Peripheral Arterial Thrombosis following Russell's Viper Bites

by Selleckchem | Nov 08 2023

Envenomings by Russell's viper ( Daboia russelii ), a species of high medical importance in India and other Asian countries, commonly result in hemorrhage, coagulopathies, necrosis, and acute kidney injury. Although bleeding complications are frequently reported following viper envenomings, thrombotic events occur rarely (reported only in coronary and carotid arteries) with serious consequences. For the first time, we report three serious cases of peripheral arterial thrombosis following Russell's viper bites and their diagnostic, clinical management, and mechanistic insights. These patients developed occlusive thrombi in their peripheral arteries and symptoms despite antivenom treatment. In addition to clinical features, computed tomography angiography was used to diagnose arterial thrombosis and ascertain its precise locations. They were treated using thrombectomy or amputation in one case that presented with gangrenous digits. Mechanistic insights into the pathology through investigations revealed the procoagulant actions of Russell's viper venom in standard clotting tests as well as in rotational thromboelastometry analysis. Notably, Russell's viper venom inhibited agonist-induced platelet activation. The procoagulant effects of Russell's viper venom were inhibited by a matrix metalloprotease inhibitor, marimastat, although a phospholipase A 2 inhibitor (varespladib) did not show any inhibitory effects. Russell's viper venom induced pulmonary thrombosis when injected intravenously in mice and thrombi in the microvasculature and affected skeletal muscle when administered locally. These data emphasize the significance of peripheral arterial thrombosis in snakebite victims and provide awareness, mechanisms, and robust strategies for clinicians to tackle this issue in patients.

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Title: Peripheral Arterial Thrombosis Following Russell's Viper Envenoming: Clinical Management and Mechanistic Insights

Abstract: Envenomings by the Russell's viper (Daboia russelii) are known to cause various medical complications, including hemorrhage, coagulopathies, necrosis, and acute kidney injury. While bleeding complications are commonly observed, thrombotic events are rare but can lead to severe consequences. In this report, we present three serious cases of peripheral arterial thrombosis following Russell's viper bites, which occurred despite antivenom treatment. These patients developed occlusive thrombi in their peripheral arteries, necessitating thorough diagnostic approaches and clinical management, including thrombectomy or amputation in severe cases with gangrenous digits. Computed tomography angiography was utilized to accurately diagnose arterial thrombosis and identify its precise locations. Mechanistic insights were obtained through investigations that revealed the procoagulant actions of Russell's viper venom in standard clotting tests and rotational thromboelastometry analysis. Interestingly, Russell's viper venom exhibited inhibitory effects on agonist-induced platelet activation. Furthermore, the procoagulant effects of Russell's viper venom were found to be inhibited by a matrix metalloprotease inhibitor, marimastat, but not by a phospholipase A2 inhibitor (varespladib). Animal experiments demonstrated that intravenous injection of Russell's viper venom induced pulmonary thrombosis in mice, while local administration caused thrombi in the microvasculature and affected skeletal muscle. These findings highlight the importance of peripheral arterial thrombosis in snakebite victims and provide clinicians with awareness, mechanistic insights, and effective strategies to manage this life-threatening complication.

Keywords: Russell's Viper, Daboia russelii, snakebite envenoming, peripheral arterial thrombosis, clinical management, diagnostic techniques, thrombectomy, amputation, procoagulant effects, platelet activation, matrix metalloprotease inhibitor, marimastat, phospholipase A2 inhibitor, varespladib, pulmonary thrombosis, microvascular thrombi, skeletal muscle involvement.