CASE REPORT Thrombotic microangiopathy in Russel’s viper envenomation S.P. Reddy 1 , S.A. Phadnis 1 , P. Kumari 1 , N. Sharma 1 , J. Sethi 2 , A.K. Pannu 1 and N. Sharma 1 From the 1 Department of Internal Medicine, Postgraduate Institute of Medical Education and Research, Chandigarh, India and 2 Department of Nephrology, Postgraduate Institute of Medical Education and Research, Chandigarh, India Address correspondence to Dr A.K. Pannu, Department of Internal Medicine, Postgraduate Institute of Medical Education and Research, Room no. 26, 4th floor, F Block, Nehru Hospital, Sector-12, Chandigarh, PIN- 160012, India. email: gawaribacchi@gmail.com Case description A 55-year-old woman, who lived in a rural area of Himachal Pradesh (India), was bitten by Russel’s viper on the left wrist. She immediately developed progressive pain and swelling over the affected limb and 6–7 episodes of vomiting. She had coagul- opathy but no bleeding tendencies (Table 1). She received anti- snake venom therapy and primary care in a local hospital. However, she developed reduced urine output with acute kid- ney injury (AKI) and was referred to our institute. At admission, the patient was alert and oriented with stable vital signs. She was initially treated with supportive care, including hemodialysis for anuric AKI. However, there was pro- gressive worsening of anemia, thrombocytopenia and AKI. Ultrasound showed normal-sized kidneys (11.2 cm and 10.8 cm) with altered echogenicity. Further workup revealed unconju- gated hyperbilirubinemia, low serum haptoglobin, elevated free plasma hemoglobin, raised lactate dehydrogenase and aspar- tate aminotransferase, and increased schistocytes on the per- ipheral blood smear, suggesting microangiopathic hemolytic anemia (MAHA). A diagnosis of thrombotic microangiopathy (TMA) was made based on MAHA, thrombocytopenia and AKI. The patient received four cycles of therapeutic plasma ex- change over 5 days with subsequent recovery (Table 1). Discussion The usual mechanisms for snakebite AKI include toxin-induced tubular injury, pigment nephropathy due to hemoglobinuria or myoglobinuria, hypotension with pre-renal AKI, acute cortical necrosis and rarely TMA. 1–3 TMA syndromes are microvascular disorders characterized by MAHA, thrombocytopenia and organ dysfunction like AKI, neurological abnormalities (altered mental status, stroke, or seizure), or cardiac ischemia. 3,4 The condition is under-recognized in snake envenomation. The majority of the snakebite TMA cases are reported from India, Sri Lanka, Australia and Brazil, and the most frequently associated species from these countries are Russell’s vipers (Daboia russelii), hump- Learning points • Thrombotic microangiopathy is an under-recognized complication of snake envenomation that is usually seen with Russell’s vipers (Daboia russelii), hump-nosed vipers (Hypnale spp.), Australian brown snakes (Pseudechis spp.) and American pit-vipers (Bothrops spp.). • Because a subset of patients with snake envenomation develops a transition from venom-induced consumptive coagulopathy to thrombotic microangiopathy, the clinicians must monitor hemoglobin, platelets, creatinine and peripheral smear for schistocytes. Submitted: 16 March 2022 VC The Author(s) 2022. Published by Oxford University Press on behalf of the Association of Physicians. All rights reserved. For permissions, please email: journals.permissions@oup.com 486 QJM: An International Journal of Medicine, 2022, 486–487 https://doi.org/10.1093/qjmed/hcac081 Advance Access Publication Date: 22 March 2022 Case report Downloaded from https://academic.oup.com/qjmed/article/115/7/486/6551991 by guest on 16 July 2022