Document Type : Case Report
Authors
- Subrata Kumar Biswas 1
- Rayeed Anan Surontee 2
- Mohammad Mahfuzul Hoque 3
- Abu Saleh Ahmed 4
- Md. Shafiqul Bari 5
1 Indoor Medical Officer, Department of Medicine, Dhaka Medical College Hospital, Dhaka, Bangladesh
2 Core Medical Trainee, Department of Medicine, Dhaka Medical College Hospital, Dhaka, Bangladesh
3 Department of Medicine, Dhaka Medical College Hospital, Dhaka, Bangladesh
4 Department of Nephrology, Dhaka Medical College Hospital, Dhaka, Bangladesh
5 Department of Medicine, Dhaka Medical College, Dhaka, Bangladesh
Abstract
Background: Russell’s viper is one of the most venomous snakes found in Bangladesh. Acute kidney injury (AKI) is a devastating complication of viper bite causing significant morbidity and mortality. We report a case of Russell’s viper bite who presented with venom-induced consumption coagulopathy (VICC), thrombotic microangiopathy (TMA) and rhabdomyolysis. He was treated with antivenom and repeated hemodialysis and subsequently discharged.
Case presentation: A 60-year-old farmer presented with history of Russell’s viper bite with local swelling without neurological involvement. His 20-minute whole blood clotting test was positive. After initial assessment, polyvalent antivenom was administered. Subsequently, he developed AKI, anasarca, high blood pressure (210/110mmHg), moderate anemia, edema (+++), bilateral crepitation at both lung fields. His blood report was suggestive of DIC, rhabdomyolysis and AKI. He was treated with blood transfusion and repeated haemodialysis. Renal biopsy revealed renal cortical necrosis with thrombotic microangiopathy. After 3 weeks of repeated hemodialysis, his condition improved and finally discharged.
Discussion: Russell’s viper causes coagulopathy, nephrotoxicity, neurotoxicity, myotoxicity and cardiotoxicity. It causes VICC leading to occlusion of small and large vessels. AKI may result from hypovolemic shock, rhabdomyolysis and acute tubular necrosis that results secondary to VICC. Our patient had local swelling, coagulation abnormality, thrombocytopenia, high CPK, high LDH, schistocytes, high D-dimer, raised indirect bilirubin and raised serum creatinine confirmed the presence of VICC, TMA and rhabdomyolysis. The findings of microangiopathic hemolytic anemia, thrombocytopenia and cortical necrosis strongly suggest DIC as the culprit for the renal lesions in the patient. Although DIC with marked thrombocytopenia had a high mortality, our patient got antivenom and hemodialysis early for which he survived.
Conclusion: TMA, cortical necrosis and rhabdomyolysis causing AKI are some of the rare but lethal complications following Russell’s viper bite. Prompt treatment with antivenom, haemodialysis and other supportive management is essential to save the life of the patient.
Keywords
- Russell’s viper
- Venom-induced consumption coagulopathy (VICC)
- Thrombotic microangiopathy (TMA), Rhabdomyolysis
- Acute kidney injury (AKI)
Main Subjects
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