Classification and clinical forms
Depending on the prevalence of the process, generalized and local (localized) DIC syndromes are distinguished. Depending on the duration of the course, three main forms are identified:
- Acute form (from a few hours to a day). It is the most severe, typically occurring against the background of shock of various origins. It consistently leads to generalized tissue damage with massive necrosis, hemorrhages, and the development of multiple organ failure.
- Subacute form (from a few days to a week). It occurs in moderate intoxication, sepsis, burn disease, trauma, intravascular hemolysis, as well as in late gestosis, leukemias, malignant tumors, immune complex pathologies, and transplant rejection. It is characterized by mosaic or local lesions. In the terminal period or during exacerbation, it can transform into the acute form.
- Chronic form (weeks and months). Accompanies malignant neoplasms, chronic leukemias, rheumatic and autoimmune diseases, prolonged intoxications, and sometimes chronic cardiovascular failure. It manifests as constant, minimal, migrating changes (rarely generalized) and slowly progressive organ failure.
A special variant is the Kasabach-Merritt syndrome (synonyms: giant hemangioma with thrombocytopenia, thrombopenia-hemangioma syndrome, multiple fibrinopoietic angioectasia). It occurs in the risk group — in newborns and young children. The cause is a large (more than 5–6 cm) capillary or cavernous hemangioma. Blood clotting occurs inside the tumor, which triggers consumption coagulopathy, thrombocytopenia, and pronounced hemorrhagic diathesis.
General morphological picture
The main target in DIC is the microvasculature. The primary morphological substrate is multiple microthrombi. Most often they consist of fibrin; hyaline, white, or red thrombi are significantly less common.
Vascular changes are manifested by pronounced blood stasis in capillaries and venules. Three types of pathological processes naturally develop in the surrounding tissues: multiple hemorrhages, cellular dystrophy, and foci of necrosis.
Changes in the lungs and kidneys
These organs are among the first to suffer due to the peculiarities of blood flow and tissue composition.
- Lungs: The organ is in the high-risk zone due to rich vascularization and an abundance of tissue thromboplastin. Microscopy reveals serous-hemorrhagic edema, erythrocyte sludging and agglutination, fibrin and hyaline thrombi. Multiple hemorrhages and small hemorrhagic infarctions occur, in the zone of which siderophages are detected. A specific sign is hyaline membranes — they are formed from fibrin that penetrates into the lumen of the alveoli.
- Kidneys: Pronounced dystrophy of the epithelium of the proximal and distal convoluted tubules is observed. In severe cases, tubulorrhexis (epithelial cell necrosis) develops, as well as focal or total symmetric cortical necrosis. The clinical equivalent of these changes is necrotizing nephrosis with acute renal failure.
Involvement of other internal organs
Multiple microthrombi and hemostatic disorders leave a mark in almost all body systems:
- Liver: Dystrophy and necrosis of hepatocytes (up to centrilobular necrosis). Fibrin thrombi are found in the central veins, and freely lying threads and strands of fibrin are found in the sinusoids.
- Adrenal glands: Characterized by the disappearance of lipids (dystrophy), necrosis of the cortex and medulla, and microthrombosis. In severe infections (e.g., meningococcemia), extensive hemorrhages occur—a condition known as Waterhouse-Friderichsen syndrome.
- Pancreas: Edema, hemorrhages, and microthrombi can progress to severe pancreatonecrosis.
- Spleen: Hemorrhages under the capsule and into the parenchyma. Hyaline and fibrin thrombi are visible in small arteries and veins, and strands of fibrin are seen in the sinusoids.
- Gastrointestinal tract and skin: Small hemorrhages, erosions, and acute ulcers appear on the mucous membranes of the GI tract. On the skin, petechial rash and small foci of necrosis caused by capillary thrombosis are observed.
- Brain and myocardium: Edema, cellular dystrophy, microthrombi, as well as punctate hemorrhages and micronecrosis are recorded.
Briefly: answers to topical questions
What stages (phases) are distinguished in the classical pathogenesis of DIC?
Four successive stages are distinguished in the classical pathogenesis of DIC.
- Stage I — hypercoagulation and thrombosis (intravascular coagulation of proteins, platelet adhesion and aggregation).
- Stage II — progressive consumption coagulopathy (depletion of procoagulants and platelets, transition to hypocoagulation).
- Stage III — profound hypocoagulation and activation of fibrinolysis (pathological fibrinolysis, lysis of microthrombi).
- Stage IV — restoration of the blood coagulation system (end of the polyuria period).
What laboratory markers are used to confirm consumption coagulopathy in DIC?
To confirm consumption coagulopathy in DIC, a complex of laboratory markers reflecting the depletion of clotting factors is used.
- Platelets — critical thrombocytopenia is detected.
- Fibrinogen — significant hypofibrinogenemia with a decrease in concentration to 1–2 g/L.
- Antithrombin III — a critical drop in blood levels.
- FDP and D-dimer — a significant increase in the content of fibrin degradation products and D-dimer.
- Coagulogram — prolongation of thrombin time to 25–50 s and blood clotting time, a decrease in prothrombin index to 30–60%, changes in INR and aPTT.
What pathogenetic mechanisms, besides the release of fibrin, participate in the formation of hyaline membranes in the lungs?
In addition to fibrin, hyaline membranes contain tyrosine-α1-antitrypsin and the C3 complement component. Immaturity and deficiency of the surfactant system also contribute to the development of hyaline membranes; during meconium aspiration, surfactant inhibition leads to atelectasis and is often accompanied by the formation of hyaline membranes.
To memorize the classical triad of tissue changes in DIC, use the abbreviation HDN: Hemorrhage, Dystrophy, Necrosis. It is precisely these processes that develop in organs following microthrombosis.
Class and exam questions
Which thrombi predominate in the microvasculature in DIC?
In the vast majority of cases, fibrin microthrombi are formed. Hyaline, white, and red thrombi are much less common.
What is Waterhouse-Friderichsen syndrome?
This is a pathological condition characterized by extensive hemorrhages in the adrenal glands followed by their necrosis. It is typical for severe infectious pathology, in particular, meningococcemia.
What specific sign of DIC can be found in the lungs?
A specific microscopic marker is hyaline membranes. They are formed from fibrin threads that have penetrated from the blood vessels into the lumen of the pulmonary alveoli.
Who is at risk for developing Kasabach-Merritt syndrome?
This special variant of DIC develops predominantly in newborns and young children against the background of large hemangiomas. In adults, it is extremely rare.
What else to study on this topic
- Pathogenesis of consumption coagulopathy in Kasabach-Merritt syndrome
- Mechanisms of hyaline membrane formation in the pulmonary alveoli
- Morphogenesis of symmetric renal cortical necrosis
- Differences between local and generalized forms of DIC
- The role of tissue thromboplastin in the development of pulmonary complications
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