sulting from microvascular (and sometimes large-vessel) thrombosis that always accompanies true DIC and that leads to end-organ failure and death (Bick, 1994). The disorder may have a spectrum of presentations, from low-grade DIC, with minimal symptoms and minor laboratory abnormalities, to fulminant DIC, with life-threatening bleeding and protein coagulation abnormalities producing end-organ dysfunction and death. Various disorders ranging from sepsis to malignancy have been described in association with DIC. Although the diagnosis of DIC is made in patients receiving massive transfusions, the diagnosis of platelet dysfunction due to hypothermia or a specific factor deficiency should be excluded before making a diagnosis of DIC.

Laboratory abnormalities in DIC are variable and are related to the many diseases that are associated with this condition. Common abnormalities include abnormal prothrombin and activated partial thromboplastin times with depressed fibrinogen levels and abnormal platelet counts. Levels of fibrin-degradation products and D-dimer are commonly elevated. Because of the continued activation of coagulation, thrombin-antithrombin complexes will be formed and their levels can be measured. Levels of thrombin-antithrombin and antithrombin III are depressed. In addition, the levels of various fragments from coagulation factor degradation are elevated, including those of F1.2 and FpA.

Low-grade DIC generally responds to management of the underlying disorder, with some patients requiring heparin therapy. The appropriate therapy for fulminant DIC remains controversial, and this is compounded by the lack of objective studies and the many underlying causes. Despite improved diagnostic and therapeutic modalities, the rate of mortality from DIC remains high and is closely related to the underlying disorder.

Conclusions and Recommendations

Traditionally, clinicians have evaluated patients for the presence and progression of cellular injury or death by assay of cellular proteins in serum that are not specific to injury processes. The new understanding of lethal cellular processes suggests that serum should be examined for the products of these processes. Indeed, immunochemical assays now exist for:

  • conjugates of lipid peroxidation products and proteins,
  • calpain-specific degradation fragments of spectrin,
  • caspase-specific degradation products from actin, and
  • phosphorylated eIF2α.

These species are all specifically pathologic and, in fact, reveal the presence of pathochemical processes for which emerging therapeutic approaches exist.

Furthermore, the processes reflected by these products (destruction of membranes by lipid peroxidation, degration of the cytoskeleton by calpain, caspase-mediated proteolysis, and apoptosis-associated blockade of normal

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