High-RiskObstetrics

Amniotic Fluid
Embolism
An Obstetric Emergency
Katherine J. Perozzi, RN, MSN
Nadine C. Englert, RN, MSN

lthough the first reported

case of amniotic fluid embolism (AFE)
was documented in 1926,1 a historic
event that received much public and
medical attention predates that case
by more than 100 years. Public
records indicate that in 1817 an obstetrician named Sir Richard Croft was
widely criticized because of the unexpected death of one of his patients
and her unborn son. The patient was
Princess Charlotte of Wales, and the
condemnation and grief Croft expe-

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rienced because of this loss apparently

led him to commit suicide. Investigations, continuing at least until the
1970s, strongly suggest that the
princess died of AFE, possibly absolving Sir Richard of mismanagement
of a difficult labor and highlighting
a senseless third tragedy.2
Even today, AFE is the leading
cause of death during labor and the
first few postpartum hours,3 and it
remains a deadly and unpreventable
obstetric emergency.4 Despite technological advances in critical care
life support, the maternal mortality
rate for AFE remains around 61%; a
large percentage of survivors have
permanent hypoxia-induced neurological damage. The fetal mortality
rate, although better than the maternal rate, is a dismal 21%, and 50% of
the surviving neonates experience
permanent neurological injury.5

Description and Etiology

Normally, amniotic fluid does not
enter the maternal circulation because
it is contained safely within the uterus,
sealed off by the amniotic sac. AFE
occurs when the barrier between
amniotic fluid and maternal circulation is broken and, possibly under a
pressure gradient, fluid abnormally
enters the maternal venous system
via the endocervical veins, the placental site (if placenta is separated),
or a uterine trauma site.6 Why this
entry into maternal circulation occurs
in some women and not in others is
not clearly understood. The devastating consequence of circulating fetal
debris (carried by amniotic fluid)
occurs only rarely, even though during normal labor and delivery,
cesarean deliveries, and minor traumatic procedures fetal tissue may
pass into maternal circulation and
cause no symptoms.7 That AFE develops in only a minute proportion of
these women suggests that either it is
an effect of the amount of exposure to
fetal debris or the type of fetal
debris (containing meconium or not)
or that some maternal factors may
play a significant role.5,8 Clark et al5
contend that AFE more closely resembles an anaphylactic reaction to fetal
debris than an embolic event, and
they propose the term anaphylacAuthors

Katherine J. Perozzi was the undergraduate perinatal nursing coordinator and a lecturer at the University of Pittsburgh School of Nursing,
Pittsburgh, Pa, when this article was written. She is now an assistant professor at the School of Nursing and Allied Health at Robert
Morris University in Moon Township, Pa. She has 17 years of experience in obstetric nursing.
Nadine C. Englert is the primary teacher and manager of the nursing skills laboratory at the University of Pittsburgh School of Nursing,
Pittsburgh, Pa. She has 13 years of experience in medical-surgical and critical care nursing.
To purchase reprints, contact The InnoVision Group, 101 Columbia, Aliso Viejo, CA 92656. Phone, (800) 809-2273 or (949) 362-2050 (ext 532); fax, (949) 362-2049;
e-mail, reprints@aacn.org.

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toid syndrome of pregnancy instead

of AFE. The exact mechanism of this
anaphylactoid reaction to amniotic
fluid is not clearly understood.
Predisposing factors once considered to be associated with AFE
include placental abruption, uterine
overdistention, fetal death, trauma,
tumultuous or oxytocin-stimulated
labor, multiparity, advanced maternal age, and rupture of membranes.4
However, in numerous documented
cases of AFE, none of these conditions or demographic characteristics
occurred or were applicable at the
time of the event. Furthermore, a
recent analysis of 46 verified cases
of AFE did not substantiate most of
these as associated factors; 12% of
the cases occurred in women with
intact membranes, 70% during
labor, 11% after vaginal delivery,
and 19% during cesarean delivery
with or without labor.5

Incidence and
Inclusion Criteria
The reported incidence of AFE
varies widely because of the obscurity of the problem and the wide
range of signs and symptoms associated with it. According to Gilbert
and Danielsen,9 AFE occurs in 1 of
every 20 646 deliveries. Thanks to
increasing awareness of the syndrome, this number is probably
more accurate than many earlier
estimates, which ranged from 1 in
8000 to 1 in 80 000. Precise reporting of incidence is extremely difficult
because no definitive clinical or laboratory test is available that can be
used to provide an exclusive diagnosis of AFE or completely rule it out.
Clark and coworkers established a
national registry for AFE in an effort
to investigate and understand this

syndrome more completely. Table 1

lists the inclusion criteria for diagnosis of AFE.

Clinical Features
and Pathophysiology
One of the major factors that
makes AFE so devastating is its total
unpredictability. Although most cases
occur after the onset of labor, some
incidents have occurred outside of
labor. As mentioned earlier, several
clinical conditions seem to be associated with AFE, but essentially
there are no definitive clues, warning
signs, or associated conditions that
indicate the risk of AFE may be
increased. Most experts agree that
AFE, as it is known now, cannot be
predicted or prevented.11
According to Gei and Hankins,11
the initial signs and symptoms have
a typical chronology, and the morbidity and mortality of the manifestations steadily decreases with time.
Most often, respiratory distress and
cyanosis occur suddenly within the
first minute and are quickly followed
by hypotension, pulmonary edema,
shock, and neurological manifestations such as confusion, loss of consciousness, and seizures. More than
80% of patients experience cardiorespiratory arrest within the first few
minutes.6 Approximately 50% of
patients do not survive this

onslaught of cardiopulmonary
injury, but of those who do, 40% to
50% have coagulopathy and hemorrhage up to 4 hours later.12 Porter et
al13 noted that in some patients,
coagulopathy may be the first indication of AFE, whereas Clark et al5
reported that seizure activity may at
times be the first manifestation.
The pathophysiology of AFE is
speculative; various theories have
been published. Gei and Hankins11
proposed a pathophysiological
course (see Figure). Three distinct
responses or a combination of clinical
responses to circulating fetal debris
are suggested.
The initial respiratory reaction
possibly begins with transient pulmonary vasospasm.14 Although this
possible transient vasospasm has
not been documented (probably
because the signs and symptoms
appear so abruptly in a seemingly
healthy person who is not being
monitored via invasive methods),
vasospasm may be caused by amniotic microemboli that trigger the
release of arachidonic acid metabolites15 and lead to pulmonary hypertension, intrapulmonary shunting,
bronchoconstriction, and severe
hypoxia.14 Exactly which components
of amniotic fluid actually cause this
effect is unknown, but Clark14 suggests that abnormal components

Table 1 National registrys criteria for diagnosis of amniotic fluid embolism 5,10
Acute hypotension or cardiac arrest
Acute hypoxia, defined as dyspnea, cyanosis, or respiratory arrest
Coagulopathy, defined as laboratory evidence of intravascular consumption or
fibrinolysis or severe clinical hemorrhage in the absence of other explanations
(although patients who died before assessment of coagulopathy are eligible)
Onset during dilatation and evacuation, labor, cesarean delivery, or within 30 minutes
postpartum
Absence of any other significant confounding condition or potential explanation of
symptoms and signs just listed

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High-RiskObstetrics

Cardiogenic and
noncardiogenic
pulmonary edema
+
Intrapulmonary
shunting
+
Bronchoconstriction

Desaturation
|
Dyspnea
Bronchospasm
Cyanosis
Pulmonary edema

Decreased coronary
blood flow

Decreased inotropism

Decreased cardiac
output
+
Pulmonary congestion
|
Hypotension
Shock

3
4

Venous
systemic
circulation

Thromboplastins

Intravascular
coagulation
|
Bleeding

Arterial
systemic
circulation

1
Amniotic fluid
enters the
circulation

Fetal hypoxia
Bradycardia
Death
5

Sequence of events:
(1) For reasons not completely understood, amniotic fluid reaches the maternal
intravascular compartment (systemic venous system).
(2) The amniotic fluid enters pulmonary circulation via the pulmonary artery. This
contaminated blood crosses to the left atrium through a patent foramen and
probably through intrapulmonary shunts once the embolism is significant, as
shown in cases of massive amniotic fluid embolism at autopsy.
(3) The exposure of the pulmonary vasculature to both soluble (leukotrienes, surfactant,
thromboxane A2, endothelin, etc.) and insoluble components (squames, vernix, hair,
mucin, etc.) of the amniotic fluid and possibly other mediators released locally
induces capillary leak, negative inotropism, and bronchospasm. This results in
sudden onset of respiratory distress and cyanosis.
(4) Within minutes, the negative inotropic effect becomes prevalent (probably due to
myocardial ischemia). Pulmonary venous pressure (congestion) increases and a
drop in cardiac output are manifested by pulmonary edema and hypotension to the
point of shock.
(5) The exposure of the intravascular compartment to amniotic fluid thromboplastin and
to other mediators freed in the circulation by the presence of amniotic fluid induces
a consumptive coagulopathy in a large proportion of the first-phase survivors. This
disseminated intravascular coagulation often results in severe uterine bleeding.
(6) The resultant systemic hypotension decreases the uterine perfusion. Abnormalities
of the fetal heart tracing will rapidly follow and may result in fetal death.

Pathophysiology of amniotic fluid embolism.

Reprinted from Gei and Hankins,11 with permission.

such as meconium may play a role.

Many experts16-22 speculate that
maternal mediators also may have
an influence.
The second manifestation
includes negative inotropism and
left ventricular failure resulting in
increasing pulmonary edema and
hypotension quickly leading to shock.
The third manifestation is a neurological response to the respiratory
and hemodynamic injury, which may
include seizures, confusion, or coma.11
About 40% to 50% of patients
who survive to this point have severe
coagulopathy, usually disseminated
intravascular coagulation, which
results in uncontrollable uterine
bleeding along with bleeding from
puncture sites such as insertion
sites for intravenous and epidural
catheters.11 This coagulopathy is
thought to be precipitated by several procoagulant components of
amniotic fluid, most notably thromboplastin, which initiate the extrinsic pathway of the clotting cascade
and result in excessive fibrinolytic
activity.8,11,23,24
Possibly before the onset of
maternal signs and symptoms, but
most certainly as they appear, initial changes in fetal heart rate patterns become evident on the electronic
fetal monitor. These changes are due
to decreased uterine perfusion and
the resultant decreased placental
blood flow associated with maternal
hypotension.11 Fetal reserve necessary
to compensate for this decreased
perfusion is quickly depleted, and
the fetus shows signs of hypoxiainduced distress. The normal fetal
heart rate is from 110/min to 160/min
with moderate short-term variability
of 6/min to 25/min. (Short-term
variability is defined as the difference

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between successive heartbeats as

measured by the R-R interval of the
QRS cardiac cycle and is reliably
assessed only via internal fetal monitoring. Short-term variability gives
the fetal heart rate tracing a zigzag
appearance on the monitor strip.) A
decrease in fetal oxygenation, in this
situation due to maternal hypotension and hypoxia, can rapidly lead to
the appearance of nonreassuring
patterns in fetal heart rate (Table 2).
Correction of the cause of these
changes, that is, maternal hypotension and hypoxia, is the only remedy.
Therefore, resuscitation of the mother
and stabilization of her condition
are the priorities. When fetal heart
rate is being assessed, the appearance
of nonreassuring patterns should be
viewed in the context of the overall
clinical picture. Each of the patterns
listed in Table 2 may have more than
a single cause; some of the causes are
relatively benign and easily correctable.
For example, simply changing the
mothers position, providing her with
fluids for volume expansion, and/or
initiating oxygen supplementation
may improve matters. However, the
seriousness of AFE is quickly made
evident by the rapid deterioration in
fetal status and the apparent futility
of measures normally implemented
to improve it.

Diagnosis
Immediate recognition and diagnosis of AFE is essential to improve
maternal and fetal outcomes. Until
recently, the diagnosis of AFE was
made only after an autopsy of the
mother revealed squamous cells,
lanugo hair, or other fetal and amniotic material in the pulmonary arterial
vasculature.11,28 Although laboratory
data may indicate that AFE is likely,

Table 2 Possible changes in fetal heart rate patterns associated with fetal hypoxia25-27
Pattern

Description

Tachycardia
Late decelerations

Decreased short-term variability

Prolonged variable decelerations

Bradycardia

Fetal heart rate maintained at >160/min for 10

minutes or longer
Decelerations in fetal heart rate from baseline, of
uniform shape, that begin after the peak of
contraction and recover back to baseline well
after the contraction ends
Beat-to-beat change is less than 6/min; accurately
assessed only through electrode placed on fetal
presenting part
Fetal heart rate intermittently decreases from baseline for 2-10 minutes before returning to
baseline; variable in timing and shape
Fetal heart rate maintained <110/min for 10
minutes or longer

ive measures should be implemented

as noted previously, no single labopromptly. In the event of cardiac
ratory or clinical finding can be used
arrest, the resuscitation team should
to diagnose or exclude it.6,7 Diagnosis,
follow standard Advanced Cardiac
therefore, must be based on clinical
Life Support protocols for obstetric
features, and AFE should not be conpatients.23 Ideally, overall managefused with other pregnancy-related
complications or medical conditions
ment of AFE should take place in an
(Table 3). Obstetric nurses and critiobstetric intensive care unit. Many
cal care nurses caring for obstetric
hospitals lack obstetric intensive care
patients should familiarize themselves
units and so the patient must be
with this condition, as Gei and Hancared for in a medical or surgical
11
kins imply
that an
Table 3 Differential diagnosis of amniotic fluid embolism
increased
Respiratory distress
awareness of
Pulmonary embolism (thrombus, fluid, air, fat)
this syndrome
Pulmonary edema
Anesthesia complications
has resulted in
Aspiration
earlier diagnosis, aggressive
Hypotension and shock-related symptoms
Septic shock
intervention,
Hemorrhagic shock
and probably a
Anaphylactic reaction
Myocardial infarction
better chance
Cardiac arrhythmias
of survival.

Management
Once the
signs and symptoms are recognized and a
presumptive
diagnosis is
made, support-

Hemorrhage and bleeding disorders

Disseminated intravascular coagulation
Placental abruption
Uterine rupture
Uterine atony
Neurological and seizure-related conditions
Eclampsia
Epilepsy
Cerebrovascular accident
Hypoglycemia

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High-RiskObstetrics
intensive care unit. Critical care
nurses without obstetric expertise
often become anxious when caring
for pregnant patients; however, the
initial principles of dealing with
obstetric emergencies are the same as
for any emergency: airway, breathing,

started at 5 cm H2O and increased

by increments of 2 to 3 cm H2O until
satisfactory levels of PaO2 are
reached.11 The goal of oxygen therapy
is to maintain arterial PaO2 higher
than 60 mm Hg and arterial oxygen
saturation at 90% or higher.6,24,30

The fetus is very vulnerable to maternal

hypoxia, which is initially profound in AFE.
and circulation. The major difference
for this particular emergency is the
need to care for 2 patients.
The fetus should be monitored
continuously for signs of compromise
(preferably by an obstetric nurse with
expertise in electronic fetal monitoring). Specific to pregnant women is
the importance of positioning. In
order to ensure optimal uterine perfusion throughout the management of
AFE, the mothers hips should be displaced to the left to prevent the
weight of the gravid uterus from compressing the inferior vena cava and
compromising blood flow.29
Oxygenation
The fetus is very vulnerable to
maternal hypoxia,28 which is initially
profound in AFE. Therefore, the first
priority is resuscitation of the mother4
and administration of oxygen by any
means available at concentrations of
100%.7,24
A more aggressive approach
includes securing an airway through
endotracheal intubation, providing
mechanical ventilation for the patient
with a high inspired fraction of oxygen
(>60%), and the addition of positive
end-expiratory pressure.6,7,11 Positive
end-expiratory pressure is typically

Circulation
Maintaining cardiac output and
blood pressure involves several simultaneous interventions. Gei and Hankins11 recommend positioning the
patient flat or in a slight Trendelenburg position to improve the venous
blood return and perfusion of the central nervous system. Supportive measures include the initiation of fluid
therapy, administration of pharmacological agents (Table 4), and electrocardiographic monitoring to detect
and treat arrhythmias; most patients
with AFE initially have electromechanical dissociation or bradycardia.5 Placement of a pulmonary artery
catheter is highly recommended for
monitoring cardiac output, central
venous pressure, and pulmonary
artery pressures (Table 5). In addition, pulmonary artery catheters provide direct access for blood samples
to be sent for cytological analysis for
amniotic fluid and fetal debris.36
Volume replacement with isotonic
crystalloid solution is a first-line therapy for maintaining blood pressure.24
Fluid therapy should be based on the
findings of central venous monitoring,
so as to avoid overhydration in these
patients, who are predisposed to pulmonary edema.6 Therapy for left ventricular dysfunction should be directed

toward improving inotropy.37 Gillie

and Hughes32 recommend several
inotropic agents as drugs of choice for
maintaining cardiac output and blood
pressure (Table 4). A clinical guideline for supporting critically ill
obstetric patients is to maintain
systolic blood pressure at or higher
than 90 mm Hg,24 with acceptable
organ perfusion, as indicated by a
urine output of 25 mL/h or more.30
Control of Hemorrhage
and Coagulopathy
The results of hematologic studies can be used to diagnose and
monitor the course of bleeding and
disseminated intravascular coagulation.7 According to Martin et al,23
control of uterine bleeding can often
be accomplished with uterine massage
and the administration of pharmacological agents (Table 4). If bleeding
is profuse and pharmacological
intervention is unsuccessful, a hysterectomy may be necessary.
Administration of blood transfusions and blood components is considered the first line of treatment for
correcting coagulopathy associated
with AFE.6 Blood products include
packed red blood cells, fresh-frozen
plasma, platelets, and cryoprecipitate to maintain organ perfusion
and urinary output until bleeding
due to disseminated intravascular
coagulation resolves.30 Cryoprecipitate is particularly useful in AFE
because it can be used to replenish
clotting factors in lieu of fresh-frozen
plasma in volume-restricted patients.
In addition, cryoprecipitate contains
both fibrinogen and fibronectin,
which facilitate the removal of cellular and particulate matter (eg, amniotic fluid debris) from the blood via
the reticuloendothelial system.6

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Table 4 Pharmacological support in amniotic fluid embolism31-33

Medications used
Inotropic agents to
maintain cardiac output
and blood pressure
Dopamine

Recommended dosages

Pharmacological action

Nursing considerations

Initial intravenous infusion: 2-5

g/kg per minute
Increase in increments of 5-10
g/kg per minute as needed

Stimulates 1-adrenergic receptors;

causes release of
epinephrine, which increases
myocardial contraction, cardiac
output, and stroke volume
Stimulates 1-adrenergic receptors;
increases cardiac function, cardiac
output, and stroke volume

Dopamine is a potent drug; be

sure to dilute before
administration; dopamine
should never be given as a
bolus dose
Reconstitute solution
according to manufacturers
directions; reconstitution
requires 2 stages

Intravenous infusion: 2-40

g/kg per minute
Rate of administration depends
on patients response,
including heart rate, blood
pressure, cardiac output, and
urine output
Norepinephrine (Levophed) Intravenous infusion: 2-4
g/min
Effect on blood pressure
determines dosage
Dobutamine

Oxytocic agents used to

control uterine atony and
bleeding
Oxytocin (Pitocin)

Stimulates -adrenergic receptors;

Continue infusion until blood
produces vasoconstriction and
pressure is maintained
increased blood pressure; moderate without therapy; avoid abrupt
increase in myocardial contraction
withdrawal
caused by stimulation of 1Observe catheter insertion site
adrenergic receptors
frequently for extravasation;
have phentolamine available
to minimize local necrosis

Dilute 10-40 U in 1000 mL

isotonic sodium chloride or
dextrose solution
Titrated to control uterine
atony, usually 0.02-0.1 U/min
0.2 mg intramuscularly or
intravenously every 2-4
hours

Stimulates the uterus; increases the

number of contracting uterine
myofibrils

An antidiuretic effect with

volume overload may
develop with high cumulative
doses

Stimulates the rate, tone, and

amplitude of uterine contractions
and decreases uterine bleeding

Prostaglandin F2 (PGF2)
(Hemabate)

250 g intramuscularly
May be repeated every 15-90
min as needed for bleeding

Stimulates uterine contractions and

decreases bleeding

Misoprostol (Cytotec)

1000 g rectally

Synthetic prostaglandin E1;

stimulates uterine contractions and
decreases bleeding

Administer intravenously
slowly over 1 minute; check
vital signs for evidence of
shock or hypertension after
intravenous administration
Because of hypertensive
response, use cautiously with
norepinephrine
A major contraindication to
use is asthma, which may be
exacerbated because of the
drugs bronchoconstrictive
properties
Limited studies are available
on the clinical efficacy of
misoprostol in treating
postpartum hemorrhage

Steroids to control
inflammatory response
Hydrocortisone sodium
succinate (Solu-Cortef)

500 mg intravenously every 6

hours

Pharmacological doses have marked Administer direct intravenous

anti-inflammatory effect because of
solution at a rate of 100
their ability to inhibit prostaglandin
mg/30 s; doses larger than
synthesis
500 mg should be infused
over 10 minutes

Methylergonovine
(Methergine)

McCance and Huether38 explain that

the reticuloendothelial system, now

referred to as the mononuclear phagocyte system, consists of a line of cells

that ingest and destroy (by phagocytosis) unwanted materials in the blood.

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High-RiskObstetrics

Table 5 Hemodynamic monitoring 34,35

Measures

Normal pressures

Right atrial pressure (essentially

the same as central venous
pressure)
Pulmonary artery pressure

1-7 mm Hg

Pulmonary artery wedge pressure

6-15 mm Hg

Cardiac output
(heart rate x stroke volume)
Cardiac index
(cardiac output/body surface
area, expressed in L/min per
square meter)

4-8 L/min

20-30/10-15 mm Hg

Abnormal pressure indications

Elevated in right-sided heart failure, fluid overload, pulmonary hypertension,
cardiac tamponade
Decreased in hypovolemia
Increased pulmonary artery systolic pressure with right-sided heart failure,
cardiac tamponade, pulmonary hypertension, pulmonary edema or
embolus, adult respiratory distress syndrome
Decreased pulmonary artery systolic pressure with hypovolemia
Increased pulmonary artery diastolic pressure with left ventricular failure,
pulmonary hypertension
Decreased pulmonary artery diastolic pressure with hypovolemia
Elevated with left ventricular failure, septal defects, mitral insufficiency,
cardiac tamponade
Decreased with hypovolemia

2.5-4.2 for adults

3.5-6.5 for pregnant
women

Another pharmacological intervention is the use of intravenous

steroids. Amniotic fluid not only displaces blood and reduces oxygen and
waste exchange but also introduces
antigens, cells, and protein aggregates
that trigger inflammation within the
bloodstream.39 In consideration of the
potential inflammatory response and
similarities to anaphylaxis, the administration of corticosteroids (Table 4)
may be helpful in AFE.5,11,24
In summary, the 3 main goals of
treatment are (1) oxygenation, (2)
maintaining cardiac output and blood
pressure, and (3) correcting coagulopathy. Intensive care nurses, including those without obstetric training,
are expected to learn the critical assessment-management actions beginning
with the primary and secondary surveys of critically ill patients. Once the
mothers condition is stabilized, the
focus of attention is fetal delivery.

Fetal Considerations
In some instances, and of course
most favorable for the fetus, AFE

does not occur until after delivery.

When AFE occurs before or during
delivery, however, the fetus is in
grave danger from the onset because
of the maternal cardiopulmonary
crisis. In addition to concern for
fetal well-being, delivery of the fetus
increases the chances for a good outcome for the mother because the
weight of the gravid uterus on the
inferior vena cava impedes blood
return to the heart and decreases
systemic blood pressure.23,40 Therefore, as soon as the mothers condition is stabilized, delivery of the
viable infant should be expedited. If
resuscitation of the mother is futile,
an emergency bedside cesarean
delivery may be necessary to save
the infant. Undeniably, the sooner
after maternal cardiopulmonary
arrest that the fetus is delivered, the
more favorable is the fetal outcome.5,41 Therefore, as difficult as it
may be, and even though the
mother may be viewed as the primary patient, prolonged resuscitation efforts should be discouraged.

Family Support
Because the maternal and fetal
mortality rates are so high, most
likely an intensive care nurse will be
called on to support the patients
family members through crisis and/or
loss. When the mother and infant
are gravely ill, keeping their family
members well informed and allowing
as much access to the loved ones as
possible are important. Warren42
reported that accessibility to physicians, unrestricted visits, and caring
conveyance of adequate information
were important to families satisfaction with the intensive care unit
experience. When possible, providing and encouraging contact and
interaction between parents and the
newborn are essential in promoting
parent-infant attachment.
In many cases, the mother dies
but the infant survives. It is important
to understand that an event that was
anticipated with much hope and joy
has gone terribly awry and that validating the wide range of emotions
that the family might experience can

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facilitate grieving. In addition, the

stages of normal grieving, anger and
blame, can interfere with the normal
parent-infant attachment and
decrease the frequency of nurturing
behaviors. Referral to counseling and
support groups is most often helpful.
When both the mother and the
infant die, it is important to allow the
father and other family members time
with their deceased loved ones. Staff
members should be present to facilitate the initial contact and to answer
questions, but they should also allow
families to be alone. Pictures of the
infant should be taken and offered to
the family for keeping. Any infant
clothing or blankets used, as well as
infant identification bands, should be
saved and given to the family. Many
obstetric units have special memory
boxes specifically for this purpose.

Summary
AFE is an unpredictable, unpreventable, and, for the most part, an
untreatable obstetric emergency.
Management of this condition
includes prompt recognition of the
signs and symptoms, aggressive
resuscitation efforts, and supportive
therapy. Any delays in diagnosis and
treatment can result in increased
maternal and/or fetal impairment or
death. Whereas once the invariable
outcome of AFE was death of the
mother, today the prognosis is somewhat brighter thanks to increased
awareness of the syndrome and
advances in intensive care medicine.
In any case, intensive care nurses are
called on to provide physical, lifesaving care to the patient and her
fetus. Both during and after the event,
supportive care must be administered
to the patients family members, who
are dealing with crisis and loss.

References
1. Meyer JR. Embolus pulmonar-caseosa. Braz
J Med Biol Res. 1926;2:301-303.
2. Humphrey A. Princess of Wales: a royal
tragedy. Midwives Chron. 1989;102:304305.
3. Gogola J, Hankins GDV. Amniotic fluid
embolism in progress: a management
dilemma. Am J Perinatol. 1998;8:491-493.
4. Sisson MC. Amniotic fluid embolism. Crit
Care Obstet. 1992;4:667-673.
5. Clark SL, Hankins GDV, Dudley DA, Dildy
GA, Porter TF. Amniotic fluid embolism:
analysis of the national registry. Am J Obstet
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CRITICALCARENURSE Vol 24, No. 4, AUGUST 2004 61

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Amniotic Fluid Embolism: An Obstetric Emergency

Katherine J. Perozzi and Nadine C. Englert
Crit Care Nurse 2004, 24:54-61.
2004 American Association of Critical-Care Nurses
Published online http://www.cconline.org

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