8. Amniotic Fluid Embolism Flashcards
You are the anaesthetist on-call for delivery suite.
You are called urgently to a delivery room where a woman in the second stage of labour
has collapsed.
Just prior to this she became extremely breathless and went blue, according to the midwife.
She is now not breathing.
What is your immediate management?
RESUSCITATION – this should be easy marks because it is ‘bread and
butter’.
ALWAYS follow the ABC approach. You can be talking about this whilst
thinking about the differential diagnosis.
Call for immediate help from a senior obstetrician and anaesthetist.
If not breathing and no pulse – commence CPR and get defibrillator.
Establish an airway – the trachea should be intubated if appropriate.
Establish breathing with100% oxygen.
Circulation – Large-bore intravenous cannulae should be sited with blood
sent for cross-match, coagulation screen, full blood count, urea, electrolytes
and blood glucose.
Commence fluid resuscitation.
Left lateral tilt/Manual uterine displacement.
After 5 minutes, consideration should be given to caesarian section to aid resuscitation attempts.
There is no evidence of blood loss. What is the differential diagnosis?
The causes of sudden cardiovascular collapse in pregnancy are:
- Amniotic fluid embolism
- Pulmonary thrombo-embolism
- Venous air embolism
- Occult haemorrhage such as
placental abruption or hepatic rupture in a
patient with fulminating pre-eclampsia/HELLP - Intra-cerebral bleed
- Drug toxicity (including local anaesthetics)
- Sepsis
- Myocardial infarction
What do you know about amniotic fluid embolism?
Rare (1:20 000 deliveries) but devastating complication of labour or early
puerperium.
Presents with severe dyspnoea, cyanosis and sudden cardiovascular
collapse (with or without bleeding).
Seizures may also occur.
Cardiac arrest occurs in up to 87%.
Up to 50% die in the first hour and the overall mortality is 60–80%.
Most survivors have a neurological injury.
AFE patho
Amniotic fluid contains fetal debris, prostaglandins and leukotrienes which
block pulmonary vessels, cause pulmonary vasoconstriction, pulmonary
hypertension and acute right ventricular failure. Hypoxia causes global
myocardial ischaemia and acute lung injury. There is widespread
complement activation.
Women who survive these events may enter a second haemorrhagic phase
characterized by massive haemorrhage with uterine atony and DIC.
The US national registry concluded that the pathophysiology was more
in-keeping with an anaphylactoid reaction rather than purely an embolic
process as fetal squames have been found in the lungs of women without
AFE syndrome.
Three major factors contribute to the problems encountered in this condition:
- Acute pulmonary embolism.
- Disseminated intravascular coagulation (DIC)
- Uterine atony
What causes Hypoxia
Extreme hypoxia is caused by pulmonary and cardiac shunts.
Pulmonary shunt
The transient increase in PVR may cause a redistribution of blood flow
from blocked pulmonary vessels to patent ones,
resulting in incomplete oxygenation as the blood-flow through them
overwhelms their maximum rate of oxygenation.
The fall in cardiac output results in a fall in mixed
venous O2 saturation returning to the heart,
compounding oxygenation problems.
There may be direct myocardial depression with pulmonary oedema.
Cardiac shunt
A (potentially) patent foramen ovale is present in 35%
of the population.
Very high PA pressures may cause
mixed venous blood to pass through it.
Coagulopathy
Severe left-sided heart failure (mechanism unclear) causes hypotension.
Coagulopathy (in up to 83%) is probably caused by tissue factor or
trophoblasts in the amniotic fluid stimulating the clotting cascade.
Diagnosis
is based on clinical presentation and laboratory findings.
Monoclonal antibody TKH-2 has been used to demonstrate fetal mucin in
the pulmonary vasculature, but it may still not be specific for the syndrome.
Infant outcome
Future successful pregnancy
The intact infant survival rate is 70%. Neurological status of the infant is
directly related to the time elapsed between maternal arrest and delivery.
Risk of recurrence is unknown. Successful subsequent pregnancies have
been reported. Recommending elective caesarean for future pregnancies in
an attempt to avoid labour is controversial.
How would you manage this lady after delivery of the fetus?
Intensive care
Survivors of the initial event are at risk of:
ARDS
Circulatory failure
DIC
Treatment is supportive:
Ventilation
Inotropic support
Clotting factors
Factor VIIa for massive haemorrhage**
Uterine atony may necessitate oxytocin and carboprost
(HemabateTM) (PGF2).
No form of therapy has been found to improve outcome.
Hydrocortisone and adrenaline have been recommended due to the
similarity of the condition with anaphylaxis.
