Disseminated intravascular coagulation

Introduction to diffuse intravascular coagulation Diffuse intravascular coagulation (DIC) is not a single disease, but a complex pathological process and clinical syndrome caused by multiple causes. It is characterized by extensive platelet aggregation and fibrin deposition in the microcirculation, resulting in diffuse microthrombus formation, secondary coagulation factors and massive consumption of platelets, and fibrinolysis, resulting in microcirculatory disorders, hemorrhage, hemolysis A series of serious clinical manifestations. The condition of acute disseminated intravascular coagulation is progressing rapidly, and if it is not treated in time, it is often life-threatening. basic knowledge The proportion of illness: 0.001% Susceptible people: no special people Mode of infection: non-infectious Complications: cerebral embolism, coma, respiratory failure, hematuria, nausea and vomiting, abdominal pain, intracranial hemorrhage, anemia, shock

Diffuse intravascular coagulopathy

There are many causes of DIC. According to the analysis of a group of materials in China, infection is common, accounting for more than 1/3 of the total number of cases, followed by malignant tumors (including acute promyelocytic leukemia). About 2/3 of the cause, extensive surgery, tissue damage, obstetric accidents, and extracorporeal circulation are also common causes of DIC.

Infection (35%):

Both Gram-negative and positive bacterial sepsis can be caused, but Gram-negative bacteria are more common, such as Escherichia coli, Proteus, Pseudomonas aeruginosa, and bacillus, Gram-positive bacteria such as Staphylococcus aureus, typhoid fever Bacillus, etc., Gram-positive bacteria such as Staphylococcus aureus, hemolytic streptococcus, Clostridium, etc., are less common caused by non-bacterial infections, such as viruses, ricketts, protozoa, spirochetes and fungal infections, etc. The pathogenesis of bacterial infection mainly includes the factors of bacterial infection itself and the endotoxin produced. After bacterial infection, vascular endothelial cell damage can release a large amount of tissue factor into the blood, promote blood coagulation, and complement activation of coagulation, fibrinolysis and kinin system. It is also related to endotoxin. It has been proved in experiments that the addition of endotoxin from Gram-negative bacteria to blood in test tubes can cause tissue factor activity on the primary membrane of monocytes, if a large amount of alkylating agent is used in rabbits. After consuming mononuclear cells, endotoxin does not produce DIC, and endotoxin exposure to vascular endothelial cells also produces tissue factor activity, but It has also been found that the ratio of Peptidogyciw (a peptide sugar that induces DIC) to the content of techoic acid in the cell wall of the bacteria-positive bacteria is also related to the occurrence of DIC. It is obvious that the pathology of DIC caused by infection is complicated and multi-faceted. Bradykinin has a strong relaxing effect on blood vessels and is one of the causes of blood pressure drop and shock in infection.

Malignant tumors (25%):

In cancer, pancreas, kidney, prostate, bronchial and other cancers, DIC is more common, acute promyelocytic leukemia is also easy to develop DIC, in cancer DIC is particularly prone to cases with extensive metastasis or massive tissue necrosis, This is because in these cases, tumor cells secrete a large amount of mucin, tissue factor, procoagulant, proteolytic enzyme, which has the pathological effect of promoting coagulation and promoting DIC. Trousseau syndrome is a case of chronic DIC in malignant tumor. , manifested as recurrent migratory arteriovenous thrombosis, and even the performance of the first.

Obstetric accident (15%):

Including amniotic fluid embolism, early exfoliation of placenta, hypertonic saline abortion, pregnancy toxemia, death of stillbirth, uterine rupture, caesarean section, etc., DIC can be seen, the mechanism of the disease is mainly due to a large number of tissue factors in tissues such as amniotic fluid and placenta Into the blood circulation, promote blood coagulation, in addition, hypercoagulable state and abnormal changes in blood vessels and blood flow may also be the cause of the disease.

The pathogenesis of DIC in various causes is not exactly the same. The main mechanisms for causing DIC are as follows:

1 severe head injury complicated by DIC may pass through the damaged blood-brain barrier, enter the blood circulation, promote blood coagulation, 2 venomous snake bite causes DIC, in addition to tissue damage, release a large amount of tissue factor, into the blood In addition to promoting blood clotting, the secretory substances of snake venom itself also have the effect of converting fibrinogen into fibrin. 3 immune diseases such as systemic lupus erythematosus, rejection of grafts, etc. cause DIC, mainly due to the abnormal immune mechanism in diseases. Vascular endothelial cell injury, complement activation is related to the promotion of coagulation mechanism, 4 liver diseases such as acute liver necrosis, cirrhosis and other cases with severe liver damage, DIC is also prone to occur, except for the similar vascular endothelial damage And the effect of procoagulant substances, on the other hand, the reason is due to the weakening of the function of phagocytosis and clearance of procoagulant substances in liver diseases, 5 body temperature rise, acidosis, shock, hypoxia-induced damage of vascular endothelial cells, can be induced Or aggravate DIC, hemolytic disease or hemolytic reaction, red blood cells can also promote procoagulant substances Onset or worsening DIC.

The most important change in the pathogenesis of DIC is due to the consequences of thrombin and plasmin. The effects of the two in the body produce a lot of blood coagulation and fibrinolytic activity, the role of the two can be due to different causes The severity of the disease varies greatly, and it can also produce different changes in different phases of the disease. It is found through a series of laboratory tests. In the role of thrombin, the fibrinogen is first decomposed into protein peptide A. Forming fibrin monomer, the monomers polymerize into fibrin and form a thrombus under the cross-linking of factor VIII, but fibrin (original) can also form a soluble complex with fibrin cleavage product (FDP), thrombin It can also activate factors V, VIII, XIII, protein C system and platelets, and stimulate the production of various active mediators such as platelet activating factor (PAF), prostacyclin, VW factor, etc. Thrombin can also affect the fiber through vascular endothelial cells. Solubilization system, therefore, changes in the body's thrombin activity will cause various changes in the body related to biochemical coagulation active substances, the combined result is fibrinogen, Factor II, V, VIII, XIII, protein C and platelets are reduced due to large consumption, platelet dysfunction, plasminogen is activated by various activators and also by tissue plasminogen activator It turns into lysozyme, and fibrinolytic enzyme acts on fibrin (former) to form FDP/fdp. FDP can inhibit the formation and polymerization of fibrin, inhibit platelet activation, and can decompose and inactivate blood coagulation factors, so that fibrin, factor V, The content of VIII, IX is reduced. From the results of the above two effects, the changes in coagulation and fibrinolysis in the body are extremely complicated in the occurrence of DIC.

In addition, the reduction of anticoagulant substances in DIC includes antithrombin III, a component of protein C system, and tissue pathway inhibitory factor.

Diffuse intravascular coagulation prevention

It is necessary to pay attention to changes in cold and warm, regulate cold and dampness, have a happy spirit, and have a mild condition. It can be properly active. If there is strong heat, hemorrhage is severe, and the patient is extremely depleted, the condition should be carefully observed for early diagnosis. Late patients should try to reduce acupuncture. On the diet, if it is true heat and yin deficiency and blood stasis, it is necessary to avoid spicy and irritating products so as not to seriously harm the body fluid and aggravate the condition.

Diffuse intravascular coagulation complications Complications cerebral embolism coma respiratory failure hematuria nausea and vomiting abdominal pain intracranial hemorrhagic anemia shock

Common complications of this disease are:

1. When the brain is embolized, coma, convulsions, etc. may occur, such as liver dysfunction, terminal necrosis, etc.;

2. Sudden difficulties, cyanosis, respiratory failure, or right heart failure due to pulmonary hypertension may occur when the lung is involved;

3. When the kidney is involved, it shows oliguria, hematuria, and even kidney failure.

4. Nausea, vomiting, abdominal pain and gastrointestinal bleeding occur when the gastrointestinal tract is involved;

5. Severe urinary tract bleeding or intracranial hemorrhage, more bleeding can be anemia or shock, or even death.

Diffuse intravascular coagulation symptoms common symptoms aortic blood supply disorder dry necrosis of the ear shell jaundice skin bleeding point of consciousness disorder diarrhea abdominal pain drowsiness bleeding tendency

Clinical Classification

(1) acute type: acute onset, often in a few hours or 1 ~ 2d onset, the condition is dangerous, rapid progress, bleeding, shock and other symptoms are obvious

Serious, common in acute infections, acute trauma and major surgery, acute hemolysis caused by blood transfusion, amniotic fluid embolism and other causes of diffuse intravascular coagulation.

(2) Subacute type: the disease occurs within days to weeks, and the condition is more moderate than the acute type. It is common in various cancers and acute leukemia, and the stillbirth remains.

(3) Chronic type: slow onset, sometimes up to several months to several years, seen in chronic liver disease, pregnancy poisoning, connective tissue disease, giant hemangioma, etc., clinical bleeding is light, shock and thrombosis are rare, often need It was discovered after laboratory inspection.

The above clinical types are often related to the amount and speed of the procoagulant into the bloodstream. If the procoagulant substance enters the bloodstream rapidly, it often appears as an acute type. When a small amount of procoagulant substance is added and slowly enters the bloodstream, it is often expressed as Subacute or chronic.

Clinical manifestation

(1) Bleeding: The bleeding of this disease is characterized by spontaneous and extensive bleeding. The bleeding site can only see the bleeding point of the skin. In severe cases, it can be seen in a wide range of skin, mucosal hemorrhage or hematoma. It can also have gastrointestinal tract, lung and urinary tract. Genital bleeding, there may be fulminant local gangrene, the characteristic of bleeding is surgical incision, wound, acupuncture site bleeding, bleeding or bleeding during childbirth, clinical bleeding severity, cerebral hemorrhage, Gastrointestinal bleeding and pulmonary hemorrhage are often the cause of death.

(2) shock: shock or hypotension is common in acute and subacute types, ranging from mild to severe, may occur in a short period of time or irreversible development, more common in diffuse intravascular coagulation caused by vascular endothelial injury, tissue damage ( Such as tumor, leukemia, the disease is rarely accompanied by hypotension, the disease is characterized by: 1 majority of refractory shock; 2 pulmonary artery and portal pressure increased, and central venous pressure and arterial pressure decreased; 3 micro Circulatory dysfunction, blood stasis, increased capillary pressure, extracorporeal fluid, blood volume reduction, shock will increase the disease, resulting in a vicious circle, poor prognosis.

(3) Embolization: extensive microvascular embolism, causing hemodynamic disorders, leading to ischemia and hypoxia, metabolic disorders, and dysfunction of various tissues and organs. The general symptoms of embolism are local congestion, hemorrhage or acromegaly. Long-term embolization of the tip can cause rhinitis, dry necrosis of the ear shell, visceral embolism is common in the liver, kidney, lung, brain, gastrointestinal tract or multiple organs at the same time, manifested as oliguria, respiratory difficulties, confusion, Coma, convulsions, abdominal pain, diarrhea and low back pain.

(4) Hemolysis: intravascular hemolysis can lead to the disease, and conversely, the formation of microthrombus and fibrin deposits during disseminated intravascular coagulation causes red blood cells to deform, break and hemolyze, and may have fever and jaundice during acute hemolysis. Low back pain, hemoglobinuria, severe oliguria or anuria, a large amount of hemolysis and hemorrhage, so that anemia and its accompanying symptoms can also be seen clinically.

(5) Nervous system: cerebral hypoxia, edema, and hemorrhage caused by extensive thrombosis and shock in the intracranial microvessels, reflecting a series of neurological symptoms and signs, such as lethargy, irritability, disturbance of consciousness, coma, Convulsions, cranial nerve palsy and limb paralysis, cerebral hemorrhage, cerebral edema, and large arterial blood supply disorders can directly cause death.

Diffuse intravascular coagulation examination

Laboratory inspection

(1) Tests reflecting coagulation factors and platelet consumption: 1 platelet count: in this disease, due to the massive consumption of platelets to form microthrombus, the platelet count is reduced, 2 clotting time: in the early stage of disseminated intravascular coagulation, the blood is in a high coagulation State, clotting time is often shortened within 5min, even in the needle tube when the blood is collected, this phenomenon is very helpful for the early diagnosis of the disease, the late secondary fibrinolysis, blood hypocoagulable state, so blood coagulation Most of the time is prolonged, 3 prothrombin time (PT): prolonged prothrombin time in most patients, some patients are normal early, prolonged with the development of the disease, 4 thrombin time (TY): patients with acute disseminated intravascular coagulation Prolonged, individual patients may also be normal or shortened, 5 fibrinogen (Fg) is quantitatively determined: most patients are less than 150mg / dL, some patients are normal or shortened in the early stage, and gradually prolonged in the course of disease, 6 part of the white clay soil coagulation Live enzyme time (KPTT): Prolonged factors suggesting a decrease in the factor involved in the production of thromboplastin, but in patients with chronic disseminated intravascular coagulation, KPTT can be normal .

(2) Examination of fibrinolytic hyperactivity: 1FDP determination: secondary coagulation test - 3P test: more false positives, but less false negatives; ethanol gel test: soluble complex of fibrinogen and FDP combined with ethanol When there is a gel formation, this test has a false negative result, but its specificity is high, false positives are less, 2 euglobulin lysis time (ELT) determination: this test reflects the level of plasmin, normal > 120min The positive rate of this test is low, about 30% to 50%, 3 plasminogen determination: normal plasma is rich in plasminogen, pre-activin is activated during diffuse intravascular coagulation, plasminogen conversion Fibrinolytic enzyme, so plasminogen decreased, tyrosine as a substrate to determine its viability, the normal value of 7 ~ l1U / Iml.

(3) Determination of antithrombin III (AT-III): The determination methods include coagulation method, radioimmunoassay and chromogenic substrate assay. The latter is sensitive and accurate, and the blood collection is only a few microliters, which can provide rapid clinical delivery. diagnosis.

(4) Blood film: Peripheral blood smear is observed under the microscope. If there are red blood cell fragments, spines, helmets, triangles or irregular red blood cells, it is also helpful for the diagnosis of this disease.

(5) Determination of fibrin peptide A (FPA) and peptide B (FPB): thrombin can cleave fibrinogen aA chain and aB chain, and release FPA and FPB successively, so plasma FPA and FPB content increase, reflecting thrombin The activity is enhanced, and the incidence of FPA is increased in 100% of patients.

(6) Determination of fibrin peptides B1-42 and B15-42: At the time of onset, due to the hyperfibrinolysis, the plasma level of plasmin increased, hydrolyzing the fibrinogen B chain, releasing B1-42; Lysozyme hydrolyzed soluble fibrin monomer released B15-42, so plasma B1-42 and B15-42 levels increased, reflecting the enhancement of fibrinolytic activity.

(7) D-dimer assay: plasmin activity enhances hydrolysis of factor VIII, cross-linked fibrin, which produces D-dimer, so the plasma content of D-dimer is increased or positive, indicating Diffuse intravascular coagulation has fibrin degradation and secondary fibrinolysis.

Diagnostic diagnosis of diffuse intravascular coagulation

Diagnostic criteria

(1) There are primary diseases that can induce diffuse intravascular coagulation and factors that contribute to the onset of disseminated intravascular coagulation.

(2) Have more than two of the following clinical manifestations: 1 repeated, severe or multi-site bleeding tendency; 2 unexplained refractory hypotension or shock; 3 emergence of lung, brain, liver, skin, subcutaneous and limb embolism, Symptoms and signs of microcirculatory disorders, especially acute renal function or pulmonary insufficiency that is not consistent with the primary disease; 4 rapid development of progressive anemia that is difficult to explain; 5 heparin or other anticoagulation The treatment is effective.

(3) Laboratory tests meet the following criteria: 1 The following three abnormalities occur simultaneously: one is that the platelet count is less than 100×109/L or progressively decreased; the other is that plasma fibrinogen is less than 150 mg/dl or progressively decreased; Third, the prothrombin time is prolonged by more than 3 s; 2 if only 2 of the above 3 experimental examinations are abnormal, then 1 to 2 of the following 4 items must be abnormal; the clotting time is prolonged by more than 5 s; the 3P test is positive, or Ethanol gel test, staphylococcal aggregation test, FDP quantification one of them is abnormal; euglobulin dissolution time is less than 70min or plasma plasminogen content is reduced; more than 2% of fragment red blood cells and various abnormal red blood cells can be seen in blood samples.

Differential Diagnosis

1. Primary fibrinolysis: This disease is clinically rare. It is due to certain factors that enhance the activity of plasminogen activin, resulting in the conversion of a large amount of plasminogen to plasmin, causing fibrinogen and Factor V, VIII and other factors caused by the decomposition of blood coagulation factors, clinical manifestations of bleeding at various sites, primary fibrinolysis is common in severe liver disease, liver-free liver transplantation, anti-plasminogen activin and liver disease The production of anti-plasmin is reduced, and the disease can also be seen in the lungs, prostate, uterus and other serious diseases, or certain drug poisoning, profibrosis can occur, there are also unexplained fibrinolysis, but organ function Obstacles are not obvious, generally do not lead to acute renal failure and shock, the main clinical manifestations of fibrinolysis are extensive severe bleeding, normal or slightly lower platelet counts in the laboratory, negative in the 3P test, euglobulin lysis The time was significantly shortened, FVIII: C was normal, platelet -TG was normal, and treatment with anti-fibrin solvent was effective, and heparin treatment was ineffective.

2. Insufficient fibrinogen production: if the normal plasma fibrinogen content is less than 60% to 80%, there will be bleeding in the clinic, and hereditary fibrinogen deficiency is rare. Patients will have different degrees of life. The bleeding symptoms, half of the patients with post-natal umbilical cord bleeding as the first symptom, in addition to this may have nasal discharge, blood in the stool, vomiting blood or blood in the urine, about 21% of patients have joint bleeding, menorrhagia is rare, laboratory tests: no Decreased platelet count and hyperfibrinolysis; prolonged clotting time; complete lack of fibrin determination, no blood coagulation; prolonged prothrombin time.

3. Severe liver disease bleeding.

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