Abnormal hemostasis in dengue hemorrhagic fever.

Abstract. Abnormal hemostasis in dengue hemorrhagic fever includes:- 1. Vasculopathy which occurs during the early febrile to pre-shock and shock phase. The evidences support are: 1.1 Increased anaphylatoxin, released by complement activation causing leakage of intravascular fluid in to serous space. 1.2 Positive tourniquet test, some of which occur preceeding thrombocytopenia in the acute phase of DHF. 1.3 Excessive increased in PGI2 which is the most potent vasodilator and platelet aggregation inhibitor. 2. Platelets: 2.1 Thrombocytopenia due to 2.1.1 The bone marrow hypocellularity with increased in all forms of megakaryocytes but the vacuolated and disintegrated ones. 2.1.2 Destruction by the liver and spleen. 2.1.3 Immune-mediated injury as demonstration of dengue antibody complexes on the platelet surface. 2.1.4 The in vitro spontaneous aggregation to vascular endothelial cell pre-infected by dengue virus inducing platelet aggregation, causing lysis and platelet destruction. 2.2 Dysfunction shown by 2.2.1 Increased release of betathromboglobulin (BTG), PF4 and PGI2. 2.2.2 In vitro hypoaggregation stimulated by ADP and defect in ADP-releasing ability. 3. Coagulopathy including: 3.1 Prothrombin complex deficiency due to liver damage. 3.2 Consumptive coagulopathy due to the activation by mononuclear phagocytes, PF3 released from platelet aggregation. DIC is seen in prolonged shock cases of DSS.

Hemodynamic response to high-dose methyl prednisolone and mannitol in severe dengue-shock patients unresponsive to fluid replacement.

Nine children; 4 males and 5 females, aged ranging from 2 1/2 to 13 years presented with signs and symptoms of poor tissue perfusion associated with dengue shock syndrome. All these 9 patients were subjected to the therapeutic trial of high dose methyl prednisolone (MP; 9/9) and mannitol (M; 6/9) after their failure to the saline and plasma replacement. Following the high dose MP and M, a significant increment in the effective circulatory blood volume as reflected by the sustained increment in CVP, widening of PP and declining in PR as well as improvement in clinical tissue perfusion were established in 7 of these nine patients so treated.

Clinical features of viper bites in 72 Thai children.

A study of snake bites in 72 children admitted to Department of Paediatrics Chulalongkorn Hospital, during January 1972 to December 1977, was investigated in depth. In 29 cases, snakes were definitely identified as green pit viper. Nature of the bite was demonstrated. Their two main clinical manifestations were local swelling and bleeding diathesis. The former was graded I to IV in increasing severity. The latter consisted of ecchymosis, haematoma, haematemesis, haematuria, bleeding gums, epistaxis and bloody stool. Each of these two clinical signs seemed to be caused by a different component of the venom as they did not always manifest in association. Swelling, though not a specific sign, was however generally the sign that heralded the envenomization. 88.1% and 94.5% of systemic bleeding episodes occurred respectively within 24 and 48 hours after the bite. Only 6 episodes, 5.5%, occurred beyond 48 hours.

Effect of five Thai snake venoms on coagulation, fibrinolysis and platelet aggregation.

The effects of five Thai snake venoms--Malayan pit viper--MPV (Ancistrodon rhodostoma); Russell's viper--RVV (Vipera russelli); cobra--CV (Naja naja); king cobra--KCV (Naja hannah) and banded krait--BKV (Bungarus fasciatus)--on blood coagulation fibrinolysis and platelet aggregation were studied. MPV has strong thrombin-like coagulant action. RVV has activating effect most probably on factor X. Other three venoms--CV, KCV and BKV have been shown to be anti coagulant, on both intrinsic and extrinsic clotting pathways. MPV has strong lytic activity on normal euglobulin clot while CV has mild accelerating action. RVV and BKV inhibit the lysis of euglobulin clot. KCV has no effect on fibrinolysis. None of the five venoms has direct aggregating activity on platelets. All except MPV inhibit ADP-induced platelet aggregation at their higher concentrations.