Amniotic Fluid Embolism

Amniotic fluid embolism is a rare obstetric emergency in which amniotic fluid, hair or other
debris, fetal squamous cell, mucus, vernix, meconium is entered into the maternal circulation via
the placental bed of the uterus forming an embolus which obstructs on to the pulmonary arteries
or alveolar capillaries causing cardiorespiratory (heart and lung) collapse and coagulopathy. It is
a rare obstetric emergency.
It was first formally characterized in 1941. While it is estimated to be the fifth most common
cause of maternal mortality in the world, there has been discrepancy with respect to the incidence
and mortality of amniotic fluid embolism.

Epidemiology
1. The incidence of clinically detectable AFE is low.
2. Estimated to be 1 in 8000 and 1 in 80,000 deliveries Maternal mortality approaches 80% ,
although more recent studies show 1 in 20,464 deliveries for a more precise number
3. 5% - 10% of maternal mortality in the USA is due to AFE.
4. Among them 50% die within the first hour of onset of symptoms and survivors of the initial
cardiorespiratory phase and 50% develop a coagulopathy. If the fetus is alive at the time of
the event, nearly 70% will survive the delivery but 50% of the survived neonates will

incure

neurologic

damage.

Presentation

It is believed however that once the fluid and fetal cells enter the maternal pulmonary circulation
in general terms there will be profound respiratory failure with deep cyanosis and cardiovascular
shock followed by convulsions and profound coma, however this does occur in two phases
detailed below:

First phase
The patient experiences acute shortness of breath and hypotension. This rapidly progresses to
cardiac failure leading to a reduction of perfusion to the heart and lungs. Not long after this stage
the patient will lapse into a coma. While previously believed to have a maternal mortality rate of
60-80%, more recently it has been reported at 26.4%.
Amniotic fluid enter the maternal circulation
Biochemical mediators
Pulmonary artery vasospasm
Pulmonary hypertension
Elevated right ventricular pressure
Hypoxia (myocardial and pulmonary capillary damage)
Left heart failure
Acute respiratory distress syndrome

Second phase
Although many women do not survive beyond the first stage, about 40 percent of the initial
survivors will pass onto the second phase. This is known as the hemorrhagic phase and may be
accompanied by severe shivering, coughing, vomiting, and the sensation of a bad taste in the
mouth. This is also accompanied by excessive bleeding as the blood loses its ability to clot.
Collapse of the cardiovascular system leads to fetal distress and death unless the child is
delivered swiftly.
Biochemical mediators

DIC
Haemorrhagic phase characterized by massive bleeding and uterine atony
Resulting in depletion of fibrinogen, platelets and coagulation factors especially factors V, VII
and XIII
Most patients will have hypofibrinogenemia, abnormal PT and PTT and low platelet count.

Causes
It is mostly agreed that this condition results from amniotic fluid entering the uterine veins and in
order for this to occur there are three prerequisites:

Ruptured membranes (a term used to define the rupture of the amniotic sac)

Ruptured uterine or cervical veins

A pressure gradient from uterus to vein

Although exposure to fetal tissue is common and thus finding fetal tissue within the maternal
circulation is not significant, in a small percentage of women this exposure leads to a complex
chain of events resulting in collapse and death.

Risk factors
1. Advanced maternal age of 35 years or older
2. Abdominal trauma]or amniocentesis
3. Use of drugs to induce labor, such as misoprostol, oxytocin
4. Caesarean or instrumental vaginal delivery
5. Polyhydramnios
6. Cervical laceration or uterine rupture
7. Placenta previa or abruption
8. Eclampsia, and fetal distress
9. Multiparity
10. Meconium present in amniotic fluid
11. IUFD
12. Tetanic uterine contraction
13. Sudden fetal expulsion
14. Placenta accrete
Clinical features

1. Sudden onset of maternal respiratory distress such as, severe dyspnea, tachypnea, cough,
2.
3.
4.
5.

cyanosis and sign of pulmonary edema may occur.

Hypotension
Hyertonic uterine contraction
Fetal bradycardia: in response to uterine hypoxia
Sign of cardiovascular collapse such as rapid pulse without fluid loss, hypotension and

right sided heart failure.

6. Uterine atony usually occurs after delivery
7. A sudden drop in O2 saturation cab be initial incication of AFE in C/S
8. 10-15%
patient will develop
gradnmal seizures (tonic-clonic

seizures)

9. Severe haemorrhage after delivery due to blood coagulation disorder.

Diagnosis
1.
2.
3.
4.

Amniotic fluid detected in maternal blood

X-ray may shows effusions, enlarged heart or pulmonary edema
ECG may show a right strain pattern with ST-T changes and tachycardia.
Maternal sputum contain fetal squamous.

Management
Goals of management
1. Restoration of cardiovascular and pulmonary equilibrium.
2. Re-establishing uterine tone
3. Correct coagulation abnormalities
Immediate management
1.
2.
3.
4.
5.
6.
7.
8.
9.

Set up IV infusion
Oxygen administration
Resuscitation should be done
Airway control endotrachial intubation for maximal ventilation and oxygenation.
Send blood for CBC, ABG, PT, PTT, fibrinogen, FDP for laboratory investigation
Treat hypotension with crystolloids.
Steroid may be indicated.
Dopamine infusion for myocardial support if patient remains hypotensive.
Moniter central venous pressure to diagnose right ventricular overload and guide fluid

infusion.
10. Monitor pulmonary artery and capillary wedge pressure and echocardiography to
evaluate left ventricular function.
11. Suction the patient to remove secretion.
12. Monitor fetal heart rate continuously.
13. Monitor mothers vital signs.
14. Delivery of the fetus quickly by immediate caesarean section.

15. Treat coagulopathy with fresh frozen plasma (FFT) for prolonged PTT, and transfuse
platelets for platelet count less than 20,000 ml.
16. Restoration of uterine tone such as massage, oxytocin or prostaglandin.
17. Improve cardiac output and uterine perfusion helps to restore uterine tone.
18. Repeated blood sampling and blood gases should be done to evaluate the efficacy of
resuscitation.
Prognosis
Prognosis is not so good. Although early recognition and prompt resuscitation may lead to
saving of womans life but lead to permanent neurological impairment, 50% cases die in first
hour of symptoms whereas 50% of survivors of phase may develop DIC and neurological
complication. Neonatal survival 79% seen.
Complication
1. Cardiopulmonary failure
2. DIC
3. Acute renal failure due to excessive blood loss.
4. Neurological complication