1217 Obesity Hypoventilation Syndrome in a 4-Year-Old Child

Abstract

Introduction four-year-old boy with morbid obesity was referred to pediatric sleep for nocturnal hypoxemia during inpatient admissions. He was found to have daytime hypoventilation, likely secondary to obesity hypoventilation syndrome (OHS). Report of Case During two inpatient admissions (wheezing, gastroenteritis), he desaturated to the 70s during sleep. At home, he received blow-by oxygen as he could not tolerate other interfaces. He underwent adenotonsillectomy. However, snoring, daytime sleepiness, hyperactivity and aggressive behavior persisted. Birth history was unremarkable, though he became progressively more obese over time. His father had obesity and obstructive sleep apnea. Physical exam was notable for elevated blood pressure of 122/68 mmHg (above 99th percentile), weight and height above 99th percentile, and BMI of 32 kg/m2 (z-score ~4.3). Despite extensive counseling, family declined polysomnography and labs. Awake end-tidal CO2s were elevated at 47 mmHg. Echocardiogram showed half-systemic PA pressures, right ventricular hypertrophy, and right atrial dilation. Family began desensitization protocol in preparation for future PAP therapy and polysomnography. Pediatric endocrinology consultation revealed low suspicion for hormonal/metabolic concerns. He entered a pediatric weight loss program. Conclusion This 4-year-old boy demonstrated daytime hypoventilation, systemic and pulmonary hypertension, likely consequences of his severe obesity. OHS is defined as BMI >95th percentile in children and awake hypercapnia (PaCO2 > 45 mmHg) in absence of alternative hypoventilation causes (e.g. pulmonary, cardiac, neurologic, pharmacologic). Presenting symptoms may include hypersomnolence, morning headaches, cognitive deficits, and signs of cor pulmonale1. The literature consists primarily of case reports; prevalence of pediatric OHS is unknown. Obesity afflicts 18.5% of children in the United States2. Given the severity of OHS sequelae, maintaining a high index of suspicion is crucial. Consider further work-up in patients with unexplained low oxygen saturations, signs of pulmonary hypertension (unexplained dyspnea on exertion, pedal edema), polycythemia, and elevated bicarbonate1.

Overview on Pediatric Obesity Hypoventilation Syndrome

“…Even while these are clearly present, sleep disturbed breathing and a weakened brain response to hypoxia and hypercapnia provide the strongest evidence for etiology. To explain the onset of this illness, Norman and associates suggested a mathematical model that incorporates sleep disturbed breathing, renal buffering, and central respiratory dive [7].…”

“…A formal respiratory evaluation, including arterial blood gases, should be performed as part of the preoperative evaluation in individuals with sleep disorders and individuals who are super obese (BMI > 50) considering this issue, according to available therapeutic guidelines for people experiencing bariatric surgery [33]. Despite these suggestions, the ideal clinical screening approach for identifying OHS in patient populations remains unknown [7]. Due to costs and a lack of facilities in many countries, simple respiratory observing and auto titrating pressure strategies are being used more and more for the diagnosing and management of OSAS.…”

“…Obese people who experience hypoventilation while sleeping but not awake hypercapnia may really be experiencing a "prodromal" form of OHS that eventually leads to persistent hypercapnia. This may resemble the clinical picture seen in patients with neuromuscular illness and sleep disordered breathing [7][8][9]. Ventilatory control in children with the obesity-hypoventilation syndrome has not been examined, but subnormal ventilatory response to hypercapnia is regarded as a component of the condition in adults.…”