We report the second case of Hb Titusville in a family of Northern European background. This variant hemoglobin caused by an a-globin gene mutation has decreased oxygen affinity. Correct diagnosis is clinically important to spare affected individuals extensive investigations into other causes of low oxygen saturation in peripheral blood. Am.
This study aimed to assess the effects of dugite envenoming on blood coagulation and platelet count in a canine model, and the efficacy of fresh frozen plasma (FFP) in reversing the clotting disorder after both adequate and inadequate venom neutralization. Following initial dosing and administration studies, an intravenous venom dose of 1μg/kg was administered to eleven dogs. This was followed 30 minutes later by antivenom in either adequate or inadequate doses. A further 30 minutes later, the animals were given either two units of their own FFP or saline. Fibrinogen, aPTT and platelet levels were monitored for eight hours. Of the six study dogs given antivenom plus FFP, two died at around 60 to 90 minutes post envenoming, at the end of the FFP infusions, and all but one of the survivors had persistent afibrinogenaemia. Of the five study dogs given antivenom and no FFP, all but one had return of detectable fibrinogen at eight hours after envenoming. The platelet count fell in all animals with recovery independent of antivenom dose, administration of FFP, or regeneration of fibrinogen. Post mortem examinations of dogs that died during dosage and administration studies showed massive intracardiac clots. We conclude that early death from Brown Snake envenoming may be due to massive intravascular clotting. FFP administration was associated with persistent afibrinogenaemia regardless of antivenom dose. In the absence of any evidence for its efficacy, this study suggests that the role of FFP after Brown Snake envenoming should be reconsidered.
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