Viper bites cause consumptive coagulopathy resulting in hypofibrinogenaemia. Whole-blood clotting time is a standard test used to assess bleeding risk. Prothrombin time (PT) and activated partial thromboplastin time (APTT) are better standardised assays that are widely available, but their diagnostic accuracy in viper bites remains unknown. Adult patients presumed bitten by green pit vipers (Cryptelytops sp.) were enrolled. Conventional venous clotting time (VCT), 20min whole-blood clotting time (20WBCT), PT with international normalized ratio (INR) and APTT were determined. A fibrinogen level below 1.0g/litre was used as the gold standard. There were 97 patients. The average age was 46.1 years and 49.5% were men. VCT >30min, INR >1.2 and fibrinogen level <1.0g/litre were found in 9.3, 10.3 and 7.2%, respectively. The sensitivities of VCT >30min, 20WBCT (N=55), INR and APTT were 57.0%, 85.7%, 85.7% and 57.1%, respectively. The respective specificities were 94.4%, 95.8%, 95.6% and 72.4%. Three hypofibrinogenaemic patients who did not receive antivenom because of VCT <30min had persistently normal VCT and went home without clinical bleeding. In conclusion, PT with INR can be an alternative test for evaluation of coagulopathy in green pit viper bitten patients with potentially improved inter-laboratory standardisation.

SummaryPlatelet aggregation and fibrinogen binding were studied in 15 individuals before and 7 days after the oral administration of ticlopidine (250 mg b.i.d.). Ticlopidine significantly inhibited platelet aggregation induced by adenosine diphosphate (ADP), the endoperoxide analogue U46619, collagen or low concentrations of thrombin, but did not inhibit platelet aggregation induced by epinephrine or high concentrations of thrombin. Ticlopidine inhibited 125I-fibrinogen binding induced by ADP, U46619 or thrombin (1 U/ml). The ADP scavengers apyrase or CP/CPK, added in vitro to platelet suspensions obtained before ticlopidine, caused the same pattern of aggregation and 125I-fibrihogen binding inhibition as did ticlopidine. Ticlopidine did not inhibit further platelet aggregation and 125I-fibrinogen binding induced in the presence of ADP scavengers. After ticlopidine administration, thrombin or U46619, but not ADP, increased the binding rate of the anti-GPIIb/IIIa monoclonal antibody 7E3 to platelets. Ticlopidine inhibited clot retraction induced by reptilase plus ADP, but not that induced by thrombin or by reptilase plus epinephrine, and prevented the inhibitory effect of ADP, but not that of epinephrine, on the PGE1-induced increase in platelet cyclic AMP. The number of high- and low-affinity binding sites for 3H-ADP on formalin-fixed platelets and their K d were not modified by ticlopidine. These findings indicate that ticlopidine selectively inhibits platelet responses to ADP.

Green pit viper bite is a common public health problem in Southeast Asia. Although most patients experience only local swelling, some may suffer from severe systemic bleeding that can be delayed. Venom antigenaemia was measured by enzyme-linked immunosorbent assay and correlated with clinical findings in 42 patients. Initial venom antigenaemia was not predictive enough for clinical uses. A kinetic study (n = 27) showed highest levels at presentation and, then, progressive decline. The average half-life was 27.5 h during the first three days and over 50 h on days 5-7 after bite. Two small subsets (7.4% each) showed persistently detectable venom on day 14 and a subsequent rise in venom antigenaemia. They were associated with prolonged thrombocytopaenia and coagulopathy, respectively. These data demonstrated the long half-life of the venom, suggesting that waiting for spontaneous resolution of coagulopathy is not preferable. In addition, the delayed venom disappearance, not the initial values, was correlated with haemostatic disorders.

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