Disseminated intravascular coagulation
key lab features
Thrombocytopenia
LOW fibrinogen
HIGH INR
Prolonged PT, APTT, thrombin time
Signs of haemolysis - MAHA?
pathophysiology
copied shamelessly from deranged physiology i think
- Activation of coagulation by inflammation
- Proinflammatory cytokines are secreted by immune cells
- Tissue factor (a potent procoagulant) is expressed on macrophages and monocytes
- Due to inflammation, endothelial dysfunction exposes more of the procoagulant surfaces behind the endothelium
- Exposed phosphatidylserine on the surface of damaged cells is also procoagulant
- All of these processes are systemic, and lead to the depletion of clotting factors by their consumption
- Inactivation of anticoagulant systems
- Depletion of the glycocalyx disrupts its normal anticoagulant activity (it's usually full of heparin-like molecules and antithrombin)
- Circulating antithrombin is rapidly depleted
- Trombomodulin and protein C anticoagulant systems are also vulnerable to depletion
- Thus, as the result of consumption of clotting factors, all the anticoagulant factors are also consumed
- Inactivation of fibrinolysis (this is mainly seen in septic DIC)
- Vascular endothelial cells usually secrete plasminogen activator inhibitor-1
- Endothelial dysfunction leads to increased circulating soluble plasminogen activator inhibitor-1
- This prevents fibrinolysis; the result is a failure to degrade microvascular thrombi, which persist and therefore cause organ dysfunction
- Platelet aggregation
- Because of the widespread activation of the coagulation cascade there is also widespread platelet activation
- Organ system dysfunction
- Disseminated activation of platelets and clotting factors leads to the formation of numerous microthrombi
- Because of the inactivated fibrinolytic system, these tend to lodge in the microcirculation and remain there, decreasing regional blood flow
- At the same time, blood flow to other regions increases because of uncontrolled vasodilation
- This results in microvascular shunting
management
- Treat underlying cause
- FFP - replaces fibrinogen
etiologies
How much time do you have?