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.