Russell’s viper is one of the ‘big four’ most dangerous poisonous snakes in India. The farmer and snakes, especially the Russell's viper, coexist in tenuous relationship in the ecosystem. The clinical manifestations of viper bite are localized pain and swelling, coagulopathy, and renal impairment. The venom induced consumption coagulopathy (VICC) following Russell’s viper bite can result in a syndrome consistent with thrombotic microangiopathy (TMA), manifesting with thrombocytopenia, microangiopathic hemolytic anemia (MAHA) and acute kidney injury (AKI). TMA is rarely reported as a complication of Russell’s viper envenoming. Our patient, a farmer, was bitten by Russell’s viper and was brought to a nearby hospital within an hour. He was administered anti-snake venom (ASV) and supportive therapy. As his renal function declined, he was transferred to our hospital. He developed thrombocytopenia, and MAHA as evidenced by progressive anemia, schistocytes on peripheral smear, increased levels of lactate dehydrogenase (LDH), and AKI unresponsive to fluid management and diuretic administration. He was managed with sustained low-efficiency dialysis (SLED) and therapeutic plasma exchange (TPE). After three cycles of TPE and seven cycles of SLED over the next three weeks, the patient recovered completely and has been asymptomatic for more than six-months during follow up. The case is reported for rarity of TMA in the Russell’s viper envenomation, and the role of TPE in such cases.
Key words: Acute kidney injury, Plasmapheresis, Snakebite, Thrombotic microangiopathy, Venom induced consumptive coagulopathy
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