A 45-year-old Asian-Indian man with a history notable for morbid obesity (body mass index [BMI] = 52) and back pain presents with worsening fatigue over the last few years. He is a non-smoker and takes oxycodone as needed for back pain. His initial exam is notable for the following: heart rate of 92 beats/minute, blood pressure of 156/92 mm Hg, respiratory rate of 18, and pulse oximetry of 91%. Breath sounds are diminished, and there is no accessory muscle use. His heart sounds are distant, with an unremarkable exam. He has neither jugular venous distention nor lower extremity edema.
Figure 1
His laboratory results are as follows: normal hematology, chemistry profile, thyroid-stimulating hormone. Pulmonary function tests are notable for reduced total lung capacity, functional reserve capacity and expiratory reserve volume. His arterial blood gas (ABG) on room air shows pH= 7.32; pCO2 = 50 mm Hg, pO2 = 61 mm Hg; bicarbonate = 31. He undergoes overnight polysomnography, which shows moderate sleep apnea with apnea-hypopnea index = 20 episodes/hour with several hypopneic episodes (Figure 1).
Which of the following options is NOT recommended to manage this patient?
Show Answer
The correct answer is: A) Initiate nocturnal oxygen supplementation.
This patient has obesity hypoventilation syndrome (OHS), which is defined as obese patients with awake alveolar hypoventilation PaCO2 >45 mm Hg, after excluding other causes such as pulmonary, endocrine, musculoskeletal, and neurological etiologies.1 An awake oxygen saturation <93% should raise suspicion for OHS.2 Over 50% patients with BMI >50 have OHS.3 Pulmonary function tests are often restrictive owing to morbid obesity. Obstructive sleep apnea (OSA) often co-exists in about 90% of patients with OHS.4
OHS management revolves around normalization of arterial carbon dioxide tension with prevention of oxygen desaturation during wakefulness and sleep. This is achieved by providing nocturnal positive pressure ventilation and weight loss measures. Supplemental nocturnal oxygen supplementation without positive pressure ventilation worsens acidemia and hypercapnia in OHS.5 Prescribing supplemental oxygen does not address underlying pathophysiology of altered chemo-responsiveness, impaired respiratory drive and upper airway obstruction. Therefore, oxygen supplementation should be avoided, unless in conjuction with noninvasive positive pressure ventilation.6 Hence, initiating nocturnal oxygen supplementation is not a recommended management strategy for this patient. Alcohol, opiates and barbiturates worsen sleep-related breathing disorders and should be avoided. Progestins and acetazolamide are reserved for patients who do not respond to NIPPV. Progestins improve awake hypercapnia and acetazolamide improves alveolar hypoventilation.7-9
Given the high rate of mortality, and progression to right heart failure, pulmonary hypertension, and angina with OHS, early recognition and initiation of treatment are vital.1
References
Bickelmann AG, Burwell CS, Robin ED, Whaley RD. Extreme obesity associated with alveolar hypoventilation; a Pickwickian syndrome. Am J Med 1956;21:811-8.
Piper AJ, Grunstein RR. Obesity hypoventilation syndrome: mechanisms and management. Am J Respir Crit Care Med 2011;183:292-8.
Nowbar S, Burkart KM, Gonzales R, et al. Obesity-associated hypoventilation in hospitalized patients: prevalence, effects, and outcome. Am J Med 2004;116:1-7.
Banerjee D, Yee BJ, Piper AJ, et al. Obesity hypoventilation syndrome: hypoxemia during continuous positive airway pressure. Chest 2007;131:1678-84.
Wijesinghe M, Perrin K, Healy B, et al. Pre-hospital oxygen therapy in acute exacerbations of chronic obstructive pulmonary disease. Intern Med J 2011;41:618-22.
Hollier CA, Maxwell LJ, Harmer AR, et al. Validity of arterialised-venous P CO2, pH and bicarbonate in obesity hypoventilation syndrome. Respir Physiol Neurobiol 2013;188:165-71.
Sutton FD Jr, Zwillich CW, Creagh CE, et al. Progesterone for outpatient treatment of Pickwickian syndrome. Ann Intern Med 1975;83:476-9.
Raurich JM, Rialp G, Ibáñez J, et al. Hypercapnic respiratory failure in obesity-hypoventilation syndrome: CO₂ response and acetazolamide treatment effects. Respir Care 2010;55:1442-8.
Powers MA. Obesity hypoventilation syndrome: bicarbonate concentration and acetazolamide. Respir Care 2010;55:1504-5.
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