A 65-year-old, obese male with a 40 pack-year tobacco history as well as hypertension requiring four drugs for control presented with a postbronchodilator FEV1 of 45% predicted. His resting oxygen saturation by pulse oximeter measured 92%. He used his short-acting bronchodilator up to five times per day for exertional dyspnea. He complained of daytime fatigue and sleepiness as well as morning headaches and attributed this to his age and COPD. Regarding his history, the patient had a fragmented sleep pattern and reported frequent napping. On examination he had pretibial edema. A polysomnogram was performed and showed evidence of OSA with significant desaturations as depicted in Figure 5. A CPAP titration was performed, but hypoxemia independent of apnea or hypopnea events persisted, resulting in the addition of supplemental oxygen. On follow-up consultation, he reported improvement in his fatigue, daytime sleepiness, and improved walking distance without dyspnea.
This case highlights the coexistence of OSA in a patient with COPD. The patient has poor symptom control of COPD but also has symptoms consistent with OSA, including daytime somnolence and morning headaches. Fatigue and sleepiness should not be attributed to COPD. Given the extent of symptoms and relative hypoxia by daytime pulse oximetry, a polysomnogram should be performed in similar patients to evaluate for OSA. It is important to note that when evaluating a patient with potential overlap syndrome, intermittent nocturnal oxygen desaturations may resolve with treatment of the underlying sleep apnea. Priority should be given to the treatment of OSA before instituting supplemental oxygen. When appropriate, patients with potential overlap syndrome who are already using nocturnal supplemental oxygen should initially have their polysomnogram and subsequent PAP titration study performed without supplemental oxygen. If, as in this case, PAP therapy alone does not correct the patient's nocturnal hypoxemia, the additional use of supplemental oxygen may be required to support their oxygen needs.
A second clinical case involved a 55-year-old postmenopausal female who was an active smoker with moderate COPD. She had undergone attempts at smoking cessation. She had weight gain of 18 pounds over 8 months, and she complained of new onset of daytime sleepiness and increased caffeine use. Her bed partner reported that she had frequent snoring. A polysomnogram was performed with evidence of moderate OSA. She was initiated on CPAP therapy with improvement in symptoms.
This case highlights the potential of OSA to develop in COPD patients with significant weight gain. In addition, as in this case, it is important to recognize risk factors for OSA beyond obesity such as in a female patient who has completed menopause. Symptoms may be misconstrued as COPD, but history-taking may reveal symptoms typically associated with sleep apnea including snoring, gasping efforts during sleep, fragmented sleep patterns, and daytime sleepiness. Often patients will mask symptoms of excessive daytime sleepiness with gradually increased caffeine consumption. This history can be as important as a complaint of daytime sleepiness. A polysomnogram is warranted to diagnose OSA given the change in symptoms.