Are your COPD patients benefiting from best practices?
Spirometry makes the diagnosis and determines therapy choices, yet it is vastly underused.
Alpha-1 antitrypsin deficiency is an autosomal recessive disorder that causes COPD and liver cirrhosis.17 Alpha-1 antitrypsin protects the lungs from proteases released from inflammatory processes such as pneumonia and from inhaled toxic particles. When this glycoprotein is absent, proteases destroy airways and alveoli. Consider the diagnosis with younger patients. The disease is easily confused with asthma or smoking-induced COPD. It predominantly affects the lower lobes. Diagnosis is made by testing blood levels for the enzyme or genetic analysis.
Treatment is the same as for other causes of COPD. Although no evidence-based recommendations are available at this time, replacement of alpha-1 antitrypsin is indicated for certain patients. Smoking cessation is critical.
In our initial assessment of the patient, his FEV1 was <50%. There was no need to repeat spirometry, as the evidence does not support ongoing spirometric evaluation.2,3 Symptomatic patients with significant airflow obstruction (FEV1 <60% predicted) are the ones most likely to benefit from therapy (ACP grade: strong recommendation, moderate-quality evidence).2,3 Conversely, there is little evidence to justify treating asymptomatic patients who have airflow obstruction.
Monotherapy with long-acting inhaled beta-agonists, inhaled corticosteroids, or long-acting inhaled anticholinergics has been shown to reduce exacerbations and is preferable to short-acting, inhaled beta-agonists or short-acting anticholinergics (ACP grade: strong recommendation, high-quality evidence).2,3 At this time, evidence is insufficient to support the use of combined therapies—eg, inhaled steroids plus long-acting beta-agonists.2,3
For patients with a PaO2 ≤55 mm Hg, survival is improved by using supplemental oxygen therapy for 15 or more hours a day. (ACP grade: strong recommendation, moderate quality evidence).2,3
Finally, for symptomatic patients with an FEV1 <50%, pulmonary rehabilitation may reduce hospitalizations and increase exercise capacity (ACP grade: weak recommendation, moderate-quality evidence).2,3
For Mr. Jones, we prescribed 1 inhalation daily of the long-acting anticholinergic inhaler, tiotropium.
Smoking cessation critical
COPD progresses with aging and with continued smoking, and smoking cessation is critical to any management strategy.
CASE: Tiotropium, 1 inhalation daily, and a smoking cessation plan
We referred Mr. Jones to an outpatient smoking cessation program and gave him American Academy of Family Physicians patient education materials to review. His exercise tolerance improved with 1 inhalation daily of the long-acting anticholinergic inhaler, tiotropium, and he is making progress in his efforts to quit smoking.
Correspondence
Dean Gianakos, MD, Lynchburg Family Medicine Residency, 2097 Langhorne Road, Lynchburg, VA 24501; deangianakos@yahoo.com
