Acute DIC Labs:
platelet count: reduced <100,000 and rapidly declining
▲ PT, ▲ aPTT, ▲ TT
▼ plasma fibrinogen (may be nl in acute phase), ▼ factors V and ▼ VIII
▲ FDP, ▲ Fibrin monomers, ▲ D-dimer. Most sensitive test. If normal, DIC unlikely.
High-grade DIC is also associated with reduced levels of antithrombin III or plasminogen activity: < 60% of normal
Perpheral smear: schistocytes
▲ LDH
▼ haptoglobin
Screening Test Abnormalities in Inherited and Acquired Coagulopathies
Chronic DIC Labs:
Platelet count: variable. Mild thrombocytopenia or normal counts.
aPPT, PT, TT: normal or high.
plasma fibrinogen: normal or high.
factors V, VIII: normal
▲ FDP, D-dimer
Presence of shistocytes but a lower degree in acute DIC.
DIC: Disseminated Intravascular Coagulation.
Etiology:
Septicemia
Multiple trauma, burns, shock
Obstetric emergencies (amniotic fluid embolism, abruptio placenta, eclampsia, and retained fetus syndrome)
Malignancy (e.g., acute promyelocytic leukemia)
Pathophysiology:
In DIC, widespread endothelial damage occurs exposing tissue factor to circulation → generation of excess thrombin and activates the endogenous coagulation cascade and the fibrinolytic system. This can result in a severe coagulopathy characterized by widespread microvascular thrombosis accompanied by depletion of circulating platelets and procoagulant proteins (protein C, protein S, antithrombin).
In chronic DIC → able to replete factors and platelets → thrombosis.
Clinical features: bleeding, multiorgan dysfunction 2° microvascular thrombi and ischemia. Less often, they may be large arterial and venous thrombosis.
Scoring system for DIC by International Society on Thrombosis and hemostasis
Useful if ▲ PT or ▲ PTT.
Mix Pt's plasma 1:1 with normal plasma and retest. PT/PTT normalizes which means there is a factor deficiency. If PT/PTT remains elevated, it implies that there is a factor inhibitor.
Coagulation factor levels are useful if mixing study suggest factor deficiency. In DIC all factors are consumed; therefor ▼ factor V and VIII.
Vitamin K deficiency → ▼ factors II, VII, IX, X (and protein C, S); therefore normal factor V and VIII.
Tx:
Advanced DIC is fatal.
Treat underlying cause, supportive care.
Replace platelets, FFP, cryoprecipitate coagulation factors (10 units of cryoprecipitate provides 2.5 gms of fibrinogen), but this rarely helps, and consumption of platelets and coagulation proteins can aggravate the microvascular thrombosis. Goal fibrinogen >100 mg/dL.
Heparin is usually ineffective in retarding the microvascular thrombosis probably because of depletion of ATIII. Thus, ATIII concentrates can be given with heparin (ATIII dose is 90-120 units as a load, then 90-120 units daily x 4 days), but there is no evidence that this practice improves survival. Heparin may be given if there is evidence of thrombosis, ischemia, or oliguria despite good SBP or in some malignancies. Also, if there is a large vessel thrombosis in DIC. No heparin if there is head trauma.
Recombinant activated protein C (Xigris - drotrecogin alfa) can reduce mortality in Pts with severe sepsis and DIC.