Abstract
BackgroundRussell’s viper envenoming is a major problem in South Asia and causes venom induced consumption coagulopathy. This study aimed to investigate the kinetics and dynamics of venom and clotting function in Russell’s viper envenoming.Methodology/Principal FindingsIn a prospective cohort of 146 patients with Russell’s viper envenoming, we measured venom concentrations, international normalised ratio [INR], prothrombin time (PT), activated partial thromboplastin time (aPTT), coagulation factors I, II, V, VII, VIII, IX and X, and von Willebrand factor antigen. The median age was 39y (16–82y) and 111 were male. The median peak INR was 6.8 (interquartile range[IQR]:3.7 to >13), associated with low fibrinogen [median,<0.01g/L;IQR:<0.01–0.9g/L), low factor V levels [median,<5%;IQR:<5–4%], low factor VIII levels [median,40%;IQR:12–79%] and low factor X levels [median,48%;IQR:29–67%]. There were smaller reductions in factors II, IX and VII over time. All factors recovered over 48h post-antivenom. The median INR remained >3 at 6h post-antivenom but had reduced to <2, by 24h. The aPTT had also returned to close to normal (<50sec) at 24h. Factor VII, VIII and IX levels were unusually high pre-antivenom, median peak concentrations of 393%, 307% and 468% respectively. Pre-antivenom venom concentrations and the INR (r = 0.20, p = 0.02) and aPTT (r = 0.19, p = 0.03) were correlated (non-parametric Spearman analysis).ConclusionsRussell’s viper coagulopathy results in prolonged aPTT, INR, low fibrinogen, factors V, VIII and X which recover over 48h. Severity of clotting abnormalities was associated with venom concentrations.
Highlights
Snake envenoming is a major health issue in the Asia-Pacific region with between 250,000 and 1 million cases occurring annually.[1]
Russell’s viper coagulopathy results in prolonged activated partial thromboplastin time (aPTT), international normalised ratio (INR), low fibrinogen, factors V, VIII and X which recover over 48h
Previous studies have shown that venom induced consumption coagulopathy (VICC) resulting from Russell’s viper envenoming causes overall haemostatic disturbances which manifest in prolonged prothrombin time (PT)/international normalised ratio (INR) and activated partial thromboplastin time, as well as decreased levels of fibrinogen, factor V and factor X and elevated D-Dimer concentrations.[14,15,16,17]
Summary
Snake envenoming is a major health issue in the Asia-Pacific region with between 250,000 and 1 million cases occurring annually.[1]. Russell’s viper envenoming results in local effects, venom induced consumption coagulopathy (VICC), mild neurotoxicity and renal injury.[3, 4] VICC is the commonest systemic manifestation and in some cases results in mucosal bleedings and less commonly major bleeding including intracranial haemorrhage.[3, 5,6,7]. The in vitro procoagulant effects of Russell’s viper venom have been well characterised and a number of procoagulant toxins have been isolated and used in laboratory assays for decades. Russell’s viper envenoming is a major problem in South Asia and causes venom induced consumption coagulopathy. This study aimed to investigate the kinetics and dynamics of venom and clotting function in Russell’s viper envenoming
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