Article Text

Download PDFPDF
Management of scorpion sting
  1. Bawaskar Hospital & Research Centre Mahad
  2. Raigad, Maharashtra India 402301

Statistics from

Request Permissions

If you wish to reuse any or all of this article please use the link below which will take you to the Copyright Clearance Center’s RightsLink service. You will be able to get a quick price and instant permission to reuse the content in many different ways.

Editor,—We read with great interest the haemodynamic pattern in patients with scorpion envenomation.1 We have studied this acute time sensitive medical emergency since 1976 and have tried various regimens including antiscorpion venom.2 Since the advent of prazosin (1983–84)—an α adrenergic blocker which acts as an antidote to venom—the mortality of scorpion sting victims is less than 1%.3

In the pre-prazosin era (1961–83) a fatality rate of 25–30% was reported from western India,4 acute pulmonary oedema causing death. We were therefore surprised by the 25% mortality reported by Karnad,1 and that two victims died on the third day of hospitalisation; we has similar findings in 1978–82—that is, before prazosin treatment.5

We have reported that the severity of scorpion sting depends on the victim’s age, the season, and the time between sting and administration of prazosin. The symptoms following the sting are hypertension, tachycardia, pulmonary oedema, and shock (autonomic storm).6 We believe that the transport of Karnad’s patients to the nearest major hospital contributed to their deaths5; seven of eight had acute pulmonary oedema owing to a delay in reaching a tertiary care hospital.1

Scorpion venom inhibits angiotensin converting enzyme (ACE), resulting in accumulation of bradykinin, which is implicated in the development of pulmonary oedema and acute reversible pancreatitis.7Captopril (an ACE inhibitor) has a similar action resulting in hypotension resistant to dopamine agonists.1 Bradykinin further enhances noradrenaline (norepinephrine) release by a presynaptic mechanism.8

Alpha receptor stimulation plays a major role in the pathogenesis of pulmonary oedema.9 It causes hyperkalaemia and hyperglycaemia (inhibition of insulin secretions). Angiotensin II stimulates α adrenergic receptors in the myocardium and hypoxia results from coronary spasm as well as accumulation of free fatty acids and free radicals injurious to myocardium leading …

View Full Text