COPD Michigan
Transcript of COPD Michigan
-
8/10/2019 COPD Michigan
1/17
1
University of Michigan Guidelines for
Health System Clinical Care
COPD
Guideline Team
Team Leader
Davoren A Chick, MD
General Medicine
Team MembersPaul J Grant, MDGeneral Medicine
Meilan K Han, MD, MSPulmonary Medicine
R Van Harrison, PhDMedical Education
Elisa B Picken, MDFamily Medicine
Developed:May, 2010
UMMC Guidelines
Oversight Team:
Connie J Standiford, MDWilliam E Chavey, MD
R Van Harrison, PhD
Literature search service:Taubman Medical Library
For more information call:GUIDES 734- 936-9771
Regents of theUniversity of Michigan
Chronic Obstructive Pulmonary Disease
Patient population: Adults with chronic obstructive pulmonary disease (COPD).
Objectives: 1. Provide a framework for management of chronic COPD and for the treatment ofmild to moderate acute exacerbations
2. Improve symptoms, quality of life and lung function while reducing morbidity andmortality for patients with COPD.
Key Points (See Table 1 for overview of diagnosis and management of COPD.)
COPD is underdiagnosed and misdiagnosed. Routine population screening is not recommended[IIID] but early case finding is encouraged. [ID] Appropriate comprehensive treatment canimprove symptoms and quality of life. [IA]
Diagnosis.
Consider COPD in any patient with dyspnea, chronic cough or sputum production, and/or ahistory of inhalational exposures known to be risk factors. [ID]
Pulmonary function testing with post-bronchodilator assessment demonstrating a reducedFEV1/FVC ratio is required for diagnosis; severity of FEV1 decline (measured as % of predicted
FEV1) establishes severity.[ID]
Treatment.
Smoking cessation is the single most important intervention to slow the rate of lung functiondecline regardless of disease severity. [IA]
Chronic medication management includes:- Bronchodilators (B2-agonists and anticholinergics) in stepwise progression based on disease
severity (Tables 9 & 10) with the goal of improving symptoms. [IA]- Inhaled corticosteroids should be considered only for patients with severe disease (FEV1 =80% Individual may or may not be aware lung functionis abnormal
Moderate 50-80% Patients typically seek medical attention at thisstage due to respiratory symptoms or an
exacerbation
Severe 30-50% Dyspnea, reduced exercise capacity, and repeatedexacerbations impact quality of life
Very severe
-
8/10/2019 COPD Michigan
5/17
5 UMHS COPD Guideline, May, 2010
Table 9. Therapeutic Steps by Severity
Mild Moderate Severe Very Severe
FEV1/FVC
-
8/10/2019 COPD Michigan
6/17
6 UMHS COPD Guideline, May, 2010
Table 10. Inhaled Medications Commonly Used in Chronic Obstructive Pulmonary Disease
Medication Brand Name Usual Adult
Starting Dose
Solution for
Nebulizer
Duration
of Action
Cost (30 days)a
Generic Brand
Bronchodilators
2-Agonists
Short-actingAlbuterol ProAir HFA
Proventil HFA
Ventolin HFA
2 puffs q 4-6 hrs PRN(90 mcg/puff)
2 puffs q 4-6 hrs PRN(90 mcg/puff)
2 puffs q 4-6 hrs PRN(90 mcg/puff)
2.5 mg q 6-8h PRN 4-6 h NA $26-43
Levalbuterol Xopenex HFAb 2 puffs q 4-6 hrs PRN(45 mcg/puff)
0.63 mg q 6-8hPRN
4-6 h NA $50-100
Long-actingFormoterol Foradil Aerolizer
Perforomist
Brovana(R,R,fomoterol)
1 capsule bid (12mcg/dose)
20 mcg q 12h
15 mcg q 12h
12+ h
12+ h
12+ h
NA
NA
NA
$153
$365
$370
Salmeterol Serevent Diskus 1 puff bid
(50 mcg/dose)
N/A 12+ h NA $158
AnticholinergicsShort-acting
Ipratropium bromide Atrovent HFA 2 puffs qid(17 mcg/puff)
0.25 mg -0.5 mg q6-8h
6-8 h NA $128-155
Long-actingTiotropium bromide Spiriva
Handihaler1 capsule qd (18
mcg/ capsule)N/A 24+ h NA $200
Combination short-acting 2-Agonists + anticholinergicin one inhaler
Albuterol/ipratropium Combiventc
Duoneb
2 puffs tid-qid(90/18mcg/puff)
2.5/0.5 mg q 4 - 6h
6-8 h NA
$24
$140-170
$210
Inhaled Corticosteroids
Budesonide PulmicortFlexhaler
PulmicortRespules
1-2 puffs BID (180mcg/puff)
0.5-1.0 mg q 12h
12 h NA
NA
$141
$500-960
Fluticasone Flovent HFA 1-2 puffs BID (110-220 mcg/puff)
N/A 12 h NA $200
Combination Bronchodilators and Inhaled Corticosteroids
Formoterol/budesonide Symbicort 4.5/160 2 puffs BID N/A 12 h NA $200
Fluticasone/salmeterol Advair Diskus
Advair HFAc
250-500/50 1 puffBID
115-230/21 2 puffsBID
N/A 12 h
12 h
NA
NA
$210-284
$210-284
aCost = Average wholesale price based -10% for brand products and Maximum Allowable Cost (MAC) + $3 for generics for
average 30-day supply, Sources: AmerisourceBergen item catalog, 2/10, and Michigan Department of Community Health M.A.CManager, 2/10
bMay cause less tremor and tachycardia compared to albuterol, but at a higher price and no difference in major clinicaloutcomes.
cNot recommend use as a first line agent due to inability to titrate the short acting beta agonist component to a lowest necessarydose while achieving a therapeutic anticholinergic dose.
d HFA steroid inhalers should always be used with a valved holding chamber type spacer.
-
8/10/2019 COPD Michigan
7/17
7 UMHS COPD Guideline, May, 2010
Table 11. Indications for Intermittent or Continuous Use of Oxygen Therapy for Very Severe COPDa
Level of EvidenceIntermittent Use
Continuous Use
b
Strong Resting PaO2 < 55 mmHg or SaO2 < 88%
Weak Desaturation of PaO2 < 55 mmHg (SaO2 < 88%)either:
with activity at night
Resting PaO2 56-59 mmHg (SaO2 89-90%) with any onof the following:
peripheral edema suggesting congestive heart failur evidence of pulmonary hypertension polycythemia (hematocrit > 55%)
aCriteria for Center for Medicare and Medicaid Services reimbursement.bAdministered for at least 15 hours per day, preferably longer.
Table 12. Acute Exacerbation: Commonly Used Pharmacologic Therapies and Doses
Generic Name Brand Name Usual Adult Dose Cost (30 days)a
Generic Brand
Short acting 2-adrenergic agonists (SABA) Inhaled [bronchodilator]
AlbuterolMDI
ProAir (HFA)Proventil (HFA)Ventolin (HFA)
4-8 puffs q 20 min x 4 hrs prn,then 4-8 puffs q 1-4 hrs prn(90 mcg/spray)
NA $26-43
AlbuterolNebulizer solution 0.5%
AccuNeb 2.5-5 mg q 20 min x 3 doses,then 510 mg q 1-4 hrs prn
(5mg/mL)
$8 $46
Levalbuterol tartrateMDI
Xopenex (HFA) 2 puffs q 4-6 hrs prn
(45 mcg/spray)
NA $50
Levalbuterol HCl
Nebulizer solution
Xopenex 0.631.25 mg q 8hr prn
(1.25 mg/0.5 mL)
$110 $126
Short acting anticholinergicbInhaled [bronchodilator]. Can be used in addition toshort acting 2-adrenergic agonists
(SABA), however efficacy is questionable.
IpratropiumMDI
Atrovent (HFA) 2-4 puffs q 6 hrs prn
(17 mcg/spray)
NA $128
IpratropiumNebulizer solution
500 mcg q 6 hrs prn
(500 mcg/2.5 mL)
$6-20 NA
Oral Corticosteroidsc[anti-inflammatory]
Prednisone: 1, 2.5, 5, 10,20, 25 mg tabs;
1 mg/mL liquid
30-40 mg/day for 7-10 days.Regimens may vary in dosage strengthand duration
$4-20 NA
Prednisolone: 5 mg tabs;1 mg/mL, 3 mg/mLliquid
30-40 mg/day for 7-10 days.Regimens may vary in dosage strengthand duration
$6-10 $30-50
(Table continues on next page)
-
8/10/2019 COPD Michigan
8/17
8 UMHS COPD Guideline, May, 2010
Table 12. Acute Exacerbation: Pharmacologic Therapies and Doses (continued)
Generic Name Brand Name Usual Adult Dosing Cost (30 days)a
Generic Brand
Antibioticsd
Patients without risk factorse
Azithromycin250, 500 mg tabs;100, 200/5 mL liquid
Zithromax 500 mg PO on day 1, then 250 mgPO on days 2-5
$16-77 $60-85
Cephalosporins (2ndor 3rd generation)
Cefdinir300 mg tabs;
125, 250/5mL liquid
Omnicef 300 mg PO BID $60-88 $334-686
Cefpodoxime100, 200 mg tabs;100/5mL liquid
Vantin 200 mg PO BID $102-466 $522
Cefprozil250, 500 mg tabs ;250/5mL liquid
Cefzil 500 mg PO BID $150-177 $436-520
Doxycycline100 mg tabs
Doxycycline50/5 mL liquid
Vibramycin capsule
Vibramycin syrup
100 mg PO BID
100 mg PO BID
$8
$78
$355
$348
Trimethoprim/sulfamethoxazole80/400, 160/800 mg tabs;40/200 /5 mL liquid
BactrimSeptraSulfatrim (liquid)
160/800 (DS tab) PO BID160/800 (DS tab) PO BID20 mL PO BID
$13-67 (all) $120-140(all)
Patients with risk factorse(no particular order)
Amoxicillin/clavulanate250/125, 500/125, 875/125mg tabs; 200/28.5 /5mL,400/57 /5mL liquid
Augmentin 500 mg PO q8 hrs or 875 mg PO q12hrs
$60-92 (tab)
$182-212(liq)
$430-482(tab)
$273-544(liq)
Levofloxacin250, 500, 750 mg tabs;25 mg/mL liquid
Levaquin 500 mg PO daily NA $436
Patients at risk for infection withPseudomonas aeruginosaf(no particular order)
Levofloxacin250, 500, 750 mg tabs;25 mg/mL liquid
Levaquin 750 mg PO daily NA $817
Ciprofloxacin100, 250, 500, 750 mg tabs
Cipro 500-750 mg PO BID $25-36 $323-484
aCost = Average wholesale price based -10% for brand products and Maximum Allowable Cost (MAC) + $3 for generics for
average 30-day supply, Sources: AmerisourceBergen item catalog, 2/10, and Michigan Department of Community HealthM.A.C. Manager, 2/10bTiotropium does not have acute bronchodilating properties. Ipratropium is preferred for acute exacerbations.c Oral corticosteroids are not for general maintenance and should be weaned following exacerbation therapy.dAntibiotics are recommended for patients with increased sputum purulence plus either increased sputum volume or increased
dyspnea.eRisk factors include: age > 65, FEV1< 50% predicted, > 3 exacerbations/year, and presence of comorbid diseases.fRisk factors for Pseudomonas aeruginosa are:
Recent hospitalization Frequent administration of antibiotics (4 courses over the past year) Severe COPD exacerbations Isolation of P. aeruginosa during a previous hospitalization or colonization during a stable period
-
8/10/2019 COPD Michigan
9/17
9 UMHS COPD Guideline, May, 2010
Clinical Problem
and Management Issues(continued)
Management issues. Both physicians and patientsunderrecognize the potential benefits of appropriatedisease management for COPD. The lack of a large FEV1response to bronchodilation may contribute to a sense oftherapeutic nihilism. However, COPD is a chronicinflammatory disease with systemic manifestations that
affect patient function, quality of life, rate of lung functiondecline and the development of comorbidities. FEV1 is notthe sole measure of disease response. COPD is responsiveto multiple treatments. With appropriate comprehensivetreatment, patients with COPD may achieve improvedquality of life and prognosis.
Rationale for Recommendations
Etiology/Prognosis
Etiology. The pulmonary manifestations of COPD are
associated with an abnormal inflammatory response tonoxious inhaled particles or gases. The most commonlyassociated noxious agent is cigarette smoke, and cigarettesmoking is the single largest risk factor for COPD. Secondhand smoke is a recognized risk factor, as areenvironmental and occupational air pollutants. Deficiencyof alpha-1-antitrypsin is a treatable cause of abnormalinflammatory response; while uncommon, it can be animportant etiologic factor in early onset and severe disease.
Prognosis. COPD is a chronic disease characterized byacute exacerbations. Airflow limitation is usuallyprogressive, and life expectancy falls as disease progresses.In the United States, COPD is the fourth leading cause ofdeath, and the number of deaths related to COPD are rising.While FEV1 is commonly used to assess disease severity, itis imperfect for prognostic prediction. A better predictor ofsurvival is the multidimensional disease index known asBODE score (Table 6):
Body mass index,Obstruction of airflow as measured by FEV1,Dyspnea as measured by the modified Medical Research
Council scale (Table 7), andExercise capacity measured by a timed 6-min walk
distance.
Screening for COPD
Although about half of the estimated 24 million people withCOPD in the United States are undiagnosed, controversyexists regarding whether population-wide screening forCOPD actually leads to improved outcomes or is ultimatelycost effective. Screening in older populations may lead tooverdiagnosis in never smokers. The United States
Preventive Services Task Force recommends againstpopulation screening. While routine population screeningcannot be recommended, early diagnostic case finding isencouraged for persons at risk.
Diagnosis of COPD and Diagnostic studies
Risk factors and clinical history.A clinical diagnosis ofCOPD should be considered in any patient who hasdyspnea, chronic cough or sputum production, and/or ahistory of inhalational exposures known to be risk factorsfor the disease including chronic tobacco smoke,occupational dusts and chemicals, and smoke from homecooking and heating fuels (see Table 2). Likelihood of a
COPD diagnosis also increases with age.
Early diagnosis is encouraged, as the most effective therapyfor COPD in terms of slowing lung function decline issmoking cessation. Also, case finding may improvesmoking cessation rates.
Recent evidence suggests that explaining a patientspulmonary function to them in terms of relative lung-ageenhances cessation rates.
Differential diagnosis considerations for patients withchronic cough and dyspnea can be found in Tables 3 and 4.
Symptoms and Signs on Physical Exam (Table 2).Dyspnea is the symptom that most frequently leads patientsto seek medical attention and worsens with disease severity.With severe disease, dyspnea can be debilitating. Chroniccough often accompanied by sputum production mayprecede the onset of dyspnea. It frequently begins as anintermittent symptom, but later becomes persistent.Wheezing and chest tightness are nonspecific symptomsthat may or may not be present. In patients with moresevere disease, anorexia and anxiety may also develop.
The physical exam is typically unhelpful in the diagnosis ofCOPD. Early airflow limitation is typically detectable viaspirometry before it is evident on physical exam. Inpatients with more severe disease, the physical exam mayreveal decreased breath sounds, decreased air movement,wheezing, and rhonchi. Hyperinflation as indicated by abarrel chest, accessory muscle use and weight loss
typically indicate more advanced disease.
Basic Testing
Spirometry. Spirometry is required to make a diagnosis ofCOPD. Spirometry is the diagnostic gold standard
because it is the most reproducible, standardized, and
objective way of measuring airflow limitation. Spirometryshould be ordered with bronchodilator and the post-bronchodilator values used to assess both the presence ofairflow obstruction and severity. A post-bronchodilatorFEV1/FVC
-
8/10/2019 COPD Michigan
10/17
10 UMHS COPD Guideline, May, 2010
bronchodilator FEV1 improvement of 12% can also be seen
in COPD. In such cases of COPD with FEV1
bronchodilation response, the post-bronchodilator
FEV1/FVC by definition remains
-
8/10/2019 COPD Michigan
11/17
11 UMHS COPD Guideline, May, 2010
While inhaled corticosteroids may carry theoretic risk fordecreasing bone mineral density (BMD), several studiesfollowing BMD over 3 years indicate the risk is likelyminimal. For further guidance regarding osteoporosismanagement, see the UMHS Osteoporosis ClinicalGuideline.
Psychiatric disorders. Psychiatric disorders may be two tothree times more prevalent in COPD patients than the
general population. These include depression and anxiety.Studies also indicate that women, in particular, experiencegreater symptoms, worse quality of life, more depressionand more anxiety than their male counterparts with COPD.Efforts should be made to identify and treat psychiatricdisorders in COPD patients. For further guidance regardingdepression management, see the UMHS DepressionClinical Guideline.
General Management of COPD
Patient Education
Multiple nonpharmacologic care interventions have beenshown to achieve improved quality of life for patients withCOPD. Therefore, tailored and patient-focused education isgenerally recommended. Education regarding smokingcessation has the greatest capacity to influence the naturalhistory of COPD. Education also improves patientresponse to exacerbations. Prospective end-of-lifediscussions help patients understand advanced directivesand therapies at end-of-life. Specific recommended patienteducation content is noted in Table 8.
Disease management involves partnering with nurses and
respiratory therapists to assist in patient education andcompliance. Patients enrolled in pulmonary rehabilitationat the University of Michigan receive instruction in selfmanagement skills that support chronic diseasemanagement.
Preventive Care
Preventive care focuses on avoiding irritants that canaggravate COPD. The most common triggers are
smoking, second hand smoke, occupational fumes andchemicals, indoor air pollution (e.g., cooking with biomassfuels), outdoor air pollution, and infection.
Smoking Cessation. Smoking cessation is the single mostimportant intervention to slow the rate of lung decline andreduce respiratory symptoms regardless of the severity ofthe patients disease. The benefit of smoking cessation on
the natural history of COPD is greater the earlier in thedisease that cessation is achieved.
Smoking cessation should be encouraged at each visit. Thecombination of pharmacologic and psychosocial treatmentfor smoking cessation has been shown to be superior topsychosocial treatment alone in patients with COPD.Smoking cessation counseling is a billable diagnosis for
patients with COPD. For further guidance on smokingcessation, see theUMHS Smoking Cessation Guideline.
Second hand smoke. Directly measured second handsmoke (SHS) exposure appears to have an adverse impacton health outcomes in COPD, independent of personalsmoking. SHS is a modifiable risk factor. Clinicians shouldassess SHS exposure in their patients and counsel itsavoidance. In public health terms, the effects of SHS
exposure on this vulnerable subpopulation provide a furtherrationale for laws prohibiting public smoking.
Occupational fumes. Nineteen percent of COPD cases areattributed to occupational pulmonary irritant exposure.Therefore, limiting exposure to industrial fumes and dust isadvised. Limiting exposure can help slow progression ofdisease and improve symptoms. Occupational exposuresinclude organic and inorganic dusts, chemical agents, andfumes. In men with early COPD, each year of continuedoccupational fume exposure has been found to beassociated with a 0.25% reduction in post-bronchodilatorFEV1% predicted.
Particulates (air pollution). Patients with COPD shouldbe counseled to monitor the pollution index and stayindoors when pollution is high. Staying indoors when airquality is poor may help reduce symptoms. Emergencyroom visits have been shown to increase among patientswith COPD following days of high air pollution.
Patients should be counseled to avoid indoor air pollutionas well. Use of biomass fuels, such as wood, crop material,and garbage, for indoor cooking is a significant risk factorfor COPD, especially in developing countries.
Vaccination. Patients with COPD are at increased risk for
complications from pulmonary infections (e.g.,hospitalization, increased use of antibiotics). Therefore, theCDC Advisory Committee of Immunization Practicesrecommends all patients receive pneumococcalpolysaccharide vaccine and yearly influenza vaccine.
Pneumococcal polysaccharide vaccination is performedthrough an initial dose given to all COPD patients. If theinitial dose is given at an age < 65, a second dose should beadministered when the individual is 65 years old and 5
years have passed since the initial vaccination.Pneumococcal vaccine has not been shown in randomizedcontrolled trials to have significant impact on morbidity or
mortality in patients with COPD. However, the vaccineremains recommended based on consensus expert opinion.
Yearly influenza vaccination has been shown to reduceexacerbations and influenza-related respiratory infections.Influenza vaccine reduces serious illness and death frominfluenza in COPD patients by approximately 50%.
Medications for Chronic Care
Medications commonly used in COPD includebronchodilators (both short and long acting B2-Agonists
http://www.med.umich.edu/1info/fhp/practiceguides/osteoporosis.htmlhttp://www.med.umich.edu/1info/fhp/practiceguides/osteoporosis.htmlhttp://www.med.umich.edu/1info/fhp/practiceguides/osteoporosis.htmlhttp://www.med.umich.edu/1info/fhp/practiceguides/depress.htmlhttp://www.med.umich.edu/1info/fhp/practiceguides/depress.htmlhttp://www.med.umich.edu/1info/fhp/practiceguides/depress.htmlhttp://www.med.umich.edu/1info/fhp/practiceguides/smoking.htmlhttp://www.med.umich.edu/1info/fhp/practiceguides/smoking.htmlhttp://www.med.umich.edu/1info/fhp/practiceguides/smoking.htmlhttp://www.med.umich.edu/1info/fhp/practiceguides/smoking.htmlhttp://www.med.umich.edu/1info/fhp/practiceguides/depress.htmlhttp://www.med.umich.edu/1info/fhp/practiceguides/depress.htmlhttp://www.med.umich.edu/1info/fhp/practiceguides/osteoporosis.htmlhttp://www.med.umich.edu/1info/fhp/practiceguides/osteoporosis.html -
8/10/2019 COPD Michigan
12/17
12 UMHS COPD Guideline, May, 2010
and anti-cholinergics) and anti-inflammatory agents(inhaled glucocorticoids). Guidelines for inhalermanagement by disease stage are presented in Table 9.More detailed dosing and cost information by drug ispresented in Table 10. While medical therapy improvesfunctional status, no existing medications for COPD havebeen shown to modify long-term decline in lung functionand oxygen is the only treatment proven to impactmortality.
B2-agonists and anti-cholinergics. Both of these agentsare bronchodilators. Despite limited change in spirometricmeasures, treatment with bronchodilators still providesclinical benefit. In COPD, long-acting bronchodilators canprevent and control symptoms, reduce the frequency andseverity of exacerbations, improve health status, andimprove exercise tolerance. They are indicated in thetreatment of any COPD patient who is symptomatic. Allcategories of bronchodilators have been shown to increaseexercise capacity in COPD. Current evidence suggestslong-acting anti-cholinergics should be considered first lineagents for baseline bronchodilator control. Combining
different types of bronchodilators may increase the degreeof bronchodilation with equivalent or fewer side effects.
Recently several safety concerns have been raised with bothlong-acting B2-agonists and anti-cholinergics.
Long-acting B2-agonists (LABA). An FDA advisorypanel recently reviewed long-acting beta-agonists andrecommended that long-acting beta-agonists not be usedas single-agent therapy in asthma (see UMHS Asthmaguideline). While long-acting beta agonists may increaseblood pressure and heart rate, data for COPD patientsfrom the TORCH study (a three-year, placebo controlledtrial in COPD of fluticasone proprionate and salmeterol
combination versus flucticasone alone, salmeterol alone,or placebo) found no increased risk of all-cause death orcardiovascular death in the salmeterol group. Thus, forpatients with COPD, long-acting beta-agonists may stillbe used without an inhaled corticosteroid. These datafurther underscore the importance of distinguishingasthma from COPD.
Anticholinergics. A recent meta-analysis suggested thatinhaled anticholinergics (ipratropium and tiotropium) areassociated with significantly increased risk ofcardiovascular death, MI, or stroke among patients withCOPD. However, since then, data from the UPLIFTstudy (a four-year, placebo controlled trial of tiotropium)
found no significant increase in myocardial infarction orstroke in the tiotropium treated group. The clinicianshould be aware that anticholinergic drugs may alsoworsen symptoms and signs associated with narrow-angleglaucoma, prostatic hyperplasia, or bladder-neckobstruction and should be used with caution in patientswith any of these conditions.
Inhaled glucocorticosteroids (ICS). Treatment with theseanti-inflammatory agents can improve symptoms and healthstatus and decrease the frequency of exacerbations. Theyare indicated in patients with an FEV150% and frequent
(at least annual) exacerbations. ICS should not be used as
monotherapy or first-line therapy in COPD. However, ICScan provide additive benefit to bronchodilators in reducingthe frequency of exacerbations and improving health status.Withdrawal from treatment with ICS can lead to short termincrease in exacerbations in some patients.
An increase in the frequency of pneumonia, particularly inpatients 65, has also been reported. The frequency of
reported pneumonia appears to be approximately double in
several studies comparing inhaled corticosteroid/LABAcombinations versus placebo in COPD. However, in thelargest published mortality study in COPD, no increase inpulmonary related deaths were noted in the ICS/LABAcombination therapy group as compared to placebo. Inpatients with COPD being treated with ICS, particularlythose over 65, the clinician should be aware of the possibleincreased risk of pneumonia and maintain a lower thresholdfor considering a diagnosis of pneumonia when patientspresent with increased symptoms.
Inhaled corticosteroids may also increase a patients risk forcataracts or glaucoma. Regular eye exams should be
considered for patients using these medications. Patientsshould also be warned about the possibility of ICS relatedthrush and vocal changes. Rinsing the mouth after use ofICS should be encouraged. Decrease in bone density is atheoretic risk of this class of medication although there islittle long-term data in this patient population.
Interestingly, a recent head-to-head trial of tiotropiumversus salmeterol-fluticasone in COPD demonstratedsimilar reductions in exacerbation rates althoughimprovements in health status were greater and deathsfewer in the salmeterol/fluticasone treated patients. Theclinical implications of these data, however, are not yetclear; we recommend adding an ICS only in patients with
severe disease and frequent (at least annual) exacerbations.
Oral glucocorticosteroids are not generally indicated forchronic use. (See Acute Exacerbation.)
Theophylline is effective for symptom control in COPD.However, due to its narrow therapeutic window and sideeffect profile, inhaled bronchodilators are preferred. Allstudies that have shown efficacy of theophylline in COPDwere done with slow-release preparations.
Antibiotics. The use of routine prophylactic antibioticscan not currently be recommended, although the utility of
daily macrolide antibiotics in particular has recentlyreceived attention and is currently being investigated.
Leukotriene modifiers. These agents have not beenadequately tested in COPD and can not be recommended atthis time.
Oxygen Therapy
The primary goal of oxygen therapy is to maintain vitalorgan function by ensuring adequate oxygen delivery. Thisis achieved by increasing the baseline PaO2 to at least 60
http://www.med.umich.edu/1info/fhp/practiceguides/asthma.htmlhttp://www.med.umich.edu/1info/fhp/practiceguides/asthma.htmlhttp://www.med.umich.edu/1info/fhp/practiceguides/asthma.htmlhttp://www.med.umich.edu/1info/fhp/practiceguides/asthma.htmlhttp://www.med.umich.edu/1info/fhp/practiceguides/asthma.html -
8/10/2019 COPD Michigan
13/17
13 UMHS COPD Guideline, May, 2010
mmHg (or SaO2 to at least 90%) at rest. In patients withvery severe COPD, long term oxygen therapy has beenshown to improve the following outcomes:
mortality quality of life cardiovascular morbidity (i.e. pulmonary hypertension) depression cognitive function exercise capacity
frequency of hospitalizationVirtually no adverse affects occur with long term oxygentherapy.
Indications for oxygen therapy. Oxygen saturation of 88% is considered respiratory failure in need of oxygentherapy. Patients with marginal oxygenation saturation, 89-93%, should be further evaluated for possible oxygentreatment according to clinical indications. Indications forintermittent and continuous oxygen use are summarized inTable 11.
For intermittent use, no data show symptomatic benefit
from short bursts of oxygen therapy before or after exercise,although some patients may recognize an improvement indyspnea following activity. Despite this, CMS (Center forMedicare and Medicaid Services) will reimburseintermittent oxygen use for the criteria shown in Table 11.
Pulmonary Rehabilitation
Pulmonary rehabilitation should be considered in anypatient with COPD who experiences significant dyspnea orexercise limitation, regardless of severity of airflowlimitation. (Note that Medicare typically reimbursesrehabilitation only for patients who have a diagnosis ofCOPD and also meet the following criteria: FEV1%predicted 65%, FVC% predicted 65%, or DLCO %
predicted 65%. Medicare patients who continue to smokemust also be enrolled in a smoking cessation program.)
Pulmonary rehabilitation is an evidence-based,multidisciplinary, and comprehensive intervention forpatients with chronic respiratory diseases who aresymptomatic and often have decreased daily life activities.Pulmonary rehabilitation is designed to reduce symptoms,optimize functional status, increase participation, andreduce health care costs through stabilizing or reversingsystemic manifestations of disease. Pulmonaryrehabilitation programs typically involve a comprehensive
patient assessment, aerobic exercise training, strengthtraining, education, and psychosocial support. Randomizedcontrolled trials demonstrate that exercise pulmonaryrehabilitation in COPD patients can relieve dyspnea andimprove health-related quality of life. Controlled trialssuggest that pulmonary rehabilitation may reduce thenumber of hospital days and health-care utilization inpatients with COPD.
Follow Up Care
Frequency. No clear consensus exists on frequency ofoffice visits for chronic COPD care. In general, werecommend that initial chronic care visits occur at leastsemi-annually. Visits may revert to annual assessments forcurrently nonsmoking patients with mild disease who arestable on treatment (i.e. with only rare exacerbations).Frequency of follow-up can be guided based on:
worsening of symptoms not associated with anexacerbation
frequency of acute exacerbations smoking status adherence to treatment plan social support systems presence of other comorbid chronic diseases
Factors to reassess. At follow-up visits reassess: pulmonary irritant exposure risks symptoms: severity, control, new, stable or worsening
(e.g., sputum production, dyspnea, cough, activities ofdaily living)
exacerbation history and possible causes smoking cessation, if applicable current medications, dosages, adherence, and proper use vaccinations
Spirometry. Rather than routinely repeating spirometry, werecommend monitoring symptoms and functional status toguide spirometry use at routine follow up visits. No clearconsensus exists on the appropriate frequency of spirometryto guide therapy after the initial diagnosis of COPD.Systematic reviews found insufficient evidence for usingspirometry to guide therapy. Once therapy is initiated,evidence-based reviews do not support annual spirometry tomonitor disease status for otherwise stable patients. Whenpatients report symptomatic change or experience asignificant acute exacerbation, follow-up spirometry maybe warranted to detect clinically significant functionalchanges that may alter clinical therapeutic options.
Medications. Steps for increasing medical therapy basedon increased severity are summarized in Table 9 and asdescribed above under Medications for Chronic Care. Ifpatients remain symptomatic at subsequent follow-up visits,combination pharmacotherapy should be considered.
Oxygen therapy. Patients with worsening symptoms,particularly if most recent FEV1 is
-
8/10/2019 COPD Michigan
14/17
14 UMHS COPD Guideline, May, 2010
patients with significant dyspnea or exercise limitation. SeePulmonary Rehabilitation section above.
After hospitalization for acute exacerbation. Patientsshould be reassessed following hospital discharge for acuteCOPD exacerbation. The assessment should include: spirometry (significant declines in lung function can
occur with exacerbations) ability to cope in their home environment
inhaler technique and understanding of treatmentregimen.
need for oxygen
Acute Exacerbation
No single definition of acute COPD exacerbation isuniversally accepted. It can reasonably be described as anacute change in a patients baseline dyspnea, cough, and/or
sputum that is beyond normal day-to-day variability and issufficient to warrant a change in medication in a patientwith underlying COPD.
A commonly used operational classification of COPD acuteexacerbation severity is:
Level I: treated at homeLevel II: requires hospitalizationLevel III: leads to respiratory failure
This guideline will focus on Level I exacerbations, whichcan be treated as an outpatient.
Causes and differential diagnosis. Causes of acuteexacerbation include: Infection (both viral and bacterial) Environmental conditions Air pollution Lack of compliance with long-term oxygen therapy Unknown (~1/3 of cases)
When performing a differential diagnosis of acuteexacerbation of COPD, alternate diagnoses need to beconsidered including: Pneumonia Congestive heart failure Pneumothorax Pleural effusion Pulmonary embolism Cardiac arrhythmia
Assessment. The outpatient assessment for an acuteexacerbation of COPD starts with the clinical history andphysical examination. Obtaining an oxygen saturation viapulse oximetry is recommended. Ordering a chestradiograph is generally not recommended, however may bereasonable for patients >65 years of age, exposure toinhaled steroids, or the presence of fever.
There is limited utility in obtaining a sputum gram stain &culture. An exception may be patients who have recentlybeen on antiobiotics. Spirometry, arterial blood gas, andelectrocardiogram are generally not recommended.
Pharmacotherapy of Acute Exacerbation
Outpatient management of acute exacerbation involvestreatment with bronchodilators, systemic corticosteroids,and antibiotics. Specific drugs and dosing are described inTable 12.
Bronchodilators. Bronchodilators are considered first-linetherapy since they improve respiratory symptoms and
FEV1. The dose and/or frequency of short-acting 2-agonists, either inhaler or nebulizer, should be increased.An inhaled anticholinergic (ipratropium) can be added ifnot already used, although the effectiveness of combinationtherapy in the setting of acute exacerbation is questionable.Clinical response does not appear to differ betweenbronchodilator delivery via MDI with a spacer or bynebulizer.
Systemic corticosteroids. Corticosteroids can reducerecovery time, improve lung function (FEV1), and improvehypoxemia (PaO2). Prednisone 30-40mg PO daily isrecommended for 10-14 days, particularly in patients with
an FEV1 % predicted < 50%. Discontinue corticosteroidsfollowing exacerbation therapy.
Antibiotics. Antibiotics are recommended for patientswith:
increased sputum purulence
plus either
- increased dyspnea or- increased sputum volume.
Antibiotic choice should be selected for presumptivetherapy based on local resistance patterns. Sputum culturesare generally not recommended unless the patient hasrecently been taking antibiotics. For patients who meet theabove criteria for antibiotics, the selection of a specificantibiotic depends on risk factors and unusualcircumstances (see Table 12).
Indications for hospitalization. The following are reasonsfor emergency department evaluation or hospital admission: Marked increase in symptoms such as dyspnea at rest Severe underlying COPD Frequent exacerbations Significant comorbidities (e.g., older age, pneumonia,
congestive heart failure, diabetes mellitus, renal or liverfailure)
Worsening hypoxemia or hypercapnia
Changes in mental status Inadequate response to outpatient therapy Uncertain diagnosis Insufficient home support
Other Management Approaches
Surgical treatment: lung volume reduction surgery,
lung transplantation. Surgical therapeutic options includebullectomy and lung volume reduction surgery (LVRS).Bullectomy may be considered for patients with localized
-
8/10/2019 COPD Michigan
15/17
15 UMHS COPD Guideline, May, 2010
giant bullae that are associated with compression ofadjacent lung. Lung volume reduction surgery may beconsidered for patients with bilateral upper lobe disease andreduced exercise capacity as measured by formalcardiopulmonary exercise testing despite maximal medicaltherapy and pulmonary rehabilitation. Data demonstrateimproved exercise capacity, dyspnea, and quality of life at24 months; survival outcomes were favorable for those withupper lobe emphysema and reduced exercise capacity.
Cost-effectiveness of this approach is not demonstrated foreven the most favorable NETT subgroup (i.e. COPDpatients with upper lobe emphysema and reduced exercisecapacity) unless outcomes are expected to remain favorablefor 10 years. Therefore, total life expectancy should beincorporated into shared decision making regarding thepotential benefits of surgery.
Lung transplantation may be considered for patients withBODE index 7 to 10 without comorbid conditions thatwould otherwise limit the expected lifespan. Considerationof transplantation potential requires co-management with apulmonary specialist for detailed assessment of baseline
pulmonary physiology and potential contraindications.
Complementary and alternative medicine. Whilecomplementary and alternative medical therapies have beenproposed for the treatment of COPD, little evidence ofsignificant clinical benefit exists. For example, yogatraining as a strategy to reduce dyspnea in COPD has beeninvestigated with some evidence to suggest it may reducedyspnea. While usual advice regarding healthy diet isgenerally endorsed, specific nutrient supplements have noproven benefit. Creatine supplementation has not beenshown to demonstrate additive exercise capacity or musclemass benefit for patients engaged in pulmonaryrehabilitation. Pulmonary function demonstrated
statistically significant worsening immediately followingosteopathic manipulative treatment, as measured by FEV1and residual volume.
Palliative care. Severe COPD increases risk of respiratoryfailure and is a leading cause of death. Given theprogressive nature of the disease, clinicians are stronglyencouraged to engage patients in shared decision makingregarding goals of therapy, including advanced careplanning and advance directives. A palliative focus for careshould be discussed with patients desiring less aggressivetherapy, avoidance of endotracheal intubation, or comfortcare measures (symptomatic care) at the end of life.
Therapies with proven effectiveness for management ofdyspnea at the end of life include opioids and oxygen.
Referral to COPD Specialist
Consider referral to a pulmonologist/COPD specialist if:
Concurrent cardiac disease, suspected asthma, or anotherpulmonary disease complicates diagnosis ormanagement;
Alpha-1-antitrypsin deficiency is diagnosed or stronglyconsidered;
Upper airway obstruction is suspected (e.g. upper airwaywheezing or stridor, with consideration ofotolaryngology referral v. pulmonary referral);
Symptoms do not respond to optimal therapy or are outof proportion to obstructive findings;
Supplementary oxygen therapy is required;
Severe or frequent (at least one per year) exacerbationsor pneumonia complicate management;
Lung volume reduction surgery or lung transplantation is
considered (BODE of 7-10, giant bullae, or earlierreferral for monitoring and preparation if FEV1
-
8/10/2019 COPD Michigan
16/17
16 UMHS COPD Guideline, May, 2010
D. Diagnostic studies: PFTs, alpha-1-antitrypsin level, chestX-ray, 6 minute walk test, chest CT [6/05]
E. Diagnostic classification: GOLD classes, MRC orMMRC dyspnea scale, BODE index [6/05]
F. Definition and diagnosis: Acute exacerbation [12/06]G. Other diagnosis not included in CF above [6/05]H. Comorbid diseases (increased risk) [6/05]I. Prevention: Smoking cessation, vaccination (influenza,
penumocus) [1/07]
J. Prevention: Irritant avoidance [1/03]K. Pharmacologic treatment: Bronchodilators, inhailed
corticosteroids [4/07]L. Treatment: Supplemental oxygen [4/07]M Treatment: Pulmonary rehabilitation [4/07]N Treatment: Complementary and alternative medicine
[1/03]O. Treatment: Mental health, psychosocial support [1/03]P. Treatment: Acute exacerbationoutpatient
management, hospitalization [12/06]Q. Referral to pulmonary sub-specialist [4/07]R. Surgical treatment: Lung volume reduction surgery,
lung transplantation [4/07]
S. Treatment: Follow up care, monitoring, chronic diseasemanagement [1/03]T. Treatment: Palliative care [1/03]U. Other treatment not in IT above [12/06]V. Other not in AU above [12/06]
The search was conducted in components each keyed to aspecific causal link in a formal problem structure (availableupon request). The search was supplemented with veryrecent clinical trials known to expert members of the panel.Negative trials were specifically sought. The search was asingle cycle.
Conclusions were based on prospective randomized
controlled trials if available, to the exclusion of other data;if RCTs were not available, observational studies wereadmitted to consideration. If no such data were availablefor a given link in the problem formulation, expert opinionwas used to estimate effect size. The strength ofrecommendation for key aspects of care was determined
by expert opinion.
Related National Guidelines
This guideline is generally consistent with the: Screening for chronic obstructive pulmonary disease
using spirometry: U.S. Preventive Services Task Forcerecommendation statement. Ann Intern Med. Apr 1
2008;148(7):529-534.
Clinical Efficacy Subcommittee of the American Collegeof Physicians. Diagnosis and management of stablechronic obstructive pulmonary disease. Annals ofInternal Medicine, 2007; 147(9):633-638.
American Thoracic Society / European RespiratorySociety. Standards for the Diagnosis and Managementof Patients with COPD. New York, NY: Am. ThoracicSociety, 2004. (available at www.thoracic.org/sections/copd/)
Global Initiative for Chronic Obstructive Lung Disease.
Global Strategy for the Diagnosis, Management, andPrevention of Chronic Obstructive Pulmonary Disease,Executive Summary.Am J Respir Crit Care Med.,2007; 176(6):532-55.
Disclosures
The University of Michigan Health System endorses the
Guidelines of the Association of American MedicalColleges and the Standards of the Accreditation Council forContinuing Medical Education that the individuals whopresent educational activities disclose significantrelationships with commercial companies whose productsor services are discussed. Disclosure of a relationship is notintended to suggest bias in the information presented, but ismade to provide readers with information that might be ofpotential importance to their evaluation of the information.
Team Member Relationship Company
Davoren A. Chick, MD (none)
Paul J. Grant, MD (none)MeiLan K. Han, MD Consultant
Speakers
bureau
Advisoryboard
Novartis, NycomedBoehringer Ingelheim,GlaxoSmithKline,CLS Boehring
CLS Boehring
R. Van Harrison, PhD (none)
Elisa B. Picken, MD (none)
Review and Endorsement
Drafts of this guideline were reviewed in clinicalconferences and by distribution for comment withindepartments and divisions of the University of MichiganMedical School to which the content is most relevant:Emergency Medicine, Family Medicine, General Medicine,Geriatric Medicine, Obstetrics & Gynecology (Womens
Health), and Pulmonary & Critical Care Medicine. TheExecutive Committee for Clinical Affairs of the Universityof Michigan Hospitals and Health Centers endorsed thefinal version.
Annotated References
Celli BR. Update on the management of COPD. Chest,Jun 2008; 133(6): 1451-1462.
This update focuses on chronic COPD.
Sethi S and Murphy TF. Infection in the pathogenesis andcourse of chronic obstructive pulmonary disease. N Engl JMed 2008;359:2355-65
This review article focuses on the role of infection inCOPD
-
8/10/2019 COPD Michigan
17/17
Lin K, Watkins B, Johnson T, Rodriguez JA, Barton MB.
Screening for chronic obstructive pulmonary disease using
spirometry: U.S. Preventive Services Task Force
recommendation statement. Ann Intern Med. Apr 1
2008;148(7):529-534.
This systematic review provides recommendations for
this screening in primary care.
Littner MR. In the clinic: chronic obstructive pulmonary
disease. Annals of Internal Medicine, Mar 4 2008; 148(5):ITC3-1ITC3-16.
This article focuses on the practical application of
recommendations for care
Qaseem A, Snow V, Shekelle P, et al. Diagnosis and
management of stable chronic obstructive pulmonary
disease: a clinical practice guideline from the American
College of Physicians. Annals of Internal Medicine, 2007;
147(9):633-638.
Wilt TJ, Niewoehner D, MacDonald R, Kane RL.
Management of stable chronic obstructive pulmonary
disease: a systematic review for a clinical practice
guideline. Ann Intern Med. Nov 6 2007;147(9):639-653.
The first reference provides the guideline for
management of stable COPD and the second reference
provides detail on the methods and literature used to
develop the guideline.
Quon BS, Gan WQ, Sin DD. Contemporary management of
acute exacerbations of COPD: a systematic review and
metaanalysis. Chest. Mar 2008;133(3):756-766.
This review summarizes evidence and recommendations
for management of acute exacerbations.