1141 Long-Term Efficacy of Acetazolamide in Treating Central Sleep Apnea After Traumatic Brain Injury

Abstract Introduction Central sleep apnea (CSA) is characterized by recurrent cessation of breathing during sleep due to a failure of the physiological mechanisms responsible for the respiratory drive. Risk factors include congestive heart failure, high altitude, opioids, and traumatic brain injury (TBI), particularly brainstem injury. Current mainstay treatments are positive airway pressure (PAP) and oxygen therapy. Medications such as acetazolamide are presumed to enhance respiratory drive or modulate chemosensitivity. Given the high degree of nonadherence to PAP therapy, medications are an appealing alternative treatment for CSA. Report of case(s) A non-verbal 39-year-old man with spastic quadriplegia, intractable epilepsy, and static encephalopathy secondary to a TBI from a motor vehicle accident at age 10 was evaluated in the sleep clinic due to his caregiver’s concern for loud snoring, witnessed apneas, and daytime hypersomnolence. The caregiver denied the use of opioids, sleep aids or a history of parasomnias. Overnight home oximetry results demonstrated nocturnal hypoxemia with a SpO2 nadir of 71%. The initial in-laboratory polysomnography showed an apnea-hypopnea index (AHI) of 144.2 with a central apnea index (CAI) of 131.6 and no Cheyne-Stokes respiration. A subsequent in-laboratory PAP titration was difficult due to the patient’s inability to follow commands. He was then started on treatment with auto-titrating CPAP 5-10 cmH2O with a full facemask. However, the therapy was ineffective due to the patient chewing on several different masks, so he was transitioned to supplemental oxygen therapy. Due to the potential choking hazard, other options such as tracheostomy and medications were considered. Because a tracheostomy would only address the obstructive component of his sleep apnea, the patient was started on acetazolamide 250 mg per G-tube daily. Reevaluation at two months with a repeat in-laboratory polysomnography demonstrated complete resolution of sleep-related respiratory events with an AHI of 0.0 and the caregiver reported improvement in daytime hypersomnolence. Repeat polysomnography 9 months later showed continued efficacy of the therapy with an AHI of 1.7 and CAI of 0.0. Conclusion Current literature demonstrates improvement of CSA with short-term use of acetazolamide. This case highlights the potential long-term efficacy of acetazolamide for chronic management of CSA in patients with TBI. Support (if any)