From fang to lung: pulmonary embolism following snake envenomation (a case report).

Abstract

Pulmonary embolism is an uncommon complication of snake envenomation. While venom-induced consumption coagulopathy typically produces hemorrhagic manifestations, thrombotic complications can paradoxically develop, requiring careful timing of anticoagulation given competing hemorrhagic risks. We report a 65-year-old woman without thromboembolic risk factors who presented 3 days after a snake bite with progressive lower limb swelling and dyspnea. Physical examination revealed unilateral edema with visible fang marks. Despite normalized coagulation parameters, markedly elevated D-dimers prompted computed tomography pulmonary angiography, which demonstrated bilateral segmental pulmonary embolism without detectable lower extremity deep vein thrombosis. The patient was treated with therapeutic anticoagulation using low-molecular-weight heparin followed by rivaroxaban for 6 months, achieving complete resolution without hemorrhagic complications. Snake venom disrupts hemostasis through a biphasic response: initial consumption coagulopathy depleting factors and platelets, potentially followed by a compensatory prothrombotic phase with hyperfibrinogenemia and thrombocytosis. Additionally, specific venom proteases directly cleave fibrinopeptides A and B from fibrinogen while activating factor XIII, creating stable cross-linked fibrin deposits resistant to fibrinolysis. The absence of deep vein thrombosis suggests thrombogenesis occurs through in situ pulmonary mechanisms or undetectable microemboli. The favorable outcome supports safe initiation of therapeutic anticoagulation once acute coagulopathy resolves. Pulmonary embolism, though rare, can complicate snake envenomation even when coagulation parameters are normalized and deep vein thrombosis is absent. After coagulopathy resolves, anticoagulation is safe. Monitoring for thromboembolic events beyond the acute hemorrhagic phase remains essential.