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.
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.
Background:Bleeding is an important complication of cirrhosis. Currently, there is no coagulation test that can reliably predict clinical hemorrhage. However, previous studies demonstrated significant correlations between hyperfibrinolysis and following bleeding in advanced cirrhotic patients. Objectives: Estimate the prevalence of hyperfibrinolysis in cirrhotic patients at stable conditions and to assess its role in predicting subsequent hemorrhage. Methods: The prospective cohort study included 58 consecutive cirrhotic patients at the Liver Clinic, Chulalongkorn Hospital. Assays for liver functions, PT, APTT, fibrinogen, fibrin degradation products (FDPs) and euglobulin lysis time (ELT) were performed at baseline. The subjects were followed-up for 10 months to observe clinical hemorrhage and survival. Results: The mean age was 56.4 years and 47% were male. The etiologies of liver diseases were virus (62.1%), alcohol (24.1%) or unknown (8.6%). Hyperfibrinolysis as reflected by ELT<120 minutes or FDPs>10 μg/mL was present in 32.8% and 74.1%, respectively. Fibrinolytic activity was significantly correlated with platelet counts and coagulation times, but not as much with liver function tests. By 10 months, 13 cases (22.4%) showed hemorrhagic episodes and 7 (12.1%) were expired, including 2 from bleeding. The significant predictors for death were Child class B or C, presence of ascites, hyperbilirubinemia, hypoalbuminemia, and prolonged APTT. However, none of the clinical, biochemical, or hemostatic factors was associated with clinical bleeding. Conclusion: Hyperfibrinolysis is common in cirrhotic outpatients. However, it cannot predict subsequent hemorrhage or survival. Novel hemostatic tests are required to assess the probability of bleeding in this disorder.
Low-molecular-weight heparin (LMWH) is now the standard of care for prophylaxis and treatment of thromboembolic disorders. Only cases with renal failure, morbid obesity or extreme age require anti-Xa monitoring to assure the therapeutic level achievement. Because of infrequent requests, the test is usually sent to the reference laboratories and specimen handling may be delayed. Because LMWHs can be kept at ambient temperature for several days, we proposed that anti-Xa levels in plasma samples are similarly steady. Patients' plasma that was requested for anti-Xa activity was left at room temperature to repeat the test 24 hours later and compare with the result of immediate assay. The study included 86 fresh specimens from 56 participants. All patients received enoxaparin with anti-Xa levels ranging from 0.1 to 2.5 U/mL. Notably, anti-Xa activities significantly rose on the second occasions (P = 8.4 x 10(-10)). The mean change of anti-Xa was +0.15 +/- 0.21 U/mL (+24.9% +/- 37.4%). Children (age <15 years) showed more marked alterations than adults (+40.9% vs. +18.2%, P = .008). There was no statistical difference in the degrees of changes between sexes and diagnoses. The data suggest that specimens sent for anti-Xa require prompt handling to prevent falsely elevated values. This observation is new and future research is needed to find the mechanism of this alteration.
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