Master Disseminated Intravascular Coagulation (DIC) with Picmonic for Medicine

Over-activation of the coagulation cascade leads to consumption of platelets, fibrin, and clotting factors. Without these important factors for clotting, hemorrhage results.

DIC is initiated by the release of tissue factor, which activates Factor VII in the extrinsic pathway, or the intrinsic clotting pathway via large-scale endothelial injury (the resulting exposed collagen activates Factor XII). There are many different conditions that can cause either or both.

Over-activation of the coagulation cascade leads to consumption and thus deficiency of platelets, fibrin, and clotting factors.

In sepsis, bacterial endotoxins cause endothelial injury and upregulate TNF which results in tissue factor expression on endothelial cells, thus activating the extrinsic pathways.

Trauma leads to DIC via the release of tissue factor and activation of the extrinsic pathway. Extensive surgery and severe burns may also lead to DIC in a similar fashion. Hemorrhage is the major clinical presentation in trauma-induced DIC.

Tissue factor released from the placenta, dead retained fetus or amniotic fluid activates the extrinsic pathway. Hemorrhage is the major clinical presentation in obstetric-related DIC.

Pancreatitis is a hypercoagulable state and can lead to over-activation of the coagulation cascade.

Malignancy is hypercoagulable and can lead to over-activation of the coagulation cascade.

Nephrotic syndrome is hypercoagulable and can lead to over-activation of the coagulation cascade.

Acute hemolytic transfusion reactions due to ABO incompatibility may lead to DIC.