A 'double-whammy': obstructive sleep apnea and impaired arousal.

Patients with obstructive sleep apnea (OSA) depend on arousal mechanisms to restore airflow during sleep. However, loss of these arousal mechanisms can lead to life-threatening consequences. A 40-year-old man (body mass index, BMI, 23.1 kg/m2) had undergone a posterior fossa craniectomy and evacuation for a 2.1 × 3.4 × 2.5 cm posterior fossa astrocytoma (Fig. 1) that extended inferiorly to the C1 level, leaving himwith residual bulbar palsy and impaired upper airway muscle function. Several weeks after the surgery, he developed new onset snoring, associated with increasingly prolonged apneic and cyanotic episodes during sleep that culminated in respiratory arrest at home. He was emergently intubated. His initial arterial blood gas showed decompensated type 2 respiratory failure (pH 6.92, pCO2 136, HCO3 27.4, BE −9.0). His electrocardiogram, telemetry, cardiac enzymes, and electrolytes were normal. His respiratory failure was reversed rapidly after intubation andhewas extubatedwithin24 h.However, in the subsequentweeks, he had three further episodes of respiratory arrests during sleep that were rapidly reversed by endotracheal intubation, similar to the first episode. A polysomnograph (PSG) was performed (Fig. 2) as the respiratory arrests happened exclusively during sleep. The repeat brain imaging revealed a postoperative development of a hypodense collection (4.4 × 4.4 × 7.2 cm) with dilatation of the ventricles (Fig. 3), which likely affected the arousal mechanism. Given the permanent loss of upper airway reflexes, he underwent a tracheostomy instead of continuous positive airway pressure (CPAP) initiation and had no further episodes of respiratory arrests during sleep.