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Chronic Obstructive Pulmonary Disease (COPD) and HIV

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Chronic Obstructive Pulmonary Disease (COPD)

Primary Care of Veterans with HIV

Organ Systems and Metabolic

April 2009; Last reviewed/updated: October 28, 2011

Background
Evaluation
Management
References
Table 1: Treatments according to Stage
Table 2: Medications and Other Therapies
Table 3: Potential ARV Interactions

Note: Some medications mentioned in this chapter may not be available on the VHA National Formulary. Consult VA pharmacists for alternatives.

Key Points

COPD comprises emphysema, chronic bronchitis, or a combination of the two.
COPD is a common cause of morbidity in HIV-infected veterans.
Multimodal treatment may decrease symptoms and slow progression.
For smokers, smoking cessation should be emphasized.
Drug-drug interactions between PIs and inhaled corticosteroids may affect treatment.

Background

COPD is:

A general term that applies to individuals with emphysema, chronic bronchitis, or as is common clinically, a combination of the two.
Characterized by airflow limitation that is not fully reversible.
Usually progressive; it is associated with abnormal inflammatory response of the lung to irritants.
Preventable and treatable.
Diagnostically defined as a post-bronchodilator forced expiratory volume in 1 second (FEV₁) to forced vital capacity (FVC) ratio of <0.70, and lack of alternative explanation for the symptoms and airflow obstruction.

Veterans with HIV*

COPD: 11%

Emphysema: 2%

*Veterans in the VA HIV Clinical Case Registry in care in 2007 who had an ICD-9 code corresponding to these conditions

Epidemiology

COPD is the fourth leading cause of chronic morbidity and mortality in the United States.
More than 100,000 people in the United States die each year of complications from COPD.
Underdiagnosed: Approximately 50% of patients with COPD have not been diagnosed.
Smoking is estimated to be responsible for approximately 75% of COPD deaths.
Only 15-20% of individuals with a significant smoking history are ever diagnosed with COPD. This reflects underdiagnosis as well as variability in susceptibility of smokers to the disease.
HIV-infected subjects were 50-60% more likely than HIV-uninfected subjects to have COPD in a prospective observational study done at VA medical centers.
After adjustment for age, race, ethnicity, pack-years of smoking, and history of intravenous drug and alcohol abuse, HIV infection has been identified as an independent risk factor for COPD.

Types of COPD

* Irreversible airflow obstruction = post-bronchodilator FEV₁/FVC <70%
Emphysema	Abnormal and permanent enlargement of the airspaces that are distal to the terminal bronchioles Usual onset in mid-life; largely irreversible,* often progressive (particularly in smokers who continue to smoke)
Chronic bronchitis	Productive cough for 3 months in each of 2 successive years in a patient for whom other causes of cough have been excluded Usual onset in mid-life; largely irreversible; often progressive (particularly in smokers who continue to smoke)

Evaluation

Risk factors	Pack-years of smoking Increasing age History of bacterial or Pneumocystis jiroveci pneumonia History of recurrent respiratory infections Exposure to occupational or other dust and chemicals Exposure to environmental (secondhand) tobacco smoke Exposure to indoor and outdoor air pollution Low socioeconomic status
History	Dyspnea With exertion Progressive Persistent Often described as causing "gasping," "heaviness," "difficulty breathing" Chronic cough (may not be present) Intermittent or persistent Productive or nonproductive Chronic sputum production If present, any pattern of chronic sputum production (even of small amounts) can suggest COPD
Physical examination	Note: Physical examination has low sensitivity and specificity. Vital signs, including respiratory rate (may be elevated), O₂ saturation (may be low), blood pressure, heart rate, temperature (the latter 3 may be elevated in exacerbations) Observation: tachypnea, dyspnea, accessory muscle use, hyperinflation, pursed lips Lungs: prolonged expiratory phase, decreased lung sounds, basilar crackles, wheezes may be present (usually during an exacerbation) CV: distant heart sounds due to hyperinflation Extremities: clubbing, cyanosis
Imaging	Chest X rays are important to obtain but they have low sensitivity for COPD (50%). Chest films may diagnose only severe emphysema, and can establish alternative diagnoses. Radiographic features associated with COPD include flattened diaphragm, increased radiolucency of the lung, long heart shadow, bullae, prominent hilar vasculature suggestive of pulmonary hypertension and cor pulmonale
Pulmonary function tests (PFTs), including spirometry	PFTs and spirometry are the diagnostic tests of choice. Order: Spirometry: airflow loops and measurements Lung volume (increased in COPD) Diffusing capacity of the lung for carbon monoxide (DLCO) (reduced in COPD; normal in asthma) Consider arterial blood gas (ABG) test for patients with <50% of predicted FEV₁, severe symptoms, and documented or suspected hypoxemia (O₂ saturation by pulse oximetry <88%) Consider bronchodilator reversibility testing for diagnosis of airway obstruction, particularly if history of asthma symptoms; may see partial but not full reversibility in COPD Repeat spirometry if there is an increase in symptoms, or a complication
Other evaluation	α1-antitrypsin deficiency screening: patients of Caucasian descent who develop COPD before age 45 or have a strong family history of early COPD Exercise tolerance may give useful information; most COPD patients can walk 500-600 meters over a 6-minute period; increases of >50 meters indicate clinically significant response to rehabilitation
Differential diagnosis (keep in mind that patients may have multiple conditions affecting pulmonary function, eg, COPD plus congestive heart failure)	Asthma (see Asthma) Reversible airway obstruction, without other features of COPD (see Asthma for distinction between reversible and irreversible airflow obstruction) Chronic inflammatory disorder; recurrent episodes of wheezing, breathlessness, chest tightness, and coughing Onset usually in childhood; symptoms vary daily
	Heart failure Orthopnea, crackles, elevated jugular venous pulse (JVP), S3 gallop, volume restriction rather than airflow limitation on PFTs
	Bronchiectasis Large volumes of purulent sputum, bronchial dilation, and wall thickening on chest X ray; high resolution CT scan is diagnostic test of choice
	Tuberculosis Exposure risk, subacute fevers, weight loss, infiltrate on chest X ray
	Bronchiolitis obliterans Younger age, nonsmoker, fume exposure, hypodense areas on CT scan
	Diffuse panbronchiolitis Male, nonsmoker, chronic sinusitis, diffuse small centrilobular nodular opacities on CT scan

Management

Smoking Cessation: Prevention and Treatment

Smoking cessation is the single most effective and cost-efficient intervention for most people to reduce the risk of developing COPD and limit its progression.
Brief, 3-minute periods of counseling from a provider to urge a smoker to quit result in smoking cessation rates of 5-10%.
For all smokers, try to incorporate the 5 A's of brief cessation counseling at each visit:
- Ask about tobacco use
- Advise to quit
- Assess willingness to make a quit attempt within the next 30 days
- Assist patients in quitting if they are ready
- Arrange follow-up

See Smoking Cessation for more information.

Stable Chronic COPD

Goals: prevent progression, relieve symptoms, improve exercise tolerance, improve health status, prevent and treat complications, prevent and treat exacerbations, reduce mortality

Remember: Counsel for smoking cessation at all stages!

Table 1: Treatments according to Stage
* There are important interactions between some inhaled corticosteroids and certain ARVs. See Table 3: Potential ARV Interactions.
All Patients: Avoid triggers and exposures Receive annual influenza vaccine Receive pneumococcal vaccine every 5 years
Stage	Spirometric Classification	Treatment
I: Mild	FEV₁/FVC <0.70 FEV₁≥80% predicted	Short-acting bronchodilator as needed: beta-agonists such as albuterol, levalbuterol, and pirbuterol, and/or anticholinergics such as ipratropium
II: Moderate	FEV₁/FVC <0.70 FEV₁ 50-79% predicted	Short-acting bronchodilator, plus: Long-acting bronchodilator (fixed dosing schedule): beta-agonists (eg, salmeterol, formoterol, arformoterol) and/or anticholinergics (eg, tiotropium) Pulmonary rehabilitation
III: Severe	FEV₁/FVC <0.70 FEV₁ 30-49% predicted	Each of the above, plus: Inhaled corticosteroid* for repeated exacerbations (steroid in order of increasing potency: triamcinolone, flunisolide, beclomethasone, budesonide, fluticasone) For patients with significant symptoms, consider addition of theophylline: may improve symptom control
IV: Very Severe	FEV₁/FVC <0.70 FEV₁<30% predicted	Each of the above, plus: Oxygen supplementation if PaO₂<60 Consider surgical procedures
Respiratory Failure	PaO₂<60 mmHg with or without PaCO₂>50 mmHg	Same as "IV: Very Severe" above

Print table

When to Refer

Pulmonary rehabilitation (stage II and greater) - refer to Pulmonary or Physical Therapy, depending on facility practice
Lung volume reduction (stage IV) - refer to Thoracic Surgery

Acute Exacerbations of COPD

This refers to acute increases in symptoms beyond normal daily variation, including 1 or more of the following symptoms:

Cough:↑ severity and frequency
Sputum production:↑ in volume or changes in character
Dyspnea:↑

Among patients with an acute exacerbation of COPD and a PaCO₂ of >50 mmHg, the 6-month mortality rate is 33%.

Precipitants include bacterial or viral infection (50-60%), air pollution exposure (10%), and temperature changes.

In patients with COPD and advanced HIV infection, consider evaluation for respiratory opportunistic infections (eg, P jiroveci pneumonia) in the setting of an exacerbation.

Table 2: Medications and Other Therapies
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Beta-adrenergic agonists (albuterol, levalbuterol, pirbuterol)	Mainstay of therapy eg, albuterol via nebulizer (2.5 mg) or metered-dose inhaler (MDI) (180 mcg [2 puffs]) Q2H
Anticholinergic bronchodilators (ipratropium, glycopyrrolate)	In addition to beta-agonists eg, ipratropium via nebulizer (500 mcg) or MDI (34 mcg [2 puffs]) Q4H
Glucocorticoids	Methylprednisolone 60-125 mg IV Q6-12H, or prednisone 40 mg PO QD Treat for up to 14 days; studies show good outcomes with 9 days of treatment Studies show no difference in outcomes between taper vs abrupt cessation of steroids in courses up to 14 days
Antibiotics	Controversial; studies do not show convincing benefit over placebo May consider for patients with increased sputum purulence AND increased sputum volume OR for patients with increased dyspnea alone For patients with severe exacerbations requiring mechanical ventilation (invasive or noninvasive) Predominant bacteria include Haemophilus influenza, Streptococcus pneumoniae, and Moraxella catarrhalis For uncomplicated patients (FEV₁>50%, no antibiotics in past 3 months, <3 exacerbations in last year): doxycycline, TMP-SMX, 2nd or 3rd generation cephalosporin, or extended-spectrum macrolide For complicated patients (cardiac disease, FEV₁<50%, antibiotics in past 3 months, ≥3 exacerbations in past year): amoxicillin + clavulanate or fluoroquinolone Treat for 7-10 days
Theophylline	Initial dosage of 400-600 mg/day (long-acting formulation), with target blood level of 5-12 mcg/mL
Oxygen therapy	By nasal cannulae, Venturi masks, non-rebreather masks Titrate to target pulse oxygen >90% or PaO2 >60-65 mmHg
Noninvasive positive pressure ventilation (NIPPV) in hospitalized patients	Such as bilevel positive airway pressure Improves respiratory acidosis, decreases respiratory rate, severity of breathlessness, and length of hospital stay Studies suggest that NIPPV may reduce mortality and the need for invasive ventilation Consider in moderate to severe exacerbations with acidemia (pH ≤7.35) and increased work of breathing (eg, RR >25); also in patients with PaCO2 above baseline (note that patients with COPD may have stable chronic elevation in PaCO2); compare acute value with baseline

Table 3: Potential ARV Interactions
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ARVs and inhaled corticosteroids Fluticasone: PIs: Caution: ↑ serum fluticasone levels; can cause systemic corticosteroid side effects, including Cushing syndrome Avoid (or limit) use with RTV, particularly in the LPV/r, ATV/r, and DRV/r combinations Even boosting doses (eg, 100 mg BID) of RTV may ↑ fluticasone C_max by 2,500% ATV: can ↑ fluticasone levels - use with caution It is unclear whether significant interactions occur between other inhaled steroids and PIs NRTIs, NNRTIs: no significant interactions expected ARVs and theophylline RTV: ↓ theophylline AUC IDV: small ↑ in theophylline AUC Monitor and adjust theophylline dosage as needed

References

Crothers K. Chronic obstructive pulmonary disease in patients who have HIV infection. Clin Chest Med. 2007 Sep;28(3):575-87, vi.
Crothers K, Butt A, Gibert C, et al. Increased COPD among HIV-positive compared to HIV-negative veterans. Chest. 2006 Nov;130(5):1326-33.
Rabe KF, Hurd S, Anzueto A, et al. Global strategy for the diagnosis, management, and prevention of chronic obstructive pulmonary disease: GOLD executive summary. Am J Respir Crit Care Med. 2007 Sep 15;176(6):532-55.
VA/DoD Clinical Practice Guideline Working Group. Management of Chronic Obstructive Pulmonary Disease. Washington, D.C.: Department of Veterans Affairs, Office of Quality and Performance; 2007.