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Disseminated Intravascular Coagulation (DIC) Profile, Comprehensive Plus
A2-antiplasmin; antithrombin activity; D-dimer; factor V activity; factor VIII activity; fibrinogen antigen; international normalized ratio (INR); plasminogen; platelet count; prolonged activated partial thromboplastin time (aPTT); prothrombin time (PT)
Identify the presence and follow the course of disseminated intravascular coagulation (DIC), including abnormalities in platelet count, fibrinogen, fibrin split products, and fibrinolytic activity
See individual tests.
Disseminated intravascular coagulation (DIC) is an acquired disorder that typically occurs secondary to an underlying condition.6-8 DIC can develop secondary to conditions including obstetric accidents (placental abruption, septic abortion), intravascular hemolysis (transfusion reactions), septicemia, viremia, metastatic malignancy, leukemia, burns, severe trauma, acute liver disease, prosthetic devices, and vascular disorders. Low grade DIC can also be observed in cardiovascular, autoimmune, renal vascular, hematologic, and inflammatory disorders. DIC occurs when the normal hemostatic balance is disrupted as the result of a systemic activation of the procoagulant and fibrinolytic systems.7 An excessive amount of thrombin is generated as the result of the uncontrolled release of tissue factor (TF) into the circulation. This can occur as the result of damage to the vascular membrane or as a response to agents that stimulate TF release from endothelial cells. Cytokines produced in septic shock or endotoxin from gram-negative bacteria can induce excessive TF release.6 TF in turn initiates the extrinsic pathway of coagulation and, through the action of thrombin, the entire coagulation cascade. Thrombin production is normally limited by tissue factor pathway inhibitor, antithrombin, and protein C anticoagulant mechanisms. Under normal circumstances, the mononuclear-phagocyte system removes TF from the circulation while hepatocytes serve to clear activated coagulation proteases and tissue-plasminogen activator from the circulation.7 In DIC, hemostatic control by the natural anticoagulant mechanisms is overwhelmed and thrombin production is unchecked.
The clinical manifestations of DIC can be predominantly thrombotic, fibrinolytic with hemorrhage, or both.6-8 The excessive thrombin generation that occurs in DIC can result in the deposition of fibrin in the microvasculature, leading to thrombosis and tissue ischemia. Overactivation of the coagulation cascade can, in turn, result in bleeding due to the depletion of platelets, fibrinogen, prothrombin, and other hemostatic proteins in what is referred to as a consumption coagulopathy. Increased fibrin production triggers the fibrinolytic system with the conversion of plasminogen to plasmin. Plasmin, in turn, catalyzes the conversion of fibrin to D-dimer and other fibrinogen degradation products. As plasmin levels increase, the levels of its inhibitor, α2-antiplasmin, become overwhelmed until free plasmin is left to circulate uncontrolled. Free plasmin breaks down both fibrinogen and fibrin-producing degradation products that can interfere with platelet aggregation, further increasing the risk of bleeding.
The symptoms of DIC in certain conditions can be exacerbated by other aspects of the disease. Hepatic dysfunction can lead to diminished production of procoagulant factors and impair the clearance of fibrinogen degradation products, increasing the risk of bleeding.6 Abnormal bone marrow function found in leukemia can lead to reduced platelet production and can adversely impact primary hemostasis. D-dimer can be useful in distinguishing DIC from other conditions associated with bleeding, such as vitamin K deficiency and the rare condition, primary fibrinolysis, since these conditions are not associated with excessive thrombin generation.6
Whole blood and plasma, frozen
4.5 mL sodium citrate whole blood, 5 mL EDTA whole blood, and 6 mL frozen plasma (2 mL in each of two tubes), one tube citrated whole blood
Lavender-top (EDTA) tube and blue-top (sodium citrate) tubes
Citrated plasma samples should be collected by double centrifugation. Blood should be collected in a blue-top tube containing 3.2% buffered sodium citrate.1 Evacuated collection tubes must be filled to completion to ensure a proper blood to anticoagulant ratio.2,3 The sample should be mixed immediately by gentle inversion at least six times to ensure adequate mixing of the anticoagulant with the blood. A discard tube is not required prior to collection of coagulation samples, except when using a winged blood collection device (ie, "butterfly"), in which case a discard tube should be used.4,5 When noncitrate tubes are collected for other tests, collect sterile and nonadditive (red-top) tubes prior to citrate (blue-top) tubes. Any tube containing an alternate anticoagulant should be collected after the blue-top tube. Gel-barrier tubes and serum tubes with clot initiators should also be collected after the citrate tubes. Centrifuge for 10 minutes and carefully remove 2/3 of the plasma using a plastic transfer pipette, being careful not to disturb the cells. Deliver to a plastic transport tube, cap, and recentrifuge for 10 minutes. Use a second plastic pipette to remove the plasma, staying clear of the platelets at the bottom of the tube. Transfer the plasma into a LabCorp PP transpak frozen purple tube with screw cap (LabCorp No. 49482). Freeze immediately and maintain frozen until tested.
Please print and use the Volume Guide for Coagulation Testing to ensure proper draw volume.
Maintain whole blood at room temperature. Freeze plasma.
Causes for Rejection
Severe hemolysis; improper labeling; clotted specimen; specimen diluted with IV fluids; samples thawed in transit; improper sample type; sample out of stability
If the patient's hematocrit exceeds 55%, the volume of citrate in the collection tube must be adjusted. Refer to Coagulation Collection Procedures for directions.
|Order Code||Order Code Name||Order Loinc||Result Code||Result Code Name||UofM||Result LOINC|
|117853||DIC Comprehensive Plus||015040||Antithrombin Activity||%||27811-9|
|117853||DIC Comprehensive Plus||117740||Alpha-2-Antiplasmin||%||27810-1|
|117853||DIC Comprehensive Plus||001610||Fibrinogen Activity||mg/dL||3255-7|
|117853||DIC Comprehensive Plus||015172||Platelets||x10E3/uL||777-3|
|117853||DIC Comprehensive Plus||115107||INR||6301-6|
|117853||DIC Comprehensive Plus||015289||Prothrombin Time||sec||5902-2|
|117853||DIC Comprehensive Plus||015116||aPTT||sec||14979-9|
|117853||DIC Comprehensive Plus||115206||D-Dimer||mg/L FEU||48065-7|
|117853||DIC Comprehensive Plus||086249||Factor V Activity||%||3193-0|
|117853||DIC Comprehensive Plus||086264||Factor VIII Activity||%||3209-4|
|117853||DIC Comprehensive Plus||117714||Plasminogen||%||5970-9|
|Reflex Table for INR|
|Order Code||Order Name||Result Code||Result Name||UofM||Result LOINC|
|Reflex 1||115109||INR (Thromborel-S)||115109||INR (Thromborel-S)||6301-6|
|Reflex Table for Prothrombin Time|
|Order Code||Order Name||Result Code||Result Name||UofM||Result LOINC|
|Reflex 1||015290||PT (Thromborel-S)||015290||PT (Thromborel-S)||sec||5902-2|