Abstract Introduction Cardiogenic syncope from transient asystole can resemble epileptic seizures in critically ill patients, often leading to misdiagnosis and unnecessary antiseizure therapy. Recognition is essential in postoperative transplant patients, where autonomic dysregulation and hemodynamic instability predispose to arrhythmia-related cerebral hypoperfusion. Stokes-Adams attacks are an uncommon but important cause of syncope, representing up to 8% of unexplained cases, typically occurring in patients with intermittent high-grade atrioventricular block or sinus node dysfunction.Similar physiology may transiently emerge in the post-transplant setting due to autonomic instability, critical illness, or medication effects. Case Presentation A 56-year-old man with Budd-Chiari syndrome and hepatocellular carcinoma underwent orthotopic liver transplantation. His postoperative course was complicated by hemorrhagic shock, multiple re-explorations, and respiratory failure requiring tracheostomy. During ICU recovery following extubation, he developed recurrent tonic episodes of unresponsiveness despite escalating antiseizure therapy. Each event lasted 20-30 seconds, with generalized stiffening, loss of consciousness, and rapid recovery with mild confusion. Continuous EEG-ECG monitoring revealed sinus arrest lasting up to 10.4 seconds without epileptiform activity, confirming a cardiogenic mechanism. Laboratory studies—including electrolytes, thyroid function, troponin, and QTc—were normal, and no AV-nodal-blocking or vagotonic drugs were used. Echocardiography showed preserved biventricular function. Electrophysiologic evaluation confirmed sinus node dysfunction as the cause of syncope. A permanent pacemaker was implanted, leading to complete resolution of episodes and full neurologic recovery. Discussion Cardiogenic syncope secondary to sinus arrest can present with convulsive movements due to transient cerebral hypoperfusion, mimicking seizures. These episodes represent a Stokes-Adams-type convulsive syncope—a modern manifestation of the classic syndrome in which sinus node dysfunction replaces complete heart block as the precipitating rhythm disturbance. The combination of stereotyped convulsive episodes, normal EEG, documented sinus arrest, and resolution after pacing is diagnostic of Stokes-Adams-type syncope rather than true epilepsy. Misdiagnosis can lead to prolonged antiseizure therapy, avoidable morbidity, and delayed pacing. In this patient without prior cardiac or neurologic disease, post-transplant autonomic dysfunction or immunosuppressant-related bradyarrhythmia likely contributed to sinus node suppression. Conclusion Sinus node dysfunction should be suspected in post-transplant or critically ill patients presenting with seizure-like episodes lacking EEG correlation. Integrated EEG-ECG monitoring and early multidisciplinary evaluation are essential for timely pacing and prevention of recurrent syncope or sudden cardiac death. This abstract is funded by: None
Lopez et al. (Fri,) studied this question.