Disseminated intravascular coagulation in children
Introduction
Brief introduction of disseminated intravascular coagulation in children Disseminated intravascular coagulation (DIC) is a complex pathophysiological phenomenon with diffuse microvascular thrombosis, resulting in microcirculatory disorders, resulting in a variety of tissue and organ dysfunction, consumptive coagulopathy and secondary Fibrin dissolves, and shock and bleeding tend to occur as the main features. basic knowledge Sickness ratio: 0.0001% Susceptible people: young children Mode of infection: non-infectious Complications: diarrhea, hemolytic anemia, cardiogenic shock, coma, jaundice, hypotension
Cause
Pediatric disseminated intravascular coagulopathy
(1) Causes of the disease
Can occur during the following diseases:
1. Premature babies and neonatal asphyxia.
2. Bacterial infection with severe sepsis (such as meningococcal septicemia), bacillary dysentery, lobar pneumonia and urinary tract infections.
3. Viral infections with severe viral pneumonia, fulminant viral hepatitis, epidemic hemorrhagic fever, hemorrhagic measles and severe chickenpox.
4. Other infections such as falciparum malaria, leptospirosis and fungal infections.
5. Hematological acute leukemia (especially promyelocytic leukemia), faba bean disease and paroxysmal nocturnal hemoglobinuria.
6. Tumor malignancy, giant hemangioma.
7. Other critical illnesses of various shocks (infectious, hemorrhagic or allergic), respiratory distress syndrome, hemolytic uremic syndrome, renal failure, burns, brain contusion, snake bite, after major surgery, extracorporeal circulation, error Blood transfusion (blood type incompatibility), severe reaction of infusion and neonatal scleredema.
(two) pathogenesis
Under normal circumstances, the blood flowing in the microcirculation does not coagulate, mainly because there is no vascular damage, no adhesion and aggregation of platelets, no triggering factors for coagulation and thrombosis, but once in the above various factors (such as bacteria) Under the influence of toxins, vascular endothelial injury, etc., the coagulation system is activated, causing the circulating blood to appear hypercoagulable state, that is, platelet aggregation and extensive fibrin deposition occur in the microcirculation, forming a large number of microthrombus. At this time, the blood coagulation factor And the consumption of platelets, especially fibrinogen, prothrombin, V, VIII, X, XII and other factors and platelets are significantly reduced, forming a "consumptive coagulopathy", so the blood's hypercoagulable state changes to a low-coagulation state, Extensive bleeding occurs clinically. After DIC occurs, the fibrinolytic system (hereinafter referred to as fibrinolysis), which maintains a dynamic balance with coagulation, is activated by activin, which is activated by activin. The plasminogen is converted to a fibrinolytic enzyme (plasmin) for fibrinolysis, which is secondary Fibrinolytic phenomenon (Fig. 1), because plasmin is a proteolytic enzyme. When fibrinolysis is hyperactive, in addition to dissolving fibrin, many clotting factors are decomposed, which reduces the consumption of various coagulation factors. Promotes the occurrence of hemorrhage. On the other hand, fibrinogen and fibrin degradation product (FDP), which is also decomposed by fibrinolysis, is also called fibrin cleavage product (FDP), which also inhibits blood clotting. Hemorrhage is aggravated. In addition, after DIC occurs, platelets accumulate and are further consumed and reduced, which also promotes bleeding.
The two pathological phenomena, DIC and secondary fibrinolysis, occur at a certain stage in the process of different diseases. Sometimes both phenomena exist simultaneously, sometimes as a phenomenon. Therefore, pathological changes can be light and heavy, and lighter. The performance is not obvious, slightly more people with purpura or ecchymosis, severe cases of many organs can occur microcirculation embolism, necrosis and hemorrhage, more common in the lungs, kidneys, and even involving the whole body organs such as liver, brain, gastrointestinal and adrenal gland, etc., if thrombus It persists for a long time, due to severe ischemia, hypoxia, acidosis, cell disintegration, tissue necrosis and functional changes, and advanced stages can lead to multiple organ failure.
Prevention
Pediatric disseminated intravascular coagulation prevention
First, the predisposing factors for this disease should be corrected:
1. Carefully treat the primary disease to prevent hemolysis and the occurrence and development of acidosis.
2. Actively correct septic shock, improve microcirculation, and avoid the use of drugs that promote platelet aggregation such as adrenaline, norepinephrine or vasopressin.
Complication
Pediatric disseminated intravascular coagulation complications Complications diarrhea hemolytic anemia cardiogenic shock coma jaundice hypotension
In severe cases, microcirculatory embolism, necrosis and hemorrhage can occur in many organs. It is more common in the lungs, kidneys, and even in organs such as the liver, brain, gastrointestinal and adrenal glands. If the thrombus persists for a long time, due to severe ischemia, lack of Oxygen, acidosis, cell disintegration, tissue necrosis and functional changes, advanced can lead to multiple organ failure, acute DIC can be associated with fatal fulminant hemorrhage; hypotension and cardiogenic shock can occur; typical lung hyaline membrane synthesis Signs, more with obvious pulmonary dysfunction and hypoxemia, manifested as progressive dyspnea, severe pulmonary hemorrhage; hematemesis, diarrhea, jaundice; hematuria, proteinuria, oliguria or anuria, even kidney Dysfunction; and convulsions, coma, etc., Gram-negative endotoxin can cause toxic shock; decreased blood volume, decreased cardiac output can cause cardiogenic shock; microvascular hemolytic anemia can occur.
Symptom
Pediatric disseminated intravascular coagulation symptoms common symptoms hypotension microcirculatory disorder oliguria intravascular clotting shock urinary drowsiness dyspnea chills coagulopathy
According to the degree of DIC, the development process and duration, it is divided into acute, subacute DIC and chronic DIC. The acute DIC is the majority, the rapid occurrence, the rapid progress, the serious consequences, if handled properly, the recovery is also fast, the duration is longer. Short, only hours or days, especially in newborns and premature babies; subacute patients for several weeks; chronic DIC occurs slowly, development delays, recovery is slow, duration can be delayed for several months, early clotting time is shortened without Bleeding tendency, bleeding symptoms appear when there is coagulopathy in the later stage, light bleeding in the skin, severe ecchymosis, hematemesis, hemoptysis, blood in the stool, hematuria, oliguria or anuria, as well as chills, convulsions, coma Difficulty breathing, cyanosis, abdominal pain, jaundice and other symptoms.
1. Coagulation mechanism is divided into 3 phases
(1) High coagulation period: When the procoagulant enters the blood circulation, the blood coagulation is increased, or some substances that activate the blood coagulation factor enter the blood circulation. At this time, there is no bleeding symptom in the clinic, but the blood sample is often drawn when blood is drawn. Easy to solidify.
(2) Consumable low coagulation period: With the formation of a large number of microthrombus, a large number of blood coagulation factors and platelets are consumed after blood coagulation, followed by a consumptive hypocoagulable state, and patients have extensive severe bleeding.
(3) Secondary fibrinolysis period: Due to the activation of fibrinolysis system, a large amount of FDP is produced. FDP itself has strong anticoagulant effect when fibrinolysis is advanced. Therefore, clinical bleeding in this stage is more serious.
The above three issues are not completely separated and can overlap each other.
2. Clinical manifestations of diffuse extensive thrombosis in the microcirculation. Extensive hemorrhage and hemorrhagic necrosis occur in the terminal organs of microvascular thromboembolism, followed by dysfunction of major organs, including:
(1) Reduced cardiac output, heart sound weakness, hypotension and cardiogenic shock.
(2) The typical fibrin transparent microthrombus causes typical hyaline membrane syndrome, which is accompanied by obvious pulmonary dysfunction and hypoxemia, which is characterized by progressive dyspnea and severe pulmonary hemorrhage.
(3) Digestive system embolism often manifests as nausea, vomiting, diarrhea and jaundice.
(4) oliguria, hematuria, proteinuria, and even renal failure.
(5) The central nervous system has lethargy, confusion, coma and convulsions.
(6) Necrotic purpura and ecchymosis appear in the skin mucosa, which is progressively enlarged and increased. The incidence of embolism of the above organs is 20% to 70%, which causes and aggravates the factors of microthrombotic deposition.
3. Circulatory Disorder - The incidence of shock shock in DIC is 40% to 70%. The causes and mechanisms are as follows:
(1) related to the primary disease, if it is sepsis, Gram-negative endotoxin can cause toxic shock.
(2) due to decreased blood volume, cardiac output decreased severe myocardial ischemia and hypoxia cardiac output decreased cardiogenic shock.
(3) Extensive bleeding in DIC reduction in blood volume of blood loss reduction in circulating blood volume shock.
(4) XII factor, kallikrein, kinin and complement system activation cause shock, kinins destroy cell mitochondria, release lysosomal enzyme, inhibit myocardial contraction, aggravate shock, complement system activates C3a, C5a has allergic toxicity, Increases vascular permeability, and can attract neutrophils to agglomerate and release procoagulant substances and lysosomal enzymes. These factors make shock more and more serious, and often develop into irreversible shock.
4. Hemolysis caused by mechanical damage of red blood cells is also called red blood cell disruption syndrome. In DIC, because red blood cells pass through narrow microvessels, they are subjected to compression and mechanical damage, and they are deformed and broken to cause hemolysis. Red blood cells can be deformed into helmets, triangles or Spine, etc., destroyed by the spleen, this kind of anemia is also called microangiopathic hemolytic anemia. In recent years, endotoxin, fibrinolytic degradation products, and D fragments can be involved in the damage of erythrocyte membrane by activating the complement-granulocyte-free radical pathway. Hemolysis process.
5. Clinical features of chronic DIC Patients with chronic DIC have common continuation and diffuse thrombosis. Unlike acute DIC, there is usually no fatal fulminant hemorrhage. Some people call it "compensatory DIC". At this time, many hemostatic systems Accelerated component conversion, shortened survival, such as platelets, fibrinogen, V, VIII, etc. Therefore, most of the coagulation test indicators are close to normal or normal, but almost all FDP is significantly increased, therefore, blood stasis is common. Spontaneous sputum and large ecchymosis, and visible mild, moderate mucosal bleeding, such as urinary tract, gastrointestinal bleeding, etc., patients may also have single or diffuse thrombosis, and the corresponding clinical manifestations.
Examine
Pediatric disseminated intravascular coagulation examination
Along with complex pathophysiological processes, the experimental features also have high variability, complexity and difficulty in interpretation. In the evaluation of DIC patients, valuable experimental findings should generally be considered. These tests are for the diagnosis and treatment of DIC. The monitoring of the effects is of great significance.
1. Common general laboratory tests and results
(1) Experimental examination reflecting abnormal blood coagulation mechanism: 1 CT, PT, KPTT and recalcification time shortened during high coagulation period, 2 consumptive hypocoagulable phase, thrombocytopenia, decreased coagulation factor, prolonged PT and TT, thromboplastin production Poor and plasma protamine procoagulant test (3P) positive, 3 secondary fibrinolysis, 3P positive (late sometimes negative), euglobulin dissolution test (ELT) <70min (normal 90 ~ 120min), Increased FDP and markedly reduced plasma protonogen, prolonged TT, etc.
(2) The examination of red blood cell break syndrome: red blood cell reduction (anemia), blood smear see broken or helmet-shaped red blood cells > 2%, bone marrow hyperplasia, erythroid hyperplasia and reticulocyte increase.
2. Laboratory test variability
Different DIC stages, different clinical types of DIC also affect the variability of laboratory test results, which is related to the body's compensatory function. All the tests are abnormal during the decompensation period, and the tests can be normal or mild abnormal during the compensation period. The results of the high compensation period are even more than normal. Therefore, 3P negative, fibrinogen is not low (tumor, etc.) can not be denied diagnosis, dynamic observation of experimental results, common experimental changes and the following conditions.
(1) Variation of PT abnormalities: PT should be abnormal in most patients with DIC, PT should be prolonged in consumptive hypocoagulability and secondary fibrinolysis, and PT prolongation is seen in 75% of patients with acute DIC, but There are still about 25% of DIC patients with normal or shortened PT, such as the presence of clotting factors that are activated early in DIC, ie, PT is shortened or normal during high coagulation, and in addition, the ability of early degradation products to be rapidly coagulated by thrombin and rapid The function of the "agglutination" test system can also explain the PT when it is DIC, normal or shortened. Therefore, PT has a limited value for the diagnosis of DIC under normal circumstances.
(2) KPTT abnormal variation: KPTT is prolonged in acute DIC for a variety of reasons, especially in the period of consumptive hypocoagulability and secondary fibrinolysis, KPTT begins to prolong at fibrinogen <1000mg/L. However, in patients with acute DIC, KPTT does not prolong about 50%. Therefore, KPTT does not prolong the diagnosis of acute DIC. The reason is: 1 early degradation products can be quickly coagulated by thrombin and the role of "agglutination" test system 2, in acute DIC, there are activated coagulation factors in the circulation, they can avoid other factors of the KPTT detection system and directly form fibrin. Therefore, KPTT has limited value in DIC diagnosis.
(3) TT abnormality variation: In patients with acute DIC, TT should be prolonged due to the presence of circulating FDP and its interference with fibrin monomer polymerization and hypofibrinemia, but for the above reasons, Individual patients can also be normal or shortened, a simple additional supplementary test can be detected, that is, using TT, the test clot provided, allowed to stand for 5 to 10 minutes, and observe whether the blood clot is dissolved, If it does not dissolve within 10 minutes, it can be judged that there is no obvious increase in plasma plasmin in the circulation. On the contrary, there may be a presence of plasma plasmin in the plasma, which has a clinically significant increase and can confirm the presence of DIC.
(4) Variation of coagulation factor analysis results: In most patients with acute DIC, there are activated coagulation factors such as X , IX and thrombin in the circulation, so the routine method of coagulation factor detection will provide DIC patients. Non-interpretable and meaningless results, such as the detection of factor VIII in patients, due to the presence of X in the blood of DIC patients, will result in a high level of factor VIII check, because X bypasses the need for VIII:C in the test system and will quickly Fibrinogen is converted to fibrin, so, in a typical standard curve, there will be a very fast time to be recorded and will be interpreted as a high level factor VIII, and in fact no factor VIII is present, visible, clotting factor Analysis will provide erroneous and meaningless results that are of little value in the diagnosis of DIC.
(5) Analysis of FDP abnormalities: FDP is elevated in 85% to 100% of patients with acute DIC, so it is considered that a common misunderstanding of DIC is elevated in FDP. In fact, these degradation products are only plasmin organisms. Based on the degradation of fibrinogen or fibrin, FDP only indicates the presence of plasmin. In some patients with DIC, FDP can be false negative, fibrinogen is composed of A, B and bonds, and plasmin first degrades the hydroxyl group of its A chain. The terminal, which produces X fragments, is then further degraded by plasmin to form fragments Y and D, after which fragment Y is further degraded to form additional fragments D and E, or a so-called N-terminal disulfide structure, and fragments X and Y still contain fibrin peptides. They are the substrates of thrombin, and it is understandable that under certain conditions, FDP can be negative in acute and chronic DIC. Modern FDP method is used to detect fragments D and E. In acute DIC, there is obvious secondary. Fibrinolytic activity and a large amount of plasmin are present in the circulation, which causes fibrin to be degraded to fragments D and E, both of which are the final degradation products. In addition, granulocyte enzymes, collagenase and aprotinin are released in large quantities, they It also degrades all fragments D and E, which makes FDP negative in acute DIC. Therefore, FDP negative cannot exclude acute and chronic DIC. However, FDP is almost always elevated in DIC patients.
(6) Euglobulin lysis test (ELT): Due to the preparation and identification of euglobulin fragments, the destruction of fibrinolysis inhibitors is complicated, so the results obtained are often controversial and susceptible to human factors in the diagnosis of DIC. At the time, the application value is very limited. In addition, the results of laboratory tests are also affected by the compensatory function of the body. According to the state of compensatory function of the organism, DIC can be divided into three stages: overcompensation, compensation and decompensation. Reimbursement, all DIC laboratory test results can be positive; compensation period, some of the test results are not obvious, or even normal; excessive compensation period, some indicators, such as fibrinogen, platelet count can be higher Normal, the clotting time is shortened. Some tests have certain defects in the methodological method. For example, the specificity of the measured indicators is not strong. For example, thrombocytopenia can still be seen in some primary diseases of DIC such as leukemia; abnormally deformed red blood cells can also be used. Found in thromboembolic thrombocytopenic purpura (TTP) and hemolytic uremic syndrome, HUS plasma fibrin peptide A (FPA) determination, although it can reflect blood coagulation, fibrin formation, However, it is not certain whether the coagulation process occurs in a wide range of small blood vessels. Due to the variability of the above laboratory test results, it is not necessary to rely solely on a positive or negative result of laboratory tests to affirm or deny the diagnosis of DIC. Comprehensive clinical analysis, dynamic observation of changes in these indicators when necessary, and then make more objective judgments. In recent years, more research has been done on the early diagnosis of DIC (including pre-DIC), and some new experimental tests are considered. The method contributes to the early diagnosis of DIC.
3. Other new laboratory tests
(1) Determination of antithrombin III (AT-III): AT-III assay has become a key test for the diagnosis and monitoring of the efficacy of patients with acute and chronic DIC. At the time of DIC, AT-III combines with some activated clotting factors to form a complex. Substance, resulting in a significant reduction in most acute or chronic DIC functional AT-III, normal adult AT-III content of 75% to 125% (180 ~ 300mg / L), newborns are about 50% of normal adults, The level of people is reached at 6 months.
(2) Detection of platelet factor 4 (PF4) and -thromboglobulin (-TG): A large number of platelet aggregation and release during DIC increased both PF4 and -TG, and many modern studies have shown that either of these two One is helpful for the diagnosis and efficacy monitoring of DIC.
(3) Fibrin peptide A (FPA) measurement: Fibrin degradation in DIC decomposes peptide A (normal value 100 mg/L), and DIC is often specifically increased. A new detection method is to measure B15 by radioimmunoassay. The determination of 42 and related peptides, such as Bl5~42 and related levels with elevated FDP, has a greater differential diagnostic value for DIC and primary fibers.
(4) Determination of D-dimer: D-dimer is a new antigen formed when thrombin initially transforms fibrinogen into fibrin and activates factor XII to hinge fibrin. It is formed as a result of plasmin-degrading hinged fibrin, and D-dimer is specific for DIC. As a result, 93.2% of DIC patients have elevated D-dimer (>2000 g/L), and the average is The level was 2047 g/L. In patients with DIC exclusion, the abnormal rate was only 6%, and the average level was 541 g/L.
(5) Determination of protein C, protein S and fibronectin: they decreased in DIC, and its diagnostic value and role in the monitoring of efficacy still need to be further determined.
(6) Determination of VIII: ratio of C/VIIIR:Ag and ratio of VIII:C/VWF:Ag, both of which decreased most at DIC due to VIII:C consumption.
(7) Thrombin-antithrombin complex (TAT): increased in DIC, normal control 1.7 g / L ± 0.3 g / L.
(8) Plasmin-2 plasmin-inhibiting complex (PIC): increased in DIC, normal control 0.2 mg/L ± 0.1 mg/L.
(9) Determination of fibrinogen peptide fragment: In the DIC, the peptide chain B1542 fragments were increased, and the normal control was 1.56 nmol/L±1.20 nmol/L.
(10) Determination of plasma soluble fibrin: meaningful in the early diagnosis of DIC, may indicate organ-concurrent lesions.
(11) Determination of plasma thrombomodulin (TM): 42.0g/L±20.85g/L when DIC occurred, 15.36g/L±4.85g/L for normal control, TM decreased significantly during DIC remission, TM concentration at the beginning The higher prognosis is worse, and the concentration of TM in patients with organ failure is higher than that of non-associated patients. For pre-DIC problems, it has been reported that FDP(-), PT(-), fibrin in the week before the onset of DIC Original (-), the number of platelets does not decrease, and at this time, TAT ( ), PIC (plasmin-2 plasmin inhibitor) ( ), D-dimer ( ) [(-) abnormality is not obvious, ( ) abnormally significant], that TAT, PIC and D-dimer examinations are helpful for the diagnosis of pre-DIC, according to clinical needs to choose a variety of imaging methods, ECG, CT, MRI and cerebral blood flow can be used for auxiliary examination Make a diagnosis.
Diagnosis
Diagnostic diagnosis of disseminated intravascular coagulation in children
diagnosis
DIC diagnostic criteria:
1. DIC diagnosis general standard
(1) There are basic diseases that cause DIC: such as infection, malignant tumor, pathological obstetrics, large surgery and trauma.
(2) There are more than 2 clinical manifestations:
1 Severe or multiple bleeding tendency.
2 can not use the primary disease to explain microcirculatory disorders or shock.
3 extensive skin, mucosal embolism, focal ischemic necrosis, shedding and ulceration, or unexplained lung, kidney, brain and other organ failure.
4 anticoagulant therapy is effective.
(3) The experimental inspection meets the following conditions:
1 There are 3 or more experimental abnormalities at the same time:
A. Platelet count <100×109/L (leukemia, liver disease <50×109/L) or progressive decline, or the following two or more platelet activation molecular markers increased plasma levels:
a. -platelet globulin (-TG).
b. Platelet factor 4 (PF4).
c. Thromboxane B2 (TXB2).
d. Platelet granule membrane protein-140 (P-selectin, GMP-140).
B. Plasma fibrinogen content <1.5 g / L (liver disease <1.0 g / L, leukemia <1.8 g / L) or > 4.0 g / L or progressive decline.
C.3P test was positive, or plasma FDP>20mg/L (liver disease>60mg/L) or plasma D-dimer level increased more than 4 times (positive) than normal.
D.PT prolonged or shortened for more than 3s (liver disease >5s), APTT prolonged or shortened for more than 10s.
E. AT-III activity <60% (not suitable for liver disease) or protein C (PC) activity decreased.
F. Plasma plasminogen antigen (PLg: Ag) < 200 mg / L.
G. Factor VIII: C < 50% (required for liver disease).
H. Plasma endothelin-1 (ET-1) levels > 80 ng / L or thrombin regulatory protein (TM) more than 2 times higher than normal.
2 Difficulties or special cases should have the following two or more abnormalities:
A. Plasma prothrombin fragment 1 2 (F1 2), thrombin-antithrombin complex (TAT) or fibrin peptide A (FPA) levels are increased.
B. Plasma soluble fibrin monomer (SFM) levels are increased.
C. Increased plasma plasmin-plasmin inhibitor complex (PIC) levels.
D. Increased plasma tissue factor (TF) levels (positive) or decreased tissue factor pathway inhibitor (TFPI) levels.
2. Leukemia DIC experimental diagnostic criteria
(1) Platelet count <50×109/L or progressive decline, or the following two or more levels of plasma platelet activation molecular markers are elevated: 1-TG; 2PF4; 3TXB2; 4P-selectin.
(2) Plasma fibrinogen content <1.8g / L or progressive decline.
(3) Positive 3P test or elevated plasma FDP > 2.0 mg / L or elevated D - dimer (positive).
(4) PT is prolonged for more than 3s or progressively extended, or APTT is extended for more than 10s.
(5) AT-III activity is <60% or PC activity is decreased.
(6) Plasma PLg: Ag < 200 mg / L.
(7) The following levels of plasma coagulation factor activation molecular markers are elevated: 1F1 2; 2TAT; 3FPA; 4SFM.
3. Liver disease DIC experimental diagnostic criteria
(1) Platelet count <50×109/L or progressive decline, or the following two platelet activation molecular markers are elevated: 1-TG; 2PF4; 3TXB2; 4P-selectin.
(2) Plasma fibrinogen content <1.0g / L or progressive decline.
(3) Factor VIII: C < 50% (required standard).
(4) PT is extended for more than 5s, or APTT is extended for more than 10s.
(5) Positive 3P test or plasma FDP <60 mg/L, or elevated D-dimer level (positive).
(6) elevated levels of plasma coagulation factor activation molecular markers: 1F1 2; 2TAT; 3FPA; 4SFM.
4. Chronic DIC diagnostic reference standard
(1) Clinically existing chronic diseases: basic diseases of DIC, such as tumors, immune diseases, chronic kidney diseases and lung diseases.
(2) There are one or more of the following abnormalities:
1 repeated mild microvascular embolism symptoms and signs, such as skin, mucosal focal ischemic necrosis and ulcer formation.
2 recurrent appearance of mild bleeding.
3 Unexplained transient lung, kidney, brain and other organ dysfunction.
4 The course of disease is more than 14 days.
(3) The experimental inspection meets the following conditions:
1 There are more than 2 elevated plasma platelet activation molecular markers: A. -TG; B. PF4; C. TXB2; DP-selectin.
2 plasma levels of more than 2 clotting factor-activated molecular markers: A.F1 2; B.TAT; C.FPA; D.SFM.
The 33P test was positive or the plasma FDP was <60 mg/L, or the D-dimer level was more than 4 times higher than the normal (positive).
4 platelets, fibrinogen half-life shortened or the conversion speed is accelerated.
5 increased levels of molecular markers of vascular endothelial cell injury: A.ET-1; B.TM.
5. The DIC laboratory diagnostic reference standard for primary medical units has the following three or more abnormal indicators to diagnose DIC.
(1) Platelet count <100×109/L or progressive decline.
(2) Plasma fibrinogen <1.5 g / L or progressive decline.
(3) The 3P test was positive.
(4) PT is prolonged or shortened for more than 3 s or changes dynamically.
(5) Peripheral blood broken red blood cells >10%.
(6) Unexplained erythrocyte sedimentation rate or erythrocyte sedimentation rate should increase disease, but its value is normal.
6. Pre-DIC (pre-DIC) diagnostic reference standard
(1) There are basic diseases that cause DIC.
(2) Have more than one of the following clinical manifestations:
1 skin, mucosal embolism, focal ischemic necrosis, shedding, and ulcer formation.
2 microcirculatory disorders that are difficult to explain in the primary disease, such as pale skin, dampness and cyanosis.
3 Unexplained lung, kidney, brain and other mild or irreversible organ dysfunction.
4 anticoagulant therapy is effective.
(3) There are three or more abnormalities in the following experimental indicators:
1 Under normal operating conditions, the blood sample is easy to coagulate, or the yang is shortened by >3s, and the APTT is shortened by more than 5s.
2 plasma platelet activation molecular marker content increased: A. -TG; B. PF4; C. TXB2; DP-selectin.
3 increased levels of blood coagulation-activated molecular markers: A.Fl 2; B.TAT; C.FPA; D.SFM.
4 decreased anticoagulant activity:
A. AT-III activity is reduced.
B. PC activity is reduced.
5 increased levels of molecular markers of vascular endothelial cell damage: A.ET-1; B.TM.
Differential diagnosis
Mainly differentiated from primary fibrinolysis, primary fibrinolysis syndrome has no coagulation function, there is no large amount of platelet aggregation and consumption and thrombin generation and fibrin monomer formation, laboratory examination of platelet count, 3P test As well as antithrombin III concentration, PF4 and -TG are normal, B142 peptide chain is increased, D-dimer (-), while DIC, the above four indicators are abnormal, B1542 peptide chain is increased, Increased D-dimer.
