Definition and Essence of DIC
DIC (disseminated intravascular coagulation) is an acquired hemostatic disorder characterized by the massive release of thromboplastic substances from tissues, primarily tissue factor. The syndrome is also known as consumption coagulopathy and thrombohemorrhagic syndrome, which reflects its dual nature: widespread thrombosis occurs initially, followed by bleeding due to the depletion of clotting factors and platelets.
Etiology
DIC can be triggered by conditions accompanied by a massive entry of procoagulants into the bloodstream or endothelial injury:
- infections and sepsis (classic model);
- severe trauma and extensive tissue destruction;
- amniotic fluid embolism and other obstetric conditions;
- all types of shock and terminal states;
- chemotherapy, transplantation complications.
Pathogenesis Using Sepsis as an Example
In sepsis, systemic inflammatory response syndrome (SIRS) develops: concentrations of pro-inflammatory cytokines increase, alongside circulating endotoxins (cell wall lipopolysaccharides) in Gram-negative infections. The release of endotoxins is enhanced during bacterial phagocytosis by neutrophils.
Cytokines and endotoxins cause systemic endothelial injury. Damaged endothelial cells expose tissue factor, activating the extrinsic coagulation pathway, followed by platelet adhesion and aggregation with the formation of multiple microthrombi. Because bacteria and mediators circulate systemically in sepsis, thrombosis is disseminated and involves the microvasculature of various organs.
Occlusion of microvessels by fibrin thrombi leads to tissue ischemia and necrosis, presenting a picture of microangiopathic hemolytic anemia (mechanical erythrocyte destruction on fibrin strands) and multiple organ dysfunction syndrome.
Phases of DIC
- Hypercoagulation phase. Avalanche-like generation of thrombin and fibrin, massive thrombosis in the microvasculature, active consumption of coagulation factors (I, II, V, VIII) and platelets.
- Hypocoagulation phase (consumption coagulopathy). Depletion of procoagulants, platelets, and physiological anticoagulants; concomitantly, fibrinolysis is compensatorily activated with proteolysis of clotting factors, thrombin inhibition, and impaired fibrin polymerization. Hemostasis is virtually blocked, leading to hemorrhage.
Clinical manifestations
In the initial stage, signs of thrombotic occlusion and organ ischemia predominate. As the hemostatic system becomes depleted, a characteristic paradoxical picture emerges: thrombosis coexists with bleeding.
- Petechial rash and ecchymoses on the skin, bleeding from injection sites and mucous membranes;
- bleeding from surgical wounds and the gastrointestinal tract;
- neurological disorders — the patient is unable to stick out their tongue, handshake is weak, muscle weakness progresses;
- signs of multiple organ failure: respiratory, hepatic, renal, intestinal, and metabolic disorders;
- development of shock is possible.
Principles of treatment
Therapy aims to eliminate the underlying cause (eradication of the sepsis focus, antibiotic therapy), correct hemostasis, and maintain organ perfusion.
- Fresh frozen plasma — replenishment of coagulation factors and natural anticoagulants;
- Heparin — to suppress excessive microcoagulation, especially during the hypercoagulation phase;
- anti-shock therapy: glucocorticoids, analgesics, dopamine, infusion of plasma substitutes;
- in some cases — antiplatelet agents (aspirin);
- in hyperfibrinolysis — inhibitors of proteolytic enzymes (e.g., aprotinin).
Key points
- DIC is a consumption coagulopathy characterized by a massive release of tissue factor and widespread microthrombosis.
- In sepsis, the triggers are SIRS cytokines and Gram-negative bacterial endotoxins that injure the endothelium.
- Pathogenesis involves two sequential phases: hypercoagulation and hypocoagulation with activation of fibrinolysis.
- Microthrombosis leads to tissue ischemia, microangiopathic anemia, and multiple organ failure.
- The paradox of the syndrome is the combination of thrombosis with widespread bleeding (petechiae, ecchymoses, hemorrhages).
- The basis of therapy is fresh frozen plasma and heparin combined with the treatment of the underlying disease.
- Additionally, anti-shock agents, antiplatelet drugs, and protease inhibitors are used in cases of hyperfibrinolysis.