Life-threatening dysrhythmias in severe thioridazine poisoning treated with physostigmine and transient atrial pacing.

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.