Abstract
BACKGROUND: Torsades de pointes (TdP) is a polymorphic ventricular tachycardia related to congenital or acquired QT prolongation. Drug-induced electrolyte disturbances are an under-recognized cause, particularly in critically ill patients. CASE SUMMARY: A 37-year-old man underwent above-knee amputation after a road traffic accident complicated by wound infection. He received intravenous colistin for multidrug-resistant Pseudomonas aeruginosa. Three days later, he developed recurrent episodes of syncope and documented TdP. Laboratory tests revealed hypokalemia, hypocalcemia, hypomagnesemia, and metabolic alkalosis despite normal renal function-features suggestive of Bartter-like syndrome. Electrolyte repletion and repeated defibrillation were required, but arrhythmias persisted until colistin was withdrawn, after which the QT interval normalized and TdP ceased. DISCUSSION: Colistin-induced tubular dysfunction can mimic Bartter syndrome, leading to metabolic derangements and ventricular arrhythmias. Recognition of this rare adverse effect is essential, as drug discontinuation is curative. TAKE-HOME MESSAGES: Colistin may rarely cause Bartter-like syndrome with electrolyte disturbances (hypokalemia, hypocalcemia, hypomagnesemia, and metabolic alkalosis) leading to TdP. In patients with drug-refractory QT prolongation, medication review is crucial to rule out rare secondary causes.