![]() use in overdose will rapidly deplete hospital stores.~AUS$1,500 to treat a 70kg man for 4 hours.no proof of effectiveness (see evidence above).Practical issues with glucagon as an antidote Thus, there is a possibility that any benefit seen from using these glucagon preparations may have been due to the insulin that was also present.This was demonstrated in the study on HIE therapy in verapamil poisoning by Kline et al (1995).” Some vials of glucagon, when analyzed by this study group at Carolinas Medical Center, contained 100 units of insulin. “Nearly all studies examining glucagon in CCB toxicity were conducted prior to the availability of recombinant glucagon and used Eli Lilly’s standard glucagon preparations instead… The standard preparation of glucagon, made from mammalian pancreatic extract, contained insulin (also from pancreatic cells) until recombinant glucagon was available in 1998.First case report for propanolol in NEJM 1971, first for verapamil in Lancet 1982Īn interesting aside from ‘The Short Coat’ (also mentioned in Kerns, 2007):.multiple case reports/ anecdotes reporting clinical improvement following glucagon administration (causation not established).no human studies evaluating the efficacy of glucagon in BB or CCB overdose.all small studies, unblinded with variable doses of glucagon.CCB overdose: appeared to increase heart rate, cardiac output and reverse AV blocks in animal models (at least transiently), no change in mean arterial blood pressure (MAP).BB overdose: glucagon increased heart rate, no change in MAP (Kern et al, 1997).Glick et al and Luchessi both suggested glucagon as a beta blocker antidote in 1968.These effects were not blocked by propanolol catecholamine-like effects on animal organs first noted by Farah and Tuttle in 1960.We suggest that to attempt to undertake a randomised clinical trial of the use of glucagon in the compromised b blocker overdosed patient would be unethical. Nobody would suggest that naloxone should not be used for opiate overdose yet the evidence base for its use is as flimsy as that of glucagon in b blocker overdose. There is a wealth of clinical experience in support of administration of glucagon. Patients seldom take an overdose solely of a b blocker and the purist evidence base sought by Boyd is unlikely to be achievable. ![]() Glucagon activates adenyl cyclase and exerts an inotropic and chronotropic effect by a pathway that bypasses the b receptors.Įach of us has personal experience of the dramatic improvement in cardiovascular parameters that can occur following the administration of glucagon in this clinical situation. There is a sound theoretical basis for the use of glucagon in the cardiovascularly compromised patient who has taken a b blocker overdose. evidence basis is often lacking and one therefore needs to rely on a combination of practical experience, case reports and assessment of biological plausibility. RATIONALE FOR GLUCAGON USE AS AN ANTIDOTEįrom O’Connor et al (2003) in response to BestBET review by Boyd and Ghosh (2003): This page discusses glucagon as an an antidote, see Glucagon Therapy for an overview of glucagon pharmacology and other possible therapeutic uses high-dose insulin as an antidote or supportive measures) risk of distraction from the delivery of other therapies (e.g.commonly induces vomiting, with concomitant aspiration risk in the unprotected airway. ![]() In Australia, the toxicology community rarely advises the use of glucagon as an antidote, for these reasons: Glucagon has also been used in the setting of calcium channel blocker toxicity Glucagon is traditionally considered a first line antidote for beta-blocker overdose. ![]()
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