DIC BY ANOTHER NAME

Consumptive Coagulopathy (PATH PHYSIOLOGY)


EVENTS LEADING TO THE EVENTS



**In certain conditions, bleeding is caused by a decrease is platelets and / or coagulation factors resulting from their USE UP in the blood vessels, a condition known as consumptive coagulopathy. Also called DIC
Rapid fibrin deposition occurs, decreasing the fibrinogen level, and also platelets due to trapping causing thromboeytopenia.
There is recent data showing that the receptor on the liver hapatocytes are responsible for
Depleting platelets and other factors.
Hypofibrinogenemia concurrent with thrombocytopenia in a bleeding patient is good evidence for a consumptive coagulopathy.
Fibrinolysis is induced, resulting in increased fibrin degradation products in the blood.
There are many etiologies of consumptive coagulopathy, with the principle example being the syndrome of DIC. The distinction between DIC and the other etiologic conditions listed below is ill defined, and one or more of the processes may be overlapping.
1. Sepsis. These conditions are a common cause of postoperabive thrombocytopenia. The mechanism is unclear, may is part be due to endotoxin-induced aggregation and destruction of platelets in the microvasculature or by direct activation of the coagulation cascade.
Also APC is deficient and so formation of microthrombi is not inhibited.
2. Shock, Trauma, Burns, and Pancreatitis.
These conditions cause release of thromboplastic substance that increase thrombin formation and consumption of coagulation factors. They also can lead to thrombocytopenia. In addition, inadequate tissue perfusion incites the inflammatory response, which leads to coagulopathy.
3. Traumatic Brain Injury. Injured brain tissue releases its rich stores of thromboplastin, which leads to hypercoagulability by accelerating fibrin formation and microvascular thrombosis. Coagulation sustrates are consumed and further clotting is impaired.
4. Obstetric Emergencies. Placental abruption, amniotic fluid embolism, dead fetus, eclampsia, septic abortion, and hydatidiform mole all can cause release of thromboplastic substances that increase thrombin formation and consumption of coagulation factors.
5. Disseminated Intravascular Coagulation. DIC is an acquired coagulation disorder that involves diffuse activation of the coagulation system, with fibrin deposition in the microvasculature, platelet aggregation, and thrombosis.
The severity ranges from subelinical or low grade to serve and life threatening.
Clinically DIC is manifested by generalized bleeding, and end-organ failure results form the diffuse microvascular thrombosis.
The more severe form can lead to multiple organ system failure and death. Mortality is increased in septic or severely injured patients with DIC.
A variety of clinical conditions are associated with DIC. In addition to all of the process listed 1 to 4 DIC may be associated with massive transfusion, hemolysis liver discase, and malignancy (including leukemis).
The pathophysiologic process in DIC is limited through inflammatory mechanisms and cytokines, especially interleukin-6.
The systemic formation of fibrin results form three mechanisms.
-First TF activated factor VII, and the TF factor VIIa complex mediates formation of thrombin, with subsequent conversion of fibrinogen to fibrin and activation of platelets.
-Second, the natural anticoagulant mechanisms operating via antithrombin III (ATIII), protein C and TF pathway inhibitor all are impaired in DIC. This leads to a shift in the hemostatic balance toward thrombosis.
-Finally, fibrin clearance is decreased because of a relative excess of PAI-I(plasmin activator inhibiter), which inhibits plasmin formation and fibrinolysis.
Diagnosis of DIC is made by the combination of clinical finding and certain supportive laboatory tests. There is no specific test that confirms or rules out the diagnosis. Clinically one suspects DIC in paitents with a generalized coagulopathy, bleeding and the presence of an inciting factor or disease associated with DIC.
The patient usually has a low or decreasing platelet count and prolonged PF/PTT. FSPs may be present in the plasma and coagulation inhibitors such as ATIII may be deficient.
Fibrinogen levels may be low in severe DIC, but, because fibrinogen is an acute phase reactant, its production is increased as part of the stress response, and levels may be normal.
The D-dimer assay is the most sensitive test for DIC, being abnormal in up to 94% of patients with a diagnosis of DIC.
In many patients with coagulopathy who are suspected of having DIC, hypothermia needs to be considered as the primary etiology of the bleeding disorder, especially if sepsis is not present.

Treatment of DIC
Treatment is of the underlying disease process is essential.
Symptomatic treatment can be tried but is futile if the underlying disease is not treated at the same time.
Several specific strategies have been investigated as therapy of DIC.
Anticoagulation has been used as an attempt to halt the underlying hypercoagulation in DIC.
Currently there have been no controlled studies showing any benefit of.**

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