Brugada Syndrome Manifesting Only During Fever in Patient with Septic Shock Secondary to Post-Obstructive Pneumonia

Abstract

BACKGROUND Brugada syndrome is a cardiac disorder associated with sudden death due to sodium channelopathy, most commonly the SCN5a mutation. There are 3 different patterns of electrocardiogram (ECG) changes characterized as type I, II, and III. ECG patterns consist of variations of incomplete RBBB and ST elevation in anterior precordial leads only. Treatment, if warranted, consists of implantable cardioverter-defibrillator. CASE REPORT A 63-year-old male presented with abdominal pain for 4 days that was persistent, and after further imaging, he was found to have hepatic metastases from a stage IV small cell carcinoma of the lung. The patient was started on chemotherapy with carboplatin and VP-16. The patient decompensated, developed septic shock secondary to post-obstructive pneumonia, and eventually required intubation. He became tachycardic, and an ECG was ordered to evaluate the heart rhythm. It was determined that the patient had Brugada wave/syndrome. The patient's condition deteriorated with worsening septic shock, suspected type II NSTEMI, and multiorgan failure. The patient was designated DNR ("do not resuscitate") and passed away. CONCLUSIONS This case represents how channelopathies can be provoked with fever. It is believed that this occurs due to denaturing of the ion channel leading to abnormal ST segment changes typically seen on ECG and an increased risk of developing lethal arrhythmias. Spontaneous presentation of nondrug-induced Brugada syndrome carries an increased risk of deadly arrhythmia, for which this patient would have required electrophysiological studies. Unfortunately, this patient was unable to undergo genetic testing or electrophysiological studies, as he passed away.

Figure 1.

This is the ECG obtained when the patient was febrile and tachycardic. The elevated J point, seen in the septal leads only and designated by the arrows, is characteristic of Brugada wave. Full interpretation of the ECG was as follows: rate was 132; rhythm was sinus; axis was ∼60; PR was normal; QRS was Brugada in septal leads, type 1; ST, elevation in V1–V3; QRS Brugada without LBBB or RBBB or incomplete block; hypertrophy was none; P wave was no atrial enlargement; QRS wave was narrow; T wave was blunted but no deflection; U wave was absent; J point was maximum at 4 mm. Type 1 Brugada syndrome, QTc was 445.

Figure 2.

This is the ECG obtained after the patient’s fever had resolved. As you can see, the Brugada wave is no longer present. Complete interpretation is as follows: rate was 99; rhythm was sinus; axis was ∼60 degrees; QRS was incomplete RBBB; PR was normal; QRS was not prolonged; hypertrophy was none; P wave was left atrial enlargement; QRS wave was no elongation; T wave was no abnormality; U wave was not present; J point was not elevated.