Abstract Introduction Post-operative respiratory failure is a significant complication with a broad differential, including primary cardiopulmonary pathology, impaired respiratory mechanics, and other systemic causes. Here, we describe the broad etiologies explored for a patient with post-operative hypoxemic hyper-carbic respiratory failure and newly diagnosed sleep apnea. Case A teenaged male with severe eczema managed with dupilumab, shellfish allergy, obesity, hypogonadotropic hypogonadism and gynecomastia was admitted for hypoxemic hyper-carbic respiratory failure following elective gynecomastia correction surgery. He underwent general anesthesia via laryngeal mask airway (LMA) and received a total of 1.2 mg hydromorphone. Upon completion of the procedure, he was found to have decreased respiratory drive. When the LMA was removed, he developed severe hypoxemia (SpO2 70%). A venous blood gas revealed respiratory acidosis with pH 7.1 and pCO2 120. Supplemental oxygen and two doses of naloxone were administered, without improvement in gas exchange. Upon admission, exam was significant for obesity and bilateral chest drains; pulmonary exam was normal. Positive pressure was initiated; oxygenation and ventilation slowly improved with titration to BiPAP 20/9, back-up rate of 15 breaths/minute with 2 L supplemental oxygen. Polysomnography two days after admission revealed severe mixed sleep apnea with severe hypoventilation and hypoxemia. A repeat polysomnogram one week later showed resolution of central apneas, but persistent severe obstructive sleep apnea with hypoventilation and hypoxemia. Subsequent evaluation included brain magnetic resonance imaging, PHOX2B sequencing, and quantitative opiate metabolite urine testing which were all within normal limits. Otolaryngology and Endocrinology were consulted, and no etiologies of the patient’s new diagnoses were identified. One month following discharge, the patient returned to full activity without respiratory symptoms. He was tolerating BiPAP well. Pulmonary function testing revealed moderate restriction and exertional hypoxemia. Chest x-ray was obtained and within normal limits. A third polysomnogram two months later confirmed diagnosis of severe obstructive sleep apnea, hypoventilation, and hypoxemia; daytime hypercapnia was also observed. Pharmacogenetic genomic evaluation suggest the patient has impaired CYP3A5 metabolism and a UGT1A1 variant. Discussion This case highlights the diagnostic dilemma of acute hypoxemic and hyper-carbic respiratory failure as well as complex sleep apnea following anesthesia exposure. The differential included drug-induced respiratory depression, abnormal opioid metabolism, late onset central congenital hypoventilation syndrome, and obesity hypoventilation syndrome. With body mass index over 30, daytime hypercapnia, and sleep apnea, the patient meets criteria for obesity hypoventilation syndrome, though pharmacogenetic consultation is ongoing. This abstract is funded by: None
Swanson et al. (Fri,) studied this question.