Disseminated intravascular coagulation

Introduction to disseminated intravascular coagulation Under the action of certain virulence factors, coagulation factors and platelets are activated, a large amount of procoagulant substances enter the blood, thrombin increases, and a wide microthrombus forms in the microcirculation. A large number of clotting factors and platelets are consumed in microthrombus formation, and secondary fibrinolytic function is enhanced, resulting in clinical manifestations such as hemorrhage, shock, organ dysfunction and hemolytic anemia. This pathological process is called DIC. basic knowledge The proportion of sickness: 0.01% Susceptible people: no special people Mode of infection: non-infectious Complications: acute renal failure, nausea and vomiting, abdominal pain, cerebral thrombosis, shock, anemia

Diffuse intravascular coagulopathy

Infection (30%):

Epidemic hemorrhagic fever, rash virus infection (smallpox, chickenpox, measles) infectious mononucleosis, cytomegalovirus infection, typhus, solid purple-negative bacilli infection (biliary infection, typhoid fever, fulminant cell dysentery , sepsis, etc.), solid purple positive cocci infection (burst purpura caused by hemolytic streptococcus, staphylococcus aureus sepsis, etc.), warfare syndrome of epidemic cerebrospinal meningitis, falciparum malaria.

Tumor and blood diseases (30%):

Prostate cancer, lung cancer, various mucinous adenocarcinomas of the digestive tract (especially extensively metastatic advanced tumors), various acute leukemias (especially promyelocytic leukemia), thrombotic thrombocytopenic purpura, hemolytic anemia.

Heart, lung, kidney, liver and other visceral diseases (20%):

Pulmonary heart disease, cyanotic congenital heart disease, severe heart failure, cirrhosis, acute or subacute hepatic necrosis, rapid glomerulonephritis, hemolytic uremic syndrome, hemorrhagic necrotic enteritis, hemorrhagic necrotizing pancreas Inflammation, diabetic acidosis, systemic lupus erythematosus, nodular arteritis and other connective tissue diseases.

Other (10%):

Shock caused by various causes, blood transfusion and infusion reactions, heat stroke, rejection after renal shift, snake bites, giant hemangioma, drug reactions and poisoning.

Disseminated intravascular coagulation prevention

(1) Prevention and treatment of primary diseases

Prevention and removal of the cause of DIC is a fundamental measure to prevent and treat DIC, such as controlling infection, removing stillbirth or staying in the placenta, and some mild DIC, as long as the cause is removed in time, the condition can be quickly restored.

(ii) Improving the microcirculatory diaturbance (Improvment of microcirculatory diaturbance)

The use of expanding blood volume, lifting vasospasm and other measures to clear the obstruction microcirculation early.

(3) Establishing a new equilibrium between coagulation and fibrolysis (Establish new balance between coagulation and fibrolysis)

In the high coagulation period, anticoagulant drugs such as heparin, low molecular weight dextran, aspirin, etc. can be used to prevent the initiation and progression of the blood coagulation process, prevent the formation of new blood clots, patients with very serious bleeding tendency, blood transfusion or supplementation of blood coagulation substances such as platelets. And the use of fibrinolysis inhibitors.

Disseminated intravascular coagulation complications Complications acute renal failure nausea and vomiting abdominal pain cerebral thrombosis shock anemia

1, skin thromboembolism: the most common, fingertips, toe end, nose tip, auricle skin blemishes, skin plaque hemorrhagic necrosis, dry necrosis.

2, renal thrombosis: oliguria, anuria, azotemia and other acute renal failure are the most common manifestations.

3, pulmonary thrombosis: difficulty breathing, cyanosis, hemoptysis, severe cases can occur acute lung failure.

4, gastrointestinal thrombosis: gastrointestinal bleeding, nausea, vomiting and abdominal pain.

5, cerebral thrombosis: irritability, lethargy, disturbance of consciousness, coma, convulsions, cranial nerve palsy and limb paralysis.

6, shock: limbs chills, bruising, oliguria and blood pressure drop. DIC caused by vascular endothelial injury is more common.

7, hemolysis: due to microvascular disease, red blood cells through mechanical damage, deformation and rupture and hemolysis. Clinically, there may be jaundice, anemia, and hemoglobin.

Disseminated intravascular coagulation symptoms Common symptoms Coagulation factor function disorders Abdominal pain Dyspnea convulsions Gastrointestinal bleeding coma Hair loss Sleepiness Nausea without urine

1, bleeding: light can only have a few skin bleeding points, severe cases can be seen in a wide range of skin, mucosal ecchymosis or hematoma, typically large skin ecchymosis, visceral bleeding, bleeding at the wound site.

2, thrombosis related performance:

(1) skin thromboembolism: the most common, fingertip, toe, nose, auricle skin blemishes, skin plaque hemorrhagic necrosis, dry necrosis.

(2) renal thrombosis: oliguria, anuria, azotemia and other acute renal failure are the most common manifestations.

(3) Pulmonary thrombosis: difficulty breathing, purpura, hemoptysis, severe acute lung failure may occur.

(4) Gastrointestinal thrombosis: gastrointestinal bleeding, nausea, vomiting and abdominal pain.

(5) cerebral thrombosis: irritability, lethargy, disturbance of consciousness, coma, convulsions, cranial nerve palsy and limb paralysis.

3, shock: acral chills, bruising, oliguria and blood pressure decreased, DIC caused by vascular endothelial injury is more common.

4, hemolysis: due to microvascular disease, red blood cells through mechanical damage, deformation and rupture and hemolysis, clinically may have jaundice, anemia, hemoglobin.

5, the symptoms of the primary disease.

Diffuse intravascular coagulation examination

The results of DIC laboratory tests vary according to their severity. Subacute DIC findings are thrombocytopenia, PT is normal or mildly prolonged, PTT is shortened, fibrinogen levels are normal or moderately reduced, and fibrin degradation products are elevated ( Since the stimulation of the lesion enhances fibrinogen synthesis, a low level of fibrinogen in the normal range, for example, 175 ml/dl) is not normal for the patient, and thus it is proposed to reduce fibrinogen production due to liver disease or to increase fiber due to DIC. The possibility of proteinogen consumption.

Acute severe DIC caused significant abnormalities in the test results, including thrombocytopenia; blood clots in the test tube were extremely small (sometimes even no visible blood clots); PT and PTT were significantly prolonged, plasma containing fibrinogen was insufficient, and was not recorded on the coagulation instrument. At the end point, the test results are often greater than a certain value, the instrument automatically reports to the interval before the next specimen (for example, >200 seconds); plasma fibrinogen is significantly reduced; plasma protamine paracoagulation test (check fibrin monomer) The results are positive; plasma D-dimer and serum have high levels of fibrin degradation products, and special coagulation factor tests show low levels of various coagulation factors, especially factors V and VIII (due to proteins activated during DIC) C causes the two factors to lose activity).

Large area of liver necrosis, abnormal results like acute DIC may appear in laboratory tests. The level of factor VIII is decreased in DIC, but the level of factor VIII is increased in hepatic necrosis because factor VIII is an acute phase protein. It is not only produced by hepatocytes, but also by spleen and kidney cells.

Diagnostic differential diagnosis of disseminated intravascular coagulation

diagnosis

The diagnosis of DIC is basically based on the etiology, pathogenesis and clinical manifestations of DIC. It is judged by comprehensive analysis of the primary disease, clinical symptoms and laboratory test results that cause DIC. In general, the diagnosis of DIC has three. in principle:

(1) There should be a primary disease that causes DIC.

(2) There are characteristic clinical signs and symptoms of DIC, such as hemorrhage, circulatory dysfunction, symptoms of dysfunction of one or some organs or positive results.

(3) Laboratory tests, the positive results of coagulation indicators, the most basic is the significant reduction of platelets, Fbg significantly reduced (except for excessive compensation), prothrombin time (PT) significantly prolonged, prolonged clotting time, 3P Positive test and shortened blood clot lysis time, etc., if the test results are contradictory, need to increase more specific indicators, for example, quantitative determination of plasma -platelet globulin (-thromboglobulin, TG) and platelet factor 4 (Platelet) The concentration of factor 4, PF4) to understand the degree of activation of platelets in the body; determination of thrombin-anfithmmbin III complex (TAT): to resolve the dynamic changes of thrombin generation in the blood; determination of plasma plasma D-aggregation Body or plasmin-2-antiplasmin complex (PAP) content to understand the presence of secondary fibrinolysis and the extent of secondary fibrinolysis, in the diagnosis of DIC, Laboratory diagnosis is very important. Due to the complicated etiology of DIC, there are many influencing factors, and various indexes of coagulation, anticoagulation and fibrinolysis system at different stages of onset. The changes in DIC's laboratory diagnostic standards vary from country to country, but most of them are based on Colman's early criteria. Colman's diagnostic criteria are: platelet count is lower than normal, PT is prolonged, Fbg is less than 2g/L. If only two of these three items are met, it is necessary to supplement a fibrinolytic index, such as whether the 3P test is positive, whether the thrombin time (TT) is extended for more than 3 sec, or plasma euglobulin is dissolved. Is the time (ELT) shortened (<70rain).

Differential diagnosis

1. Severe liver disease: due to multiple bleeding, jaundice, disturbance of consciousness, renal failure, decreased platelets and fibrinogen, prolonged prothrombin time, easy to be confused with DIC, but no thrombosis of liver disease, negative 3P test, FDP and The euglobulin dissolution time is normal.

2, thrombotic thrombocytopenic purpura: the disease is extensively formed in the capillary microthrombotic: microvascular hemolysis, thrombocytopenic purpura, kidney and nervous system damage, very similar to DIC, but this disease has a characteristic transparent thrombus, There is no red blood in the thrombus, white blood cells, no consumptive coagulation, so prothrombin time and fibrinogen are generally normal, and sometimes abnormal, pathological biopsy can confirm the diagnosis.

3, primary fibrinolysis: this disease is extremely rare, streptokinase and urokinase treatment is a typical example, this disease and DIC is extremely difficult to identify, because 1 can be induced by the same cause; 2 both have fibrinolysis characteristics : bleeding, FDP increased, the difference between the two is mainly fibrinolytic sites, DIC secondary fibrinolysis is a physiological response to thrombosis, the typical site is limited to microcirculation; primary fibrinolysis is in the large blood vessels, endothelial cell release is alive factor.

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