02. Chronic obstructive lung disease (COPD)

Resident Editor: Monica Parks, MD

Faculty Editor: Lekshmi Santhosh, MD

BOTTOM LINE

✔ Order PFTs for anyone suspected of having COPD

✔ FEV1/FVC < 70% is virtually diagnostic

✔ Treat stable disease with inhaled bronchodilators

✔ Treat exacerbations with a burst of systemic corticosteroids and increased frequency of inhaled bronchodilators

Definition

  • Persistent (irreversible) and usually progressive airflow restriction and enhanced airway inflammatory response to noxious gases and inhalants.
  • Note that some subsets of patients have overlap syndromes with asthma.

Epidemiology

  • 3rd ranked cause of death in the US
  • Worldwide prevalence of GOLD stage 2 or higher is 10% in adults over 40
  • Most patients with mild to moderate disease are undiagnosed
  • Typically manifests in 6th decade of life
  • Risk factors: smoking (usually at least 10-15 pack years unless other risk factors present), environmental exposures, certain genetic predispositions (1-antitrypsin), and persistent asthma
  • Non-smokers comprise 20% of COPD patients

Signs and Symptoms

  • Chronic cough
  • Chronic sputum production
  • Dyspnea: usually persistent, progressive, worse with exertion. Pts may unknowingly avoid dyspnea by self-reducing activity, so get a careful activity history.
  • Some present with intermittent acute symptoms of the above.

Differential diagnosis

  • Asthma: reversible airflow limitation, begins earlier in life, comorbid allergic rhinitis and eczema common. Some patients have a COPD-asthma overlap syndrome.
  • CHF:PFTs show restriction; volume overload on exam. Frequently comorbid with COPD.
  • Bronchiectasis: Copious purulent sputum, frequent lung infections, may have predisposing condition (ie cystic fibrosis)
  • Tuberculosis: look for risk factors for exposure
  • Others: bronchiolitis obliterans, interstitial lung disease, chronic fungal or non-TB mycobacterial infection, malignancy, non-asthmatic eosinophilic bronchitis, upper airway cough syndrome (allergic and non-allergic rhinitis), GERD, medication effect (ACE-I)

Evaluation

  • History – tobacco exposure, other inhaled drugs, occupational exposures (e.g. fumes, dust, chemicals), environmental exposures (e.g. air pollution, indoor stoves), family history
  • Physical – wheezes, crackles, prolonged expiratory phase, hyperresonance/hyperinflation, distant heart sounds, “barrel chest”, decreased diaphragmatic excursion.  Later in disease course can see accessory muscle use, cyanosis, right heart failure (cor pulmonale), neck vein distention.
  • PFTs (Spirometry) – post-bronchodilator FEV1/FVC ratio <0.70 is diagnostic. May also be helpful in monitoring progression and response to therapy.
  • Other labs/tests to consider
    • If O2 sat is abnormal get ABG: typically see hypercapnia and hypoxemia (PaCO2 and PaO2 are “50/50” in advanced disease).
    • Check 1-antitrypsin levels in all cases with persistent airflow limitation on PFTs
    • CXR: increased radiolucency, flattened diaphragms, narrow heart shadow, bullae (not required for Dx)

STAGING AND TREATMENT OF STABLE DISEASE

Tables adapted from GOLD Staging of COPD (http://www.goldcopd.com)

A. ASSESS SEVERITY OF AIRFLOW LIMITATION

Stage

Characteristics

(in patients with FEV1/FVC <70%)

3-year Mortality

I (mild COPD)

FEV1 >80% predicted

 

II (moderate COPD)

FEV1 50-80% predicted

11%

III (severe COPD)

FEV1 30-49% predicted

15%

IV (very severe COPD)

FEV1 <30% predicted

24%

B. ASSESS SYMPTOM SEVERITY

  • Modified Medical Research Council Questionnaire for Assessing the Severity of Breathlessness (mMRC) – focused on dyspnea only
  • COPD Assessment Test (CAT, www.goldcopd.org) – evaluates symptomatic impact of COPD, not necessarily used to guide treatment

C. ASSESS RISK OF EXACERBATIONS

D. ASSESS COMORBIDITIES

Treatment

Non-pharmacologic:

  • Smoking cessation: single most important intervention for patients with COPD, the only intervention known to modify the long-term decline in lung function.
    • Counseling plus nicotine replacement, bupropion, or varenicline
    • The effect of e-cigarette use on COPD management remains unclear.
  • Immunizations:
    • Annual flu vaccine
    • PPSV23 before age 65, once > 65 then get PCV13 (at least 1 year from 1st dose PPSV23) then second dose PPSV23 (at least 5yrs from 1st dose PPSV23 if received)
  • Physical activity/Pulmonary Rehabilitation
  • Lung cancer screening: Annual low-dose CT in adults 55-80yo with a 30 pack-year smoking history and who currently smoke or have quit within 15 years (USPSTF Grade B)
  • End-of-life care and planning: for advanced COPD  
  • Nutrition
  • Patient education and inhaler teaching

Stable Disease:

  • Goals of treatment: symptom relief, decrease severity/frequency of exacerbation, improve exercise capacity and health status, and reduce mortality
  • Bronchodilators are the mainstay of treatment
    • Start with intermittent short-acting beta agonists (LABA) or anti-muscarinics (LAMA) for sx relief (ipratropium, albuterol)
    • If moderate or persistent symptom burden, add long-acting anti-muscarinics or beta agonists (LAMA, LABA)
      • No evidence that starting these for early COPD improves disease course.
      • LAMAs are superior to LABAs for reducing exacerbations.
    • Combination bronchodilator therapy (ie, formoterol/triotropium)are more effective than single bronchodilators.
  • Consider inhaled corticosteroids (ICS) for patients who are still symptomatic on optimal long-acting bronchodilator regimen, Consider combination therapy (Advair = salmeterol/fluticasone) for ease of use – combination long acting beta agonist (LABA) and ICS (ex: Advair, Symbicort) reduces exacerbations by additional 10% than either agent alone.
  • Consider PDE4 inhibitors if frequent exacerbations despite maximal inhaler therapy.
  • For GOLD Group D (chronic respiratory failure), home O2 leads to decreased mortality in patients with severe hypoxemia (PaO2 < 55 mmHg) and increased quality of life. Indications: O2 sat ≤ 88% or PaO2 ≤55 or PaO2 ≤60 if also with cor pulmonale, peripheral edema, or polycythemia.
  • Prophylactic antibiotics (ie, azithromycin) may reduce exacerbations and improve quality of life in selected patients, though may increase risk of drug resistance and drug side effects.
  • Consider lung volume reduction surgery or lung transplant surgery in GOLD Stage IV in adherent patients.

GROUP

GOLD STAGE

Annual Exacerbations

Symptom burden

First line treatment

A

1-2

<1

Low

SAMA or SABA PRN.

B

1-2

<1

High

LAMA or LABA.

C

3-4

>2

Low

Start with LAMAthen LAMA + LABA or LAMA + LABA + ICS. Consider long-term abx or PDE4 inhibitor.

Stage IV: consider lung reduction or transplant surgery, home O2

D

3-4

>2

High

Acute exacerbations: Exacerbations reduce quality of life, speed progression of disease, and increase risk of death.

  • Triggers: Most common = viral or bacterial infection; others include PE, heart failure, pulmonary irritants
  • Definition:

Criteria to Classify Acute COPD Exacerbations

Major Criteria

Additional Criteria

Increase in sputum volume

Increase in sputum purulence

Worsening dyspnea

URI in past 5 days

Fever of no apparent cause

Increase in wheezing/cough

Increase in RR or HR 20% above baseline

Mild = 1 major criteria plus ≥ 1 additional criteria

Moderate = 2 major criteria

Severe = 3 major criteria

  • Outpatient treatment:
    • increase frequency of inhaled short-acting beta-agonists
    • systemic corticosteroids (ie: prednisone 40 mg daily for 5 days),
    • ensure adequate oxygenation (supplemental O2 if needed)
    • consider antibiotics if meets moderate or severe exacerbation criteria as above. Check local resistance patterns.
      • uncomplicated: doxycycline or azithromycin x5 days
      • Complicated: amoxicillin-clavulanate or levofloxacin if elderly, severe COPD or heart disease x5-10 days
  • Criteria for admission: high risk comorbidities, inadequate response to outpatient management, significantly worsening dyspnea, inability to eat or sleep due to symptoms, worsening hypoxemia, worsening hypercapnia, AMS, inability to care for oneself

When to refer

  • Difficulty controlling symptoms on maximal bronchodilator/ICS regimen
  • Rapidly progressive disease course (to exclude other etiologies)
  • If considering pulmonary rehab and/or surgery and unsure if patient is an appropriate candidate

References

Global Strategy for the Diagnosis, Management and Prevention of COPD. Global Initiative for Chronic Obstructive Lung Disease (GOLD). Updated 2017. Available: http://www.goldcopd.org/ Accessed March 31, 2018.  

Littner MR. In the clinic: COPD. Annals of Internal Medicine March 4, 2008:ITC3.1-ITC3.16.

Pratter MR. Overview of common causes of chronic cough: ACCP evidence-based clinical practice guidelines. Chest. 2006;129(1 Suppl):59S-62S.

Zhou Y, et al. Tiotropium in early-stage chronic obstructive pulmonary disease. N Engl J Med. 2017;3777(10):923-935.

Vogelmeier C, et al. Tiotropium versus salmeterol for the prevention of exacerbations of COPD. N Engl J Med. 2011;364(12):1093-103.

Herath SC, et al. Prophylactic antibiotic therapy for chronic obstructive pulmonary disease (COPD). Cochrane Database Syst Rev. 2013;28(11): CD009764.