الفهرس 
IntroductionOnly 14 pages are availabe for public view
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Abstract
Normal hemostasis and coagulation is now viewed as primarily a cell-based process wherein key steps in the classical clotting cascade occur on the phospholipid membrane surface of cells (especially platelets) beginning with activation of tissue factor and factor VII at the site of vascular breach which produces an initial “priming” amount of thrombin and a subsequent thrombin burst.Coagulation and hemostasis in the liver failure patient is influenced by multiple, often opposing, and sometimes changing variables and may even produce a hypercoagulable state (Figure8). Although a bleeding diathesis is usually predominant, the assessment of bleeding risk based on conventional laboratory tests such as the PT or PT INR is inherently deficient due to simultaneous impairment of the anticoagulation pathways. Whereas the PT and PTINR are well established in measuring prognosis (albeit with yet to be resolved interlaboratory variation), their limitations in bleeding risk prediction necessitate caution in the prophylactic use of plasma and other procoagulant factors based on arbitrary “cutoff” values that lack sound physiological and clinical supportive evidence.The decision to use prophylactic therapy should take into account the predominant underlying physiology, the history of bleeding and the risk-benefit of the procedure as well as the likelihood that rescue therapy would be available should bleeding occur. Further studies are clearly essential to learn how best to measure the net activity of the coagulation cascade in a given patient in order to make best use of the available options. Only then can the clinician determine whether to use blood factor replacement, platelet augmentation or thrombin burst enhancement with rFVIIa, or to use antifibrinolytics based on the clinical situation. Until then, the authors recommend challenging unfounded dogma and to the extent that is possible, tailoring therapy to the individual situation Coagulation defects in patients with and chronic liver disease are complex and relate to an imbalance in innate bleeding and clotting tendencies. With current clinical tools, these tendencies are to a large degree unpredictable and may vary from patient to patient. Because the traditional measures of coagulation are not dependable predictors of bleeding or clotting, specific diagnostic tests must be developed and tested to help the clinician predict bleeding and clotting diseases in these patients. Well-designed clinical studies are needed to assess new testing modalities and the efficacy of common interventions. New development of prophylactic and therapeutic interventions is needed to help with the clinical management of liver disease patients. This is an exciting time for research in coagulation disorders in cirrhosis, and discoveries in the near future will very likely change the paradigm in the care of patients with chronic liver diseases.