Etiology and Triggers
DIC develops as a severe complication of underlying pathological conditions. Main triggers include:
- Shock of any etiology.
- Obstetric complications ( placental abruption, amniotic fluid embolism, fetal demise).
- Major trauma and surgical procedures, including crush syndrome.
- Malignant neoplasms and widespread metastasis.
- Severe intoxications and infectious processes.
- Incompatible blood transfusions.
- Organ transplantation and rejection reactions.
- Cardiopulmonary bypass and hemodialysis.
Classification by Trigger Mechanism
Depending on which component of hemostasis is activated first, DIC is divided into three types:
- Predominant procoagulant activation. Triggered by the massive entry of procoagulants (thromboplastin, thrombin) into the bloodstream. Characteristic of obstetric pathology, crush syndrome, and metastatic cancer.
- Predominant platelet and vascular activation. Caused by generalized vascular damage or primary platelet injury. Occurs in infectious, autoimmune, and immune complex diseases, as well as graft rejection.
- Mixed pathogenesis. Equal activation of both pathways. Observed in shock, burn disease, hematologic disorders, and cardiopulmonary bypass.
Pathogenesis and Stages
The process unfolds in four sequential stages:
1. Stage of Hypercoagulation and Thrombosis Intravascular aggregation of formed elements and disseminated blood clotting occur. Multiple microthrombi form in the microvasculature of various organs. This phase is extremely brief—lasting only 8–10 minutes—and may clinically manifest as shock.
2. Stage of Consumptive Coagulopathy (Consumption Coagulopathy) Massive thrombus formation leads to a sharp drop in fibrinogen and platelet levels as they are "consumed" by the process. Active clotting factors are cleared by phagocytes. The condition transitions from hypercoagulation to hypocoagulation, clinically expressed as a bleeding diathesis. In subclinical presentations, the only confirmation of this stage is the detection of fibrin in the cytoplasm of neutrophils and macrophages.
3. Stage of Profound Hypocoagulation and Fibrinolysis Activation Develops 2–8 hours after onset. Previously formed microthrombi undergo lysis, and circulating clotting factors undergo proteolysis. Hyperplasminemia occurs, characterized by the appearance of soluble fibrin-containing complexes and fibrin degradation products (FDPs). Fibrin monomers lose their ability to polymerize and become thrombin-resistant. FDPs themselves exert potent anticoagulant and antiplatelet effects. Clinical and laboratory findings: complete incoagulability of blood, severe bleeding and hemorrhages, microangiopathic hemolytic anemia. Capillary-trophic insufficiency develops, leading to hypoxia, acidosis, and increased vascular permeability.
4. Recovery Stage (Residual Manifestations) Characterized by hemorrhagic, dystrophic, and necrotic tissue changes. In favorable cases, these undergo regression. In severe cases, acute multiorgan dysfunction syndrome (MODS) develops: renal, hepatic, pulmonary, cardiac, and adrenal failure. Mortality reaches 50%.
Neonatal features: Mortality among preterm infants reaches 75–90% due to the immaturity of the hepatic protein-synthesizing function (deficiency of clotting factors), immature fibrinolytic and phagocytic systems, and an impaired ability to clear FDPs.