A 30-year-old previously healthy man presented with one week of fatigue, malaise, and confusion, complaining of dull neck pain. In the ED he became acutely agitated and combative, eventually requiring sedation and intubation for altered mental status. Initial vitals were normal, with BP 130/85 and HR 66, but then patient developed a fever to 101.3 and subsequently exhibited supraventricular tachycardia on telemetry. ECG revealed sinus tachycardia, incomplete right bundle-branch block, and downsloping or coved-type ST-segment elevation in leads V1 and V2 with T-wave inversion, consistent with a type 1 Brugada pattern (Figure 1).
The patient was admitted to ICU and treated empirically for meningoencephalitis with ceftriaxone, vancomycin, and acyclovir. Head CT showed diffuse increased intracranial pressure and CSF analysis revealed a lymphocytic pleocytosis with normal glucose and protein levels. With antibiotics and antipyretics, fever resolved by hospital day 2. ECG was repeated and showed complete resolution of the Brugada pattern (Figure 2). Patient was continued on antibiotics and by hospital day 5 was extubated. Because there was no personal or family history of syncope or sudden cardiac death, he was managed conservatively. He remained afebrile, in normal sinus rhythm, and was discharged with cardiology follow-up.
The Brugada ECG pattern is characterized by right bundle-branch block and J-point elevation, with a slowly descending ST-segment and flat or negative T waves in leads V1, V2, and sometimes V3. These ECG changes may be induced by fever, sodium channel blockers, tricyclic antidepressants, cocaine, and electrolyte abnormalities. Brugada syndrome is diagnosed when these ECG changes are associated with history of syncope, inducible polymorphic ventricular tachycardia or ventricular fibrillation, or family history of sudden cardiac death.
About one-fourth of cases are caused by loss of function mutations in the cardiac sodium channel gene SCN5A. The mutated sodium channels result in temperature-dependent ionic changes that cause characteristic Brugada ECG patterns during fever.
Patients who acutely present with a Brugada-type ECG are at a considerably higher risk of sudden cardiac death and should be considered a medical emergency. In one series, 51% of patients with ECG changes were symptomatic, including 38% who developed cardiac arrest. Management with antipyretics or withdrawal of offending medication is warranted. While asymptomatic patients with negative family history can be managed conservatively, patients with Brugada syndrome and history of cardiac arrest or intermediate risk factors require an automatic implantable cardiac defibrillator.
Brugada syndrome is increasingly recognized as a cause of sudden cardiac death. Many patients are undiagnosed due to its dynamic and often hidden nature. The cardiac rhythm can deteriorate into fatal ventricular arrhythmias, making it important to recognize conditions that unmask it. In our case, a Brugada pattern emerged during a febrile episode.