Schmidt_1997_Crit.Care.Med_25_1925

OBJECTIVES To describe clinical, electrocardiographic, and blood chemistry findings in a case of high-dosage thioridazine self-poisoning, focusing on the cellular mechanisms of the cardiovascular toxicity. DESIGN: Case report and literature review. SETTING: Intensive care unit (ICU) of a district hospital in Germany. PATIENT: A 68-yr-old male patient admitted to the ICU for treatment of a severe thioridazine intoxication. INTERVENTIONS: Prevention of absorption (gastric lavage), mechanical ventilation, fluids, alkalinization, catecholamines, drugs (physostigmine, neostigmine), direct current cardioversion/defibrillation, and transient pacemaker (atrial stimulation). MEASUREMENTS AND MAIN RESULTS: Central nervous, cardiovascular, and gastrointestinal systems indicated the adverse side effects of thioridazine intoxication over a period of 9 days. During high toxic thioridazine plasma concentrations (6061 to 6480 ng/mL), a life-threatening crisis occurred due to malignant ventricular arrhythmias followed by bradycardia (e.g., sinus node arrest). The electrocardiogram showed delays in all parts of the conduction system of the heart, including prolonged repolarization for several days, which disappeared completely when thioridazine plasma concentrations were within the therapeutic range.
CONCLUSIONS: An individual therapeutic approach is needed in cases of thioridazine overdose. The primary aim is to stabilize the cardiac rhythm and the circulation.