontinuation 

of inhaled corticosteroids in patients 

with chronic obstructive pulmonary disease: 

the COPE Study [published online ahead 

of print September 5, 2002]. Am J Respir Crit 

Care Med. 2002;166(10):1358-1363. doi:10.1164/ 

rccm.200206-512OC. 

37. Pauwels RA, Löfdahl CG, Laitinen LA, et al. 

Long-term treatment with inhaled budesonide 

in persons with mild chronic obstructive pulmonary 

disease who continue smoking. N Engl J 

Med. 1999;340(25):1948-1953. 

38. Vestbo J, Sørensen T, Lange P, Brix A, 

Torre P, Viskum K. Long-term effect of inhaled 

budesonide in mild and moderate chronic obstructive 

pulmonary disease: a randomised controlled 

trial. Lancet. 1999;353(9167):1819-1823. 

39. Burge PS, Calverley PM, Jones PW, Spencer 

S, Anderson JA, Maslen TK. Randomised, double 

blind, placebo controlled study of fluticasone 

propionate in patients with moderate to severe 

chronic obstructive pulmonary disease: the 

ISOLDE trial. BMJ. 2000;320(7245):1297-1303. 

40. Drummond MB, Dasenbrook EC, Pitz MW, 

Murphy DJ, Fan E. Inhaled corticosteroids in 

patients with stable chronic obstructive pulmonary 

disease: a systematic review and metaanalysis 

[published correction appears in JAMA. 

2009;301(10):1024]. JAMA. 2008;300(20):2407- 

2416. 

41. Aaron SD, Vandemheen KL, Herbert P, Dales 

R, Stiell IG, Ahuja J, et al. Outpatient oral prednisone 

after emergency treatment of chronic 

obstructive pulmonary disease. N Engl J Med. 

2003;348(26):2618-2625. 

42. Hanania NA, Darken P, Horstman D, et al. 

The efficacy and safety of fluticasone propionate 

(250 µg)/salmeterol (50 µg) combined in th Diskus 

inhaler for the treatment of COPD. Chest. 

2003;124(3):434-443. 

43. Calverley PM, Boonsawat W, Cseke Z, Zhong 

N, Peterson S, Olsson H. Maintenance therapy 

with budesonide and formoterol in chronic obstructive 

pulmonary disease [published correction 

appears in Euro Respir J. 2004;24(6):1075]. 

Euro Respir J. 2003;22(6):912-919. 

44. Kardos P, Wencker M, Glaab T, Vogelmeier 

C. Impact of salmeterol/fluticasone propionate 

versus salmeterol on exacerbations in severe 

chronic obstructive pulmonary disease [published 

online ahead of print October 19, 2006]. 

Am J Respir Crit Care Med. 2007;175(2):144-149. 

doi:10.1164/rccm.200602-244OC. 

45. Rabe KF, Timmer W, Sagkriotis A, Viel K. 

Comparison of a combination of tiotropium, plus 

formoterol to salmeterol plus fluticasone in moderate 

COPD [published online ahead of print 

April 10, 2008]. Chest. 2008;134(2):255-262. doi: 

10.1378/chest.07-2138 

46. Tarpy SP, Celli BR. Long-term oxygen therapy. 

N Engl J Med. 1995;333(11):710-714. 

47. National Emphysema Treatment Trial Research 

Group. Patients at high risk of death after 

lung-volume-reduction surgery. N Engl J Med. 

2001;345(15):1075-1083. 

48. Patterson GA, Maurer JR, Williams TJ, Cardoso 

PG, Scavuzzo M, Todd TR; The Toronto 

Lung Transplant Group. Comparison of outcomes 

after double and single lung transplantation 

for obstructive lung disease. J Thorac Cardiovasc 

Surg. 1999;110(4):623-632. 

49. Bando K, Paradis I, Keenan R, et al. Comparison 

of outcomes after single and bilateral lung 

transplantation for obstructive lung disease. J 

Heart Lung Transplant. 1995;14(4):692-698. 

50. Orens JB, Becker FS, Lynch JP III, Christensen 

PJ, Deeb GM, Martinez FJ. Cardiopulmonary 

exercise testing following allogenic lung 

transplantation for different underlying disease 

states. Chest. 1995;107(1):144-149. 

51. Hosenpud JD, Bennett LE, Keck BM, Boucek 

MM, Novick RJ. The Registry of the International 

Society for Heart and Lung Transplantation: 

eighteenth official report—2001. J Heart Lung 

Transplant. 2001;20(8):805-815. 

52. Orens JB, Estenne M, Arcasoy S, et al; Pulmonary 

Scientific Council of the International 

Society for Heart and Lung Transplantation. International 

guidelines for the selection of lung 

transplant candidates: 2006 update—a consensus 

report from the Pulmonary Scientific Council 

of the International Society for Heart and 

Lung Transplantation. J Heart Lung Transplant. 

2006;25(7):745-755. 

53. Hosenpud JD, Bennett LE, Keck BM, Edwards 

EB, Novick RJ. Effect of diagnosis on survival 

benefit of lung transplantation for end-stage 

lung disease. Lancet. 1998;351(9095):24-27. 

54. Maurer JR, Frost AE, Estenne M, Higenbottam 

T, Glanville AR; The International Society 

for Heart and Lung Transplantation, the American 

Thoracic Society, the American Society of 

Transplant Physicians, the European Respiratory 

Society. International guidelines for the selection 

of lung transplant candidates. Transplantation. 

1998;66(7):951-956. 

55. Cassaburi R, Petty TL, eds. Principles and 

Practice of Pulmonary Rehabilitation. Philadelphia, 

PA: W.B. Saunders Company; 1993. 

56. Nici L, Donner C, Wouters E, et al; ATS/ 

ERS Pulmonary Rehabilitation Writing Committee. 

American Thoracic Society/European 

Respiratory Society statement on pulmonary 

rehabilitation. Am J Respir Crit Care Med. 

2006;173(12):1390-1413. 

57. Cassaburi R, ZuWallack R. Pulmonary rehabilitation 

for management of chronic obstructive 

pulmonary disease. N Engl J Med. 

2009;360(13):329-335. 

58. Ries AL, Bauldoff GS, Carlin BW, et al. Pulmonary 

rehabilitation: Joint ACCP/AACVPR 

Evidence-Based Clinical Practice Guidelines. 

Chest. 2007;131(5 suppl):4S-42S. 

59. Ferreira IM, Brooks D, Lacasse Y, Goldstein 

RS, White J. Nutritional supplementation for 

stable chronic obstructive pulmonary disease. 

Cochrane Database Syst Rev. 2005;2:CD000998. 

60. Griffiths TL, Burr ML, Campbell I, et al. Results 

at 1 year of outpatient multidisciplinary 

pulmonary rehabilitation: a randomised controlled 

trial [published correction appears 

in Lancet. 2000;355(9211):1280]. Lancet. 

2000;355(9201):362-368. 

61. California Pulmonary Rehabilitation Collaborative 

Group. Effects of pulmonary rehabilitation 

on dyspnea, quality of life, and healthcare 

costs in California. J Cardiopulm Rehabil. 

2004;24(1):52-62. 

62. Griffiths TL, Phillips CJ, Davies S, Burr ML, 

Campbell IA. Cost effectiveness of an oupatient 

multidisciplinary pulmonary rehabilitation programme. 

Thorax. 2001;56(10):779-784. 

63. Anzueto A. Impact of exacerbations on 

COPD. Eur Respir Rev. 2010;19(116):113-118 



17


COMORBIDITIES and 

Systemic Effects in COPD 

Kartik Shenoy, MD | Fredric Jaffe, DO 

Chronic obstructive pulmonary disease (COPD) is primarily thought to be a 

disease confined to the lungs. However, recent evidence suggests that COPD 

is a systemic disease with associated comorbidities that can affect quality 

of life, morbidity, and mortality. Conditions such as cardiovascular disease, 

musculoskeletal dysfunction, osteoporosis, and diabetes mellitus are all part 

of the systemic manifestations of COPD. The present article reviews the causal 

link between COPD and these comorbid conditions and touches on management 

of these diseases in patients with COPD. 


disease (COPD) has been viewed as a 

disease that is confined to the lungs. 

However, recent evidence suggests 

that a variety of comorbidities are associated 

with COPD and can affect the 

course of disease in a patient. 1 Many of 

these comorbidities, which have smoking 

as a common risk factor, include— 

but are not limited to—cardiac disease, 

diabetes mellitus, and skeletal muscle 

dysfunction. Large epidemiologic studies 

have established an independent 

detrimental effect of these conditions 

on patients with COPD. 2 Therefore, 

treatment strategies for patients with 

COPD should include management of 

these nonpulmonary sequelae that contribute 

to the burden of COPD. 

Mortality and 

Cardiovascular Disease 

Currently, COPD is the fourth leading 

cause of death in the United States, and 

compared with other diseases, such as 

heart disease or stroke, death rates are 

on the rise. 3 In patients with COPD, it 

is unclear whether patients are more 

likely to die from other comorbidities 

or whether COPD is the main cause 

of death. Cardiovascular disease, one 

of the leading causes of death in the 

United States, is the most common comorbidity 

in patients with COPD. In a 

cohort of nearly 400,000 patients from 

Veterans Administration (VA) clinics, 

researchers found that the prevalence 

of coronary artery disease was significantly 

higher in those with COPD 

than those without COPD (33.6% compared 

with 27.1%). 4 In another study of 

45,000 patients, Sidney et al 5 found that 

those patients with COPD had a higher 

risk of hospitalization and mortality 

from cardiovascular disease. 5 Similarly, 

Holguin et al 6 studied comorbidity and 

mortality in COPD-related hospitalizations. 

They found that there was an 

increased prevalence and higher 

in-hospital mortality in patients with 

From the Division of Pulmonary and Critical Care Medicine at Temple University School of Medicine in 

Philadelphia, Pennsylvania. 


E-mail: kartik.shenoy@tuhs.temple.edu or fredric.jaffe@tuhs.temple.edu 

COPD who had ischemic heart disease 

and congestive heart failure than in 

those without COPD. 6 

It can be argued that the common 

risk factor of smoking has increased 

the incidence of cardiovascular disease 

in patients with COPD. However, 

there is evidence that patients with 

COPD have a risk that is above and beyond 

that related to smoking alone. In 

one study, 7 patients with symptoms of 

chronic bronchitis had a 50% increase 

in cardiovascular mortality when controlled 

for age, sex, and amount of 

smoking. 

There is also a link between lower 

forced expiratory volume in 1 second 

(FEV 1 

), a surrogate measure of smoking, 

and cardiovascular disease. Hole et 

al 8 found that subjects with lower FEV 1 

(


asked, risk of cardiovascular mortality 

was present whether the patients were 

current smokers, previous smokers, or 

never smokers. 

Still, questions remain as to why 

there is an elevated risk of cardiovascular 

disease in patients with COPD; 

this has not been fully elucidated. One 

reason may be related to systemic inflammation, 

as there have been strong 

links between systemic inflammation 

and cardiovascular disease. Serum 

markers of inflammation such as 

C-reactive protein (CRP) have been 

linked to increased risk of cardiac disease 

and have also been shown to be 

increased in patients with stable COPD 

as well as in those with exacerbations. 

An inflammatory link between cardiovascular 

disease and COPD can thus 

be speculated. Once again, smoking 

tobacco may play a role in that smoking 

can increase inflammatory markers. 

9 Some have postulated that in addition 

to smoking cessation, the use of 

statin medications may be of benefit in 

those with COPD by exerting an antiinflammatory 

effect. Although there 

have been no prospective studies, some 

retrospective studies have shown the 

use of statins along with angiotensinconverting 

enzyme inhibitors or angiotensin 

receptor blockers may reduce 

cardiovascular mortality in patients 

with COPD. 10 

The accurate assessment of coronary 

artery disease in a COPD patient 

can be problematic because of ventilatory 

limitations during exercise and 

inability to attain a target heart rate 

needed for accurate assessment of cardiac 

ischemia. In addition, pharmacologic 

tests can be problematic due to 

the use of adenosine or dipyridamole, 

which may cause bronchospasm in 

patients with COPD. If needed, dipyridamole 

testing may be used in select 

patients with COPD, where disease 

is less severe. Assessment of cardiac 

function with dobutamine echocardiography 

testing may be safe in the 

general population, but hyperinflation 

related to COPD can limit the accuracy 

of this testing. Lung tissue of patients 

with COPD can obscure the echocardiogram 

probe resulting in imaging 

that is difficult to interpret. Coronary 

computed tomography is an alternative 

to the above testing, but it has not 

been specifically validated in those 

with COPD. Careful consideration of 

respiratory reserve should be made before 

ordering assessment for coronary 

artery disease in patients with COPD. 

β-Blockers are a cornerstone drug 

in the medical management of coronary 

artery disease. Some clinicians fear precipitating 

bronchospasm in those with 

COPD with β-blockers. Data suggest 

that cardioselective β-blockers can be 

used safely in COPD patients for the 

management of known coronary disease. 

11 Nonetheless, caution should be 

exercised when treating patients with 

reversible airflow obstruction such as 

asthma. The large amount of data that 

support the use of these medications 

in patients with heart disease suggests 

that every effort should be taken to 

administer these medications. Coexistent 

cardiovascular disease should be 

carefully considered in a patient with 

COPD. Efforts to diagnose and treat 

cardiovascular disease likely will improve 

patient outcomes. 

Skeletal Muscle 

Dysfunction and 

Nutritional Status 

Musculoskeletal dysfunction can cause 

significant morbidity in patients with 

COPD and affects survival in these patients. 

Patients with a low body mass 

index (BMI) and decreased fat-free 

mass have been linked to increased 

mortality compared to patients with a 

normal BMI. 12 The cause of musculoskeletal 

dysfunction in COPD is multifactoral. 

A combination of malnutrition, 

decreased activity, and use of 

glucocorticoids all play a role in musculoskeletal 

dysfunction. Recent data 

point to oxidative stress and systemic 

inflammation contributing to muscle 

dysfunction. Clinicians may assume 

that musculoskeletal dysfunction only 

occurs in those with more severe disease; 

however, new evidence suggests 

otherwise. For instance, Coronell et 

al 13 assessed quadriceps endurance in 

patients with mild to moderate COPD. 

Even during normal physical activity, 

these patients had decreased strength 

and endurance. 13 Therapies that exist 

to ameliorate muscle dysfunction 

in patients with COPD consist of pulmonary 

rehabilitation, modified nutritional 

supplementation, and use of 

pharmacologic agents to increase fatfree 

mass. 

The GOLD II guidelines 14 recommend 

pulmonary rehabilitation in all 

patients with moderate COPD, but 

it is likely that even those with mild 

disease can derive benefit. Upper and 

lower extremity strength training with 

light aerobic exercise increases endurance, 

improves symptoms of dyspnea, 

and enhances quality of life. 14 Cote 

et al 15 found, in patients with severe 

COPD (mean FEV 1 

32%), that rehabilitation 

provided a survival advantage 

and decreased hospital utilization. 

15 Unfortunately, improvements 

conferred by pulmonary rehabilitation 

diminish if exercise is discontinued, 

and patients should be urged to continue 

exercises at home. Fewer data are 

available on the optimal time to begin 

rehabilitation and whether repeating 

rehabilitation program has benefit. 

Overall, patients who start to develop 

even subtle functional limitations 

should be referred to a rehabilitation 

program. 

Having a low BMI is a risk factor 

for all-cause mortality, but the optimal 

timing of referral to nutritional support 

has not been established in patients 

with COPD. Most studies of nutritional 

support involve patients whose COPD 

is well controlled without multiple exacerbations. 

More evidence suggests 

that weight loss follows a stepwise 

progression and worsening nutritional 

status may be related to acute exacerbations 

of COPD. 16 

Schols and Wouters 17 proposed a 

simple screening process that involves 

measurement of BMI and weight course 

(Figure 1). First, patients are characterized 

as underweight (BMI


than 10% loss in the past 6 months or 

greater than 5% in 1 month. Nutritional 

supplementation would then be indicated 

in specific subgroups. Nutritional 

interventions may only involve diet 

modification; however, some patients 

require energy-dense supplements. 

These products should be spaced out 

throughout the day to avoid appetite 

loss and adverse ventilatory effects due 

to higher caloric encumbrance. 

Other options to help combat musculoskeletal 

dysfunction involve the 

use of anabolic steroids and growth 

hormone replacement therapy. Unfortunately, 

most studies with these agents 

have yielded less than ideal results with 

respect to increases in weight, muscle 

mass, and exercise tolerance, but others 

have shown modest yet consistent 

increases in muscle function. In one 

study, addition of growth hormone in 

patients with COPD increased muscle 

mass but did not increase exercise tolerance. 

18 The use of testosterone in 

healthy subjects increases muscle mass 

and power, which are compounded 

by strength training; however, as with 

growth hormone, use of testosterone in 

patients with COPD has yielded mixed 

results. 

There are many factors related to 

COPD that may cause musculoskeletal 

dysfunction, including inactivity, 

steroid use, malnutrition, and oxidative 

stress. Goals of increased physical 

activity, improved nutritional intake, 

limitation of systemic steroids, and 

possible pharmacologic interventions 

may improve quality of life and possibly 

mortality in patients with COPD by 

improving skeletal muscle function. 

Osteoporosis 

Patients with COPD are at risk for osteoporosis 

for several reasons, such as 

smoking tobacco, inactivity, malnutrition, 

and a low BMI. These risk factors, 

combined with increased age and corticosteroid 

use, all play a role in putting 

these patients at high risk for the development 

of osteoporosis. For patients 

with COPD, the approach to minimize 

osteoporosis risk should involve screening, 

risk reduction, and treatment. 

SCREENING 

TREATMENT 

CONTROL 

Weight 

Loss 

Traditionally, screening was offered 

to postmenopausal women or 

patients with COPD taking oral glucocorticoids. 

However, screening a 

larger cohort of patients with COPD 

may be prudent. Evidence from Praet 

et al, 19 who studied bone mineral density 

(BMD) in men with chronic bronchitis, 

suggests more patients may be at 

risk. They found that patients who were 

on bronchodilators alone had substantially 

worse BMD than an age-matched 

control population. 19 Pino-Montes et 

al 20 also studied COPD patients who 

had no prior use of glucocorticoids and 

found that they had lower BMD compared 

to age-matched controls. 

The risk of osteoporosis in patients 

on inhaled corticosteroids is debatable. 

Studies specifically looking at patients 

with COPD who use inhaled corticosteroids 

lack conclusive evidence. 21 Some 

have found worsening BMD, while others 

have found no significant difference 

compared with placebo arms. 21 Overall 

it seems short-term use of ICS at low 

doses does not pose a statistically significant 

risk. However, those who are 

Underweight Normal Weight Overweight 

Low FFM 

Responder 

Maintenance 

Therapy 

Oral/Enteral 

Suppletion 

Anabolic 

Stimulation 

Stable 

Weight 

Weight 

Loss 

Stable 

Loss 

Stable 

Normal 

Low FFM 

Nutrition Intervention 

Control 

Normal 

Nonresponder 

Compliance 

Improvement 

Oral/Enteral 

Suppletion 

Anabolic 

Stimulation 

Figure 1. Nutritional screening and treatment algorithm for patients with chronic obstructive 

pulmonary disease. Abbreviation: FFM, fat-free mass. Reprinted with permission from Clinics in 

Chest Medicine. 17 

on inhaled corticosteroids at higher 

doses may be at a risk above and beyond 

the already increased risk of being 

a patient with COPD. 

Osteoporosis or osteopenia is often 

asymptomatic and may cause little 

morbidity. However, the fractures related 

to them can be detrimental, especially 

in patients who are respiratory 

limited. Thoracic and vertebral fractures 

can substantially alter lung function. 

Hip fractures can cause pain and 

immobility. Worsening lung function 

coupled with immobility worsens the 

quality of life for patients with COPD. 

Further studies are needed to specifically 

address morbidity and mortality 

effects of fractures in COPD. 

With the high potential for morbidity 

and mortality in patients with 

osteoporosis and COPD, physicians 

should screen and treat these patients 

aggressively. Establishing which patients 

should be screened can be difficult. 

It can be argued that screening 

every COPD patient for osteoporosis 

is important because of the fact that 

20


patients with COPD have worsened 

BMD compared to age-matched populations, 

as previously discussed. However, 

Biskobing 22 suggested a more 

narrow population of screening postmenopausal 

women, premenopausal 

women, men with hypogonadism, and 

men and women with low BMI or history 

of fracture related to osteoporosis 

(Figure 2). Screening is also recommended 

for patients who are about to 

start long-term, high-dose inhaled corticosteroids 

or an oral corticosteroid 

program (>7.5 mg/d). These patients 

should be followed with repeat BMD 

testing every 2 years. 22 Those taking 

long-term oral glucocorticoids should 

be evaluated more frequently, generally 

every 6 to 12 months. 22 

Treatment strategies involve calcium 

and vitamin D supplementation, 

physical therapy, hormonal replacement, 

and use of bisphosphonates. 

Those at risk for osteoporotic fractures 

should be started on calcium and vitamin 

D supplementation. Hormone 

replacement can be offered to those 

who have hypogonadism unless contraindicated. 

All patients who are at 

risk will benefit from physical therapy. 

Treatment for postmenopausal women 

has been established by the American 

College of Physicians. 23 Any postmenopausal 

woman with a T score on BMD 

testing of less than -2 or less than -1.5 

with risk factors should begin treatment. 

23 When it comes to men who are 

not on oral corticosteroids the data are 

less clear. Orwoll 24 suggested that men 

with T scores less than -2.0 may be candidates 

for treatment. 

Every patient on long-term oral 

corticosteroids should receive calcium 

and vitamin D supplementation. 22 The 

use of bisphosphonates in this group 

should be guided by BMD testing and 

risk factors. High-risk postmenopausal 

women with normal BMD can be offered 

hormone replacement therapy 

or bisphosphonates if contraindicated. 

Others should have bisphosphonates 

added if T score on BMD testing is less 

than -1. Women on oral corticosteroids 

with normal T scores and no other risk 

factors should be followed up every 6 

o Measure bone mineral density in the following high-risk patients at baseline: 

• Those on chronic oral glucocorticoids or high-dose inhaled glucocorticoids 

• Postmenopausal women 

• Premenopausal women with amenorrhea 

• Hypogonadal men 

• History of fracture 

• Body mass index


for acute exacerbations of COPD and 

in long-term diabetes mellitus management 

as it relates to COPD. 

Dyslipidemia, like diabetes mellitus, 

has strong links to smoking and cardiovascular 

disease. 28 Smoking is known to 

cause an increase in low-density lipoprotein 

(LDL), triglycerides, and verylow-density 

lipoproteins. However, 

studies on lipid profiles and COPD are 

lacking. It is currently unknown if dyslipidemia 

is another disease process independently 

associated with COPD. A 

systematic review 29 revealed that there 

have been small retrospective trials to 

show the benefit of statin use in COPD. 

Though most of these trials investigated 

exacerbation rates, intubations, and 

lung function, a small subset has shown 

decreased mortality rates. 29 It is unclear 

whether this mortality benefit lies in 

correcting dyslipidemia, reducing systemic 

inflammation, or halting decline 

of lung function. Further studies need 

to elucidate the relationship between 

lipid profile and COPD. 

Conclusion 

Chronic obstructive pulmonary disease 

has long been thought of as a disease 

limited to the lungs. However, emerging 

evidence elucidates the impact of 

comorbidities in this patient population. 

Strong links to cardiovascular disease, 

musculoskeletal dysfunction, and 

osteoporosis have been made. Weaker 

links have been made to dyslipidemia 

and diabetes mellitus. The concept of 

systemic inflammation is an emerging 

subject that may link COPD and 

these comorbidities. For primary care 

physicians, aggressive management of 

these comorbidities is paramount to 

the treatment of patients with COPD. 

Further data are needed in the optimal 

management of comorbidities in relation 

to COPD. Aggressive treatment 

of these conditions likely will improve 

quality of life and may alter outcomes 

in patients with COPD. 

References 

1. Chatila WM, Thomashow BM, Minai OA, 

Criner GJ, Make BJ. Comorbidities in chronic 

obstructive pulmonary disease [review]. Proc Am 

Thorac Soc. 2008;5(4):549-555. 

22 

2. van Mannen JG, Bindels PJ, Ijzemans CJ, van 

der Zee JS, Bottema BJ, Schadé E. Prevalence of 

comorbidity in patients with a chronic airway obstruction 

and controls over the age of 40. J Clin 

Epidemiol. 2001;54(3):287-293. 

3. Jemal A, Ward E, Hao Y, Thun M. Trends in the 

leading causes of death in the United States, 1970- 

2002. JAMA. 2005;294(10):1255-1259. 

4. Maple DW, Dedrick D, Davis K. Trends and 

cardiovascular comorbidities of COPD patients 

in the Veterans Administration Medical System, 

1991-1999. COPD. 2005;2(1):35-41. 

5. Sidney S, Sorel M, Quesenberry CP Jr, Deluise 

C, Lanes S, Eisner MD. COPD and incident 

cardiovascular disease hospitalizations and mortality: 

Kaiser Permanente Medical Care Program. 

Chest. 2005;128(4);2068-2075. 

6. Holguin F, Folch E, Redd SC, Mannino DM. 

Comorbidity and mortality in COPD-related 

hospitalization in the United States; 1979 to 2001. 

Chest. 2005;128(4);2005-2011. 

7. Jousilahti P, Vartiainen E, Tuomilehto J, Puska 

P. Symptoms of chronic bronchitis and the risk 

of coronary disease. Lancet. 1996;348(9027):567- 

572. 

8. Hole DJ, Watt GC, Davey-Smith G, Hart CL, 

Gillis CR, Hawthorne VM. Impaired lung function 

and mortality risk in men and women: findings 

from the Renfrew and Paisley prospective 

population study. BMJ. 1996:313(7059):711-715. 

9. Wannamethee SG, Lowe GD, Sharper AG, 

Rumley A, Lennon L, Whincup PH. Associations 

between cigarette smoking, pipe/cigar smoking, 

and smoking cessation and haemostatic and inflammatory 

markers for cardiovascular disease 

[published online ahead of print April 7, 2005]. 

Eur Heart J. 2005;26(17):1765-1773. 

10. Mancini GB, Etminan M, Zhang B, Levesque 

LE, Fitzgerald JM, Brophy JM. Reduction of 

morbidity and mortality by statins, angiotensin 

converting enzyme inhibitors, and angiotensin 

receptor blockers in patients with chronic obstructive 

pulmonary disease [published online 

ahead of print May 2, 2006]. J Am Coll Cardiol. 

2006:47(12);2554-2560. 

11. Salpeter S, Ormiston T, Salpeter E. Cardioselective 

β-blockers for chronic obstructive 

pulmonary disease. Cochrane Database Syst Rev. 

2005;(4):CD003566. doi:10.1002/14651858. 

12. Vestbo J, Prescott E, Almdal T, et al. Body 

mass, fat-free body mass, and prognosis in patients 

with chronic obstructive pulmonary disease 

from a random population sample: findings 

from the Copenhagen City Heart Study. Am J 

Respir Crit Care Med. 2006:173(1);75-83. 

13. Coronell C, Orozco-Levi M, Méndez R, 

Ramírez-Sarmiento A, Gáldiz JB, Gea J. Relevance 

of assessing quadriceps endurance in patients 

with COPD. Eur Respir J. 2004;24(1):129- 

136. 

14. Rabe KF, Hurd S, Anzueto A, et al. Global 

strategy for the diagnosis and management of 

chronic obstructive pulmonary disease: GOLD 

executive summary. Am J Respir Crit Care Med. 

2007;176(6):532-555. 

15. Cote CG, Celli BR. Pulmonary rehabilitation 

and the BODE index in COPD. Eur Respir J. 

2005;26(4):630-636. 

16. Vermeeren MA, Schols AM, Wouters EF. Effects 

of an acute exacerbation on nutritional and 

metabolic profile of patients with COPD. Eur 

Respir J. 1997;10(10):2264-2269. 

17. Schols AM, Wouters EF. Nutritional abnormalities 

and supplementation in chronic obstructive 

pulmonary disease. Clin Chest Med. 

2000;21(4):753-762. 

18. Burdet L, de Muralt B, Schutz Y, Pichard C, 

Fitting JW. Administration of growth hormone 

to underweight patients with chronic obstructive 

pulmonary disease. Am J Respir Crit Care Med. 

1997:156(6);1800-1806. 

19. Praet J, Peretz A, Rozenberg S, Famaey JP, 

Bourdoux P. Risk of osteoporosis in men with 

chronic bronchitis. Osteoporos Int. 1992:2(5);257- 

261. 

20. del Pino-Montes J, Fernandez J, Gomez F. 

Bone mineral density is related to emphysema 

and lung function in chronic obstructive pulmonary 

disease [abstract]. J Bone Miner Res. 

1999;14(suppl):SU331. 

21. Gartlehner G, Hansen RA, Carson SS, Lobr 

KN. Efficacy and safety of inhaled corticosteroids 

in patients with COPD: a systematic review and 

meta-analysis of health outcomes. Ann Fam Med. 

2006:4(3);253-262. 

22. Biskobing DM. COPD and osteoporosis [review]. 

Chest. 2002:121(2);609-620. 

23. Qaseem A, Snow V, Shekelle P, Hopkins R, 

Forclea M, Owens D; Clinical Efficacy Assessment 

Subcommittee of the American College 

of Physicians. Pharmacologic treatment of low 

bone mineral density or osteoporosis to prevent 

fractures: a clinical practice guideline from the 

American College of Physicians. Ann Intern Med. 

2008:149(6);404-415. 

24. Orwoll ES. Treatment of osteoporosis in men 

[review] [published online ahead of print July 29, 

2004]. Calcif Tissue Int. 2004:75(2);114-119. 

25. Walter RE, Beiser A, Givelber RJ, O’Connor 

GT, Gottlieb DJ. Association between glycemic 

state and lung function: the Framingham 

Heart Study. Am J Respir Crit Care Med. 

2003:167(6);911-916. 

26. Bolton CE, Evans M, Ionescu AA, et al. Insulin 

resistance and inflammation—a further systemic 

complication of COPD. COPD. 2007:4(2);121- 

126. 

27. Baker EH, Janaway CH, Phillips BJ, et al. Hyperglycemia 

is associated with poor outcomes in 

patients admitted to hospital with acute exacerbation 


[published online ahead of print January 31, 

2006]. Thorax. 2006:61(4);284-289. 

28. Craig WY, Palomaki GE, Haddow JE. Cigarette 

smoking and serum lipid and lipoprotein 

concentrations: an analysis of published data. 

BMJ. 1998:298(6676);784-788. 

29. Janda S, Park K, FitzGerald JM, Etminan M, 

Swiston J. Statins in COPD: a systematic review 

[published online ahead of print April 17, 2009]. 

Chest. 2009:136(3);734-743.


OSTEOPATHIC PRINCIPLES 

and Practice in Chronic Obstructive 


Stephen J. Miller, DO, MPH 

The author reviews the literature to identify investigations on the use of 

osteopathic principles and practice in patients with or suspected of having chronic 

obstructive pulmonary disease (COPD). The author primarily sought to determine 

the impact of osteopathic structural diagnosis as a guide to treatment and the 

role of manipulative interventions in the treatment of patients with COPD. Some 

studies tested the use of osteopathic manipulation in a test population of patients 

with COPD vs a control population; however, no studies tested a fully integrated 

approach that combined osteopathic principles with osteopathic manipulative 

treatment. Because successful management of COPD requires substantial lifestyle 

changes, including smoking cessation, diet, exercise, occupational, family, and 

other considerations, studies are needed that consider physicians’ practice of both 

osteopathic principles and OMT appropriately targeted to patients with COPD. 


disease (COPD) is caused by chronic 

bronchial and parenchymal inflammation 

that progressively obstructs 

expiratory airflow and is not fully reversible. 

1 The prevalence of COPD is 

increasing worldwide. It was the sixth 

leading cause of death worldwide in 

1990, and it is projected to be the third 

leading cause of death by 2020. 2 Because 

of the condition’s prevalence, 

thousands of published studies related 

to the diagnosis and management of 

chronic obstructive pulmonary disease 

exist. However, there are relatively few 

studies that approach treatment from 

an osteopathic perspective—specifically, 

the use of osteopathic principles and 

practice (OPP), of which osteopathic 

manipulative treatment (OMT) is a 

very important and useful modality. 3,4 

Osteopathic medicine’s philosophy 

is based on the following 4 principles 3,4 : 

1. The human being is a dynamic unit 

of function. 

2. The body possesses self-regulatory 

mechanisms that are self-healing in nature. 

3. Structure and function are interrelated 

at all levels. 

4. Rational treatment is based on these 

principles. 

The Educational Council on Osteopathic 

Principles (ECOP) developed 

a curriculum for osteopathic medical 

Dr Miller discloses that he sees patients with COPD and uses OMT as part of his treatment plan, for which 

LMU-DCOM bills and receives payment for in the course of usual healthcare delivery. 

Address correspondence to Stephen J. Miller, DO, MPH, Lincoln Memorial University-DeBusk College of 

Osteopathic Medicine, 6965 Cumberland Gap Parkway, Harrogate, TN 37752-8245. 

E-mail: stephen.miller@lmunet.edu 

education based on these principles 

designed to create physicians who are 

health—rather than disease—oriented 

by treating each patient as an equal 

partner (adult-to-adult) in attaining 

health. The ECOP developed “five basic 

integrative and coordinated body 

functions … that were considered in a 

context of healthful adaptation to life 

and its circumstances” to nurture such 

physician growth. These functions are 

as follows 3 : 

1. Posture and motion 

2. Gross and cellular respiratory and 

circulatory factors 

3. Metabolic processes of all types 

4. Neurologic integration 

5. Psychosocial, cultural, behavioral, 

and spiritual elements. 

When practiced together, these 

functions represent a holistic approach 

to patient care. 3,4 I conducted the 

23


present review to uncover studies that 

used or supported the use of OPP and 

OMT with COPD patients. 

Methods 

Between July 2010 and September 2010, 

I conducted a search on PubMed using 

the following MeSH terms: pulmonary 

disease, chronic obstructive; lung diseases, 

obstructive; primary health care; 

physicians, family; manipulation, osteopathic; 

manipulation, orthopedic; 

smoking cessation; and counseling. I 

also conducted searches in UpToDate, 

ClinicalTrials.gov, OSTMED.DR, and 

http://www.osteopathic-research.com/ 

using the same terms. During this time, 

articles were also found by examining 

the bibliographies of helpful articles. 

Review articles, trials with results, and 

other articles were chosen based on 

their containing relevant content. Articles 

with similar content, such as management 

techniques for smoking cessation, 

were sometimes excluded when 

another article provided more relevant, 

more extensive, or newer coverage of 

the topic. Findings were grouped to 

better understand the role of OPP in 

COPD management. 

Results 

Two articles were found through the 

PubMed search on the use of OPP and 

OMT in patients with COPD. The bibliographies 

of the articles were used to 

find additional articles. The PubMed 

24 

search was expanded to include MeSH 

terms for lung diseases, primary care, 

family physicians, and orthopedic manipulation 

as well as appropriate keywords. 

Of the more than 300 articles 

found, recent articles were chosen 

based on relevance and other criteria. 

A PubMed MeSH search that incorporated 

terms for smoking cessation, 

primary healthcare, family physicians, 

and COPD yielded 34 articles, which 

are referenced in the remainder of the 

present article. 

Recognizing the Presence of 

Disease 

Despite its common occurrence, 

COPD remains difficult to diagnose in 

its prodromal and early stages. Clinical 

signs may be vague, 1,5-7 and spirometry 

remains underutilized as a simple, 

office-based diagnostic tool because of 

reimbursement issues and other factors. 

8,9 Clinical guidelines such as the 

Global Initiative for Chronic Obstructive 

Lung Disease (GOLD) have set 

objective standards for diagnosis and 

staging of COPD by pulmonary function. 

1 In addition, several researchers, 

such as Stallberg et al, 10 have developed 

clinical questionnaires in an effort to 

improve disease recognition and to encourage 

treatment. 

Osteopathic physicians appear to 

underutilize their palpatory skills to aid 

in diagnosis or management of COPD. 

In an Ohio study published in 2003, few 

osteopathic physician specialists used 

OMT in patients with COPD. 11 This 

behavior may represent an observed 

downward trend by residents in osteopathic 

graduate medical education 

programs to practice their skills while 

in training. 12 Likewise, a 2003 study by 

Chamberlain and Yates 13 found that 

most osteopathic medical students 

believed they would use palpatory diagnosis 

and osteopathic manipulative 

treatment (OMT) for fewer than 25% 

of their patients (and primarily for 

structural complaints). These studies 

suggest a downward trend in perceived 

usefulness of manipulation as a current 

medical best practice. The value of detecting 

and treating viscerosomatic reflexes 

14-17 appears to be on the decline 

in daily osteopathic medical practice. 

Recognizing and Addressing 

Risk Factors 

Patients at risk of developing COPD 

frequently have clinical signs that include 

chronic cough (with or without 

sputum production), wheeze, and exertional 

dyspnea. 6 These signs should 

alert physicians to the possibility of 

COPD. The additional presence of 

smoking tobacco in 80% to 90% of 

patients with these chronic symptoms 

should be an obvious signal of increased 

risk of COPD. 5 Nonetheless, 

physicians routinely fail to recognize 

and act on these important clues to the 

absence of health in their patients and 

prevent progression to COPD. 1 

In a 2003 review, Mannino found 

that nearly half of patients with chronic 

cough suggesting COPD were undiagnosed, 

despite exhibiting symptoms 

that might have led their physicians to 

perform pulmonary function testing. 6 

van der Molen 7 cited a study by van 

Schayck, 18 in which pulmonary function 

testing found that 1049 of 3016 

smokers had COPD undiagnosed by 

their physicians. Holistic emphasis is 

an important part of osteopathic medical 

training. Dating back to Andrew 

Taylor Still, MD, DO, we understand 

that practicing healthy behaviors leads 

to wellness, and we recognize the importance 

of detecting symptoms that 

signal incipient disease. We are trained 

to help the ill patient back to health, 

rather than just treat disease. 19 This 

training is especially helpful as we craft 

treatments with our patients. 

Crafting Evidence-Based 

Treatment Options With Your 

Patients 

Smoking Cessation—Smoking cessation 

remains the cornerstone for 

treatment of patients with COPD and 

are the major interventions known to 

reduce disease morbidity and mortality. 

20 However, patients face a difficult 

task in the decision to quit smoking. 

They may be emotionally drained, frequently 

blaming themselves for their


illness, and they may despair that the 

onset of symptoms heralds an irreversible 

decline that smoking cessation will 

not stop. 21 They may have a history of 

several failed attempts to quit that further 

haunts them. The primary care 

physician who elicits and addresses 

these emotional cues in their patients 

may empower them to successfully quit. 

Education for accurate self-assessment 

of disease risk, co-morbid conditions, 

and family support are also 

important factors that the primary 

care physician must help their patients 

address as part of their empowerment. 

Self-help programs and cessation medication 

can be beneficial as well. 22,23 

Pulmonary rehabilitation programs 

are another possible intervention. One 

such activity led by Bourbeau et al 24 

in the late 1990s found statistically 

significant improvements in patients’ 

health status through in-home weekly 

visits by health professionals. Another 

by Norrhall et al 25 in 2009 enrolled 

84 smokers with COPD in a lifestyle 

modification course with healthcare 

professionals. According to the study, 

47% of the patients quit smoking tobacco 

and remained smoke-free up to 

1 year after the intervention. A 2008 

review of Canadian pulmonary rehabilitation 

programs using inspiratory 

muscle training and exercise training 

showed improved quality of life of the 

programs’ participants and a nearly 

50% reduced risk of hospitalization for 

acute exacerbations. 26 

All of these examples highlight the 

importance of knowing your patients’ 

needs in order to craft treatment with 

the most likelihood for success. That 

success comes most often when physician, 

patient, family, and available 

healthcare and community supports 

work together, yet another example of 

osteopathic principles in practice. 

Pharmacotherapy—The goal of 

pharmaceuticals in treating patients 

with COPD is to improve quality of 

life—no medication has been shown 

to reduce COPD-related mortality. 2,21 

β-Agonists, anticholinergics, combination 

therapy, and inhaled corticosteroids 

all are given to reduce patient 

symptoms, ease exacerbations, enhance 

possible exercise, and improve 

ability to perform activities of daily 

living. Physicians who reduce patients’ 

symptoms and improve their abilities 

to perform activities of daily living incur 

trust. Creating patient trust is an 

important outcome. 21 The physician 

who practices the holistic approach will 

emphasize these positive outcomes not 

as chronic disease treatment, but rather 

as paths to better health. A patient so 

motivated and who has well-founded 

trust in a physician is more likely to 

consider attempting the most beneficial, 

but hardest to accomplish, treatment 

option—smoking cessation. 

Osteopathic Manipulative Treatment—Several 

articles have chronicled 

the use of OMT in diagnosis and management 

of chronic COPD. In 1973, 

Howell et al 27 reported results of OMT 

in a patient with COPD diagnosed by 

clinical symptoms. The authors progressively 

applied OMT in the areas 

of greatest restriction in the thoracic 

spine and chest cage for 16 months. 

There was a reported reduction in the 

patient’s clinical symptoms and improvement 

in his oxygen saturation, 

but objective measures did not support 

the clinical improvement. 27 A followup 

study 28 of 11 patients followed for 

9 months with a similar protocol had 

similar results. 

In a small study of COPD patients, 

Miller 29 found that 92% of patients 

treated with spinal manipulation and 

thoracic lymph drainage had improvement 

in their physical work capacity. 

Similar to other studies, there was a 

worsening of patients’ residual volume 

and total lung capacity. 

More recently, in 2006, Noll et al 30 

conducted a study of 35 patients with 

COPD based on GOLD criteria. Eighteen 

patients received a session of OMT 

and 17 had a sham treatment. Again, 

the OMT group had a worsening of 

residual volume and total lung capacity 

following this single treatment session 

of 7 protocol techniques, which 

included thoracic lymphatic pump 

(TLP) with activation. Patients also 

had a statistically significant decrease 

in forced expiratory flow at 25% and 

50% of vital capacity and at the midexpiratory 

phase. The authors postulated 

that the worsening residual volume 

and total lung capacity were due 

to overmanipulation. In a follow-up 

study in 2009, Noll et al 31 tested this 

hypothesis in 25 patients with TLP and 

activation, TLP without activation, rib 

raising, and myofascial release in sequential 

sessions of 4-week intervals. 

Again, all OMT sessions worsened pulmonary 

function mildly, with the TLP 

with activation group having the most 

deleterious effect on residual volume. 31 

Despite the worsening objective data, 

all patients reported an easing of symptoms. 

31 None of these studies identified 

or determined long-term impact on the 

subjects. 

Monitoring Management Efforts 

With Evidence-Based Modalities 

The most successful monitoring may 

be diaries that chronicle patients’ abilities 

to perform activities of daily living 

and exercise and that showcase reduced 

symptoms alongside smoke-free days. 21 

Conversely, efforts to link objective 

data such as peak flow measurements 

with smoking cessation have had mixed 

results. 32,33 The holistically practicing 

primary care physicians’ task then 

is to help patients focus on daily life 

successes such as symptom improvement, 

better work capacity, and fewer 

exacerbations as a result of smoking 

cessation. Crane 34 suggests managing 

tobacco addiction as a chronic illness 

requiring expert care, adding counseling 

to patient-individualized plans and 

psychosocial support that is overseen 

by the patient’s primary care physician. 

Pederson and Blumenthal 35 stressed 

the need for primary care physicians 

to ask patients about tobacco use—the 

primary intervention a clinician can do 

to motivate a patient to quit. Pederson 

and Blumenthal 35 also highlighted the 

US public health service “five R” clinical 

guidelines (relevance, risks, rewards, 

roadblocks, and repetition) 36 for those 

patients who are pre-contemplative or 

contemplative as a useful method for 

helping such patients reach the conclusion 

to plan for and attempt cessation. 

25


Research published in 2009 by Secades-Villa 

et al 37 showed success using 

these strategies. Patients randomly assigned 

to a smoking cessation program 

consisting of 20-minute sessions with 

a psychologist weekly for 5 weeks and 

overseen by their primary care physician 

maintained a cessation rate of 

42.8% 12 months after the intervention. 

The intervention tasked patients 

to compare their subjective view of 

health to number of days abstaining 

from smoking, social reinforcement of 

abstinence to number of days abstaining, 

social reinforcements available and 

used to continue abstinence, and physiologic 

feedback on cigarette abstinence 

through reductions in carbon monoxide 

levels. 37 

A 2005 Cochrane review included 

an analysis of 58 trials where treatment 

conditions differed in format (self help, 

individual counseling with person-toperson 

contact, proactive telephone 

counseling, or group counseling) and 

estimated an odds ratio of 1.7 (95% 

confidence interval, 1.4-2.0) for successful 

cessation with individual counseling 

compared to no intervention. 38 

The 2008 update for managing tobacco 

use and dependence by the US Agency 

for Healthcare Research and Quality 39 

showed that adding tobacco use status 

to vital signs in typical patient encounters 

with primary care physicians 

dramatically increased the incidence 

26 

of physician-driven interventions. This 

intervention was shown to be effective 

even when the only assessment to determine 

patients’ readiness to quit was 

to simply ask if the patient is ready to 

quit. It was successful when it involved 

patient-physician discussion of at least 

3 minutes duration delivered during 4 

or more separate encounters. Therefore, 

if possible, clinicians should address 

tobacco use each visit and schedule 3 

to 4 follow-up visits with any patient 

expressing a willingness to consider 

quitting. 39 Lastly, Conroy et al 40 found a 

direct correlation between patient satisfaction 

with their primary care physician 

and their physician’s efforts to help 

them quit smoking. We found no studies 

that combined such simple sequential 

intervention with OMT. 

Comment 

Many studies have demonstrated a 

beneficial therapeutic effect of OMT 

in acute pulmonary conditions such as 

pneumonia. 41-43 However, in the treatment 

of patients with chronic COPD, 

there has been a clear trend that symptomatic 

improvement occurs with mild 

worsening of objective pulmonary 

measurements of lung function. Study 

design may be a factor—multiple treatment 

protocols, small patient numbers, 

and overmanipulation have been postulated 

as potential explanations for 

these spirometric findings. Thus, there 

appears to be a symptomatic benefit 

from manipulative interventions that 

may be useful in the clinical setting. 

The only treatment modality that 

has been shown to reduce morbidity 

and mortality in COPD is smoking 

cessation. Osteopathic principles and 

practice strongly support treating the 

person as a whole, using techniques 

specific to osteopathic physicians as 

well as more standard interventions 

(eg, smoking cessation). Unfortunately, 

the established benefit of OMT interventions 

to date is relatively marginal 

and primarily affects symptomatic improvement. 

Conclusion 

In the future, osteopathic manipulative 

medicine protocols might be designed 

to facilitate smoking cessation as part 

of a holistic, patient-centered approach 

to management and support. This may 

be the best approach and strength of 

osteopathic manipulative medicine for 

patients with COPD. 

Acknowledgments 

I would like to thank Gregory Smith, 

DO, for his support and guidance. I 

would also like to thank the Lincoln 

Memorial University-DeBusk College of 

Osteopathic Medicine medical librarian, 

Lisa Travis, MS, EdS, for her editorial 

assistance and help with data collection 

and processing. 

References 

1. Chavez PC, Shokar NK. Diagnosis 

and management of chronic obstructive 

pulmonary disease (COPD) in a primary 

care clinic. COPD. 2009;6(6):446-451. 

doi:10.3109/15412550903341455. 

2. Ferguson GT, Make B. Management of stable 

chronic obstructive pulmonary disease. In: 

Stoller JK, Hollingsworth H, eds. UpToDate. 18.2 

version. Waltham, MA: UpToDate; 2010. 

3. Seffinger MA, King HH, Ward RC, Jones JM, 

Rogers FJ, Patterson MM. Osteopathic philosophy. 

In: Chila AG, ed. Foundations of Osteopathic 

Medicine. 3rd ed. Philadelphia, PA: Wolters Kluwer 

Lippincott Wiliams & Wilkins; 2011. 

4. Nelson KE, Glonek T, eds. Somatic Dysfunction 

in Osteopathic Family Medicine. Philadelphia, PA: 

Lippincott Williams & Wilkins; 2007. 

5. Yawn B, Mannino D, Littlejohn T, et al. 

Prevalence of COPD among symptomatic 

patients in a primary care setting. Curr 

Med Res Opin. 2009;25(11):2671-2677. 

doi:10.1185/03007990903241350. 

6. Mannino D. Chronic obstructive pulmonary 

disease: definition and epidemiology [review]. 

Respir Care. 2003;48(12):1148-1191. http://www. 

rcjournal.com/contents/12.03/12.03.1185.pdf. Accessed 

May 27, 2011. 

7. van der Molen T, Schokker S. Primary prevention 


in primary care [review]. Proc Am Thorac Soc. 

2009;6(8):704-706. http://pats.atsjournals.org/cgi/ 

reprint/6/8/704.pdf. Accessed May 27, 2011. 

8. Jenkins C. Spirometry performance in primary 

care: the problem, and possible solutions [editorial]. 

Prim Care Respir J. 2009;18(3):128-129. 

http://www.thepcrj.org/journ/vol18/18_3_128_129.pdf. 

Accessed May 27, 2011. 

9. Miller MR. Spirometry in primary care [editorial]. 

Prim Care Respir J. 2009;18(4):239-240. http:// 

www.thepcrj.org/journ/vol18/18_4_239_240. 

pdf. Accessed May 27, 2011.


10. Ställberg B, Nokela M, Ehrs PO, Hjemdal P, 

Jonsson EW. Validation of the clinical COPD 

Questionnaire (CCQ) in primary care. Health 

Qual Life Outcomes. 2009;7:26. http://www.hqlo. 

com/content/pdf/1477-7525-7-26.pdf. Accessed May 

27, 2011. 

11. Spaeth DG, Pheley AM. Use of osteopathic 

manipulative treatment by Ohio osteopathic 

physicians in various specialties. J Am Osteopath 

Assoc. 2003;103(1):16-26. http://www.jaoa.org/cgi/ 

reprint/103/1/16. Accessed May 27, 2011. 

12. Fennig GA Jr, Shubrook JH Jr. Inpatient osteopathic 

structural examinations: is “red tape” 

getting in the way of personalized patient care? J 

Am Osteopath Assoc. 2008;108(7):327-332. http:// 

www.jaoa.org/cgi/content/full/108/7/327. Accessed 


13. Chamberlain NR, Yates HA. A prospective 

study of osteopathic medical students’ attitudes 

toward use of osteopathic manipulative treatment 

in caring for patients. J Am Osteopath Assoc. 

2003;103(10):470-478. http://www.jaoa.org/ 

cgi/reprint/103/10/470. Accessed May 27, 2011. 

14. Beal MC. Viscerosomatic reflexes: a review. J 

Am Osteopath Assoc. 1985;85(12):786-801. 

15. Korr IM. Somatic dysfunction, osteopathic 

manipulative treatment, and the nervous system: 

a few facts, some theories, many questions. J Am 

Osteopath Assoc. 1986;86(2):109-114. 

16. Korr IM. The spinal cord as organizer of disease 

processes: some preliminary perspectives. J 

Am Osteopath Assoc. 1976;76(1):35-45. 

17. Korr IM. The spinal cord as organizer of 

disease processes: II. The peripheral autonomic 

nervous system. J Am Osteopath Assoc. 

1979;79(2):82-90. 

18. Van Schayck CP, Loozen JM, Wagena E, Akkermans 

RP, Wesseling GJ. Detecting patients at 

a high risk of developing chronic obstructive pulmonary 

disease in general practice: cross sectional 

case finding study. BMJ. 2002;324(7350):1370. 

http://www.bmj.com/content/324/7350/1370.1.long. 


19. Stefano L. Greenman’s Principles of Manual 

Medicine. 4th ed. Philadelphia, PA: Wolters Kluwer 

Lippincott Wiliams & Wilkins; 2011. 

20. Anthonisen N. Chronic obstructive pulmonary 

disease. In: Goldman L, Ausiello DA, Arend 

W, et al, eds. Cecil Medicine. 23rd ed. Philadelphia, 

PA: Saunders Elsevier; 2008:619-627. 

21. Belfer MH, Reardon JZ. Improving exercise 

tolerance and quality of life in patients with 

chronic obstructive pulmonary disease. J Am Osteopath 

Assoc. 2009;109(5):268-278. http://www. 

jaoa.org/cgi/reprint/109/5/268. Accessed May 27, 

2011. 

22. Mohanasundaram UM, Chitkara R, Krishna 

G. Smoking cessation therapy with varenicline 

[review]. Int J Chron Obstruct Pulmon Dis. 

2008;3(2):239-251. http://www.ncbi.nlm.nih.gov/ 

pmc/articles/PMC2629973/pdf/COPD-3-239.pdf. Accessed 


23. Ebbert JO, Wyatt KD, Zirakzadeh A, Burke 

MV, Hays JT. Clinical utility of varenicline for 

smokers with medical and psychiatric comorbidity 

[review] [published online ahead of print 

November 29, 2009]. Int J Chron Obstruct Pulmon 

Dis. 2009;4:421-430. http://www.ncbi.nlm.nih. 

gov/pmc/articles/PMC2793070/pdf/copd-4-421.pdf. Accessed 


24. Bourbeau J, Julien M, Maltais F, et al; Chronic 

Obstructive Pulmonary Disease axis of the Respiratory 

Network Fonds de la Recherche en Santé 

due Québec. Reduction of hospital utilization in 

patients with chronic obstructive pulmonary disease: 

a disease-specific self-management intervention. 

Arch Intern Med. 2003;163(5):585- 591. 

http://archinte.ama-assn.org/cgi/reprint/163/5/585. 


25. Norrhall MF, Nilsfelt A, Varas E, et al. A 

feasible lifestyle program for early intervention 

in patients with chronic obstructive pulmonary 

disease (COPD): a pilot study in primary 

care [original research]. Prim Care Respir J. 

2009;18(4):306-312. http://www.thepcrj.org/journ/ 

vol18/18_4_306_312.pdf. Accessed May 27, 2011. 

26. Ambrosino N, Casaburi R, Ford G, et al. 

Developing concepts in the pulmonary rehabilitation 

of COPD. J Respir Med. 2008;102(suppl 

1):S17-S26. doi:10.1016/S0954-6111(08)70004-0. 

27. Howell RK, Kappler RE. The influence of osteopathic 

manipulative therapy on a patient with 

advanced cardiopulmonary disease. J Am Osteopath 

Assoc. 1973;73(4):322-327. 

28. Howell RK, Allen TW, Kappler RE. The influence 

of osteopathic manipulative therapy in 

the management of patients with chronic obstructive 

lung disease. J Am Osteopath Assoc. 

1975;74(8):757-760. Accessed May 27, 2011. 

29. Miller WD. Treatment of visceral disorders 

by manipulative therapy. In: Goldstein M, ed. The 

Research Status of Spinal Manipulative Therapy; 

1975. Bethesda, MD: Government Printing Office. 

295-301. NINCDS monograph 15, DHEW 

publication (NIH) 76-998. 

30. Noll DR, Degenhardt BF, Johnson JC, Burt 

SA. Immediate effects of osteopathic manipulative 

treatment in elderly patients with chronic 

obstructive pulmonary disease. J Am Osteopath 

Assoc. 2008;108(5):251-259. http://www.jaoa.org/ 

cgi/content/full/108/5/251. Accessed May 27, 2011. 

31. Noll DR, Johnson JC, Baer RW, Snider EJ. 

The immediate effect of individual manipulation 

techniques on pulmonary function measures in 

persons with chronic obstructive pulmonary disease. 

Osteopath Med Prim Care. 2009;3:9. http:// 

www.om-pc.com/content/3/1/9. Accessed May 27, 

2011. 

32. Tashkin DP, Murray RP. Smoking cessation in 

chronic obstructive pulmonary disease [review]. 

Respir Med. 2009;103(7):963-974. doi:10.1016/j. 

rmed.2009.02.013. 

33. O’Hara P, Grill J, Rigdon MA, Connett JE, 

Lauger GA, Johnston JJ. Design and results of the 

initial intervention program for the Lung Health 

Study. The Lung Health Study Research Group. 

Prev Med. 1993;22(3):304-315. doi:10.1006/ 

pmed.1993.1025. 

34. Crane R. The most addictive drug, the most 

deadly substance: smoking cessation tactics for 

the busy clinician. Prim Care. 2007;34(1):117- 

135. doi:10.1016/j.pop.2007.02.003. 

35. Pederson LL, Blumenthal D. Smoking cessation: 

what works in primary care settings. Ethn 

Dis. 2005;15(2 suppl 2):S10-S13. http://www.ishib. 

org/journal/ethn-15-2s-10.pdf. Accessed May 27, 2011. 

36. Fiore MC, Bailey WC, Cohen SJ, et al. Treating 

Tobacco Use and Dependence: Clinical Practice 

Guideline. Rockville, Md: US Department of 

Health and Human Services, Public Health Service; 

2000. http://www.surgeongeneral.gov/tobacco/ 

treating_tobacco_use.pdf. Accessed May 31, 2011. 

37. Secades-Villa R, Alonso-Pérez F, García-Rodríguez 

O, Fernández-Hermida JR. Effectiveness 

of three intensities of smoking cessation treatment 

in primary care. Psychol Rep. 2009;105(3 pt 

1):747-758. 

38. Lancaster T, Stead LF. Individual behavioural 

counseling for smoking cessation [review]. 

Cochrane Database Syst Rev. 2005;(2):CD001292. 

doi:10.1002/14651858.CD001292.pub2. 

39. US Department of Health & Human Services, 

Agency for Healthcare Research and Quality. 

Treating Tobacco Use and Dependence: 2008 

Update. Rockville, MD: Agency for Healthcare 

Research and Quality; 2008. http://www.ncbi.nlm. 

nih.gov/bookshelf/br.fcgi?book=hsahcpr&part=A28163. 


40. Conroy MB, Majchrzak NE, Regan S, 

Silverman CB, Scheider LI, Rigotti NA. The 

association between patient-reported receipt 

of tobacco intervention at a primary care visit 

and smokers’ satisfaction with their health 

care. Nicotine Tob Res. 2005;7(suppl 1):S29-S34. 

doi:10.1080/14622200500078063. 

41. Noll DR, Shores JH,Gamber RG, Herron KM, 

Swift J Jr. Benefits of osteopathic manipulative 

treatment for hospitalized patients with pneumonia. 

J Am Osteopath Assoc. 2000;100(12):776- 

782. http://www.jaoa.org/cgi/reprint/100/12/776. Accessed 


42. Knott EM, Tune JD, Stoll ST, Downey HF. Increased 

lymphatic flow in the thoracic duct during 

manipulative intervention. J Am Osteopath 

Assoc. 2005;105(10):447-456. http://www.jaoa.org/ 

cgi/reprint/105/10/447. Accessed May 27, 2011. 

42. Noll DR, Degenhardt BF, Fossum C, Hensel 

K. Clinical and research protocol for osteopathic 

manipulative treatment of elderly patients 

with pneumonia [brief report] [published 

correction appears in J Am Osteopath Assoc. 

2008;108(11):670]. J Am Osteopath Assoc. 

2008;108(9):508-516. http://www.jaoa.org/cgi/ 

reprint/108/9/508.pdf. Accessed May 27, 2011. 



27

September 2011 - Osteopathic Physicians' Guide: COPD - American ...

Create successful ePaper yourself

Delete template?

Save as template?