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Review Article

Amniotic fluid embolism

Girendra Sadera,
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: Key words: Amniotic, embolism, fluid, pregnancy


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
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,
mortality in developed countries.[1] Although the first case varied clinical presentations and rarity of the condition. Frati
of amniotic fluid entering the maternal circulation was et al. recently compared nine studies and arrived at a mean
published in 1926 by Meyer,[2] it was recognized as a distinct 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
clinical entity only in 1941 when Steiner and Lushbaugh
of AFE in UK is about 2/100,000 maternities.[5]
made a detailed description of the syndrome based on their
autopsy findings. They postulated that pulmonary embolism World Health Organization defines maternal death as death of
by amniotic fluid was the reason for death in eight women a woman during pregnancy or within 42 days after pregnancy
who died unexpectedly during labor.[3] Despite being known due to causes related to pregnancy or aggravated by it.[6]
for so many years now, it remains a medical mystery even Maternal deaths can be divided into direct or indirect based
today with no consensus on the exact pathogenesis of the on the etiology. A direct death is one resulting from obstetric
syndrome. There is a recent surge of research to find novel complications of the pregnant state (example: Preeclampsia),
biomarkers which can help in predicting and diagnosing AFE. while an indirect death is due to an associated disease which may
This article aimed to provide a comprehensive review of the be aggravated by physiological effects of pregnancy (example:
Pre-existing cardiac disease). AFE is one among the top five
available knowledge on AFE.
leading causes of direct obstetric deaths in developed countries.
Busardo et al. examined seven different national registries and
Access this article online
concluded that fatal cases of AFE amounted to a mean of 12.8%
Quick Response Code:
(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
DOI: in UK is 0.33/100,000 (2010-2012).[6] It is the fifth leading cause
10.4103/2249-4472.155192 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 this could not explain the entire clinical manifestations of the
syndrome. Moreover, this mechanism could not be proved in
Many risk factors have been associated with AFE, but causality animal studies.[15,16]
has not been proved for most of them though a consistent
At present, AFE is thought to result from an immune-mediated
association has been observed with older maternal age and
mechanism, given its similarity to septic shock or anaphylactic
medical induction of labor.[1] According to data from the UK
shock. It results from an abnormal immunological response of
and Ireland, confidential enquiries into maternal deaths and
the mother following exposure to fetal antigens leading to the
morbidity 2009-2012 labor induction or augmentation was done
release of various pro-inflammatory mediators.[13] Clark et al. even
in six out of eleven women who died of AFE in 2009-12 and three
proposed to rename the syndrome as “anaphylactoid syndrome
out of eleven had uterine hyper-stimulation.[6] The associated risks
of pregnancy,”[11] though it was not widely accepted. The exact
are mentioned in Table 1.[8-12] Instrumental delivery, caesarean
immunological mechanism is still unknown. Amniotic fluid itself
delivery, cervical trauma or uterine rupture may be the result
contains various vasoactive and prothrombotic substances such as
of attempting to deliver the fetus after an AFE and may not
platelet activating factor, interleukin 1 (IL-1), tumor necrosis factor-
be causative.[8] Some authors are of the opinion that uterine
alpha (TNF α), leukotrienes C4 and D4, endothelin, tissue factor,
stimulation is the least likely time for amniotic fluid to come into
arachidonic acid, and others which when released into the maternal
contact with the maternal circulation, thereby questioning the
circulation can lead to vasoconstriction, bronchoconstriction and
causative role of uterine stimulation.[13] Thus, no significant risk coagulation.[17] An anaphylactic mechanism is supported by
factor has been proved yet to change the current obstetric practice. studies showing increased mast cell degranulation[18] and refuted
The risk of recurrence of the condition is also not known, though by studies that failed to show a rise in serum tryptase levels.[19]
there are a few reports of successful subsequent pregnancies.[14] Complement activation as the primary mechanism has been
proposed.[20] The levels of complement factors C3 and C4 have
PATHOGENESIS been found to be reduced in patients with AFE. Furthermore, mast
cells can be secondarily activated after complement activation.
Exposure of the maternal circulation to amniotic fluid or fetal Platelet aggregation and neutrophil activation are also other
antigens is universally accepted as a prerequisite for AFE to occur. mechanisms proposed for the release of inflammatory mediators
This can occur through one of the three routes - uterine trauma that ultimately lead to the clinical syndrome.[17]
sites, endocervical veins or placental attachment site.[14] Minor
uterine trauma occurs at the time of normal labor as well as The reason for activation of the coagulation cascade is
instrumental or cesarean delivery. The exact mechanism underlying incompletely understood. Tissue factor in amniotic fluid and
the occurrence of AFE after this exposure is still not known. apoptotic amniotic cells may initiate the coagulation cascade,
but it is still doubtful if the small quantities of these factors
Historically, AFE was thought to be caused due to mechanical could lead on to the disseminated intravascular coagulation
obstruction of pulmonary vessels by amniotic fluid embolus (DIC) picture that is seen in AFE.[13]
consisting of fetal squames, vernix caseosa, lanugo hair,
trophoblasts, fetal gut mucin, and bile stained meconium. But Recently, an integrated mechanism was proposed. According
to this theory, activation of the coagulation cascade can
Table 1: Risk factors associated with amniotic fluid
lead to microthrombi in pulmonary vessels and add on to
embolism the mechanical obstruction by amniotic fluid components.
Age >35 years This, along with the various inflammatory mediators like
Multiparity leukotrienes can cause the complete picture of the syndrome.[21]
Male fetus An overview of the pathogenesis of AFE is shown in Figure 1.
Medical induction of labor
Instrumental delivery CLINICAL FEATURES
Caesarean delivery
Cervical trauma
Uterine rupture About 70% of cases occur during labor, 19% during cesarean
Uterine hyperstimulation section, and 11% after delivery in the immediate postpartum.[22]
Preeclampsia There have been reports of delayed AFE occurring up to 48 h
Eclampsia after delivery.[14] There are also reports of cases occurring after
Placenta previa second-trimester abortions, amniocentesis, blunt abdominal
Placental abruption trauma, abdominal surgeries, dilatation and evacuation, and
Ethnic minority
intrapartum amnioinfusion with normal saline.[23,24]

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Sadera and Vasudevan: Amniotic fluid embolism

The classical form of AFE presents as a sudden onset respiratory with the classical subtype which was associated with a higher
distress followed by a sudden cardiovascular collapse. This incidence of sudden death.[26]
is followed by cardiac arrest and/or coagulopathy.[13] The
signs and symptoms in this early phase include dyspnea, DIAGNOSIS
desaturation, hypotension, cardiac arrhythmias, seizures, loss
of consciousness, bleeding, and cardiac arrest.[13] Fetal hypoxia Amniotic fluid embolism is essentially a clinical diagnosis and a
and bradycardia are almost universal if AFE occurs prior diagnosis of exclusion as there is no available laboratory test to
to delivery. Premonitory symptoms of tingling, numbness, confirm the diagnosis. The classical triad of respiratory distress,
restlessness, and agitation have been described and are thought cardiovascular collapse, and coagulopathy makes it easy to
to occur from early hypoxia.[9] The cause of cardiac arrest can be diagnose the classical form.[13] Different national registries
hypoxia, direct myocardial suppression or excessive bleeding.[11] have their own entry criteria but share common features
Lung injury and acute respiratory distress syndrome (ARDS) involving the classical triad along with a criterion to describe
are seen in the late phase. Multiple organ dysfunction and the timing of occurrence of the syndrome.[11,25] Other similar
hypoxic brain damage are common in those who survive the conditions need to be excluded before a diagnosis of AFE is
initial cardiac arrest. Infants born to these mothers are at risk made [Table 2].[6,14,27,28] The UK Obstetric Surveillance System
for hypoxic ischemic encephalopathy and cerebral palsy.[25] 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
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,
Obstetric causes
Tsunemi et al. attempted to classify 136 cases of AFE into
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
Maternal hemorrhage
Premonitory symptoms
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
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

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Sadera and Vasudevan: Amniotic fluid embolism

LABORATORY TESTS Table 4: Adjuvant laboratory tests in amniotic fluid

There is no confirmatory laboratory test available at present Complete blood counts
Peripheral smear
for diagnosing AFE. Earlier, demonstration of fetal tissues
Coagulation profile - PT, aPTT, D-dimer, fibrin degradation products,
in maternal blood by aspiration through the distal port of fibrinogen
a pulmonary artery catheter was considered confirmatory. Thromboelastography/thromboelastometry
But it is now known that it’s not specific for AFE.[13] Many Serum electrolytes
biomarkers are presently under study, and some are available ABG
commercially. [29] Their clinical use is doubtful and not ECG
Cardiac enzymes
recommended routinely. Some of the currently available
Echocardiography (transthoracic/transesophageal)
biomarkers are discussed below.
Chest radiograph
aPTT: Activated partial thromboplastin time, PT: Prothrombin time, ABG: Arterial
TKH2 is a monoclonal antibody against Sialyl Tn (STN) blood gas, ECG: Electrocardiogram
antigen. Immunohistochemical staining using TKH2 antibody
can help in detecting meconium and the amniotic fluid mucin
in lung secretions.[30] as soon as signs and symptoms arise and should not wait for
laboratory tests. These patients are ideally managed in an
Sialyl Tn is a known antigen in meconium and amniotic fluid intensive care setting by a multi-disciplinary team.
mucin. Detection of STN in maternal serum can act as a
diagnostic evidence for amniotic fluid in maternal circulation.[30] In the event of cardiac arrest, cardiopulmonary resuscitation
(CPR) should be done according to advanced cardiac life
Zinc coproporphyrin-1 (ZnCP-1) is a known component support guidelines with special consideration to pregnancy.
in meconium and fetal urine. The maternal plasma levels of Left lateral displacement of the uterus or left lateral tilt should
ZnCP-1 have been found to be high in patients with AFE. It be done to relieve aortocaval compression and hands should
can be detected by high-performance liquid chromatography be placed higher up on the chest during chest compressions.
and can act as a sensitive diagnostic tool.[31]
Hypoxia and respiratory distress are to be managed with 100%
oxygen. Early intubation and mechanical ventilation are to
Levels of complement factors C3and C4 are decreased in
be considered.[34] The level of respiratory support needed will
patients with AFE while serum mast cell tryptase has been
depend on the severity of presentation.[35] Early intubation
found to be high.[29] Measuring the levels of these proteins can
can help preventing aspiration, the risk of which is higher
play a useful role. Levels of other nonspecific factors found to
in pregnant women. A difficult airway is to be anticipated
be high in amniotic fluid include IL-6 and 8, TNF α soluble
given the physiological changes in pregnancy, and appropriate
preparedness is necessary.[36] Mechanical ventilation should
follow lung protective strategy protocol as these patients are
Insulin-like growth factor binding protein-1 (IGFBP-1)
at risk for ARDS.[35]
is a protein synthesized in the decidua. Normally, its level
in amniotic fluid is approximately 150 times more than in
Hemodynamic instability needs to be treated with careful
maternal plasma.[32] Higher levels in maternal plasma can point
volume expansion, vasopressors and inotropes. Invasive arterial
towards AFE. A combination of maternal serum IGFBP-1,
pressure monitoring, central venous, and pulmonary artery
alpha-fetoprotein, and fetal fibronectin has been postulated catheters can help in the management. Echocardiography
as a confirmatory test for AFE.[33] helps in assessing the cardiac status and guiding fluid
therapy.[35] Noninvasive advanced hemodynamic and cardiac
Other adjuvant laboratory tests can help in exclusion of other
output monitors may be helpful. Intraaortic balloon counter
conditions and also help in the management. These are listed pulsation, cardiopulmonary bypass, and extracorporeal
in Table 4.[14] membrane oxygenation have all been used with reported
success in cases of AFE.[37-41] These modalities may be tried
MANAGEMENT when available in the event of worsening cardiopulmonary
status not responding to other treatment modalities.
Management of AFE is supportive, and thus a final diagnosis is
not required to manage these patients. Supportive management Transfusion of blood products forms the cornerstone of
based on the pathophysiological changes should be started treating coagulopathy. Massive blood transfusion protocol

6 Journal of Obstetric Anaesthesia and Critical Care / Jan-Jun 2015 / Vol 5 | Issue 1
Sadera and Vasudevan: Amniotic fluid embolism

needs to be initiated.[42] Damage control resuscitation in CONCLUSION

the form of packed cells, plasma, and platelets in the ratio
of 1:1:1 is recommended by some in cases of uncontrolled Amniotic fluid embolism remains a clinical diagnosis of
hemorrhage.[43] Transfusion of fresh frozen plasma (FFP) exclusion and management is only supportive. There is no
should be done at an initial rate of 15 mL/kg body weight. clearly proven risk factor to predict or prevent its occurrence.
Severe hypofibrinogenemia (<1 g/L) persisting after FFP Though the mortality rate has decreased over the years due to
transfusion may be treated with fibrinogen concentrates or better resuscitation and critical care,[35] it still remains high at
cryoprecipitate. Fibrinogen assessments are recommended as 12.8%.[7] An encouraging light of hope is the recent increase in
they correlate with the severity of bleeding, with fibrinogen research to find the exact pathogenesis of this condition and
levels <2 g/L predicting more severe bleeding.[42] Repeated also to discover clinically relevant biomarkers that can help in
monitoring of coagulation status is necessary and point-of- earlier diagnosis and prompt treatment.
care devices like thromboelastometry are especially useful
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Cite this article as: Sadera G, Vasudevan B. Amniotic fluid embolism. J Obstet
Anesth 2013;22:329-36.
Anaesth Crit Care 2015;5:3-8.
36. Johnston TA, Grady K. Maternal Collapse in Pregnancy and the
Puerperium. Green-top Guideline No. 56. London (UK): Royal College Source of Support: Nil, Conflict of Interest: None declared.

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