What Is an Amniotic Fluid Embolism?

Amniotic fluid embolism refers to the severe labor complications of acute pulmonary embolism, anaphylactic shock, disseminated intravascular coagulation, renal failure or sudden death caused by amniotic fluid suddenly entering the mother's blood circulation during delivery. The incidence rate is 4 / 100,000 to 6 / 100,000. Amniotic fluid embolism is caused by the pollution of tangible substances in the amniotic fluid (fetal hair, keratinized epithelium, fetal fat, meconium) and procoagulant substances into the mother's blood circulation. In recent years, studies have suggested that amniotic fluid embolism is mainly an allergic reaction, which is a series of allergic reactions caused by the mother to fetal antigens after the amniotic fluid enters the maternal circulation, so it is suggested to be named "pregnancy allergic reaction syndrome".

Basic Information

English name: amniotic fluid embolism
Visiting department: Obstetrics and Gynecology
Common causes: Contaminates tangible substances in amniotic fluid, procoagulant substances enter the maternal blood circulation

Common symptoms: Chills, irritability, cough, shortness of breath, cyanosis, vomiting
Contagious: no

Causes of amniotic fluid embolism

Amniotic fluid embolism mostly occurs at the time of delivery or rupture of the membrane, and can also occur postpartum. It is more common in term labor, but also in mid-term induction of labor or forceps and curettage. Most of them occur suddenly and the disease is dangerous.

The occurrence of amniotic fluid embolism usually requires the following basic conditions: increased pressure in the amniotic cavity (excessive uterine contraction or tonic uterine contraction); rupture of the membrane (of which 2/3 is premature rupture of the membrane, 1/3 is self-rupture of the membrane) ); There are open veins or sinuses in the cervix or cervix.

The occurrence of amniotic fluid embolism is usually caused by the following factors: most women who have undergone maternal birth; premature rupture of membranes or history of artificial rupture of membranes; common cases of excessive uterine contraction or inappropriate application of oxytocin (oxytocin); Rupture or surgery is prone to amniotic fluid embolism.

Clinical manifestations of amniotic fluid embolism

The rapid onset of amniotic fluid embolism, often too late to do many laboratory tests, patients have died, so early diagnosis is extremely important. In most cases, some prodromal symptoms such as chills, irritability, cough, shortness of breath, cyanosis, and vomiting first appear at the time of onset. If the amount of amniotic fluid invasion is very small, the symptoms are mild and sometimes they can recover on their own. Such as the ambiguous amniotic fluid or a large amount of amniotic fluid, typical clinical manifestations occur one after another.

Respiratory cycle failure

According to the condition is divided into two types of fulminant and slow. After the fulminant symptoms are prodromal symptoms, dyspnea and cyanosis will soon appear. Acute pulmonary edema includes cough, spitting pink foamy sputum, fast heart rate, decreased blood pressure, and even disappears. In a few cases, only one scream was heard and cardiac arrest followed by death. Symptoms of the slow respiratory circulatory system are mild, and there are no obvious symptoms. They are not diagnosed until the postpartum bleeding occurs and the blood does not condense.

2. Systemic bleeding tendency

Some amniotic fluid embolism patients survived the respiratory and circulatory failure period, and subsequently developed DIC, which manifested as a tendency of systemic bleeding mainly caused by vaginal bleeding, such as mucosa, skin, needle and eye bleeding, and hematuria. However, some cases of amniotic fluid embolism lack clinical symptoms of the respiratory circulatory system. The onset of vaginal bleeding is difficult to control postpartum, and it is easy to be mistaken for weak uterine contraction caused by postpartum hemorrhage.

3. Multiple system organ damage

All organs of the disease are damaged, and the kidney is the most commonly damaged organ except the heart. Due to hypoxia in the kidney, oliguria, urinary occlusion, hematuria, and azotemia may occur due to renal failure. Patients may experience irritability, convulsions, and coma during cerebral hypoxia.

Amniotic fluid embolism examination

Non-specific inspection

(1) Electrocardiogram The right ventricle and right atrium are dilated, and the performance of myocardial strain can also be seen. At the same time there is tachycardia.

(2) The chest radiograph may show no abnormalities. 70% of patients may have mild pulmonary edema, which is manifested as diffuse, point-like infiltration shadows on both sides, distributed along the hilum, and the lungs are slightly enlarged. Heart shadow may increase.

(3) A sudden drop in blood oxygen saturation can often indicate a problem with pulmonary embolism.

(4) There are many differences in the test results of blood coagulation function , and the results depend on the survival time of patients and the degree of clinical bleeding. Platelet count <100 × 10 ⁹ / L; Prothrombin time prolonged, more than 10 seconds is diagnostic; Plasma fibrinogen <1.5g / L; Observe clot, take 5mL of normal maternal blood into test tube The blood clot formation was observed in the incubator for 8 to 12 minutes. The blood of patients with low fibrinogen was not easy to coagulate, and the blood clot was less in 30 minutes. The diffusion showed that the platelets were quite low and secondary fibrinolysis. Prolonged bleeding time and clotting time. The increase of fibrin degradation products, plasma protamine paracoagulation test (3P test) and ethanol gel test were positive.

2. Specificity check

(1) Detection of amniotic fluid components in the maternal circulation or lung tissue. Because the occurrence of amniotic fluid embolism is mainly caused by the presence of amniotic fluid and its constituents in the maternal blood, which results in pulmonary embolism and spasm. In uterine blood vessels and lung tissues, components derived from the fetus such as fetal squamous epithelial cells, hairs, and mucus were used as diagnostic criteria.

(2) Neuraminic-N-acetylgalactose (SialylTn) antigen detection in maternal serum and lung tissues In recent years, with the continuous development of immunological technology, this is a new diagnostic method for amniotic fluid embolism. Kobayashi et al. Found that the monoclonal antibody TKH-2 of mucin glycoprotein can recognize the oligosaccharide structure of mucin glycoprotein in amniotic fluid. Using immunoblot technology, TKH-2 can detect very low concentrations in meconium supernatant SialylTn antigen. Antigens that can be recognized by TKH-2 are not only abundant in meconium, but also appear in clear amniotic fluid. Immunohistochemical detection revealed that fetal small intestine, colon, and respiratory mucosal epithelial cells contained antigens that reacted with TKH-2. SialylTn was detected in meconium-contaminated amniotic fluid and clear amniotic fluid by radioimmunoassay. Antigen, but the former is significantly higher than the latter, SialylTn antigen is now found to be one of the characteristic components of meconium and amniotic fluid, SialylTn antigen accounts for about one tenth of meconium. The source of SialylTn antigen in amniotic fluid is still not very clear. Because of the expression of SialylTn antigen in the mucosal epithelium of the digestive tract and respiratory tract, it is thought that in addition to meconium, which is the main source of SialylTn antigen in amniotic fluid, some may be derived from mucus proteins of the fetal respiratory tract. The concentration of SialylTn antigen in pregnant women's serum after pregnancy is different. If there is meconium pollution in amniotic fluid, the concentration of SialylTn antigen in pregnant women's serum [(20.3 ± 15.4) U / ml] is slightly higher than those with clear amniotic fluid [(11.8 ± 5.6) U / ml]. However, the diagnostic value is that in the serum of patients with amniotic fluid embolism or those with amniotic fluid embolism-like symptoms, the SialylTn antigen is significantly increased, about (105.6 ± 59.0) U / ml. Therefore, the quantitative determination of SialylTn antigen in serum by a sensitive radioimmunocompetitive detection method is a simple, sensitive and non-traumatic method for the diagnosis of amniotic fluid embolism, which can be used for the early diagnosis of amniotic fluid embolism.

Histological diagnosis after maternal death is still very important. Immunohistochemical staining of lung tissue with TKH-2 found that patients with amniotic fluid embolism or patients with amniotic fluid embolism-like symptoms showed strong staining of the pulmonary vessels. The positive staining was completely suppressed by the submandibular gland mucin, suggesting that it was immunospecific.

(3) Determination of tissue anticoagulant factors As mentioned earlier, the formation of amniotic fluid is not the main cause of amniotic fluid embolism, and some humoral factors such as tissue factor-like procoagulant substances, leukotriene, etc. play a role in the pathophysiology. Played a very important role. Approximately 40% of patients with amniotic fluid embolism develop fatal coagulopathy. The coagulation activity of tissue factors can be antagonized by anti-tissue factor proteins, so theoretically, the detection of tissue factors in maternal blood can be used as a basis for distinguishing other obstetric DICs.

(4) Measurement of mast cells in lung tissue In recent years, there are a large number of literature reports on the mechanism of amniotic fluid embolism, and it is believed that the occurrence of amniotic fluid embolism is an allergic reaction of the body to fetal components in amniotic fluid, causing mast cells to degranulate and release histamine. Trypsin and other mediators cause severe pathophysiological changes in the body. Tryptase is a neutral protease and the main component of granules secreted by T cells and mast cells. Fineschi et al. Used a special immunohistochemical method to detect mast cell tryptase in the pulmonary circulation and found that the number of mast cells in the lung tissue of patients who died of amniotic fluid embolism and anaphylactic shock was significantly increased, there was no difference between the two, and they died of traumatic The number of mast cells in lung tissue of shock patients was significantly lower than that of patients with amniotic fluid embolism and anaphylactic shock, and there were significant differences. It is shown that the use of immunohistochemical detection of trypsin in lung mast cells can diagnose amniotic fluid embolism.

Amniotic fluid embolism diagnosis

It can occur after ruptured membranes, during or after childbirth, and in the case of intravenous induction of oxytocin or mid-pregnancy forceps, etc., sudden maternal irritability, chills, vomiting, cough, dyspnea, cyanosis, rapid shock . Those with acute onset can die within minutes.

After the blood pressure rises in some patients, postpartum hemorrhage often occurs, the blood does not congeal, and sometimes there is a tendency for systemic bleeding, and finally kidney, lung, and heart failure may occur.

Differential diagnosis of amniotic fluid embolism

Amniotic fluid embolism is easily misdiagnosed as other diseases:

Eclampsia

There is usually a history of hypertension, edema, and proteinuria, which can occur before, during, and after delivery. There is no factor of rupture of the membranes, and auscultation of both lungs is generally free of snoring. DIC examinations are usually normal.

2. Congestive heart failure

He has a history of heart disease, and the cause of increased heart burden. The patient has sudden panic shortness of breath, coughing foamy sputum, and generally has no convulsions, bleeding and renal failure. Symptoms can improve after heart failure control.

3. Cerebrovascular accident

The patient has a history of hypertension, headache, dizziness, sudden coma, and hemiplegia may occur.

4. Epilepsy

Patients often have a history of convulsions and inducement of mental factors. Patients are generally free of DIC and renal failure.

5. Postpartum hemorrhage caused by other non-DIC causes

A clear cause can usually be found without changes in the coagulation mechanism.

6. Thromboembolic disease

Patients often have a hypercoagulable state, deep vein thrombosis of the lower extremities, and generally no bleeding.

Amniotic fluid embolization treatment

The key to successful rescue of amniotic fluid embolism is early diagnosis, early treatment, early treatment with heparin, and early treatment of pregnant uterus. Summarized into the following aspects.

Anti-allergic

In the case of anaphylactic shock, high-dose corticosteroids should be used, and dexamethasone is usually administered intravenously. However, hormones can inhibit the function of the reticuloendothelial system, and the activated coagulation factors cannot be cleared in time to aggravate DIC. Therefore, it should be noted when repeated application, it is better to apply this drug on the basis of heparin treatment.

Oxygen

Should strive to provide positive pressure to continue to provide oxygen, at least with a mask or using a respirator, oxygen supply can reduce pulmonary edema, improve brain hypoxia and other tissue hypoxia.

3. relieve pulmonary hypertension

Oxygen supply can only solve the alveolar oxygen pressure, but can not solve the hypoperfusion of pulmonary blood flow. The pulmonary hypertension must be relieved as soon as possible to fundamentally improve hypoxia and prevent acute right heart failure, peripheral circulation failure and acute respiratory failure. The commonly used drugs are the following:

(1) Aminophylline has the effect of relieving pulmonary vasospasm, dilating coronary arteries and diuretics, as well as relieving bronchial smooth muscle spasm.

(2) Papaverine has an expansion effect on coronary blood vessels, lungs, and cerebral blood vessels, and is an ideal drug to relieve pulmonary hypertension.

(3) Atropine relieves pulmonary vasospasm, but also suppresses the secretory function of the bronchi and improves microcirculation.

(4) phentolamine relieves pulmonary vasospasm.

4.Anti-shock

Shock caused by amniotic fluid embolism is more complicated and is related to various factors such as allergies, pulmonary origin, cardiogenic origin, and DIC. Therefore, it must be comprehensively considered when handling.

(1) Expansion of blood volume There is insufficient effective blood volume during shock, and blood volume should be expanded as soon as possible. It is best to use a pulmonary artery floating catheter to measure the pulmonary capillary wedge pressure (PCWP), and replenish blood volume while monitoring the heart load. If PCWP is measured unconditionally, infusion can be guided according to central venous pressure. No matter which method of monitoring is used, 5 mL of blood should be drawn at the same time as intubation, a blood sedimentation test, smear staining to look for amniotic fluid components, and related DIC laboratory tests. The choice of volume expansion fluid, began to use dextran-40, intravenous drip, those with blood loss should be replenished with fresh blood and balance fluid.

(2) Correction of acidosis For the first time, 5% sodium bicarbonate can be given, and 1/2 to 2/3 of the calculated amount is injected first. It is best to measure arterial blood gas and acid-base, and to administer according to imbalance.

(3) Adjust vascular tone. Those with severe and severe shock symptoms or blood pressure that is still unstable despite the blood volume being replenished can be selected from vasoactive drugs. Dopamine is usually given intravenously to ensure blood supply to important organs.

5. Prevention and treatment of DIC

Once the diagnosis of amniotic fluid embolism is established, anticoagulation therapy should be started and heparin should be used as soon as possible to inhibit intravascular coagulation and protect renal function. Application of heparin intravenous drip. Amniotic fluid embolism can occur before, during, or after childbirth. Should be alert to the occurrence of severe postpartum hemorrhage, the safest measure is to give fresh blood on the basis of heparin, and supplement fibrinogen, platelet suspension, and fresh lyophilized plasma to supplement clotting factors to prevent postpartum hemorrhage.

6. Prevention of Heart Failure

Rapid digitalis preparations can be injected intravenously and repeated once every 4 to 6 hours if necessary. In addition, furosemide is injected intravenously to prevent heart failure, which is of great significance to improve the success rate of rescue.

7. Prevention and treatment of multiple organ damage

In the case of amniotic fluid embolism, except the lungs and heart, followed by the kidneys. To prevent renal failure, it is necessary to pay attention to the blood perfusion of the kidney when anti-shock. Do not use or cautiously use vasoconstrictor drugs before blood volume is replenished. When blood volume is replenished, blood pressure rises and urine output is still less than 17 mL per hour Diuretics should be given. Ineffective patients often suggest acute renal failure, and emergency measures such as hemodialysis should be used as soon as possible.

8. Prompt and proper use of antibiotics

To prevent infection.

9. Obstetric treatment

Timely obstetric treatment is extremely important to the success of the rescue. Amniotic fluid embolism occurs before the fetus is delivered, and it should actively improve the respiratory and circulation functions, prevent DIC, and rescue shock. If the cervix is not open or not fully opened, cesarean section should be performed to relieve the cause and prevent the disease from worsening; those with a full cervix opening and the fetal first exposed under the ischial spine can use forceps to assist delivery. Pay close attention to uterine bleeding during operation and postpartum. If there is no bleeding, continue conservative treatment; if there is uncontrollable postpartum hemorrhage and the blood is not condensed, hysterectomy should be performed decisively to control blood sinus hemorrhage on the placenta peeling surface and block the amniotic fluid sediment from continuing to enter the blood circulation, making the disease worse. Opinions on the use of tocolytics are still inconsistent, and users do not agree that strengthening the contractions can cause the amniotic fluid stored in the uterine wall to enter the maternal blood circulation, resulting in worsening of the condition.

Amniotic fluid embolism prevention

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

1. Do not perform peeling during artificial rupture to reduce the damage of small vessels in the cervical canal.

2. Do not perform artificial rupture in uterine contraction.

3. Grasp the indications for cesarean section, protect the open blood vessels on the uterine incision before puncturing the amniotic membrane during the operation.

4. Master the indications for oxytocin application.

5. The situation of stillbirth and early stripping of placenta should be closely observed.

6. Avoid birth injuries, uterine rupture, cervical laceration, etc.

(1) Do not make the uterine contraction too strong during delivery. The uterine contraction will increase the intrauterine pressure, which may cause the endometrium of the lower uterus to rupture. Then the amniotic fluid enters the mother from the gap during uterine contraction. Sedatives and uterine contraction agents need to be given appropriately to reduce uterine contractions.

(2) Artificial peeling and artificial rupture, care should be taken to avoid injury when expanding the cervix and peeling. After the rupture of the membrane, the amniotic fluid can directly contact the open vein, and it is easy for the amniotic fluid to enter the mother's blood circulation when the contraction is enhanced. The artificial rupture of the membrane must be performed during the uterine contractions to reduce the chance of amniotic fluid entering the maternal blood circulation.

(3) Use oxytocin correctly and observe closely to prevent excessive uterine contraction. Special care should be taken when using oxytocin.

(4) For those with predisposing factors, closely observe and watch out for the occurrence of this disease, such as cesarean section, placenta previa, early stripping of placenta, and sudden delivery.

Prognosis of amniotic fluid embolism

Amniotic fluid embolism is because amniotic fluid enters the mother's blood circulation during delivery. Amniotic fluid has tangible substances such as fetal fat and epithelial cells, which can directly block blood vessels and can also be used as strong coagulation substances, causing pulmonary embolism, severe shock and blood loss The coagulation situation caused the mother to have uncontrollable bleeding. Once amniotic fluid embolism occurs, even with active rescue, the mortality rate is still very high, and the maternal mortality rate can be as high as 80%. The time of death is as fast as several minutes to several hours. About 1/3 of the patients die within half an hour of the onset, and another 1/3 die within 1 hour of the onset, mostly due to pulmonary vascular embolism, and the remaining 1/3 die from Non-coagulated blood or renal failure. Amniotic fluid embolism is the most dangerous complication of obstetrics. Because this situation is often not expected before delivery, the mother should be closely observed during delivery, especially in the case of fetal death, giant children, placenta previa, placenta Precautions must be taken when premature ablation or excessive uterine contraction is present. ^[1]