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Journal Article

Citation

Isbister GK, Scorgie FE, O'Leary MA, Seldon M, Brown SG, Lincz LF. J. Thromb. Haemost. 2010; 8(11): 2504-2513.

Affiliation

School of Medicine and Public Health, University of Newcastle, Newcastle, NSW Department of Clinical Toxicology and Pharmacology, Calvary Mater Hospital, Newcastle, NSW Tropical Toxinology Unit, Menzies School of Health Research, Charles Darwin University, Darwin, NT Hunter Haematology Research Group, Calvary Mater Hospital, Newcastle, NSW Centre for Clinical Research in Emergency Medicine, Western Australian Institute for Medical Research, Royal Perth Hospital and the University of Western Australia, Perth, WA, Australia.

Copyright

(Copyright © 2010, John Wiley and Sons)

DOI

10.1111/j.1538-7836.2010.04050.x

PMID

20831619

Abstract

Background: Limited information exists on the dynamics of haemostasis in patients with venom induced consumption coagulopathy (VICC) from snake envenomation.Objective: The study aimed to investigate specific factor deficiencies and their time course in Australasian elapid envenomation. Methods: We measured coagulation parameters and factor concentrations in patients recruited to the Australian Snakebite Project, an observation cohort study. There were 112 with complete VICC, defined as an international normalised ratio(INR)>3, and 18 with partial VICC. Serial citrated plasma samples were collected from 0.5-60h post-bite. INR, activated partial thromboplastin time (aPTT), coagulation factors I,II,V,VII,VIII,IX,X,vWF antigen and D-dimer concentrations were measured. Results: Complete VICC was characterised by near/total depletion of fibrinogen, factor V and VIII, with an INR and aPTT that exceeded the upper limits of detection, within 2h of snakebite. Prothrombin levels never fell below 60% of normal, suggesting that the toxins were rapidly eliminated or inactivated and re-synthesis of clotting factors occurred irrespective of antivenom. Partial VICC caused limited depletion of fibrinogen and factor V, and almost complete consumption of factor VIII. Onset of VICC was more rapid with brown snake (Pseudonaja spp.) venom, which contains a group C prothrombin activator toxin, compared to the tiger snake group, which contains a group D prothrombin activator toxin and requires human factor Va formation. Resolution of VICC occurred within 24 to 36h irrespective of snake type. Conclusions: The results suggest that Australasian elapid prothrombin activators have a potent but short duration of action. Antivenom is unlikely to be administered in time to prevent VICC.


Language: en

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