A 55-year-old previously healthy man from the western province of Sri Lanka was admitted to Colombo South Teaching Hospital (CSTH) 18 h after an HNV bite. He was initially managed in a peripheral hospital and later transferred as he was anuric for 8 h. He also had vomiting and loose stools. Fang marks were seen on the fifth left toe with pain, minimal swelling and two blisters on the dorsum of the foot. The killed snake was identified by the medical officer as an HNV. He was conscious and rational with a pulse rate of 100 bpm, blood pressure 150/100 mmHg and oxygen saturation of 98%. There was no bleeding tendency or neurological manifestations. Bedside whole blood clotting time was less than 20 min on admission to the peripheral hospital and at 18 h when seen at the CSTH. Polyvalent antivenom was not given as it is ineffective in neutralizing HNV toxicity and carry a high risk of side effects. Initial investigations revealed, haemoglobin 13.2 g/dl, white cells 13.2 × 109/L, platelets 68 × 109/L, serum sodium 143 mmol/L, serum potassium 4.2 mmol/L and serum creatinine 3.2 mg/dl. On the 2nd day, haematological investigations revealed, haemoglobin 10.5 g/dl, white blood cells 14.1 × 109/L and platelets 58 × 109/L, whole blood clotting time > 20 min, PT/INR 1.7 (reference range: < 1.1) and APTT 48 s (30–40s). Total bilirubin 62.14 μmol/L (5–21) with direct bilirubin 10.08 μmol/L (< 3.4), serum alanine aminotransferase (ALT) 171 U/L (10–40), serum aspartate aminotransferase (AST) 808 U/L (10–35), Creatine kinase (CK) 750 U/L (15–105), serum lactate dehydrogenase (LDH) 2370 U/L (230–460) and serum creatinine was 409 μmol/L (70–120). Blood picture revealed fragmented red cells and thrombocytopenia suggestive of microangiopathic haemolytic anaemia (MAHA). In view of thrombotic microangiopathy (TMA), he was transfused with fresh frozen plasma with the improvement of INR and APTT. The patient was commenced on haemodialysis due to acute kidney injury (AKI). On the 3rd day, he became tachypneic with de-saturation and blood gases revealed PH 7.21, PCO2 45 mmHg, PO2 31 mmHg HCO3 12.4 mEq/L. He was intubated and started on mechanical ventilation. Bleeding through the endotracheal tube was noted but there was no bleeding from elsewhere. Chest x-ray revealed bilateral alveolar shadowing suggestive of pulmonary haemorrhages. At this time his platelet count was 56 × 109/L, INR 1.1, APTT 40 s, thrombo-elastometry showed only a deficiency of platelets. Due to the life-threatening nature of the situation, he was commenced on intravenous methylprednisolone 1 g pulse therapy daily along with FFP and platelet transfusions. There was a rapid improvement of hypoxia with the resolution of chest x-ray changes during the next 48 h. We discontinued steroid therapy after 3 days as there was no further bleeding and chest x-ray changes were resolving. Because of, persistent TMA as evidenced by a further drop in haemoglobin (8 mg/dl) and platelets (28 × 109/L) plasmapheresis was commenced and continued for 6 cycles. Despite the effective treatment of TMA, the patient went on to develop dry gangrene of toes on both feet. Renal function did not improve and required long term maintenance haemodialysis. He underwent renal transplantation 11 months after the incident due to end-stage renal disease.