The individual has always had to struggle to keep from being overwhelmed by the tribe. If you try it, you will be lonely often, and sometimes frightened. But no price is too high to pay for the privilege of owning yourself. ----Friedrich Nietzsche

DIC is a confusing clinical syndrome wherein systemic intravascular coagulation removes red cells from blood circulation and exhausts essential coagulation precursors such as fibrinogen, fibronectin, and vitronectin, causing defective clot formation that disrupts tissue perfusion and oxygenation, undermines coagulation, and causes sudden, unexpected, uncontrolled bleeding.

In arteries, blood coagulability is affected by the opposing factors of blood turbulence that inhibits clot formation, red cell mass that inhibits turbulence, and insoluble fibrin generation that entangles red cells into a clot.

Inadequate red cell mass exaggerates turbulence, as in the chronic anemia of renal failure, which damages von Willebrand Factor and disrupts insoluble fibrin polymerization so as to paralyze hemostasis.

Excessive dosage with erythropoietin or excessive transfusion with packed red cells can reduce turbulence below a critical threshold whereupon systemic coagulation begins spontaneously. This rapidly removes red cells from circulation and consumes coagulation precursors including fibrinogen, fibronectin and vitronectin, causing defective clot formation and systemic paralysis of hemostasis. 

Trauma victims often experience pain, fear, hypothermia and sepsis that promotes DIC by releasing tissue factor into systemic circulation that activates factor VII and simultaneously exaggerating sympathetic tone and activity that increases factor VIII activity, causing a deadly combination of systemic inflammation, tissue edema, tissue hypoxemia, and hypercoagulability.

Critical illnesses such as pneumonia, influenza, sepsis, ARDS, and MOFS are sometimes complicated by DIC. 

Normal pregnancy is a stressful condition that invites eclampsia and DIC. It exaggerates factor VIII activity, and the placenta is rich in tissue factor that escapes into systemic circulation and activates factor VII. Amniotic fluid is rich in tissue factor, so that the abnormal entry of amniotic fluid into systemic circulation triggers an intense interaction of factors VII, VIII, IX and X that generates excessive quantities of insoluble fibrin in systemic circulation, depletes its precursors, and variously exaggerates blood viscosity, undermines tissue perfusion, and paralyzes coagulation.