Obesity hypoventilation syndrome (OHS) has been defined as obesity (BMI >30) associated with hypoventilation (awake arterial carbon dioxide tension [Paco2] > 45) not attributed to other obvious causes, such as hypothyroidism, kyphoscoliosis, or severe COPD. The syndrome has been recognized for more than 50 years, but the significant morbidity and mortality associated with this syndrome has only recently been appreciated.
It is important to note that OHS is not obstructive sleep apnea (OSA). Though the majority of patients with OHS has OSA, the prognosis associated with the diagnosis of OHS appears to be significantly worse than that of OSA. Although comparative studies are lacking, reported mortality associated with OHS ranges between 3% at 18 months, in patients highly adherent to therapy, to 23% at 18 months, in patients not receiving appropriate therapy. This significant mortality associated with OHS far exceeds that associated with OSA.
Diagnosis of OHS requires a measurement of Paco2. At this time, direct measurement with arterial blood gas (ABG) testing is the accepted standard. Dr. Littleton and Dr. Mokhlesi compiled available epidemiologic data and report that patients with OHS tend to be severely obese (BMI equal to or greater than 40), hypersomnolent, and, if diagnosed with OSA, have an apneahypopnea index > 30 (Clin Chest Med 2009;30(3):467). The diagnosis of OHS should be sought after in this patient population; however, less obese patients and patients without OSA may also develop OHS.
The discomfort associated with ABG testing often causes physicians to seek alternate diagnostic options. Elevated serum bicarbonate levels and awake hypoxemia are strongly suggestive of OHS in the appropriate clinical setting but are not specific for the hypoventilation necessary to diagnose the disorder. Transcutaneous capnometry is a promising tool but, as of yet, has not been utilized in the diagnosis of OHS. Thus, given the lack of other reliable and readily available tests, ABG testing remains the gold standard for diagnosis and needs to be utilized.
Treatment of OHS is primarily aimed at treating the associated sleepdisordered breathing, usually present in the form of OSA.
Thus, continuous positive airway pressure (CPAP) is often part of the treatment plan. Since many patients with OHS require high CPAP pressures to address their OSA, CPAP intolerance becomes a significant concern. In that case, bilevel PAP therapy should be the next therapeutic consideration. Bilevel PAP may also be used to treat the hypoxemia that sometimes persists in these patients, despite adequate CPAP therapy for underlying OSA.
In patients with OHS without concomitant OSA, bilevel PAP may be used to address their sleep-related hypoventilation.