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BackgroundHump-nosed viper bite is the commonest cause of venomous snakebite in Sri Lanka. Despite initially being considered a moderately venomous snake more recent reports have revealed that it could cause significant systemic envenoming leading to coagulopathy and acute kidney injury. However, myocardial infarction was not reported except for a single case, which occurred immediately after the snakebite.Case presentationA 50-year-old previously healthy Sri Lankan woman had a hump-nosed viper bite with no evidence of systemic envenoming during initial hospital stay. Five days later she presented with bite site cellulitis with hemorrhagic blisters, acute kidney injury, and evidence of microangiopathic hemolytic anemia and thrombocytopenia with normal coagulation studies. She was managed with supportive care that included intravenously administered antibiotics, blood transfusions, and hemodialysis; both her microangiopathic hemolytic anemia and thrombocytopenia improved without any specific intervention. On day 10 she developed: a non-ST elevation myocardial infarction complicated with acute left ventricular failure evidenced by acute shortness of breath with desaturation despite adequate ultrafiltration; new onset lateral lead T inversions in electrocardiogram; raised troponin I titer; and hypokinetic segments on echocardiogram. She was managed with low molecular weight heparin and antiplatelet drugs, which were later discontinued due to upper gastrointestinal bleeding. Her hospital stay was further complicated by hospital-acquired pneumonia and deep vein thrombosis involving her ileofemoral vein. She died on day 33 from the snakebite.ConclusionsMyocardial infarction after snakebites is rarely reported. This is the first case report of a patient developing a myocardial infarction during the recovery phase of thrombotic microangiopathy following a hump-nosed viper bite. The possibility of thrombotic risk related to thrombotic microangiopathy following hump-nosed viper bite is an area that is poorly studied; it needs further attention.

Acute renal failure (ARF) is a well-recognized complication of paroxysmal nocturnal hemoglobinuria (PNH). The predominant mechanism is intravascular hemolysis resulting in massive hemoglobinuria ARF. We report a case of acute tubular necrosis (ATN) developed in the absence of overwhelming evidence of intravascular hemolysis in a 21-year-old man with anemia, who was eventually diagnosed to have PNH. The patient presented with rapidly deteriorating renal functions in the background of iron deficiency anemia, which was attributed to reflux esophagitis. There was no clinical or laboratory evidence of intravascular hemolysis. Renal biopsy revealed ATN with deposition of hemosiderin in the proximal tubular epithelial cells. Diagnosis of PNH was confirmed with a positive Ham's test and flow cytometry. Our case emphasizes the need to consider ATN as a possible cause for ARF in patients suspected to have PNH even in the absence of overwhelming evidence of intravascular hemolysis.