alexa Glucagon in beta-blocker and calcium channel blocker overdoses: a systematic review.
Diabetes & Endocrinology

Diabetes & Endocrinology

Endocrinology & Metabolic Syndrome

Author(s): Bailey B

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Abstract BACKGROUND: Glucagon is usually accepted as part of the standard treatment in the management of patients with beta-blocker and calcium channel blocker overdoses. METHODS: A systematic review was done in order to evaluate the evidence supporting glucagon use in beta-blocker and calcium channel blocker overdoses. Studies evaluating glucagon for those uses were identified using the Cochrane Database of Systematic Reviews, the Cochrane Controlled Trials Register, MedLine, ToxLine, and EMBASE searches, as well as reviewing medical toxicology textbooks and references of identified articles. Only controlled studies of human or animal studies were included, the latter only when it was an in vivo model of acute poisoning. The quality of the included studies was assessed. RESULTS: The search found no study in humans but identified 30 in animals. In the five studies of animal models of beta-blocker overdose included, glucagon appeared to consistently increase the heart rate at least transiently but appeared to have no effect on mean arterial pressure even though it possibly increased cardiac output. Its effect on the survival rate in animal models of beta-blocker overdose was unclear. In the six studies of animal models of calcium channel blocker overdose included, glucagon appeared to increase heart rate and cardiac output and reverse second and third degree AV blocks, all at least transiently. There appeared to be no effect of glucagon on mean arterial pressure although it did increase in one model. Glucagon appeared to have no effect on survival rate. The included studies for both overdoses were not blinded, had limited numbers of animals, and some had inadequate glucagon regime. CONCLUSION: The evidence supporting the use of glucagon in the management of patients with beta-blocker and calcium channel blocker overdoses is limited to animal studies.
This article was published in J Toxicol Clin Toxicol and referenced in Endocrinology & Metabolic Syndrome

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