An article on amniotic fluid embolism

I believe that many pregnant mothers, whether they choose natural childbirth or cesarean section, will be informed of the risks of childbirth and surgical anesthesia by obstetricians or anesthesiologists before entering the hospital for delivery. Among them, amniotic fluid embolism is indispensable. Amniotic fluid embolism is a rare but most serious complication in obstetrics. Below I will introduce the relevant knowledge about amniotic fluid embolism in detail.

Amniotic fluid embolism (AFE) refers to a serious complication of delivery during which amniotic fluid suddenly enters the maternal blood circulation, causing acute pulmonary embolism, anaphylactic shock, disseminated intravascular coagulation, renal failure or sudden death. The incidence rate is 4/100,000 to 6/100,000. Amniotic fluid embolism is caused by the entry of tangible substances (fetal vellus, keratinized epithelium, vernix caseosa, meconium) and procoagulants in the contaminated amniotic fluid into the maternal blood circulation. Studies have shown that amniotic fluid embolism is mainly an allergic reaction, which is a series of allergic reactions of the mother to fetal antigens after the amniotic fluid enters the maternal circulation. Therefore, it is recommended to name it "pregnancy allergic reaction syndrome."

1. Risk factors:

1. Premature labor

2. Older pregnant women.

3. Cesarean section and instrumental delivery

4. Placenta previa and placental abruption.

5. Multiple parity (≥5 times).

6. Cervical laceration

7. Fetal distress

8. Eclampsia

9. Drug-induced labor

II. Pathophysiology: Entry of amniotic fluid into the maternal circulation

1. Cardiogenic shock (acute pulmonary hypertension and right heart failure, followed by left heart failure)

2. Respiratory failure: hypoxemia, ventilation-perfusion ratio imbalance, non-cardiogenic pulmonary edema

3. Inflammation: The body produces an immune or inflammatory response to the amniotic fluid.

3. Clinical manifestations:

1. Hypotension caused by cardiogenic shock: a prominent feature, the cause of death in 85% of patients, and arrhythmia makes treatment more complicated.

2. Hypoxemia and respiratory failure: Common early manifestations, detected by pulse oxygen saturation. Clinical manifestations also include confusion, agitation, drowsiness, dyspnea, cyanosis, etc., and moist rales may be found in both lungs. Severe hypoxemia can lead to permanent neurological damage or maternal brain death.

3.DIC: It may occur in 80% of patients, appearing tens of minutes or hours after the onset of cardiopulmonary symptoms. Common manifestations include ecchymosis, prolonged bleeding time and massive bleeding at the site of invasive operation.

4. Coma or convulsions.

IV. Outcome: The overall maternal mortality rate is close to 20%. Up to 85% of the survivors suffer from severe neurological damage caused by cerebral hypoxia. In developed countries, maternal deaths caused by amniotic fluid embolism account for 10% of total maternal deaths, and neonatal mortality is 20%~60%.

5. Treatment:

1. Supportive treatment: correct hypoxia, improve cardiopulmonary function, and maintain hemodynamic stability.

2. Correct hypoxia: oxygen inhalation through mask or mechanical ventilation.

3. Correct pulmonary hypertension: use drugs such as papaverine hydrochloride and phentolamine.

4. Cardiotonic treatment: drugs such as digoxin can prevent heart failure.

5. Anti-shock treatment: Perform cardiopulmonary resuscitation if necessary.

6. Correct coagulation dysfunction: transfusion of fresh frozen plasma, cryoprecipitate, fibrinogen, etc.

7. Anti-allergic treatment.

6. Anesthesia precautions:

Intraoperative anesthesia management

1. Immediately activate a multidisciplinary rescue team

Obstetrics, anesthesiology, neonatology, ICU, and blood bank work together to prioritize the goal of maintaining maternal circulation and oxygenation and delivering the fetus quickly.

2. Monitoring points

Basic monitoring: continuous ECG, SpO₂, invasive arterial blood pressure (IBP), central venous pressure (CVP).

Advanced monitoring: echocardiography (TEE/TTE) to assess cardiac function, pulmonary artery pressure and volume status; dynamic monitoring of coagulation function (PT/APTT, fibrinogen, D-dimer, platelets).

Blood gas analysis: Review every 15-30 minutes, paying attention to lactate, electrolytes and coagulation indicators.

3. Choice of anesthesia method

General anesthesia (preferred): It is suitable for patients with hemodynamic instability or abnormal coagulation function to avoid the risk of epidural hematoma caused by intrathecal anesthesia.

Spinal anesthesia: only for patients in the early stage of AFE with stable vital signs, and coagulation function needs to be carefully assessed.

In an emergency: No need to wait for anesthesia to fully take effect; saving lives is the priority.

4. Circulation support

Fluid management: limit crystalloid infusion (to avoid pulmonary edema), mainly colloid fluid or blood products, with a target CVP of 8-12 mmHg.

Vasoactive drugs:

- First-line drug: norepinephrine (maintain MAP ≥ 65 mmHg).

- Severe hypotension: Combined with epinephrine (0.05-0.1 μg/kg/min).

- Right heart failure: dobutamine (2-10 μg/kg/min) or milrinone.

- Anti-allergic treatment: Early intravenous injection of epinephrine (10-50 μg) and hydrocortisone (200 mg).

5. Correction of coagulation disorders

- Target: fibrinogen>1.5 g/L, platelets>50×10⁹/L.

- Infusion strategy:

- Fibrinogen: 4-6 g (or cryoprecipitate 10 U).

- Fresh frozen plasma (FFP): 15-20 mL/kg.

- Platelets: 1-2 therapeutic doses.

- Tranexamic acid (TXA): 1 g intravenous drip (first dose).

-Avoid heparin unless a thrombotic event is identified.

6. Respiratory support

- High-flow oxygen inhalation or non-invasive ventilation, and immediate endotracheal intubation if necessary (for patients with hypoxemia or impaired consciousness).

- Mechanical ventilation strategy: low tidal volume (6-8 mL/kg), appropriate PEEP (5-10 cmH₂O), to avoid excessive airway pressure that increases the right heart load.

- Treatment of pulmonary hypertension: papaverine hydrochloride, atropine, aminophylline, α-adrenergic inhibitors (phentolamine), etc.

7. Fetal delivery and uterine management

- 5-minute emergency cesarean section: If the mother's heart stops beating or has severe hypoperfusion, the fetus is delivered immediately to improve maternal circulation.

- Management of postpartum hemorrhage: uterotonics (oxytocin, carbetocin), uterine compression, B-Lynch suture, and uterine artery embolization or resection if necessary.

VII. Conclusion

The core of prevention and management of amniotic fluid embolism is standardized prenatal examinations, scientific delivery and timely treatment, which requires cooperation between mothers and medical institutions. Medical staff need to remain highly vigilant, especially in high-risk deliveries, to maximize the safety of mothers and babies.

Yan Weina, attending physician of the Department of Anesthesiology, Zunhua People's Hospital

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