Disseminated intravascular coagulation: Difference between revisions
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Revision as of 18:48, 12 October 2011
Background
- Widespread and inappropriate activation of the coagulation and fibrinolytic systems
- Thrombosis
- Tissue factor activation -> thrombin -> fibrin clots in microcirculation
- Activation of the coagulation system leads to consumption of plts and coag factors
- Tissue factor activation -> thrombin -> fibrin clots in microcirculation
- Bleeding
- Thrombin/fibrin actives tPA and the fibrinolytic system
- Degree of fibrinolysis can be excessive -> bleeding
- Thrombin/fibrin actives tPA and the fibrinolytic system
- Thrombosis
Causes
- Infection
- Most common cause of DIC
- 10%–20% of pts w/ Gram-neg sepsis have DIC
- Septic pts more likely to have bleeding than thrombosis
- More likely to develop in asplenic pts or cirrhosis
- Carcinoma
- DIC is often chronic and compensated
- Thrombosis is more common than bleeding
- Leukemia
- More likely to have bleeding than thrombosis
- Trauma
- Brain injury, crush injury, burns, rhabdo, fat embolism
- Liver disease
- May have chronic compensated DIC; acute DIC may occur in setting of acute liver failure
- Pregnancy
- Abruption, amniotic fluid embolus, septic abortion, HELLP syndrome
- Envenomation
- Rattlesnakes and other vipers
- Bleeding not as serious as expected from lab values
- ARDS
- 20% of pts with ARDS develop DIC; 20% of pts with DIC develop ARDS
- Transfusion reactions
Clinical Features
Diagnosis
- PT high
- PTT high
- Platlet low
- Fibrinogen low
- FDP high
- D-dimer high
- RBCs fragmented
Treatment
See Heme: Bleeding Treatment
Source
1/26/06 DONALDSON (addapted from Tintinalli)