Bicarbonate Level for Early Diagnosis of Obesity Hypoventilation Syndrome: Still Defining Boundaries

To the Editor:

Given the current epidemic of obesity, it is likely that obesity hypoventilation syndrome (OHS), the form of chronic respiratory failure specifically attributable to obesity, is becoming the second leading cause of chronic respiratory insufficiency worldwide after COPD.¹ As opposed to the latter, no large public health campaign has yet been conducted to improve the diagnostic process of OHS, and the disease is largely underrecognized, usually discovered at an advanced stage when acute respiratory failure occurs.² In their prospective observational study, Bingol et al³ compare the clinical characteristics and polysomnographic parameters of OHS subjects with those of obese subjects with pure OSAS. Finding that bicarbonate level in plasma was higher and the nadir S_pO2 at night was lower in the OHS group compared with the obstructive obesity sleep apnea syndrome group, they concluded that these parameters can help in improving the diagnosis of OHS in specialized sleep medicine centers without the use of an arterial puncture to obtain arterial blood gas analysis.⁴ We think that, although attractive for specialists in sleep medicine, this study missed its target. What is interesting is that the present study confirms the opinion of a panel of international experts regarding the diagnostic value of bicarbonate level to assess OHS in obese snorers.⁵ However, the diagnosis of OHS is not a difficult issue reserved for specialists in sleep medicine. In this line, some key practical aspects need to be taken into account in this study. First, it is largely underdetected by general practitioners, and only a minority of the numerous obese patients at risk are referred early to a specialized center for a polygraphic sleep study. Second, even when admitted to the ICU for an episode of acute respiratory failure, up to 75% of the morbidly obese patients with OHS are misdiagnosed as having COPD or asthma.³ So the point is not to prevent a puncture of the radial artery to make the diagnosis less invasive in specialized sleep centers; this seems from a practical point of view crucial when some respiratory diseases like pulmonary hypertension require a pulmonary arterial catheter for assessment. Furthermore, these patients will continue to have many arterial punctures in the ICU and sometimes an endotracheal tube as a bonus if we do not improve the early diagnostic process and management of the disease. Manuel et al⁵ have recently described a new phenotype of obese subjects with high bicarbonate level (>27 mmol/L) and normal P_aCO2 (<45 mm Hg) that can be considered as developing an incipient form of OHS. Determining bicarbonate level in obese patients at risk may improve the early detection of OHS by general practitioners, who can then refer these patients to a pulmonologist early in the course of the disease. Finally, the therapeutic goals include facilitating the use of noninvasive ventilation and extending its practice and always treating OHS as one of the multiple disorders associated with obesity.

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