Abstract | November 8, 2021
A Case of Central Alveolar Hypoventilation Secondary to Traumatic Brain Injury that Improved After Treatment with Ondansetron
Learning Objectives
- Define central alveolar hypoventilation and its pathophysiology.
- Describe a possible mechanism by which Ondansetron improves central respiratory control.
Introduction: Approximately 1.5 million Americans sustain a traumatic brain injury (TBI) every year. TBIs comprise a large portion of surgical critical care patients, who often require mechanical ventilation. Central alveolar hypoventilation (CAH), a serious complication caused by disruption of neuromodulatory respiratory brainstem control and neural signal initiation and integration, may lead to difficulty weaning patients from ventilators and subsequent prolonged ventilation. Ondansetron, a selective 5-HT3 receptor antagonist, has been shown in mouse studies to prevent apnea by blocking inhibitory afferent signals from the vagus nerve to the ventral respiratory group. Here, we describe a patient with TBI who developed CAH and ultimately improved after treatment with Ondansetron.
Case presentation: A 26-year-old female with a past medical history of motor vehicle accident six months prior resulting in TBI and seizures, presented to our trauma bay following a subsequent motor vehicle accident involving a semi-truck. In the trauma bay, the patient exhibited agonal breathing with a GCS of 8. She was intubated for airway protection and underwent 3 surgeries to manage injuries sustained. During the recuperative phase, the patient developed ventilator dyssynchrony and difficulty weaning off mechanical ventilation.
Final/working diagnosis: The patient was diagnosed with CAH secondary to TBI and subsequent prolonged ventilator course and difficulty weaning from mechanical ventilation.
Management/Outcome/Follow-up: On hospital day 13, the patient was started on 4 mg of Ondansetron intravenously every 6 hours for ventilator dyssynchrony. After 3 days of treatment with Ondansetron, the patient was weaned from the ventilator and transitioned to Aerotrach without respiratory distress. Ondansetron was discontinued on discharge, and on follow-up 120 days after discharge, the patient no longer required tracheostomy or any other form of ventilatory support. Our case shows the promise of Ondansetron in preventing a prolonged ventilatory course in CAH caused by TBI. Further research is required to assess the benefit of treatment with Ondansetron in such cases.