what are the causes of disseminated intravascular coagulation in obstetrics and what are the causes of disseminated intravascular coagulation in obstetrics
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Etiology of disseminated intravascular coagulation in obstetrics
First, the cause of the disease
Obstetrical DIC mostly occurs in serious complications and complications in obstetrics. Common diseases are found in:
1. Infectious abortion
During illegal abortion and intrauterine injection of drugs in the second trimester of pregnancy, infection causes bacteria and bacterial toxins to enter the blood, choriitis, amnionitis and septicemia, which causes damage to vascular endothelial cells, platelet aggregation and tissue necrosis to release thromboplastin.
2. Overdue abortion fetal death in utero
Pritchard (1959) reported that about 25% of pregnant women who died in utero for more than 4 weeks developed hypofibrinogonemia, and almost no coagulation disease was found in those who delivered before 4 weeks. The occurrence of hypoproteinemia is due to the survival of stillbirth and the release of tissue thrombin, which leads to DIC.
3. Early placental abruption
It is an obstetric emergency that endangers the lives of mothers and children. The incidence rate was 0.46% ~ 2.1% in China and 0.46% ~ 1.3% in the southern United States. There are differences due to different diagnostic criteria, Intrauterine fetal death was 1.2% and 9.2%, respectively. The causes of placental abruption were unknown, but most of them occurred in patients with hypertension. Because of spastic contraction of spiral arterioles, decidual ischemia, hypoxia injury and necrosis, release of thromboplastin, retroplacental hematoma and consumption of fibrinogen, there was a tendency to bleed and organ embolism when fibrinogen【小于】1 ~ 1.5 g/l.
4. Amniotic fluid embolism
Amniotic fluid contains epithelial cells, hair, keratinite, fetal fat, meconium, mucus and other particulate matter. Amniotic fluid entering the blood circulation can trigger the internal and external coagulation system, destroy platelet aggregation, promote blood coagulation, and activate coagulation factor VII, which forms endogenous thromboplastin through the contact of vascular endothelial surface, and has a strong coagulation promoting effect. Amniotic fluid contains not only procoagulant substances, but also fibrinolytic activating enzyme, which activates fibrinolytic system, converts plasminogen into fibrinolytic enzyme, dissolves fibrin into fibrin degradation product (HDP), and also dissolves fibrinogen. A large amount of coagulation factors are consumed, especially platelets and fibrinogen. On the other hand, fibrin dissolves and makes blood? It changed sharply from high pour point state to low pour point and high solubility state. Therefore, amniotic fluid embolism leads to DIC, which is dangerous, develops rapidly, falls into deep shock, and even dies within a few minutes.
In the late stage of shock, microcirculation congestion, slow blood flow, increased blood concentration and viscosity, easy aggregation of red blood cells, severe ischemia, hypoxia and accumulation of a large number of acidic metabolites can damage vascular endothelial cells and activate endogenous coagulation system, resulting in DIC. Traumatic shock, damaged tissue can also activate exogenous coagulation system.
6. Severe hypertensive disorder complicating pregnancy
Pathophysiological changes, Severe vasospastic contraction, Blood concentration, ischemia, hypoxia and endothelial cell injury lead to the decrease of eprostacyclin synthase, the relative increase of tromboxane (TXA2) synthase, the decrease of PGI2/TXA2 ratio and the increase of collagen, which activate platelets, trigger platelet adhesion and aggregation, and release adenosine diphosphate (ADP), 5-hydroxytryptamine (5-HT) and catecholamine to further aggregate platelets and reduce platelets. Therefore, severe hypertensive disorder complicating pregnancy has the condition of activating endogenous coagulation system. Clinical manifestations include bleeding symptoms, hematemesis and hematuria, but there is no hypofibrinogen in laboratory examination, but hemolytic anemia and thrombocytopenia, so hemolytic anemia is not secondary to hyperfibrinolysis. However, for hypertensive disorder complicating pregnancy complicated with microangiopathy hemolysis, non-expendable coagulation disease should be differentiated from DIC. Hemolytic anemia, thrombocytopenia and increased liver enzymes are collectively called Hellp syndrome. Whether there is a causal relationship between Hellp and DIC remains to be further observed and studied.
Second, the pathogenesis
The above factors usually cause DIC through the following ways.
1. First, a large number of tissue factors enter the blood circulation and start exogenous coagulation pathways, such as severe trauma during surgery, placental abruption, fetal death, etc. In these cases, a large number of tissue factors (i.e., coagulation factor III, or tissue thromboplastin (TTP)) are released into the blood and Ca2 in plasma. And coagulation factor VII form a complex to start the exogenous coagulation system. At present, it is believed that the activation of coagulation system is mainly mediated by TTP. Monocytes or macrophages, like endothelial cells, have TTP expression on the cell surface when stimulated by pathogenic factors or mediators.
2. The second is to activate coagulation factor VII and start endogenous coagulation pathway. For example, bacterial endotoxin can damage vascular endothelial cells and expose subintimal collagen during infectious abortion. Coagulation factor XII contacts collagen or endotoxin, and the guanidine configuration on arginine changes, and serine residues in active sites are exposed and activated. In addition, Factor XII and activated Factor XII A may also form fragment XII F under the action of soluble lumbrokinase (proteolytic enzyme) such as kallikrein, fibrinolysis or trypsin, which is called enzymatic activation. F is a kallikrein activator, which can activate plasma kallikrein into kallikrein, which further activates factor XII, thus accelerating the response of endogenous coagulation system. A and F can also activate fibrinolytic, kinin and complement systems, and further promote the development of DIC.
3. When infectious abortion and amniotic fluid embolism occur, bacterial endotoxin and some granular matter in amniotic fluid enter the blood circulation, which can activate platelets, make their membrane glycoprotein ⅱ b ~ ⅲ a complex function express as fibrinogen receptor, combine with fibrinogen, and promote platelet aggregation. The vascular endothelial cells were injured by pathogenic factors, and collagen and microfibers under endothelium were exposed, which were linked with platelet membrane glycoprotein ⅰ b directly by von Willebrand factor (vWF) or by von Willebrand factor (vWF)Combined, so that platelets adhere. Activated platelets release adenosine diphosphate (ADP), 5-hydroxytryptamine (5-HT) and tromboxane (TXA2), which can further activate platelets and form microaggregates. In addition, when platelets are activated, membrane phospholipids change, that is, negatively charged phospholipids transfer from the inner layer to the outer layer of the membrane, and interact with factors XI, XA, X and II through Ca2, which promotes thrombin formation with the participation of cofactors V and VIII. Usually, platelets play a secondary role in the pathogenesis of DIC. But it can also play a primary role.
4. Vascular endothelial cells (VEC) have bidirectional interaction with vascular tension, coagulation and fibrinolysis. Under the action of pathogenic factors, such as severe infectious abortion (pathogens can be bacteria, viruses, fungi, protozoa, spirochetes or rickettsia), vascular endothelial cells are often damaged and their physiological balance is out of balance. For example, endotoxin can act directly on VEC, or through the release of tumor necrosis factor (TNF) from monocytes and neutrophils. VEC can also be damaged by interleukin 1 (IL-1), platelet activating factors (PAF) and complement (C5a). TNF and IL-1 can change the surface properties of VEC and promote the adhesion of neutrophils, monocytes and T cells on the surface. PAF induces platelet aggregation and release, promotes chemotaxis and granule secretion of neutrophils and monocytes, and promotes interaction between endothelial cells and neutrophils. C3a and C5a can induce monocyte to release IL-1, C5a can enhance the activation of neutrophils to produce oxygen free radicals, resulting in damage to endothelial cells, and promote the occurrence of DIC.
In a word, coagulation is activated during DIC, so that thrombin and fibrinolytic enzyme appear in circulating blood. On the one hand, thrombin cuts fibrin peptides A and B from fibrinogen, and the rest is fibrin monomer, which polymerizes into fibrin in microcirculation, forming thrombus, interfering with blood flow, peripheral ischemia, damaging organs, and at the same time, thrombocytopenia. On the other hand, fibrinolytic enzyme cuts the C-terminal of fibrin (proto) and produces FDP (fibrinogen degradation product), which forms soluble complex with fibrin monomer, interferes with monomer polymerization and leads to bleeding. Fragments D and E have high affinity with platelet membrane, which makes platelets lose function and also leads to bleeding. Fibrinolytic enzyme can also degrade coagulation factors V, VII, IX and IX, as well as growth hormone, ACTH and insulin in plasma. Fibrinolytic enzyme activates complement system to dissolve red blood cells, release ADP and membrane phospholipids to promote coagulation; Dissolve platelets to reduce them and provide procoagulant substances. These are the pathophysiological basis of thrombosis, bleeding and organ dysfunction in DIC.
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