Disseminated Intravascular Coagulation (DIC) Profile, Comprehensive Plus

Create a Free Account to View Prices


Turnaround Time: 2 - 3 days
CPT Code:


Test Type: Whole blood and plasma, frozen


Identify the presence and follow the course of disseminated intravascular coagulation (DIC), including abnormalities in platelet count, fibrinogen, fibrin split products, and fibrinolytic activity.

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

1. Adcock DM, Kressin DC, Marlar RA. Effect of 3.2% vs 3.8% sodium citrate concentration on routine coagulation testing. Am J Clin Pathol. 1997 Jan; 107(1):105-110. PubMed 8980376

2. Reneke J, Etzell J, Leslie S, Ng VL, Gottfried EL. Prolonged prothrombin time and activated partial thromboplastin time due to underfilled specimen tubes with 109 mmol/L (3.2%) citrate anticoagulant. Am J Clin Pathol. 1998 Jun; 109(6):754-757. PubMed 9620035

3. National Committee for Clinical Laboratory Standardization. Collection, Transport, and Processing of Blood Specimens for Coagulation Testing and General Performance of Coagulation Assays; Approved Guideline. 5th ed. Villanova, Pa: NCCLS; 2008. Document H21-A5:28(5).

4. Gottfried EL, Adachi MM. Prothrombin time and activated partial thromboplastin time can be performed on the first tube. Am J Clin Pathol. 1997 Jun; 107(6):681-683. PubMed 9169665

5. McGlasson DL, More L, Best HA, Norris WL, Doe RH, Ray H. Drawing specimens for coagulation testing: Is a second tube necessary? Clin Lab Sci. 1999 May-Jun; 12(3):137-139. PubMed 10539100

6. Carey MJ, Rodgers GM. Disseminated intravascular coagulation: Clinical and laboratory aspects. Am J Hematol. 1998 Sep; 59(1):65-73. PubMed 9723580

7. Yu M, Nardella A, Pechet L. Screening tests of disseminated intravascular coagulation: Guidelines for rapid and specific laboratory diagnosis.Crit Care Med. 2002 Jun; 28(6):1777-1780. PubMed 10890618

8. Mammen EF. Disseminated intravascular coagulation (DIC). Clin Lab Sci. 2000 Fall; 13(4):239-245. PubMed 11586511

Collection Details:

Collection Instructions:

If the patient's hematocrit exceeds 55%, the volume of citrate in the collection tube must be adjusted.

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.

Maintain whole blood at room temperature. Freeze plasma.