A 74-year-old man comes to the office due to increasing shortness of breath, especially on exertion. The patient also has cough with mucoid expectoration, especially in the morning. He has had no orthopnea, paroxysmal nocturnal dyspnea, or chest pain. The patient was hospitalized for community-acquired pneumonia 2 years ago. Other medical conditions include glaucoma, benign prostatic hyperplasia, and hypertension. He smoked a pack of cigarettes daily for 40 years and quit 2 years ago. Temperature is 37.2 C (98.9 F), blood pressure is 144/96 mm Hg, pulse is 82/min, and respirations are 16/min. Pulse oximetry shows an oxygen saturation of 89% on room air at rest. The patient's face appears ruddy and plethoric. The chest is barrel-shaped with an increased anteroposterior span. Breath sounds are diminished throughout, and the expiratory phase is prolonged. Heart sounds are distant but regular, and there are no murmurs or gallops. There is no peripheral edema or jugular venous distension. Laboratory results are as follows:
| Complete blood count | |
| Hematocrit | 58% |
| Hemoglobin | 18.2 g/dL |
| Platelets | 240,000/mm3 |
| Leukocytes | 7,500/mm3 |
| Serum chemistry | |
| Sodium | 140 mEq/L |
| Potassium | 4.2 mEq/L |
| Blood urea nitrogen | 18 mg/dL |
| Creatinine | 1.2 mg/dL |
Which of the following interventions will have the maximum impact on this patient's survival?
Management of stable chronic obstructive pulmonary disease | |
Nonpharmacologic |
|
Surgical |
|
Medications |
|
*Reduces mortality. **Reduces hospitalizations for patients with frequent exacerbations. ICS = inhaled corticosteroid; LABA = long-acting β2 agonist; LAMA = long-acting muscarinic antagonist; mAb = monoclonal antibody; PDE4 = phosphodiesterase 4. | |
This patient with a long smoking history has a chronic productive cough, prolonged expiratory phase, and evidence of hyperinflation (barrel chest with increased anteroposterior span). These features are highly suggestive of chronic obstructive pulmonary disease (COPD).
Long-term supplemental oxygen therapy (LTOT) has been shown to improve survival and quality of life in patients with COPD who have significant chronic hypoxemia. The criteria for initiating LTOT include:
Arterial oxygen tension (PaO2) ≤55 mm Hg or pulse oxygen saturation (SaO2) ≤88% on room air at rest, with normal exertion, or during sleep
PaO2 ≤59 mm Hg or SaO2 ≤89% in patients with cor pulmonale or secondary polycythemia (hematocrit >55%, as in this patient)
The mechanism of mortality reduction is unclear but appears to be related to alleviation of hypoxic pulmonary vasoconstriction, which prevents right ventricular failure resulting from pulmonary hypertension. Oxygen is titrated to maintain SaO2 between 90%-94%. The greatest impact on survival is seen in patients with more severe baseline hypoxemia, and maximum benefit achieved by those using oxygen for ≥15 hours a day.
Additional interventions with proven mortality benefit in COPD include smoking cessation, pulmonary rehabilitation, and vaccination against certain respiratory pathogens. Lung volume reduction surgery and noninvasive ventilation also improve survival in selected patients.
(Choice A) Vaccination against influenza and COVID-19 are strongly linked to decreased acute exacerbations of COPD (AECOPD) and reduced mortality; immunization against Streptococcus pneumoniae may also have similar benefits. However, Bordetella pertussis is a very infrequent cause of AECOPD or death. Similar to the general population, patients with COPD should be revaccinated for B pertussis (TdaP) every 10 years.
(Choices B, C, and D) Therapies that target the airways in COPD include inhaled bronchodilators and corticosteroids and mucus-clearing interventions (eg, chest physiotherapy, mucolytic agents). These treatments may improve symptoms and potentially reduce AECOPD but have no demonstrated impact on survival.
(Choice E) Periodic phlebotomy is sometimes indicated for profound secondary polycythemia if there is evidence of hyperviscosity syndrome (eg, blurred vision, confusion, heart failure), which generally develops with hematocrit >65%. This patient is ruddy/plethoric but has no symptoms of hyperviscosity; his moderate polycythemia is compensatory for chronic hypoxemia and should improve with LTOT.
(Choice F) Prophylactic macrolides (eg, azithromycin) can prevent AECOPD, and appear to do so through pleiotropic anti-inflammatory effects rather than antibacterial activity. However, no survival benefit has been demonstrated.
Educational objective:
Long-term oxygen therapy improves survival in patients with chronic obstructive pulmonary disease and significant chronic hypoxemia, especially if there is concurrent cor pulmonale or secondary polycythemia.