Obesity Hypoventilation Syndrome

摘要

Obesity Hypoventilation Syndrome (OHS) refers to a state of chronic daytime hypoventilation associated with obesity. Criteria for the diagnosis include persistently elevated PaCO2 > 45 mmHg, a body mass index > 30 kg/m2 and no other cause for hypoventilation. The exact pathophysiology has not been clearly defined, but the syndrome has been attributed to a combination of abnormal respiratory mechanics resulting in increased work of breathing, depressed central ventilatory control, and neurohormonal effects. Most patients with OHS have obstructive sleep apnea (OSA) and respond to CPAP therapy with significant improvement in daytime oxygenation and reduction in PaCO2. Those without OSA or who do not respond appropriately to CPAP, may require BIPAP therapy. Some OHS patients who initially require BIPAP can be switched to CPAP at a later time. Alternative methods of positive airway pressure treatment, such as average volume-assured pressure support or surgical interventions such as bariatic surgery or tracheostomy can be offered to patients who are refractory to CPAP or BIPAP. Introduction Obesity Hypoventilation Syndrome (OHS) refers to a state of chronic daytime hypoventilation associated with obesity that is usually extreme (body mass index (BMI) ≥ 40 kg/m2). The disorder has also been known as the Pickwickian Syndrome after Burwell’s 1956 case report (1) of an obese patient with hypercapnia, hypersomnolence and cor pulmonale noted the similarity to a character described by Charles Dickens in the Posthumous Papers of the Pickwick Club. The criteria for diagnosis of OHS include persistent elevation of arterial carbon dioxide tension (PaCO2) greater than 45 mmHg, a BMI that exceeds 30 kg/m2 (in some patient series, 35 kg/m2 ), and no other identifiable cause of hypoventilation (Table 1). The term simple obesity (SO) is used to describe obese individuals without OHS or OSA. For those with sleep-disordered breathing, there is a strong association between OHS and OSA (Figure 1). About 90% of patients with OHS who have polysomnography are found to have OSA (2). Conversely, the prevalence of OHS in patients with OSA has been in the 10-20% range in most series (3,4). Overlap syndrome, OSA in patients with chronic obstructive pulmonary disease, is another hypercapnic sleep disorder. Hypercapnia may develop at a lower BMI in patients with Overlap Syndrome, but many of these patients are overweight or meet obesity criteria. OHS and Overlap Syndrome are each considered to be distinct clinical conditions.The prevalence of OHS in the general population is not known, but has been estimated at approximately 0.5% for women and 1% for men (5). It seems to be a common, but under-recognized problem for persons with extreme obesity. Nowbar et al (6) found that 31% of a group of hospitalized patients with a BMI greater than 35 kg/m2, and 48% with a BMI greater than 50 kg/m2, had a PaCO2 greater than 43 mmHg and no other reason for hypercapnia. It has been suggested that the widespread use of pulse oximetry without consideration of the possibility of hypercapnia may contribute to the under-recognition of chronic hypoventilation in obese hospitalized patients (7). Clinical Features The clinical presentation of OHS is similar to that of OSA: disturbed sleep, snoring, excessive daytime sleepiness, morning headaches, depression and cognitive difficulties. But in addition, patients with OHS often develop sequelae of chronic hypoxia: polycythemia, pulmonary hypertension and cor pulmonale.Untreated, OHS has been associated with substantial morbidity and early mortality. Affected patients are at risk for acute or subacute decompensation that usually requires hospitalization, often in an intensive care unit. Acute hypercapnic respiratory failure in patients with OHS is characterized by severe hypoxia and uncompensated hypercapnia with cor pulmonale, and sometimes, massive edema and altered mental status. In the series of hospitalized patients reported by Nowba