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On the management of scorpion stings
  2. A B ALEX
  1. Department of Physiology
  2. Institute of Medical Sciences
  3. Banaras Hindu University
  4. Varanasi-221005, India
  5. email: desh{at}

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    Editor,—We read with great interest Karnad's paper,1 and also the responses in the correspondence columns2 concerning the same article. We have the following points to make based on our 12 years' experience of scorpion envenomation in experimental animals.

    According to Karnad's study,1 scorpion envenomed patients exhibited haemodynamic changes in terms of right or left ventricular failure. However, our results with experimental animals have shown two stages of envenomation—namely, a stage of immediate respiratory failure and a delayed stage of circulatory failure.3Respiratory failure occurred within two to three minutes in all 10 of the animals we studied. Nearly 40% of them died within five minutes; the remaining 60% recovered from the initial respiratory arrest and survived for a further two to three hours. In this 60%, however, respiration never returned to normal, and it was associated with ischaemia-like ECG patterns. At the same time, the mean arterial pressure gradually decreased until it dropped abruptly along with respiratory arrest. Eventually, ventricular fibrillation occurred resulting in the animal's death. The initial stage appears to be mediated by the neuronal components, as reported elsewhere.4 The circulatory failure may be due to increased kinins decreasing the blood pressure, or to irreversible shock syndrome associated with multiorgan failure, or myocardial ischaemia leading to ventricular failure. At this stage, we have observed increased secretions (lacrimation, salivation, and tracheal secretion), passing of urine and stool, etc. Our results indicate that respiratory failure is more critical in determining the mortality and time of death than circulatory failure.

    We are not able to comprehend the exact mechanisms by which captopril reverted the circulatory derangements and the improvement of scorpion stung patients.1 Rather, we anticipated a fall in blood pressure with captopril, as it increases endogenous kinin concentrations. We have showed that captopril mimicks the action of venom.4 However, Karnad1 and Bawaskar5 missed our reports on Buthus tamulus envenomation.4 6 7 Further, it has also been shown that kallikrein-kinin inhibitor (aprotinin) countered the scorpion toxicity.4 6 8 In addition, we have shown that scorpion venom increased the afferent vagal activity that can be blocked by aprotinin.6 This evidence indicates that aprotinin blocks the underlying pathology of scorpion envenomation, and is therefore better than other drugs for treating envenomation. Prasozin, an α1 adrenergic receptor blocker, can only block the increased adrenergic activity seen after envenomation at the postsynaptic sites, but it cannot reverse the underlying pathology generated by kinins or other mediators. Contrarily, there are reports of the successful use of insulin9 10 in patients stung by scorpions, and these reports do not find a place in the discussions of Karnad1 or Bawaskar.5 Therefore, we feel that insulin still has a place as a therapeutic agent in the treatment of scorpion toxicity unless disproved otherwise.

    Regarding pulmonary oedema associated with scorpion envenomation, we have recently demonstrated pulmonary oedema afterButhus tamulus envenomation (detected by physical and histological evidence).11 Further, pulmonary oedema was due to the involvement of kinins as pretreatment and aprotinin, which blocked the venom induced pulmonary oedema and other features of scorpion toxicity.11 The decreased ventilation seen at this stage of delayed circulatory failure further favours the formation of pulmonary oedema.

    In conclusion, captopril should be avoided in the treatment of scorpion toxicity until we understand the precise mechanisms behind its action. Aprotinin is a better choice as it blocks or counters the pathophysiological processes of scorpion envenomation and is also easily available in developing countries like India, where antivenom has yet to find a place in the market. The proven efficacy of insulin has to be considered with greater openness for the benefit of scorpion stung patients.


    This letter was shown to the author and Dr Bawaskar responds as follows:

    Our experience and rational approach to the management of life threatening, acute medical emergencies caused by scorpion envenomation is entirely different, and we do not agree with the use of aprotinin advocated by Deshpande and Alex. Aprotinin is not available in India; it is currently only licensed for cardiac operations that have a large risk of perioperative bleeding. In human scorpionism, which is entirely different from experimental, the clinical manifestations are related to many factors such as the weight of the victim, the size of the scorpion, the season, and the time lapsed between sting and administration of prazosin.1-1 By the time they are hospitalised, all patients exhibit some cardiovascular manifestations, many have full blown pulmonary oedema.1-2 We have been treating scorpion sting victims since 1976, and have treated more than 1500 severe cases. In our series, no victim had respiratory depression, arrest, or cardiac arrhythmia once prazosin had taken effect.1-3 Respiratory failure is a secondary phenomenon.1-4

    Scorpion venom stimulates neuronal sodium channels, resulting in autonomic storm. Both branches of the autonomic system are stimulated, resulting in vomiting, sweating, salivation, fasciculations, priapism in men, hypotension, hypertension, bradycardia or tachycardia, ventricular premature contractions, cool extremities, pulmonary oedema, and shock (fig 1-1).1-2

    Figure 1-1

    Pathophysiology of scorpion sting.

    It has been proved beyond doubt that pulmonary oedema, as a result of scorpion envenomation, is due to myocardial dysfunction.1-5Bradykinin induced secretory pulmonary oedema is secondary, and occurs as a result of the stimulation of kalikrenin due to tissue damage caused by anoxia and the accumulation of oxygen free radicals, if cardiogenic manifestations are not managed earlier with prazosin.1-6

    α Receptor stimulation plays an important role in the pathogenesis of scorpion stings resulting in an inotropic (hypertension) phase, which, if not treated, progresses to a hypokinetic (pulmonary oedema, hypotension, tachycardia, and shock) phase. The hypokinetic phase is due to the liberation of oxygen free radicals, fatty acids, and insulin deficiency.1-3 Prazosin enhances insulin secretion by blocking α receptors over β cells of the pancreas. Hyperkalaemia and hyperglycaemia exist in the victim due to autonomic storm. Prazosin increased endogenous insulin secretion thus acts like a glucose–insulin potassium drip and protects and prevents myocardium injury caused by liberated fatty acids and oxygen free radicals, and prevents lethal cardiac arrhythmia and sudden death (fig 1-2).1-7

    Figure 1-2

    Effects of prazosin (venom antidote).

    Atropine, which is similar to aprotinin, enhances cardiovascular morbidity and mortality by blocking acetyl choline action (vagolytic).1-8

    Recently, Abroug et al reported that scorpion antivenom is no better than placebo.1-9 Similarly, in our series, scorpion antivenom (available since 1997) did not prevent cardiovascular manifestations as a result ofMesobuthus tamulus sting.1-10Primary care doctors need full understanding of pathophysiology and a rational approach to this type of medical emergency to avoid high morbidity and mortality.

    Prazosin, a pharmacological antidote to venom, which reverses both inotropic and hypokinetic phases induced by severe scorpion stings, is simple, scientific, easily available, and does not cause anaphylaxis. Since its advent, mortality due to scorpion stings has been reduced to less than 1%. It should be the first line of treatment for severe scorpion stings.1-11


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