DIC is probably more appropriately referred to as consumptive coagulopathy.
The cascade will usually begin with exposure of blood to some sort of procoagulant
like tissue factor or malignant cells. Fibrin will then form in the
circulation. This is rapidly followed by normal fibrinolysis leading
to the depletion of clotting factors. The concern is that this rapid
turnover of clotting factors can lead to end organ damage through clotting
and bleeding.
The deposition of fibrin will cause the microangiopathic hemolytic
anemia. In order of most to least common, manifestations of DIC are
bleeding, renal, hepatic, and pulmonary dysfuntion, thromboemboli and CNS
manifestations.
The most common causes of DIC are:
The diagnosis of DIC is difficult and takes a high clinical
suspicion, about 1% of hospitalized patients will develop DIC. The
classic triad would be a suspicious clinical history, thrombocytopenia
and a microangiopathic hemolytic anemia.
The platelet count is reduced as thrombin and fibrin fix and activate
platelets. Elevated FDP and D-dimer are the sine qua non of DIC as
they are the marker of increased turnover of clotting factors. D-dimer
is more specific while FDP is more sensitive. PT, PTT and thrombin
times are all prolonged because of depletion of clotting factors further
up in the pathway. Fibrinogen tends to be a difficult test to read.
Although it is classically reduced, it is also an acute phase reactant.
(Other tests which you may see: Reptilase time, essentially the
same as the thrombin time but not affected by the presence of heparin.
Specific inhibitors, if a mixing study does not normalize coagulation parameters.
Treatment is really just treatment of the underlying disease. There is a role for platelet and factor repletion in patients who are actively bleeding or at very high risk of bleeding.
Adam Cifu