Fatal Diffuse Thrombotic Microangiopathy after a Bite by the “Fer-de-Lance” Pit Viper (Bothrops lanceolatus) of Martinique

Abstract

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.

Suspicious Neuroimaging Pattern of Thrombotic Microangiopathy

“…8 Multifocal TMA with intimal-medial dissection by thrombi extending from foci of endothelial damage in small cerebral arteries and arterioles can be secondary to toxins. 10,11 A drug as the toxin is a rare cause of TMA.…”

Posterior fossa infarct following Viper bite: a paradox

“…As in early disseminated intravascular coagulopathy (DIC), direct action of toxins causes vascular endothelial damage, with probable release of vascular endothelial growth factor and von Willebrand's factor that also promote thrombus formation and subsequent infarcts (3). Another possibility is a preexisting procoagulant state, due to a mutation in factor V, deficiencies of proteins C or S, or antithrombin III or antiphospholipid antibodies (5). Direct cardiotoxic effect of viper venom leading to dysrhythmias, which provoke cardiac thromboembolism, also has been implicated in ischemic sequelae (5).…”

“…Several hypotheses attempt to explain the occurrence of infarcts following viper envenomation. Hypotension was documented in all series as one of the causes of infarcts (3,5). This is due to vasodilatation and loss of vasomotor tone provoked by the viper toxin.…”

“…Another possibility is a preexisting procoagulant state, due to a mutation in factor V, deficiencies of proteins C or S, or antithrombin III or antiphospholipid antibodies (5). Direct cardiotoxic effect of viper venom leading to dysrhythmias, which provoke cardiac thromboembolism, also has been implicated in ischemic sequelae (5).…”

Reversible Posterior Leukoencephalopathy in a Venomous Snake (Bothrops asper) Bite Victim

“…Different mechanisms, including toxin-induced hypercoagulability, systemic hypotension, thrombotic microangiopathy, and immune-mediated vasculitis, have been proposed to explain the occurrence of cerebral infarctions in snake bite victims. 5,7,8 Alternatively, venom-induced endothelial damage may be the cause of ischemic strokes in these patients. 9 This case is the first case of posterior reversible leukoencephalopathy in a venomous snake victim to be reported, and it provides more insights into the pathogenesis of venomous snake bite-induced cerebral ischemia.…”