Discussion

This was an observational study rather than a strict scientific trial. Because mortality is so high in patients with cardiological symptoms and treatment reduced it to 1.6% we believe that it would be unethical to without treatment.

Scorpion stings occur in tropical and subtropical regions and are common in rural India. The hemodynamic and myocardial effects of scorpion venom have been reported in experimental animals as well as in humans. The red scorpion (mesobuthus tamulus) was responsible for the stings reported autonomic nervous system causing a sudden outpouring of endogenous catecholamines into the circulation. The venom initially causes transient cholinergic stimulation (vomiting, profuse sweating, bradycardia, priapism, hypersalivation, and hypotension) which is followed by sustained adrenergic hyperactivity (hypertension, tachycardia, and myocardial failure). The adrenergic phase but not the cholinergic phase is a dose dependent phenomenon.

On the basis of clinical manifestations and known pathophysiology if scorpion envenomation we devised an approach to management that did not use antivenin. We treated patients in our facility with what was available to us. We believe that transporting these patients to the nearest big hospital can contribute to their death. Nifedipine, a calcium channel blocker, is useful for the immediate treatment of hypertension and helps to reduce the myocardial contractility enhanced by autonomic stimulation. In addition nifedipine may protect the heart muscle from the toxic effects of scorpion venom. Experimental studies showed that myocardial damage after a scorpion envenomation is caused by an influx of calcium ions into the heart muscle cells. Sudden rebound of hypertension in some patients an be explained by recurrent envenoming. Prazosin, a post synaptic x blocker, is known to reduce preload and left ventricular impedance. Its hypotensive action may also be due to inhibition of adrenaline. Plasma renin activity was not significantly increased in response to blood pressure lowering action of prazosin.

Nifedipine alone does not prevent myocardial damage unless the peripheral action of venom is blocked by the sympathetic x blocker, prazosin. Although blood pressure was controlled by nifedipine , subsequent myocardial failure responded only after the addition of oral pazosin. Most of the electrocardiographic abnormalities in human scorpion sting, including ST–T changes, closely resemble the electrocardiograms in patients with congenital QT interval syndrome. The outpouring of catecholamines in response to the scorpion sting is probably a major factor in the pathogenesis of ST–T changes. The possibility of a direct effect of the toxin on the myocardium, however, cannot be excluded.

In dogs various metabolic disturbances caused by scorpion venom were reversed by the specific scorpion antivenin essentially through the release of insulin. Prazosin inhibits the suppression of insulin secretion caused by scorpion envenoming. As a consequence of this action it helps to reverse the metabolic changes and arrest myocardial damage caused by liberated free fatty acids and phospholipids. We have found that the combination of nifedipine and prazosin is a pharmacological antidote to the action of venom. This treatment is quick acting, easily available, relatively cheap and does not risk anaphylaxis.

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