Obstetrics - Amniotic Fluid Embolism

Question 1

What is amniotic fluid embolism?

Answer 1

Amniotic fluid embolism (AFE) is a rare, catastrophic obstetric emergency that can present with sudden maternal collapse, associated with hypoxaemia, shock and
coagulopathy. It occurs when amniotic fluid or cells enter the maternal circulation.

Question 2

What is the incidence of AFE?

Answer 2

Studies estimate an incidence between 1 and 12 cases per 100,000 deliveries.

Question 3

What are the pathogenic mechanisms of AFE?

Answer 3

The pathophysiology of AFE is still poorly understood. The syndrome was
previously thought to have an embolic mechanism, due to fetal tissue/amniotic fluid forcibly entering the maternal circulation and resulting in physical consequences similar to that of a pulmonary embolus. However, it is now thought to be a two-phase immune response to the antigens contained in fetal tissue, resulting in a systemic response similar to that of anaphylaxis:

Phase 1
Vasoactive substances are produced in response to fetal tissue antigens.
This results in pulmonary artery vasospasm leading to acute right heart
failure, hypotension and hypoxaemia. This phase may last up to
30 minutes.

Phase 2
Right ventricle recovers, but left ventricular failure and pulmonary
oedema occur. Biochemical mediators and severe hypoxaemia lead to
increased capillary permeability, DIC, uterine atony and massive
haemorrhage.

Question 4

What are the clinical features of AFE?

Answer 4

The classical triad of an AFE is hypoxaemia, cardiovascular collapse and coagulopathy.
It may present with breathlessness, cyanosis, hypotension, dysrhythmias, DIC or sudden maternal collapse. However, presentation may be more subtle,
with non-specific symptoms including vomiting and anxiety

Question 5

What are the risk factors for AFE?

Answer 5

There are no proven risk factors, but the following are associated with an
increased risk of AFE:
1 Advanced maternal age
2 Placental pathology (praevia/abruption)
3 Induction of labour
4 Operative delivery
5 Multiparity
6 Polyhydramnios
7 Uterine rupture
8 Intrauterine death
9 Trauma (cervical lacerations etc.)
The syndrome is considered to be largely unpredictable and unpreventable.

Question 6

What are the principles of management of AFE?

Answer 6

The key features of the management of AFE focus on early recognition with prompt resuscitation of the mother, and expedited delivery of the fetus.
Treatment is predominantly supportive.
1 Rapid intravenous filling and the use of directly acting vasopressors are
usually required
– Left lateral tilt is essential in the antenatal patient to reduce aortocaval
compression by the gravid uterus
2 Rapid delivery of the fetus (do not delay delivery by transferring to theatre)
3 Activation of the major haemorrhage protocol should be considered as
plasma, cryoprecipitate and platelets are frequently required alongside
packed red cells (DIC is likely, secondary to activation of tissue factor and
factor X)
– Surgical intervention may be necessary for haemorrhage control
– Maintenance of uterine tone with oxytocin, ergometrine and prostaglandins
is essential
4 Establishing invasive monitoring can be hazardous due to rapidly developing
consumptive coagulopathy

Question 7

What are the differential diagnoses?

Answer 7

There are a number of differential diagnoses that can be divided into obstetric
and non-obstetric in aetiology.

Obstetric causes:
1 Placental abruption
2 Eclampsia
3 Uterine rupture
4 Peripartum haemorrhage

Non-obstetric causes:
1 Anaphylaxis
2 Total spinal anaesthesia
3 Septic shock
4 Massive pulmonary embolus