Case presentation
A 40-year-old Ethiopian man with no previous history of cardiac disease presented with a 7-days history of profuse watery diarrhea associated with vomiting and crampy abdominal pain. He denied a history of shortness of breath, orthopnea, paroxysmal nocturnal dyspnea, and palpitation. He had no family history of sudden cardiac death and cardiac illness.
On physical examination, the patient appeared acutely ill and his vital signs were as follows: blood pressure (BP)-70/50 mmHg, pulse rate (PR)-104 beat per minute which was feeble, respiratory rate-20, temperature- 35-degree Celsius, and saturation of 96% on room air. There was conjunctival pallor. There were signs of peripheral hypoperfusion such as cold extremities and delayed capillary refill. Cardiac and nervous system examinations were non-revealing.
Laboratory work-up revealed; serum potassium: 2.27mmol/L, sodium: 127mmol/L, chloride: 99.7mmol/L, serum creatinine: 2.33mg/dl, and blood urea nitrogen: 108.8 mg/dl. White cell count (WBC) level was 8800 and Hemoglobin (Hgb) was 10.2 g/dl. Liver enzymes were within the normal range and total and direct bilirubin level was 1.62 mg/dl and 1.05 mg/dl, respectively. There were numerous puss cells on microspic stool exam. Blood and stool culture were sent.
With this finding, a working diagnosis of septic shock of GI focus, acute kidney injury, severe hypokalemia, and hypovolemic hyponatremia was established.
The patient was admitted and managed as follows: intravenous (IV) epinephrine infusion was started after BP failed to respond to initial fluid resuscitation, IV ceftriaxone 1 gram BID and metronidazole 500 mg TID, IV potassium chloride infusion 40 meq in 400 ml of normal saline TID, and Oral rehydration solution 300 ml per loss.
Despite the above management, there was poor clinical response, and laboratory work-up 2 days after admission revealed a high WBC level (28, 080) and Hgb level of 6.2 g/dl. Serum potassium become 3.72 mmol/l. There was no growth on blood and stool culture. Subsequently, the initial antibiotics were discontinued and IV ciprofloxacin 400 mg BID and vancomycin 1g BID was initiated. He was transfused with 2 units of packed red blood cell and given IV hydrocortisone 100mg TID. IV potassium chloride infusion was discontinued. The remaining treatment was continued.
Within 16 hours of ciprofloxacin initiation, he developed sudden onset shortness of breath followed by loss of consciousness. On examination, he was unresponsive, pulse was not palpable, BP was unrecordable, and had no spontaneous breathing effort. The random blood sugar level was 195 mg/dl. ECG done at this time revealed a sustained polymorphic tachycardia with a feature of torsade de pointes (Figure 1).
With a diagnosis of sudden cardiac arrest due to polymorphic ventricular tachycardia induced by ciprofloxacin, cardiopulmonary resuscitation (CPR) was started immediately; epinephrine infusion at a rate of 0.3 microgram/kg/minute commenced and amiodarone 150 mg IV bolus was administered. After 5 cycles of CPR and defibrillation return of spontaneous circulation was achieved. However, 30 minutes later he developed additional episodes of recurrent torsade de pointes and cardiac arrest. CPR and defibrillation were attempted but it was not successful and the patient passed away. The possible cause of death was cardiac arrest secondary to torsade de pointes induced by ciprofloxacin.