Barefoot children and farm laborers are at special risk of being stung. Scorpions often live in places sheltered from heat – for example, under tiled roofs and in piles of dry husks. These husks are frequently handled by farmers between October and November, which accounts for the high incidence of stings during this period. There is another peak of scorpion–stings between March and June.
Dr. Bawaskar, while in charge of a primary health center in birwadi, in colaba district of Maharashtra State, studied this problem between August, 1976, and December, 1984. He studied 214 patients (age range 8 to 25 years) with scorpion–sting who presented with pain at the site of sting, sweating, tachycardia, irregular pulse, breathlessness, dilated pupils, occasional vomiting and priapism. Over half the patients, notably the young, had pulmonary edema and five patients died despite rigorous treatment with frusemide, digitalis and atropine.
Pulmonary edema developed in 24/41 patients ant time between 30 minutes to 29 hours of the sting (mean: 11 hours). Pulmonary edema resulted from extensive myocarditis and gross left ventricular failure. Dr. Bawaskar studied the available literature on scorpion–stings.
Scorpion venom is a potent stimulator of the autonomic nervous system. An initial transient cholinergic stimulation (clinically manifested as vomiting, sweating, salivation and bradycardia) is followed by sustained adrenergic hyperactivity (clinically manifested by hypertension, tachycardia, arrhythmia and ECG changes: Left anterior hemiblock, hypoxic ST–T changes and prolonged QRS and QT).
Studies have shown that myocardial damage following scorpion–sting results from calcium ion influx into the heart muscle cells, hence a calcium channel blocker such as nifedipine was a rational choice of treatment. Dr. Bawaskar found sublingual nifedipine very suitable, particularly in severely anxious and agitated children with poor peripheral circulation.
A report by Gueron and Yaron from Israel in 1970 had shown that scorpion venom is a potent sympathetic stimulator resulting in high serum catecholamine levels. Prazosin produces decrease in preload and afterload by alpha receptor blockade. By introducing rational therapy with nifedipine and prazosin (and also by discontinuing the use of atropine and digoxin), Dr. Bawaskar has achieved significant success there has not been a single death in his region due to scorpion–sting. For massive life threatening pulmonary edema, he has used a sodium nitroprusside drip.
Working in a rural setting, Dr. Bawaskar had to rely entirely on clinical observations for monitoring his patients and their response to therapy. This he did by observing and recording blood pressure every 30 minutes, heart rate, auscultation of the heart for systolic murmur and S3 gallop, auscultation of lung bases for evidence of rales indicating pulmonary edema, warmth of the extremities and ECG changes, and chest radiographs to document pulmonary edema and its clearance after therapy. Thus he could document that pulmonary edema took three to six hours to disappear and at the end of 72 hours radiography still showed cardiomegaly. The action of prazosin started to appear at the end of the first hour, peaked after three hours and persisted for six hours, as shown by reduction in heart rate and blood pressure, disappearance of systolic murmur and basal rates and warming of the extremities. Priapism took four to six hours to disappear after three hours and persisted for six hours, as shown by reduction in heart rate and blood pressure, disappearance of systolic murmur an basal rates and warming of the extremities. Priapism took four to six hours to disappear after an oral dose of prazosin.
Antivenom therapy has been advocated as the only specific treatment for scorpion–sting, on the analogy of antivenin for snake–bite. Dr. Bawaskar believes this approach to be incorrect. Although in an experimental setting antivenom given before injection of scorpion toxin almost totally prevents the cardiac effects in rats, in the clinical situation this cannot be reproduced. Using radio–labeled antivenom, the peak tissue concentrations of venom are reached in 37 minutes. When patients are admitted with cardiac manifestations (which means the toxic venom has already released pharmacologically active substances) it seems more rational to use a pharmacological approach with specific effector blockers, which is more rapid than serotherapy given after symptoms have set in. Anti–scorpion serum is not available.
Although ethical considerations do not allow Dr. Bawaskar to undertake controlled clinical trials in his rural setting, his own experience between 1976 and 1984 (6 out of 11 patients died of pulmonary edema with digoxin and diuretics and steroids) and between 1986 and 1991 (no death among 79 victims with cardiac manifestations) using sublingual nifedipine and oral prazosin, is a significant original contribution to clinical research with practical utility.
The toxicity of the sting depends upon the dose of venom, size, age, state of nutrition of the scorpion as well as climatic conditions. Dr. Bawaskar made some interesting clinical observations on a daughter and mother, and a brother and sister coming simultaneously with a sting by the same scorpion. The first–bitten had systemic symptoms and signs (vomiting, sweating, hypertension, cold limbs) while the second had only local pain at the site of sting but had no systemic manifestations. Presumably, the scorpion had virtually evacuated its telson in the first victim, with very little toxin left for the second victim.