Clotting disorders in liver disease

Blood clotting is one of the main mechanisms by which bleeding is spontaneously controlled. This involves mainly three components : platelets, clotting factors and fibrinolytic factors. A stable effective clot is formed when platelets are adequate in number and function, clotting factors are available in adequate quantity and fibrinolytic mechanisms are downregulated. In liver disease particularly cirrhosis any or all of these mechanisms may be deranged. Bleeding may be a result of low platelet count or function, reduced synthesis of clotting factors ( mainly II, VII,IX and X) as well as excessive production of fibrinolytic factors( protein C,S and tissue plasminogen activator). Elevated pressure in splanchnic vessels resulting from portal hypertension makes them more liable to rupture under minimal stress or spontaneously. Curiously in some cases coagulation may be hyperactive leading to thrombosis due to overproduction of procoagulants or deficiency of fibrinolytic factors. Monitoring and maintenance of coagulation is critical in patients with severe liver disease particularly during surgery or liver transplantation. Massive blood transfusion is associated with a poor prognosis in the short and long term and hence irrational blood and component therapy has fallen into disrepute. Germane and need based timely blood or component therapy can salvage difficult situations while avoiding the effects of massive transfusions. Most centres now apply real-time point-of-care coagulation monitoring to guide their component therapy as opposed to lab report based correction. While reproducibility between different systems is lacking the clinical correlation has been encouraging. In fact one of the major successes in liver transplantation surgery has been the reduction of blood loss which has played a significant role in improving the safety and success of the procedure.