What Is Coagulopathy?

Consumptive coagulopathy (abbreviated as DIC) is a syndrome, not an independent disease. It is caused by extensive fibrin deposition and platelet aggregation in capillaries, arterioles, and small veins under the action of various pathogenic factors. Microthrombus. Causes circulatory and other visceral dysfunction, wasting coagulopathy, secondary fibrinolysis, and produces clinical manifestations such as shock, bleeding, embolism, and hemolysis. In the past, it was called defibrination, consumption coagulopathy, and recently it was thought that consumption thrombohemorrhagic disease was appropriate, but the most commonly used is diffuse intravascular coagulation.

Wasting coagulopathy

Consumptive coagulopathy is a syndrome. It is caused by a variety of pathogenic factors, extensive fibrin deposition and platelet aggregation in capillaries, arterioles, and small veins, forming extensive microthrombus. Causes circulatory and other visceral dysfunction, wasting coagulopathy, secondary fibrinolysis, and produces clinical manifestations such as shock, bleeding, embolism, and hemolysis.

Introduction to wasting coagulopathy

Causes of wasting coagulopathy

There are many causes of DIC. According to data analysis, infection is the most common in China, followed by malignant tumors (including acute leukemia), both of which account for 2/3 of the etiology. Reports abroad show that malignant tumors, especially those with metastatic disease, are the first. Extensive tissue trauma, cardiopulmonary bypass, and obstetric accidents are also common causes of DIC. The etiology of DIC involves blood itself and other factors, which can be summarized as follows:

(I) Endothelial injury and tissue trauma

1. Infections A variety of serious bacterial infections (such as Staphylococcus aureus, Gram-negative bacilli, toxic bacteria, typhoid, etc.) can cause DIC. Both bacteria and their toxins can damage tissues and vascular endothelial cells. The activation factors kinin and bradykinin activate the coagulation system, which also has a strong vasomotor effect, which can dilate blood vessels and lower blood pressure. Cause shock. The kinin system has a strengthening effect on the coagulation process. Complement is also closely related to coagulation, fibrinolysis, and plasma kallikrein system, which is also one of the factors of thrombosis. Recently found that white blood cells also play an important role in the mechanism of activating coagulation. It is affected by endotoxin and can release tissue factors. When combined with factor , it can activate factor X to promote coagulation. Viral infections (such as epidemic hemorrhagic fever, severe Japanese encephalitis, etc.), malaria, leptospirosis, rickettsial disease, and rickettsial infections can also cause DIC. Its pathogenesis is roughly similar to bacterial infections. 2. The formation of antigen-antibody complexes. Various immune reactions and immune diseases can damage vascular endothelial cells, activate complement, can also cause platelet aggregation and release reactions, and activate coagulation mechanisms, such as systemic lupus erythematosus, graft rejection or other immune Sexually transmitted diseases.

3 Others such as elevated body temperature, acidosis, shock or persistent hypotension, and hypoxia can damage the endothelial cells of the blood vessel wall.

(B) A large number of procoagulant substances entering the blood circulation are common in obstetric accidents, such as amniotic fluid embolism, early placental dissection, and stillbirth. Tissue factors released by amniotic fluid, placenta, etc. enter the blood circulation in large quantities and induce DIC. Severe trauma is also a common cause of DIC, such as severe burns, extensive surgery, crush syndrome, poisonous snake bites, etc. can release a large number of tissue factors from the damaged tissue into the blood and promote coagulation. In addition, in the extensive metastasis of cancer and tissue necrosis (especially pancreatic, stomach, prostate and bronchial cancer), the tissue coagulation active substances contained in tumor cells activate the exogenous coagulation system, produce a large amount of thrombin and promote coagulation. Proteases in tumor cells can also activate coagulation factors and promote coagulation. Chemotherapy and radiotherapy kill tumor cells to release procoagulant substances, and DIC is more likely to occur.

(3) The destruction of a large number of red blood cells, platelets and white blood cells or damage of red blood cells and platelets releases phospholipids similar to tissue factors. After red blood cells are destroyed, erythropoietin is released, which has similar tissue thromboplastin activity, and can be released after platelet destruction A series of procoagulant active substances was produced. Recently discovered that neutrophil damage is also an important part of the pathogenesis of DIC, and may also be a necessary condition for the formation of microthrombus. The involvement of neutrophils in the occurrence of DIC may be related to the role of factor IXa in activating complement. When activated, complement can damage granulocytes, release protease-like coagulation active substances from it, and promote blood coagulation.

(4) Other factors

1. Impaired monocyte function can promote the development of DIC. Under normal circumstances, the monocyte-macrophage system, including Kupffer cells in the liver, can engulf or clear procoagulant substances such as thrombin, fibrin particles, and endotoxins that enter the blood. Diseases such as acute liver necrosis or cirrhosis have impaired liver function, weaken their phagocytosis and clearance functions, and are prone to DIC. Long-term use of a large number of adrenocortical hormones can easily induce DIC, which is related to the obstruction of the monocyte-macrophage system. 2. The original health status of patients with original health status also has important effects, such as pregnant women often have a tendency to hypercoagulability, malnutrition, especially glucose metabolism disorders, prone to DIC. 3 The fibrinolytic system is inhibited, such as the long-term use of large amounts of anti-fibrinolytic drugs, such as 6-aminocaproic acid, tranexamic acid, p-carboxybenzylamine, can induce DIC. There are also blood stasis, acid-base imbalances, electrolyte disorders and endocrine disorders, which are all related to the occurrence of DIC.

Pathogenesis of wasting coagulopathy

When the human body is affected by certain pathogenic factors, the blood coagulation system is activated, blood coagulation activity is increased, platelet aggregation and fibrin deposition occur in the microcirculation, and disseminated microthrombuses are formed. This feature is also known as: Defibrin syndrome; Consumptive coagulopathy; Intravascular coagulation-fibrinolysis syndrome. Currently collectively referred to as disseminated intravascular coagulation.

Normal human body has a complete coagulation, anticoagulation and fibrinolytic system. Coagulation and anticoagulation are both opposite and unified, maintaining a dynamic balance. In normal human blood, if a small amount of active coagulation intermediates are formed, they are quickly eliminated by the monocyte-macrophage system or neutralized by anticoagulants in the blood. The fibrinolytic system can continuously dissolve a small amount of fibrin formed in small blood vessel damage. The occurrence of DIC is due to the action of various pathogenic factors, a process that promotes and activates blood coagulation in the blood circulation, and produces excessive thrombin. The blood's coagulability is too high, which disrupts the balance between coagulation and anticoagulation in the body. The pathological changes include: extensive fibrin deposits in microvessels throughout the body, forming microthrombus, causing microcirculation disorders, mechanical damage to red blood cells, and hemolysis; when coagulation occurs in the microcirculation, a large number of platelets and coagulation factors are consumed, thereby The state of high coagulation is changed to the state of low coagulation; secondary fibrinolysis in the body produces a large amount of plasmin, which causes fibrinogen to be broken into X, A, B, and C lobes, and then further broken into Y, D, and E lobes. . The anticoagulant effects of these fibrin (pro) degradation products can aggravate bleeding. In addition to a large amount of bleeding, thrombus in the microcirculation can cause microcirculation obstruction, leading to the failure of lungs, kidneys, liver, brain, heart and other organs.

Wasting coagulopathy

About 90% of DIC cases can be found at the time of autopsy with microthrombosis or fibrin deposition in the blood vessels, which are more common in the lungs, kidneys, gastrointestinal tract, and adrenal glands. In a group of 52 autopsy results, the incidence of pulmonary embolism was 54.6%, the kidney was 36.5%, and the gastrointestinal tract was 34.6%. The smaller microthrombus was easily ignored when hematoxylin-eosin stained. Need to stain with Mallory phosphotungstate hematoxylin, etc. or confirm with electron microscope. Microthrombus can sometimes be seen only in some local organs, but not found in circulating blood, and there are some cases of clinically confirmed DIC, but there is no thrombosis in autopsy, which may be caused by fibrinolysis after death. To. If using electron microscopy, combined with special staining, fibrin deposits can still be found on the surface of vascular endothelium. Renal lesions can be manifested as localized tubular necrosis or severe cortical necrosis on both sides, with a few cases of non-embolic endometritis or hyaline pulmonary lesions in the lungs.

Classification and staging of wasting coagulopathy

According to the speed and duration of intravascular coagulation, it can be divided into 3 types:

1. The acute type is characterized by: sudden onset, usually lasting several hours or days; dangerous condition, can be violent; severe bleeding tendency; often accompanied by shock; common in fulminant meningitis, epidemics Hemorrhagic fever, pathological obstetrics, sepsis, etc.

2. The subacute type is characterized by: acute onset, which develops within a few days or weeks; slow progress, common in malignant diseases, such as acute leukemia (especially promyelocytic leukemia), tumor metastasis, and stillbirth And local thrombosis.

3 The chronic type is rare clinically: the onset is slow; the course of the disease can be months or years; the period of hypercoagulation is obvious, the bleeding is not heavy, and there can be only stasis spots or stasis.

According to blood coagulation, bleeding and fibrinolysis, DIC can be divided into 3 stages:

1. Hypercoagulable phase only increases blood coagulation during blood draw, and more common is chronic type, which can also be seen in subacute type, and acute type is not obvious.

2. The consumptive hypocoagulation period is due to the large consumption of plasma coagulation factors and platelets, which reduces blood coagulability and obvious bleeding symptoms.

3 In the secondary fibrinolytic phase, due to intravascular coagulation, the fibrinolytic system is activated, causing secondary fibrinolysis and bleeding symptoms are more obvious.

Clinical manifestations of wasting coagulopathy

Although the causes of DIC are different, the clinical manifestations are similar. In addition to the signs of the primary disease, there are mainly four aspects of bleeding, shock, embolism and hemolysis.

DIC is divided into three types: acute, subacute and chronic. Among them, acute is the most common. It is common in Gram-negative bacillus infection, sepsis, epidemic hemorrhagic fever, obstetric accident, acute hemolysis, incompatible blood transfusion type, poisonous snake bite, extensive major surgery. , Cardiopulmonary bypass, severe crush injuries and compound trauma, the disease is dangerous. Subacute DIC is seen in leukemia, various cancers, cancer metastasis, or stillbirth, and the condition is relatively mild. Chronic patients are rare. The clinical manifestations can be masked by primary diseases, and they are easily missed or misdiagnosed. They are often found in autopsy. They are more common in systemic lupus erythematosus, ovarian cancer, giant hemangioma, and advanced diabetes.

(A) Bleeding Bleeding is one of the most common clinical manifestations in acute DIC. It is characterized by sudden and massive bleeding at multiple sites, with only a few being insidious. The incidence of bleeding is 80-90%, which is one of the important basis for the diagnosis of this disease. The bleeding site varies depending on the primary lesion. It is most common on the skin and presents one or more large ecchymoses and hematomas. There is a large amount of vaginal bleeding during an obstetric accident. During the operation, the wound does not stop bleeding or the blood does not coagulate. Local injection may have continuous pinhole bleeding. Acute DIC can also be accompanied by severe bleeding from the gastrointestinal, lung, or urinary tract. According to a group of domestic reports, skin accounts for 85.1% of bleeding sites, gum bleeding, epistaxis, wound and injection site bleeding of 60.1%, digestive tract 46.8%, respiratory tract 23.4%, urinary tract 19.1%, intracranial 13.8%, The vagina was 6.4%, with multiple sites accounting for 62.8%. The blood can be completely non-condensing. Outbreaks of fulminant purpura are mainly in the lower limbs and buttocks, and chronic DIC bleeding with skin necrosis and lower limb gangrene is not as severe as acute, often manifested as recurrent ecchymosis or hematoma, which is ineffective with general hemostatic drugs. A few minor or early DICs can be without bleeding. The mechanism of bleeding is: Consumption of a large number of platelets and coagulation factors after extensive coagulation in blood vessels, causing coagulation disorders; A large amount of fibrin degradation; Fibrinogen and fibrin degradation products have various aspects of anticoagulation; Hypoxia and acidosis can damage capillaries and increase permeability.

(II) Symptoms of microvascular embolism In a few acute cases, microvascular embolism can be a prominent feature, but most of them occur at a later stage. Chronic may have recurrent attacks. For example, when there is extensive thrombus in the microvessels, the blood circulation is impaired, resulting in ischemic damage to tissues and organs, hypoxia, metabolic dysfunction, and even organ failure. Clinical manifestations vary according to the different sites involved. Superficial skin embolism causes dry necrosis that occurs in the fingers, toes, nose, cheeks, and ears. Visceral embolism is most common in the lungs and kidneys. When there is extensive thrombus in the glomerular circulation, acute renal failure can occur, manifested as low back pain, oliguria, proteinuria, hematuria, cast urine, and even anuria and uremia. Lung microcirculation embolism can cause acute respiratory failure, manifested as respiratory distress syndromes such as sudden onset of dyspnea, chest tightness, and cyanosis. Gastrointestinal mucosa ischemia and necrosis cause gastrointestinal bleeding. Focal necrosis of the liver. Patients with cerebral embolism may have headaches, convulsions, coma, and pupil sizes. Hypofunction occurs when pituitary and adrenal cortex are formed.

(3) Hypotension and shock are more common in the acute type, the degree of shock varies, and it is not proportional to the amount of bleeding. It often occurs in DIC caused by vascular endothelial injury, with Gram-negative bacillus sepsis being the most common. Several groups of domestic reports have an incidence of 50%. Shock often occurs suddenly, the condition rapidly deteriorates, coma occurs, and renal, respiratory, and circulatory failure occur. Shock rarely occurs due to tissue damage and leukemia. The mechanism of shock is mainly due to the embolism of the internal organs and surrounding small blood vessels such as the liver and lungs, which leads to increased pressure in the pulmonary arteries and portal veins and a decrease in returning blood volume, leading to a decrease in cardiac output and tissue blood perfusion. In addition, when the endogenous coagulation system is activated, factor is activated, and kallikrein is converted to kallikrein, which converts bradykinin to bradykinin, causing vasodilation and also a cause of lowering blood pressure. Once shock occurs, it will aggravate DIC and form a vicious circle.

(4) Hemolytic anemia caused by hemolytic DIC is usually mild, and it is often difficult to detect at an early stage. When the microvascular pathological changes are complicated, the red blood cells forcibly pass through the vascular reticulum structure and suffer mechanical damage, which may cause obvious hemolytic symptoms. Acute attacks are manifested by chills, fever, jaundice, hemoglobinuria, decreased red blood cell counts, increased reticulocyte counts, and a large number of red blood cell fragments and various deformed red blood cells such as helmet-shaped, triangular, polygonal, or spherical in the surrounding blood.

The symptoms of primary disease can be confused with those of DIC. The above four types of manifestations can occur simultaneously or sequentially. Acute patients often have any of the two clinical manifestations described above. In the early stages of onset of DIC, organ dysfunction caused by shock and microthrombus is the main cause; in the later stage, bleeding is the most prominent symptom. Subacute and chronic DIC are mainly manifested by bleeding, while shock and organ dysfunction are rare.

Wasting coagulopathy laboratory test

There are many DIC examination items, but they lack specificity, high sensitivity, and simple and fast methods. Some tests are more accurate, but it takes too much time to adapt to the requirements of emergency diagnosis. Due to the rapid development and large changes of DIC, the test results must be timely and accurate, and if necessary, repeated inspections and dynamic observations are needed, because the test results at different stages of DIC are not the same, due to different strengths of the body's compensation function. . When the test results are inconsistent with clinical manifestations, the significance of the test results should be properly evaluated. Sometimes clinical manifestations may be more important than a positive test result. DIC's laboratory tests are mainly divided into the following:

(I) Examination of wasting coagulopathy 1. Thrombocytopenia is present in about 95% of cases, generally below 100,000 / mm3. If the continuous decline of platelets is found in dynamic observation, the diagnosis is of great significance. If DIC is not completely treated, the platelet count does not increase despite transfusion of blood or platelets. Conversely, if the number of platelets is above 150,000 / mm3, it is unlikely that DIC is present. In some patients with liver disease or leukemia, platelets have been significantly reduced before the occurrence of DIC, so platelet counts are not helpful in the diagnosis of DIC.

2. Prolonged prothrombin time When exogenous system factors , , , and X are consumed in large amounts, fibrinogen degradation products and anticoagulant substances in plasma increase, prothrombin time is significantly prolonged, and the positive rate can reach 90%. The diagnosis of DIC is generally not supported unless the prothrombin time measurement is normal in the very early stages of DIC. The normal prothrombin time is 12.0 ± 0.1 seconds, and it is meaningful to extend it for more than 3 seconds.

3 Fibrinogen is reduced by about 70% of DIC cases, and fibrinogen is less than 200 mg / dl. In the original high fibrin level or in the early stages of DIC, the fibrinogen reduction was not significant, and the quantitative measurement was normal. Dynamic observations can see the tendency of continuous reduction of fibrinogen, generally below 150 mg / dl, it has diagnostic significance. . The method of semi-quantitative fibrinogen titer is simple and practical.

4 Others, such as prolonged bleeding time, prolonged coagulation time, poor clot withdrawal, and prolonged clotting time, are also of reference significance to the diagnosis and help the diagnosis of DIC.

(B) Examination of fibrinolysis

1. Prolonged thrombin time When the fibrinogen is significantly reduced or the fibrinogen (proto) degradation products (FDP) are increased, the thrombin time is prolonged, but the measurement results can be affected by heparin treatment. The use of continuous thrombin time is a more sensitive indicator for the diagnosis of FDP.

2. Plasma snake venom coagulation time The thrombin time was measured using an enzyme (Reptilase) extracted from snake venom instead of thrombin. When the FDP increases, the clotting time is prolonged, and the advantage of this method is that it is not affected by heparin.

3 Inspection of fibrin degradation products There is only a trace amount of FDP in normal human serum. If FDP is significantly increased, it means that there is an increase in fibrinolysis, which indirectly reflects DIC. There are many methods for determination, including the immunoassay Fi test (ie latex particle agglutination test, normal titer <1: 8), FDP flocculant test, radioimmunoassay, staphylococcus hedgehog test (normal FDP value is 0.57 ± 0.1 g / dl, up to 60 g / dl in DIC), indirect hemagglutination inhibition test of tannic acid ratio to red blood cells (normal serum FDP value <10 g / dl, more than 20 g / dl in DIC), enzyme membrane immunoadsorption technology, etc. An increase in FDP indicates the possibility of acute DIC.

4 Plasma protamine paracoagulation test (referred to as 3P test) and ethanol gel test This is a test that reflects the soluble fibrin complex in plasma. When intravascular coagulation occurs, FDP combines with fibrin monomers to form a soluble complex that cannot be coagulated by thrombin. Protamine can separate the complex and re-precipitate the fibrin monomer. As a result, the self-polymerization of fibrin monomer and FDP occurred, forming a flocculent precipitate visible to the naked eye, which is called a paracoagulation test. The principle of the ethanol gel test is the same as the 3P test. Domestic data report that the positive rate of the 3P test is 72.6-88.2%, and the positive rate of the ethanol gel test is low. Both methods can have false positive or false negative results. In contrast, the ethanol gel test is less sensitive, but more reliable; while the 3P test has poor specificity and many false positives. If the molecular weight of the FDP lobes is small, the 3P test can also be negative. It is better to compare the two with each other for greater significance.

5. Euglobulin dissolution time Euglobin is a protein component of plasma precipitated in an acidic environment. It contains fibrinogen, fibrinolysin and its activin, but does not contain fibrinolytic inhibitors. It can be used to determine fibrinolytic enzymes. Whether the original activator is increased. The normal value should exceed 2 hours. If dissolved within 2 hours, it indicates that fibrinolysis is excessive. When hyperfibrinolysis is increased, plasminogen is reduced and plasmin is increased. Euglobulin is rapidly dissolved by a large amount of plasmin. The positive rate reported in domestic data is 25 to 42.9%.

(3) Hemolytic examination of microangiopathy shows abnormal red blood cells, such as fragmented cells and armor cells, in the serum. When the blood film shows that the proportion of broken and deformed red blood cells exceeds 2%, it is of reference value for the diagnosis of DIC.

(4) Other recent new experimental methods include: Determination of the content of antithrombin III (AT): In DIC, AT is consumed in large quantities, which is significantly reduced in the early stage. The measurement results are not affected by FDP. The measurement methods are: There are two methods of coagulation activity and agar diffusion method. Use 51Cr to label platelets or 125I to label fibrinogen to determine whether platelet life is shortened. Measurement of platelet -globulin (-TG) and platelet factor 4 (PF4) content: -TG and PF4 can be released into the blood circulation during platelet aggregation. Increased -TG and PF4 reflect hypervascular platelet function, which decreases during consumption. Measurement of fibrin breakdown products: When there is blood clot in blood vessels and thrombin activity is increased, the breakdown of fibrinogen increases and fibrin peptide A (FPA) increases. Can be measured by radioimmunoassay. An increase in fibrin monomers, dimers, and multimers can be found in chromatographic analysis.

Wasting coagulopathy

DIC's condition is serious, it is dangerous, and it develops rapidly. It must be actively rescued, otherwise the condition can develop into irreversibility. Both the primary disease and DIC are causal to each other, and both must be taken into account during treatment, and the clinical manifestations and laboratory test results must be closely observed.

(1) Elimination of the cause and treatment of the primary disease Treatment of the primary disease is a fundamental measure for the treatment of DIC. It is also important to control the adverse factors of the primary disease, such as actively controlling infection, clearing stillbirths in the uterus, and anti-tumor treatment. Others such as supplementing blood volume, preventing shock, improving hypoxia and correcting water and electrolyte disorders also have positive effects. Hemolytic reactions should be prevented during blood transfusion. After removing the cause, the condition can be quickly relieved, and eliminating the causes of DIC is also conducive to preventing the occurrence and development of DIC.

(2) Heparin treatment Heparin and antithrombin III (ATIII) in the blood form a complex, which strengthens the inactivation of thrombin and active coagulation factors a, Xa, a, and a by AT, resulting in anticoagulation. Therefore, in the treatment of heparin, the blood AT level must be considered. If the AT level is too low, even if given a large amount of heparin, it will not be effective. In recent years, heparin has been found to promote fibrinolysis and hinder platelet aggregation. Indications regarding the use of heparin include: clear diagnosis of DIC, including when the primary disease or the cause cannot be controlled or removed, the latter is used as symptomatic treatment of DIC; if the cause of DIC has been confirmed to occur, in order to prevent intraoperative or After the procoagulant substance enters the blood circulation and aggravates DIC, it can also be used in a short period of time. When preparing to apply a fibrinolytic inhibitor or supplement the coagulation substance, if the procoagulant substance has already played a role in the blood, heparin should also be used first. After giving fibrinolytic inhibitor, blood transfusion and fibrinogen. For acute DIC, especially those with complicated conditions such as fresh wounds and wounds, heparin should be used with caution. If used incorrectly, there is a risk of exacerbating bleeding. For chronic or subacute DIC, there is no vascular injury and fresh wounds. Use safer. For patients with suspected DIC, such as those with a tendency to DIC and a negative 3P test or other laboratory tests, or a positive 3P test without clinical bleeding symptoms, heparin may not be used for the time being. When the test results and clinical manifestations clearly support DIC, heparin is used. treatment. At present, there are no unified views on the indications for heparin application, but most people believe that those who have a clear diagnosis and useful drug indications should strive for early use. According to a report of 47 cases of DIC treated with heparin in Shanghai Ruijin Hospital in 1986, the cure rate of obstetric accidents was as high as 72.2%, and infectious diseases were 42.2%. In addition to the above diseases, treatment of heparin in most DIC cases is not helpful and sometimes even harmful. The reasons for the failure of heparin treatment include: improper indications for medication, especially with a poorly defined diagnosis; the time of medication is too late, and the disease has become irreversible; the exhaustion of AT in the body prevents heparin from functioning normally; improper dose control ; acidosis is not corrected, making heparin inactive.

In the following cases, heparin should be applied with caution to avoid exacerbating bleeding: In the later stage of DIC, pathological changes have been mainly fibrinolysis and bleeding mainly involves the relationship between fibrinolysis and a large number of FDPs, rather than the consumption of coagulation factors; The surgical wound has not healed; the original severe bleeding such as tuberculosis hemoptysis, ulcer bleeding or cerebral hemorrhage; those with obvious liver and kidney dysfunction; the original hematopoietic dysfunction and thrombocytopenia.

Dosage and usage of heparin: Generally, a medium dose is used. Intravenous injection of 50 mg every 4 to 6 hours or continuous intravenous drip (about 10 mg per hour). The 24-hour dosage is 200 300mg (each 100mg = 12500u), and the coagulation time (test tube method) needs to be measured before each intravenous injection, so that the control is between 20-30 minutes, the heparin dose is appropriately adjusted, and it is used until the DIC check index is restored. normal. Recently it has been suggested that the amount of heparin should not be too large. In Japan, 80-120 mg / d is used more. For those who still cannot control, it may be because of the reduction in AT. It is necessary to give blood transfusion and plasma to increase the level of AT-. Regarding low-dose heparin treatment, some people have proposed to use 5000ul of heparin and subcutaneous injection 2 to 3 times a day. It can also be administered intravenously. After using a small dose of heparin, the blood concentration began to rise after 15-60 minutes, peaked in 1 to 5 hours, and gradually disappeared after 7 hours. There may be differences among individuals. The advantage of low-dose heparin treatment is that it has no bleeding complications and does not require laboratory monitoring. It has been suggested that ultra-low doses for the prevention of thrombosis can also be effective, with 1 unit subcutaneous injection per kilogram per hour. For those who are effective in heparin treatment, the clinical situation generally improves after coagulation defects have been corrected, such as stable blood pressure and disappearance of cyanosis, before discontinuation of treatment. If the coagulation time is prolonged beyond 30 minutes, and the bleeding is exacerbated, it means that the amount of heparin is excessive, and the drug should be discontinued and the protamine sulfate should be intravenously injected to neutralize the amount of heparin. Once every 12 hours, it can be corrected after 1-2 times. After stopping the drug, follow-up coagulation time for 3 to 5 consecutive days to understand whether there is recurrence. In patients with acute DIC, heparin is effective, and prothrombin time can return to normal within 24 hours. Fibrinogen rises within 1-3 days, and platelets rise slowly, which takes about 7 days.

(3) Commonly used antiplatelet agglutination drugs are pansentine, 400-600mg / d, orally divided into 3 times, or 100-200mg is intravenously infused in 100ml glucose liquid, repeated once every 4-6 hours. Aspirin was orally administered in divided doses of 1.2 to 1.5 g / d. The combination requires a reduction in dose. It is suitable for patients with mild DIC or highly suspected DIC who have not confirmed the diagnosis. Low-molecular dextran reduces blood viscosity and inhibits platelet aggregation. The general dosage is 500-1000ml intravenous infusion. It is mainly used for early DIC. If the diagnosis is not completely certain, it can also be used in combination with pansentin.

(IV) Application experiments of AT- concentrates and synthetic antithrombin agents prove that when AT- drops to a certain level, even if the amount of heparin is increased, its anticoagulant effect cannot be improved. Some people think that AT- levels are low to normal. At 50%, AT- should be supplemented. Some people in Japan are intravenously injecting heparin at 10,000u / d, while intravenously injecting AT-III 1500u / d, which is equivalent to 1500ml of plasma.

Japan has recently synthesized anticoagulant preparations, and its effect has nothing to do with AT-. It has obvious effect on DIC and has few side effects.

(5) Supplementation of platelets and coagulation factors can provide blood coagulation matrix for microthrombus when transfusion or fibrinogen is given before heparin is used, and promote the development of DIC. However, if the clotting factor is too low, the use of heparin can aggravate bleeding. Blood transfusion (preferably fresh blood) or fibrinogen supplementation should be used, the latter can increase plasma fibrinogen by 25 mg / dl per gram of preparation, and the hemostatic effect can only be achieved when the fibrinogen concentration exceeds 100 mg / dl.

(6) Application of antifibrinolytic drugs In the early days of DIC, fibrinolytic itself is a physiological protective mechanism, so it is generally not recommended to use antifibrinolytic drugs. Early use may worsen the condition. However, when secondary fibrinolysis becomes the main contradiction of bleeding in the late stage of DIC, antifibrinolytic drugs can be appropriately applied. Such drugs should be used under adequate heparin treatment. Antifibrinolytic drugs can be applied alone only when there is no more blood coagulation and secondary fibrinolysis continues. Commonly used drugs include 6-6 aminocaproic acid (6EACA) 2-6 g / d, intravenous drip, antifibrinolytic aromatic acid (p-carboxylamine, abbreviated as PAMBA) 200 400mg / d, or hemostatic acid (AMCHA) 200 500mg / d, diluted slowly with glucose solution or intravenous injection. Some people claim that aprotinin can be used when there is a large amount of plasmin in the blood. The trial dose is 80 to 100,000 u. It is injected intravenously, and it is reduced after improvement, and 10,000 u is used every 2 hours.

(7) Traditional Chinese medicine used for activating blood circulation and removing blood stasis are traditional Chinese medicines such as compound salvia miltiorrhiza, hepatic hydrazine, Shenfu injection, and acid mucopolysaccharide of sea cucumber, which have certain curative effect in the treatment of DIC.

(8) In other domestic cases of treating DIC complicated with shock, it has been reported that anisodamine, scopolamine or phenbenzamine can relieve vasospasm. Low-molecular dextran has a good effect on unblocking blood vessels. It has also been proposed to use a variety of different therapies such as urokinase, blood exchange, plasmapheresis, hemodialysis, etc., but the efficacy is still uncertain and needs further research.