Review Article

Amniotic fluid embolism

Girendra Sadera,
ABSTRACT
Bharathram Vasudevan1

Consultant, Critical Care and Amniotic fluid embolism (AFE) is a rare complication of pregnancy carrying a high mortality
Anaesthesia, Wirral University Teaching rate. The exact pathogenesis of the condition is still not known. Diagnosing AFE needs a
Hospital, NHS Foundation Trust, high suspicion as it is essentially a clinical diagnosis of exclusion. Patients with AFE are
Upton, Wirral, UK, 1Department of best-managed in a critical care unit by a multidisciplinary team and management is largely
Anaesthesiology, All India Institute of supportive. This review compiles the currently available information on AFE.
Medical Sciences, New Delhi, India
Address for correspondence:
Dr. Girendra Sadera,
Consultant, Critical Care and Anaesthesia,
Wirral University Teaching Hospital, NHS
Foundation Trust, Upton, Wirral, CH49 5PE, UK.
E-mail: girendra.sadera@nhs.net Key words: Amniotic, embolism, fluid, pregnancy

INTRODUCTION EPIDEMIOLOGICAL DATA

A mniotic fluid embolism (AFE) is an uncommon

complication of pregnancy with a high mortality
rate, making it one of the leading direct causes of maternal
mortality in developed countries.[1] Although the first case
of amniotic fluid entering the maternal circulation was
published in 1926 by Meyer,[2] it was recognized as a distinct
clinical entity only in 1941 when Steiner and Lushbaugh
made a detailed description of the syndrome based on their
autopsy findings. They postulated that pulmonary embolism
by amniotic fluid was the reason for death in eight women
who died unexpectedly during labor.[3] Despite being known
for so many years now, it remains a medical mystery even
today with no consensus on the exact pathogenesis of the
syndrome. There is a recent surge of research to find novel
biomarkers which can help in predicting and diagnosing AFE.
This article aimed to provide a comprehensive review of the
available knowledge on AFE.
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DOI:
10.4103/2249-4472.155192
The reported incidence of AFE varies widely among different
studies, as is the reported mortality rates. The wide variation is
due to the absence of universally accepted diagnostic criteria,
varied clinical presentations and rarity of the condition. Frati
et al. recently compared nine studies and arrived at a mean
incidence of 5.5/100,000 deliveries (range 2-15.2) and a mean
case fatality rate of 24.8% (range 13.3-48%).[4] The incidence
of AFE in UK is about 2/100,000 maternities.[5]
World Health Organization defines maternal death as death of
a woman during pregnancy or within 42 days after pregnancy
due to causes related to pregnancy or aggravated by it.[6]
Maternal deaths can be divided into direct or indirect based
on the etiology. A direct death is one resulting from obstetric
complications of the pregnant state (example: Preeclampsia),
while an indirect death is due to an associated disease which may
be aggravated by physiological effects of pregnancy (example:
Pre-existing cardiac disease). AFE is one among the top five
leading causes of direct obstetric deaths in developed countries.
Busardo et al. examined seven different national registries and
concluded that fatal cases of AFE amounted to a mean of 12.8%
(range 4.7-24.3%) of maternal deaths.[7] It was the leading cause
of maternal mortality in the Japanese registry while it was among
the top five in other registries.[7] The mortality rate due to AFE
in UK is 0.33/100,000 (2010-2012).[6] It is the fifth leading cause
of direct obstetric death in UK after thromboembolism, sepsis,
hemorrhage, and preeclampsia/eclampsia.[6]

Journal of Obstetric Anaesthesia and Critical Care / Jan-Jun 2015 / Vol 5 | Issue 1 3
 Sadera and Vasudevan: Amniotic fluid embolism
RISK FACTORS
Many risk factors have been associated with AFE, but causality
has not been proved for most of them though a consistent
association has been observed with older maternal age and
medical induction of labor.[1] According to data from the UK
and Ireland, confidential enquiries into maternal deaths and
morbidity 2009-2012 labor induction or augmentation was done
in six out of eleven women who died of AFE in 2009-12 and three
out of eleven had uterine hyper-stimulation.[6] The associated risks
are mentioned in Table 1.[8-12] Instrumental delivery, caesarean
delivery, cervical trauma or uterine rupture may be the result
of attempting to deliver the fetus after an AFE and may not
be causative.[8] Some authors are of the opinion that uterine
stimulation is the least likely time for amniotic fluid to come into
contact with the maternal circulation, thereby questioning the
causative role of uterine stimulation.[13] Thus, no significant risk
factor has been proved yet to change the current obstetric practice.
The risk of recurrence of the condition is also not known, though
there are a few reports of successful subsequent pregnancies.[14]
PATHOGENESIS
Exposure of the maternal circulation to amniotic fluid or fetal
antigens is universally accepted as a prerequisite for AFE to occur.
This can occur through one of the three routes - uterine trauma
sites, endocervical veins or placental attachment site.[14] Minor
uterine trauma occurs at the time of normal labor as well as
instrumental or cesarean delivery. The exact mechanism underlying
the occurrence of AFE after this exposure is still not known.
Historically, AFE was thought to be caused due to mechanical
obstruction of pulmonary vessels by amniotic fluid embolus
consisting of fetal squames, vernix caseosa, lanugo hair,
trophoblasts, fetal gut mucin, and bile stained meconium. But
Table 1: Risk factors associated with amniotic fluid
embolism
Age >35 years
Multiparity
Male fetus
Medical induction of labor
Instrumental delivery
Caesarean delivery
Cervical trauma
Uterine rupture
Uterine hyperstimulation
Preeclampsia
Eclampsia
Placenta previa
Placental abruption
Ethnic minority
4 Journal of Obstetric Anaesthesia and Critical Care / Jan-Jun 2015 / Vol 5 | Issue 1
this could not explain the entire clinical manifestations of the
syndrome. Moreover, this mechanism could not be proved in
animal studies.[15,16]
At present, AFE is thought to result from an immune-mediated
mechanism, given its similarity to septic shock or anaphylactic
shock. It results from an abnormal immunological response of
the mother following exposure to fetal antigens leading to the
release of various pro-inflammatory mediators.[13] Clark et al. even
proposed to rename the syndrome as “anaphylactoid syndrome
of pregnancy,”[11] though it was not widely accepted. The exact
immunological mechanism is still unknown. Amniotic fluid itself
contains various vasoactive and prothrombotic substances such as
platelet activating factor, interleukin 1 (IL-1), tumor necrosis factor-
alpha (TNF α), leukotrienes C4 and D4, endothelin, tissue factor,
arachidonic acid, and others which when released into the maternal
circulation can lead to vasoconstriction, bronchoconstriction and
coagulation.[17] An anaphylactic mechanism is supported by
studies showing increased mast cell degranulation[18] and refuted
by studies that failed to show a rise in serum tryptase levels.[19]
Complement activation as the primary mechanism has been
proposed.[20] The levels of complement factors C3 and C4 have
been found to be reduced in patients with AFE. Furthermore, mast
cells can be secondarily activated after complement activation.
Platelet aggregation and neutrophil activation are also other
mechanisms proposed for the release of inflammatory mediators
that ultimately lead to the clinical syndrome.[17]
The reason for activation of the coagulation cascade is
incompletely understood. Tissue factor in amniotic fluid and
apoptotic amniotic cells may initiate the coagulation cascade,
but it is still doubtful if the small quantities of these factors
could lead on to the disseminated intravascular coagulation
(DIC) picture that is seen in AFE.[13]
Recently, an integrated mechanism was proposed. According
to this theory, activation of the coagulation cascade can
lead to microthrombi in pulmonary vessels and add on to
the mechanical obstruction by amniotic fluid components.
This, along with the various inflammatory mediators like
leukotrienes can cause the complete picture of the syndrome.[21]
An overview of the pathogenesis of AFE is shown in Figure 1.
CLINICAL FEATURES
About 70% of cases occur during labor, 19% during cesarean
section, and 11% after delivery in the immediate postpartum.[22]
There have been reports of delayed AFE occurring up to 48 h
after delivery.[14] There are also reports of cases occurring after
second-trimester abortions, amniocentesis, blunt abdominal
trauma, abdominal surgeries, dilatation and evacuation, and
intrapartum amnioinfusion with normal saline.[23,24]
 Sadera and Vasudevan: Amniotic fluid embolism

The classical form of AFE presents as a sudden onset respiratory
distress followed by a sudden cardiovascular collapse. This
is followed by cardiac arrest and/or coagulopathy.[13] The
signs and symptoms in this early phase include dyspnea,
desaturation, hypotension, cardiac arrhythmias, seizures, loss
of consciousness, bleeding, and cardiac arrest.[13] Fetal hypoxia
and bradycardia are almost universal if AFE occurs prior
to delivery. Premonitory symptoms of tingling, numbness,
restlessness, and agitation have been described and are thought
to occur from early hypoxia.[9] The cause of cardiac arrest can be
hypoxia, direct myocardial suppression or excessive bleeding.[11]
Lung injury and acute respiratory distress syndrome (ARDS)
are seen in the late phase. Multiple organ dysfunction and
hypoxic brain damage are common in those who survive the
initial cardiac arrest. Infants born to these mothers are at risk
for hypoxic ischemic encephalopathy and cerebral palsy.[25]
with the classical subtype which was associated with a higher
incidence of sudden death.[26]
DIAGNOSIS
Amniotic fluid embolism is essentially a clinical diagnosis and a
diagnosis of exclusion as there is no available laboratory test to
confirm the diagnosis. The classical triad of respiratory distress,
cardiovascular collapse, and coagulopathy makes it easy to
diagnose the classical form.[13] Different national registries
have their own entry criteria but share common features
involving the classical triad along with a criterion to describe
the timing of occurrence of the syndrome.[11,25] Other similar
conditions need to be excluded before a diagnosis of AFE is
made [Table 2].[6,14,27,28] The UK Obstetric Surveillance System
diagnostic criteria for AFE are given in Table 3.[10]

In the atypical form, coagulopathy manifesting as severe bleeding Table 2: Differential diagnoses of AFE
occurs in the absence of cardiopulmonary manifestations.[13] Nonobstetric causes
Uterine atony can additionally contribute to the hemorrhage. Pulmonary embolism (air, fat, thrombi)
Pulmonary edema
Tension pneumothorax
Studies utilizing transesophageal echocardiography have
Cardiac - myocardial infarction, heart failure, arrhythmias, tamponade
found that the cardiac abnormalities in AFE are biphasic – an
Anaphylaxis
early transient phase of intense pulmonary vasoconstriction, Septic shock
pulmonary hypertension, and right ventricular failure, and a Aspiration
late phase of left ventricular dysfunction leading to hypotension Anesthesia related - local anesthetic toxicity, high spinal
and cardiogenic pulmonary edema.[14] Other reversible causes - toxins, hypo/hyperkalemia, metabolic,
hypothermia
Obstetric causes
Tsunemi et al. attempted to classify 136 cases of AFE into
Eclampsia
three subtypes: Abruptio placenta
1. Classical subtype with early respiratory distress and hypoxia, Uterine rupture
2. Anaphylactoid subtype with early cardiac dysfunction and Postpartum hemorrhage
arrhythmias and Peripartum cardiomyopathy
3. DIC subtype with coagulopathy. AFE: Amniotic fluid embolism

They found considerable overlap of features in many patients. Table 3: UKOSS diagnostic criteria
The DIC subtype carried a lesser mortality when compared Either - In the absence of any other clear cause
Acute maternal collapse with one or more of the following
Acute fetal compromise
Cardiac arrest
Cardiac arrhythmias
Hypotension
Maternal hemorrhage
Coagulopathy
Premonitory symptoms
Seizure
Shortness of breath
Excluding women with maternal hemorrhage as the first presenting
feature in whom there was no evidence of early coagulopathy or
cardio-respiratory compromise
Or
Women in whom the diagnosis was made at postmortem examination
with fetal squames or hair in the lungs
Figure 1: Pathophysiology of amniotic fluid embolism UKOSS: UK obstetric surveillance system

Journal of Obstetric Anaesthesia and Critical Care / Jan-Jun 2015 / Vol 5 | Issue 1 5
 Sadera and Vasudevan: Amniotic fluid embolism
LABORATORY TESTS
There is no confirmatory laboratory test available at present
for diagnosing AFE. Earlier, demonstration of fetal tissues
in maternal blood by aspiration through the distal port of
a pulmonary artery catheter was considered confirmatory.
But it is now known that it’s not specific for AFE.[13] Many
biomarkers are presently under study, and some are available
commercially. [29] Their clinical use is doubtful and not
recommended routinely. Some of the currently available
biomarkers are discussed below.
TKH2 is a monoclonal antibody against Sialyl Tn (STN)
antigen. Immunohistochemical staining using TKH2 antibody
can help in detecting meconium and the amniotic fluid mucin
in lung secretions.[30]
Sialyl Tn is a known antigen in meconium and amniotic fluid
mucin. Detection of STN in maternal serum can act as a
diagnostic evidence for amniotic fluid in maternal circulation.[30]
Zinc coproporphyrin-1 (ZnCP-1) is a known component
in meconium and fetal urine. The maternal plasma levels of
ZnCP-1 have been found to be high in patients with AFE. It
can be detected by high-performance liquid chromatography
and can act as a sensitive diagnostic tool.[31]
Levels of complement factors C3and C4 are decreased in
patients with AFE while serum mast cell tryptase has been
found to be high.[29] Measuring the levels of these proteins can
play a useful role. Levels of other nonspecific factors found to
be high in amniotic fluid include IL-6 and 8, TNF α soluble
receptor.
Insulin-like growth factor binding protein-1 (IGFBP-1)
is a protein synthesized in the decidua. Normally, its level
in amniotic fluid is approximately 150 times more than in
maternal plasma.[32] Higher levels in maternal plasma can point
towards AFE. A combination of maternal serum IGFBP-1,
alpha-fetoprotein, and fetal fibronectin has been postulated
as a confirmatory test for AFE.[33]
Other adjuvant laboratory tests can help in exclusion of other
conditions and also help in the management. These are listed
in Table 4.[14]
MANAGEMENT
Management of AFE is supportive, and thus a final diagnosis is
not required to manage these patients. Supportive management
based on the pathophysiological changes should be started
6 Journal of Obstetric Anaesthesia and Critical Care / Jan-Jun 2015 / Vol 5 | Issue 1
Table 4: Adjuvant laboratory tests in amniotic fluid
embolism
Complete blood counts
Peripheral smear
Coagulation profile - PT, aPTT, D-dimer, fibrin degradation products,
fibrinogen
Thromboelastography/thromboelastometry
Serum electrolytes
ABG
ECG
Cardiac enzymes
Echocardiography (transthoracic/transesophageal)
Chest radiograph
aPTT: Activated partial thromboplastin time, PT: Prothrombin time, ABG: Arterial
blood gas, ECG: Electrocardiogram
as soon as signs and symptoms arise and should not wait for
laboratory tests. These patients are ideally managed in an
intensive care setting by a multi-disciplinary team.
In the event of cardiac arrest, cardiopulmonary resuscitation
(CPR) should be done according to advanced cardiac life
support guidelines with special consideration to pregnancy.
Left lateral displacement of the uterus or left lateral tilt should
be done to relieve aortocaval compression and hands should
be placed higher up on the chest during chest compressions.
Hypoxia and respiratory distress are to be managed with 100%
oxygen. Early intubation and mechanical ventilation are to
be considered.[34] The level of respiratory support needed will
depend on the severity of presentation.[35] Early intubation
can help preventing aspiration, the risk of which is higher
in pregnant women. A difficult airway is to be anticipated
given the physiological changes in pregnancy, and appropriate
preparedness is necessary.[36] Mechanical ventilation should
follow lung protective strategy protocol as these patients are
at risk for ARDS.[35]
Hemodynamic instability needs to be treated with careful
volume expansion, vasopressors and inotropes. Invasive arterial
pressure monitoring, central venous, and pulmonary artery
catheters can help in the management. Echocardiography
helps in assessing the cardiac status and guiding fluid
therapy.[35] Noninvasive advanced hemodynamic and cardiac
output monitors may be helpful. Intraaortic balloon counter
pulsation, cardiopulmonary bypass, and extracorporeal
membrane oxygenation have all been used with reported
success in cases of AFE.[37-41] These modalities may be tried
when available in the event of worsening cardiopulmonary
status not responding to other treatment modalities.
Transfusion of blood products forms the cornerstone of
treating coagulopathy. Massive blood transfusion protocol
 Sadera and Vasudevan: Amniotic fluid embolism
needs to be initiated.[42] Damage control resuscitation in
the form of packed cells, plasma, and platelets in the ratio
of 1:1:1 is recommended by some in cases of uncontrolled
hemorrhage.[43] Transfusion of fresh frozen plasma (FFP)
should be done at an initial rate of 15 mL/kg body weight.
Severe hypofibrinogenemia (<1 g/L) persisting after FFP
transfusion may be treated with fibrinogen concentrates or
cryoprecipitate. Fibrinogen assessments are recommended as
they correlate with the severity of bleeding, with fibrinogen
levels <2 g/L predicting more severe bleeding.[42] Repeated
monitoring of coagulation status is necessary and point-of-
care devices like thromboelastometry are especially useful
Thromboelastometric measurements can help in early
detection of a hypercoagulable or a hyperfibrinolysis state
and can direct therapy with FFP, factor concentrates and
tranexamic acid.[44] The role of heparin and factor VIIa are
controversial and should be used with caution.
Treatment of uterine atony is equally important to control
bleeding. Initially, uterine massage and drugs such as
oxytocin, methylergometrine, and carboplast can be tried.
Uterine tamponade, manual exploration, and uterine artery
embolization may be helpful in some cases. Hysterectomy as
an early resort is recommended to remove the main source of
bleeding especially when there are no experienced personnel
to perform the less definitive procedures.[6]
Isolated case reports of successful management of AFE with
other treatment modalities such as inhaled nitric oxide,
inhaled prostacyclin, aprotinin, exchange transfusion,
continuous hemodiafiltration, cell salvage, and pulmonary
thromboembolectomy have been published.[45-50] The extent
of their usefulness in AFE is uncertain.
PERIMORTEM CAESAREAN DELIVERY
Perimortem cesarean delivery in cases of maternal cardiac
arrest is vital in resuscitation of the mother and also in saving
the fetus. Royal College of Obstetricians and Gynaecologists
guideline states that perimortem cesarean section should
be done in cases of maternal collapse where return of
spontaneous circulation does not occur after 4 min of effective
CPR and the fetus should be delivered within 5 min of arrest.
The viability of the fetus is not a matter of concern in such
cases. It should be done then and there without shifting the
patient to operating room.[36] In the case of cardiopulmonary
instability without overt cardiac arrest, the role of cesarean
section is controversial. The mother may not tolerate stress
of surgery. If not delivered, the fetus is at risk for hypoxia
and intrauterine death. The decision needs to be made on a
case to case basis.[27]
Journal of Obstetric Anaesthesia and Critical Care / Jan-Jun 2015 / Vol 5 | Issue 1 7
CONCLUSION
Amniotic fluid embolism remains a clinical diagnosis of
exclusion and management is only supportive. There is no
clearly proven risk factor to predict or prevent its occurrence.
Though the mortality rate has decreased over the years due to
better resuscitation and critical care,[35] it still remains high at
12.8%.[7] An encouraging light of hope is the recent increase in
research to find the exact pathogenesis of this condition and
also to discover clinically relevant biomarkers that can help in
earlier diagnosis and prompt treatment.
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Cite this article as: Sadera G, Vasudevan B. Amniotic fluid embolism. J Obstet
Anaesth Crit Care 2015;5:3-8.
Source of Support: Nil, Conflict of Interest: None declared.
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