Can scorpions be useful?

Abstract

At 1000 h on June 14, 2005, a 10-year-old boy, breathless and cold, was brought to our hospital by his father. The father reported that at 2000 h, the boy had been stung by a red scorpion—causing excru ciating pain, which decreased in the following hour, as an ice pack was applied to the site. However, the boy then vomited twice, and started to sweat profusely. The father took the boy to the village tantrik (traditional healer), who recited a healing spell. By 0230 h, the boy’s hands and feet were cold, and he felt short of breath. He was unable to sleep. The father car ried his son 2 km to the nearest road, and then travelled the remaining 46 km to hospital by hired autorickshaw. On arrival, the boy was propped up, and given supplementary oxygen. The pulse was weak; the electrocardiogram (ECG) showed a heart rate of 188 beats per min. The systolic blood pressure and respiratory rate were 70 mm Hg and 60 breaths per min respectively. A loud summation gallop was heard over the praecordium; bubbling, low-pitched crackles were heard all over the chest. Priapism was noted. The boy was given furosemide 20 mg intravenously, a slow bolus of aminophylline 50 mg, and prazosin 250 μg orally. He was also given a 12-h infusion of dobutamine, at 10 μg/kg per min. The pulmonary oedema resolved within 12 h, and the tachycardia within 36 h. Blood tests showed normal electro lyte concentrations. However, between 36 h and 60 h after admission, although the patient had no fever, the ECG showed a pattern diagnostic of Brugada syndrome— with raised, upwardly convex ST segments descending into inverted T waves in leads V1–V3 (fi gure). This pattern had resolved by 72 h; the patient was discharged on June 18, 2005, with a systolic blood pressure of 110 mm Hg, and a heart rate of 75 beats per min. Although the patient was treated free of charge, and the family was off ered a day’s earnings and free transport to attend, they declined follow-up. The patient was visited at home in October, 2007, and was well, with a normal ECG. Brugada syndrome is an inherited disorder characterised by ST-segment elevation in the right praecordial leads, and associated with sudden cardiac death. 10–30% of cases are caused by mutations in the SCN5A gene, on chromosome 3, which codes for the α-subunit of the cardiac voltage-dependent sodium channel. Mutations usually reduce the sodium current. Brugada syndrome can sometimes be unmasked by the administration of a sodium-channel blocker, such as ajmaline. In this case, Brugada syndrome may have been serendipitously unmasked by scorpion toxin. Toxin from scorpions such as Mesobuthus tamulus (the Indian red scorpion) activates sodium channels and inhibits potassium channels— leading to intense and persistent depolarisation of autonomic nerves. The resulting autonomic storm is characterised by transient parasympathetic (vomiting, sweating, priapism, hypotension, cardiac dysrhythmias) and prolonged sympathetic (hypertension, tachycardia, cold hands and feet, pulmonary oedema, shock) features. Scorpion envenoming is therefore treated with prazosin, a postsynaptic α blocker—even though at present an intravenous preparation of this drug is not available. I postulate that in this patient, the initial surge in sodium current depleted intracellular sodium, and caused Brugada syndrome to manifest later—although ECG patterns diagnostic of Brugada syndrome can appear intermittently, even without a drug challenge. Perhaps drugs derived from scorpion toxin could increase the sodium current, and treat Brugada syndrome.