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.