1/5. Persistent coagulopathy in snake bite.Bleeding diathesis is a cardinal feature of viperine bite, which has been thought to last not more than 24 hours. There is scarcity of literature about prolonged bleeding disorder in snake envenomation. Various explanations suggested in the literature include-temporary decrease in antivenin levels, rapid elimination of antivenin from circulation or continuous release of unneutralised venom from the envenomated site. Two children with prolonged coagulopathy lasting for more than a week, correction of which required more than 300 ml of antisnake venom are reported here.- - - - - - - - - - ranking = 1keywords = circulation (Clic here for more details about this article) |
2/5. Pulmonary haemorrhage causing rapid death after bothrops jararacussu snakebite: a case report.A 36-year old woman was bitten on the left ankle by a bothrops jararacussu, and died 45 min after the bite. At necropsy, there were local signs of envenoming with haemorrhage, thrombosis and necrosis of the subcutaneous and muscular tissue. Multiple fibrin and platelet thrombi were found in the microcirculation of the heart and lungs, suggesting the occurrence of disseminated intravascular coagulation. Pulmonary haemorrhage probably secondary to the action of haemorrhagins, consumption coagulopathy and disseminated intravascular coagulation was the immediate cause of death. Intravenous inoculation of the venom could have occurred in the present case, which would explain the rapid onset of coagulation disorders, haemorrhage and death.- - - - - - - - - - ranking = 1keywords = circulation (Clic here for more details about this article) |
3/5. Coagulopathy after snake bite by bothrops neuwiedi: case report and results of in vitro experiments.Coagulation studies were performed in a patient who had been bitten by a snake of the species bothrops neuwiedi. The patient presented with hemorrhagic necrosis at the envenomization site and considerable bleeding from venous puncture sites. He developed a severe defibrination syndrome with a clottable fibrinogen level of approximately 0.1 g/l. fibrinogen was not measurable by clotting time assay. Fibrin degradation products were greatly elevated. Treatment with antivenom caused an anaphylactic reaction within ten minutes and serum sickness after three days. in vitro experiments revealed that B. neuwiedi venom directly activates Factors II and X, but does not activate factor xiii. In vivo consumption of factor xiii after B. neuwiedi envenomization is ascribed to the action of Factor IIa. At low venom concentrations clotting is initiated by activation of prothrombin by the venom either directly or via Factor X activation. Treatment with heparin might be beneficial in coagulopathy secondary to snake bite by reducing circulating active thrombin. The venom contains thrombin-like proteases which cause slow clotting of fibrinogen, and plasmin-like components causing further proteolysis of fibrinogen and fibrin. Antivenom has no effect on the proteolytic action of the snake venom. The in vivo effects of antivenom are presumably caused by acceleration of the elimination of venom components from the circulation. Intravenous administration of antivenom caused normalization of blood coagulation parameters within 48 h.- - - - - - - - - - ranking = 1keywords = circulation (Clic here for more details about this article) |
4/5. A retrospective study of 40 victims of crotalus snake bites. Analysis of the hepatic necrosis observed in one patient.Forty patients with a diagnosis of snake bite were studied at the Infectious and Parasitic disease Service of the faculty of medicine of Botucatu. Thirty were males and 10 females, ranging in age from 16 to 70 years. All were farm laborers and 35 of them were bitten in the lower limbs. Two of the 9 patients seen more than 6 hours after the bite died. The low mortality rate (5%) observed could be explained by the early care provided, by the use of appropriate doses of anti-crotalus serum, parenteral hydration, urine alkalinization with sodium bicarbonate and induction of osmotic diuresis with a mannitol solution. Anatomopathological examination of one of the patients who died revealed extensive hepatic necrosis. The authors discuss the possibility of the effect of a factor of snake venom in the genesis of hepatic necrosis and in the increased transaminase levels.- - - - - - - - - - ranking = 0.064379930477294keywords = hepatic (Clic here for more details about this article) |
5/5. Circulating immune complexes, complement activation kinetics and serum sickness following treatment with heterologous anti-snake venom globulin.Consecutive serum and plasma samples, from a patient receiving 100 ml polyvalent horse anti-venom globulin after a rattlesnake bite, were analysed for circulating immune complexes (IC) and activation of complement factors. IC were determined by two independent methods, a complement consumption assay and a Clq-binding assay. Rapidly rising levels of complement-fixing circulating IC were detected as early as 4--5 days after the serum treatment and distinct IC-activity was recorded in both assays on day 8 when clinical symptoms of serum sickness were observed. The IC remained in circulation for at least 5 weeks. Signs of intravascular C-activation in the form of low C3, C4 and C5 values was noted on day 1 after treatment. Factor B was demonstrable 3--4 days after the snake bite and this factor and C3c attained a peak around day 8, just before maximal suppression of native C3 and C4. 14 days after the globulin treatment C3c and B were declining rapidly while C3 and C4 approached normal values first 36 days after treatment. An increase in heterophilic antibodies to sheep erythrocytes was observed after treatment with anti-venom globulin.- - - - - - - - - - ranking = 1keywords = circulation (Clic here for more details about this article) |