• Tuberculosis and Respiratory Diseases
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• v.53 no.5
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• pp.561-568
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• 2002

Severe obesity can produce a marked impairment of respiratory function. The obesity hypoventilation or Pickwickian syndrome comprises of extreme obesity, alveolar hypoventilation, somnolence, plethora, pulmonary hypertension and right heart failure. It is sometimes associated with obstructive sleep apnea but can be distinguished from obstructive sleep apnea by the presence of awake $CO_2$ retention. Alt hough uncommon, it is important to recognize this syndrome because due to its potential life threatening nature and because can be reversed by appropriate treatment. Here, we report 3 cases of obesity hypoventilation syndrome.

• Sleep Medicine and Psychophysiology
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• v.29 no.1
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• pp.4-8
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• 2022

Obesity hypoventilation syndrome (OHS) is defined as the triad of obesity (body mass index, [BMI] ≥ 30 kg/m²), daytime hypercapnia (PaCO2 ≥ 45 mm Hg), and sleep breathing disorder, after excluding other causes for hypoventilation. As the obese population increases worldwide, the prevalence of OHS is also on the rise. Patients with OHS have poor quality of life, high risk of frequent hospitalization and increased cardiopulmonary mortality. However, most patients with OHS remain undiagnosed and untreated. The diagnosis typically occurs during the 5th and 6th decades of life and frequently first diagnosed in emergency rooms as a result of acute-on-chronic hypercapnic respiratory failure. Due to the high mortality rate in patients with OHS who do not receive treatment or have developed respiratory failure, early recognition and effective treatment is essential for improving outcomes. Positive airway pressure (PAP) therapy including continuous PAP (CPAP) or noninvasive ventilation (NIV) is the primary management option for OHS. Changes in lifestyle, rehabilitation program, weight loss and bariatric surgery should be also considered.

• Sleep Medicine and Psychophysiology
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• v.22 no.1
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• pp.30-34
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• 2015

Obesity hypoventilation syndrome (OHS) is characterized by severe obesity, excessive daytime sleepiness, hypoxemia and hypercapnea. Because OHS mimics pulmonary hypertension or cor pulmonale, clinicians should recognize and treat this syndrome appropriately. A 58-year-old female visited the emergency room because of dyspnea. She was obese and had kyphoscoliosis. The patient also experienced snoring, recurrent choking during sleep and daytime hypersomnolence which worsened after gaining weight in the recent year. The arterial blood gas analysis showed she experienced hypoxemia and hypercapnea not only during nighttime but also daytime. We suspected OHS and the patient underwent polysomnography to confirm whether obstructive sleep apnea was present. During the polysomnography test, sleep obstructive apnea was observed and apnea-hypopnea index was 9.2/hr. The patient was treated with bilevel positive airway pressure therapy (BiPAP). After BiPAP for 4 days, hypoxemia and hypercapnia were resolved and she is currently well without BiPAP. We report a case successfully treated with clinical improvement by presuming OHS early in a patient who had typical OHS symptoms, even while having other conditions which could cause hypoventilation.

• Journal of mucopolysaccharidosis and rare diseases
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• v.1 no.2
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• pp.35-39
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• 2015

Sleep problems occur frequently among patients with Prader-Willi syndrome (PWS). The most common problem is excessive daytime sleepiness (EDS) that are closely related to of sleep-related breathing disorder (SRBD) such as obstructive sleep apnea (OSA) and congenital hypoventilation syndrome. Obesity, craniofacial dysmorphism and muscular hypotonia of patients with PWS may increase the risk of SRBD. Sleep apneas can interrupt the continuity of sleep, and these disruptions result in a decrease in both the quality and quantity of sleep. In addition to SRBD, other sleep disorders have been reported, such as hypersomnia, a primary abnormality of the rapid eye movement (REM) sleep and narcolepsy traits at sleep onset REM sleep. Patients with PWS have intrinsic abnormalities of sleep-wake cycles due to hypothalamic dysfunction. The treatment of EDS and other sleep disorders in PWS are similar to standard treatments. Correction of sleep hygiene such as sufficient amount of sleep, maintenance of regular sleep-wake rhythm, and planned naps are important. After comprehensive evaluation of sleep disturbances, CPAP or surgery should be recommended for treatment of SRBD. Remaining EDS or narcolepsy-like syndrome are controlled by stimulant medication. Bright light therapy might be beneficial for disturbed circadian sleep-wake rhythm caused by hypothalamic dysfunction.