American Journal of Tropical Medicine and Hygiene · 2008 · 75 citations · 24 references
MedicineHematologyPathologyAutopsy PathologyHematopathologyHistopathologyCerebrovascular DiseasePlatelet FunctionPlatelet PhysiologyThromboembolic DiseaseThrombosisThrombotic DisordersCerebral ComplicationsCerebral VesselsClinical Manifestations Of SnakebiteEndothelial Cell DamageLeft Ventricular FailureMetalloproteinase ToxicityThrombosis PathophysiologyVascular Endothelial Dysfunction
In Martinique, a man bitten two days earlier by a pit viper (Bothrops lanceolatus) was hospitalized with impaired consciousness and tetraplegia. Investigations confirmed cerebral and myocardial infarctions. Resolving thrombocytopenia was associated with virtually normal blood prothrombin time/activated partial thromboplastin time but increasing hyperfibrinogenemia. Despite specific antivenom treatment, he developed fatal left ventricular failure six days after the bite. At autopsy, multiple cerebral, myocardial and mesenteric infarctions were found. Rupture of mitral chordae tendinae was the likely cause of death. Histopathologic examination showed multi-focal thrombotic microangiopathy with intimal-medial dissection by thrombi extending from foci of endothelial damage in small cerebral, myocardial, pulmonary, mesenteric, and interlobular renal arteries and arterioles. These findings were the causes of infarctions. There was intense angiogenesis in organizing cerebral infarcts. Immunohistochemical analysis showed platelet aggregates and endothelial cells within microthrombi. Viperidae venoms contain vascular endothelial toxins, notably metalloproteinase hemorrhagins, but von Willebrand factor activators or vascular endothelial growth factor-type factors are more likely to have been implicated in this case.
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