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Heparin Like Effect in Acute Variceal Bleeding

2019-10-07 08:56:52 | BioPortfolio

Summary

This study attempts to clarify the pathophysiology of haemostasis in relation to the evidence of sepsis in liver disease, and compares the accuracy of various available laboratory tests in assessment of these patients. Further research is needed for proper understanding of the influence of sepsis on coagulation disorders in acute variceal bleeding in cirrhosis, to correctly identify the type and optimal quantity of blood product requirement in at risk patients.

Thromboelastography (TEG) /Sonoclot has been proposed as a superior tool to rapidly diagnose and help guide resuscitation with blood products. Secondly, the study of derangement in coagulopathy after the onset of sepsis is of paramount importance because of increased mortality after the onset of sepsis. In the present study, patients with cirrhosis who present with acute variceal bleeding, will be included in the study cohort, and will undergo a baseline diagnostic workup as described. They will be followed for development of any signs of infection after hospitalization. Then the effect of sepsis on their coagulation and thrombin generation response swill be assessed. Thus the effect of sepsis on the progression and outcome of coagulopathy in patients with acute variceal bleeding will be studied.

Study Design

Conditions

Coagulation Disorder

Intervention

SONOCLOT, coagulation factor assays for VIII/X, XIII, TPA/ PAI

Location

Postgraduate Institute of Medical Education and Research
Chandigarh
Choose Any State/Province
India
160012

Status

Not yet recruiting

Source

Postgraduate Institute of Medical Education and Research

Results (where available)

View Results

Links

Published on BioPortfolio: 2019-10-07T08:56:52-0400

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Medical and Biotech [MESH] Definitions

Blood-coagulation factor VIII. Antihemophilic factor that is part of the factor VIII/von Willebrand factor complex. Factor VIII is produced in the liver and acts in the intrinsic pathway of blood coagulation. It serves as a cofactor in factor X activation and this action is markedly enhanced by small amounts of thrombin.

A deficiency of blood coagulation FACTOR XIII or fibrin stabilizing factor (FSF) that prevents blood clot formation and results in a clinical hemorrhagic diathesis.

Storage-stable glycoprotein blood coagulation factor that can be activated to factor Xa by both the intrinsic and extrinsic pathways. A deficiency of factor X, sometimes called Stuart-Prower factor deficiency, may lead to a systemic coagulation disorder.

The classic hemophilia resulting from a deficiency of factor VIII. It is an inherited disorder of blood coagulation characterized by a permanent tendency to hemorrhage.

Storage-stable blood coagulation factor acting in the intrinsic pathway. Its activated form, IXa, forms a complex with factor VIII and calcium on platelet factor 3 to activate factor X to Xa. Deficiency of factor IX results in HEMOPHILIA B (Christmas Disease).

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