2025 FSA Podium and Poster Abstracts

Introduction/Background: Acute spinal cord injury (SCI) disrupts sensory, motor, and autonomic function below the level of injury, often resulting in significant cardiovascular instability. Disruption of autonomic pathways can impair sympathetic tone and blunt compensatory reflexes, predisposing patients to hemodynamic collapse. The Bezold-Jarisch reflex (BJR), a vagally mediated response to decreased ventricular filling, typically causes bradycardia, vasodilation, and hypotension. In SCI, impaired sympathetic compensation exacerbates this response, particularly in the setting of anesthesia-induced venodilation and hypovolemia. We present a case of a 40-year-old male with a T7 ballistic spinal cord injury and mandibular fracture who suffered catastrophic cardiovascular collapse following anesthetic induction, despite preoperative hemodynamic stability.

Methods: This case report highlights key anesthetic considerations in acute SCI. A literature review was conducted using PubMed and UpToDate with the search terms: acute spinal cord injury, neurogenic shock, autonomic dysfunction, Bezold-Jarisch reflex, and anesthesia. Relevant articles were reviewed to contextualize autonomic and hemodynamic considerations in SCI patients undergoing general anesthesia.

Results: Acute SCI predisposes patients to cardiovascular instability due to autonomic dysfunction. Reflex mechanisms—including unopposed vagal tone, the Bezold-Jarisch reflex, impaired baroreceptor response, and catecholamine depletion—when combined with anesthetic-induced vasodilation and hypovolemia, can result in severe circulatory collapse.

Discussion: The perioperative management of SCI patients requires careful consideration of autonomic dysfunction. While high thoracic and cervical injuries are classically associated with neurogenic shock, lower thoracic injuries can still result in significant autonomic instability. Induction of general anesthesia, which blunts sympathetic tone and reduces venous return, can unmask autonomic dysfunction, leading to circulatory collapse. Management strategies include aggressive volume resuscitation, vasopressor support, cautious titration of anesthetic agents, and invasive monitoring in high-risk patients. Given the risk of exaggerated vagal responses, anticholinergic agents should be readily available.

Conclusion: This case underscores the importance of anticipating autonomic dysregulation in SCI patients, even when they appear hemodynamically stable preoperatively. A proactive anesthetic approach with vigilant hemodynamic management is essential to mitigate the risk of perioperative cardiovascular collapse.