(189) Brugada Syndrome Unmasked in Critically Ill Wounded Warrior

Introduction: Brugada syndrome (BrS) is a rare autosomal dominant cause of ST elevation (STE) due to a defective myocardial sodium channel, increasing the risk of malignant ventricular arrhythmias and death. BrS is defined on electrocardiogram (ECG) as >0.2mV coved-type STE in the right precordial leads with three distinctive patterns. BrS is a challenge in critically ill patients as it can be provoked by fever, increased autonomic tone, and medications [1]. This case highlights the diagnosis of this life-threatening condition in a polytrauma patient.

Description: A 23-year-old healthy male was admitted to the ICU with polytrauma following a blast injury requiring multiple operative interventions. On day 3 the patient was noted to be febrile to 102.1F while sedated on propofol. Telemetry and EKG reveled acute STE in leads V1-V3. High sensitivity troponins during one-hour intervals were 208.0, 211.4 and 213.8 ng/L. Bedside ultrasound (US) demonstrated no wall motion abnormalities and no right heart strain. STE’s dissipated within 36 hours of ceasing propofol and managing the patient’s temperature but returned during later fevers and Propofol. The patient later reported syncope during both exertion and rest and a distant relative with sudden cardiac death at the age of 40. He was ultimately referred to an electrophysiologist.

Discussion: The STE’s demonstrated on EKG in this case were characteristic of a Type I Brugada pattern. Acute coronary syndrome, coronary dissection, and fat embolism were considered less likely given the above troponins and US. BrS was considered most likely diagnosis given inciting factors, recent syncope episodes, and family history. Propofol has especially been noted to precipitate tachydysrhythmias [2]. Additionally, increased body temperature during heat illness can have similar effects as febrile illness leading to another possible explanation for his prior syncope during exertion [3,4]. Furthermore, febrile patients have shown a higher prevalence for BrS and fever is noted to increase risk of tachydysrhythmias leading to recommendations that these patients be managed aggressively with anti-pyrectics [1,5,6,7]. Attention to detail is critical in identifying and mitigating risks of this possibly fatal condition unmasked by common inciting factors such as fever.