Pathophysiology (Costello & Nehring, 2023)

The pathophysiology behind DIC involves a complex imbalance between coagulation and bleeding. When the body is exposed to trauma, cancer treatments, bacterial endotoxins, or cytokines, tissue factor (TF) activates coagulation factor VII into VIIa in the coagulation pathway. Thrombin and fibrin are formed in the extrinsic pathway creating clots in the circulation, resulting in a constant feedback loop of coagulation stimulation, inhibition, and consumption. In other words, clotting factors are consumed and synthesis of new platelets in the bone marrow cannot keep up with demand, leading to excessive bleeding. 

DIC typically progresses through two stages: overactive clotting followed by bleeding (National Heart, Lung, and Blood Institute, 2022).

• Stage 1: excessive clotting leads to blood clots in the vasculature. Blood clots decrease or block blood flow which can damage organs.
• Stage 2: uncontrolled clotting uses up platelets and clotting factors, leading to bleeding.

Acute (decompensated) DIC occurs when blood is exposed to significant amounts of tissue factor (or other procoagulant substances) over a short timeframe, with an excessive generation of thrombin. This results in rapid consumption of coagulation factors that outpace their production. Fibrin degradation products (FDPs) interfere with fibrin clot formation and platelet aggregation.
 
Chronic (compensated) DIC develops when blood is continuously or intermittently exposed to smaller amounts of tissue factor. Coagulation factors and platelets are consumed, but new synthesis can compensate, and the liver can clear FDPs. Clotting times may be normal, and thrombocytopenia mild or absent. Many patients are asymptomatic with abnormal lab tests showing increased thrombin production and fibrinolysis. Chronic DIC is seen in patients with advanced malignancy.

Physical Examination Findings (Costello & Nehring, 2023)

Consider DIC if your patient exhibits generalized oozing or unexplained thrombosis.

• Bleeding from a variety of areas such as nose, gums, mouth, sites of trauma or surgery, wound sites, the vagina, the rectum, or through devices such as urinary catheters and intravenous lines
• Kidney failure, hematuria, oliguria, and anuria
• Acute lung injury, dyspnea, and hemoptysis secondary to pulmonary hemorrhage or pulmonary embolism
• Neurologic dysfunction, coma, delirium, and transient focal neurologic symptoms or mental status changes secondary to thrombi or hemorrhage in the brain
• Chest pain if coronary artery occlusion occurs
• Skin lesions, ecchymosis, hematoma, necrosis, gangrene, purpura, petechiae, and cyanosis
• Liver dysfunction, jaundice
• Adrenal failure from adrenal hemorrhage or infarction
• Purpura fulminans – a rare, life-threatening condition with tissue thrombosis and hemorrhagic skin necrosis