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DISSEMINATED INTRAVASCULAR COAGULATION
Definition: Simultaneous systemic circulation of THROMBIN & PLASMIN(1).
| TEST | CLOTTING | LYSIS | DIC | LIVER |
| Platelet Count | N - Dec | N | Dec | N |
| Protime | N - Inc | N | N - I | Inc |
| PTT | N - Inc | N | N - I | Inc |
| Fibrinogen | N - Dec | N | DEC | DEC |
| Fibrin Monomer | POS 1 -3 + | N | POS | N |
| D-Dimer | N | INC | INC | N |
| Euglob Lysis Time | N | DEC | N - DEC | N |
| ATIII | N - Dec | N | N - D | N - D |
| 2-AntiPlasmin | N | DEC | DEC | N - D |
| Factor V | N - Dec | N | N - D | DEC |
| Factor VII | N - Dec | N | N - D | DEC |
| Factor VIII | N - Dec | N | N - D | N - I |
TYPES OF CONSUMPTIVE COAGULOPATHY(2)
Type I: DIC plus secondary fibrinolysis - Acute DIC
Type II: DIC (circulating thrombin) - Compensated/Chronic DIC
Type III: Primary fibrinolysis (circulating plasmin)
DIC TESTING
DIC PANEL I: FM, Fib, D-Dimer, ATIII & 2-AntiPlasmin
DIC PANEL II: FM, Fib, D-Dimer, ATIII, 2-AP, Factors V,
VIII
DIC PANEL III: FM, Fib, D-Dimer, ATIII, 2-AP, Factors V, VII,
VIII
Changes in any of the above analytes over 2 sequential blood draws are significant and provide much more useful diagnostic and prognostic information over any single set of data, no matter how abnormal the single values might be. Particular monitoring of the platelet count, fibrinogen, D-Dimer, ATIII & 2-AP will allow the clinician to determine therapies once a DIC diagnosis is made (positive FM & D-Dimer).
Why measure factors V, VII, VIII? In DIC, these factors may be consumed
resulting in low levels. In liver disease V & VII may be decreased
while VIII is normal or increased.
PATHOPHYSIOLOGY OF DIC
The hemostatic mechanism in the body is a finely balanced interaction between coagulation and fibrinolysis. Both of these mechanisms allow for the local repair and remodeling of tissues at the sites of injury, ie, surgical incision or local trauma. Both are specifically programmed to prevent dissemination of the constituents of the focal hemostasis process. Since both thrombin and plasmin are potent and non specific protease enzymes, nature provides several down regulatory mechanisms. For thrombin, the down regulation includes the protein C & S pathway, release of heparinoid substances and inactivation by ATIII, and heparin cofactor II, acting as intravascular scavengers for free thrombin in blood. Plasmin is primarily regulated by 2-Antiplasmin.
A significant increase in systemic thrombin levels is usually accompanied by Disseminated Intravascular Fibrin Formation (DIFF). DIFF can rapidly saturate and deplete the capacity of ATIII to neutralize thrombin, resulting in consumption of circulating coagulation factors in the production of fibrin. The fibrinolytic response to this production of fibrin is to generate systemic plasmin, which further destroys some of the key components of the hemostatic response and bleeding ensues.
A key step in reversing this physiological situation is to neutralize free thrombin and prevent fibrin formation while replacing the other hemostatic factors, using platelets, FFP and Cryo to promote normal hemostasis and down regulate the secondary fibrinolysis. This latter effect is also enhanced by the 2-Antiplasmin contained in the FFP. Multiple clinical situations associated with DIC can initiate this activation by different stimuli, ie, endotoxin, tissue factor, cytokine release. All lead to increased generation of thrombin and/or plasmin. In order to stop the DIC, the clinician must treat the underlying initiating cause as well as treating the hemostatic defects.
REPLACEMENT THERAPIES
FFP, platelet concentrates, cryoprecipitate, ATIII conc & Protein C conc (when available) as needed to correct deficiencies.
ATIII CONCENTRATE: (from ASH Symposia, Anaheim, CA, 12/92) A hemostatic level of at least 65% ATIII is necessary to prevent thrombosis. The half life of ATIII is 3 days, but in a consumptive coagulopathy, a plasma level of 80% should be maintained to prevent clotting or thromboembolism. Despite the long half life, it is usually necessary to dose a patient every 12-24 hours until a stable clinical state is reached. There are no known contra-indications and no signs or complications have been identified with elevated levels (150-210%). One vial may increase levels about 7-10% in a 70kg adult, depending on the initial value. ATIII concentrate administration should be followed by plasma ATIII levels. Concentrate may be used to control clotting, DIC (Positive Fibrin Monomer) or hereditary ATIII deficiency.
1 Bick, Roger L: Disorder of Hemostasis & Thrombosis. Theime, NY,
1985, p 165.
2 Mammen, Eberhard: DIC Monograph, Murex Diagnostics, 1993.