Pattern of coagulopathy in viperidae snake bite

The study was carried out in the Department of Physiology, Isra University, Hyderabad. Seventy three cases of viperidae snake bite were studied to observe the pattern of coagulopathy. All had prolonged clotting time at the time of admission. Prothrombin time was increased in 56 cases, activated partial thromboplastin time was increased in 63 cases, bleeding time was normal in all cases. Platelet count was decreased in 28 cases and fibrinogen levels were decreased in 36 cases. Disseminated intravascular coagulation was found to be the predominant pattern of coagulopathy in viperidae snake bite cases

Acute renal failure in viperidae snake bite victims

This study included 10 cases of viperidae snake bite that developed acute renal failure out of 73 cases admitted to various wards of Liaquat Medical College hospital during the last two years. All these patients reported to the hospital 3-5 days after the bite. All had signs of severe envenomation with incoagulable blood and prolonged PT and APTT. All has bleeding manifestations. Blood urea and serum creatinine were increased in all patients and four were anuric. Leucocytosis and thrombocytopenia were found in 7 cases, serum bilirubin was increased in 4 cases, 4 patients required dialysis and 4 out of 10 cases expired. Bad prognostic features included severe envenomation, leucocytosis, thrombocytopenia, and necessity for dialysis. We conclude that acute renal failure is a serious complication of viperidae snake bite with high mortality rate and it necessitates early and effective treatment

Effects of prolonged poisoning by cobra venom on blood coagulation, platelets and fibrinolysis

The effects of Cobra Venom [CV] on blood coagulation, platelets and fibrinolytic system were studied in rabbits after injecting repeated doses of 0.05 MLD of the Venom. Thrombocytopenia was the earliest change to appear. It was followed by rise in serum fibrinogen degradation products and prolongation of prothrombin time, [PT] activated partial thromboplastin time [APTT] and thrombin time [TT] indicating a progressive consumption coagulapathy and activation of fibrinolysis. Red blood cell morphology was unchanged during first three weeks; whereas fragmentation appeared after fourth week and it increased in severity with further envenomations i.e., when chronic disseminated intravascular clotting was established

Síndrome hemorragíparo por exposición a raticida: comunicación de un caso / Bleeding disorder caused by exposure to a rodenticide: report of 1 case

We report a 22 years old male, admitted to the emergency room due to a life threatening coagulation disorder, with prothrombin times fluctuation between 5 and 37 percent and very low activity of factors II, VII, IX and X. In the month prior to the admission, the patient had used the rodenticide difethialone, without any precaution to avoid accidental exposure. The patient was maintained with fresh frozen plasma until oral vitamin K1 was obtained. This medication corrected the coagulation disorder

Laboratory assessment of thrombolytic therapy in acute myocardial infarction.

Hemostatic profiles and cardiac enzymes were studied in 55 acute myocardial infarct (AMI) patients to assess SK and rt-PA therapy. Hypofibrinogenemia occurred 85% in SK group and 55% in rt-PA group with high FDP and D-Dimer, indicating systemic fibrinogenolysis and local crosslinked fibrin clot lysis. The incidence of bleeding in SK and rt-PA groups combined with anticoagulants were the same but lower in rt-PA with antiplatelet. The mean FDP was significantly higher in the bleeding group (p < 0.01). Cardiac enzymes: CK, CK-MB peak values indicated reperfusion were 26.6%, 60% and 90% in conventional, SK and rt-PA therapy, respectively. Early and late occlusion did not occur either in SK or rt-PA followed by anticoagulants. Late occlusion was found in patients treated with rt-PA and antiplatelet. Mortality rate was 20% in conventional therapy.

Aluminium phosphide poisoning. Two cases with rare presentation.

We report two cases of aluminium phosphide poisoning who presented with rare manifestations, one with bleeding diathesis, hepatitis and acute tubular necrosis and the other with acute respiratory failure.