Causes (Etiology)
DIC syndrome develops as a severe complication of other pathological conditions. The main triggers include:
- Shock of any genesis.
- Obstetric pathology (premature placental abruption, amniotic fluid embolism, intrauterine fetal death).
- Extensive trauma and surgical procedures, including crush syndrome.
- Malignant tumors and multiple metastases.
- Severe intoxications and infectious processes.
- Incompatible blood transfusion.
- Organ transplantation and rejection reactions.
- Use of cardiopulmonary bypass (CPB) machines and artificial kidney.
Classification by triggering mechanism
Depending on which component of hemostasis is activated first, three types of the syndrome are distinguished:
- With predominance of the procoagulant link. Triggered by massive entry of procoagulants (thromboplastin, thrombin) into the bloodstream. Typical for obstetric pathology, crush syndrome, and metastatic cancer.
- With predominance of the vascular-platelet link. Based on generalized vascular damage or primary impact on platelets. Occurs in infectious, autoimmune, and immune complex diseases, as well as in transplant rejection.
- Mixed pathogenesis. Equal activity of both links. Observed in shock, burn disease, blood disorders, and the use of artificial circulation.
Pathogenesis and Stages of Development
The process proceeds as a sequential change of four stages:
1. Stage of hypercoagulation and thrombosis Intravascular aggregation of blood cells and disseminated blood coagulation occur. Multiple thrombi form in the microvasculature of various organs. This phase is very short — lasting only 8–10 minutes and may clinically manifest as shock.
2. Stage of increasing consumption coagulopathy Massive thrombus formation leads to a sharp decrease in fibrinogen and platelet levels — they are literally "consumed" by the process. Active coagulation factors are removed by phagocytes. There is a transition from hypercoagulation to hypocoagulation. Clinically, this is expressed by hemorrhagic diathesis. In a mild/latent course, the only confirmation of the stage is the detection of fibrin in the cytoplasm of neutrophils and macrophages.
3. Stage of deep hypocoagulation and activation of fibrinolysis Develops 2–8 hours after the onset of the syndrome. Previously formed microthrombi undergo lysis, and circulating clotting factors are subjected to proteolysis. Hyperplasminemia occurs: easily soluble fibrin-containing complexes and fibrin degradation products (FDPs) appear. Fibrin monomer loses its polymerization capacity and becomes resistant to thrombin. FDPs themselves exhibit strong anticoagulant and antiplatelet effects. Clinical and laboratory presentation: complete incoagulability of blood, pronounced bleeding and hemorrhages, microangiopathic hemolytic anemia. Capillarotrophic insufficiency develops, leading to hypoxia, acidosis, and increased vascular permeability.
4. Recovery stage (residual manifestations) Characterized by hemorrhagic, dystrophic, and necrotic changes in tissues. In a favorable case, they undergo reverse development. In severe situations, acute multiple organ dysfunction syndrome (MODS) develops: renal, hepatic, pulmonary, cardiac, adrenal. Mortality reaches 50%.
Features in newborns: Mortality among premature infants reaches 75–90%. This is associated with the immaturity of the liver's protein-synthesizing function (lack of clotting factors), imperfection of fibrinolysis and phagocytosis systems, as well as the body's inability to effectively excrete FDPs.
Briefly: answers to topical questions
What types of microthrombi by morphological composition form in the vessels during DIC syndrome?
Multiple microthrombi of various morphological compositions form in the microvasculature vessels during DIC syndrome, among which specific types predominate:
- Fibrin thrombi (thrombi fibrinosi) — the most frequently encountered substrate of the process.
- Hyaline thrombi (thrombi hyalini) — form less frequently, consist of precipitated plasma proteins and agglutinated formed elements.
- White and red thrombi (thrombi albi et rubri) — are identified in vessels less often than other types.
What macroscopic and microscopic changes occur in the kidneys during DIC syndrome?
Pronounced vascular, dystrophic, and necrotic changes develop in the kidneys during DIC syndrome against the background of impaired intravascular blood coagulation:
- Microscopic changes (mutationes microscopicae) — fibrin thrombi in glomerular capillaries, as well as dystrophy of the epithelium of the proximal and distal convoluted tubules.
- Severe changes (mutationes graves) — necrosis of tubular epithelial cells (tubulorrhexis) and symmetrical focal or total cortical necrosis.
- Clinical equivalent (aequivalens clinicum) — manifestations of necrotizing nephrosis, leading to the development of acute renal failure.
What pathomorphological changes develop in the lungs during DIC syndrome?
Characteristic microscopic changes and structural disorders of the respiratory department develop in the lungs during DIC syndrome:
- Serous-hemorrhagic edema (oedema seroso-haemorrhagicum) — accumulation of protein-rich fluid in the alveolar lumens.
- Thrombosis and stasis (thrombosis et stasis) — fibrin and hyaline thrombi in vessels, sludging and agglutination of erythrocytes.
- Hemorrhagic manifestations (manifestationes haemorrhagicae) — multiple hemorrhages and small hemorrhagic infarctions with the presence of siderophages.
- Hyaline membranes (membranae hyalinae) — a specific sign formed from fibrin that has penetrated into the alveolar lumens.
The essence of pathogenesis can be remembered through the phrase: "First everything clots, so that later everything bleeds". Multiple microthrombi take up all fibrinogen and clotting factors, leaving the blood liquid and defenseless against hemorrhages.
Class and exam questions
Why do pronounced bleeding occur in DIC syndrome if thrombi initially form?
Due to consumption coagulopathy. In the first stage, clotting factors (especially fibrinogen) and platelets are massively consumed for the formation of microthrombi. As a result of their deficiency and subsequent activation of fibrinolysis, the blood loses its ability to clot.
How to confirm the second stage of the syndrome with a latent clinical picture?
In the absence of overt hemorrhagic diathesis, the only confirmation of the second stage can be the detection of fibrin threads in the cytoplasm of macrophages and neutrophils.
What is the reason for extremely high mortality in DIC syndrome in premature newborns?
High mortality is due to the immaturity of liver function, which leads to an initial deficiency of clotting factors. In addition, their phagocytosis and fibrinolysis processes are imperfect, due to which the body is unable to remove activated factors and fibrin degradation products.
What else to study on this topic
- Mechanisms of development of microangiopathic hemolytic anemia.
- Pathogenesis of capillarotrophic insufficiency and its effect on tissue acidosis.
- Anticoagulant and antiplatelet effect of fibrin degradation products (FDPs).
- Morphological manifestations of acute multiple organ dysfunction syndrome (MODS) as an outcome of DIC syndrome.
- The role of macrophages and neutrophils in the removal of active clotting factors.
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