Nursebob’s MICU/CCU Survival Guide
Hematology In Critical Care
Disseminated Intravascular Coagulation
2/3/2006©
1. Disseminated Intravascular Coagulation (DIC)
A.Inappropriatied accelerated systemic activation of coagulation
B. Always a secondary disease.
a. A consequence of many other primary problems.
C. DIC once referred to secondary activation of the coagulation system with fibrin deposition in the microvascularture.
a. Massive,
prolonged spillage of thromboplastin.
b.
Extensive damage or alteration in the vascular endothelium.
c.
Damage to blood cells.
D. DIC that has changed to describe a varying clinical picture.
a. Most serious form.
- Extensive consumption of coagulation proteins
- Signifant deposition of fibrin
- Bleeding.
b. Mild forms of DIC.
- Endogenous markers of thrombin generation
- With little or no obvious coagulation problems.
2. Patients at increased risk for DIC.
A, Trauma Patients.
a. Widespread areas of tissue damage (particularly the brain).
- Head Injury common cause of DIC in infants and children
= Because of the high thromboplastin content of the brain
= Proportionately increased ratio of surface area of the head to total BSA.
B. Sepsis
a. Sepsis may occur in about 40% of trauma patients
b. Primary cause of DIC in all patients
C. Multiple organ failure.
a. Worsened by secondary fibrinolysis
b. Results in the formation of FDP's (fibrinogen / fibrin degradation products or "D - dimers)
- Interfere with normal fibrin formation and platelet function.
c. Fibrin deposition in DIC may lead to further organ dysfunction.
d. DIC is a major cause of acute renal failure and it also contributes to multiple system organ failure.
e. Damaged organs contributing to DIC.
3. DIC Detection
A. Markers of endogenous thrombin generation.
a. Prothrombin fragment F1.2, is released when thrombin is generated from prothrombin.
b. Thrombin is neutralized by binding to Antithrombin III (ATIII), its most important inhibitor, and fibrinopeptide
c. Forming thrombin-antithrombin III complexes.
B. In the practical management of patients, cruder measures of DIC are often used.
a. Prothrombin time (PT) and activated partial thromboplastin time time (aPTT)
-May be prolonged reflecting consumptionof many coagulation proteins.
b. Plasma concentrations of coagulation proteins known to be consumed in DIC All show decreases in concentration
- Fibrinogen
- Factor V
- Factor VIII..
C. Fibrinogen/fibrin degradation products (FDP's) or D-dimers
a. A fragment from fibrin alone, which are both increased in concentration.
b. Fibrin monomer (the remaining fibrinogen molecule when fibrinopeptide A has been removed) which may be present.
D. The Thrombin clotting time, which may be prolonged, reflecting hypofibrinogenemia and the presence of FDP's.
4. DIC Treatment
A. Cornerstone treatment of DIC is the alleviation of the primary disorder.
B. Without control, DIC will continue despite forms of therapy directed at correcting the bleeding or thrombotic problem.
C. Replacement therapy is helpful until the primary problem is controlled
a. Fresh frozen plasma (FFP)
b. Cryoprecipitate
c. Platelet concentrates.
D. The use of heparin in DIC.
a. Controversial and at this time not generally indicated in patients with underlying problem of trauma.
b. Interrupts the cascade.
c. Helps prevent microemboli. (“disseminated intravascular *coagulation*.”
d. Use a combination of heparin and replacement therapy (platelets, cryoprecipitate or plasma, depending on labs)
e. Prognosis depends on the underlying disease.
f. Heparin rapidly interrupts the clotting cascade, thus preventing further consumption of clotting products in the body by the DIC
g.
The benefit is that you (hope to) stop the intravascular clotting to prevent
infarcts hither and yon caused by clotted-off little blood
vessels
all over (uh, disseminated