amniotic fluid embolism


Introduction to amniotic fluid embolism Amniotic fluid embolism refers to the serious complications of childbirth caused by acute pulmonary embolism, anaphylactic shock, disseminated intravascular coagulation, renal failure or sudden death during sudden delivery of amniotic fluid into the maternal blood circulation. The incidence rate is 4/100,000 to 6/100,000. Amniotic fluid embolism is caused by tangible substances (fetal hair, keratinized epithelium, fetal fat, meconium) and procoagulant substances in the contaminated amniotic fluid. In recent years, it is believed that amniotic fluid embolism is mainly an allergic reaction. It is a series of allergic reactions caused by maternal body to the fetal antigen after the amniotic fluid enters the maternal circulation. Therefore, it is recommended to name it "pregnancy allergic reaction syndrome", which is a low incidence of obstetrics and a mortality rate. Very high complications, maternal mortality rate of more than 80%, amniotic fluid embolism onset, acute disease, more than a short time after the onset of death, to avoid predisposing factors, timely diagnosis, early organization of rescue, treatment, is the key to rescue survival. basic knowledge The proportion of sickness: 0.0045% Susceptible people: maternal Mode of infection: non-infectious Complications: pulmonary hypertension, acute renal failure, pulmonary embolism, acute pulmonary edema, pulmonary failure, disseminated intravascular coagulation, anaphylactic shock, sudden death


Causes of amniotic fluid embolism

1, the cause:

Amniotic fluid embolism occurs in the time of birth or membrane rupture, but also occurs in postpartum, more common in term, but also in mid-term induction or forceps, most of the sudden onset, the condition is dangerous.

The occurrence of amniotic fluid embolization usually requires the following basic conditions: increased pressure in the amniotic cavity (over-uterine contraction or tonic uterine contraction); membrane rupture (2/3 of which is premature rupture of membranes and 1/3 of the membranes are broken) ); open vein or sinus at the cervix or uterine body injury.

Amniotic fluid embolism usually has the following incentives: majority of maternal; many cases of premature rupture of membranes or artificial rupture of membranes; common in hypertrophic or oxytocin (oxytocin) improper application; early placenta stripping, placenta previa, uterus Amniotic fluid embolism is prone to rupture or surgery.

2. The way the amniotic fluid enters the mother body:

The amount of amniotic fluid entering the maternal circulation has not been calculated yet, but the pathways for amniotic fluid to enter the mother are as follows:

(1) Intracervical vein: During the labor process, cervical dilatation may cause the internal cervix to tear, or when the operation of the cervix is dilated, the membrane is removed, the internal monitor is placed to cause damage to the internal cervix, and the vein wall is broken and opened. It is an important way for amniotic fluid to enter the mother.

(2) At or near the placenta attachment: There is a rich sinus at the placenta attachment. If the placenta is ruptured near the placenta, the amniotic fluid may enter the uterine vein through the fissure.

(3) Peripheral membrane blood vessels: If the membrane has ruptured, the decidua of the subdural membrane is open, and strong contractions may also force the amniotic fluid into the sinus and enter the maternal circulation. In addition, cesarean section uterine incision is increasingly becoming one of the important ways for amniotic fluid to enter the mother. Of the 46 amniotic fluid embolisms reported by Clark (1995), 8 occurred just after the end of cesarean section. Of the 53 amniotic fluid embolisms reported by Gilbert (1999), 32 (60%) had a history of cesarean section.

3. Pathogenesis:

(1) Pulmonary hypertension: acute respiratory circulatory failure amniotic fluid and its contents such as epithelial cells, mucus, bristles, fetal fat, fetus and other particulate matter once the blood into the blood first embolizes the pulmonary small vessels to cause mechanical infarction, followed by the chemistry of particulate matter Media characteristics stimulate lung tissue production and release of prostaglandin E2, prostaglandin F2, serotonin, histamine and leukotrienes, causing pulmonary vasospasm, resulting in increased pulmonary artery pressure, increased right heart load, right heart failure Pulmonary hypertension causes pulmonary perfusion to decrease, effective gas exchange is insufficient, alveolar capillary ischemia and hypoxia increase pulmonary capillary permeability, and fluid exudation leads to pulmonary edema and pulmonary hemorrhage, acute respiratory failure, left Atrial recurrent blood volume and left ventricular discharge decreased rapidly and circulatory failure occurred. All tissues and organs were hypoxic and hypoxic, and eventually multiple organ failure occurred. Seventy-five percent of deaths die from this cause. In addition, the antigenic substance acting on the fetus in amniotic fluid can cause an allergic reaction leading to shock.

(2) Disseminated intravascular coagulation: amniotic fluid causes coagulation dysfunction after entering the maternal circulation. It is generally believed that the procoagulant substance contained in amniotic fluid is similar to tissue thromboplastin (factor III), which activates the exogenous coagulation system and leads to DIC. In addition to amniotic fluid, it also contains factor X activating substances, pulmonary surfactants, and trypsin-like substances in meconium. These procoagulant substances promote the accumulation of platelets, convert prothrombin to thrombin, and also pass the external coagulation system of blood. Activated blood clotting and acute DIC, blood fibrinogen is consumed and decreased, and the fibrinolytic system is activated to cause hyperfibrinolysis and coagulopathy. In addition, fibrin cleavage products accumulate, and amniotic fluid itself inhibits uterine contraction, causing the uterus to decrease in tension, resulting in uterine blood not condensing and bleeding, which aggravates shock.

(3) anaphylactic shock: With the development of immunological techniques, Sialyl Tn antigen can be detected regardless of meconium contamination in amniotic fluid, amniotic fluid with meconium contamination is higher, and these micro-plug substances in amniotic fluid are allergic Originally, it can stimulate the body to produce anaphylactic shock such as histamine, leukotriene and other chemical mediators, which are characterized by impaired cardiopulmonary function, blood pressure and other shock performance and blood loss.

(4) multiple organ failure: pathological changes such as DIC often cause multiple organ involvement, such as shock kidney, acute tubular necrosis, extensive hemorrhagic hepatic necrosis, lung and spleen hemorrhage are the most common. The clinical manifestations are acute liver and kidney failure. When two or more vital organs are simultaneously or sequentially failing, they are called mutiple system organ failure (MSOF), and the mortality rate is almost 100%.

Amniotic fluid enters the blood vessels, blocks the small blood vessels of the lungs, causes pulmonary hypertension, abnormal type I allergic reaction and coagulation mechanism, resulting in a series of pathophysiological changes in the body.


Amniotic fluid embolism prevention

If you can pay attention to the following items, it is beneficial to prevent amniotic fluid embolism.

1, disable artificial stripping, uterine contraction period, the use of acupuncture artificial rupture.

2, to avoid hypertonic uterine contractions

(1) Avoid pressing the bottom of the palace to force the baby to deliver irregular operations.

(2) Strictly grasp the indications for oxytocin use, the medication should start from a small dose (2mU / min), special personnel monitoring, special records, according to contractions, fetal, cervical dilatation and head basin relationship, adjust the drug concentration, the maximum dose <20mU/min.

(3) small dose of misoprostol (25 ~ 50g) to promote cervical ripening and planned delivery, if necessary, repeat 1 or 2 times every 6 hours, closely monitor the labor.

3, grasp the indications of vaginal midwifery, operating specifications, if bleeding, blood is not condensate, difficult to control, should be alert to amniotic fluid embolism.

4, after labor or rupture of the membrane, the contraction is too strong, after the exclusion of obstructive dystocia, it is estimated that a short time can not be delivered, can be used intramuscular injection of meperidine, or a little bit of magnesium sulfate to reduce the contraction strength.

5, strict control of cesarean section indications, surgical operation specifications, gentle, cut the uterus, first absorb the amniotic fluid and then give birth to the placenta, if there is a large sinus exudation should be clamped closed.

6, when the mid-pregnancy clamp is scraped, the membrane should be broken first, and the amniotic fluid should be drained and then scraped.

7, for the stillbirth, early exfoliation of the placenta, etc., should be closely observed.

8. Avoid birth injury, uterine rupture, cervical laceration and so on.


Amniotic fluid embolism complications Pulmonary hypertension, acute renal failure, pulmonary embolism, acute pulmonary edema, pulmonary failure, disseminated intravascular coagulation, anaphylactic shock, sudden death

1. Prenatal or postpartum onset: common in hypertensive uterine contractions or rupture of membranes, pulmonary hypertension, shock mainly, patients with irritability, difficulty breathing, cyanosis, convulsions, coma, blood pressure, shock, etc., a few The case only screamed, the heart stopped breathing and died, and some cases were mildly slow. First, there were chills, irritability, cough, chest tightness and other prodromal symptoms, followed by cyanosis, difficulty breathing, convulsions, coma, shock state, and degree. After this period, death due to coagulopathy or acute renal failure.

2, postpartum disease: bleeding, shock-based, cardiopulmonary insufficiency symptoms are mild.

3, organ failure: If the condition is not controlled, continue to deteriorate, and eventually develop into multiple organ failure, complicated by acute renal failure, life-threatening.


Amniotic fluid embolism symptoms common symptoms shock cyanosis circulatory failure coma dyspnea convulsion renal failure cerebral hypoxia fatigue pale

Typical symptoms of acute amniotic fluid embolism include: difficulty breathing, cyanosis, cardiovascular dysfunction, hemorrhage and coma, fetal components found in maternal blood, and "amniotic embolism-like syndrome" for undetected fetal components. Amniotic fluid embolism is actively treated. The onset time can be during pregnancy, time of birth and postpartum. The above typical symptoms may not be available to all patients. Therefore, it is difficult to express chills, chest tightness, microcough or cough, pale, bleeding and blood. Condensed patients should be highly alert to the occurrence of amniotic fluid embolism.

Amniotic fluid embolism occurs at the end of the first stage of labor, and when the second stage of labor is strong, it can also occur in a short time after the delivery of the fetus, and there may be manifestations of cardiopulmonary failure and shock, DIC and renal failure.

1. Respiratory circulatory failure: According to the condition, it is divided into two types: fulminant and slow type. After the fulminant is a prodromal symptom, it will soon have difficulty breathing, cyanosis, cough in acute pulmonary edema, vomiting pink foam, fast heart rate, blood pressure. Decline or even disappear, a few cases only screamed, heartbeat respiratory arrest and death, slow-type respiratory circulatory system symptoms are mild, or even no obvious symptoms, until the bleeding occurs after delivery, blood is not found when the blood is not condensed.

2, systemic bleeding tendency: some amniotic fluid embolism patients survived the period of respiratory and circulatory failure, followed by DIC, showing a large number of vaginal bleeding mainly systemic bleeding tendency, such as mucosa, skin, needle eye bleeding and hematuria, and blood is not Condensation, it is worth noting that some cases of amniotic fluid embolism, lack of symptoms of the respiratory circulatory system, the main manifestation of vaginal bleeding that is difficult to control after childbirth, do not simply mistake the uterine contraction caused by postpartum hemorrhage.

3, multiple system organ damage: the disease of the whole body organs are damaged, except the heart outside the kidney is the most commonly damaged organs, due to kidney hypoxia, oliguria, urinary closure, hematuria, azotemia, cause Renal failure and death; patients with cerebral hypoxia can have irritability, convulsions, and coma.



First, non-specific inspection

1. Electrocardiogram: right ventricle, right atrium dilatation, and the manifestation of myocardial strain, and tachycardia.

2, chest X-ray: may have no abnormal performance, 70% of patients may have mild pulmonary edema symptoms, manifested as bilateral diffuse punctate infiltration shadows, distributed around the hilum, lungs slightly enlarged, heart shadow may Increase.

3, blood oxygen saturation: sudden drop can often indicate the problem of pulmonary embolism.

4, blood coagulation function test: the results vary greatly, the results depends on the patient's survival time and the extent of clinical bleeding, 1 platelet count <100 × 109 / L; 2 prolonged prothrombin time, 10 seconds is diagnostic 3 plasma fibrinogen <1.5g / L can be diagnosed, in fact, often more serious, Clark and other data in 8 cases of fibrinogen can not be detected or the lowest value ever recorded in the laboratory, 4 coagulation Block observation, take 5ml of normal maternal blood in a test tube, observe the formation of blood clots for 8 to 12 minutes in the incubator, the blood of patients with low fibrinogen is not easy to coagulate, the blood clot is less in 30 minutes, and the diffuse shows that the platelets are quite low, secondary Fibrinolysis, 5 bleeding time and prolonged clotting time, 6 fibrin degradation products, plasma protamine paracoagulation test (3P test) and ethanol gel test positive.

Second, specificity check

1. Detection of amniotic fluid in maternal circulation or lung tissue: Because amniotic fluid embolism occurs mainly because of the formation of amniotic fluid and amniotic fluid into the maternal blood, causing pulmonary vascular embolism and paralysis, therefore, people put in maternal blood In the uterine blood vessels and lung tissue, components derived from the fetus such as fetal squamous epithelial cells, bristles and mucus are used as diagnostic criteria. The positive rate of maternal blood is about 50%, and the positive result of autopsy is 73%, in maternal blood. The method for finding amniotic fluid is as follows: blood specimens are taken from the right ventricle. Clinically, the central venous pressure can be used to take the upper or lower vena cava blood, or the pulmonary artery floating catheter can be used for blood collection, or cardiac arrest. Blood is taken during intracardiac injection, and the blood is centrifuged and divided into three layers, which are blood cells, amniotic fluid, and the surface layer is plasma. The middle layer is stained for microscopic examination, and the auxiliary staining method, such as oil red staining, can be used to find fetal fat. Ayoub-Shklar staining keratin, anti-human keratin serum can detect the presence of keratin in maternal lung tissue by immunoperoxidase method, but this method The specificity and sensitivity are poor. At the same time, many scholars hold the opposite opinion. Clark and other scholars have observed a large number of clinical cases and animal experiments, and found that normal pregnant women have squamous epithelial cells and other amniotic fluid components in their blood. Amniotic fluid embolism does not occur, suggesting that squamous epithelial cells or bristles appear in the pulmonary circulation may not be pathological. Therefore, the presence of squamous epithelial cells in the pulmonary circulation alone cannot diagnose amniotic fluid embolism.

2, detection of neuronal-N-acetylgalactosamine (Sialyl Tn) antigen in maternal serum and lung tissue: In recent years, with the continuous development of immunological technology, this is a new diagnostic method for amniotic fluid embolism, Kobayashi et al. The study found that the monoclonal antibody TKH-2 of mucin glycoprotein can recognize the oligosaccharide structure in mucus glycoprotein in amniotic fluid. By immunoblotting, TKH-2 can detect very low concentration of Sialyl in meconium supernatant. Tn antigen, an antigen recognized by TKH-2 is not only present in meconium, but also in clear amniotic fluid. It is found by immunohistochemical detection in fetal small intestine, colon, and respiratory mucosal epithelial cells. The antigen that reacts with TKH-2 can be detected by radioimmunoassay in meconium-stained amniotic fluid and clear amniotic fluid, but the former is significantly higher than the latter. It is found that Sialyl Tn antigen is meconium and amniotic fluid. One of the characteristic components, Sialyl Tn antigen accounts for about one-tenth of meconium. The source of Sialyl Tn antigen in amniotic fluid is still not very clear. Because of the Sialyl Tn in the mucosal epithelium of the digestive tract and respiratory tract. The original expression, in addition to meconium is the main source of Sialyl Tn antigen in amniotic fluid, some may be derived from the mucus protein of the fetal respiratory tract. The concentration of Sialyl Tn antigen in the serum of pregnant women after pregnancy is different. If meconium is contaminated in amniotic fluid, The serum concentration of Sialyl Tn in pregnant women [(20.3±15.4) U/ml] is slightly higher than that of amniotic fluid clear [(11.8±5.6) U/ml], but the diagnostic value is in amniotic fluid embolism patients or amniotic fluid embolism-like symptoms In the serum of patients, Sialyl Tn antigen was significantly increased, which was about (105.6±59.0) U/ml. Studies by Kobayashi et al confirmed that the serum level of Sialyl Tn antigen was significantly higher in patients with amniotic fluid embolism than in non-amniotic embolism patients. The serum Sialyl Tn antigen mainly comes from the destruction of the maternal-fetal barrier or the Sialyl Tn in the fetal serum passes through the placenta to the maternal blood circulation. The Sialyl Tn antigen in the amniotic fluid enters the maternal blood circulation in a small amount, which is not enough to cause amniotic fluid embolism. It seems to indicate the occurrence of amniotic fluid embolism and the entry into the mother. The amount of Sialyl Tn antigen in the blood circulation is related, so it is simple to quantify the Sialyl Tn antigen in serum by sensitive radioimmunoassay. , sensitive, non-invasive diagnosis of amniotic fluid embolism, can be used for early diagnosis of amniotic fluid embolism, histological diagnosis after maternal death is still very important, immunohistochemical staining of lung tissue with TKH-2, found amniotic fluid embolism or In patients with amniotic fluid embolism-like symptoms, pulmonary vascular blood vessels showed strong positive staining, and this strong positive staining was completely inhibited by the submandibular gland mucin protein, indicating that it is immunospecific.

3, the determination of tissue anticoagulant factor: As mentioned above, the formation of amniotic fluid is not the main cause of amniotic fluid embolism, and some body fluid factors such as tissue factor-like procoagulant substances, leukotrienes, etc. A very important role, about 40% of patients with amniotic fluid embolism have fatal coagulopathy, the coagulation activity of tissue factor can be antagonized by anti-tissue factor protein, so in theory can be determined by detecting tissue factor in maternal blood The basis of other obstetric DIC.

4. Determination of mast cells in lung tissue: In recent years, there have been a lot of reports on the mechanism of amniotic fluid embolism. It is believed that amniotic fluid embolism is caused by the body's allergic reaction to fetal components in amniotic fluid, which leads to degranulation of mast cells to release histamine. Tryptase and other mediators cause serious physiological changes in the body. Tryptase is a neutral protease, which is the main component of T cell and mast cell secretory granules. Fineschi et al. used special immunohistochemical method to detect pulmonary circulation. The medium mast cell tryptase was found to have a significant increase in the number of mast cells in the lung tissue of amniotic fluid embolism and anaphylactic shock. There was no difference between the two groups. The number of mast cells in the lung tissue of patients with traumatic shock was significantly lower than that of amniotic fluid. There are significant differences between embolization and anaphylactic shock, indicating that amniotic fluid embolism can be diagnosed by immunohistochemical detection of lung mast cell tryptase.


Diagnosis and identification of amniotic fluid embolism


Mainly based on the typical clinical manifestations, rapid initial diagnosis and immediate rescue, the necessary auxiliary examinations at the same time as the rescue, but can not wait for the results of the inspection to deal with the opportunity to rescue.

The diagnosis of amniotic fluid embolism is a very complicated problem. As early as 1948, the famous obstetrician Eastman published the following opinion: "We must be careful not to let it (diagnosis of amniotic fluid embolism) become a trash can. All deaths that are difficult to explain in the labor process, especially those that have not been confirmed by autopsy, can be thrown inside. "To date, there have been hundreds of cases of amniotic fluid embolism reported in the literature. Pregnant women are pregnant as early as 20 weeks of gestation. Sudden death in abortion, but also died 48 hours after delivery, some make it difficult to explain, although some people believe that only by clinical symptoms, no need to confirm the autopsy can diagnose amniotic fluid embolism, but at present the relevant pathogenesis and clinical detection means Before it was unclear and resolved, its diagnostic criteria were difficult to fully harmonize.

1, medical history

It should be known whether oxytocin has been used, whether there is excessive contraction in the labor process or has been pressed in the abdomen, early exfoliation of the placenta, premature rupture of membranes, etc. In recent years, the cesarean section rate has increased, after cesarean section Unexplained bleeding should also take into account the possibility of the disease.

2, clinical manifestations

Patients may have symptoms such as chills, coughing, cyanosis, etc. If there is no prodromal symptoms, sudden breathing difficulties, cyanosis, foamy bloody sputum, wet sputum in the lungs, increased heart rate, decreased blood pressure, and even convulsions and coma should be considered. And the possibility of this disease, as for the heartbeat, sudden stop of breathing, although rare, should also suspect the disease.

The severity of the disease is related to the amount of amniotic fluid entering and the composition and speed. If the amount of entry is small and the speed is slow, the performance may be delayed amniotic fluid embolism after delivery.

For the diagnosis of AFE, some scholars such as Clark et al (1995) believe that only clinical symptoms and some laboratory tests can be performed without pathological evidence, and the inclusion criteria for diagnosis are established. Locksmith (1999) briefly summarizes them as follows: Acute hypotension and cardiac arrest; 2 acute hypoxia; 3 coagulopathy; 4 no other clinical manifestations that can be explained; 5 occurring within 30 minutes of labor or delivery or surgical abortion.

Locksmith believes that other diseases with the same symptoms and signs as AFE have hemorrhagic shock, early placental ablation, sepsis, pulmonary infarction, inhaled stomach contents, eclampsia, less common allergies, anesthetic toxicity, myocardial infarction Air embolism, cerebral embolism and cerebral hemorrhage can be seen. If you only rely on clinical manifestations, you can misdiagnose AFE as AFE and throw it into the "trash bin".

3. Auxiliary inspection

(1) Finding tangible substances in amniotic fluid in maternal blood and maternal tissues: The rapid and very sensitive and specific methods for the presence of amniotic fluid in maternal blood have not yet been confirmed, so the traditional methods of the past are still of great value. In particular, if typical AFE symptoms and signs appear, and the contents of amniotic fluid are found in maternal blood or maternal tissue, the diagnosis will be more certain if there are some unexplained symptoms and signs, such as DIC that is difficult to interpret and in the mother. The presence of more amniotic fluid in some tissues will also contribute to the diagnosis of AFE.

1 maternal blood: usually in the rescue of patients often for jugular vein puncture or femoral vein incision, can be used for venous cannulation to the inferior vena cava part of the blood pumping 10ml, centrifugal sedimentation or static precipitation after taking the supernatant smear Wright-Giemsa staining, looking for bristles, squamous epithelial cells, if found to be diagnosed, you can also use Sudan III staining to find fat particles, or use Ayoub-Shklar staining for keratin, if found with fat particles and keratin, there are also Help with diagnosis.

However, some scholars have suggested that squamous cells can not be found in maternal blood or certain tissues to diagnose AFE. Clark et al. (1988) found squamous cells in blood samples taken from pulmonary artery intubation in non-pregnant women and pregnant women. Therefore, it is advisable to use a squamous cell in the blood to diagnose AFE.

2 resected uterus: AFE or DIC occurs during cesarean section and AFE or DIC occurs after natural delivery, and the uterus is removed. The paracervical venous plexus and the lower part of the uterus are around the incision in the lower part. The amniotic fluid may be found in the lower lip venous plexus. The contents, such as squamous cells, fetal fats, etc., are unlikely to be found in the squamous cells of the mother. It is reported that the amniotic fluid content is about 50% here and within the broad ligament plexus.

(2) Coagulation dysfunction check: When the patient enters the coagulopathy period, the main examination contents are as follows:

1 platelet count: less than 100 × 109 / L (100,000 / mm3) is abnormal, less than 50 × 109 (50,000 / mm3) for critically ill patients.

2 fibrinogen determination: below 2g / L (200mg / dl) is abnormal, less than 1g / L (100mg / dl) for critically ill patients.

3 prothrombin time measurement: normal for 13s, if extended to 16s or more has clinical significance.

4 coagulation test: pumping patients with venous blood 5ml, coagulation in 6min, normal fibrinogen levels, 10 ~ 15min coagulation in 1 ~ 1.5g / L (100 ~ 150mg / dl), more than 30min non-coagulated <1g / L (100mg/dl), the latter two are abnormal and have clinical significance.

5 plasma protamine sub-agglutination test (3P test): normal soluble fibrin monomer complex (SFMC) content is low, 3P test negative; DIC, SFMC increased, 3P test positive.

In the above test, the clot test is simple, the doctor can observe by himself, if the platelet count and fibrinogen measurement values are low, the prothrombin time is prolonged, the 3P test is positive, and the DIC diagnosis can be established.

In addition, in order to understand whether the fibrinolytic activity is increased, the euglobulin lysis time and thrombin time can be determined.

(3) X-ray chest radiograph: slow development of the disease, after 6 hours of onset, if circumstances permit, you can make a chest radiograph at the bedside; if there is diffuse point in the lung, flaky shadow infiltration, distributed around the hilum, right Heart enlargement, mild atelectasis and other manifestations can help diagnose.

(4) Electrocardiogram: suggesting that there is a right atrium, the right ventricle is enlarged, and the myocardium is hypoxic.

4. Diagnosis after death

(1) Right ventricular blood test to test: If the patient died quickly, the diagnosis is unclear, you can take right ventricular blood for testing, the method is already described, find the tangible substances in amniotic fluid, especially the mane can be diagnosed as amniotic fluid embolism.

(2) Autopsy: typical manifestations of significant enlargement of the right ventricle, pulmonary edema, alveolar hemorrhage, squamous epithelial cells containing fetal skin, mane, fetal fat and from microvessels and capillaries with a diameter of <1 mm in the lung The mucin of the fetal intestine, the bile microtubule in the meconium, which is found in the kidney, heart, and brain tissue of the patient, and is commonly found in the uterus and its veins.

5, special examination of TKH-2 monoclonal antibody, meconium and amniotic fluid containing Sialyl Tn antigen, the antigen can be identified by radioimmunoassay inhibition method with TKH-2 monoclonal antibody, serum and non-pregnant women's Sialyl Tn concentration after pregnancy The same, but the concentration of Sialyl Tn antigen in amniotic fluid embolization is higher, reaching 105.6±59.0v/ml, so AFE can be diagnosed with TKH-2 monoclonal antibody, but this method is difficult to apply in AFE emergency diagnosis and treatment.

Differential diagnosis

1, eclampsia convulsions: usually have high blood pressure, edema and proteinuria history, in prenatal, postpartum, postpartum can occur, no fetal membrane rupture factors, chest examinations generally no Luoyin, DIC examination is generally no abnormalities.

2, congestive heart failure: a history of heart disease, an increased burden of heart burden, patients suddenly flustered, shortness of breath, cough foamy phlegm, generally no convulsions, bleeding and renal failure, after the heart failure control symptoms can be improved.

3, cerebrovascular accident: the patient has a history of hypertension, headache, dizziness, sudden coma, can occur hemiplegia.

4, epilepsy: patients often have a history of convulsions, there are incentives for mental factors, patients generally have no DIC and renal failure.

5, other postpartum hemorrhage caused by non-DIC causes: generally can find a clear cause, no change in blood coagulation mechanism.

6, thromboembolic disease: patients often have hypercoagulable state, the performance of lower extremity deep vein thrombosis, generally no bleeding.

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