High-RiskObstetrics

Amniotic Fluid
Embolism Description and Etiology
Normally, amniotic fluid does not
enter the maternal circulation because
An Obstetric Emergency it is contained safely within the uterus,
sealed off by the amniotic sac. AFE
occurs when the barrier between
Katherine J. Perozzi, RN, MSN
amniotic fluid and maternal circula-
Nadine C. Englert, RN, MSN
tion is broken and, possibly under a
pressure gradient, fluid abnormally

A
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 obste-
trician named Sir Richard Croft was
widely criticized because of the unex-
pected death of one of his patients
and her unborn son. The patient was
Princess Charlotte of Wales, and the
condemnation and grief Croft expe-
Online
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rienced because of this loss apparently
led him to commit suicide. Investi-
gations, continuing at least until the
1970s, strongly suggest that the
princess died of AFE, possibly absolv-
ing 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 tech-
nological advances in critical care
life support, the maternal mortality
rate for AFE remains around 61%; a
large percentage of survivors have
permanent hypoxia-induced neuro-
logical damage. The fetal mortality
rate, although better than the mater-
nal rate, is a dismal 21%, and 50% of
the surviving neonates experience
permanent neurological injury.5
enters the maternal venous system
via the endocervical veins, the pla-
cental 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 devastat-
ing consequence of circulating fetal
debris (carried by amniotic fluid)
occurs only rarely, even though dur-
ing normal labor and delivery,
cesarean deliveries, and minor trau-
matic procedures fetal tissue may
pass into maternal circulation and
cause no symptoms.7 That AFE devel-
ops 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 resem-
bles an anaphylactic reaction to fetal
debris than an embolic event, and
they propose the term “anaphylac-

Authors
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.

54 CRITICALCARENURSE Vol 24, No. 4, AUGUST 2004

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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 con-
sidered to be associated with AFE
include placental abruption, uterine
overdistention, fetal death, trauma,
tumultuous or oxytocin-stimulated
labor, multiparity, advanced mater-
nal age, and rupture of membranes.4
However, in numerous documented
cases of AFE, none of these condi-
tions 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 obscu-
rity of the problem and the wide
range of signs and symptoms associ-
ated with it. According to Gilbert
and Danielsen,9 AFE occurs in 1 of
every 20 646 deliveries. Thanks to
increasing awareness of the syn-
drome, this number is probably
more accurate than many earlier
estimates, which ranged from 1 in
8000 to 1 in 80 000. Precise report-
ing of incidence is extremely difficult
because no definitive clinical or lab-
oratory test is available that can be
used to provide an exclusive diagno-
sis of AFE or completely rule it out.
Clark and coworkers established a
national registry for AFE in an effort
to investigate and understand this
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syndrome more completely. Table 1 onslaught of cardiopulmonary
lists the inclusion criteria for diag- injury, but of those who do, 40% to
nosis of AFE. 50% have coagulopathy and hemor-
rhage up to 4 hours later.12 Porter et
Clinical Features al13 noted that in some patients,
and Pathophysiology coagulopathy may be the first indi-
One of the major factors that cation of AFE, whereas Clark et al5
makes AFE so devastating is its total reported that seizure activity may at
unpredictability. Although most cases times be the first manifestation.
occur after the onset of labor, some The pathophysiology of AFE is
incidents have occurred outside of speculative; various theories have
labor. As mentioned earlier, several been published. Gei and Hankins11
clinical conditions seem to be asso- proposed a pathophysiological
ciated with AFE, but essentially course (see Figure). Three distinct
there are no definitive clues, warning responses or a combination of clinical
signs, or associated conditions that responses to circulating fetal debris
indicate the risk of AFE may be are suggested.
increased. Most experts agree that The initial respiratory reaction
AFE, as it is known now, cannot be possibly begins with transient pul-
predicted or prevented.11 monary vasospasm.14 Although this
According to Gei and Hankins,11 possible transient vasospasm has
the initial signs and symptoms have not been documented (probably
a typical chronology, and the mor- because the signs and symptoms
bidity and mortality of the manifes- appear so abruptly in a seemingly
tations steadily decreases with time. healthy person who is not being
Most often, respiratory distress and monitored via invasive methods),
cyanosis occur suddenly within the vasospasm may be caused by amni-
first minute and are quickly followed otic microemboli that trigger the
by hypotension, pulmonary edema, release of arachidonic acid metabo-
shock, and neurological manifesta- lites15 and lead to pulmonary hyper-
tions such as confusion, loss of con- tension, intrapulmonary shunting,
sciousness, and seizures. More than bronchoconstriction, and severe
80% of patients experience cardiores- hypoxia.14 Exactly which components
piratory arrest within the first few of amniotic fluid actually cause this
minutes.6 Approximately 50% of effect is unknown, but Clark14 sug-
patients do not survive this gests that abnormal components
Table 1 National registry’s 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
CRITICALCARENURSE Vol 24, No. 4, AUGUST 2004 55
High-RiskObstetrics

such as meconium may play a role.

Cardiogenic and Many experts16-22 speculate that
noncardiogenic 3 Decreased coronary
pulmonary edema blood flow
maternal mediators also may have
+ 4 ↓ an influence.
Intrapulmonary Decreased inotropism
shunting
The second manifestation
↓
+ Decreased cardiac includes negative inotropism and
Bronchoconstriction output left ventricular failure resulting in
↓ +
Desaturation Pulmonary congestion
increasing pulmonary edema and
| | hypotension quickly leading to shock.
Dyspnea ? Hypotension
Bronchospasm
2 The third manifestation is a neuro-
Shock
Cyanosis logical response to the respiratory
Pulmonary edema and hemodynamic injury, which may
include seizures, confusion, or coma.11
About 40% to 50% of patients
5 who survive to this point have severe
Thromboplastins
coagulopathy, usually disseminated
↓ intravascular coagulation, which
Venous Arterial Intravascular results in uncontrollable uterine
systemic systemic coagulation
circulation circulation bleeding along with bleeding from
|
Bleeding puncture sites such as insertion
sites for intravenous and epidural
catheters.11 This coagulopathy is
6 thought to be precipitated by sev-
1
eral procoagulant components of
Amniotic fluid Fetal hypoxia
amniotic fluid, most notably throm-
enters the Bradycardia boplastin, which initiate the extrin-
circulation Death sic pathway of the clotting cascade
and result in excessive fibrinolytic
5
activity.8,11,23,24
Sequence of events:
(1) For reasons not completely understood, amniotic fluid reaches the maternal Possibly before the onset of
intravascular compartment (systemic venous system). maternal signs and symptoms, but
(2) The amniotic fluid enters pulmonary circulation via the pulmonary artery. This
contaminated blood crosses to the left atrium through a patent foramen and
most certainly as they appear, ini-
probably through intrapulmonary shunts once the embolism is significant, as tial changes in fetal heart rate pat-
shown in cases of massive amniotic fluid embolism at autopsy. terns become evident on the electronic
(3) The exposure of the pulmonary vasculature to both soluble (leukotrienes, surfactant,
thromboxane A2, endothelin, etc.) and insoluble components (squames, vernix, hair, fetal monitor. These changes are due
mucin, etc.) of the amniotic fluid and possibly other mediators released locally to decreased uterine perfusion and
induces capillary leak, negative inotropism, and bronchospasm. This results in
sudden onset of respiratory distress and cyanosis.
the resultant decreased placental
(4) Within minutes, the negative inotropic effect becomes prevalent (probably due to blood flow associated with maternal
myocardial ischemia). Pulmonary venous pressure (congestion) increases and a hypotension.11 Fetal reserve necessary
drop in cardiac output are manifested by pulmonary edema and hypotension to the
point of shock. to compensate for this decreased
(5) The exposure of the intravascular compartment to amniotic fluid thromboplastin and perfusion is quickly depleted, 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
the fetus shows signs of hypoxia-
disseminated intravascular coagulation often results in severe uterine bleeding. induced distress. The normal fetal
(6) The resultant systemic hypotension decreases the uterine perfusion. Abnormalities heart rate is from 110/min to 160/min
of the fetal heart tracing will rapidly follow and may result in fetal death.
with moderate short-term variability
Pathophysiology of amniotic fluid embolism. of 6/min to 25/min. (Short-term
Reprinted from Gei and Hankins,11 with permission.
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 moni-
toring. 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 hypoten-
sion 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 hypoten-
sion 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
mother’s 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 diag-
nosis 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 amni-
otic material in the pulmonary arterial
vasculature.11,28 Although laboratory
data may indicate that AFE is likely,
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Table 2 Possible changes in fetal heart rate patterns associated with fetal hypoxia25-27
Pattern Description
Tachycardia Fetal heart rate maintained at >160/min for 10
minutes or longer
Late decelerations 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
Decreased short-term variability Beat-to-beat change is less than 6/min; accurately
assessed only through electrode placed on fetal
presenting part
Prolonged variable decelerations Fetal heart rate intermittently decreases from base-
line for 2-10 minutes before returning to
baseline; variable in timing and shape
Bradycardia Fetal heart rate maintained <110/min for 10
minutes or longer
as noted previously, no single labo- ive measures should be implemented
ratory or clinical finding can be used promptly. In the event of cardiac
to diagnose or exclude it.6,7 Diagnosis, arrest, the resuscitation team should
therefore, must be based on clinical follow standard Advanced Cardiac
features, and AFE should not be con- Life Support protocols for obstetric
fused with other pregnancy-related patients.23 Ideally, overall manage-
complications or medical conditions ment of AFE should take place in an
(Table 3). Obstetric nurses and criti- obstetric 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 Han- cared for in a medical or surgical
kins imply
11
that an Table 3 Differential diagnosis of amniotic fluid embolism
increased
awareness of Respiratory distress
Pulmonary embolism (thrombus, fluid, air, fat)
this syndrome Pulmonary edema
has resulted in Anesthesia complications
Aspiration
earlier diagno-
sis, aggressive Hypotension and shock-related symptoms
intervention, Septic shock
Hemorrhagic shock
and probably a Anaphylactic reaction
better chance Myocardial infarction
Cardiac arrhythmias
of survival.
Hemorrhage and bleeding disorders
Management Disseminated intravascular coagulation
Placental abruption
Once the Uterine rupture
signs and symp- Uterine atony
toms are recog- Neurological and seizure-related conditions
nized and a Eclampsia
presumptive Epilepsy
Cerebrovascular accident
diagnosis is Hypoglycemia
made, support-
CRITICALCARENURSE Vol 24, No. 4, AUGUST 2004 57
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,
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 monitor-
ing). Specific to pregnant women is
the importance of positioning. In
order to ensure optimal uterine perfu-
sion throughout the management of
AFE, the mother’s hips should be dis-
placed to the left to prevent the
weight of the gravid uterus from com-
pressing 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
58 CRITICALCARENURSE Vol 24, No. 4, AUGUST 2004
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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
Circulation
Maintaining cardiac output and
blood pressure involves several simul-
taneous interventions. Gei and Hank-
ins11 recommend positioning the
patient flat or in a slight Trendelen-
burg position to improve the venous
blood return and perfusion of the cen-
tral nervous system. Supportive meas-
ures include the initiation of fluid
therapy, administration of pharmaco-
logical agents (Table 4), and electro-
cardiographic monitoring to detect
and treat arrhythmias; most patients
with AFE initially have electro-
mechanical dissociation or bradycar-
dia.5 Placement of a pulmonary artery
catheter is highly recommended for
monitoring cardiac output, central
venous pressure, and pulmonary
artery pressures (Table 5). In addi-
tion, pulmonary artery catheters pro-
vide 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 ther-
apy 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 pul-
monary edema.6 Therapy for left ven-
tricular 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 guide-
line 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 stud-
ies can be used to diagnose and
monitor the course of bleeding and
disseminated intravascular coagula-
tion.7 According to Martin et al,23
control of uterine bleeding can often
be accomplished with uterine massage
and the administration of pharmaco-
logical agents (Table 4). If bleeding
is profuse and pharmacological
intervention is unsuccessful, a hys-
terectomy may be necessary.
Administration of blood transfu-
sions and blood components is con-
sidered the first line of treatment for
correcting coagulopathy associated
with AFE.6 Blood products include
packed red blood cells, fresh-frozen
plasma, platelets, and cryoprecipi-
tate to maintain organ perfusion
and urinary output until bleeding
due to disseminated intravascular
coagulation resolves.30 Cryoprecipi-
tate 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 cellu-
lar and particulate matter (eg, amni-
otic fluid debris) from the blood via
the reticuloendothelial system.6
 Table 4 Pharmacological support in amniotic fluid embolism31-33
Medications used Recommended dosages
Inotropic agents to
maintain cardiac output
and blood pressure
Dopamine Initial intravenous infusion: 2-5
µg/kg per minute
Increase in increments of 5-10
µg/kg per minute as needed
Dobutamine Intravenous infusion: 2-40
µg/kg per minute
Rate of administration depends
on patient’s response,
including heart rate, blood
pressure, cardiac output, and
urine output
Norepinephrine (Levophed) Intravenous infusion: 2-4
µg/min
Effect on blood pressure
determines dosage
Oxytocic agents used to
control uterine atony and
bleeding
Oxytocin (Pitocin) 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
Methylergonovine 0.2 mg intramuscularly or
(Methergine) intravenously every 2-4
hours
Prostaglandin F2 (PGF2) 250 µg intramuscularly
(Hemabate) May be repeated every 15-90
min as needed for bleeding
Misoprostol (Cytotec) 1000 µg rectally
Steroids to control
inflammatory response
Hydrocortisone sodium 500 mg intravenously every 6
succinate (Solu-Cortef) hours
McCance and Huether38 explain that referred to as the mononuclear phago-
the reticuloendothelial system, now cyte system, consists of a line of cells
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Pharmacological action Nursing considerations
Stimulates β1-adrenergic receptors; Dopamine is a potent drug; be
causes release of sure to dilute before
epinephrine, which increases administration; dopamine
myocardial contraction, cardiac should never be given as a
output, and stroke volume bolus dose
Stimulates β1-adrenergic receptors; Reconstitute solution
increases cardiac function, cardiac according to manufacturer’s
output, and stroke volume directions; reconstitution
requires 2 stages
Stimulates α-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 β1- Observe catheter insertion site
adrenergic receptors frequently for extravasation;
have phentolamine available
to minimize local necrosis
Stimulates the uterus; increases the An antidiuretic effect with
number of contracting uterine volume overload may
myofibrils develop with high cumulative
doses
Stimulates the rate, tone, and Administer intravenously
amplitude of uterine contractions slowly over 1 minute; check
and decreases uterine bleeding vital signs for evidence of
shock or hypertension after
intravenous administration
Because of hypertensive
response, use cautiously with
norepinephrine
Stimulates uterine contractions and A major contraindication to
decreases bleeding use is asthma, which may be
exacerbated because of the
drug’s bronchoconstrictive
properties
Synthetic prostaglandin E1; Limited studies are available
stimulates uterine contractions and on the clinical efficacy of
decreases bleeding misoprostol in treating
postpartum hemorrhage
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
that ingest and destroy (by phagocyto-
sis) unwanted materials in the blood.
CRITICALCARENURSE Vol 24, No. 4, AUGUST 2004 59
High-RiskObstetrics

Table 5 Hemodynamic monitoring 34,35

Measures Normal pressures Abnormal pressure indications

Right atrial pressure (essentially
the same as central venous
pressure)
Pulmonary artery pressure
Pulmonary artery wedge pressure
Cardiac output
(heart rate x stroke volume)
Cardiac index
(cardiac output/body surface
area, expressed in L/min per
square meter)
1-7 mm Hg Elevated in right-sided heart failure, fluid overload, pulmonary hypertension,
cardiac tamponade
Decreased in hypovolemia
20-30/10-15 mm Hg 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
6-15 mm Hg Elevated with left ventricular failure, septal defects, mitral insufficiency,
cardiac tamponade
Decreased with hypovolemia
4-8 L/min
2.5-4.2 for adults
3.5-6.5 for pregnant
women

Another pharmacological inter-
vention is the use of intravenous
steroids. Amniotic fluid not only dis-
places 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 admin-
istration 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 coagu-
lopathy. Intensive care nurses, includ-
ing those without obstetric training,
are expected to learn the critical assess-
ment-management actions beginning
with the primary and secondary sur-
veys of critically ill patients. Once the
mother’s 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 out-
come 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 There-
fore, as soon as the mother’s condi-
tion 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 out-
come.5,41 Therefore, as difficult as it
may be, and even though the
mother may be viewed as the pri-
mary patient, prolonged resuscita-
tion 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 patient’s
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 physi-
cians, unrestricted visits, and caring
conveyance of adequate information
were important to families’ satisfac-
tion with the intensive care unit
experience. When possible, provid-
ing 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 vali-
dating 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 facili-
tate 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, unpre-
ventable, 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 some-
what 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, life-
saving care to the patient and her
fetus. Both during and after the event,
supportive care must be administered
to the patient’s family members, who
are dealing with crisis and loss.
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Amniotic Fluid Embolism: An Obstetric Emergency
Katherine J. Perozzi and Nadine C. Englert
Crit Care Nurse 2004;24 54-61
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