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An Atypical Clinical Manifestation of a Hump-Nosed Pit Viper Envenomation
N D B Ehelepola1, C N Karunathilaka1, G L H S Liyanage1
1Teaching (General) Hospital Kandy, Kandy, Sri Lanka.
Envenomations by hump-nosed pit vipers (HNVs) are frequent in Sri Lanka and in South India. Until recently, HNV was considered a moderately venomous snake. Here, we report a case of a previously healthy female developing all the known serious complications, plus some previously unreported complications following a HNV envenomation. She had muscarinic symptoms like profuse sweating and salivation within a couple of minutes and a seizure several minutes after envenomation. Her acute kidney injury (AKI) was swift onset and progressed to end-stage renal failure at three months. She had mild parotid swelling, crepitations in her lungs, and edema of the bitten leg. She had evidence of microangiopathic hemolytic anemia and hemolytic uremic syndrome as well. She developed local tissue necrosis, a non-ST-elevation myocardial infarction (non-STEMI), and anterior ischemic optic neuropathy (AION) following the envenomation. We believe the best explanation for her swift onset complication is intravascular injection of venom. We believe ischemia due to thrombotic microangiopathy has contributed to local tissue necrosis. Those ischemia and kidney failure have contributed to non-STEMI and AION. We illustrate the issue of the sluggish progress made by medicine in understanding the complications of envenomation by using HNV as an example.
Envenomations by hump-nosed pit vipers (HNVs) are frequent in Sri Lanka and in South India. Until recently, HNV was considered a moderately venomous snake. Here, we report a case of a previously healthy female developing all the known serious complications, plus some previously unreported complications following a HNV envenomation. She had muscarinic symptoms like profuse sweating and salivation within a couple of minutes and a seizure several minutes after envenomation. Her acute kidney injury (AKI) was swift onset and progressed to end-stage renal failure at three months. She had mild parotid swelling, crepitations in her lungs, and edema of the bitten leg. She had evidence of microangiopathic hemolytic anemia and hemolytic uremic syndrome as well. She developed local tissue necrosis, a non-ST-elevation myocardial infarction (non-STEMI), and anterior ischemic optic neuropathy (AION) following the envenomation. We believe the best explanation for her swift onset complication is intravascular injection of venom. We believe ischemia due to thrombotic microangiopathy has contributed to local tissue necrosis. Those ischemia and kidney failure have contributed to non-STEMI and AION. We illustrate the issue of the sluggish progress made by medicine in understanding the complications of envenomation by using HNV as an example.
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