DISSEMINATED INTRAVASCULAR COAGULATION (DIC)
Disseminated intravascular coagulation is a consumptive coagulopathy secondary to an underlying disease process, most commonly obstetric complications, malignancy, sepsis or severe trauma and burns. In this disorder, there is activation of the coagulation cascade that leads to the formation of fibrin with subsequent lysis within the vascular system and resultant microthrombosis and consumption of platelets and clotting factors. Clinically, this disorder manifests as hemorrhaging and microemboli. The bleeding is evidenced as ecchymoses, petechiae or purpura. The bleeding occurs from all wounds, even venipuncture, and continues for hours or days despite local pressure. Uncontrollable bleeding induced by venipuncture is often times the first manifestation of DIC. Multiple organ failure secondary to ischemia is the result of the widespread microthrombi occluding the microcirculation.
DIC may occur as the result of one of two possible mechanisms: (1) release of tissue factor or thromboplastic substances into the circulation, or (2) widespread injury to the endothelial cells. In certain adenocarcinomas, the mucus they release may activate factor X and thus serve as a thromboplastic substance. Gram-negative bacteria may release endotoxins, which cause the release of thromboplastic substances contained within endothelial cells or the lysosomes of granulocytes and monocytes. In obstetric-related disorders, thromboplastin is derived from the placenta, dead retained fetus, or amniotic fluid. Widespread endothelial injury may occur as a result of the deposition of antigen-antibody complexes (systemic lupus erythematosus), temperature extremes (burns), or microorganisms (meningococci or rickettsiae).
Common laboratory abnormalities include elevations of fibrin degradation products (FDP), D-dimers, PST, PT, PTT, and thrombin time along with thrombocytopenia and decreased fibrinogen levels. Also of note is the association of a microangiopathic hemolytic anemia with DIC. The elevation of both the thrombin time and FDP are very sensitive indicators of DIC. Elevation of the thrombin time results from interference with fibrin polymerization by fibrin degradation products. Symptomatology includes dyspnea, cyanosis, respiratory failure, convulsions, coma, oliguria, acute renal failure, shock, and signs of diffuse hemorrhaging or thrombosis.
Treatment of DIC entails correcting the underlying inciting disease process. Approximately 50% of patients with DIC are suffering from obstetric complications, and in these cases, delivery of the fetus, fetal parts, or placenta results in a reversal of this disorder. Acute treatment for severe bleeding entails transfusions with platelets, fresh frozen plasma, and cryoprecipitate. Heparin use is necessary when treating thrombotic complications.