Disseminated intravascular coagulation (DIC)

A systemic process with activation of the blood coagulation system, resulting in generation and deposition of fibrin, leading to micro vascular thrombi in many organs and leading to multiorgan failure.

Normally the process of coagulation is controlled at many levels to ensure appropriate amount of hemostasis at appropriate locations.

DIC refers to the process that disrupts fine tuning, leading to unregulated coagualtion.

Its presence indicates the presents of another underlying disease.

Results in the consumption and depletion of coagulation proteins and platelets due to the ongoing process of coagulation activity.

May be associated with significant bleeding complications.

Can present with a spectrum of findings ranging from asymptomatic abnormal laboratory results to florid bleeding or thrombosis.

A manifestation of inappropriate thrombin activation.

Activation of thrombin leads to: conversion of fibrinogen to fibrin, activation of platelets, consumption of platelets, activation of factors V and VIII, activation of protein C, degradation of factors Va and VIIIa, activation of endothelial cells, and activation of fibrinolysis.

With excessive activation of thrombin there is conversion of fibrinogen to fibrin leading to formation of fibrin monomers and excessive thrombus formation.

Thrombi that are formed are rapidly dissolved by excessive fibrinolysis in most patients.

Thrombin is the most potent physiologic activator platelets.

Activated platelets are consumed in DIC, resulting in thrombocytopenia.

Fibrin degradation products in DIC can bind to GP IIb/IIa and inhibit further platelet aggregation.

In some patients the fibrinolysis system is inhibited with intravascular clot formation, but may also lead to acceleration of the process with bleeding.

Patients may have simultaneous clotting and bleeding problems.

Fibrin deposition occurs as the result of tissue factor mediated thrombin generation and impaired physiologic anticoagulant mechanisms such as antithrombin system and protein C system which should balance thrombin generation.

Associated with an impaired fibrinolytic system caused by high circulating levels of fibrinolytic inhibitor PAI-1, although in some cases fibrinolytic activity may be increased.

3-5 hours after bacteremia thrombin generation is noted to be present as tissue factor/Factor VIIa system initiates its production.

Activation of factors V, VIII, XI, and XIII can promote thrombosis, but they are then rapidly cleared by anti-thrombin or activated protein C or by binding to the fibrin clot.

The above process can lead to the depletion of all the prothrombotic clotting factors and anti-thrombin, which in turn lead to both thrombosis and bleeding.

Can cause ischemia and loss of digits and extremities typically with disseminated infection and shock.

Driven by tissue factor and is associated with systemic inflammatory states, including sepsis and viral hemorrhagic fevers.

In response to a microbiologic pathogen or liposaccharide induced toll-like receptor activation, macrophages and monocytes up regulate tissue factor to trigger intravascular coagulation.

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