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AUGUST 15, 2001 / VOLUME 64, NUMBER 4 w w w .aafp.org/afp AMERICAN FAMILY PHYSICIAN 603

years.6 Emphysema is characterized bychronic dyspnea resulting from the

destruction of lung tissue and the enlarge-ment of air spaces. Asthma, which alsofeatures airflow obstruction, airway in-flammation and increased airway respon-siveness to various stimuli, may be distin-guished from COPD by reversibility of pulmonary function deficits.5

Outpatient management of patientswith stable COPD should be directed atimproving quality of life by preventingacute exacerbations, relieving symptomsand slowing the progressive deteriorationof lung function. The clinical course of

COPD is characterized by chronic disabil-ity, with intermittent acute exacerbationsthat occur more often during the wintermonths. When exacerbations occur, theytypically manifest as increased sputumproduction, more purulent sputum andworsening of dyspnea.7 Although infec-tious etiologies account for most exacer-bations, exposure to allergens, pollutants

Despite public educationabout the dangers of

smoking, chronic ob-structive pulmonary dis-ease (COPD) continues

to be a major medical problem and isnow the fourth leading cause of death inthe United States.1Approximately 20 per-cent of adult Americans have COPD.2

Acute bronchitis and acute exacerbationsof COPD are among the most commonillnesses encountered by family physi-cians and account for more than 14 mil-lion physician visits annually.3,4

To date, widespread agreement on the

precise definition of COPD is lacking.TheAmerican Thoracic Society (ATS) definesCOPD as a disease process involving pro-gressive chronic airflow obstruction be-cause of chronic bronchitis, emphysema,or both.5 Chronic bronchitis is definedclinically as excessive cough and sputumproduction on most days for at least threemonths during at least two consecutive

Acute exacerbations of chronic obstructive pulmonary disease (COPD) are treated with oxy-

gen (in hypoxemic patients), inhaled beta2agonists, inhaled anticholinergics, antibiotics and

systemic corticosteroids. Methylxanthine therapy may be considered in patients who do not

respond to other bronchodilators. Antibiotic therapy is directed at the most common

pathogens, including Strept ococcus pneumoniae , Haemophilus inf lu enzae and Moraxella

catarrhalis . Mild to moderate exacerbations of COPD are usually treated with older broad-

spectrum antibiotics such as doxycycline, trimethoprim-sulfamethoxazole and amoxicillin-

clavulanate potassium. Treatment with augmented penicillins, fluoroquinolones, third-gener-

ation cephalosporins or aminoglycosides may be considered in patients with more severe

exacerbations. The management of chronic stable COPD always includes smoking cessation

and oxygen therapy. Inhaled beta2 agonists, inhaled anticholinergics and systemic cortico-

steroids provide short-term benefits in patients with chronic stable disease. Inhaled cortico-

steroids decrease airway reactivity and reduce the use of health care services for manage-

ment of respiratory symptoms. Preventing acute exacerbations helps to reduce long-term

complications. Long-term oxygen therapy, regular monitoring of pulmonary function and

referral for pulmonary rehabilitation are often indicated. Influenza and pneumococcal vac-

cines should be given. Patients who do not respond to standard therapies may benefit from

surgery. (Am Fam Physician 2001;64:603-12,621-2.)

O A patient information handout on

chronic obstructive

pulmonary disease,

written by the

authors of this

article, is provided

on page 621.

COPD: Management of Acute

Exacerbations and Chronic Stable DiseaseMELISSA H.HUNTER,M.D., and DANA E. KING, M.D.Medical University of South Carolina College of Medicine, Charleston, South Carolina

COVER ARTICLEPRACTICAL THERAPEUTICS

Members of various

fam ily practice depart-

ment s develop articles fo r “Practical Therapeu-

tics.” This article is one

in a series coordinated

by the Department of

Family Medicine at t he

Medical University of

Sout h Carolina,

Charleston . Guest edi-

to r of the series is

William Hueston, M.D.

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or inhaled irritants may also play a role.8 Thisarticle reviews the management of acute ex-acerbations and stable COPD.

Epidemiology

COPD is one of the most serious and dis-

abling conditions in middle-aged and elderlyAmericans.Cigarette smoking is implicated in90 percent of cases and, along with coronaryartery disease, is a leading cause of disability.9

Two thirds of patients with COPD have seri -ous chronic dyspnea, and nearly 25 percenthave profound total body pain.10

COPD has a major impact on the familiesof affected patients. Caring for these patientsat home can be difficult because of their func-tional limitations and anxieties about airhunger. Furthermore, patients with COPDcan have frequent exacerbations that often

require medical intervention. Ult imately,caregivers may have the burden of consider-ing end-of-life decisions.

Pathophysiology

COPD is a subset of obstructive lung dis-eases that also includes cystic fibrosis,bronchiectasis and asthma. COPD is charac-terized by degeneration and destruction of the lung and supporting tissue,processes thatresult in emphysema, chronic bronchit is, orboth. Emphysema begins with small airway

disease and progresses to alveolar destruc-tion, with a predominance of small airwaynarrowing and mucous gland hyperplasia.

The pathophysiology of COPD is not com-pletely understood. Chronic inflammation of the cells lining the bronchial tree plays aprominent role. Smoking and, occasionally,other inhaled irr itants, perpetuates an ongo-ing inflammatory response that leads to air-way narrowing and hyperactivity. As a result,airways become edematous, excess mucusproduction occurs and cilia function poorly.With disease progression, patients have

increasing difficulty clearing secretions. Con-sequently, they develop a chronic productivecough, wheezing and dyspnea. Bacterial colo-nization of the airways leads to fur therinflammation and the formation of divert ic-ula in the bronchial tree.

Exacerbations of COPD can be caused bymany factors, including environmental irr i-tants, heart failure or noncompliance withmedication use.11 Most often, however, ex-acerbations are the result of bacterial or viralinfection (Table 1).12 Bacterial infection is afactor in 70 to 75 percent of exacerbations,

with up to 60 percent caused by Streptococcus pneumoniae , Haemophilus influenzae orMoraxella catarrhal is.13 Atypical organismssuch as Chlamydia pneumoniae have beenimplicated in about 10 percent of exacerba-tions.The remaining 25 to 30 percent of casesare usually caused by viruses.14 More seriousexacerbations requiring mechanical ventila-tion have been associated with Pseudomonas

604 AMERICAN FAMILY PHYSICIAN w w w .aafp.org/afp VOLUME 64, NUMBER 4 / AUGUST 15,2001

Exacerbations of COPD typically manifest as increased sputum

production, more purulent sputum and worsening of dyspnea.

TABLE 1

Most Common Infectious Causesof COPD Exacerbations

Mild to moderate exacerbations

Strept ococcus pneumoniae

Haemophilu s influ enzae

Moraxella catarrhalis

Chlamydia pneumoniae

Mycoplasma pneumoniae

Viruses

Severe exacerbationsPseudom onas species

O ther gram -negative enteric bacilli

COPD = chronic obstructive pu lmonary disease.

Adapted w ith permission from Fein A, Fein AM .

Management of acute exacerbations in chronic

obstruct ive pulmonary disease. Curr Opin Pulm Med

2000;6:122-6.

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species. These exacerbations are more com-mon in patients with severe disease and a his-tory of frequent exacerbations.13

Prognostic Indicators

Over the past 40 years, numerous studieshave attempted to determine which factorsinfluence survival in patients with COPD.Most of these studies have examined survivalin stable outpatients. The long-term progno-sis for patients with symptomatic chronicbronchit is is not promising. Data from the

past decade indicate that 60-year-old smokerswith chronic bronchitis have a 10-year mor-tality rate of 60 percent, which is four timeshigher than the mortality rate for age-matched nonsmoking asthmatics.15

Several studies have shown that thestrongest predictors of mortality are older ageand a decreased forced expiratory volume persecond (FEV1)16,17 (Table 2).18 Youngerpatients with COPD generally have a lowermortality rate unless they also have alpha1-antitrypsin deficiency, a rare genetic abnor-mality that causes panlobular emphysema in

younger adults.Alpha1-antit rypsin deficiencyshould be suspected when COPD develops ina patient younger than 45 years who does nothave a history of chronic bronchit is ortobacco use, or when multiple family mem-bers develop obstructive lung disease at anearly age. Reversible changes after bron-chodilator administration are a sign of lessadvanced disease and improved survival.

Decreases in FEV1on serial testing are asso-ciated with increased mortality (i .e., patientswith a faster decline of FEV1 have a higherrate of death). Cigarette smoking is the major

risk factor associated with an accelerateddecline of FEV1. Smoking cessation inpatients with early COPD improves lungfunction initially and slows the annualdecline of FEV1.19-21 Other factors found torelate positively to survival include a higherpartial pressure of arterial oxygen (PaO2), ahistory of atopy and higher diffusion andexercise capacity.16,22-24 Factors found to

decrease survival include malnutrition andweight loss, dyspnea, hypoxemia (PaO2 lessthan 55 mm Hg), right-sided heart failure,tachycardia at rest and increased partial pres-sure of arterial carbon dioxide (PaCO2 higherthan 45 mm Hg).16,25,26

Recommendations for the clinical moni-toring of patients with COPD include serialFEV1 measurements, pulse oximetry andtimed walking of predetermined distances,although a decline in the FEV1 has the mostpredictive value.27 An FEV1 of less than 1 L

signifies severe disease, and an FEV1 of lessthan 750 mL or less than 50 percent predictedon spirometric testing is associated with apoorer prognosis.

COPD


TABLE 2

Factors Influencing Survival in Patients with COPD

Risk factor Effect on survival

Postbronchodilator FEV 1 D ecreases m ortality w ith increased FEV 1,

decreases m ortality w ith reversible com ponent

of obstruction

Rate of FEV 1 decline D ecreases m ortality w ith slow er decline; FEV1 < 1 L

generally considered severe disease

History of atopy Decreases m ortality

H igher diffusion capacity D ecreases m ortality

PaO 2 level Decreases m ortality w ith increased level; PaO 2 4 5 m m H g)

Right-sided heart failure Increases m ortality

M alnutrition Increases m ortality

Resting tachycardia Increases m ortality

COPD = chron ic obstru ctive pu lmonary disease; FEV 1 = f orced expiratory volume

per second; Pa O 2 = partial pressure of arterial oxygen; Pa CO 2 = partial pressure of

arterial carbon dioxide.

Adapt ed wit h permission from Hughes JR, Goldstein MG, Hurt RD, Shiff man S.

Recent advances in the pharmacot herapy of smok ing. JAMA 1999 ;281 :72-6 .

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Pharmacologic Managementof Exacerbations

Because no curative therapy is available,management of severe exacerbations of COPDshould be directed at relieving symptoms andrestoring functional capacity (Figure 1).5

Patients with COPD often have poor baselinefunctional status with few respiratoryreserves. Infections can worsen their condi-tion and lead to a quick decline in pulmonaryfunction.

The ATS has recommended strategies formanaging acute exacerbations of chronicbronchitis and emphysema.5 These strategiesinclude beta2 agonists, the addition of anti-cholinergics (or an increase in their dosage),the intravenous administration of corticos-teroids, antibiotic therapy when indicated,and the intravenous administration of

methylxanthines such as aminophylline.11Hospitalization of patients with COPD may

be necessary to provide antibiotic therapy,appropriate supportive care and monitoringof oxygen status.Oxygen supplementation viaexternal devices or mechanical ventilation

may be indicated to maintain oxygen deliveryto vital tissues.

OXYGENATION

Initial therapy should focus on maintainingoxygen saturation at 90 percent or higher.Oxygen status can be monitored clinically, aswell as by pulse oximetry.Oxygen supplemen-tation by nasal cannula or face mask is fre-quently required.With more severe exacerba-tions, intubation or a positive-pressure maskventilation method (e.g., continuous positive

airway pressure [CPAP]) is often necessary toprovide adequate oxygenation. Such interven-tions are more likely to be needed whenhypercapnia is present, exacerbations are fre-quent or altered mental status is evident.12

BRONCHODILATORS

Inhaled beta2 agonists should be adminis-tered as soon as possible during an acuteexacerbation of COPD. Use of a nebulizer toprovide albuterol (Ventolin) or a similaragent with saline and oxygen enhances deliv-ery of the medication to the airways.28

Beta2agonists can be delivered effectively bymetered-dose inhaler if patients are able to useproper technique, which may be difficult dur-ing an exacerbation. Salmeterol (Serevent), along-acting beta2 agonist, has been shown torelieve symptoms in patients with COPD.29

Twice-daily dosing is an added benefit andmay be convenient for many patients.

Orally administered beta2 agonists havemore side effects than inhaled forms. Hence,oral agents generally are not used to treatexacerbations of COPD.

ANTICHOLINERGICS

Compared with beta2agonists, inhaled anti-cholinergics such as ipratropium (Atrovent)provide the same or greater bronchodilation.These agents have been shown to be beneficialin patients with COPD.12Anticholinergics canbe delivered by nebulizer or metered-doseinhaler.In inhaled forms,anticholinergics havefew adverse effects because of minimal sys-


The Aut ho rs

M ELISSA H. H U N TER, M .D ., is assistant professor in the D epartm ent of Fam ily M edi-

cine at the M edical U niversity of South C arolina C ollege of M edicine, Charleston. She

received her m edical degree from the M edical University of South C arolina and com -

pleted a fam ily m edicine residency at M cLeod Regional M edical Center, Florence, S.C .

D r. H unter also com pleted a faculty developm ent fellow ship in fam ily m edicine at theU niversity of North C arolina at C hapel H ill.

D AN A E. KING , M .D ., is associate professor in the D epartm ent of Fam ily M edicine at

the M edical U niversity of South C arolina C ollege of M edicine. H e received his m edical

degree from the U niversity of Kentucky C ollege of M edicine, Lexington, and com -

pleted a fam ily practice residency at the U niversity of M aryland H ospital, Baltim ore,

w here he w as co-chief resident. In addition, D r. King com pleted a faculty developm ent

fellow ship in fam ily m edicine at the U niversity of N orth C arolina at C hapel H ill.

Add ress correspondence to M elissa H. Hunter, M.D., Un iversity Family M edicine, 9298

Medical Plaza Dr., Charleston , SC 2940 6 (e-mail: hunt [email protected]). Reprint s are not

available from the auth ors.

Compared with beta 2 agonists, inhaled anticholinergics such

as ipratropium provide the same or greater bronchodilation .

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Management of COPD

Treat obstruction.

Variable tom ild sym ptom s

Beta2 agonist byM D I as needed

M ild to m oderatecontinual sym ptom s

A nticholinergic by M D I,or beta2 agonist

Suboptim al response

A dd long-acting beta2 agonist.


C onsider m ethylxanthine.

Severe exacerbations

Increase beta2 agonist by M D Ito up to 6 to 8 puffs every1 to 2 hours; considernebulizer for delivery.

Increase anticholinergic byM D I to up to 6 to 8 puffsevery 3 to 4 hours.

Intravenously or orallyadm inistered corticosteroid

C onsider m ethylxanthine.

A ppropriate antibiotictherapy

Refer patient for m ultidisciplinarypulm onary rehabilitation.

Provide patient w ith periodic m onitoring(i.e., pulm onary function tests) andcontinuing care.


C onsider orally adm inisteredcorticosteroid.

Im provem ent

W ean patient to low est dosageor consider inhaled corticosteroid.

N o im provem ent

A ssess patient’s response to treatm ent.

Severe sym ptom s or im paired functional capacity

Stop corticosteroid.

A ssess patient

for hypoxem ia.

Encourage

nonpharm acologicm easures: patienteducation, exercise,sm oking cessation,nutrition, andinfluenza andpneum ococcalvaccines.

C onsider supplem entaloxygen therapy ifPao2 is < 55 m g H gor nocturnal oxygensaturation is < 88% .

Establish diagnosis of C O PD and assess patient’s sym ptom s.

N oYes

FIGURE 1. Algo rithm for the ma na ge ment of chronic ob structive pulmona ry disea se (COPD). (MDI = mete red-dose inha ler;

Pa o2 = pa rtial pressure of a rteria l oxygen)

Adapt ed wit h permission from Standards fo r the diagnosis and care of pat ients with chronic obstruct ive pulmonary disease. American

Thoracic Society. Am J Respir Crit Care Med 1995;152(5 pt 2):S77-121.

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temic absorption. Use of a combination prod-uct such as ipratropium-albuterol (Com-bivent) may simplify the medication regimen,thereby improving compliance.

ANTIBIOTICS

Antibiotic therapy has been shown to havea small but important effect on clinical recov-ery and outcome in patients with acute ex-acerbations of chronic bronchitis and emphy-sema.30 Therefore, antibiotic administrationshould be considered at the beginning of

treatment for exacerbations of COPD.12

A recent meta-analysis30of nine clinical tri-als demonstrated the benefit of antibiotictherapy in the management of COPD. Ther-apy for moderate acute exacerbations of chronic bronchitis and emphysema should bedirected at S. pneumoniae , H. influenzae andM. catarrhalis , which are the most common

pathogens, with C. pneumoniae and Myco- plasma pneumoniae occurring less often.

Initial outpatient management may includeorally administered doxycycline (Vibramy-cin), tr imethoprim-sulfamethoxazole (Bac-tr im DS, Septra DS) or amoxicillin-clavu-lanate potassium (Augmentin).12 Patientswho are older than 65 years of age or havemore frequent exacerbations (four or moreepisodes per year) may need an augmentedpenicillin or a fluoroquinolone.

Hospitalized patients should receive intra-

venous treatment with an antipseudomonalpenicillin, a third-generation cephalosporin,a newer macrolide or a fluoroquinolone, asdetermined by local bacterial resistance pat-terns. In more severe exacerbations,infectionswith gram-negative bacteria (especially Kleb-siella and Pseudomonas species) are morecommon. Thus, treatment should include a


TABLE 3

Antibiotics Commonly Used in Patients with COPD Exacerbations

Mild to moderate exacerbations*

First-line antibiotics

D oxycycline (Vibram ycin), 100 m g tw ice daily

Trim ethoprim -sulfam ethoxazole (Bactrim D S,

Septra D S), one tablet tw ice daily

A m oxicillin-clavulanate potassium (A ugm entin),

one 500 m g/125 m g tablet three tim es daily

or one 875 m g/125 m g tablet tw ice daily

M acrolides

C larithrom ycin (Biaxin), 500 m g tw ice daily

A zithrom ycin (Zithrom ax), 500 m g initially,

then 250 m g daily

Fluoroquinolones

Levofloxacin (Levaquin), 500 m g dailyG atifloxacin (Tequin), 400 m g daily

M oxifloxacin (A velox), 400 m g daily

IV = intravenous.

*—For orally administered ant ibiot ics, the usual duratio n of t herapy is five to 10 days.

†—Drugs are often used in combination for synergy; IV therapy is usually employed.

Information f rom references 12, 28 and 29.

Moderate to severe exacerbations†

C ephalosporins

C eftriaxone (Rocephin), 1 to 2 g IV daily

C efotaxim e (C laforan), 1 g IV every 8 to 12 hours

Ceftazidim e (Fortaz), 1 to 2 g IV every 8 to 12 hours

A ntipseudom onal penicillins

Piperacillin-tazobactam (Zosyn), 3.375 g IV every

6 hours

Ticarcillin-clavulanate potassium (Tim entin),

3.1 g IV every 4 to 6 hours

Fluoroquinolones

Levofloxacin, 500 m g IV daily

G atifloxacin, 400 m g IV daily

A m inoglycoside

Tobram ycin (Tobrex), 1 m g per kg IV every 8 to

12 hours, or 5 m g per kg IV daily

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third-generation cephalosporin or an aug-mented penicillin, plus a fluoroquinolone oran aminoglycoside for synergy.

Some of the antibiotics most commonlyused to treat acute exacerbations of chronicbronchitis and emphysema are listed in Table 3.12,28,29Antibiotic resistance poses an increas-ing problem,especially in infections caused byS. pneumoni ae , beta-lactamase–producingH. influenzae and M. catarrhalis. Conse-quently, physicians often are forced to usebroader spectrum antibiotics for empiric

therapy.31

Cultures of respiratory samples areuseful for guiding antibiotic therapy inpatients who require mechanical ventilation.13

CORTICOSTEROIDS

Short courses of systemic cort icosteroidsmay provide important benefits in patientswith exacerbations of COPD. A recent clinicaltrial32 involving 271 patients in Veterans Affairshospitals showed that steroid therapy resultedin moderate improvement of clinical out-comes,with shorter hospital stays and increasesin FEV1. The fact that there were no significant

differences between patients treated for twoweeks and those treated for eight weeks justifiesthe use of a shorter course of corticosteroids toreduce the occurrence of adverse effects.Adverse effects can include hyperglycemia,sec-ondary infection and behavioral changes.33

For severe exacerbations of COPD requir-ing inpatient therapy, methylprednisolonesodium succinate (Solu-Medrol) is com-monly used init ially. The steroid is adminis-tered intravenously in a dosage of 1 to 2 mgper kg every six to 12 hours.After two to threedays of intravenous therapy, the patient can

be switched to orally administered pred-nisone in a starting dosage of 60 mg daily fora total of two weeks of therapy. Taperingdoses of prednisone should then be givenover a two-week period to avoid adverseeffects from sudden withdrawal.

Currently,no cri teria have been establishedfor deciding which patients benefit mostfrom corticosteroid therapy.Thus,all patients

without serious contraindications shouldreceive systemic corticosteroids for severeexacerbations of COPD.

METHYLXANTHINES

The use of methylxanthines such as amino-phylline and theophylline is controversialin patients with exacerbations of COPD.Although methylxanthines can be of somehelp in improving diaphragmatic function,they are potentially toxic and are associatedwith serious drug effects.34

Nevertheless, with close monitoring andattention to potential adverse effects, methyl-xanthines may have a place in the treatmentof patients who do not respond to otherbronchodilators. They may also have a rolein the management of patients with chronicstable disease who cannot operate metered-dose inhalers or use other medicationsbecause of adverse drug effects.

Dosages of aminophylline ranging from10 to 15 mg per kg daily are required toachieve therapeutic levels of 10 to 20 mg permL. Increased serum levels can be expected

with concomitant use of cimetidine (Taga-met), ciprofloxacin (Cipro) or erythromy-cin.35 Smoking promotes methylxanthinemetabolism and decreases serum drug levels.9

Management of Chronic Stable Disease

NONPHARMACOLOGIC INTERVENTIONS

Patients with COPD should be encouragedto adopt and maintain a healthy lifestyle.Reg-ular exercise should be promoted, and nutri -tional management should be provided.Patients who smoke should stop smoking.Weight loss should be encouraged in obese

patients labeled as “blue bloaters,” and nutri -tional supplementation should be consideredin thin patients labeled as “pink puffers.” Com-prehensive pulmonary rehabilitation alsoshould be considered.

Home health care services are key to suc-cessful management in outpatient settings.Hospice care may be appropriate for selectedpatients.

COPD


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Smoking cessation is the most important,and probably the most difficult, factor in pre-venting or treating COPD. Interventionsavailable to help patients stop smokinginclude behavioral modification programsand pharmacologic agents such as nicotine

replacement products and antidepressants(e.g., bupropion [Zyban]). A combination of pharmacologic and behavioral approachesappears to yield the best quit rates. The effec-tiveness of nicotine patches is improved inpatients who also receive even minimal coun-seling from a health care provider.36

PHARMACOLOGIC INTERVENTIONS

Pharmacologic interventions used in thetreatment of stable COPD include essentiallythe same medications for the management of acute exacerbations of chronic bronchitis and

emphysema (Figure 1).5 Based on clinical evi-dence, at least short-term benefi ts result fromtreatment that includes inhaled beta2 ago-nists, inhaled anticholinergics and orally ad-ministered corticosteroids.

Anticholinergics such as ipratropium seemto provide some short-term improvement inairway obstruction but have no significanteffect on the rate of decline of FEV1.37 Bothshort-acting and long-acting beta2 agonistsproduce short-term bronchodilation, relievesymptoms and improve quality of life inpatients with COPD.38 The use of combined

beta2 agonists and anticholinergic agents hasbeen found to provide small additional bron-chodilation compared with the use of eithermedication alone.39

Treatment with orally administered corti-costeroids for two to four weeks has been cor-related with a 20 percent or greater improve-ment of the baseline FEV1 in patients withCOPD.40 However, no current evidence is

available on the long-term effects of steroidtherapy on lung function.

The effectiveness of inhaled corticosteroidsremains controversial. Recent investigationsin the Lung Health Study41 have shown noslowing of the rate of decline of FEV1. How-ever, inhaled steroids seem to improve airwayreactivi ty and respiratory symptoms, andthey also have been found to decrease the useof health care services for treatment of respi-ratory problems.

If long-term cort icosteroid therapy is con-

templated, it is important to consider possibleadverse effects.These include potential effectson bone mineral density, weight gain and thedevelopment of glucose intolerance.

Antibiotics are generally reserved for use inepisodes of acute exacerbations of chronicbronchit is and emphysema. Theophyll inemay induce short-term improvement of theFEV1, but the benefits of methylxanthinetherapy should be weighed against potentialside effects and possible toxicity.

HYPOXEMIA

Apart from smoking cessation, supplemen-tal oxygen therapy is the only measure that hasbeen shown to reduce mortality in patientswith COPD.42Supplemental oxygen should begiven to patients who are hypoxemic with aPaO2 of 55 mm Hg or less, or an oxygen satu-ration of 88 percent or less while sleeping.

Oxygen therapy, with delivery by nasal can-nula or CPAP, may be provided in the home.Continuous long-term oxygen therapy(LTOT) should be considered in patients witha PaO2 below 55 mm Hg while at rest andawake, and in patients with accompanying

polycythemia,pulmonary hypertension,right-sided heart failure or hypercapnia (PaCO2above 45 mm Hg). CPAP is generally reservedfor patients with chronic hypercapnia.

One set of investigators43 found significantdecreases in hospital admissions and lengthof hospital stays for acute exacerbations of COPD in patients treated with CPAP andLTOT.Home health care services and nursing


Smoking cessation is the most important factor in the pre-

vention or t reatment of COPD.

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care are essential to assist patients in theproper use of these measures.

PULMONARY REHABILITATION

Pulmonary rehabilitation and exercise maybe beneficial as adjunct treatment in patientswhose symptoms are not adequatelyaddressed wi th pharmacologic therapy. Thegoals of pulmonary rehabilitation are to en-hance standard medical therapy and maxi-mize functional capacity. Rehabil itation exer-cises can also improve exercise tolerance.44

Pulmonary rehabil itation may be most usefulin patients who have limited activity and de-creased quali ty of li fe.

Rehabilitation programs should includethe following: patient and family education;smoking cessation; physical, nutrit ional andoccupational therapy; and, in selectedpatients, LTOT or CPAP.

Long-term management and monitoringshould include periodic spirometry and mea-surement of arterial blood gases to assess theneed for supplemental LTOT or CPAP oncethe PaO2 is below 55 mm Hg or the PaCO2 is

above 45 mm Hg. The use of sedatives andhypnotics should be avoided.

Annual influenza immunization is recom-mended for patients with COPD. Pneumo-coccal vaccine should be given at least once,with consideration of re-vaccination everyfive to 10 years.

SURGERY

Surgical interventions in COPD includelung transplantation and lung volume reduc-tion procedures. Recent advances in immunesuppression and an improved understanding

of the timing of interventions and the selec-tion of appropriate recipients have madetransplantation a realistic option.

The goal of lung volume reduction surgeryis to reduce hyperinflation of one or bothlungs by surgical and/or laser resection. Theresults of one study45 showed a one-year 45percent increase in FEV1,a 25 percent decreasein total lung capacity and an improvement of

exercise performance in patients who under-went the procedure. Preliminary findings inother studies have shown improvement indyspnea, quality of life and lung function.46

However, the perioperative mortality rate canbe as high as 10 percent,and cost-effectivenessshould be considered before lung volumereduction surgery becomes widely used.47

The authors indicate that t hey do not have any con-

flicts of int erest. Sources of funding: none reported.

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