Disseminated Intravascular Coagulation

Place in the classification of coagulopathies

The state of the hemostatic system critically determines the severity of any blood loss. In marked clotting disorders, massive blood loss can occur even with damage to small blood vessels. All clotting disorders (coagulopathies) are divided into two polar groups according to their clinical orientation:

• Hemorrhagic disorders — conditions accompanied by isolated bleeding.
• Thrombophilias (thrombotic disease) — conditions with an increased tendency to form blood clots.

Separately, thrombohemorrhagic syndromes are distinguished as phase-specific hemostatic disorders. DIC is the most clinically significant representative of this group. In DIC, hypercoagulation is paradoxically combined with a severe deficiency of clotting factors.

Etiology and clinical presentation

DIC is always a secondary, acquired condition. It occurs in severe diseases and terminal states accompanied by massive tissue damage. The main causes include:

• Hemodynamic shock of various origins;
• Severe sepsis;
• Massive trauma and fractures;
• Crush syndrome;
• Massive blood transfusions.

Clinical manifestations of the syndrome are associated with microcirculatory and hemostatic disorders. Patients experience profuse tissue bleeding directly during surgical operations, spontaneous gastrointestinal and uterine bleeding. The appearance of hemorrhages in the skin, subcutaneous tissue, and injection sites is characteristic.

Pathogenesis and stages of DIC

The pathogenesis is based on massive activation of coagulation, which triggers a cascade of destructive reactions. The chain of events looks as follows: formation of multiple microthrombi $\rightarrow$ depletion of clotting factors $\rightarrow$ development of hypocoagulation $\rightarrow$ uncontrolled bleeding.

According to its stages, the process is classified as follows:

1. Stage I — hypercoagulation (massive formation of microthrombi in the vascular bed).
2. Stage II — consumption coagulopathy (due to thrombus formation, hemostatic system reserves are rapidly depleted).
3. Stage III — hypocoagulation and fibrinolysis (blood stops clotting, profuse bleeding begins).
4. Stage IV — recovery.

Forms of the syndrome by rate of development

Acute form Develops with a massive release of thromboplastic substances into the bloodstream. The initial stages of the pathology alternate so quickly that the protective and adaptive reactions of hemostasis do not have time to activate. Normally, natural clotting inhibitors (antithrombin III, $\alpha$1-antitrypsin, and $\alpha$2-macroglobulin) should stop the process, but in the acute form, their action is insufficient. Hemodynamic shock occurs, followed by massive bleeding. The causes of bleeding in this phase are complex: hypo- and afibrinogenemia, progressive consumption coagulopathy, consumption thrombocytopenia, and additional loss of factors along with escaping blood.

Subacute and chronic forms The subacute form unfolds more slowly — over the course of several days or weeks. The chronic form can last for months. It often develops subclinically, without dramatic hemorrhagic events, and is detected primarily by laboratory tests. A chronic course is most characteristic of oncological processes and systemic connective tissue diseases.

Class and exam questions

What else to study on this topic

• Hereditary coagulopathies: Hemophilia A (factor VIII deficiency) and Hemophilia B (factor IX deficiency)
• Hereditary coagulopathies: von Willebrand disease
• Thrombocytopenias: Werlhof disease (idiopathic thrombocytopenic purpura)
• Qualitative defects: Glanzmann thrombasthenia and gray platelet syndrome
• Vasopathies: Rendu-Osler-Weber teleangiectasia and hemorrhagic vasculitis

Prepared by WhiteCoat Pro faculty in accordance with the medical school curriculum. For educational purposes only.