Disseminated intravascular coagulation (DIC) is a pathological process or clinical syndrome caused by various diseases and observed in the course of multiple conditions. Its main features include activation of the coagulation mechanism, widespread microvascular thrombosis, massive consumption of plasma coagulation factors and platelets, and activation of the fibrinolytic system, leading to secondary hyperfibrinolysis. This results in clinical manifestations such as extensive bleeding, shock, organ embolism, and hemolysis. DIC can be classified into acute, subacute, and chronic types based on the speed of progression. Acute DIC is more common in children, often seen in severe acute infections or after major surgeries. Subacute DIC may last from days to weeks and can occur in conditions like acute leukemia or malignant tumors. Chronic DIC may persist for months and is observed in cases such as giant hemangiomas or systemic lupus erythematosus.

bubble_chart Clinical Manifestations

1. Manifestations of the primary disease (or underlying disease), such as severe infections caused by various viruses, bacteria, and other pathogens.
2. Presence of two or more of the following clinical manifestations of DIC:
   1. Multiple bleeding tendencies: Often the initial symptom, ranging from skin petechiae to spontaneous bleeding in multiple sites, including skin ecchymosis, epistaxis, gastrointestinal or urinary tract bleeding, etc. Wounds often continue to ooze blood. Significant bleeding usually indicates progression to the consumptive hypocoagulable state phase, and bleeding worsens further in the advanced stage (hyperfibrinolysis phase).
   2. Microcirculatory failure or shock that cannot be easily explained by the primary disease.
   3. Symptoms and signs of multiple microvascular thrombosis: Due to widespread microthrombi formation in the microcirculation of various organs and tissues, leading to ischemia, hypoxia, metabolic disturbances, and functional impairment. Kidney involvement may present as oliguria, hematuria, or even renal failure; lung involvement may cause dyspnea or hemoptysis; gastrointestinal involvement may manifest as abdominal pain or hematochezia; cerebral embolism may lead to unconsciousness or convulsions. The formation of numerous fibrin strands and meshes in the microvasculature mechanically injures passing red blood cells, resulting in hemolysis (microvascular nature of disease hemolysis), which may lead to anemia in severe cases. Peripheral blood smears may reveal abnormal red blood cells (>2%).
   4. Effective response to anticoagulant therapy.

bubble_chart Auxiliary Examination

The main diagnostic criteria include the following three abnormalities simultaneously:

1. Platelet count <100×10⁹/L, or a progressive decline (in patients with liver disease or leukemia, DIC is indicated when platelets are below 50×10⁹/L). Alternatively, two or more of the following plasma platelet activation markers are elevated:
   1. β-thromboglobulin (βTG);
   2. platelet factor 4 (PF4);
   3. thromboxane B2 (TXB2);
   4. granule membrane protein 140 (GMP-140).
2. Plasma fibrinogen <1.5g/L或呈進行性下降(肝病DIC時<1Ig/L )，或>4g/L.
3. Prothrombin time is shortened or prolonged by more than 3 seconds compared to the normal control (or prolonged by more than 5 seconds in liver disease), or shows dynamic changes, or the activated partial thromboplastin time (APTT) is prolonged or shortened by more than 10 seconds.
4. 3P test is positive or plasma FDP > 20mg/L (>60mg/L in liver disease with DIC), or plasma D-dimer is elevated (positive) by more than 4 times.
5. Plasminogen content and activity are reduced.
6. Antithrombin III (AT-III) activity is decreased (<60%)，或蛋白C活性降低。
7. plasma factor VIII:C activity <50%(肝病者為必需項目)。
8. plasma endothelin-1 (ET-1) level > 80ng/L or thrombomodulin (TM) is elevated by more than 2 times.

For difficult or special cases, two or more of the following abnormalities should be present:

1. Factor VIII:C is decreased, AT:Ag is increased, VIII:C/vWF:Ag ratio is decreased.
2. Plasma thrombin-antithrombin complex or prothrombin fragment 1+2 (F1+2) levels are elevated, or fibrinopeptide A (FPA) levels are elevated.
3. Plasma plasmin and plasmin inhibitor complex (HC) concentration is elevated.
4. Plasma tissue factor (TF) level is elevated, or tissue factor pathway inhibitor (TFPI) level is decreased.

bubble_chart Diagnosis

Due to the lack of specific diagnostic indicators, a comprehensive diagnosis must be made by combining clinical and laboratory examinations. To date, there is no unified diagnostic standard. The following diagnostic criteria, established at the 7th National Conference on Thrombosis and Hemostasis of the Chinese Society of Hematology (1999), are provided for reference.

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1. Treating the primary disease and eliminating the disease cause are the fundamental measures for treating DIC. If the primary disease cannot be controlled, other treatments are unlikely to be effective. This includes the rational use of antibiotics, anti-allergy measures, anti-tumor therapies, etc.
2. Improve microcirculation
   1. Low molecular weight dextran can protect damaged vascular endothelium, reduce platelet adhesion and aggregation, decrease red blood cell aggregation, increase blood volume, reduce blood viscosity, and improve microcirculation. The dosage is 10–15 ml/kg intravenously, once or twice daily, or every 6–8 hours depending on the condition. It is contraindicated in the advanced stage of DIC as it may exacerbate bleeding.
   2. Vasodilators may be appropriately used. For microvascular spasm, tangut anisodus alkaloid (654-2) can be administered at 0.5–1 mg/kg per dose.
   3. Correct acidosis and improve hypoxia.
3. Block the progression of intravascular coagulation
   1. Anti-platelet aggregation drugs: Options include: (1) Dipyridamole: 10 mg/(kg·d), added to glucose solution for intravenous drip or divided into three oral doses. (2) Aspirin: 10–20 mg/(kg·d), divided into three oral doses. (3) Low molecular weight dextran: dosage as mentioned above.
   2. Use of heparin: (1) Indications: (a) Early-stage cases in a hypercoagulable state; (b) Cases with progressive consumption of coagulation factors and platelets and worsening bleeding; (c) Middle and advanced-stage cases may be treated in combination with replacement therapy and antifibrinolytic drugs; (d) For DIC prevention, such as during chemotherapy for acute leukemia. (2) Contraindications: (1) Contraindicated in cases of pulmonary subcutaneous nodule hemoptysis, ulcer bleeding, or neonatal birth trauma; (2) Contraindicated in cases with large-area wound bleeding. (3) Dosage and administration: Various methods can be chosen based on the condition: (a) General dosage: 0.5–1 mg (1 mg ≈ 125 U)/kg per dose, dissolved in 50–100 ml of 5–10% glucose or saline and infused intravenously over about 1 hour, or if necessary, dissolved in 20 ml of fluid and slowly injected intravenously, every 4–6 hours; (b) Low dose: 0.5–1 mg/(kg·d), divided into two doses, subcutaneously every 12 hours. This method has gained more support in recent years, especially for prophylactic administration. (4) Precautions: (a) Closely monitor the patient’s condition during use and adjust the dosage based on lab results; (b) Measure clotting time via the test tube method before each dose, aiming for a prolongation of 15–20 minutes; (c) Monitoring clotting time is generally unnecessary with low-dose use; (d) If bleeding worsens after administration, 10 ml of 10% calcium gluconate (diluted twofold) can be given intravenously. If ineffective, protamine can be used for neutralization, with a dosage equal to the last dose of heparin, usually starting with half the dose and giving the other half 15 minutes later if necessary; (e) Heparin can be discontinued once the condition improves, bleeding stops, and prothrombin time and fibrinogen levels return to normal; (f) If heparin is ineffective, consider whether the primary disease remains uncontrolled, acidosis is uncorrected, or plasma AT-III levels are too low. Low molecular weight heparin (LMWH) is increasingly recommended, as it has a longer duration of action, stronger affinity for AT-III, and is less affected by interfering factors.
   3. Other anticoagulants: Reports abroad describe the use of FOY and MD805, which are also effective in cases with significantly reduced AT-III levels where heparin is ineffective. Since heparin’s anticoagulant effect depends on normal AT-III levels, and AT-III decreases in DIC, AT-III should be supplemented, preferably using concentrated preparations (500–1000 U/d, dissolved in sterile distilled water and injected intravenously).
4. Supplemental therapy: During the hypocoagulable phase, coagulation factors and platelets should be supplemented when they are too low, but this must be done on the basis of anticoagulant therapy.
   1. Transfuse fresh plasma or whole blood, 10-15 ml/kg each time. If necessary, administer concentrated platelets at 1-2 units/10 kg, which can increase platelet count by 40-90×10⁹/L.
   2. Coagulation factor preparations such as fibrinogen and factor VIII preparations.
5. Use of fibrinolytic agents: For cases with obvious organ embolism symptoms (e.g., renal failure, cerebral embolism, etc.), urokinase or streptokinase may be selected.
6. Use of antifibrinolytic drugs: Only applicable in the advanced stage of DIC where hyperfibrinolysis is the primary cause of bleeding. These should be used in combination with heparin or after heparin therapy. They are contraindicated in the early stage of DIC, especially in cases with existing organ embolism. Commonly used drugs include 6-aminocaproic acid, tranexamic acid, and aprotinin (80,000–120,000 U per dose, followed by 10,000 U every 2 hours via intravenous drip).
7. Use of adrenal corticosteroids: Opinions remain divided. Generally, short-term use may be considered when the primary disease requires it, when platelet counts are significantly reduced with obvious bleeding tendencies, or during the advanced stage of DIC with hyperfibrinolysis. This should be administered based on anticoagulation therapy with heparin.