DISSEMINATED INTRAVASCULAR COAGULATION
SETTING THE SCENE FOR DIC
In the normal body, there are small bleeds occurring regularly as we bump into things or cut ourselves. Small blood vessels tear exposing an inner substance called "tissue factor." Tissue factor initiates a blood clotting cascade involving assorted blood proteins such that blood clots (made of a protein called "fibrin") form and patch these small blood vessel tears. Bleeding stops and the clots become stronger and more permanently bound to the injury. Eventually, the healing process involves replacing the clot with scar tissue and the original tissue tear is patched up nearly as good as new.
In disease conditions where there is a great deal of tissue destruction (crushing injury, widespread bacterial infection, cancer, snake bite, etc.), a lot of tissue factor is exposed leading to a lot of activated coagulation. Microclots form all over the body's vasculature float around freely. Eventually they get stuck and plug up small blood vessels so that normal circulation cannot get through. Cells in these tissues begin to die from lack of oxygen. This creates more tissue death and more tissue factor exposure and compounds the problem. It is easy to see where the term "Disseminated Intravascular Coagulation" comes from.
Eventually there is so much clot activation that clotting factors are used up. Without the normal clotting mechanisms in place, spontaneous bleeding results. Unless the underlying cause of the tissue destruction can be controlled, death is common.
Typical conditions that are associated with DIC include those involving dying internal tissue, widespread inflammation, red blood cell destruction, poor circulation, particulate matter in the bloodstream, or loss of blood vessel integrity. Some of the more classic conditions are listed below:
The sooner DIC is recognized, the more likely the chance of a positive outcome. At first, there are no signs at all, just subtle blood test changes. It is important for the medical staff to watch for these lab changes in patients known to have diseases associated with DIC.
There are several factors that go into the diagnosis of DIC and a patient need not have them all:
The absence of D-Dimer rules out DIC with 95% confidence in dogs but is less reliable in cats.
Fibrinogen is a fibrin precursor and its absence suggests depletion. The use of fibrinogen reduction as a marker for DIC has been questioned because there are numerous other factors that can reduce fibrinogen.
A SPECIAL NOTE ON THROMBOELASTOGRAPHY ("TEG" TESTING) - In this kind of testing a gadget called a thromboelastograph hemostasis analyzer accepts a sample of blood, forms a clot with it, and measure the strength and elasticity of the clot. The test determines if there is an excessive tendency to clot or a reduced tendency to clot. Dogs with reduced ability to clot on the TEG test have a much higher mortality rate. This test may help determine the prognosis with DIC at least in dogs.
Ultimately what all this clotting and bleeding comes down to is loss of blood flow to the tissues and treatment centers on restoring normal circulation. This means intravenous fluid administration is crucial to restore tissue perfusion. In the past, heparin (an anticoagulant) was used to treat DIC as well as plasma transfusions. These treatments have become more controversial. There is no definitive treatment for DIC beyond maintaining tissue perfusion with fluids and general critical patient support.
The most significant factor in the treatment of DIC is removal of the original disease that predisposed the patient to DIC in the first place. If this can be achieved, it would be the best chance at resolving DIC.
Page posted: 3/25/2009