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Glucagon use in β blocker overdose
  1. Niall O’Connor1,
  2. Shaun Greene2,
  3. Paul Dargan3,
  4. Alison Jones3
  1. 1Our Lady of Lourdes Hospital, Drogheda, Ireland
  2. 2Emergency Department, Guys and St Thomas’ NHS Trust
  3. 3National Poisons Information Service, Guys and St Thomas’ NHS Trust
  1. Correspondence to:
 Niall O’Connor

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The Best Evidence Topic Reports series is intended to provide evidence-based answers to clinical questions. The recent best evidence topic report by Boyd1 concluded that there is not enough evidence to support the use of glucagon in β blocker overdose. However, clinical toxicology is an area in which the evidence basis is often lacking and one therefore needs to rely on a combination of practical experience, case reports and assessment of biological plausibility. There is a sound theoretical basis for the use of glucagon in the cardiovascularly compromised patient who has taken a β blocker overdose. Glucagon activates adenyl cyclase and exerts an inotropic and chronotropic effect2 by a pathway that bypasses the β receptors.

Each of us has personal experience of the dramatic improvement in cardiovascular parameters that can occur following the administration of glucagon in this clinical situation.

Patients seldom take an overdose solely of a β blocker and the purist evidence base sought by Boyd is unlikely to be achievable. There is a wealth of clinical experience in support of administration of glucagon. 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 β blocker overdose. We suggest that to attempt to undertake a randomised clinical trial of the use of glucagon in the compromised β blocker overdosed patient would be unethical.

By acting on the recommendation of this best evidence topic report, the unwary reader may deny patients a potentially life-saving treatment, which is universally recommended by toxicologists.2–4


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