Search

Abstract  Brugada syndrome (BS) is characterized by an electrocardiographic (ECG) pattern consisting of elevated ST segments in leads V1–V3 and a morphology similar to right bundle branch block. BS is associated with a risk of sudden cardiac death. A genetic defect (e.g., SCN5A) seems to be a requirement for occurrence of this syndrome. Together with factors like electrolyte disturbances, bradycardia or febrile illness, this defect leads to increased ventricular vulnerability resulting in ventricular arrhythmias. A 38-year-old so far healthy male suffered a second to third degree burn over 40% of his body surface. The patient was in an excellent physical condition before the trauma. Burns were treated with multiple split-thickness skin grafts. The patient was ventilated artificially on the ICU of the local casualty hospital. After several days, patient developed septic shock requiring low dose catecholamine infusion. During sepsis with fever up to 40°C even under calculated antibiosis, recidivating polymorphic ventricular tachycardias which degenerated to ventricular fibrillation in terms of an electrical storm had to be treated electrically several times a day. Therapy according to the guidelines of advanced life support was ineffective. Sinus rhythm ECG revealed a Brugada pattern and repolarization abnormalities suspicious for cardiac ischemia. Therefore BS and cardiac ischemia were taken into account as the trigger for the ventricular tachyarrhythmias. By reason of the inconspicuous anamnesis we assessed a low feasibility of a coronary heart disease but acute myocardial ischemia during sepsis could not be fully excluded. However, because of the large area of burned skin, transfer to the cath lab would have been a considerable effort for our patient. Fully aware of fever as a predisposing factor of electrocardiographic and arrhythmic manifestation of a BS, fever treatment was our first therapeutical effort. After effective fever treatment including physical cooling and intravenous paracetamol, Brugada pattern and tachyarrhythmias disappeared within a few hours. No further ventricular arrhythmias were registered during ongoing inflammation as long as body temperature was normal. Four months after these acute events, we invasively excluded coronary heart disease. A supplementary positive ajmaline test ensured the correct diagnosis of BS. No currently described mutation typical for BS was found in the genetic screening. No history of syncope, sudden cardiac death or lifethreatening arrhythmias was reported from blood relatives. According to current guidelines, a cardioverter-defibrillator (ICD) was implanted. At the 12-month follow-up, interrogation of the ICD revealed no further tachyarrhythmias. ECG has completely normalized. Sufficient documentation of ECG and body temperature is a necessity in the ICU, especially in a patient with a clinical picture of sepsis and ventricular tachycardia. Unfortunately, registration of ECGs of distinctively morbid patients showing Brugada pattern is often difficult although the ECG pattern is quite characteristic. If a BS is diagnosed, antiarrhythmic therapy diverges from the usual therapeutical approach, instead of adjustment of serum electrolytes and a medicamentous antiarrhythmic regime, normalization of body temperature and sepsis treatment is urgent and can be life-saving. [ABSTRACT FROM AUTHOR]