I. Physiology of Disseminated intravascular coagulation (DIC):
DIC is the syndrome that occurs when the clotting cascade goes awry. This is a clotting and bleeding disorder that results from the generation of tissue factor activity within the blood. This trigger of the coagulation cascade quickly leads to significant thrombin production which perpetuates its own formation. In very little time, the existing regulatory factors such as antithrombin III, protein C, and protein S are consumed. As a result, large amounts of thrombin are generated, leading to a hypercoagulable state. In the normal physiological state, plasmin is responsible for breaking fibrin into fibrin split products, thereby limiting the amount of fibrin clot being formed. In DIC, the quantity of plasmin is significantly increased, leading to the generation of significant quantities of fibrin degradation products. This often results in bleeding.
II. DIC usually occurs because of an underlying cause. It often arises in one of the following three clinical situations.
A. Complications of obstetrics where uterine material with tissue factor activity gains access to the maternal circulation such as in abruptio placentae.
B. Infection with gram negative bacteria which secrete an endotoxin that induces the generation of tissue factor.
C. Malignancy - particularly adenocarcinoma of the pancreas or prostate as well as promyelocytic leukemia.
D. Another less common cause is head trauma.
III. Clinical features
A. Subacute DIC - associated with thromboembolic complications such as DVT and PE as well as with vegetations on heart valves.
B. Acute DIC
1. Thrombocytopenia and depletion of coagulation factors leads to bleeding tendency.
2. This is worsened by increased degradation of fibrin to fibrin split products which interefere with fibrin polymeration and with platelet function.
3. Fibrin deposition into small blood vessels leads to tissue ischemia. The most vulnerable organ is the kidney, where fibrin deposition can lead to acute renal failure.
4. Hemolysis can occur through mechanical damage to the red blood cells secondary to the fibrin deposits.
5. Patient may experience neurological phenomena caused by ischemic injury to the brain.
IV. Laboratory findings
A. Subacute DIC
1. Thrombocytopenia
2. Normal or slightly prolonged aPT
3. Short aPTT
4. Decreased fibrinogen
5. Increased fibrin split products
B. Acute DIC
1. Thrombocytopenia
2. Markedly prolonged aPT and aPTT (over 200 seconds) secondary to insufficient fibrinogen.
3. Very high levels of D-dimers and fibrin split products
4. Low levels of the specific clotting factors
V. Treatment of DIC
A. Identify and treat the underlying cause
1. Uterine evacuation for abruptio placentae
2. Broad spectrum antibiotics for gram negative sepsis
3. Replacement therapy with cryoprecipitate (for FXIII and fibrinogen) and platelets
B. Uses of heparin
1. Can be used if thrombotic complication (ex: oliguria secondary to acute renal failure or cyanosis of
digits)
2. Can use heparin to prevent thrombotic complications if DIC is occurring secondary to a malignancy that is not quickly treatable.
3. Never use heparin in patients with head injury or with CNS bleeding.
|
|
