Abstract
Toxins from Bothrops venoms targeting hemostasis are responsible for a broad range of clinical and biological syndromes including local and systemic bleeding, incoagulability, thrombotic microangiopathy and macrothrombosis. Beyond hemostais disorders, toxins are also involved in the pathogenesis of edema and in most complications such as hypovolemia, cardiovascular collapse, acute kidney injury, myonecrosis, compartmental syndrome and superinfection. These toxins can be classified as enzymatic proteins (snake venom metalloproteinases, snake venom serine proteases, phospholipases A2 and L-amino acid oxidases) and non-enzymatic proteins (desintegrins and C-type lectin proteins). Bleeding is due to a multifocal toxicity targeting vessels, platelets and coagulation factors. Vessel damage due to the degradation of basement membrane and the subsequent disruption of endothelial cell integrity under hydrostatic pressure and tangential shear stress is primarily responsible for bleeding. Hemorrhage is promoted by thrombocytopenia, platelet hypoaggregation, consumption coagulopathy and fibrin(ogen)olysis. Onset of thrombotic microangiopathy is probably due to the switch of endothelium to a prothrombotic phenotype with overexpression of tissue factor and other pro-aggregating biomarkers in association with activation of platelets and coagulation. Thrombosis involving large-caliber vessels in B. lanceolatus envenomation remains a unique entity, which exact pathophysiology remains poorly understood.
Highlights
Introduction iationsBothrops snakes, called lanceheads, are the main genus of medical importance in the Neotropical Americas
High levels of PAI-1 and tissue plasminogen activator (tPA) as well as increase in von Willebrand factor (vWF) and thrombomodulin were recorded in patients bitten by B. jararaca evolving with systemic bleeding with or without incoagulable blood, suggesting that the fibrinolysis is due to vascular endothelial damage [45,52]
Venoms of B. lanceolatus and B. caribbaeus, rather associated with the occurrence of thrombosis, mainly contain snake venom metalloproteinases (SVMP), phospholipases A2 (PLA2), snake venom serine proteinases (SVSP), L-amino acid oxidases (LAAO) [97] and do not differ significantly in the composition from other venoms belonging to this genus responsible for systemic bleeding (Table 1)
Summary
A discrete trickle of blood from the fang punctures starts minutes after the bite with venom injection, even in the absence of systemic signs and blood incoagulability [28,29,32,33]. A local ecchymosis around the bite site is another classical feature and seems more frequent in children [28,33]. Blisters around or far from the bite in the affected limb may appear within the first 24 h and contain a serohematic or a bloody content, to be considered as manifestation of local hemorrhagic syndrome [13]
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