Disseminated Intravascular Coagulation (DIC) Profile, Comprehensive Plus
| Disseminated Intravascular Coagulation (DIC) Profile, Comprehensive Plus | | | |
| Number | | 117853 |
| CPT | | 85049; 85220; 85240; 85300; 85379; 85384; 85410; 85420; 85610; 85730 |
| Related Information | | Disseminated Intravascular Coagulation (DIC) Profile Hemostasis and Thrombosis Appendix |
| Test Includes | | Alpha2-antiplasmin; antithrombin activity; D-dimer; factor V activity; factor VIII activity; fibrinogen, quantitative; international normalized ratio (INR); plasminogen; platelet count; prolonged activated partial thromboplastin time (aPTT); prothrombin time (PT); prothrombin time (PT) and partial thromboplastin time (PTT) |
| Special Instructions | | 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. |
| Specimen | | Whole blood and plasma, frozen |
| Volume | | 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 |
| Container | | Lavender-top (EDTA) tube and blue-top (sodium citrate) tubes |
Collection | | 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.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 and carefully remove the plasma
using a plastic transfer pipette, being careful not to
disturb the cells. Transfer the plasma into a LabCorp PP
transpak frozen purple tube with screw cap (LabCorp
No 49482). Freeze immediately and maintain
frozen until tested. To avoid delays in turnaround time
when requesting multiple tests on frozen samples, please
submit separate frozen specimens for each test requested.
Please print and use the Specimen
Collection Bulletin as a tube-filling guide. |
| Storage Instructions | | Maintain whole blood at room temperature. Freeze plasma. |
| Patient Preparation | | Avoid warfarin (Coumadin®) therapy for 2 weeks and heparin therapy for 2 days prior to the test. |
| Causes for Rejection | | Hemolysis; clotted specimen; improperly filled specimen tube; thawed tube; specimen not properly identified |
| Use | | Identify the presence and follow the course of disseminated intravascular coagulation (DIC), including abnormalities in platelet count, fibrinogen, fibrin split products, and fibrinolytic activity |
| Methodology | | See individual tests. |
| Additional Information | | Disseminated intravascular coagulation (DIC) is an acquired disorder that typically occurs secondary to an underlying condition.6,7,8 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 the 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.6,7,8 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, alpha2-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 |
| Footnotes | | - Adcock DM, Kressin DC, and Marlar RA, “Effect of 3.2% vs 3.8% Sodium Citrate Concentration on Routine Coagulation Testing,” Am J Clin Pathol, 1997, 107(1):105-10.
- Reneke J, Etzell J, Leslie S, et al, “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, 109(6):754-7.
- “National Committee for Clinical Laboratory Standardization: Collection, Transport, and Processing of Blood Specimens for Coagulation Testing and General Performance of Coagulation Assays; Approved Guideline,” Third Edition, Villanova: NCCLS Document H21-A3:11(23), 1999.
- Gottfried EL and Adachi MM, “Prothrombin Time and Activated Partial Thromboplastin Time Can Be Performed on the First Tube,” Am J Clin Pathol, 1997, 107(6):681-3.
- McGlasson DL, More L, Best HA, et al, “Drawing Specimens for Coagulation Testing: Is a Second Tube Necessary?” Clin Lab Sci, 1999, 12(3):137-9.
- Carey MJ and Rodgers GM, “Disseminated Intravascular Coagulation: Clinical and Laboratory Aspects,” Am J Hematol, 1998, 59(1):65-73.
- Yu M, Nardella A, and Pechet L, “Screening Tests of Disseminated Intravascular Coagulation: Guidelines for Rapid and Specific Laboratory Diagnosis,” Crit Care Med, 2002, 28(6):1777-80.
- Mammen EF, “Disseminated Intravascular Coagulation (DIC),” Clin Lab Sci, 2000, 13(4):239-45
|
|