Bilateral leg edema, pulmonary hypertension, and obstructive sleep apnea

Our data raise the question of a possible causal relationship between obstructive sleep apnea and leg edema. Most of the participants in our study have not used nasal continuous positive airway pressure (CPAP) for long. However, using nightly nasal CPAP, 4 edematous patients experienced reduced leg edema, and 3 have stopped using diuretic medication (Blankfield, unpublished data). This small subset of obstructive sleep apnea patients suggests that obstructive sleep apnea may be a cause of edema.

Making a diagnosis of obstructive sleep apnea does not necessarily mean that treatment is indicated. An abnormal apnea-hypopnea index without excessive daytime sleepiness does not warrant treatment.¹¹ The results of this study have unclear clinical relevance for patients with obstructive sleep apnea and edema who lack symptoms of daytime somnolence because no study has evaluated whether treating obstructive sleep apnea alters morbidity or mortality in these individuals. Accordingly, it may be prudent for clinicians to refer edematous patients for polysomnography only if they have symptoms of excessive daytime sleepiness, desire a remedy for their edema, use diuretic medication, or develop complications of edema formation such as cellulitis, stasis dermatitis, or venous stasis ulcers.

However, if obstructive sleep apnea contributes to or causes pulmonary hypertension or edema, then it may be advisable to treat patients who have these cardiovascular complications, regardless of the presence or absence of symptoms of sleep-disordered breathing. Previous research is inconclusive regarding a causal relationship between obstructive sleep apnea and pulmonary hypertension. Most of the literature favors the premise that obstructive sleep apnea is not a cause of pulmonary hypertension,^12-17 but some studies suggest otherwise.^18,19

If subsequent research demonstrates that obstructive sleep apnea causes either pulmonary hypertension or edema, then clinical trials will be necessary to document whether morbidity and mortality rates improve after appropriate treatment of the obstructive sleep apnea. This information will be essential to determine if treatment is warranted for obstructive sleep apnea patients who have pulmonary hypertension or edema, but who lack symptoms of excessive daytime sleepiness.

Acknowledgments

The authors appreciate data collection assistance by Louise Wiatrak, MA and Simone Powers, data entry assistance by Amy Tapolyai, MBA, and Gregory Zyzanski, and manuscript assistance by Kurt Stange, MD, PhD.