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Biomedical subjects

C Mitrakul

Publications and source records attributed to C Mitrakul.

At least 19 recordsLinked to original sources
PubMed1993

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.

Dengue↗
PubMed1991

Antivenom therapy in Russell's viper bite.

Bleeding and renal failure are the two main manifestations responsible for the high morbidity and mortality in untreated Russell's viper bite victims. This study was an effort to find prognostic factors and a practical therapeutic approach for the care of such patients. Early detection of abnormalities in the clot quality test and/or evidence of systemic bleeding followed by immediate correction of the clotting defects using specific antivenom can reduce morbidity in Russell's viper envenomation.

Adolescent↗
PubMed1987

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.

Child↗
PubMed1984

Clinical features of neurotoxic snake bite and response to antivenom in 47 children.

Among 47 children admitted to the Chulalongkorn Medical School Hospital for neurotoxic snake bite, the attackers were identified in 15; the cobra (Naja naja) was the snake involved in all cases. Clinical manifestations in all 47 children appeared to follow a similar pattern. Drowsiness heralded the systemic effects in most of the patients. The characteristic systemic signs were those resulting from the neuromuscular effects of the venom and included ptosis, frothy saliva, slurred speech, respiratory failure, and paralysis of the skeletal muscles. These episodes occurred within 8 hours in 94% of the cases, and at the latest 19 hours following the bite. In some cases unconsciousness accompanied respiratory failure. Necrosis in the region of the bite, the prominent local sign, developed in 40% of the cases at the end of the 1st week after the bite. Infusion of specific antivenom was an effective therapeutic measure for the neuromuscular changes. Respiratory assistance was mandatory in cases of respiratory failure. Edrophonium chloride demonstrated a supportive role as a countermeasure against the neuromuscular effects.

Antivenins↗
PubMed1983

Neonatal lead poisoning. An unusual clinical manifestation.

A case of lead encephalopathy in a 2-month-old child is reported. Modes of poisoning are discussed and the unusual clinical manifestations of metallic brownish discoloration of nails and subdural effusion are presented. The possibility of lead poisoning as a cause of convulsions in neonates should be considered by doctors caring for these patients. Detailed history of lead exposure in prenatal and postnatal periods aids in early diagnosis and treatment which, thus, prevent severe neurological sequelae.

Adult↗
PubMed1982

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.

Adolescent↗
PubMed1979

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.

Adenosine Diphosphate↗
PubMed1978

Focal sclerosing glomerulonephritis: a kinetic evaluation of hemostasis and the effect of anticoagulant therapy: a controlled study.

Seventeen children, 12 boys and 5 girls with histopathologic confirmation of focal sclerosing glomerulonephritis (FSG) presented with nephrosis (100%), hypertension (64.7%), intermittent hematuria (58.8%) and associated infection (82.3%). The coagulation-profile study in these patients revealed a hypercoagulable state characterized by significant elevation of fibrinogen and factor V concentrations and platelet count (P less than .002--.02). Increased blood viscosity (13.64 +/- 3.3 cp) was also noted in the patients (controls 10.8 +/- 0.9 cp). Determination of platelet half-life and fibrinogen half-life demonstrated that these were both shortened (P less than .001). Predominant shortening of platelet half-life was observed in 3 of the 4 patients during heparin therapy but this reverted to normal during therapy with the antiplatelet agent (Persantin). These findings signify the presence of a low-grade intravascular coagulation which perhaps occurs in the glomerular capillaries. Significant increments in creatinine clearance (CCr) and renal blood flow (RBF) were observed with treatment in the 9 anticoagulant-treated patients but not in the 8 control patients treated with prednisone and cyclophosphamide.

Adolescent↗
PubMed1977

Hemostatic and platelet kinetic studies in dengue hemorrhagic fever.

In an attempt to reveal certain aspects of the pathogenesis of the bleeding disorder in dengue hemorrhagic fever, hemostatic and platelet kinetic studies were carried out in 61 children with this disease. As has been shown by others, thrombocytopenia and hypofibrinogenemia were the two most prominent hemostatic defects constantly discovered. Increased intravascular clotting seemed to be one responsible factor, though not an outstanding one. This was evidenced by mildly and variably low factors II, V, VII, VIII, IX, X, and XII, and by mild to moderate increase of fibrin degradation products as well as low platelet counts and fibrinogen. In 11 cases platelet kinetic study revealed increased destruction as a main cause for the thrombocytopenia, most probably due to the underlying immunologic mechanism, i.e., via the immune complexes formed. Another factor was platelet dysfunction--the release of adenosine diphosphate.

Adenosine Diphosphate↗