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Obesity Hypoventilation Syndrome: Simple to Diagnose, Potentially Deadly if Overlooked


Obesity hypoventilation syndrome (OHS) shares clinical symptoms with obstructive sleep apnea (OSA) such as daytime sleepiness, headaches, and memory problems. Both the symptoms and their sequelae, however, can be much more severe in OHS. Here, guidance on what to look for and how to manage OHS.

Obesity hypoventilation syndrome (OHS) is associated with some of the same clinical symptoms seen in obstructive sleep apnea (OSA), such as excessive daytime sleepiness, headaches, and memory problems. These symptoms and their clinical consequences, however, can be much more severe in OHS, and may include dyspnea, peripheral edema, daytime hypoxemia, and a higher incidence of pulmonary hypertension than is seen in OSA.1

OHS is relatively simple to diagnose, yet is underrecognized and often overlooked.
Criteria for the diagnosis are2:1. Obesity (BMI >30)
2. Hypoventilation (pCO2 >45 mm Hg)
3. The presence of sleep-disordered breathing
4. The exclusion of other causes of hypoventilation

Obesity, the first criterion, is common, and far more prevalent today than ever before. The incidence of OHS may be as high as 50% in individuals with a BMI of greater than 50 kg/m2.

Hypoventilation, the second diagnostic criterion, requires an arterial blood gas (ABG) determination to document a pCO2 of more than 45 mm Hg. Since arterial blood gases aren’t routinely measured and can be more painful than routine venous blood draws, a screening test would be helpful to help decide when to order an ABG. A serum bicarbonate level of more than 27 mmol/L has been proposed.2 This test is convenient because it is available with routine chemistries and is a fairly sensitive marker of elevated pCO2.

The third diagnostic criterion, sleep-disordered breathing, manifests as OSA in about 90% of patients. The remaining 10% of patients with OHS don’t have clear-cut OSA, but may demonstrate nocturnal hypoventilation.

The last component of the definition requires the exclusion of other causes of hypoventilation, including lung disease and neuromuscular weakness, which may elevate pCO2. To better evaluate and rule these out, consider a good neurologic history and exam and pulmonary function tests and a chest radiograph in patients with elevated pCO2.

Why does OHS affect some obese people, but not others?
Morbid obesity and OSA can lead to impaired respiratory mechanics and alterations in the respiratory drive. However, it isn’t clear why OHS develops in some but not others with the same level of obesity and OSA. The protein leptin, produced by adipose tissue, may be the answer. A mouse model in which mice lack leptin results in a syndrome with all the same features of OHS. Leptin replacement can reverse this syndrome in mice.

Of course, the situation is more complicated in humans. Patients with obesity and OHS have very high levels of the hormone leptin, which implies problems with leptin resistance rather than deficiency. In fact, leptin levels correlate with degree of hypoventilation and hypercapnia. This leptin resistance probably contributes to a blunted respiratory drive and hypercapnia in patients with OHS. Researchers continue to examine the relationship of leptin and OHS and hopefully this will lead to the development of new treatments.

Why and how should OHS be treated?
Nocturnal positive airway pressure is the mainstay of therapy for sleep-disordered breathing. While most people with OSA are treated with continuous positive airway pressure (CPAP) therapy, patients with OHS more often require bilevel positive airway pressure (BiPAP). Some patients also require supplemental oxygen therapy. The goal of nocturnal positive airway pressure (PAP) is to eliminate nocturnal hypoventilation and hypoxemia, decrease sleepiness, and improve daytime gas exchange. Most patients improve when PAP is closely monitored and titrated.

Some patients require tracheostomy to manage severe hypoxemia and hypercarbia. Tracheostomy can improve both of these measures; however, there still can be residual hypoventilation. This procedure is thus reserved for the most serious of cases.

The other main therapy for OHS is weight loss. While dietary and exercise measures are important, bariatric surgery is often needed. This surgery can help decrease daytime hypercapnia and improve daytime oxygenation; however, it is associated with increased morbidity and mortality, and sleep-disordered breathing may increase these risks. Therefore, a surgical approach has to be carefully considered and is optimally performed in a center with much experience.

The take-home message for primary care clinicians
It is imperative to recognize OHS: if untreated, the disorder leads to significantly increased mortality and morbidity. Early treatment may improve symptoms, improve quality of life, decrease hospitalizations, improve gas exchange, and save money in health care costs. Because of these benefits, consider asking obese patients about sleep-related symptoms to screen for OSA. In patients with OSA or morbid obesity, look at the serum bicarbonate level (and if it exceeds 27 mmol/L, obtain an ABG) to evaluate for hypoventilation.

1.  Khan M, Wood KL, Bhatt NY. Obesity hypoventilation syndrome. Sleep Med Clin. 2008;3:525-539.

2. Mokhlesi B, Tulaimat A. Recent advances in obesity hypoventilation syndrome. Chest. 2007;132:1322-1336.

3. Piper AJ, Grunstein RR. Obesity hypoventilation syndrome: mechanisms and management. Am J Respir Crit Care Med. 2011;183:292-298.



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