Discussion
Fluoroquinolones are commonly used antimicrobial agents because of their wide antimicrobial efficacy in common respiratory, gastrointestinal, and genitourinary infections. However, cardiac toxicity can occur as an unintended consequence of therapy with quinolone. Case reports and other studies have reported several quinolone-induced arrhythmia-related cardiac effects, including QT interval prolongation, TdP, ventricular tachycardia, ventricular fibrillation, and SCD [4, 8-9]. Fluoroquinolones prolong the QT interval by blocking the cardiac voltage-gated rapid potassium channels (IKr). This adverse effect can be potentiated by the presence of predisposing factors such as female gender, structural heart disease, concomitant use of QT-interval-prolonging medication, reduced drug elimination (due to drug interaction, renal, or hepatic dysfunction), electrolyte abnormalities (hypokalemia, hypomagnesemia), bradycardia, prolonged QTc interval before therapy, and congenital LQTS.
The risk of QT prolongation and TdP varies among quinolones; moxifloxacin appears to have the greatest risk followed by levofloxacin and ofloxacin. Ciprofloxacin has been associated with the lowest risk for QT prolongation and torsade de pointes [4-6, 9-10]. Even though ciprofloxacin is considered to be the safest quinolone in terms of TdP, there are several case reports on ciprofloxacin-induced TdP [11-15]. This case report suggests that ciprofloxacin should be used with great caution in patients who are at risk for QT prolongation and QT-mediated arrhythmias.
The diagnosis of quinolone-induced TdP requires the presence of a clear temporal relationship between exposure and onset of the ECG features. Typical ECG features of TdP include an antecedent prolonged QT interval, particularly in the last heartbeat preceding the onset of the arrhythmia. Additional typical features include a ventricular rate of 160 to 250 beats per minute, irregular RR intervals, and cycling of the QRS axis through 180 degrees every 5 to 20 beats. In our case, TdP developed within 16 hours of ciprofloxacin administration and the patient had predisposing factors such as hypokalemia and acute kidney injury.
Prevention of ciprofloxacin-induced QT-interval prolongation and TdP in a high-risk patient includes, whenever possible alternative antibiotics that don’t prolong QT interval should be used, serum potassium and magnesium should be maintained in the normal range, and monitoring the QT-interval before and at least every 8 to 12 hours after initiating the drug [16].
The management of quinolone-induced QT-interval prolongation includes discontinuation of the offending drug and aggressive correction of any metabolic and electrolyte abnormalities. Prompt defibrillation in hemodynamically unstable and in those with syncope due to torsade de pointes. In conscious patients’ treatment with intravenous magnesium infusion, beta-blockers, and temporary transvenous pacing are indicated [17].
The major limitations in the management of this case were; initiation of full dose of ciprofloxacin in the presence of acute renal failure and severe hypokalemia, inadequate monitoring of QT interval after starting culprit drug, failure to withdraw ciprofloxacin, and inappropriate treatment of TdP namely failure to administer IV magnesium sulfate and inappropriate administration of IV amiodarone. Since there is no baseline ECG before administration of ciprofloxacin, congenital LQTS can’t be ruled out completely.