Fatal exertional heat stroke in a patient receiving zuclopenthixol, quetiapine and benztropine.

Can J Clin Pharmacol

Critical Care Trauma Centre, Victoria Hospital, London Health Sciences Centre, Ontario.

Published: January 2008

Objective: To report a case of fatal exertional heat stroke associated with the use of zuclopenthixol, quetiapine and benztropine.

Case Summary: A 36-year-old male with a history of schizophrenia and bipolar disease was working as a roofer during the third day of a heat wave. His medications included zuclopenthixol, quetiapine, benztropine, carbamazepine and levothyroxine. He developed loss of consciousness late in the day and presented to hospital with a Glasgow Coma Scale 3 and a rectal temperature of 42.2 degrees C. He progressed to severe multiple organ dysfunction and asystole, and expired the following morning. Neuroleptic and anticholinergic agents have long been associated with heat alteration, but there are few reports involving the newer antipsychotic agents. Physicians and pharmacists should ensure that appropriate counseling is given to patients receiving these medications regarding early recognition of signs and symptoms and prompt treatment of heat related illness and heat stroke.

Download full-text PDF

Source

Publication Analysis

Top Keywords

heat stroke
12
zuclopenthixol quetiapine
12
fatal exertional
8
exertional heat
8
quetiapine benztropine
8
heat
6
stroke patient
4
patient receiving
4
receiving zuclopenthixol
4
benztropine objective
4

Similar Publications

Background: The roles of the Pink1/Parkin pathway and mitophagy in lung injury during heat stroke remain unclear. In this study, we investigated the role of Pink1/Parkin-mediated mitophagy in acute lung injury (ALI) in rats with exertional heat stroke (EHS).

Methods: Sixty Sprague Dawley rats were randomly divided into control (CON), control + Parkin overexpression (CON + Parkin), EHS, and EHS + Parkin overexpression (EHS + Parkin) groups.

View Article and Find Full Text PDF

The Role of Key Molecules of Pyroptosis in Liver Damage of Rats With Exertional Heat Stroke.

Gastroenterol Res Pract

January 2025

Department of Hepatobiliary Disease, 900th Hospital of Joint Logistics Support Force, Fuzhou General Clinical Medical College of Fujian Medical University, Fuzhou, Fujian, China.

This study is aimed at investigating the role of key molecular elements involved in pyroptosis in liver injury caused by exertional heat stroke (EHS). We established a model of EHS-induced liver injury in Sprague-Dawley rats, with a control group (receiving no treatment) for comparison and 12 rats in each group. Alanine transaminase (ALT) and aspartate transaminase (AST) levels in the blood were detected.

View Article and Find Full Text PDF

Heat stroke (HS) represents a life‑endangering condition that is due to an imbalance between heat generation and dissipation, owing to exposure to hot environments or strenuous exercise. HS is a medical condition that is gaining increased prevalence throughout the world due to a steady rise in temperature, and massive mortalities have been recorded among vulnerable populations. In 2024, extreme heat waves led to increased cases of HS and related fatalities globally, particularly in Karachi, Pakistan.

View Article and Find Full Text PDF

Heat Stroke Warning System Prototype for Athletes: A Pilot Study.

Sensors (Basel)

January 2025

Department of Sports Science and Sports Development, Faculty of Allied Health Sciences, Thammasat University, Pathumthani 12120, Thailand.

This research has developed a heat stroke warning system prototype for athletes utilizing the following sensors: DHT22, GY-906-BAA MLX90614, MAX30102. The device calculates the heat stroke risk and notifies users. The data is recorded, stored, displayed on a free-access website which graphs body temperature, ambient temperature, humidity, heart rate and heat stroke risk, and provides notifications for athletes engaged in outdoor activities.

View Article and Find Full Text PDF

In maximally Ca-activated demembranated fibres from the mammalian skeletal muscle, the depression of the force by lowering the temperature below the physiological level (~35 °C) is explained by the reduction of force in the myosin motor. Instead, cooling is reported to not affect the force per motor in Ca-activated cardiac trabeculae from the rat ventricle. Here, the mechanism of the cardiac performance depression by cooling is reinvestigated with fast sarcomere-level mechanics.

View Article and Find Full Text PDF

Want AI Summaries of new PubMed Abstracts delivered to your In-box?

Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!