MORPHOLOGYInDIC,microthrombi aremostoftenfoundinthearteriolesandcapillariesofthekidneys,adrenals,brain,andheart,butnoorganisspared.Theglomerulicontainsmallfibrinthrombi.Thesemaybeassociatedwithonlyasubtle,reactiveswellingoftheendothelialcellsorvaryingdegreesoffocalglomerulitis.Themicrovascularocclusionsgiverisetosmallinfarctsintherenalcortex.Inseverecasestheischemiacandestroytheentirecortexandcausebilateralrenalcorticalnecrosis.InvolvementoftheadrenalglandscanproducetheWaterhouse-Friderichsen syndrome (Chapter20).Microinfarctsalsoarecommonlyencounteredinthebrainandareoftensurroundedbymicroscopicorgrossfociofhemorrhage.Thesecangiverisetobizarreneurologicsigns.Similarchangesareseenintheheartandoftenintheanteriorpituitary.DICmaycontributetothedevelopmentofSheehan postpartum pituitary necrosis (Chapter19).ThebleedingtendencyassociatedwithDICismanifestednotonlybylarger-than-expectedhemorrhagesnearfociofinfarctionbutalsobydiffusepetechiaeandecchymosesontheskin,serosalliningsofthebodycavities,epicardium,endocardium,lungs,andmucosalliningoftheurinarytract.
As might be imagined, depending on the balance between clotting and bleeding tendencies, the range of possible clinical manifestations is enormous. In general, acute DIC (e.g., that associated with obstetric complications) is dominated by bleeding, whereas chronic DIC (e.g., as occurs in those with cancer) tends to manifest with signs and symptoms related to thrombosis. The abnormal clotting usually is confined to the microcirculation, but large vessels are involved on occasion. The manifestations may be minimal, or there may be shock, acute renal failure, dyspnea, cyanosis, convulsions, and coma. Most often, the onset of DIC is announced by prolonged and copious postpartum bleeding or the presence of petechiae and ecchymoses on the skin. These may be the only manifestations, or there may be severe hemorrhage into the gut or urinary tract. Laboratory evaluation shows thrombocytopenia and prolongation of the PT and the PTT (from depletion of platelets, clotting factors, and fibrinogen). Fibrin split products are increased in the plasma.
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The prognosis varies widely depending on the nature of the underlying disorder and the severity of the intra-vascular clotting and fibrinolysis. Acute DIC can be life threatening and must be treated aggressively with anticoagulants such as heparin or the coagulants contained in fresh frozen plasma. Conversely, chronic DIC is sometimes identified unexpectedly by laboratory testing. In either circumstance, definitive treatment must be directed at the underlying cause.
Isolated thrombocytopenia is associated with a bleeding tendency and normal coagulation tests. A count less than 150,000 platelets/µL generally is considered thrombocytopenia. However, only when platelet counts fall to 20,000 to 50,000 platelets/µL is there an increased risk of posttraumatic bleeding, and spontaneous bleeding is unlikely until counts fall below 5000 platelets/µL. Most bleeding occurs from small, superficial blood vessels and produces petechiae or large ecchymoses in the skin, the mucous membranes of the gastrointestinal and urinary tracts, and other sites. Larger hemorrhages into the central nervous system are a major hazard in those with markedly depressed platelet counts.
The major causes of thrombocytopenia are listed in