Disseminated Intravascular Coagulation
Disseminated intravascular coagulation (DIC) is a serious condition that is most commonly experienced by doctors of acute medicine treating patients in serious and critical conditions.
First, it is necessary to know some information about the process of blood clotting. The coagulation process depends mainly on function of blood platelets and coagulation factors.
In case of a vascular integrity disruption the platelets form a primary clot that is reinforced by protein known as fibrin produced by the clotting factors. The fibrin is outcome of a complicated coagulation cascade. There also exists a blood clot dissolving system that prevents inadequately frequent blood clots formation. The balance of these systems should ensure that the blood coagulates only if needed.
The actual initiation of blood coagulation is caused by some factors such as the tissue factor. The tissue factor is a substance released from cells of damaged vascular wall. It is logical - if there is damage of the vascular wall, it is necessary to initiate clotting to prevent the blood leak. However, in some pathological conditions, an undesirable massive release of tissue factor into the bloodstream may occur causing a major disruption of the blood coagulation system. Such conditions may include sepsis (cell damage during the whole-body inflammatory response, bacterial cell decay, etc.), large tumor processes (disintegration of tumor cells) and conditions after major surgery and extensive injuries.
Uncontrolled release of tissue factor causes too powerful activation of the clotting system leading to formation of multiple blood clots in small vessels in the majority of organs. These blood clots impair the oxygen supply, cause ischemia and affected organs' failure. The excessive blood clotting consumes platelets and clotting factors (consumption coagulopathy) and this results in paradoxical tendency to increased bleeding (bruising, bleeding in the digestive tract, bleeding into urogenital tract and internal bleeding).
The DIC is suspicious in patients in severe conditions with signs of increased bleeding and failure of vital organs. It is important to do the blood test and examine the concentration of certain blood components participating in blood coagulation such as blood platelets, fibrinogen and D-dimers. In a classic case of DIC, platelet numbers are low, fibrinogen level also decreases (fibrinogen transforms to active molecule of fibrin) and D-dimers level elevates (D-dimers are compounds arising by fibrin disintegration) as the organism tries to dissolve the produced blood clots.
There are two main tests that evaluate the activity of coagulation factors - PT and APTT. The higher their values the slower is the coagulation. In case of DIC, the values are higher as blood with depleted coagulation factors coagulates slower.
The patient should be treated, usually in department of critical care. Vital functions and blood clotting parameters must be monitored. If there is a clear cause of the DIC, it must be treated, if possible.
The therapy of DIC itself is a bit paradoxical .It would be seemingly logical to stop the bleeding in the first place. However, we administer on the contrary the anticoagulation drugs (like heparin). The anticoagulants should stop the formation of further blood clots and so stop the vicious circle of unnecessary excessive clotting. In conditions with a significant bleeding, we deliver the missing clotting factors in form of frozen blood plasma transfusion.
Plasma contains the needed clotting factors and helps to stabilize the disorganized coagulation system of a patient with DIC.