Westmead Hospital Topic Summary

2014 Version

Amniotic Fluid Embolism

Introduction
also referred to as anaphylactoid syndrome of pregnancy
catastrophic condition which occurs during pregnancy or shortly after
delivery
characterized by abrupt onset of hypotension,hypoxia &consumptive
coaugulopathy..
Incidence between 1 and 12 cases per 100,000 deliveries
maternal mortality rate: 20 to 60%.
many survivors suffer irreversible neurologic sequelae caused by cerebral
hypoxia
40% fetal mortality
50% of surviving infants have long-term neuro impairment mostly due to
cerebral hypoxia.
Of those who survive the first hour, 40% will develop a coagulopathy.
can occur in any trimester
squamous cells and mucin of fetal origin can be found in the maternal
pulmonary vasculature, kidneys, liver, spleen, pancreas, and brain

Risk factors
Hypertonic uterine action
effect of amniotic fluid embolism rather than the cause
uterine blood flow ceases completely when IUP exceeds 35 to 40mmH
least likely time for fetomaternal exchange to take place.
Caesarean section
Polyhydramnios
Precipitate labour.
Oxytocin stimulated labour
Rupture of membrane
Multiparity
Placental abruption
Most cases do not have risk factors as mentioned above
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Is also reported with mothers with intact membranes, uncomplicated 2

trimester pregnancies

nd

Clinical Presentation
linked to precipitous labor, uterine hyperstimulation, and the use of
oxytocin
analysis of national registry data has questioned the strength of these
associations.
12% of the cases occurred in women with intact membrane, 70% during
labour, 11% after vaginal delivery and 19% during C/S with or without
labour
onset usually during labor and delivery or in the immediate postpartum
period
classically a women in the late stages of labour or immediately postpartum
begins gasping for air &then rapidly suffers seizures or cardiorespiratory
arrest complicated by DIC.
Rarely, has been reported up to 48 hours postpartum, or following
cesarean delivery, first and second trimester abortions, or amniocentesis.
abrupt and fulminant onset of:
Hypoxia and respiratory failure
Cardiogenic shock
Disseminated intravascular coagulation
Rapid cardiorespiratory collapse.
Nonspecific symptoms
chills, nausea, vomiting, agitation, may precede the onset of
dyspnea and hypotension
tonic-clonic seizure activity may be present. Clinical
presentation similar to septic or anaphylactic shock but a clear
etiologic agent or antibody-mediated reaction has not been
identified.

Hypoxaemia
Results from severe ventilation/perfusion mismatching.
Bronchospasm in 15% of patients.
Hypoxia accounts for approximately 50% of the deaths observed in the first
hour after presentation, and may also result in severe neurologic
impairment or brain death in the mother.
Up to 70% of patients who survive the first several hours develop
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noncardiogenic pulmonary edema coincident with improvement in left

ventricular dysfunction.
Evidence for damage to the endothelial-alveolar membrane and a capillary
leak syndrome includes the high protein concentration in edema fluid and
the presence of amniotic fluid debris in the sputum and alveolar spaces.
While noncardiogenic edema appears to result from widespread damage to
the alveolar-capillary membrane, AFES does not usually produce a clinical
pattern typical of the acute respiratory distress syndrome (ARDS).
Patients who survive the first hours of AFES tend to recover rapidly; this is
in contrast to the generally protracted course of ARDS.

Cardiovascular collapse
Primarily the result of left ventricular dysfunction.
Cardiac dysrhythmias, including pulseless electrical activity, bradycardia,
ventricular fibrillation, and asystole, may further complicate management.
Pulmonary artery catheter data usually show a diminished cardiac output
with relatively small increases in pulmonary vascular resistance.
Approximately 86% of patients diagnosed with AFES die from cardiogenic
shock or its complications.
Disseminated intravascular coagulation - as many as 80% of patients
develop DIC Causes haemorrhage.

Diagnosis
No single clinical or laboratory finding is available.
Primarily a clinical diagnosis.
Profound shock and severe respiratory compromise during labor or
immediately postpartum.
At postmortem,demonstrate fetal squames or debris in the pulmonary
artery vasculature.
Surviving patients identification of amniotic fluid debris in the bronchial
washings or blood from right atrium or ventricle washings or fetal squames
in sputum.
ECG (R ventricular strain pattern,tachycardia),blood gas-(reduced
PaO2,PaCO2 &metabolic acidosis),coagulation screen(evidence of
DIC),CXR-(perihilar infiltrates) may be helpful.
Other causes of sudden cardiorespiratory failure, such as air or pulmonary
embolism, hemorrhage, anesthetic complications, anaphylaxis, sepsis,
aspiration of gastric contents, and myocardial infarction, must be excluded
Some authors require amniotic fluid debris (squamous and trophoblastic
cells, mucin, and lanugo) in samples from the distal port of a pulmonary
artery catheter in order to make the diagnosis. However, amniotic fluid
components commonly are present in the maternal circulation in women
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without clinical evidence of AFES, and thus should not be considered

pathognomonic.
Serological assays and immunohistochemical staining employing the
monoclonal antibody TKH-2 to detect a common fetal antigen appear to
have a high sensitivity for AFES. However, these methods are not fully
validated and cannot be recommended in routine practice.

Differential Diagnosis
PTE, septic shock, MI, aspiration pneumonia, allergy to anaesthetic
agents.

Pathophysiology
Because AFES is an uncommon clinical event, understanding the cause of
this syndrome has been based to a large degree upon animal models.
Introduction of amniotic fluid into the venous circulation of laboratory
animals results in the rapid development of pulmonary hypertension, acute
cor pulmonale, and systemic hypotension.
These responses appear secondary to occlusion and vasospasm of the
maternal pulmonary vasculature due to the local presence of amniotic
fluid.
Passage of amniotic fluid debris into the maternal circulation during or just
after childbirth,together with surrounding platelet-fibrin thrombi,obstructs
pulmonary circulation.This results in,
brief initial phase of pulmonary & systemic hypertension,there is
decreased systemic vascular resistance & left ventricular stroke work
index.
Transient but profound oxygen desaturation seen in initial phase result in
neurological injury in most survivors.
Who live beyond the initial CV collapse, a secondary phase of lung injury
occurs in 70% which may in turn lead to ARDS & coagulopathy in 40%
which may manifest by persistent bleeding from IV sites or surgical
incisions, often ensues.

Haemodynamic changes
In humans, amniotic fluid most commonly enters the maternal circulation
through the endocervical veins, the placental insertion site, or at a site of
uterine trauma.
In humans, the principal hemodynamic alteration in AFES is left ventricular
failure rather than pulmonary hypertension with right ventricular failure:
pulmonary artery and pulmonary capillary wedge pressures are elevated,
cardiac output is decreased, and the left ventricular stroke work index is
severely reduced, indicating left ventricular dysfunction.
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Although some cardiovascular symptoms in AFES may be in part caused

by pulmonary vascular occlusion by amniotic fluid debris, additional
explanations are required for the diverse manifestations of this clinical
syndrome.
An initial period of pulmonary hypertension may exist, which then
resolves in 15 to 30 minutes.
This is followed by left heart failure, cardiogenic pulmonary edema,
and cardiogenic shock.
The mechanism of left heart failure is unclear, but some animal data
suggest that it may result from hypoxic injury to the left ventricle,
release of maternal inflammatory mediators, or a direct depressant
effect of amniotic fluid on the myocardium.

Inflammation
Immunologic or inflammatory events may be required for the clinical
syndrome to develop.
Asymptomatic embolization of amniotic material is not uncommon,
supporting the theory that specific maternal responses are necessary to
produce AFES.
Several mechanisms have been proposed to explain the time lag between
amniotic fluid embolism and disease as well as the inconsistent
occurrence of the clinical syndrome:
Abnormal amniotic fluid may be required.
Exposure to atypical substances within the amniotic fluid, such as
leukotrienes or other arachidonic acid metabolites, may produce the
principal hemodynamic responses, including left heart failure,
pulmonary capillary injury, and coagulopathy.
Host immune responses may be necessary to affect organ function.
Variability in severity and intensity of clinical features may reflect
varied immunologic stimulation by fetal-associated antigens.

Management
The three main goals of the treatment are:
oxygenation
maintaining cardiac output and BP
correcting coagulopathy- give uterotonics, and uterine massage,
blood transfusion and blood components (FFP, cryoprecipitate,
platelets)
As per management of cardiorespiratory arrest, resuscitation consists of
the A, B and Cs
securing airway through endotracheal intubation
mechanical ventilation with high inspired fraction oxygen, and the
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addition of positive end-expiratory pressure

position the patient flat or slight Trendelenburg, IVF, inotropes, ECG
to monitor and to detect arrhythmias. Placement of a pulmonary
artery catheter is recommended.
AFES remains unpredictable, unpreventable, and without specific
treatment.
Women at high risk for AFES cannot be easily identified, and no
prophylactic measures are available.
No data that any type of intervention improves maternal prognosis with
amniotic fluid embolism.
Management is supportive and focuses on rapid cardiorespiratory
stabilization.
The maternal mortality rate is 60 to 90 percent.
In one review of 61 cases, neurologically intact survival occurred in only
15 percent; of the fetuses in utero at the time of the event, only 39%
survived.

Monitoring
Monitoring should include continuous pulse oximetry, electrocardiography,
arterial blood pressure monitoring, and electronic fetal monitoring, if illness
occurs prior to delivery.
Invasive hemodynamic monitoring with pulmonary artery catheterization is
essential to the management of both the cardiovascular and respiratory
components of AFES.
Serial measurements of the pulmonary capillary wedge pressure and
cardiac output are useful in the fluid management of this syndrome, and
can guide therapy in cases of cardiogenic and noncardiogenic pulmonary
edema.
Central venous pressure assessment alone is generally not sufficient for
the management of these complex, hemodynamically compromised
patients.

Prevention of fetal hypoxia

Adequate level of maternal oxygenation must be maintained to protect the
mother and prevent adverse fetal consequences secondary to hypoxia,
should be ventilated with highest concentration of O2 available..
Any factor that impairs maternal oxygen delivery to the placenta (eg,
anaemia, hypoxaemia, diminished cardiac output, leftward shifts in the
oxyhaemoglobin dissociation curve) increases the hypoxic risk to the
fetus.
Despite a relatively low umbilical vein PO2 (in the range of 32 mmHg),
fetal oxygen content is close to maternal oxygen content.
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Low oxygen tensions in the fetus are compensated by an elevated fetal

haemoglobin concentration and cardiac output.
These compensatory mechanisms allow adequate oxygen supply to the
fetus under normal conditions, but are overwhelmed during periods of
significant maternal hypoxia.
In healthy women exposed to low fractions of inspired oxygen, fetal
umbilical vein PO2 begins to fall when maternal PO2 is below 47 mmHg.
Because these values lie on the steep part of the oxyhaemoglobin
dissociation curve, small changes in maternal PO2 in this range may
cause significant changes in fetal oxygen content.
Assuming there are no significant alterations in maternal cardiac output,
hemoglobin, or pH, a maternal PO2 in the range of 65 mmHg is
acceptable for adequate fetal oxygenation.
If maternal oxygenation is inadequate on high flow rates of oxygen by
facemask, prompt endotracheal intubation is indicated.
Therapy of noncardiogenic pulmonary edema requires judicious fluid
management, application of PEEP in intubated patients, and avoidance of
barotrauma.
Management of DIC involves replacement of blood products & FFP.
IV bolus heparin to reverse the tendency towards coagulopathy is
uncertain.

Pharmacologic therapy
Cardiogenic shock requires the use of inotropic and vasoactive agents.
Norepinephrine and dopamine are the drugs of choice for the initial
maintenance of cardiac output and blood pressure.
In the patient with severe left ventricular dysfunction and pulmonary
edema, dobutamine may offer the potential advantage of increasing the
low cardiac output and decreasing the high filling pressures.
Dobutamine infusion may result in hypotension caused by a drop in
systemic vascular resistance, and use of a vasopressor (generally
norepinephrine) in combination with this inotrope may be required.
Patients with AFES who are managed with appropriate inotropic support
and use of vasoactive agents as guided by central haemodynamic
monitoring may have an overall improved survival rate.

Fluid management
Vigorous fluid resuscitation should be withheld, if possible, until a
pulmonary artery catheter can guide management.
Intravenous fluids may result in, or exacerbate, pulmonary edema, and
initial management with vasopressors is preferred.
Blood product transfusion may be required for the correction of clinically
significant coagulopathy.
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Delivery of the fetus

Approximately 65 % of cases of fatal AFES present before delivery.
In this situation, immediate delivery of the fetus should be considered,
particularly when there is significant maternal hypoxemia or hemodynamic
compromise that may affect the fetus.
Delivery should also be considered if there is rapid and progressive
deterioration of the mother's condition, or if delivery of the fetus would
facilitate maternal resuscitative efforts.
Delivery of the fetus may often facilitate the resuscitation of the mother by
relieving the weight of the gravid uterus on the IVC, hence increasing
venous return to the heart to improve cardiac output.
If the resuscitation of the mother is deemed futile an emergency
perimortem C/S is indicated to ensure the well-being of the baby.

References

AFE an obstetric emergency Critical care Nurse 4/24, Aug 2004

Up to date2014
Williams Obstetrics.
Clark, Steven L. Amniotic fluid embolism, Obstetrics and Gynecology, Feb
2014

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