The clinical pathology of intravascular coagulation

A variety of mechanisms may cause intravascular coagulation. Fibrinolysis is nearly always secondary to the initial clotting. In the acute form, ICF is characterized by depletion of platelets and several coagulation factors together with active fibrinolysis. There is a decrease in Factors V and VIII because they are sensitive to coagulation. The stable coagulation factors may be decreased as well because after activation they are removed from the circulation by the liver and reticuloendothelial system. Severe bleeding is the usual accompaniment of the acute syndrome, which may also occur in cancer and infection of all types. The acute syndrome may also occur in prolonged, extensive operations, after transfusion of incompatible blood, heat stroke, acute injury, certain snake bites, and with the administration of certain drugs. The chronic syndrome of intravascular coagulation is much more common and is associated with many diseases, including collagen diseases or immune diseases and malignancy. Many patients with chronic intravascular coagulation have normal or even increased levels of coagulation factors, and these patients have no unusual bleeding. The diagnosis depends on the demonstration of circulating complex of "soluble" fibrin revealed by the ethanol gel and protamine sulfate gelation tests. The secondary fibrinolysis results in elevation of FSP. Many laboratories are investigating the use of other procedures in the diagnosis of intravascular coagulation, including fibrinopeptides A and B, the VIII:C VIIIR:AG ratio, antithrombin III, PF 4, beta-thromboglobulin, D dimer, urinary FSP, and fibrinogen chromatography.