Tinjauan pustaka

Definisi
Amniotic fluid embolism (AFE) is a rare, unpredictable and potentially catastrophic condition that
is unique to pregnancy. The clinical syndrome of AFE was first described by Meyer in 1926, then
again by Steiner and Luschbough in 1941.2 It has since been shown to encompass a wide spectrum
of presentations, from subtle clinical vents to sudden and fatal maternal cardiac arrest. It is
characterised by the acute onset of combined cardiorespiratory compromise and coagulation
disorders, occurring in the pregnant or recently pregnant state.1

Because of the infrequency of the condition and the lack of a reliable animal model, much of the
information about AFE is derived from case reports, case series and registries. Consequently, there
are significant variations in the reported incidence, risk factors and outcomes, which are also
contributed to by different diagnostic criteria and potential false-positive cases.1

Although the appearance of a syndrome suggestive of amniotic fluid embolism was reported as
early as 1926, this condition received its first systematic description in 1941 in a small series of
patients reported by the pathologists Steiner and Luschbaugh. These authors reported 32 cases of
women dying of “obstetrical shock” during labor. In eight of these women, careful autopsy
examination revealed squamous cells or other debris of presumed fetal origin in the maternal
pulmonary arterial circulation in addition to other findings. Despite widely disparate clinical
presentations, these authors viewed all patients as having died of a unique clinical syndrome based
solely on similar pulmonary histologic findings. They concluded that the patients had died as a
result of pulmonary embolism by “amniotic fluid,” giving rise to the term amniotic fluid
embolism.2\

In subsequent decades, the assumptions of these authors regarding the pathognomonic nature of
such pulmonary findings and their pathophysiologic implications went largely unchallenged.
Patients with pathologic findings similar to those described in the report of Steiner and Luschbaugh
were often diagnosed as having amniotic fluid embolism regardless of clinical presentation; reports
describing such cellular debris in the circulation of women with conditions unrelated to amniotic
fluid embolism were largely ignored. As a result, numerous case reports appeared in the medical
literature describing an incredible variety of presumed clinical presentations of “amniotic fluid
embolism” based solely on the detection of fetal cells or other debris of presumed fetal origin in
the pulmonary arteries at autopsy. However, a critical review of the clinical details provided in the
original report of Steiner and Luschbaugh reveals that in seven of the eight reported cases, the
patients appear to have died from a condition such as sepsis or hemorrhage from undiagnosed
uterine rupture, yet were considered as index cases of a new condition (amniotic fluid embolism)
based exclusively on pulmonary histologic findings.2

Against this background of erroneous diagnostic criteria and flawed animal models, it is not
surprising that little progress was made for decades in the understanding of this condition, its
diagnosis, or treatment. The modern era of amniotic fluid embolism was heralded in the 1980s
with the publication of several studies made possible by the development of clinical techniques for
pulmonary artery catheterization of critically ill women, basic science investigations into
maternal–fetal physiology, and the establishment of the first systematic case registry of amniotic
fluid embolism. These studies revealed several surprising results that led to a reevaluation and
rejection of earlier theories of pathogenesis.2

Etiologi
Whilst the underlying mechanisms of AFE are poorly understood, it is relatively well accepted
that the aetiology relates to the transfer of amniotic fluid into the maternal circulation, whereby an
idiosyncratic reaction is triggered. For amniotic fluid to gain access to the maternal circulation
there must be a breech of the physical barriers within the utero-placental unit, for examples the
endocervical veins uterine trauma site or the site of placental attachment. There must also be a
pressure gradient favouring transfer into the maternal circulation. These theories are supported by
a number of identified risk factors for AFE that involve breeches of these barriers (e.g. placenta
praevia and placental abruption) or that are associated with increases in intra uterine pressure (e.g.
uterine contractions, augmentation of labour).1

Once amniotic fluid is present in the maternal circulation the process by which an AFE reaction is
triggered remains unclear. Two main theories have evolved to explain the clinical consequences.
The first and more traditional view is that the amniotic fluid and cellular components (squames,
vernix, mucin, lanugo) create an obstruction to the pulmonary circulation, leading to decreased
 cardiac output with consequent maternal collapse –
hence the term ‘‘embolism’’. However, this theory
fails to support all of the clinical manifestations of
AFE and whilst a physical obstruction to pulmonary
blood flow may be a component of a reaction,
especially with meconium-stained amniotic fluid, it
does not appear to be the primary mechanism.1

The second theory is that the reaction is

immunemediated, this being supported by a number
of factors. Amniotic fluid has been shown to be
present in the maternal circulation without any
Gambar 1. Kemungkinan penyebab clinical consequences and in attempts to develop
terjadinya emboli air ketuban3
animal models of AFE, the injection of amniotic fluid
has not reliably triggered a reaction. Amniotic fluid contains many vasoactive and procoagulant
substances, such as platelet activating factor, cytokines, bradykinin, thromboxane, leukotrienes
and arachadonic acid so it may require only small amounts of such substances to enter the maternal
circulation to produce the events of an AFE. In addition, AFE reactions have been shown to be
more common in women carrying a male fetus and. in cases of rhesus isoimmunisation Clark
suggests that differences in the nature or severity of the presentation of AFE may be a result of
variations in antigen exposure and individual response. Because of the similarities of some cases
of AFE to anaphylaxis, Clark suggested that a more appropriate name for the condition is
‘‘anaphylactoid syndrome of pregnancy’’.1

Faktor – Faktor Resiko

A large number of risk factors for AFE have been identified. These include maternal age over 35
years, multiple pregnancy, caesarean birth, assisted delivery, placenta praevia, placental abruption,
eclampsia, fetal distress, polyhydramnios, uterine rupture and ethnic minority Labour induction
has received recent particular attention as a possible risk factor. Data from the UK Obstetric
Surveillance System (UKOSS) suggested that induction of labour greatly increased the risk of
AFE. (OR 3.86, 95% CI 2.04–7.31). This finding supported a Canadian study that also showed an
increased risk. (OR 1.8, 95% CI 1.3–2.7) However, a large USA population study of 3 million
births and 227 cases of AFE did not find a significant association (adjusted OR 1.5,95% CI 0.2–
2.3). The plethora of associations means that identification of risk factors for AFE has an
exceptionally low positive predictive value and is of no benefit in the acute setting. Further, as
many risk factors are not potentially modifiable, identification may not prove useful in reducing
the incidence of AFE.1

Berdasarkan penelitian yang dilakukan di jepang oleh Oi hidekazu dkk. There were 65 deaths
(mortality rate: 48.0%). The mean maternal age of the AFE study group was 32.2 years. The
maternal age distributions were similar for the fatal AFE group (mean: 32.8 years; range: 21–42
years) and the nonfatal AFE group (mean: 31.1 years; range: 16– 43 years). Nineteen of 65 women
with fatal AFE were having their first baby, indicating that fatal cases were more likely to be
multiparous (p = 0.009). The gestational age at delivery among the fatalities was greater than 37
weeks in 50 out of 65 cases, while 5 (7.7%) cases were delivered before 37 weeks. Among the 70
nonfatal AFE cases, 16 (22.9%) were women who delivered before 37 weeks of gestation. A
gestational time of over 37 weeks appeared to correlate significantly with fatality (p = 0.002). In
the fatal AFE group, only 4 cases (6.2%) were delivered by cesarean section. This difference was
statistically significant (p < 0.0001) compared with the rate of cesarean section (41.4%) in the
nonfatal cases.4 Menurut data penelitian di Inggris oleh Knight et al, memiliki beberapa
karakteristik (tabel 2).5

Epidemiologi
The published incidence of AFE varies widely, likely because of a number of factors such as the
methodology used for case ascertainment (e.g. voluntary registries population-linked data), non-
specific diagnostic criteria, uncertainty as to how the condition has been diagnosed, and differences
in reporting as a result of varying levels of awareness. Recent data suggest that the incidence ranges
from 1:12,953 deliveries, in the US to 1:52,600 deliveries in the UK with Australia reporting a
figure within this range of 1:16,393 (tabel 3). Knight et al. noted the variation in the incidence of
AFE between countries based on the methodology used for case ascertainment. The lowest rates
of AFE were obtained with prospective case identification, suggesting there may be a significant
number of false-positive cases reported. They recommended that future comparisons of incidence
data between countries be based on use of similar methodology and case definitions.1
 Tabel 1 Distribution of fatal and nonfatal AFE cases according to selective characteristics4

The analysis of the national registry reveals that 70% of cases of amniotic fluid embolism occur
during labor, 11% after a vaginal delivery, and 19% during a cesarean elivery. These figures
suggest that the mode of delivery may alter the timing of amniotic fluid embolism but not its
Tabel 2 Characteristics of Women With Amniotic-Fluid Embolism5

occurrence. In rare instances, amniotic fluid embolism may occur during the first or second
trimesters of pregnancy, at the time of pregnancy termination, or amniocentesis.6

Patofisiology
AFE can occur at any time during pregnancy or in the immediate postpartum period, with reports
of cases also at the time of amniocentesis, at induction of labour for miscarriage and termination
of pregnancy. Knight et al. noted that in their UK study population of 60 cases, AFE generally
occurred between two hours before delivery and four hours after delivery. In 56% of cases AFE
Tabel 3 Incidence of amniotic fluid embolism and case presented at or before delivery and when
fatality rates in published series1
it occurred after delivery, 73% of cases
were at caesarean delivery, making this a
significant risk factor (adjusted OR 8.84,
95% CI 3.70–21.1)1

Cardiovascular changes associated with

AFE may be complex and the detail is
open to debate. Currently, it is thought
that there is likely to be a biphasic
response In the initial phase of an AFE
reaction there may be severe pulmonary
hypertension associated with acute right
ventricular failure, which can lead to
severe impairment of left ventricular filling due to deviation of the interventricular septum into the
left atrium and ventricle. These findings are likely to explain the sudden cardiovascular collapse
seen in some AFE reactions. If the patient survives this initial insult, the second phase is thought
to involve continuing left ventricular failure, without severe pulmonary hypertension. Clark et al.
found only mildly increased pulmonary artery pressures and increased central venous and
pulmonary capillary wedge pressures. The mechanism of the on-going left ventricular failure is
unclear, but has been a postulated to be a result of myocardial ischaemi or the presence of
substances that depress myocardial function.1

A number of vasoactive mediators are present in amniotic fluid and may explain the potential for
pulmonary hypertension. Hankins et al. were able to demonstrate that the injection of homologous
amniotic fluid into the maternal circulation of goats caused marked in creases in both the
pulmonary and systemic vascular resistances. This response was more intense in the presence of
meconium. This may explain why in Clark et al.’s initial case series, worse maternal outcomes
were seen in women with meconium-stained amniotic fluid Endothelin has also been implicated
in the pathophysiology, because amniotic fluid contains high concentrations, which may be
sufficient to generate the vasoconstriction seen during AFE. Other humoral factors such as
proteolytic enzymes, histamine, serotonin, prostaglandins and leukotrienes may also have a role.1
 Coagulation disorders in
AFE occur in the majority of
cases, occurring in over 80%
of cases and are sometimes
the presenting feature. The
coagulopathy seen with AFE
is postulated to occur as a
result of both procoagulant
and anticoagulant factors
and is likely to be
multifactorial. Amniotic
fluid contains a number of
factors that influence
coagulation, including
activated clotting factors II,
VII and X and tissue factor.

Gambar 2 Proposed pathophysiology of amniotic fluid embolism6 It is not clear whether the
coagulopathy is due primarily to a
consumptive process or massive fibrinolysis. The procoagulant thromboplastin is found in
amniotic fluid and might contribute to a consumptive coagulopathy. Significant early-onset
hyperfibrinolysis has recently been demonstrated in a case of AFE and may be secondary to
increased levels of urokinase-like plasmin activator, thrombin-antithrombin complexes and
plasminogen activator inhibitor-1 found in amniotic fluid.1

Respiratory symptoms are a feature of AFE and can range from mild dyspnoea to respiratory arrest.
Intrapulmonary shunting is seen acutely in many women, leading to low arterial oxygenation
despite oxygen therapy. In severe reactions pulmonary oedema may be a consequence of left
ventricular failure or potentially from capillary damage.1

Clinical manifestasion
Amniotic fluid embolism can present with a wide range of symptoms and signs, from cardiac arrest
through to relatively minor or possibly sub-clinical events. In Clark’s initial analysis of clinical
features, hypotension and fetal distress were
universal findings, with cardiac arrest, pulmonary
oedema and coagulation disturbances also
common.1

with Knight et al. reporting that the most common

manifestations are (tabel 4) premonitory symptoms
(30%), shortness of breath (20%) and acute fetal
compromise (20%). However, as the condition
progresses or when it is more severe, other features
typical of AFE may be apparent, particularly
maternal haemorrhage, hypotension, marked
dyspnoea, severe coagulopathy and acute fetal
compromise.1

Diagnosis
Gambar 3 Proposed pathophysiology of
Historically, the diagnosis of AFE was usually made amniotic fluid embolism oleh clark et al2
at autopsy when fetal squames were found within
the pulmonary vasculature. With the improved survival rate, most cases are now diagnosed on
clinical grounds. In addition, the relevance of detection of fetal squamous material in the
pulmonary vasculature, as an indicator of AFE, is uncertain. AFE is considered to be a diagnosis
of exclusion, with the entry criteria used by some of the AFE registries summarising the key
diagnostic features. Whilst there are minor differences between registries, they tend to have the
following fourinclusion criteria: (1) acute hypotension or cardiac arrest; (2) acute hypoxia; (3)
coagulopathy or severe clinical haemorrhage in the absence of other explanations; and (4) an event
during labour, caesarean delivery, uterine surgery or within a defined postpartum period and with
no other explanation for the findings. Alternative explanations for maternal compromise that may
need to be ruled out are broad and are both obstetric and non-obstetric. A range of investigations,
such as haematological studies, electrocardiograms, chest X-rays, CT scans and echocardiographs
may be required.1

There is no recognised or readily available diagnostic test for AFE. With the potential
immunological involvement, there has been interest in the measurement of markers such as
complement, tryptase and amniotic fluid. The sensitivity and specificity of the tests is poor, so they
should currently be considered as investigational tools rather than clinical tests to confirm or
exclude AFE. Activation of the complement system is demonstrated by decreased complement
levels during AFE episodes and this has been suggested as a possible trigger of events. Decreased
levels of C3, C3a and C4 have been found. Complement activation also occurs during normal
labour and delivery, although the decrease does not appear to be as large as during an AFE episode.
Elevated serum tryptase levels have been reported in a small number of cases but this does not
appear to be a common finding, so tryptase levels are likely to be more useful in ruling out
anaphylaxis.1

Additional diagnostic tests described include zinc coproporphyrin (Zn-CPI) (a component of

meconium) and sialyl Tn (STN), a fetal antigen present in both meconium and amniotic fluid.1

Tabel 4 Features of Amniotic-Fluid Embolism Tabel 5 Signs and symptoms of amniotic fluid embolism1
at Presentation5
Levels of Zn-CPI may be elevated in women with AFE and this test may indicate the passage of
meconium into the maternal circulation. serum STN levels have been examined in a number of

studies and show high sensitivity and specificity for AFE. In addition, higher levels of STN have
been found in non-survivors of AFE, raising the possibility of utility in predicting the severity or
mortality from AFE.1

Tabel 4 kriteria diagnosis emboli ketuban7

Tabel 5 differential diagnosis berdasarkan gejala klinis7

Gambar 4 kriteria diagnostik untuk emboli ketuban menurut clark1

Gambar 5 kriteria emboli ketuban menurut jepang8

Indeed, several reports have described the delayed onset of AFE. The delayed reaction caused by
the slow-reacting substance of anaphylaxis has been well established and the mechanism was

Gambar 6 serum marker sebagai tambahan
untuk penegakan diagnosis emboli ketuban8
considered to also be the cause of AFE
pathophysiology. To explain the cases presenting
in the late post partum period, Courtney suggested
that AF may be trapped in the uterine veins during
uterine contractions during delivery. The fluid
may then be released into the circulation during
normal postpartum uterine involution. There is no
standard diagnostic test to confirm the presence of
AFE. Depending on the clinical presentation,
laboratory investigations including serum level of
STN and Zn-CPI may be useful for the accurate
diagnosis of AFE.

Tatalaksana
At our present level of understanding all recommendations are treatment oriented, as there are no
effective prophylactic options to prevent the development of AFE. Early recognition and prompt
initiation of proper management is critical in optimizing outcomes for the patient with AFE. The
treat ment is supportive.
The airway should be
rapidly controlled and
therapy undertaken to
prevent or correct
hypoxemia. Aggressive
resuscitative efforts should
be pursued to support and
maintain hemodynamic
sufficiency, and ensure
8
adequate tissue perfusion. In the Gambar 7 Klasifikasi AFE di jepang
face of severe hemorrhage coagulopathies must be treated. To reduce the impact of aortocaval
compression on venous return, left uterine displacement should be done either manually or by
placing a wedge under the parturient’s right hip. Moreover, the Managing Obstetric Emergencies
and Trauma (MOET) course recommends that fetal delivery (i.e., perimortem caesarean section or
PMCS) be undertaken within 5 minutes of maternal cardiac arrest to decrease fetal toxicity and
improve resuscitation efforts by removing aorto caval compression. This will also potentially
facilitate the efficacy of cardiopulmonary resuscitation. The fetus should be continuously
monitored for any signs of hypoxia or distress.9

In general, an approach based on traditional A-B-Cs (i.e., airway-breathing-circulation) of life

support is the safest way to proceed. Immediate administration of high flow oxygen to prevent
hypoxia is critical. Depending on patient status, this may be accomplished via high flow nasal
cannula, face-mask, non-invasive positive pressure ventilation, or bag-valve mask ventilation.
Most patients will require endotracheal intubation and positive pressure ventilation with 100%
oxygen – at least initially. The decision to intubate is better made earlier than later. In severe cases,
advanced ventilatory strategies may be required to treat severe hypoxia, non-cardiogenic
pulmonary edema or ARDS. Besides lung protective strategies with use of a conventional
ventilator, other approaches such as high frequency oscillatory ventilation, or even extracorporeal
membrane oxygenation (ECMO) may be required. Veno-venousECMO intervention for purely
pulmonary support and veno-arterial EMCO intervention for cardiac support (with or without
pulmonary decompensation) should be considered. The potential airway difficulties present in a
parturient should be kept in mind and physicians should be ready to secure the airway by use of a
fiberoptic scope or even tracheotomy.9

After the airway and respiratory status have been addressed, management focuses on treatment of
hypotension and restoration of maternal circulation. Besides two large bore intravenous lines,
central venous access should be established with serious consideration given to the use of a
pulmonary artery catheter . Also, an arterial line and a urinary catheter should be placed to help
guide therapy. Recent reports suggest that the use of transthoracic echocardiography or TEE may
be beneficial when evaluating left ventricular contractility and filling. These modalit ies may also
be useful in guiding the administration of intravenous fluid therapy and/or vasopressor/inotrope
administration.9

The physician should rapidly administer isotonic solutions to maxim ize preload. Vasopressors
and inotropes will usually be needed, as refractory hypotension is highly probable. In the early
phases of AFE circulatory vasodilation occurs. Phenylephrine and vasopressin may be appropriate
therapies. Inotropic support, including dobutamine, dopamine, epinephrine, or norepinephrine may
be required to treat ventricular contractile impairment. Milrinone may be an appropriate choice for
right heart support through its positive effect on inotropy as a phosphodiesterase inhibitor, and
through its vasodilatory effect on the pulmonary vasculature. Inhaled nitric oxide or inhaled
epoprostenol should be considered for pulmonary vasodilation to treat refractory hypoxemia and
to unload the right ventricle. Should this strategy fail, an intraaortic balloon pump, right ventricular
assist device and/or ECMO (see above) should be considered.9

Hemorrhage in the setting of AFE should prompt early and aggressive blood product
administration. Packed red blood cells and platelets should be administered to maintain oxygen
carrying capacity and prevent thrombocytopenic bleeding. In cases of persistent bleeding,
coagulopathy, or DIC treatment should proceed with a combination of fresh frozen plasma,
cryoprecipitate, fibrinogen, and factor replacement. The exact products to be administered should
be guided by laboratory studies, which may include fibrinogen levels, functional platelet counts,
and thromboelastogram (TEG) as well as the standard INR and PTT. The use of recombinant
activated factor VII has been reported in patients with AFE and bleeding unresponsive to
conventional blood product therapy; however, due to significantly worse associated outcomes,
factor VIIa should be restricted to cases where hemorrhage cannot be stopped by massive blood
component replacement. Antifibrinolytic d rugs such as tranexamic acid or aminocaproic acid have
been used in the past for obstetrical bleeding, but their efficacy in AFE is undetermined.9

Medical therapy should be provided for uterine atony. If the bleeding cannot be controlled,
hysterectomy may be necessary, but uterine artery embolization has been described in selected
cases.After initial stabilization, almost all patients with AFE require transfer to the intensive care
unit. High-quality, modern maternal care using targeted approaches to potential sequelae and
complications of AFE is the likely reason for improving outcomes associated with AFE.9

Left uterine displacement is crucial in resuscitation efforts if the fetus remains in utero. It has been
reported that immediate cesarean section will improve neonatal neurologic recovery and overall
maternal outcome if performed within 5 min of maternal cardiovascular arrest. Maternal
resuscitative efforts are also enhanced by relief of aortocaval compression at delivery.10

Other novel approaches for the treatment of AFE have been successfully used which included
exchange transfusion, extracorporeal membrane oxygenation (ECMO), cardiopulmonary bypass,
a right ventricular assist device, uterine artery embolization, intraaortic balloon pump with ECMO
have recently been reported with successful outcomes. Continuous hemofiltration, cell-salvage
combined with blood filtration and serum protease inhibitors are few other recommended
treatment in literature.10

Hysterectomy may be required in patients with persistent uterine hemorrhage to control blood loss.
rfVII has also been described as a treatment for hemorrhage occurring with AFE, but should be
used with caution because a recent review of case reports has suggested worsened outcomes. Both
aerosolized prostacyclin and inhaled nitric oxide (NO) act as direct pulmonary vasodilators, and
have been successfully used to treat the acute pulmonary vasoconstriction of AFE its
administration is still controversial. This controversy arises because of the manifestation of both
DIC and embolism in patients of AFE.Besides heparin, in few animal studies aspirin have been
tried. Heparin prophylaxis maintained platelet count whereas aspirin prophylaxis did not. They
concluded that the aspirin is not an effective prophylactic drug.10

Gambar 8 Alogaritma terapi perdarahan postpartum11

Prognosis
Survival after AFE has improved significantly with early recognition of this syndrome and rompt
and early resuscitative measures. Previously, it was documented that 50% of patients die within
the first hour and about two-third within 5 h of the event with high incidence of severe and
permanent neurological damage among survivors. Although mortality rates have declined,
morbidity remains high with severe sequelae. Beside neurologic impairment, acute oliguric or
nonoliguric renal failure, cardiac failure with left ventricular impairment, cardiogenic pulmonary
edema, arrhythmias, myocardial ischemia or infarction have been reported. Respiratory failure
with noncardiogenic pulmonary edema and refractory bronchospasm are other reported sequelae:
•The prognosis after AFE is very poor, and most women
do not survive.
•If patient survives the embolism, most survivors have
neurologic deficits.
•The infant survival rate is 70%. Neurologic status of
the infant is directly related to the time elapsed between
maternal arrest and delivery.
•Risk of recurrence is unknown. Successful subsequent
pregnancies have been reported.
Despite our lack of understanding of the pathophysiologic processes of AFE, it is very clear that
early and aggressive management (including immediate cesarean section) of patients with
clinically suspected AFE enhances both fetal and maternal resuscitation and improves survival. It
is important to always consider AFE in the differential diagnosis of sudden maternal
cardiopulmonary instability and remember that the lack of development of DIC and hemorrhage
does not exclude the diagnosis of AFE.

Pencegahan
Risk factors found in several studies to be significantly associated with an increased risk of AFE
included maternal age of 35 years or older, cesarean delivery, forceps/vacuum delivery, placenta
previa, abruption placenta, eclampsia and fetal distress. It is assumed that the rupture of the
membranes followed by the inflow of amniotic fluid into maternal circulation occurs easily in
cases of cesarean delivery, forceps/ vacuum delivery, placenta previa, abruption placenta and
eclampsia because these conditions are ascribed to injury of the birth canal or injury of
trophoblasts. The amniotic membrane and chorion membrane form an important barrier that
prevents amniotic fluid from flowing into the maternal circulatory system. The egg membrane,
especially the amniotic membrane, restricts contact of the amniotic fluid with maternal allergy
associated cells. In the event of rupture of the egg membrane, an anaphylactoid reaction is likely
to occur in the mother’s body, and routine delivery management should be employed. Unless the
membrane is ruptured, the maternal allergy-associated cells, including mast cells, eosinophils and
basophils, are not exposed to a large amount of amniotic fluid. If the membrane is ruptured and
amniotic fluid flows into the vagina, the possibility of contact with maternal allergy-inducing cells
decreases because, as with the skin, the vagina is lined by thick, stratified, squamous epithelium
and rarely comes into contact with maternal immune cells. If the membrane is ruptured, and
amniotic fluid comes into contact with the cervical tissues or uterine muscles, either major or minor
allergic-like reactions are induced in some parts of the uterus. In the vent of rupture of the
membrane, the contact between the amniotic fluid and the mother’s body should be prevented as
much as possible. Timely rupture of the membrane, which is defined as ‘complete dilation of the
uterine cervix followed by rupture of the membrane’, is regarded as normal. This conventional
process ensures safe delivery management. Artificia rupture of the membrane at the higher station
of the presenting part of the fetus or rupture of the membrane without effacement of the cervix
enables contact with the endocervical columnar epithelium or stroma (in the presence of laceration)
and increases the possibility of allergic reaction. Therefore, obstetricians should recognize the
increased risk of inflow of amniotic fluid into maternal blood in the event of an injury, vacuum
delivery and forceps delivery. The pathological conditions that increase the risk for development
of AFE include pregnancy accompanying allergy-related condition, pregnancy-induced
hypertension syndrome, low-lying placenta and placenta previa. Treating obstetricians should
carefully follow-up with pregnant women with these risks and direct special attention to the
progress in the event of rupture of the membrane.

Based on those risk factors of AFE we manage the patients during labor to prevent AFE as below:
1 Measuring the volume of bleeding is not reliable. Always consider the possibilities of internal
bleeding and blood leakage toward the back, which makes it difficult to measure volume
accurately. Measuring the volume of bleeding during delivery also is occasionally inaccurate.
2 Direct special attention to the pulse and shock index. Carefully consider pulse rate. Make it a
rule to calculate the shock index as amatter of routine practice. A timely diagnosis of shock cannot
be made if attention is directed only to blood pressure.
3 Restlessness, respiratory discomfort, severe lower abdominal pain and fetal dysfunction of
unknown origin appear before AFE manifests.
4 Check for atonic bleeding and incoagulable vaginal bleeding of unknown origin. In the obstetric
field patients suffer severe bleeding characteristic of DIC after uterine atony or incoagulable
vaginal bleeding resulting from consumption of coagulation factors.
5 Pay particular attention to a rupture of the membrane that can result in AFE. Carefully observe
the mother and her baby for some time after the rupture of the membrane.
6 Do not rupture the membrane using a non physiological or artificial technique. As mentioned
before, contact of the amniotic fluid with the lumen of the cervix entails the risk for AFE.
Therefore, rupture of the membrane at stations higher than station 1 and artificial rupture in a state
of insufficient dilation of the uterine cervix (<5 cm) should be avoided.
7 In the event of early rupture of the membrane, induced delivery should be carefully monitored.
Because amniotic fluid easily flows into maternal blood, this type of delivery should be managed
as a high-risk delivery.
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from: https://www.ncbi.nlm.nih.gov/pubmed/24622759
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