Introduction

Pregnancy is an undoubtedly magical period in a woman's life with its unique set of joys and
challenges. There is something quite remarkable about the process, the excitement mingling
with fear, delight with discomfort, preparedness with the feeling that nothing you do is just
quite enough.
As peaceful as she may want it to be, it can be a stressful time too, filled with trepidation for
the baby's health and her own.
Every pregnant woman faces the risk of unforeseeable complications that can harm her or her
unborn baby. These women represent a vulnerable section of our population, where early
childbearing age, poor nutrition, and limited access to healthcare, education, and sanitation
pose threats to pregnant women.
Therefore, the healthcare system needs to be geared to combat complications and effectively
prepare the mother for birth and requires widespread community support to do so. It becomes
increasingly vital to characterize the spectrum of pregnancy-related emergencies to minimize
maternal and infant mortality.
Pregnant women presenting to the Emergency Department (ED) require thorough evaluation
for early identification of life-threatening complications.
Common obstetric issues seen in ED are hyperemesis gravidarum, abortions,
eclampsia/preeclampsia, etc.
Non-obstetric causes include urinary tract infections including pyelonephritis, lower
respiratory tract infections, acute undifferentiated febrile illnesses, deep venous thrombosis,
etc.
The majority of the emergencies in these women have been found to be symptoms suggestive
of a miscarriage, some of which can be prevented if early and efficient treatment is instituted.
Improved access to preventive care in India, particularly in rural areas, could be beneficial to
countering high rates of maternal and child morbidity.(1)

Obstetric Emergencies- An Overview of the Indian context

According to recent studies, India had an estimated institutional delivery of 78.9% in 2015-16
with a maternal mortality ratio of 174 and infant mortality rate of 44.
These numbers have improved due to the schemes and interventions implemented by the
Indian government under various acts including the Reproductive and Child Health-2
program and Janani Suraksha Yojana where Community health workers (CHW) have been an
integral part.
The Indian government has worked to fix this urban-rural gap by starting various initiatives
to improve health outcomes in rural and remote areas, particularly through promoting the use
of CHW.
In addition to educating health care professionals, what is a growing demand and urgent need
is the dissemination of knowledge to pregnant women and their caretakers as well as the
community as a whole. This builds self-reliance among people and promotes early
recognition of issues that are otherwise either ignored or go unnoticed.
Unfortunately, studies done on this subject show most pregnant women and their families
either lack knowledge or lack concern regarding pregnancy-related complications. We must
strive to ensure a healthy, informed outlook among the community toward pregnancies and
their challenges.
Obstetric emergencies have exhaustive effects on the mother and fetus which can cause
significant maternal and fetal/infant morbidity and mortality. Maternal mortality is a vital
index of the quality and efficiency of obstetric services prevailing in a country. Women face a
multitude of problems during pregnancy ranging from simple physiological symptoms to life-
threatening complications. Globally, about 800 women die every day of preventable causes
related to pregnancy and childbirth; 20% of these women are from India and this remains a
major public health challenge. Annually, it is estimated that 44,000 women die due to
preventable pregnancy-related causes in our country. (2)

Recent data related to MMR

Globally, maternal mortality declined by almost 38% from 2000 to 2017. Yet an estimated
810 women continue to die each day due to complications of pregnancy and childbirth with
the majority of deaths in low- and middle-income countries.
For every woman who dies of pregnancy-related causes, many more suffer from morbidity,
disabilities, and long-term ill-health. The Sustainable Development Goal (SDG) 3.1 sets out
that by 2030, the global maternal mortality ratio (MMR) will be reduced to less than 70 per
100,000 live births, and no country should have an MMR of more than 140 per 100,000 live
births.
Coverage targets for 2025
To achieve high-quality maternal and newborn healthcare, i.e., antenatal care, childbirth care,
and postnatal care as well as improvement in some broader determinants, such as gender
equality, women’s empowerment, and others, five targets are set for three levels: Global,
National, and Sub-national.
The first three of the five targets are common with the ENAP targets, given the importance of
maintaining the maternal and newborn dyad.
Call for action
Achieving the ambitious targets and goals will require urgent acceleration of progress.
EPMM partners call on all stakeholders to take action and increase sustained commitment
and investment to improving maternal and newborn survival and well-being. This will require
context-specific actions at national and sub-national levels. EPMM will be working closely
with Every Newborn Action Plan (ENAP) to assess the status and advancements along the
pathway to achieve the targets.
The EPMM Partners urges governments and the maternal and newborn health stakeholders
to:
• Adopt the EPMM coverage targets in their national policies and strategies to improve
maternal health along the continuum of care and reduce maternal mortality in their specific
contexts
• Convene national stakeholder groups to establish national and subnational tracking and
accountability mechanisms that will guide progress toward agreed-upon goals
• Enhance domestic fiscal resources and empower domestic human resources to address
disparities in maternal health
• Exert leadership within the donor community to drive more effective use of cooperative
resources for maternal health along the continuum of care, and
• Strengthen intersectoral policy dialogues encompassing female education and security, a
human rights-based approach to sexual, reproductive, maternal, and newborn health, and
comprehensively address the barriers in progress.

Obstetric emergencies
Obstetric emergencies refer to clinical conditions that require immediate interventions to
prevent mortality or morbidity to a mother and or her baby.
Easy access to an appropriate healthcare facility, problem recognition and provision of the
best possible standard of care is the sine qua non to 'successful' management.
The bane of success is usually lack of and or delay in one or more of the following:
 Information provision,
 Primary Prevention (where applicable),
 Resuscitation,
 Access to a healthcare facility,
 Diagnosis and Treatment.
The management of emergencies is usually the responsibility of hospital obstetricians. As
more maternity care is now given in the community, however, midwives, general
practitioners, and paramedics may be involved and must know the outlines of the
management of emergencies and the possible side effects.
If such a situation occurs outside the hospital, arrangements must be made to safely and
promptly transport the woman to the obstetric unit safely and promptly. All emergency
protocols should have been considered beforehand and mutually agreed upon by
obstetricians, midwives, general practitioners, and paramedics.
Everybody then knows their immediate priority, and hazards to the woman can be minimized.
The first principles of dealing with obstetric emergencies are the same as for any emergency
(see to the airway, breathing, and circulation), but remember that in obstetrics there are two
patients; the fetus is very vulnerable to maternal hypoxia.
Types-
In the virtual issue of Case Reports in Women's Health, reflective cases on obstetric
emergencies are highlighted. These include
1. Retinal detachment without hypertension,
2. Pulmonary oedema from ritodrine use,
3. Pre-eclampsia with severe features (HELLP syndrome, sub-capsular hematoma) and
one of its precursors (mirror syndrome) and an imitator (fatty liver disease).
4. Ectopic pregnancies,
5. Advanced extra-uterine pregnancy,
6. Placenta accreta spectrum disorders,
 7. Intra-placental choriocarcinoma,
8. Uterine dehiscence/rupture,
9. Premature rupture of membranes,
10. Acute abdominal pain,
11. Obstetric haemorrhages,
12. Delayed-interval delivery in monochorionic diamniotic twin and
13. Infections such as pyoderma gangrenosum.(3)

First trimester Second trimester Third trimester

1. Ectopic pregnancy 1. Abortion 1. Placenta previa
2. Molar pregnancy 2. Abruptio
3. Rupture of uterus placenta
4. Abortion 3. PPH
4. Inversion of
uterus
5. Uterine rupture
6. Hypertensive
disorder
7. Amniotic fluid
embolism
8. Obstetrical shock
9. Cord
presentation and
prolapse
10. Shoulder
dystocia
11. Vasa Previa
12. DIC

Abruption of placenta
Definition-
An abruption is a death threat to the fetus and a hazard to the mother. When the placenta
separates from its bed (probably because of the rupture of a malformed blood vessel), the
damage to the fetus follows not just because of the barrier that the clot makes between the
placental bed and villi but also because the release of prostaglandins causes a major degree of
uterine spasm.
Clinical features-
This interferes with the perfusion of the placenta, which remains attached. Blood tracking
into the myometrium often goes as far as the peritoneum over the uterus, causing much pain
and shock, with spasms of the uterine muscle. In major degrees of placental abruption, the
woman is shocked well beyond the apparent amount of blood loss and needs urgent transport
into the hospital.
Usually, the placenta is implanted on the anterior wall of the uterus, but sometimes it is
posterior when the abruption is less painful and not so severe that the mother is shocked; the
fetus may still be at risk, however.

Diagnosis in these cases is by recognition of the excessively frequent contractions produced

by the prostaglandin release and the abnormal pattern of the fetal heart rate secondary to fetal
hypoxia; these are best shown with cardiotocography, a priority investigation in all women
admitted with abdominal pain in pregnancy.
Treatment must be aimed at the shock and at preventing disseminated intravascular
coagulopathy.
Emergency management-
o A wide-bore intravenous line should be set up and blood sent for cross-matching of at
least six units of blood.
o Until this blood arrives, other plasma-expanding fluids, such as Haemaccel, should be
used.
o If the fetus is still alive and gestation is sufficiently advanced, cesarean section is the
best management.
o However, if the fetus is dead, conservative management can be pursued provided that
the woman does not continue deteriorating—for example, by developing a
coagulopathy.

o Most women with a severe abruption that kills the fetus will go into spontaneous labor
soon and have an easy delivery, but cesarean section is occasionally necessary for
maternal indications alone.
Placenta previa

The blastocyst occasionally implants in the lower part of the uterus. Stretching and thinning
of the uterine muscle of the lower segment in the third trimester may sheer off part of the
placental attachment. This is accompanied by painless bleeding.
Often the fetus is not affected by the first small bleeds, but they should be taken seriously for
there is a risk that the mother could have a much larger bleed.
Hence, women with bright red, painless vaginal bleeding are considered to have placenta
praevia until proven otherwise and should be admitted to hospital.
Vaginal ultrasound examination is the best technique for investigating possible placenta
praevia, but, although it has a high sensitivity and specificity for central placenta praevia in
the third trimester, it is much less precise in the late second trimester or for marginal placenta
praevia.
Management should therefore always be based on appropriate clinical judgment.
If placenta praevia is confirmed the woman should stay in hospital for at least 48 hours after
the bleeding has stopped. Management is conservative, even to the level of giving blood
transfusions for severe bleeds until the fetus is mature (at about 36 weeks).
Studies do not show any benefit in keeping women in hospital until delivery, provided that
they have a telephone at home and live close enough to the hospital to be brought in by the
emergency services within 20 minutes if they start bleeding again.
Unless it is very obvious—for example, a complete placenta praevia on ultrasound
examination, together with a transverse lie of the fetus—placenta praevia is sometimes
confirmed by examination under general anaesthesia in the at, proceeding in most instances
to caesarean section performed by a senior obstetrician.
Occasionally, if the placenta is anterior and only just engaging in the lower segment, the
membranes may be ruptured and a vaginal delivery expected, as the head coming down into
the mother's pelvis will compress the bleeding placental bed against the back of the pubis
symphysis.
The same cannot be said for any degree of posterior placenta praevia. After delivery, a
postpartum hemorrhage is likely because the placental bed is situated over less well-
contracting uterine muscle and may be well bleed despite oxytocic stimulation. This often
requires a blood transfusion.(4)
Postpartum haemorrhage
After a normal delivery a woman commonly loses up to 300ml of blood. As her blood
volume has increased because of fluid retention during pregnancy, this is a loss which can be
coped with readily.
However, a loss of >500ml measured clinically in the first 24 hours is considered to be a
primary postpartum haemorrhage.
Blood loss is commonly underestimated by the attending practitioners. The mother should be
watched carefully and treatments given to prevent any further loss. If the uterus has not
contracted firmly, manual stimulation may work by rubbing up a contraction, and a further
oxytocic is given.
If the placenta is incomplete the uterine cavity is explored for the remaining lobules whose
presence in the uterine cavity may prevent the organ contracting down. If neither of these
conditions exists, trauma to the lower uterus, cervix, or upper vagina may be the cause of the
bleeding.
Such traumas should be looked for (in theatre with a good light) and sutured appropriately. A
rare cause of continuing primary postpartum haemorrhage is a rupture of the uterus.
This needs diagnosis and treatment with either hysterectomy or abdominal re-suturing.
After the first 24 hours, any bleeding is a secondary postpartum haemorrhage. It is
commonly associated with infection, which should be treated vigorously with intravenous
antibiotics. If it persists, suction evacuation of the uterus should be undertaken by a senior
obstetrician; perforation of the soft uterus is a major risk in this situation.
A complication of severe and prolonged blood loss is a consumptive coagulopathy, when
the mother's blood does not clot owing to interference with the clotting cascade. The
continuing cooperation of a senior haematologist is essential. The mother continues to bleed
not just from the placental bed but from other sites in the body. This needs firm and prompt
correction so that full coagulation can be restored. Giving cryoprecipitate (frozen precipitate)
provides the missing components.(4)
Infection
After delivery, the genital tract has several sites of potential ingress of bacteria. The placental
bed itself is a large raw area, and ascending infection from the lower genital tract may be
assisted by previous intrauterine procedures—for example, forceps delivery.
Infection of the cervix or, uncommonly, of the episiotomy site, may also occur; the breast can
also be a site of infection in the puerperium.(4)
Umbilical cord prolapse
(Simulation)
Umbilical cord prolapse is when the umbilical cord exits the cervical os before the fetal
presenting part.
Compression of the cord results in vasoconstriction and resultant fetal hypoxia, which can
lead to fetal death or disability if not rapidly diagnosed and managed.

Objectives:
 Describe the clinical presentation of umbilical cord prolapse.
 Outline the key steps in the acute management of umbilical cord prolapse.
 Review alternative management strategies that can be utilized after initial attempts at
funic decompression have failed or in cases where obstetric care is not immediately
available.
 Explain strategies to improve care coordination between the interprofessional teams
caring for patients with umbilical cord prolapse to improve outcomes.

 Aetiology
Certain features of pregnancy increase the risk for the development of umbilical cord
prolapse by preventing appropriate engagement of the presenting part with the
pelvis. These include
 fetal malpresentation,
 multiple gestations,
 polyhydramnios,
 preterm rupture of membranes,
 intrauterine growth restriction,
 preterm delivery, and
 fetal and cord abnormalities.
Nearly half of the cases of umbilical cord prolapse can be attributable to iatrogenic
causes.
Iatrogenic risk factors include
 amniotomy without an engaged fetal presenting part
 attempted external cephalic version in the setting of ruptured membranes,
  amnioinfusion,
 placement of a fetal scalp electrode or intrauterine pressure catheter, or
 the use of a cervical ripening balloon.

Cord prolapse vs. cord presentation

Epidemiology
Estimates of the incidence of umbilical cord prolapse range from 1.4 to 6.2 per 1000. The
majority of cases of umbilical cord prolapse occur in single-gestation pregnancies; in twin
gestations, the incidence increases in the second twin.
Most prolapses occur shortly after rupture of membranes; one study estimates that 57%
occur within five minutes of membrane rupture while 67% occur within one hour of rupture.
The incidence of umbilical cord prolapse is on a downward trend, which is thought to be
secondary to the widespread use of cesarean sections for many of the risk factors of cord
prolapse, such as fetal malpresentation.
It is associated with high perinatal mortality, ranging from 23% to 27% in low-income
countries to 6% to 10% in high-income countries.(5)
Decreasing rates of grand multiparity worldwide are also thought to contribute to the reduced
incidence.

Types of cord prolapse

In 2021 Wong et al. revised the definition and management of umbilical cord prolapse and
classified the situation into three distinct categories:
 cord prolapse (when the cord is below the cervical os),
 cord presentation (when the cord is above the cervix but below the presenting part),
and
 compound cord presentation (when the cord is above the cervix and lateral to the
presenting part).(6)
The occurrence of fetal bradycardia in the setting of ruptured membranes should prompt
immediate evaluation for potential cord prolapse.
There are two forms of umbilical cord prolapse-
 The first, overt prolapse, occurs when the cord exits the cervix before the fetal
presenting part;
 The second, occult prolapse, occurs when the cord exits the cervix with the fetal
presenting part.
Overt cord prolapse-
 In overt prolapse, the cord is palpable as a pulsating structure in the vaginal vault.
 In overt prolapse, the diagnosis is clinical and made by palpation of a pulsating
structure in the vaginal vault or visibly protruding from the vaginal introitus.
 This is typically accompanied by fetal bradycardia or severe variable
decelerations, though fetal heart rate changes are only present in approximately two-
thirds of cases.
Occult cord prolapse-
 In occult prolapse, the cord is not visible or palpable ahead of the fetal presenting
part.
 In occult prolapse, only fetal heart rate abnormalities may appear, as the cord will
not be palpable or visible on examination.
 The diagnosis should be a consideration in cases of unexplained fetal heart rate
changes in the setting of recent membrane rupture or other maneuvers that
increase the risk of prolapse (for example, placement of a fetal scalp electrode).
Evaluation
Umbilical cord prolapse is a clinical diagnosis and should be considered in the case of fetal
bradycardia or recurrent variable decelerations, especially if they occur immediately after the
rupture of membranes.
The diagnosis is confirmed by palpation of a pulsatile mass in the vaginal vault.
No radiographic or laboratory confirmation is available, and funic decompression should be
attempted as soon as the diagnosis is suspected.
Antenatal ultrasound for cord presentation has been demonstrated to be a poor predictor of
umbilical cord prolapse.

Case report 1 (Umbilical cord prolapse associated with acute bradycardia.)

 We present a case of a para 3 patient who was admitted in active labor at 8 cm
dilation with intact membranes. On vaginal examination, the cervix was fully effaced
with bulging membranes, and therefore she was directed to a labor room.
 CTG trace was normal, and therefore she was proposed for controlled ARM
(artificial rupture of membranes) which she declined. During monitoring,
spontaneous rupture of membranes occurred and the fetal heart rate (FHR)
trace suddenly dropped to 60–70 bpm.
 On emergency vaginal examination, the umbilical cord loop was found beneath
the fetal head and between the cervix and the fetal skull. Because the patient was
in active labor, it was impossible to mobilize the fetal head upwards.
 Emergency cesarean section was performed, and a healthy baby was delivered
within 15 min of diagnosis with Apgar scores 6 and 9 at 1 and 5 min. When
analyzing the trace, we can classify this CTG trace as normal (stable baseline, normal
variability, and no signs of evolving hypoxia) therefore we can theoretically estimate
a normal cord blood pH (for example 7.2).
  When the acute event happened, a diagnosis was made/established in less than 3
min. With an acute hypoxia pattern (prolonged deceleration) the pH drops by 0.1
every 10 min, and therefore, in less than 20 min the pH will still be above 7,
which is considered normal.(6)

Case report 2 (Abnormal CTG (recurrent decelerations) associated with

compound cord presentation)
A G2 P2 patient with ruptured membranes one hour before being admitted to the labor
ward in the early stage due to an intermediary CTG trace—recurrent variable
decelerations chemoreceptor-type.
She had 3–4 unpainful irregular uterine contractions in 10 min.
On vaginal examination, the cervix was 2 cm dilated. Lateral to the fetal head, an
umbilical loop was palpated (a compound cord presentation).
An emergency cesarean section was performed with a healthy baby delivered in normal
conditions.
After delivery, when analyzing the CTG trace we found an abnormal clinical association
with the subacute hypoxia model which is often seen in the active first stage of labor.
At 2 cm dilation, the intermediary trace is usually associated with subacute pathology
(temporary umbilical cord obstruction), but in our presented case the fetus started to activate
a compensation mechanism, releasing catecholamines with tachycardia, and therefore a
clinical examination of the cervix was performed.(6)
Case report 3 (Prolonged deceleration associated with umbilical cord
prolapse.)
This case is about a primiparous patient in the latent first stage of labor. She was admitted for
regular contractions at 36 weeks with rupture of membranes, cephalic presentation at −1
station, and the cervix 5 cm dilated.
CTG trace was classified as normal with a stable baseline and reassuring variability with
decelerations. Fetal heart rate in the upper segment of the normal range was considered
normal given the gestational age.
Suddenly, the patient reported the loss of a large amount of clear amniotic fluid. Immediately
after, a prolonged deceleration was noted on the continuous CTG trace, the patient was
examined, and a loop of the umbilical cord was detected in the upper third of the
vagina.
Tocolysis (hexoprenaline 10 mcg iv) was administered, and a member of the team was
holding the presenting part to release cord compression while preparations for
emergency cesarean section were in progress.
An emergency cesarean section was performed, and the fetus was delivered with Apgar
scores of 7 and 8 at 1 and 5 min.(6)
Discussion about the cases

 In all presented cases the umbilical cord prolapse was diagnosed based on the
sudden changes in the CTG traces. However, all patients had risk factors for this
pathology which were spotted during the initial clinical and anamnestic
assessment.

 Cord prolapse is an obstetrical emergency where an expedited delivery is needed

to minimize the hypoxic-ischemic risk to neonatal brain tissue.
 The risk is associated with complete or partial umbilical blood flow obstruction
which corresponds with specific changes on the CTG trace. The complete
obstruction of the umbilical cord is relatively rare (0.14–0.62%) and therefore the
risk of brain injury is also low. However, given the fact that it is a life-threatening
clinical condition, a high level of suspicion is needed when the risk factors are
associated with intermediary CTG traces.

 Healthcare practitioners from the labor ward department should also distinguish
between other causes of abnormal CTG traces and prepare for immediate action.
An acute hypoxia pattern (prolonged deceleration or bradycardia) should expedite
the delivery in irreversible cases such as uterine rupture and abruption and
immediate treatment or intrauterine resuscitation is needed in hypertonia or
epidural-induced maternal hypotension. In all other cases, the 3–6–9–12–15 min
rule should be applied
 In the acute hypoxia pattern, the umbilical artery pH drops by 0.1 every 10 min. In
this situation, the 3–6–9–12–15-min rule must be applied (intrauterine
resuscitation by 6 min, move the patient to a suitable delivery location by 9 min, if
CTG trace is persistently bradycardic, commence delivery procedures by 12 min
and deliver the baby by 15 min), but only after acute accidents have been
excluded. (6)

Management
The definitive management of umbilical cord prolapse is expedient delivery; this is usually
by cesarean section. In rare cases, vaginal delivery or operative vaginal delivery may be
faster and, thus, preferable, but this should only occur under the presence and guidance of
an experienced obstetrician.
Until delivery is possible, the cornerstone of management of umbilical cord prolapse is
funic decompression, relieving the pressure on the cord by elevation of the fetal presenting
part. Studies suggest that the interval to funic decompression may be more important to
outcomes than interval to delivery.
 Decompression should be done manually by the medical provider through the placement
of their finger or hand in the vaginal vault and gentle elevation of the presenting part off
the umbilical cord. The provider should be conscientious not to place any additional
pressure on the cord, as this can cause vasospasm and worsen outcomes.
Placement of the mother in a steep Trendelenburg or knee-chest position can also aid in
cord decompression. In cases of a potentially prolonged interval to delivery (i.e., the need
for transfer to a hospital with obstetric capabilities), saline infusion into the bladder may
aid in funic decompression and remove the need for continuous manual elevation by the
provider.
If fetal decelerations persist and delivery is not imminent, the administration of a tocolytic
can be attempted to relieve pressure on the umbilical vessels and to improve placental
perfusion, thereby improving blood flow to the fetus.
Reduction of the cord into the os, which was common before the widespread availability of
cesarean sections, has been associated with increased fetal mortality and is not routinely
recommended except in cases of an expected long interval to delivery where other
maneuvers have failed.
If the cord is visibly protruding from the introitus, it should remain warm and moist because
the ambient temperature is significantly colder than the temperature in the uterus and can
result in vasospasm of the umbilical arteries, contributing to fetal hypoxia. One method
described as preventing this is the replacement of the cord into the vaginal vault followed by
the insertion of a moist tampon to keep it in place.
In very rare cases of umbilical cord prolapse in peri-viable pregnancies, case studies
demonstrate that conservative management may allow the continuation of the pregnancy
until reaching a more desirable gestational age. However, a frank discussion should take
place with the patient regarding the experimental nature of this treatment and its potential
risks.
Pre-viable gestational age, lethal fetal abnormalities, or fetal demise are not indications for
expedient delivery, and instead, a dilation and evacuation or labor induction should be the
therapeutic choice, dependent on gestational age or maternal preference.

Vasa previa
Vasa previa occurs when fetal blood vessels that are unprotected by the umbilical cord or
placenta run through the amniotic membranes and traverse the cervix. Two types of vasa
previa have been described. Type I occurs when a velamentous cord is inserted between the
umbilical cord and placenta, and fetal vessels that run freely within the amniotic membranes
overlie the cervix or are near it. Pregnancies with resolved placenta previa or low-lying
placenta are at risk for type I vasa previa. Type II occurs when the placenta contains a
succenturiate lobe or is multilobed (typically bilobed), and fetal vessels that connect the 2
placental lobes course over or near the cervix. Although there are no standardized criteria
for how close the fetal vessels must be to the internal os to constitute vasa previa, a
threshold of 2 cm has been proposed. In 1 series, all emergent deliveries with vasa previa
had a fetal vessel within 2 cm of the cervical os.

Clinical implications of vasa previa

Approximately 1 per 2500 deliveries are complicated by vasa previa. If membranes rupture,
these vessels may rupture, with resultant fetal hemorrhage, exsanguination, or even death.
In addition, fetal asphyxia could occur if sufficient pressure is applied to vessel(s) overlying
the cervix and circulation is compromised.
In the most recent case series, the perinatal mortality rate for pregnancies that are
complicated by vasa previa is in part to these survival differences because of patient self-
reporting of postnatal diagnoses that were complicated by adverse outcomes. In cases with
prenatal diagnosis, 3.4% of newborn infants required transfusion, compared with 58.8% in
those infants without prenatal diagnosis.
In a series of 56 cases with prenatal diagnosis, preterm bleeding occurred in 42% of cases
with emergent delivery that occurred in 4.1% of singleton and 28.6% of twin pregnancies. In
another large series, 28% of cases with prenatal diagnosis were delivered emergently.

Risk factors for vasa previa

The 2 major risk factors for vasa previa are velamentous cord insertion, which accounts for
the majority of reported cases, and succenturiate placental lobe or bilobed placenta.
Approximately 60% of women with vasa previa at delivery had a placenta previa or low-lying
placenta identified during the second-trimester ultrasound scan. In addition, 20% with vasa
previa have a low-lying placenta at delivery. Another risk factor that has been identified
consistently is in vitro fertilization, which may increase the risk for type 1 vasa previa to
approximately 1 in 250, regardless of whether the gestation is a singleton or a multiple. An
increased prevalence of vasa previa has also been described with multiple gestations.
However, in many cases, this occurred in the setting of in vitro fertilization. Thus, the risk
appears to be more modest with spontaneous twins.

How is vasa previa diagnosed?

The diagnosis of vasa previa by ultrasound scanning was first reported in 1987. Routine
ultrasound evaluation of the placenta and lower uterine segment permits the detection of
the majority of cases.
In a recent systematic review of 8 series that included>400,000 pregnancies and 138 cases of
vasa previa, the median detection rate was 93%, with a specificity of 99%. Although it can be
diagnosed antenatally by transvaginal ultrasound scanning, vasa previa can be missed even
under optimal circumstances. Prenatal diagnosis of vasa previa by ultrasound scanning is
most often made at 18 and 26 weeks of gestation, and identification is less effective if the
ultrasound examination is performed only in the third trimester. If diagnosed in the second
trimester, approximately 20% of cases are resolved before delivery.3,8 The following
algorithm is recommended to facilitate the diagnosis of vasa previa and applies to all
pregnancies
At the time of mid-trimester ultrasonography, the placental location and the relationship
between the placenta and internal cervical os should be evaluated.
The American Institute of Ultrasound in Medicine and the American College of Obstetricians
and Gynecologists also recommend that the placental cord insertion site be documented
when technically possible.
A follow-up ultrasound should be performed at 32weeks of gestation for women who were
diagnosed with placenta previa or low-lying placenta at the mid-trimester ultrasound ex
amination.
Since placenta previa detected in the middle of the second trimester that later resolves and
low lying placenta, even it it later resolves, are associated with vasa previa and consequently
high perinatal mortality rates, transvaginal ultrasonography with color and pulsed Doppler is
recommended to rule out vasa previa.
These recommendations are for asymptomatic women, an earlier ultrasound may be
indicated in women who are bleeding. If vasa previa is suspected, trans vaginal ultrasound
scans with color and pulsed Doppler should be used to facilitate the diagnosis.
The diagnosis of vasa previa is confirmed if an arterial vessel is visualized over the cervix,
either directly overlying the internal os or in close proximity to it, and color Doppler
demonstrates a rate consistent with the fetal heart rate
The course of the vessel should be evaluated carefully to visualize it within the membranes
and to exclude other possible causes of a vessel in close proximity to the cervix, such as funic
presentation, marginal vein, or venous sinus.

How should the pregnancy with prenatal diagnosis of vasa previa be

managed?
The goal of management of vasa previa is to prolong pregnancy safely while avoiding
potential complications related to rupture of membranes or labor. Two other national
societies have existing clinical guidelines, but these recommendations regarding
management are also based on observational data, decision analyses, and expert opinion.
Given the risk-benefit profile of ante natal corticosteroids, if indications do not develop
earlier, it is reasonable to consider treatment at 28-32 weeks of gestation in case of need for
urgent preterm delivery.
Antenatal hospitalization has also been proposed, beginning at 30 to 34 weeks of gestation;
in 1 series, more than one-half of the women who were observed as outpatients
subsequently required hospitalization for a complication.
The purpose of hospitalization is to allow for closer surveillance for signs of labor and then a
more timely performance of cesarean delivery to avoid membrane rupture. However, quality
data to support this as standard practice (compared with outpatient treatment) are lacking;
a decision for prophylactic hospitalization may be individualized and based on a combination
of factors such as presence or absence of symptoms (eg, preterm contractions, vaginal
bleeding), a history of spontaneous preterm birth, logistics (distance from the hospital), and
the balancing of the risks that are associated with bedrest and activity restriction.

How and when should a pregnancy complicated by vasa previa be delivered?

The ultimate goal is to deliver before the rupture of the membrane while minimizing the
impact of iatrogenic prematurity. Amniocentesis is not recommended to evaluate fetal lung
maturity because delaying delivery is not helpful or recommended if fetal lung maturity is
not confirmed.
The optimal timing of cesarean delivery remains unknown. In the largest retrospective
series, fetuses who were diagnosed prenatally had a 97% survival rate, and the mean
gestational age at delivery was 34.9 2.5 weeks of gestation.
Data from a decision analysis study suggested that delivery at 34e35 weeks balances the
risk of premature rupture of the membranes and subsequent fetal hemorrhage and death vs
the risks of prematurity; the authors found no benefit to expectant management beyond 37
weeks of gestation.
Based on available data, planned cesarean delivery for a prenatal diagnosis of vasa previa at
34-37 weeks of gestation is reasonable. If a woman with pregnancy at viable gestational age
has an antenatal diagnosis of vasa previa and then develops premature rupture of
membranes or labor, cesarean delivery should be performed.
In addition, vasa previa should be suspected when there is vaginal bleeding combined with
either a sinusoidal FHR pattern or sudden FHR bradycardia. Delivery of a pregnancy that is
complicated by vasa previa should occur by cesarean birth at a center that is capable of
providing immediate neonatal blood transfusion if needed.
The surgical team should make the hysterotomy mindful of the location of the placenta and
aberrant blood vessels. In the event that a fetal vessel has been lacerated inadvertently
during delivery, immediate cord clamping is recommended to prevent fetal/neonatal blood
loss. Delayed clamping of the umbilical cord is not recommended. In selected cases,
preparations for delivery should include immediate availability of type O negative blood, in
case of delivery of severely anemic neonate. (7)
Shoulder dystocia

Shoulder dystocia is an obstetric emergency that can complicate vaginal delivery and is
characterized by the failure to deliver the fetal shoulders solely using gentle downward
traction following expulsion of the head.

Shoulder dystocia results from the anterior fetal shoulder becoming impacted behind the
maternal pubic symphysis, or less commonly, the posterior fetal shoulder becoming lodged
behind the maternal sacral promontory.

Most shoulder dystocias are unpredictable and unavoidable; therefore, any clinician involved
with a vaginal delivery must have the clinical knowledge to promptly identify shoulder
dystocia and be prepared to perform any additional obstetric maneuvers required to effect
delivery.

When this vaginal delivery complication arises, competency in the recommended sequence
of maneuvers and coordinated management with interprofessional clinicians can prevent
permanent neonatal injury and asphyxiation.

However, clinicians deficient in this clinical knowledge may become a mechanism of greater
maternal and neonatal injury by attempting to resolve shoulder dystocia inappropriately.

Objectives:

 Identify the relevant anatomy, physiology, and risk factors of shoulder dystocia.
 Effectively implement the proper sequence of obstetric maneuvers recommended in
managing a shoulder dystocia.
 Employ appropriate evaluation and management strategies for patients with shoulder
dystocia injuries.
 Delineate how to effectively collaborate and communicate among the
interprofessional team when shoulder dystocia occurs to optimize outcomes for the
parturient and infant.

Etiology

The underlying cause of shoulder dystocia is the persistent anterior-posterior position of the
fetal shoulders as they enter the pelvic inlet or descent of the fetal shoulders simultaneously.
According to the American College of Obstetricians and Gynecologists (ACOG), the
following are the 3 primary mechanisms of this:

 Increased resistance between the vaginal walls and the fetus (eg, fetal macrosomia)
 A large fetal chest relative to the fetal head (eg, neonates of diabetic women)
 Rapid descent prevents rotation of the bisacromal diameter within the pelvis (eg, a
precipitous delivery)
Risk factors

Unfortunately, shoulder dystocia can be challenging to predict and cannot be reliably

prevented. The most significant risk factors are maternal diabetes, previous shoulder
dystocia, and fetal macrosomia.

Maternal diabetes causes elevated glucose levels in the fetus, which stimulates it to produce
excess insulin, insulin-like growth factors, and growth hormone, potentially leading to large
for gestational age infants or infants with larger shoulders and increased abdominal-to-head
circumference ratios.

Larger infants may have difficulty traversing the fixed diameters of the maternal pelvis.
Despite this, the majority of shoulder dystocias still occur in nondiabetic mothers with
average-size infants, while many patients with diabetes or macrosomic infants do not have
shoulder dystocias.

For patients with a history of shoulder dystocia, operative (ie, forceps or vacuum) vaginal
delivery, or an infant with a brachial plexus injury in a prior pregnancy, the risk of recurrence
is estimated to be ≥10%.

For this reason, primary elective cesarean delivery may be considered after careful
evaluation of the entire clinical picture. For patients who elect to proceed with a trial of
labor, the delivering team must maintain heightened awareness and prepare for recurrent
shoulder dystocia.

Prophylactic use of the McRoberts maneuver may be considered in these situations. No

advantage, though, has been observed with its use before the appearance of clinical signs
suggestive of shoulder dystocia. However, there are minimal risks in using the maneuver
prophylactically at the time of delivery.

Additional risk factors for shoulder dystocia include prior operative (ie, forceps or vacuum)
vaginal delivery, delivery of a large birthweight infant, increased maternal weight gain,
maternal obesity, and intrauterine fetal death. These factors, however, are often present
concurrently with other more significant risk factors (eg, fetal macrosomia and maternal
diabetes), making it difficult to isolate the individual risk associated with each clinical
feature.

Intrapartum conditions that may signal the possibility of impending shoulder dystocia include
a prolonged second stage of labor, failure of the fetal head to descend, and need for the
operative (ie, forceps or vacuum) vaginal delivery of the fetal head.
 However, while it is essential to remain mindful of the risk factors for shoulder dystocia to
prepare for delivery properly, attempts to predict shoulder dystocia based on risk factors have
shown poor reliability and have a poor predictive value.

Epidemiology

Shoulder dystocia is thought to occur in approximately 0.2% to 3% of all vaginal deliveries in

which the fetus is in a vertex presentation. The incidence of shoulder dystocia increases as the
size of the infant increases. The incidence of shoulder dystocia in deliveries with infants
weighing <4,000 g is approximately 1%. However, for deliveries with infants weighing 4,000
to 4,500 g, this increases to about 5% to 9% and rises to approximately 14% to 23% for
infants weighing more than 4,500 g.

Pathophysiology

Familiarity with the bony female pelvis is essential in understanding how shoulder dystocia
develops and provides insight into why the correct application of various maneuvers can
relieve shoulder dystocia.

Composition of the Pelvic Girdle

The pelvic girdle is comprised of 4 bones and 3 joints. The bones consist of the sacrum, the
coccyx, and the two innominate bones formed by the fusion of the ilium, ischium, and pubic
rami. The joints include the sacroiliac joints bilaterally located between the sacrum and each
ilium, and the pubic symphysis joint, where the right and left pubic rami meet anteriorly.

Pelvic Spaces: The Lesser Pelvis and Greater Pelvis

The space enclosed by the pelvic girdle has a bowl-like shape and is divided into the greater
and the lesser pelvis. The greater pelvis (ie, false pelvis) refers to the superior portion
between the iliac wings. The lesser pelvis (ie, true pelvis) lies inferior to the greater pelvis
and is located between the sacrum and coccyx posteriorly and the pubic and ischial bones
anteriorly and laterally.

A somewhat round, bony ridge known as the pelvic brim is at the boundary between the
greater and lesser pelvis; it is comprised of the sacral promontory, the arcuate line on the
ilium, and the superior border of the pubic rami. The pelvic brim circumscribes an opening
known as the pelvic inlet. The pelvic inlet is thus the "entrance" into the lesser, or true,
pelvis. The pelvic outlet is the opening at the lower margin of the lesser pelvis. This margin
is made up posteriorly of the coccyx, posterolaterally of the sacrotuberous ligaments, laterally
of the ischial tuberosities, and anteriorly of the pubic arch. Thus, during labor and delivery,
the fetus must descend through the pelvic inlet, traverse the lesser pelvis, and emerge through
the pelvic outlet. Shoulder dystocia occurs when one of the fetal shoulders gets stuck behind
the pelvic brim.
Fetal Rotation Through the Lesser Pelvis

The obstetric (ie, true) conjugate is the distance between the sacral promontory and the
widest portion of the pubic symphysis, located between the superior and inferior margins of
the symphysis. The obstetric conjugate represents the smallest fixed distance through the
pelvic inlet. The obstetric conjugate in the average gynaecoid pelvis is approximately 11.5 to
12 cm, while the average transverse diameter is typically slightly larger at 13 cm. The largest
diameters of the fetal head are in the A-P plane, while the largest diameter of the fetal
shoulders is in the transverse plane. For the largest diameters of the fetal head and shoulders
to pass through the larger transverse diameter of the maternal pelvis, the fetus must rotate
through the true pelvis.

The fetal head typically passes through the pelvic inlet in a transverse position (ie, facing one
of the maternal sides). The fetus then internally rotates, more directly aligning its head and
shoulders in an A-P orientation (ie, facing either the maternal abdomen or back), which
allows its bisacromial diameter to align with the transverse diameter of the maternal pelvis.
The fetal head then extends with delivery and restitutes, realigning the fetal head, shoulders,
and rest of the body, which represents an external rotation. In some cases, especially with
larger infants, the fetal shoulders get stuck behind the bones of the pelvic inlet while
attempting to rotate, resulting in shoulder dystocia.

Effect of Shoulder Dystocia on Fetal Oxygenation

After delivery of the fetal head, the fetal trunk, including the chest, abdomen, and umbilical
cord, becomes compressed within the vaginal canal resulting in decreased fetal oxygenation
due to reduced blood flow through the umbilical cord. Additionally, the compression prevents
the fetus from expanding its lungs effectively until the body is fully delivered. Consequently,
rapid relief of shoulder dystocia to avoid fetal asphyxiation is critical in reducing infant
morbidity and mortality.

History and PE

On admission, a comprehensive maternal history, focused physical examination, and review

of all imaging should be obtained in an attempt to identify potential risk factors, such as:

 Maternal diabetes, obesity, and weight gain during pregnancy

 History of shoulder dystocia with a prior delivery
 Estimated fetal weight of 5,000 g in women without diabetes or 4,500 g in women
with diabetes

During labor and delivery, it is always prudent for the delivering clinician to monitor the
position of the fetus and its overall progress as it descends into the pelvis, which will assist
with correctly performing the obstetric maneuvers required to relieve a shoulder dystocia,
should one occur.

Clinical Features
Retraction of the fetal head toward the perineum may be noted following the delivery of the
fetal head. The "turtle sign" is usually a significant clinical sign of impending shoulder
dystocia, but it is not necessarily diagnostic. Although there is no consensus on the clinical
criteria that are diagnostic of a shoulder dystocia, it is typically characterized by one of the
following parameters:

 The delivering clinician is unable to deliver the fetal shoulders solely using gentle
downward traction.
 Additional obstetric maneuvers become necessary to deliver the neonate successfully.
 There is a documented head-to-body delivery interval of >1 minute

Pelvimetry and Pelvic Diameters

Pelvimetry is the measured assessment of the dimensions of the pelvis; it is most often used
to evaluate the risk of cephalopelvic disproportion in a pregnant individual. The 3 diameters
primarily used in pelvimetry to assess the pelvic inlet are the anterior-posterior (A-P), the
transverse, and the oblique diameters. Furthermore, the pelvic inlet's A-P diameter (ie,
conjugate) can be measured in 3 different ways. By measuring the distance from 3 separate
points along the pubic symphysis to the central point of the sacral promontory, various
aspects of the A-P diameter, also known as A-P conjugates, can be assessed. These
conjugates are the anatomical, diagonal, and obstetric conjugates.

The anatomic conjugate is the distance between the sacral promontory and the superior
margin of the pubic symphysis. Katanozaka et al. reported that parturients with an anatomic
conjugate of <12 cm were more likely to have a cesarean delivery due to labor dystocia than
those with larger conjugates. The diagonal conjugate is the distance between the
sacral promontory and the inferior margin of the pubic symphysis; it is the only conjugate
that can be directly assessed on a physical examination. This is done by palpating the sacral
promontory with the middle finger on a vaginal exam and then noting the distance from the
fingertip to the point the examining hand contacts the pubic arch, which is approximately
12.5 cm on average.

The obstetric (ie, true) conjugate is the distance between the sacral promontory and the
widest portion of the pubic symphysis, located between the superior and inferior margins of
the symphysis. The obstetric conjugate represents the smallest fixed distance through the
pelvic inlet. Although it cannot be measured directly on physical exam, it can be estimated by
measuring the diagonal conjugate and subtracting 1 to 2 cm; the average obstetric conjugate
measures approximately 10.5 cm. Some studies have demonstrated ultrasound imaging as an
effective, safe, and simple way to assess the obstetric conjugate antenatally to identify
patients who should be delivered by cesarean section due to a high risk for cephalopelvic
disproportion. Current guidelines, however, generally do not recommend making decisions
regarding the mode of delivery based on pelvimetry assessments, as a Cochrane review found
no evidence that pelvimetry imaging assessment improved outcomes.

Intrapartum Evaluation
Intrapartum conditions that may signal the possibility of impending shoulder dystocia include
a prolonged second stage of labor, failure of the fetal head to descend, and need for the
operative (ie, forceps or vacuum) vaginal delivery of the fetal head. However, while it is
essential to remain mindful of the risk factors for shoulder dystocia to prepare for delivery
properly, attempts to predict shoulder dystocia based on risk factors have shown poor
reliability and have a poor predictive value.

Therefore, shoulder dystocia remains a clinical diagnosis made after it occurs (eg, failure to
deliver the fetal shoulders solely with gentle downward traction, additional obstetric
maneuvers become necessary). Although professional societies have no agreed criteria to
diagnose shoulder dystocia, maneuvers to manage a shoulder dystocia should be initiated if a
shoulder dystocia is suspected due to characteristic signs (eg, turtle sign). Furthermore,
suspicion of shoulder dystocia should be announced to the rest of the obstetrical team. Also,
the delivery time of the fetal head should be noted so the team can track how much time has
elapsed before shoulder delivery occurs. After delivery, careful clinical assessment is
required for the infant (as well as the parturient) to look for potential traumatic injuries.

Treatment / Management

Shoulder dystocia is an obstetric emergency requiring preparation and training for proper
management by the delivering clinician and other obstetric team members. Not only does the
infant need to be delivered quickly, but healthcare professionals must also use a careful and
calm approach to mitigate the risk of injury to the parturient and the neonate.

Once a shoulder dystocia is identified, it is important for the delivering clinician to clearly
inform the other team members so they can immediately call for additional support (eg,
neonatal and anesthesia clinicians), assist with any maneuvers, and begin proper
documentation. The delivering clinician can then attempt specified obstetric maneuvers in a
sequential order to relieve the shoulder dystocia. Maneuvers are typically divided into first-
line, second-line, and heroic maneuvers. Fundal pressure should be avoided during shoulder
dystocia maneuvers. Not only does it not help with the delivery of the fetal shoulders, it may
worsen the shoulder impaction and increase the risk of uterine rupture. Furthermore, patients
should be instructed to stop pushing while the maneuvers are being performed.

First-Line Maneuvers

 The McRoberts maneuver: ACOG recommends this be the first maneuver

performed; suprapubic pressure may be applied concurrently. This maneuver involves
two assistants, one holding each maternal leg, to hyperflex the patient's thighs onto
the abdomen by bringing the patient's knees up toward her armpits. This increases the
pelvic conjugates, resulting in a more open pelvic outlet. It also causes a cephalad
rotation of the pubic symphysis; this results in a significant increase in the angle of
inclination (ie, the angle relative to the x-axis) between the superior border of the
pubic symphysis and the superior border of the sacral promontory. The angle between
L5 and the sacral promontory flattens as the pelvis rotates with the McRoberts
maneuver. As the sacral promontory flattens, the posterior shoulder of the fetus has
additional space to move posteriorly and inferiorly into the true pelvis. Combined
 with the cephalad rotation of the pubic symphysis anteriorly, this allows the anterior
shoulder to drop out from under the pubic symphysis, especially if suprapubic
pressure is applied simultaneously, reducing stretch on the fetal brachial plexus, and
facilitating delivery. Flattening the sacral promontory also enables the force produced
by spontaneous uterine contractions to become more effective by aligning the fetus
with the maximal expulsive uterine force vectors. Additionally, the position can
significantly increase the intrauterine pressure generated during contractions and
make maternal pushing efforts more effective; this is hypothesized to occur because
the position brings the uterus closer to the diaphragm, which electromyographic
studies have shown has a far more significant impact than the rectus muscles on
generating increased intraabdominal and intrauterine pressure during
Valsalva. Therefore, when applied during contractions and maternal pushing efforts,
the McRoberts maneuver significantly increases expulsive force, reducing mechanical
resistance and facilitating delivery.
 Suprapubic pressure: The goal of suprapubic pressure is to decrease the fetal
bisacromial diameter by adducting the anterior fetal shoulder and dislodging the
impacted shoulder. Continuous pressure is applied to the suprapubic area with the
palm or fist in a downward and oblique direction toward the patient's right or left side,
depending on which way the fetus is faced. The delivering clinician should know the
position of the fetus and communicate to the assistants the direction in which
suprapubic pressure should be applied and who should apply it based on where each
assistant is standing. For example, if the infant is in the right occiput anterior (ROA)
position, facing down and toward the left maternal leg, then the left fetal shoulder is
impacted under the pubic symphysis; the neonate should be rotated in a clockwise
direction by the assistant holding the maternal right leg, who can more easily apply
the suprapubic pressure by pushing down and slightly away from themselves, toward
the maternal left hip. Conversely, if the neonate is in the left occiput anterior (LOA)
position, the assistant holding the maternal left leg should apply pressure toward the
maternal right hip and rotate the neonate in a counterclockwise direction.

Second-Line Maneuvers

 Delivery of the posterior arm: Some authors recommend this maneuver be used
before other second-line maneuvers if the McRoberts maneuver and suprapubic
pressure fail to result in delivery since some studies have suggested it may be most
effective in this group. To perform this maneuver, the obstetrical clinician slides a
hand along the posterior fetal shoulder and arm, grasps the forearm or wrist, and
sweeps the arm across the fetal chest to deliver the posterior arm. With the successful
delivery of the posterior arm, the relevant transverse diameter changes from the
bisacromial diameter (ie, shoulder-to-shoulder) to the acromial-axillary diameter (ie,
axilla-to-shoulder), which can be up to 3 cm shorter. This dislodges the anterior fetal
shoulder and allows for delivery. If the fetal forearm is not easily accessible (eg, when
the fetal arm is extended), the following additional maneuvers can be attempted to
gain access to the forearm or deliver the posterior fetal arm through alternative means:
o Fetal arm flexion: The delivering clinician slides a hand down the posterior
fetal arm until the antecubital fossa is palpated; pressure can then be applied to
the antecubital fossa, typically leading to flexion of the fetal arm and allowing
access to the forearm.
 o Menticoglou maneuver: The delivering clinician places their middle fingers
under the posterior axilla and applies outward traction, which leads to delivery
of the posterior shoulder, followed by delivery of the posterior arm.
o Posterior axilla sling traction: A suction catheter or a soft urinary catheter
is positioned under the axilla of the posterior fetal arm and used as a sling.
Traction is applied to the sling to deliver the posterior shoulder, followed by
the arm. Alternatively, the sling can rotate the shoulders by applying lateral
traction toward the baby's back. At the same time, the other hand is placed on
the anterior shoulder, applying pressure toward the fetal chest.

 Rotational maneuvers (Rubin or Woods screw)

o The Rubin maneuver: This is performed by the delivering clinician placing a
hand into the vagina and applying pressure to the scapula of the posterior fetal
shoulder towards the fetal chest. This will lead to the adduction of the fetal
shoulder, allowing the anterior shoulder to rotate and deliver from behind the
pubic bone where it is impacted.
o The Woods screw maneuver: This is performed by placing one hand on the
clavicular aspect of the posterior fetal shoulder and rotating the shoulder
toward the fetal back. This allows the anterior fetal shoulder to descend while
the rotation is occurring.

 Gaskin maneuver: The patient is placed onto her hands and knees (ie, an "all fours"
or "table-top" position); either gentle downward traction to the fetal shoulder closest
to the maternal sacrum or upward traction to the fetal shoulder against the maternal
symphysis pubis is then applied. If this is unsuccessful, other maneuvers (eg, delivery
of the posterior arm, rotational maneuvers) can also be attempted from this position.
This maneuver should only be used in patients without epidural analgesia.

 Routine episiotomy: Although some experts have recommended wide episiotomies

be used before performing second-line maneuvers in all patients to gain more access,
ACOG and the Royal College of Obstetricians and Gynecologists (RCOG) both
recommend against universally performing an episiotomy in shoulder dystocia cases.
This is because shoulder dystocia is, fundamentally, a boney obstruction, and incising
the soft tissue of the perineum does not relieve this obstruction. ACOG and RCOG
recommend considering an episiotomy only if the delivering clinician believes it will
help them perform the second-line maneuvers better.

Heroic Measures: Extraordinary measures may need to be considered for severe or

catastrophic shoulder dystocias that do not resolve with all other maneuvers. These
maneuvers are associated with extremely high rates of fetal morbidity and mortality and high
rates of significant morbidity for the parturient. They should only be used when multiple
attempts at first- and second-line maneuvers have failed. The delivering clinician should have
an assisting physician available and be aware of the time needed to prepare the operating
room and administer general anesthesia.

 Intentional clavicular fracture: The fetal clavicle is intentionally fractured by

manually pulling the anterior clavicle outward. If successful, this will decrease the
 bisacromial diameter. This maneuver, however, is difficult to perform and may injure
the underlying vascular and pulmonary structures.

 Zavanelli maneuver: The fetal head is rotated to the occiput anterior position, flexed,
and pushed back up the vagina and into the uterus, effectively reversing the cardinal
movements of labor and relieving the compression on the umbilical cord. This fetus is
held in place until emergent cesarean delivery is performed.

 Abdominal rescue: If a cephalic replacement (ie, the Zavanelli maneuver) is

unsuccessful, a low transverse hysterotomy is performed, and the fetal shoulder is
dislodged and manually rotated through the transabdominal incision, followed by
vaginal delivery.

 Symphysiotomy: A Foley catheter is placed with the patient in the lithotomy

position. The urethra is retracted laterally with the Foley catheter. The pubic
symphysis is then incised, and the anterior fibers and cartilage are divided in two.
This is recommended only as a last resort when all the other measures have failed or
in cases where immediate access to an operating room for Zavenelli or abdominal
rescue is not available.

Documentation of Shoulder Dystocia

Documentation by a member of the obstetrical team of delivery times and sequence of events
is vital not only to the delivering clinician but also to the patient and their future healthcare
practitioners. Furthermore, following the delivery, proper documentation assists clinicians in
reviewing what occurred during the delivery and counseling patients on subsequent
pregnancy risks. It also provides any future obstetrical clinicians involved in that patient's
care insight into the delivery events. Clinical information important to post-delivery
documentation includes pre-pregnancy maternal weight, total maternal weight gain, estimated
fetal weight, duration of active labor, duration of the second stage, and delivery time of the
fetal head and body.

Differential Diagnosis

When retraction of the fetal head against the perineum is noted (ie, the "turtle sign"),
differential diagnoses include a tight nuchal cord, fetal malposition, or normal delivery; these
can be excluded with a brief examination for a nuchal cord following delivery of the head and
when delivery of the anterior fetal shoulder is attempted.

Prognosis

Once a shoulder dystocia is relieved, the fetal and maternal prognosis depends on the severity
of complications that may develop. Maternal morbidities (eg, obstetric anal sphincter injury,
bladder laceration) may result in long-term issues, such as fecal incontinence. The most
common neonatal injuries, humerus and clavicle fractures and brachial plexus injuries, often
resolve without permanent disability. However, approximately 10% may result in permanent
neurologic injury. Simulation-based training has decreased the overall rate of shoulder
dystocia-related complications.

The risk of recurrent shoulder dystocia is estimated at ≥10%. A comprehensive analysis of

risk factors and the overall clinical picture should be reviewed and discussed with the patient
in subsequent pregnancies. The risks and benefits of cesarean delivery should also be
discussed with the patient since this is the only way to prevent recurrent shoulder dystocia
confidently. According to ACOG, cesarean delivery should not be universally recommended
to all patients with previous shoulder dystocia as it often does not reoccur; rather, decisions
regarding the mode of delivery in future pregnancies should be individualized based on
clinical factors and the patient's preferences.

Complications

Maternal Complications

Shoulder dystocia can result in several maternal morbidities and are more frequent when
"heroic maneuvers" are performed. Maternal complications include:

 Postpartum hemorrhage
 Obstetric lacerations, including urethral, bladder, and 3rd- and 4th-degree perineal
lacerations with resulting urinary and fecal incontinence
 Femoral and lateral femoral cutaneous neuropathies from prolonged use of the
McRoberts position secondary to nerve compression underneath the inguinal ligament
 Symphiseal separation secondary to hyperflexion of maternal legs
 Uterine rupture

Neonatal Complications

Neonatal complications associated with shoulder dystocia include traumatic injuries,

asphyxia, and death. Traumatic injuries, including brachial plexus injuries and clavicle and
humerus fractures, occur at a total rate of 5.2% following delivery. Injuries to the brachial
plexus during birth can be categorized as upper lesions involving C5-C6 (ie, Erb palsy),
lower lesions involving C8-T1 (ie, Klumpke palsy), or total plexopathies involving C5-T1.
Horner syndrome and facial nerve injuries may accompany brachial nerve injuries. Of
these, C5-C6 injuries and clavicle fractures are significantly more common. Children with
upper lesions have the highest rates of full recovery, while those with total plexus palsies
have the worst prognosis. Brachial plexus injuries typically resolve in up to 20% of cases
with conservative measures, but persistent deficits are noted in approximately 10% of
neonates.

Fetal asphyxia, hypoxic encephalopathy, and death are fortunately much less common. They
most often occur after an average head-to-body delivery time of 10.75 minutes or using >5
maneuvers but are less common when the dystocia is relieved after the first maneuver. Head-
to-body delivery time is not predictive of the severity of neonatal injury, however, as neonatal
death has been seen to occur after intervals of <5 minutes.
Deterrence and Patient Education

Prevention of Shoulder Dystocia

 Prophylactic use of shoulder dystocia maneuvers: Some clinicians have attempted to

prevent shoulder dystocia by implementing the McRoberts maneuver or suprapubic
pressure before the fetal head is delivered in patients with risk factors for shoulder
dystocia (eg, a macrosomic fetus, maternal diabetes). However, a Cochrane review
found no clear evidence for or against this practice as the studies analyzed were
underpowered, and maternal outcomes were not adequately addressed.
 Labor induction and cesarean delivery: Early labor induction and planned cesarean
delivery have also been proposed as strategies to prevent the occurrence of shoulder
dystocia in high-risk patients. However, studies have failed to demonstrate clear
benefits with either of these measures while increasing costs and cesarean rates for
most patients. In diabetic patients with estimated fetal weights >4,500 g or
nondiabetic patients with estimated fetal weights >5,000 g, though, ACOG
recommends that a planned cesarean delivery be considered due to the increased
specificity in detecting fetal macrosomia. Due to insufficient evidence, early labor
induction at any gestational age is not recommended.

Patient Counseling

Patients should be informed of risk factors for shoulder dystocia. Good glycemic control
during pregnancy and healthy weight gain should be emphasized, especially in patients with
gestational diabetes and obesity. For patients with a prior delivery complicated by shoulder
dystocia, it is crucial to convey to the mother that she has a 6- to 30-fold increased risk of
shoulder dystocia recurrence with any subsequent vaginal delivery.

Key facts to keep in mind about shoulder dystonia are as follows:

 Shoulder dystocia is an obstetric emergency where the anterior fetal shoulder

becomes stuck on the maternal pubic symphysis, delaying the birth of the baby’s
body.
 The most common findings include slow delivery of the fetal head or chin and the
turtle sign.
 Risk factors include previous dystocia, macrosomia, diabetes mellitus, and maternal
obesity. However, most shoulder dystocia are unpredictable.
 Management includes calling for help, stopping maternal pushing, first-
line McRoberts maneuver with or without suprapubic pressure, followed by second-
line internal maneuvers.
 If first- and second-line maneuvers are unsuccessful, the sequence should be repeated
before resorting to heroic maneuvers.
 Avoid applying fundal pressure during obstetric maneuvers, as this only serves to
impact the anterior fetal shoulder further into the pubic bone, making the shoulder
dystocia worse.
  When performing the Zavanelli maneuver, inhalational anesthetics or nitroglycerin
may help to relax the uterus, although this is not well supported.
 Maternal complications include third- or fourth-degree tears or postpartum
hemorrhage.
 Fetal complications include fractures of the humerus or clavicle, brachial plexus
injury, and hypoxic brain injury.
 The delivery should be thoroughly documented in the medical record, including the
duration of the second stage and the time of delivery from head to body.

Enhancing Healthcare Team Outcomes

ACOG recommends developing an obstetric rapid response team and protocols that can be
instituted based on clinical triggers. This team should include obstetric clinicians and nurses,
anesthesia personnel, and neonatal team members who will care for the infant immediately
after delivery.

Furthermore, having anesthesia clinicians immediately available in case initial maneuvers

fail and the presence of neonatal team members in the room at delivery can be critical in
providing optimal infant resuscitation if needed. Hospital guidelines should also identify and
address the need for additional personnel (eg, operating room technicians, blood bank and
laboratory staff, and page-system operators). Suspected shoulder dystocia is an appropriate
indication to summon a rapid response team if the dystocia is not resolved rapidly.

Effectively performing maneuvers to manage shoulder dystocia is a team effort. Management

algorithms should be practiced regularly with simulation training by all personnel that may be
present in a delivery room, including physicians, midwives, nurses, technicians, and trainees.

This training should focus on correctly performing maneuvers, including heroic ones, and
practicing clear, standardized communication between team members. Regular practice in
managing emergencies through simulations can help ensure that all obstetric healthcare team
members are adequately trained in their respective roles when performing shoulder dystocia
maneuvers.

Participation in emergency drills can identify clinical errors frequently made during
emergencies, increase effective communication between healthcare team members, and
reinforce proper protocol. Several studies have shown that simulation training also reduces
maternal and neonatal morbidity.

Additionally, teams should always discuss the potential for shoulder dystocia in patients with
risk factors before delivery. Advanced consideration and planning will allow team members
to be mentally and physically prepared to act quickly as needed. The delivering clinician
should assess the fetal position during pushing and clearly communicate before delivery of
the fetal head which direction suprapubic pressure should be applied in case shoulder
dystocia becomes apparent.
Documentation by a member of the obstetrical team of delivery times and sequence of events
is vital not only to the delivering clinician but also to the patient and their future healthcare
practitioners. Furthermore, following the delivery, proper documentation assists clinicians in
reviewing what occurred during the delivery and counseling patients on subsequent
pregnancy risks. It also provides any future obstetrical clinicians involved in that patient's
care insight into the delivery events.

Children who suffer from obstetric brachial plexopathies have a generally good outcome with
conservative management and observation, though some may have permanent impairments.
In these cases, orthopedic surgeons, pediatricians, and therapists need to work closely in
concert with one another to optimize outcomes for the patient.

Uterine inversion

Uterine inversion is one of the most serious complications of childbirth. It refers to the
collapse of the fundus into the uterine cavity. Although it is rare, it carries a high risk of
mortality due to hemorrhage and shock.

Objectives:

 Determine the etiology of uterine inversion.

 Identify the presentation of a patient with uterine inversion.
 Determine the treatment and management options available for uterine inversion.
 Communicate the need for a well-integrated, interprofessional team approach to
improve care for patients with uterine inversion.

Etiology
Excessive umbilical cord traction with a fundal attachment of the placenta and fundal
pressure in the setting of a relaxed uterus are the 2 most common proposed aetiologies
for uterine inversion. Other possible risk factors for uterine inversion include rapid labor,
invasive placentation, manual removal of placenta, short umbilical cord, use of uterine-
relaxing agents, uterine overdistension, fetal macrosomia, nulliparity, placenta previa,
connective tissue disorders (Marfan syndrome and Ehlers-Danlos syndrome), and history
of uterine inversion in the previous pregnancy. However, in most cases, no risk factors are
identified, thus making this condition unpredictable.

Degrees of Uterine Inversion

 Incomplete: Fundus inverts but does not herniate through the level of the internal os
 Complete: The internal lining of the fundus crosses through the cervical os with no
palpable fundus abdominally
 Prolapsed: Entire uterus prolapsing through the cervix with the fundus passing out of
the introitus

Classification

 Acute: 24 hours or less after delivery

 Subacute Longer than 24 hours postpartum)
 Chronic: Longer than 1 month postpartum

Epidemiology

A uterine inversion is rare, complicating about 1 in 2000 to 1 in 23,000 deliveries. Ironically,

most are seen with “low-risk” deliveries. The incidence is 3 times higher in India than in the
United States. Uterine inversion has decreased fourfold after the introduction of active
management during the third stage.

Pathophysiology

Three possible events explain the pathophysiology of acute uterine inversion:

1. A portion of the uterine wall prolapses through the dilated cervix or indents forward
2. Relaxation of part of the uterine wall
3. Simultaneous downward traction on the fundus leading to the uterine inversion

History and Physical

Uterine inversion is a clinical diagnosis and should be suspected when the fundus is not
palpable abdominally. The sudden onset of brisk vaginal bleeding leads to hemodynamic
instability in the mother. Traditionally, the shock has been considered disproportionate to
blood loss, possibly mediated by parasympathetic stimulation caused by the stretching of
tissues. However, careful evaluation of the need for blood transfusion should be made
because blood loss is greatly underestimated. The other symptoms are mainly severe lower
abdominal pain with a strong bearing down sensation, though most women may not be able
to complain due to severe shock. It may occur before or after placental detachment.

Evaluation

The diagnosis is often made clinically with a bimanual examination, during which
the uterine fundus is palpated in the lower uterine segment or within the vagina. If a clinical
examination is equivocal, then an ultrasound can be used to confirm the diagnosis.

Treatment / Management

Once the diagnosis of uterine inversion is made, immediate intervention to control

hemorrhage and restore hemodynamic stability in the mother is required because a delay
leads to an increase in the mortality rate appreciably. The following actions should be taken
urgently and simultaneously:

 Call for help and call for an anesthesiologist immediately.

 A large-bore cannula achieves hemodynamic stability, and crystalloid and blood are
given to combat hypovolemia.
 The recent uterine inversion with the placenta already separated from it may often be
replaced by manually pushing up on the fundus with the palm and fingers in the
direction of the long axis of the vagina. A delay renders replacement more difficult
and increases the risk of hemorrhage.
 If the placenta is still attached, it is usually not removed until fluids are given
and uterine-relaxing anesthetics, such as a halogenated inhalation agent, have been
administered. Other tocolytic agents, such as magnesium sulfate or beta-mimetic and
nitroglycerine, have been used successfully for uterine relaxation and repositioning.
Any portion of the inverted uterus prolapsed beyond the vagina is replaced within the
vagina.
 After the placenta is removed, steady pressure with the fist is applied to the inverted
fundus to push it into the dilated cervix. Alternatively, 2 fingers can be extended
rigidly to push the center of the fundus upward. Undue force is not applied to avoid
perforation of the uterus with the fingertips. This is followed by the administration of
uterotonic agents, which help uterine contraction, thereby preventing the recurrence of
the inversion.

An appropriate antibiotic is administered to prevent infection. Other options include

hydrostatic reduction and surgical correction if manual repositioning is unsuccessful due to a
dense constriction ring.

Hydrostatic reduction: If manual reduction alone is not successful, simple hydrostatic

pressure may be of great assistance in pushing the fundus back to its normal anatomical
position. Warmed sterile saline is infused into the vagina. The clinician’s hand or a silicone
ventouse cup is used as a fluid retainer to generate intravaginal hydrostatic pressure and
resultant inversion correction. The bag of fluid should be elevated about 100 to 150 cm above
the vagina to guarantee sufficient pressure for insufflation. It also prevents blood loss and
prevents the uterus from inverting again. The possible complications of the procedure include
infection, failure, and saline embolus.

Surgical options include Huntington and Haultain procedures, laparoscopic-assisted

repositioning, and cervical incisions with manual uterine repositioning. The Huntington
procedure involves laparotomy by gradually pulling on the round ligaments to restore the
uterus to its proper position. If the cervical ring is tight, repositioning may be more easily
achieved by incising the ring posteriorly with a vertical incision and manually pushing the
fundus. As with manual repositioning, after replacing the fundus, the anesthetic agent used to
relax the myometrium is stopped, and uterotonic therapy is administered immediately,
followed by the repair of the uterine incision. If these procedures are performed, then
pregnancies in the future require a cesarean delivery. If the placenta is not separated from the
uterus, then a hysterectomy may be necessary.

Differential Diagnosis

The conditions that cause a lump in the vagina and lead to postpartum collapse need to be
excluded. These include:

 Severe atony of the uterus

 Uterovaginal prolapse
 Fibroid polyp
 Neurogenic collapse
 Postpartum collapse
 Retained placenta without inversion
 Coagulopathy

Prognosis

Acute cases can lead to hemorrhagic shock, but prompt management usually mitigates long-
term sequelae. It is unknown whether the condition affects future pregnancy prospects, but
case reports exist of uncomplicated pregnancies.

Complications

Complications associated with uterine inversion can be due to the condition (primary) or its
management (secondary). The condition's complications primarily revolve around
hemorrhage and its associated risks, including multi-organ damage, shock, Sheehan
syndrome, and hysterectomy). The condition can result in significant, persistent blood loss
and tissue necrosis without treatment. Complications accompanying treatment relate to
general anesthesia and blood transfusions.

Deterrence and Patient Education

Women who have experienced uterine inversion need to be counseled that they run the risk of
recurrence in subsequent pregnancies.
Enhancing Healthcare Team Outcomes

Uterine inversion is a true obstetric emergency that requires immediate treatment if the
patient's life is to be saved. An interprofessional team, including ICU nurses, best manages
the condition. The patient needs immediate resuscitation, a patent airway, blood transfusion,
and either manual or surgical management. The outcomes for most patients are guarded. (8)

Rupture of uterus

A uterine rupture is a complete division of all three layers of the uterus.

Most uterine ruptures occur when the uterus is gravid in the setting of a trial of labor after
cesarean delivery. Clinicians must remain vigilant for signs and symptoms of uterine rupture
as it is associated with serious morbidity and mortality for both the mother and fetus.

Objectives:

 Summarize the etiology of uterine rupture.

 Outline the typical presentation of a patient with a uterine rupture.
 Describe the management options available for uterine rupture.

Uterine dehiscence is a similar condition characterized by incomplete division of the uterus

that does not penetrate all layers. Uterine dehiscence can produce a uterine window—a
thinning of the uterine wall that may allow the fetus to be seen through the myometrium.
Often uterine dehiscence is an occult finding in an asymptomatic patient. There is no
standard for managing uterine dehiscence in a parturient with a stable fetal heart rate
tracing. Uterine dehiscence in a full-term pregnancy is often managed by cesarean delivery,
while expectant management has been shown to be successful when there
is uterine dehiscence in the preterm period. While the terms uterine dehiscence
and uterine rupture are, at times, used interchangeably, we will keep them separate.
Interest in uterine rupture has increased in recent years due to a desire to offer more patients
a trial of labor after cesarean delivery (TOLAC). A TOLAC refers to a plan to have a vaginal
birth in any subsequent pregnancy after cesarean delivery. The risk of uterine rupture is one
of the main considerations when counseling patients on TOLAC. If successful vaginal
delivery occurs, the turn VBAC, or vaginal birth after cesarean, is used to describe the
delivery.

Etiology

Within pregnant women, there are two populations at risk for uterine rupture: those who
have a myometrial scar from previous surgery and those with an unscarred uterus. The cause
and risk factors for each group are different.

Great attention has been paid to the large increase in the cesarean section rate in the United
States over the past five decades. The cesarean section rate increased by 25% between 1970
and 2016.

TOLAC is one strategy to decrease the rate of cesarean births. The TOLAC has been shown
to reduce maternal morbidity and mortality during the index pregnancy as well as future
deliveries. While a successful vaginal birth resulting from TOLAC is associated with less
morbidity than a scheduled cesarean delivery, a failed TOLAC that ends in cesarean delivery
is associated with more morbidity than a scheduled cesarean delivery.

Thus, the safety of TOLAC is directly tied to the probability of successful vaginal birth.
Amongst the complications associated with TOLAC, uterine rupture is associated with the
largest increase in maternal and neonatal morbidity. Furthermore, it is estimated that the rate
of uterine rupture is approximately 15-30 times higher when women undergo a TOLAC
compared to a scheduled repeat cesarean delivery.

In women who attempt a TOLAC, those with a previous midline (inverted T or J shaped or
classical cesarean section) incision are at two to three times higher risk for uterine rupture
than those with a previous low segment transverse incision. Misoprostol administration is
associated with an increased rate of uterine rupture. The American College of Obstetricians
and Gynecologists now recommends against administering misoprostol to women undergoing
a TOLAC, with the exception only given to those women with a fetal demise. Interestingly, a
history of prior vaginal delivery significantly reduces the risk of subsequent uterine rupture.

While the incidence of unscarred uterine rupture is low, the rate is increasing. The rupture of
an unscarred uterus causes significantly more maternal and neonatal morbidity than the
rupture of a scarred uterus. Most ruptures involving unscarred uteri can be traced to one of
the following etiologies: (1) trauma, (2) a genetic disorder associated with uterine wall
weakness, (3) a prolonged induction or augmentation of labor, or (4) overstretching of
the uterine wall.

In the United States, most major abdominal trauma that occurs during pregnancy is due to
falls and motor vehicle accidents. Concern for uterine rupture is one reason fetal monitoring
is required after blunt abdominal trauma. Uterine rupture is also a concern during internal
podalic and external cephalic versions. For this reason, some obstetricians avoid neuraxial
anesthesia because they believe a uterine rupture may be missed if neuraxial anesthesia
conceals rupture-associated pain. Neuraxial anesthesia for external cephalic version has been
shown to improve patient comfort and improve the rate of successful version.

The uterine wall, or myometrium, is weakened in conditions such as Ehlers-Danlos and

Loeys-Dietz, which increases the risk of rupture. A uterine rupture in a woman that has not
had a previous cesarean section is now a criterion that is used to diagnose vascular Ehlers-
Danlos syndrome.

Prolonged uterine exposure to oxytocin and other uterotonic medications

increases uterine wall stress and can lead to rupture, especially in the setting of obstructed
labor. Women who experience a uterine rupture are more likely to have received oxytocin
for induction or augmentation of labor compared to women without a rupture.

Conditions such as gestational diabetes with macrosomia, polyhydramnios, multiple gestation

pregnancy, and uterine anomalies such as fibroids can stretch the myometrium beyond its
optimal range. These conditions are associated with a higher risk of uterine rupture. There is
also evidence that serial stretching of the uterine wall, such as occurs in multiparous women,
may increase the risk of rupture.

Epidemiology

Overall, it is estimated that one uterine rupture occurs for every 5,000 to 7,000 births. The
incidence of uterine rupture in both scarred and unscarred uteri is increasing worldwide

Uterine rupture is more common in women with prior cesarean delivery. The rate
of uterine rupture is highly dependent upon the number of cesarean deliveries a woman has
had and the type of uterine incision present. The rate of uterine rupture is approximately 1%
for women with one previous cesarean delivery versus 3.9% for those with greater than one
previous cesarean delivery.

The rate of uterine rupture with an unscarred uterus has been found to be approximately one
rupture per 10,000 to 25,000 deliveries. The incidence of uterine rupture in an unscarred
uterus is higher in developing countries. It is hypothesized that this rate is higher because
techniques to manage obstructed labor, such as instrument-assisted and cesarean delivery, are
less readily available.

Pathophysiology

Uterine rupture refers to the complete division of all three layers of the uterus: the
endometrium (inner epithelial layer), myometrium (smooth muscle layer), and perimetrium
(serosal outer surface). Generally speaking, the term uterine rupture implies that a gravid
uterus is involved—though ruptures have been reported in nonpregnant uteri.
A uterine rupture can allow a part of the fetus, amniotic fluid, or the umbilical cord to enter
the peritoneal cavity or broad ligament. A uterine rupture can cause abdominal pain, vaginal
bleeding, a change in the contraction pattern, or a nonreassuring fetal heart rate tracing.

History and Physical

The presentation of a woman with a uterine rupture is highly dependent upon whether they
have a labor epidural, a scared or unscarred uterus, and the location of the rupture.

For women with a suspected uterine rupture, the initial assessment is for hemodynamic
stability. Blood pressure and heart rate should be obtained to assess for hypotension and
tachycardia. Common symptoms of hypotension include lightheadedness, dizziness, nausea,
vomiting, and anxiety. Most of the bleeding associated with a uterine rupture is
intraabdominal and cannot be detected by the patient. When vaginal bleeding occurs, it is
helpful to differentiate between light spotting and significant blood-soaked linen.

Bladder injury is not uncommon with uterine rupture. Patients with a

suspected uterine rupture should have their urine examined for hematuria. Pink, red, or
brown urine can imply the presence of red blood cells. Blood clots can also pass through the
urethra—these can be painful.

Patients with a uterine rupture may describe acute onset abdominal pain that begins with a
“ripping” sensation. Subsequent contracts are often quite painful. Chest pain may occur if
blood enters the peritoneum. Blood in the peritoneum can irritate the diaphragm and cause
referred to shoulder or chest pain similar to ischemic cardiac pain. A labor epidural may mask
the pain associated with a uterine rupture and lead to delayed diagnosis.

The fetal heart rate provides insight into both the health of the fetus and the health of the
woman—the fetal heart rate is one of the most sensitive indicators of maternal end-organ
perfusion. Reduced blood flow to the fetus can present as fetal bradycardia, reduced
variability, or late decelerations. Fetal bradycardia is the most common abnormality
associated with uterine rupture. No fetal heart rate tracing is pathognomonic
for uterine rupture. The absence of fetal heart sounds is obviously an ominous sign and
requires an ultrasound to confirm absent cardiac activity.

Palpating the abdomen to localize the area of most pain and guarding can be helpful in
women with a suspected uterine rupture. A uterine rupture should cause midline pain. Most
women with a uterine rupture will have a tender abdomen, even when receiving labor
epidural analgesia. Palpation of the abdomen can also provide insight into whether the
contraction pattern or uterine shape has changed. Uterine contraction amplitude may
decrease, and contractions may stop altogether in women who experience a uterine rupture.

An internal examination can identify products of conception, fresh blood, or clots in the
vaginal canal. In a uterine rupture, the vaginal canal is usually not full of blood—unless the
tear extends into the vagina or cervix. Speculum examination may help diagnose non-
pregnancy related bleeding such as a laceration or abnormal cervical growth. A vaginal exam
can also identify loss of fetal station (movement of the fetal presenting part towards the
abdominal cavity), which can occur with a uterine rupture if part of the fetus enters the
peritoneum.

Evaluation

Due to the potential for serious maternal and neonatal morbidity, uterine rupture must be
excluded in all cases of vaginal bleeding during pregnancy. The classic symptoms described
for uterine rupture include acute onset abdominal pain, vaginal bleeding, a non-reassuring
fetal heart rate tracing, and a change in the contraction pattern on
tocodynamometry. Unfortunately, these symptoms are often not present. Radiographic and
laboratory tests can be helpful in diagnosing a minor uterine rupture. Imaging is not
appropriate when there is a significant rupture because of the emergent need for delivery and
hemorrhage control.

The most important initial laboratory test is hemoglobin or hematocrit. If significant bleeding
has occurred, coagulation tests (prothrombin time, activated partial thromboplastin time,
fibrinogen, thromboelastogram) should be considered. If significant bleeding has not yet
occurred, baseline hemoglobin or hematocrit can be used to monitor for ongoing blood loss.

In a stable patient with a possible minor rupture, an ultrasound can be helpful to rule out other
etiologies for vaginal bleeding, such as placenta previa, placental abruption, or spontaneous
abortion. The following findings on abdominal ultrasound support the diagnosis
of uterine rupture: an abnormality in the uterine wall, a hematoma next to a hysterotomy
scar, free fluid in the peritoneum, anhydramnios, or fetal parts outside the uterus.

Ultimately, the diagnosis of uterine rupture is often confirmed when hemoperitoneum and
fetal parts are identified during laparotomy.

Treatment / Management

A uterine rupture must prompt immediate action. A delay in delivery, resuscitation, or

surgery increases maternal and fetal risk. A uterine rupture will typically be associated with
fetal bradycardia. Thus, the initial treatment step is an emergent cesarean delivery—with or
without an exploratory laparotomy. General endotracheal anesthesia is typically required to
facilitate quick delivery—even when a labor epidural is in place. Labor epidurals take 5 to 15
minutes to achieve a surgical block; this is typically an unacceptable delay in the setting
of uterine rupture. General anesthesia has the added advantages of allowing for better
management of the maternal acid-base status through adjustment of minute ventilation,
stabilizing the airway, and providing neuromuscular blockade to facilitate laparotomy. Lastly,
neuraxial anesthesia is contraindicated in the setting of hemodynamic instability and in
patients with severe bleeding diathesis.

A uterine rupture requires simultaneous delivery and treatment of maternal hemorrhage. A

second large-bore intravenous line should be placed, and blood should be ordered and
brought to the operating room. If large-bore intravenous access cannot be obtained, central
venous access with a large bore sheath introducer should be considered. Initial resuscitation is
often provided by infusing Lactated Ringer's electrolyte solution. Brisk and large volume
blood loss should prompt early blood transfusion. If bleeding is not quickly controlled, an
arterial line will improve the accuracy and frequency of blood pressure monitoring, lead to a
shorter response to hypotension, and facilitate serial laboratory tests.

A midline abdominal incision, as opposed to the Pfannenstiel incision, should be considered

when intraperitoneal bleeding is suspected. A midline incision provides better surgical
exposure for the identification of the bleeding source and may shorten the time interval
between surgical incision and delivery. In a smaller rupture, the uterus may be amenable to
repair. When there is hemodynamic instability or significant uterine injury, a hysterectomy is
indicated. Approximately one in three women who experience uterine rupture require a
hysterectomy.

Differential Diagnosis

The differential diagnosis for second and third trimester vaginal bleeding in the setting of
acute abdominal pain includes spontaneous abortion, bloody show associated with normal
labor, placenta previa, placental abruption, and uterine rupture.

A spontaneous abortion (also referred to as an early pregnancy loss or a miscarriage) can be

diagnosed by finding fetal tissue in the cervical canal either by palpation or visualization
during the speculum exam within the first 20 weeks of gestation.

Bloody show refers to mucus mixed with blood that is discharged prior to the onset of labor.
Bloody show may precede labor by as much as three days. The blood loss associated with
bloody show is small, and patients remain hemodynamically stable.

Placenta previa refers to the placenta attaching to the uterus over the cervical opening. A
placenta previa is one of the more common causes of second and third trimester
bleeding. The classic description of placenta previa is painless vaginal bleeding
unaccompanied by uterine contractions. However, some patients with placenta previa may
have crampy contraction pain. Most placenta previas can be diagnosed by ultrasound. It is
important not to perform a digital examination in patients with 2nd or 3rd trimester vaginal
bleeding until a placenta previa has been ruled out. Digital examination of the cervix when a
placenta previa is present may result in life-threatening maternal hemorrhage.

A placental abruption refers to the placenta separating from the uterus before delivery. Most
placental abruptions occur around 25 weeks. In an abruption, maternal blood vessels tear
away from the decidua basalis, the uterine endometrium at the site of placentation, and push
the placenta and uterus apart.

Patients may report vaginal bleeding, acute onset abdominal pain, and continuous crampy
contractions due to blood irritation. Similar to a uterine rupture, placental abruption may
cause non-reassuring fetal heart rate changes. However, placental abruption is more likely to
be associated with tetanic uterine activity than a uterine rupture.
Significant blood can accumulate behind a placental abruption and remain undetectable by
ultrasound examination. Ultrasonography has poor sensitivity for diagnosing a placental
abruption. If blood loss is significant, an abruption can be life-threatening for both the woman
and the neonate.

Uterine rupture occurs rarely but must be ruled out in all cases of 2 and 3 trimester vaginal
bleeding. The biggest risk factor for a uterine rupture is TOLAC. Most uterine ruptures
occur during labor. A uterine rupture should be considered in all women undergoing a
TOLAC who present with any of the following: hypotension, a sudden change in contraction
pattern, fetal bradycardia, sudden abdominal pain, hematuria, loss of fetal station, or vaginal
bleeding.

Prognosis

With quick surgical intervention and resuscitation, most women survive a uterine rupture.
The maternal mortality rate associated with the rupture of an unscarred uterus is higher (10%)
than the mortality rate associated with the rupture of a scarred uterus (0.1%).The neonatal
mortality rate after uterine rupture is 6% to 25%.

The risk of recurrent rupture after the uterine repair is not well described. This is because the
incidence of rupture is low, and many women with a significant uterine rupture require a
hysterectomy. In a few small case series conducted outside the United States, the incidence of
repeat rupture was 33% to 100%. There is low-level evidence that the repeat rupture rate may
be higher when the initial rupture occurs in the uterine fundus. Due to the maternal and fetal
risk of repeat rupture, most obstetricians recommend repeat cesarean delivery between 36 and
37 weeks—before labor is allowed to begin.

Complications

The incidence of serious fetal and maternal morbidity depends upon the location and
magnitude of the rupture as well as the speed of surgical intervention. Lateral ruptures are
associated with worse outcomes than midline ruptures—perhaps because of increased
vascularity of the lateral uterine wall. A longer time to surgical intervention is associated
with more maternal blood loss, a higher risk of coagulopathy, and longer fetal exposure to
hypoxia.

Rupture of unscarred uteri is associated with more blood loss, a higher incidence of
hysterectomy, and a higher rate of composite maternal morbidity (death, hysterectomy, blood
transfusion, or urologic injury) than rupture of scarred uteri. The incidence of composite fetal
neurologic injury (intraventricular hemorrhage, seizure, death, or brain ischemia) is also
higher for ruptures involving an unscarred uteri, compared to scarred uteri. The rate of fetal
mortality is 10% for unscarred uteri and 2% for scarred uteri.

Postoperative and Rehabilitation Care

The plan for postoperative care is based upon the impact of blood loss on coagulation, acid-
base balance, and hemodynamic stability. Most patients who experience uterine rupture will
be previously healthy. Accordingly, blood loss is often well tolerated. Patients with ongoing
blood loss, an elevated (greater than 2 mmol/L) and rising blood lactate, and vasopressor
requirements should be considered for postoperative intensive care unit admission.

Consultations

A multidisciplinary team approach is recommended to manage complications associated

with uterine rupture. An anesthesia provider with familiarity on labor and delivery is
necessary to provide anesthesia for cesarean delivery, place lines, lead resuscitation efforts,
administer vasoactive medications, and secure the airway (when necessary). A pediatric
provider with familiarity with neonatal resuscitation is recommended because many babies
born in the setting of uterine rupture will have been deprived of oxygen for an extended
period of time. In the setting of massive blood loss or the development of disseminated
intravascular coagulation, a hematologist may help secure clotting factor concentrates. A
urology consultation is recommended if the uterine rupture extends into the bladder or
damages one of the ureters.

Deterrence and Patient Education

Given the potential for maternal and fetal morbidity associated with a uterine rupture,
prevention strategies are prudent. Women at higher risk for uterine rupture (e.g., multiparity,
multiple gestations, advanced maternal age, connective tissue disorders) should receive
oxytocin judiciously. Likewise, procedures that may cause a uterine rupture, such as the
internal podalic and external cephalic version, should be performed gently and with careful
consideration for the type of anesthesia. Lastly, significant pressure applied to the uterus
during the second stage of labor should be avoided. This practice has not been shown to
shorten the second stage of labor, and it increases the risk for uterine rupture.

Women with risk factors for uterine rupture should be educated on the early signs and
symptoms of rupture. It is recommended that women at high risk for uterine rupture reside
near their delivery hospital.

Enhancing Healthcare Team Outcomes

Uterine rupture is a life-threatening complication associated with pregnancy. Should one

occur, a multidisciplinary response is required to minimize risk for maternal and fetal
morbidity. A suspected uterine rupture requires immediate attention and should be treated
with urgent laparotomy [Level 5 evidence].

Due to the potential for uterine rupture and significant fetal and maternal morbidity the
availability of providers in obstetrics, anesthesia, pediatrics, as well as operating room
personnel should be considered when making a plan for a TOLAC [Level 5 evidence]. Due to
the risk of uterine rupture, TOLAC should be performed in locations where emergent
cesarean delivery is offered [Level 5 Evidence]. (9)
Amniotic fluid embolism

Amniotic fluid embolism (AFE) is a rare but serious condition with high mortality and
morbidity rates and is the second leading cause of peripartum maternal death. It occurs when
amniotic fluid enters the maternal bloodstream.

Objectives:

 Identify the various risk factors for amniotic fluid embolism.

 Assess the triggering pulmonary pathology initiated by the inflammation associated
with amniotic fluid embolism.
 Implement evidence-based evaluation and treatment methods for amniotic fluid
embolism, ensuring prompt and effective responses to this critical obstetric
emergency.
 Collaborate in improving care coordination among an interprofessional team to
enhance the delivery of care for a patient affected by an amniotic fluid embolism.

Introduction

Amniotic fluid embolism (AFE) is a critical obstetric emergency marked by sudden

cardiorespiratory collapse and disseminated intravascular coagulation (DIC). Often referred
to as the anaphylactoid syndrome of pregnancy, AFE is distinct from a direct embolism or the
presence of amniotic fluid itself. The global occurrence of AFE ranges from 1 in 8000 to 1 in
80,000 deliveries, though the exact incidence remains unclear due to diagnostic and reporting
inaccuracies.

The initial description of AFE dates back to 1941 when Steiner and Luschbaugh noted fetal
cells in the maternal pulmonary circulation of women who died during labor. Data from the
National Amniotic Fluid Embolism Registry indicates that the condition shares similarities
with anaphylaxis rather than a typical embolism.

Notably, fetal tissue or amniotic fluid components are not consistently detected in women
displaying signs and symptoms of AFE. Traditionally, AFE diagnosis occurred postmortem,
relying on the presence of fetal squamous cells in the maternal pulmonary artery
blood. However, as fetal squamous cells are also found in the circulation of laboring women
who do not develop AFE, the diagnosis is exclusionary and based on clinical presentation
after ruling out other causes of hemodynamic instability.

Etiology

AFE remains unpredictable, with an elusive origin. Various factors contribute to its
development, encompassing maternal age (especially older than 35 to 40 years), grand
multiparity, male fetuses, early gestational age, cervical ripening, polyhydramnios, multiple
gestation, gestational diabetes, operative delivery, manual placental extraction, regional
disparities (western U.S.), Asian and Black races, asthma, illicit substance use, and trauma.
Induction of labor and conditions such as cerebrovascular disorders and cardiac disease
heightens the risk of AFE, with strong associations observed in placenta previa, eclampsia,
uterine rupture, fetal growth restriction, fetal death, placental abruption, maternal renal
disease, peripartum cardiomyopathy, and postpartum hemorrhage.

There is some conflicting evidence on the risk factors for AFE. Many earlier studies
concluded that cesarean delivery, particularly with a classical uterine incision, raised AFE
risk. This concept has since been reversed, with cesarean section of any type found to be
unrelated. Similarly, amniotomy was once thought to increase the risk of AFE but is now
believed to be uncoupled. One population-based case-cohort study looked at 149 cases of
AFE, 80 of which were fatal. They reported that a spontaneous vaginal delivery had 12 times
the risk of AFE than cesarean delivery, and instrumental vaginal delivery was almost 3 times
the risk of cesarean delivery. They concluded that cesarean section is a protective factor for a
fatal AFE. Amnioinfusion does correlate with a 3-fold increase in AFE risk, potentially due
to increased uterine distension. Notably, 66% of AFE patients reported prior allergies,
aligning with the condition's secondary name, "anaphylactoid syndrome of pregnancy,"
exceeding the general population's atopy rate. Additionally, 8% of AFE-affected pregnancies
stem from in vitro fertilization, surpassing the baseline IVF rate.

Placenta accreta spectrum (PAS) disorder emerges as the anomaly most strongly linked to
AFE, carrying a 10-fold increased risk. The severity of PAS correlates with a higher AFE
incidence. Introducing amniotic fluid and fetal components into maternal circulation triggers
intense pulmonary vasoconstriction and bronchoconstriction. These effects result not only
from physical obstruction but primarily from the release of inflammatory cytokines reacting
to foreign material. These mediators activate coagulation and fibrinolytic pathways,
culminating in a DIC syndrome.

Epidemiology

The estimated incidence of AFE ranges from 1.9 to 6.1 per 100,000 births, though the exact
prevalence remains uncertain due to inaccurate diagnosis and underreporting of nonfatal
cases. Notably, AFE emerged as the primary cause of death during parturition in Germany in
2011 and accounts for 24.3% of maternal deaths in Japan. In Australia, AFE is recognized as
the leading direct cause of maternal mortality, affecting between 1 in 8000 to 1 in 80,000
deliveries. The estimated incidence in the UK is 2 per 100,000 births, while in the United
States, AFE occurs at approximately 7.7 per 100,000 births.

A significant majority of AFE cases, around 70%, manifest during labor, with approximately
19% occurring during cesarean sections and 11% following vaginal deliveries. It is
noteworthy that AFE can occur up to 48 hours after delivery. Rare instances of AFE have
been reported after pregnancy termination, amniocentesis, injection of hypertonic saline into
the uterus for abortion induction, and in the first or second trimester of pregnancy.

Pathophysiology

AFE is characterized by a disruption in the placental-amniotic interface, leading to the entry

of amniotic fluid and fetal elements, such as hair, meconium, skin cells, and gut mucin, into
the maternal circulation. It is essential to note that the presence of squamous cells in the
pulmonary circulation is no longer solely diagnostic for AFE, as clinical presentation plays a
crucial role.

Accompanying the entry of amniotic and fetal substances are tissue factors with procoagulant
properties. Activation of histamine, endothelin, and leukotrienes leads to physiologic changes
that result in cardiovascular collapse. Potential portals of entry include the placental
attachment, cervical veins, or uterine surgical incisions. Once within the pulmonary arterial
tree, this triggers a pathological maternal anaphylactoid immune response, releasing
inflammatory mediators.

The initial phase involves intense and transient pulmonary vasoconstriction, possibly coupled
with bronchoconstriction. This results in acute pulmonary arterial obstruction, dilation of the
right ventricle and right atrium, and significant tricuspid regurgitation. Subsequently, hypoxia
and right heart failure ensue. There is a less common type of AFE reported, which presents
with only the hemorrhage and DIC component without maternal hemodynamic instability.

Subsequent to right ventricular enlargement, left ventricular function experiences significant

depression due to myocardial ischemia stemming from hypoxia or coronary artery spasm.
This ventricular enlargement causes the intraventricular septum to bow into the left ventricle,
resulting in obstruction and systolic dysfunction. Consequently, pulmonary artery pressure
rises, and cardiac output decreases. Dysrhythmias such as ventricular fibrillation, asystole,
and pulseless electrical activity have all been reported in association. Thus, survivors of this
critical condition may face hypoxic brain injuries or multisystem organ failure.

Sudden cardiovascular collapse is induced by hypoxemia and hypotension. The introduction

of amniotic fluid and fetal elements triggers inflammatory mediators, including platelet-
activating factor, tissue necrosis factor-alpha (TNF-alpha), interleukin 6, interleukin 1,
phospholipase A2, endothelin, plasminogen activators, thromboplastins, and complement
factors. This activation sets off the coagulation cascade and fibrinolytic systems, resulting in
a fibrinolytic form of DIC. Amniotic fluid in the maternal circulation activates platelet factor
III, leading to platelet aggregation and activation of clotting factor Xa. Amniotic fluid and
fetal elements may infiltrate the uterus, causing severe uterine atony and exacerbating
hemorrhage. The superimposed pathologic activation of the coagulation and fibrinolytic
pathways results in severe coagulopathy, observed in approximately 80% of AFE patients.
The decrease in coagulation factors may occur either immediately at the time of
cardiopulmonary collapse or in a delayed manner. Bleeding can be severe, relentless, and
fatal.

Autopsies on women succumbing to AFE reveal pulmonary edema, amniotic component

emboli in the lungs, and alveolar hemorrhage. Additional findings may include myocardial
infarction, acute renal failure from acute tubular necrosis, and cerebral infarctions.

Histopathology

Prevalence of Pulmonary Edema

  Pulmonary edema is a prevalent finding in 70% of postmortem examinations of
individuals who succumb to AFE.
 This condition constitutes a crucial pathological feature, underscoring its significance
in AFE cases.

Microscopic Presence of Amniotic Fluid Substances

 Despite the presence of amniotic fluid substances in the lungs, their microscopic
identification can be challenging due to their minute size.
 Histological examinations may not always capture these tiny particles, potentially
leading to under recognition.

Alveolar Hemorrhage

 In conjunction with pulmonary edema, alveolar hemorrhage is a common histological

manifestation in the lungs of individuals affected by AFE.
 The observation of alveolar hemorrhage adds another layer to the pathological
changes associated with this condition.

These clinical pearls shed light on the intricate pathological aspects of AFE, emphasizing the
importance of considering macroscopic and microscopic findings in diagnosing and
understanding this complex obstetric emergency.

History and Physical

The medical history or current health details of a patient experiencing an AFE may reveal
factors such as advanced maternal age, multiple pregnancies, placenta-related issues (accreta,
abruption, previa), preeclampsia, gestational diabetes, polyhydramnios, amniocentesis, use of
amnioinfusion, amniotomy, cervical lacerations, or any surgery on the gravid uterus. In the
classic scenario, women in the later stages of labor suddenly develop acute shortness of
breath accompanied by hypotension. Preceding other symptoms, there may be signs of
agitation, anxiety, altered mental status, or a sense of impending doom. Seizures may ensue,
leading to cardiac arrest, followed by massive hemorrhage associated with DIC, ultimately
resulting in death—often within an hour of onset. Statistics indicate that 53% of females with
AFE present at or just before delivery, while the remainder present, on average, 19 minutes
after delivery.

AFE commonly manifests with cardiac arrest, but other presentations include respiratory
collapse and DIC. Many patients lose consciousness, and some may exhibit seizure-like
activity (10% to 50%), likely due to brain anoxia. The physical examination typically reveals
a patient in cardiovascular collapse, marked by severe hypoxemia, hypotension, and cyanosis.
The classic triad of AFE consists of hypoxia, hypotension, and coagulopathy, with a normal
body temperature. Funduscopic examination may detect minute bubbles in retinal arteries.
Tachypnea may be present, often accompanied by the characteristic holosystolic high-pitched
murmur of tricuspid regurgitation. This murmur is loudest at the lower left sternal border,
radiating to the right sternal edge. Hemorrhage can range from massive to minimal, and
uterine atony (83%) exacerbates bleeding. Initial bleeding typically occurs from the vagina
but may also be observed in surgical incisions. Full-blown DIC is observed in approximately
83% of patients. Premonitory symptoms, such as shortness of breath or agitation, may
precede cardiovascular collapse.

Evaluation

The diagnosis of AFE relies on exclusionary criteria after the occurrence of a clinical
scenario that aligns with its characteristics. It is fundamentally a clinical diagnosis, as no
reliable, definitive test for AFE exists. The suspicion of AFE arises when sudden dyspnea,
dysphoria, hypotension, cardiovascular collapse, and coagulopathy manifest following
actions during the peripartum period, such as active labor, rupture of membranes, vaginal
delivery, or cesarean section. AFE has also been observed during or after elective pregnancy
terminations, whether induced or surgical. Initial evaluation typically occurs during
aggressive cardiopulmonary resuscitation, focusing on the 2 main system failures:
hemodynamic and hematologic.

Transthoracic echocardiography (TTE) or transesophageal echocardiography (TEE) plays a

crucial role in diagnosis when available. TEE is preferred if patient stability is achieved.
Significant echocardiographic findings in AFE include right ventricle dilatation, hypokinesis,
overload, tricuspid regurgitation, and right atrial enlargement. Early cardiac thrombi may be
identified in the enlarged right ventricle or right atrium. A characteristic feature associated
with AFE is the bowing of the intraventricular septum into the left ventricle, leading to left
ventricular obstruction and systolic dysfunction, resembling the shape of the letter 'D.'

Immediate blood collection is essential for an urgent type and crossmatch, complete blood
count, comprehensive metabolic panel, and a full coagulation panel, encompassing platelets,
prothrombin time, partial thromboplastin time, bleeding time, fibrinogen, d-dimer, and fibrin
degradation products (FDPs). The International Society on Thrombosis and Hemostasis
(ISTH) provides a formal scoring system for determining DIC presence in pregnancy
based on platelet count, international neutralization ratio (INR), and fibrinogen level.
Scores >3 indicate the presence of DIC in pregnancy.

Establishing precise criteria for diagnosing AFE has been challenging due to the absence of a
single definitive test. Various international standards have been introduced to define AFE,
with the American Society for Maternal-Fetal Medicine (SMFM) establishing objective
criteria following a consensus symposium with the Amniotic Fluid Embolism Foundation in
2016. The criteria stipulate the presence of the following conditions:

1. Sudden cardiopulmonary collapse or hypotension (systolic blood pressure <90

mmHg) with hypoxia (SpO2 <90%).
2. Severe hemorrhage or DIC according to the ISTH definition.
3. Symptomatology occurs either during labor or placental delivery (or up to 30 minutes
later).
4. Absence of fever or other explanations for the observed findings.
The SMFM acknowledges that there may be cases falling outside these parameters, such as
during pregnancy terminations. They clarify that their primary objective is to establish
standardized criteria for research reporting. While recognizing that their standards may
encompass numerous outlier cases, they hope to minimize such occurrences. The critical
clinical findings associated with AFE include coagulopathy, pulmonary hypertension, and
neurologic symptoms. Some authors have proposed a modified version of the above
definition that would consist of premonitory signs, like seizures, agitation, anxiety, feelings
of imminent death, confusion, and fainting. It has been recommended that the diagnostic
criteria proposed by SMFM be further validated in future large prospective cohort studies.

Treatment / Management

Due to the rarity of AFE, many obstetric clinicians lack experience in managing such cases.
To mitigate panic and confusion and enhance coordination among healthcare providers, it has
been proposed that a checklist could be a beneficial cognitive aid in the initial and immediate
management of a patient with an AFE. The overall treatment approach for a patient with an
AFE is supportive, with initial management aligning with the "ABC" principles, prioritizing
the support of the airway, breathing, and circulation.

Prompt and effective cardiopulmonary resuscitation is the cornerstone of managing an acute

AFE. Chest compressions should be initiated immediately, providing 100 to 120
compressions per minute with 1 ventilation every 6 seconds. It is crucial to avoid excessive
ventilation, as this can lead to a decrease in cardiac output.

During chest compressions, defibrillator pads should be applied without interruption, and a
non-synchronized shock should be administered if the cardiac rhythm is shockable.
Cardiopulmonary resuscitation should continue for 2 minutes, followed by a pause to check
for a pulse and analyze the rhythm. It is recommended to change providers, ensuring that no
one person gives chest compressions for more than 2 minutes. If indicated, a second shock
may be administered, and the process should be repeated.

In the absence of intravenous (IV) access, it is advisable to establish an interosseous line in

the humeral head for fluid and medication administration. If the cardiac rhythm persists, the
administration of epinephrine at a dose of 1 mg every 3 to 5 minutes should be initiated
through either the IV or interosseous line. In the presence of cardiac arrest with no return of
circulation within approximately 4 minutes, preparations for delivery should be made. This
can involve an operative delivery or perimortem cesarean delivery if the fetus is at a
gestational age considered viable.

The release of vasoconstrictors often results in increased pulmonary vascular resistance,

leading to right ventricular failure. TTE findings can help recognize this failure. Managing
right ventricular failure involves adjusting ventilator settings, avoiding fluid overload, and
using medications such as norepinephrine for blood pressure control. Preferred inotropic
support includes dobutamine or milrinone, and vasodilation with epoprostenol is
recommended.
Coagulopathy induced by tissue factor activation, primarily through Factor VII activation,
should be addressed with a 1:1:1 ratio of packed red blood cells, platelets, and fresh frozen
plasma to maintain fibrinogen levels above 150 mg/dL to 200 mg/dL. Tranexamic acid
should be given promptly, as this antifibrinolytic is readily available and safe to use with
obstetrical hemorrhage. Treating with large fluid volumes should be avoided. If prolonged
CPR of 10 minutes or longer is needed, or if right ventricular failure is unresponsive to
medical management, consideration may be given to extracorporeal membrane oxygenation
(ECMO). Anticoagulation treatment may be necessary to decrease clotting activation, platelet
consumption, and the consumption of coagulation factors.

The prompt evacuation of the fetus, termed "resuscitative hysterotomy," is a pivotal

component of AFE treatment, distinct from perimortem cesarean section, with the primary
aim of improving maternal hemodynamics. Given its time-sensitive nature, this procedure is
likely to be conducted at the site of the AFE, as transport to an operating room within the
optimal 1- to 2-minute window may not be feasible.

For the mother, comprehensive care involves securing the airway, effective ventilation,
appropriate fluid management, and judicious use of vasopressors. Intra-arterial lines facilitate
real-time pressure measurement and frequent arterial blood gas sampling. A central venous
pressure line aids in assessing right-sided preload. Recognizing the adverse impact of copious
fluid administration on clotting factors and bleeding, the decision to transition to vasopressors
should be contemplated earlier as compared to later when resuscitating a patient with
significant bleeding from other causes.

Pulmonary hypertension and right heart failure commonly accompany AFE, making
inotropes, pulmonary vasodilators, and after-load reducing agents paramount to treatment.
Vasopressor support should be initiated with norepinephrine if needed. Dobutamine and
milrinone, as inotropes, provide pulmonary vasculature dilation and a decrease in right
ventricular afterload. Epoprostenol, whether inhaled or intravenous, for pulmonary
vasodilation may be used instead of inhaled nitric oxide or sildenafil with similar outcomes
for right ventricular failure. Ideal management involves maintaining a mean arterial pressure
(MAP) >65 mmHg, a cardiac index >2 L per meter squared, an adequate urine output of 40
mL/hr to 50 mL/hr, and a PaO2/FiO2 ratio >250.

Extracorporeal membrane oxygenation (ECMO) life support has proven successful for
refractory cardiogenic shock secondary to AFE when severe right ventricular
dysfunction does not respond to medical management. ECMO provides respiratory and
hemodynamic support through the femoral vasculature until the right ventricle's function
improves. Any patient persisting in cardiopulmonary collapse should have femoral arterial
and venous 4 Fr sheaths placed in anticipation of ECMO. Transferring to tertiary facilities
capable of ECMO may require early decision-making and awareness of local capabilities.
Anticoagulation-free ECMO should be considered if ongoing bleeding or DIC is present.
Following fetal delivery, managing hemorrhage, uterine atony, and the resulting
coagulopathy (DIC) is the next step. Empirical administration of packed red blood cells
(pRBCs), fresh frozen plasma (FFP), and platelets in a 1:1:1 ratio has been traditional.
However, cryoprecipitate is preferred over FFP to reduce volume overload, given its
concentrated clotting factors, including factor VIII, von Willebrand factor, and fibrinogen.
Tranexamic acid may be administered for fibrinolysis. Blood products are used for fluid
resuscitation to mitigate the risk of volume overload.

Standard laboratory turnaround times for clotting parameters may be too slow for actively
bleeding patients. Viscoelastic hemostatic assay (VHA)-guided algorithms have
demonstrated reduced transfusion requirements, offering improved outcomes. Whole blood
viscoelastic hemostatic assays, such as thromboelastography and rotational
thromboelastometry, performed at the bedside, provide minute-to-minute evaluation of
clinically relevant information, aiding in the rapid assessment and treatment of major
obstetric hemorrhage, as seen in AFE. These measurements include fibrinogen levels, platelet
count and function, and evaluation of the entire extrinsic clotting pathway, guiding
appropriate administration of cryoprecipitate, fibrinogen, prothrombin complex concentrates,
platelets, FFP, and pRBCs.

While investigational, anecdotal reports in the literature cite the use of several other
medications, including rivaroxaban, a factor Xa inhibitor, C1 esterase inhibitor concentrate,
ketorolac, ondansetron, and aminocaproic acid.

Obstetrical management must prioritize the rapid evacuation of the fetus, usually by cesarean
section. The Society for Maternal-Fetal Medicine recommends this for all fetuses over
23 weeks gestational age. Evacuation of the uterus may not improve the clinical situation
with a previable fetus or even with a gestational age of less than 20 weeks. Ongoing
resuscitation of the mother in the delivery room, with an anesthesiologist or critical care
provider overseeing cardiovascular resuscitation, must continue during the infant's extraction.
Shifting the gravid uterus to the left is recommended, relieving aortocaval compression.

This multidisciplinary team, capable of initiating neonatal resuscitation, should include a

neonatologist, given that the majority of these infants are born with a low Apgar [Link]
obstetrician may opt for several procedures to alleviate ongoing uterine hemorrhage, such as
uterine artery ligation or embolization. Circumferential B-Lynch, Hayman, or Pereira
compression sutures have been used to compress the atonic uterus and staunch bleeding.
However, in the setting of massive hemorrhage and an atonic uterus, emergency
hysterectomy may be the best course, required in approximately 50% of patients with severe
and ongoing coagulopathy.
Debriefing is recommended to review processes, identify areas for improvement, and offer
emotional support to the patient, family, and medical providers. Reporting all cases of AFE to
the international AFE registry contributes to improving outcomes in future situations.
Simulations and drills are valuable in preparing the care team for these unusual yet emergent
clinical situations.

Differential Diagnosis

AFE is prone to misdiagnosis, prompting ongoing efforts to clarify its etiology, risk factors,
and pathogenesis. Vigilance must be taken for potentially reversible causes, including
hypovolemia, hypoxemia, and hypothermia. Consideration of underlying reversible diagnoses
such as myocardial infarction or tamponade, acidosis, hyperkalemia, and tension
pneumothorax is warranted. The differential diagnosis for a pregnant patient experiencing
complete cardiovascular collapse during or around the time of delivery, followed by
significant hemorrhage, should encompass the following:

 Pulmonary embolism (PE)

 Peripartum cardiomyopathy
 Septic shock
 Aortic dissection
 Magnesium toxicity
 Air or cholesterol embolism
 Myocardial infarction
 Venous air embolism
 Eclampsia
 Aspiration
 Toxic reaction to anesthetic medications
 Anaphylaxis
 Obstetrical hemorrhage causing coagulopathy and shock
 Cephalad spread of spinal anesthetic

AFE exhibits some similarities to pulmonary embolus but lacks an ongoing coagulopathy
seen in PE. Postpartum cardiomyopathy would likely manifest significant ST-T wave
changes on electrocardiography, accompanied by predominant symptoms of left-sided
congestive heart failure. Bedside echocardiography (TEE or TTE) can aid in distinguishing
AFE with its classic right ventricular dilatation, overload pattern, and septal bowing into the
left ventricle.

Septic shock typically presents with the classic systemic inflammatory response syndrome
(SIRS) picture and is unlikely to lead to sudden cardiovascular collapse. Myocardial
infarction, unless antecedent to the cardiac arrest, would display typical ST-T wave changes
and elevated serial cardiac enzymes, observable through bedside echocardiography. Venous
air embolism usually presents with wheezing, gasping, and chest pain before cardiovascular
collapse. Eclampsia may be suggested by hypertension, edema, proteinuria, headaches, or
seizures preceding the collapse. Anaphylaxis should exhibit premonitory symptoms like
wheezing, dyspnea, rash, urticaria, and a period of hypotension before cardiovascular
decompensation. Cephalad distribution of spinal anesthetic would present with an elevated
sensory level, weakness of the upper extremities, difficulty in speaking, dysphagia, and
bradycardia.

Prognosis

AFE stands as a prominent cause of maternal mortality in developed countries, with a

historical mortality rate initially reported at 61%, but recent data suggests a lower rate of
around 10%. Early and effective management of cardiac arrest significantly enhances
survival, with a case fatality rate ranging between 11% and 26% in developed nations.

Tragically, within the first hour following an AFE, an estimated 50% of patients succumb,
and two-thirds face mortality within 5 hours. The peak period of death has been noted to be 1
to 12 hours after the AFE occurs. A California-based study indicated that 26.4% of affected
pregnant patients died, while 66% developed DIC. Maternal survival remains uncommon, but
prompt recognition and resuscitation improve prognoses. The United Kingdom AFE registry
reported a 37% mortality rate, with 7% of survivors experiencing neurological impairment.

Survivors of AFE often grapple with substantial neurological, pulmonary, and cardiovascular
deficits, affecting two-thirds of these recently pregnant patients. Recurrence risks are
uncertain, but instances of successful subsequent pregnancies have been
documented. Elective cesarean delivery recommendations for future pregnancies to mitigate
labor-related risks are contentious.

Infant mortality rates hover around 30%, accompanied by elevated risks of hypoxic-ischemic
encephalopathy, cerebral palsy, and cognitive disabilities among survivors. The grim
statistics extend to stillbirth and neonatal death, reaching rates as high as 10% to
40%. Patients who survive pregnancies complicated by AFE commonly grapple with
depression and post-traumatic stress disorder (PTSD).

While initial rates of neurologically intact survival were reported at 15%, recent data suggests
an improvement, with estimates nearing 46%. Advances in diagnosis, medical management,
and a deeper understanding of AFE's pathophysiology contribute to enhanced survival rates.
Early recognition has not only benefited maternal outcomes but has also resulted in improved
neonatal mortality and morbidity rates.

Complications

Survivors of AFE may contend with a spectrum of significant complications, including the
following:

 Renal failure
 Cardiac failure
 Prolonged respiratory failure leading to adult respiratory distress
 Myocardial infarction
 Arrhythmias
 Cardiomyopathy
  Congestive heart failure
 Left ventricular systolic dysfunction
 Prolonged coagulopathy
 Respiratory failure (extended)
 Prolonged bronchospasm
 Liver failure
 Cardiogenic pulmonary edema
 Seizures
 Anoxic encephalopathy
 Various cognitive or neurologic impairments

Infants delivered emergently during maternal AFE are at heightened risk for sustaining
hypoxic-ischemic encephalopathy (HIE). This often results in a significantly cognitively
impaired child, potentially manifesting chronic epilepsy, motor impairment, and
developmental delay.

Deterrence and Patient Education

AFE is an exceptionally severe condition characterized by its sudden onset, and

unfortunately, its occurrence is largely unpredictable. Despite its unforeseeable nature, there
are limited preventive measures that can be taken. To minimize the risk of AFE, care should
be exercised during certain maneuvers, such as the insertion of a pressure catheter and
intraamniotic infusion therapy. Additionally, efforts should be made to refrain from incising
the placenta during cesarean delivery whenever possible.

Future studies are crucial to identifying individuals at the highest risk, as long-term mental
and physical health consequences are prevalent in these patients. It is noteworthy that only
around 60% of women affected by AFE manage to return to their previous state of well-
being. Further research can contribute to a better understanding of risk factors and improve
preventive strategies.

Enhancing Healthcare Team Outcomes

The abrupt onset of cardiovascular collapse and profound coagulopathy in mothers, coupled
with the imperative for neonatal resuscitation, renders the management of AFE highly
intricate and demanding for any interdisciplinary team. Successful outcomes for both the
mother and infant hinge on seamless coordination among various healthcare professionals,
including obstetricians, maternal-fetal specialists, anesthesiologists, labor and delivery
nurses, neonatologists, intensivists, hematologists, perfusionists, respiratory therapists, and
neonatal intensive care unit nurses.

A multidisciplinary approach, facilitated within a high-acuity level hospital setting, is crucial

for optimizing maternal and infant survival outcomes in cases of AFE. This collaborative
effort ensures that expertise from diverse medical specialties converges to address the
multifaceted challenges posed by AFE, thereby enhancing the overall quality of care and
response to this challenging obstetric emergency.(10)
Shock in obstetrics

Shock is defined as a state of circulatory inadequacy with poor tissue perfusion resulting in
generalized cellular hypoxia. Circulatory inadequacy is due to a disparity between the
circulating blood volume and the capacity of the circulatory bed.

The net effect of this disparity is inadequate exchange of oxygen and carbon dioxide between
the intra and extravascular compartments. The stagnation of carbon dioxide and other
metabolites in the tissue leads to metabolic acidosis and cellular death.

The series of changes observed in shock and their clinical manifestations are therefore,
dependent on two sets of changes (a) Circulatory inadequacy at the ‘filtration’ level
(microvascular compartment), (b) Cellular damage and ultimately death.

Anatomy of microvascular circulation:

Micro vascular circulation consists of circulation of blood through a tuft of capillaries with a
feeding arteriole and a draining venule at either end of the capillary bed. The f low of blood
within the capillary bed is controlled by 2 sphincters—one at the arteriolar end and the other
at the venular end. They are known as pre and postcapil lary sphincters. In addition to the tuft
of capillaries, there is a direct communication between the arteriole and the venule and this
communicating trunk bypasses the cap illary bed. This is known as metarteriole shunt or ‘thor
oughfare channel’. When the sphincters are closed, the metarteriole shunt operates to divert
blood for supply to the vital organs, like brain, heart and kidney.

Pathophysiology of shock

Pathophysiological changes in obstetric shock are pre dominantly associated with (a) general
changes due to hypovolemia, and (b) specific changes due to liberation of endotoxin.
Hypotension stimulates release of neuroendocrine mediators like adrenocorticotropic
hormone (ACTH), growth hormone (GH), b endorphin, cortisol and glucagon.

There is also sympathoadrenal response. Presence of endotoxin (lipopolysaccharide), in

septic shock activates the leukocytes through the complement system. There is the release of
inflammatory mediators such as proteases, superoxide (O2–), hydroxyl (OH–) radicals,
cytokines, prostaglandins, and many cytotoxic enzymes. These interfere with the function of
a number of enzyme systems and increase capillary permeability.

Cytokines such as interleukins (ILS) and tumor necrosis factor (TNF) interact by autocrine
and paracrine mechanisms to cause cellular or organ dysfunction. In the presence of hypoxia,
sepsis and acidosis, lysosomal enzymes which are cytotoxic, are released. They can cause
myocardial depression and coronary vasoconstriction. Prostacyclin is a vasodilator and
inhibits platelet aggregation.
Thromboxane A2 causes pulmonary vasoconstriction and platelet aggregation. Leukotrienes
cause vasoconstriction, platelet activation and increased vascular permeability. Endothelium-
derived relaxing factor (EDRF) which is identified as nitric oxide (NO) is found to produce
sustained vasodilatation and hypotension.

Thrombosis is increased due to inhibition of antithrombin III. Thrombocytopenia is common.

Metabolic changes: Hepatic glycogenolysis due to increased level of glucagon,
catecholamine and cortisol leads to hyperglycemia. There is diminished peripheral utilization
of glucose due to increased level of insulin antagonists like cortisol and growth hormone.

Inadequate oxygen supply to tissue initiates anaerobic metabolism. Consequently, there is

metabolic acidosis, the production of lactic acid and H+ ions. The sodium pump fails to
operate. Finally, the lysosomal enzymes are released. These lead to cell death.
Management of shock

HEMORRHAGIC SHOCK

Basic management of hemorrhagic shock is to stop the bleeding and replace the volume which has
been lost. Prompt diagnosis and immediate resuscitation is essential failing which multiple organ
failure develops.

Restore circulating volume (Infusion and transfusion): Blood should be transfused, especially in
hemorrhagic shock as soon as it is available. Crystalloids: Normal saline has to be infused initially for
immediate volume replacement. But they are rapidly lost from circulation. Colloids: Polygelatin
solutions (Hemaccel, Gelofusion) are isoosmotic with plasma. They do not interfere with the
coagulation system. Large volumes can be administered. They promote osmotic diuresis. Dextrans:
They are polymolecular polysaccharides.

They interfere with crossmatching and they are avoided. Human albumin solutions (4.5%)—not
generally used for volume replacement. Maintenance of cardiac efficiency: When a large vol ume of
fluid or blood is to be administered, the cardiac competence or efficiency should be ascertained, other
wise there is a risk of overloading the circulation and cardiac failure. 6 liters of crystalloids may be
needed for the loss of 1 liter of plasma volume. One or two large bore (14 or 16-gauge) cannula are
inserted for volume replacement. Packed red blood cells (specific blood component), combined with
normal saline, are used for hemorrhagic shock. Hemodynamic monitoring is aimed at maintaining.
systolic BP >90 and MAP >60 mm Hg, CVP 12–15 cm H2O and pulmonary capillary wedge pressure
14–18 mm Hg.

Administration of oxygen to avoid metabolic acidosis: In the initial phase, administration of oxygen
by nasal cannula at a rate of 6–8 liters per minute is enough but in the later phases, ventilation by
endotracheal intuba tion may be necessary. Oxygen delivery should be continued to maintain O2
saturation >92%, PaO2 80–100 mm Hg, PaCO2 30–35 mm Hg and pH >7.35.

Endotracheal intubation and mechanical ventilation may be needed for patients with septic shock.
Indications of mechani cal ventilation are: severe tachypnea (RR >40/min), altered mental status,
severe hypoxemia, despite O2 supplementation. Pharmacological agents: Use of vasopressor drugs
should be kept to a minimum, since peripheral vaso constriction is already present. The role of
vasoactive drugs, inotropes and corticosteroids in shock has been discussed in detail in connection
with management of endotoxic shock. Control of hemorrhage: Specific surgical and medical treatment
for the control of hemorrhage should start along with the general management of shock. The specific
management of each variety of obstetric hemorrhage has been outlined in the related chapters.
Monitoring: Clinical parameters like skin temperature, and visible peripheral veins can be helpful to
assess the degree of tissue perfusion. Urine output (>30 mL/hr) is a useful guide. Arterial blood
pressure is a poor indicator to assess tissue perfusion. Invasive monitoring may not be needed in a
straight forward case. In a critically ill patient, however, measurement of central venous pressure
(CVP), to assess the adequacy of patient’s circulating volume and the contractile state of the
myocardium, is essential. Pulse oximeter and blood gas analysis are useful to assess tissue perfusion.
Measurement of left atrial pressure (pulmonary artery occlusion pressure) by ‘SwanGanz’ catheters
could be done in selected cases.

ENDOTOXIC SHOCK Investigations to organize in a patient with septic shock: CBC, hematocrit,
coagulation profile, (platelet count, serum fibrinogen, FDPs, PT, APTT), liver and renal function
tests, chest radiograph, USG, CT or MRI may be needed (for localizing pelvic pathology or pelvic
abscess, pneumonia or ARDs), and also ECG monitoring.

The principles of management are: (a) to correct the hemodynamic instability due to sepsis
(endotoxin), (b) to appropriate supportive care, and (c) to remove the source of sepsis.

Guidelines for Obstetric HDU and ICU (Maternal Health Division

Ministry of Health and Family Welfare Government of India)

Any pregnant woman can develop life-threatening complications with little or no

warning. The complications of pregnancy and labor are essential of two types‐ the first set of
complications include obstetric complications like Postpartum Hemorrhage (PPH), Pre-
eclampsia/Eclampsia (PE/E), etc. which require intensive obstetric care by specially trained
providers, and the second set of complications include multi‐organ involvement/failure which
necessitates care provision by intensivist and super‐specialists such as those from nephrology
, neurology, cardiology, pulmonology etc.

Women with obstetric complications need access to quality maternal health services that
can detect and manage life-threatening obstetric complications. These women need 24/7 pers
onalized care by skilled providers, essentially led by obstetricians or Emergency Obstetric Ca
re (EmOC) trained providers. For a small proportion of women who have progressed to a
clinical condition where there is multi‐organ involvement/failure, the care has to be provided
in an intensive care unit setting led by intensivists/super‐specialists.

Types of specialized care units

 What is an Intensive Care Unit (ICU)?
ICU is a specialized area of the hospital that is specifically designed, staffed, located, furnish
ed and equipped, dedicated to the management of critically sick patients, injuries or
complications. It is a department with dedicated medical, nursing and allied staff trained in
critical care.

What is an Obstetric ICU?

It is an ICU that is dedicated to obstetric patients who have developed multi‐organ failure
necessitating specialized care by super‐specialists like intensivists/ nephrologists/ cardiologist
s, pulmonologists/ endocrinologist etc.

What is a High Dependency Unit (HDU)?

HDU is an area in a hospital where patients can be cared more extensively than in a normal
ward, but not to the point of intensive care. So, it is also known as the intermediate care unit.
Patients in HDU may require ICU admission later (step up) or at the same time, patients in IC
U who had an improvement in their condition, may be shifted to HDU (step down), before
shifting them to the general ward.

Why dedicated Obstetric HDUs are required?

 In India, most of the public health facilities do not have a separate special care unit for
high-risk pregnancies and postpartum mothers with complications. Such women are being
managed in the labor room, without a dedicated team(s) of competent providers and
appropriately equipped facilities.


To further bring down the MMR, facility of skill based services in dedicated critical care set
up, with state‐of‐the‐art equipment and technology and a team of appropriately trained
professionals are the need of the hour.

 Any pregnancy can develop life threatening complications at any time with or without any
warning.

 Out of the total complications, the incidence of high-

risk pregnancy is approximately 7 to 8%.

 Care of critically ill patients is a unique challenge in obstetrics.

 When things go wrong in obstetrics, they go wrong fast – “they fall off a cliff”.


Medical conditions might present a risk to the pregnancy, and pregnancy may also modify
the disease state.
  Drug therapy may be affected by altered pharmacokinetics during pregnancy, and may
have an impact on the fetus.

Process of Shifting of a Patient from Ward/ Triage Room to HDU or ICU/ Obstetric ICU
The key steps to be taken are:

[Link] the family/companion of pregnant woman of the decision, and take consent.

[Link] sheets containing history, examination, investigations and management should

be maintained.

3. Obstetric HDU staff should be appropriately informed.

[Link] patients should be escorted by doctor/staff with all existing treatment including
continuation of patent IV line.

5. Keep monitoring the vitals of the patient.

 6. Adequate follow‐up by the treating doctor.

7. Oxygen and supine hypotension prevention (by performing lateral tilt to 15‐
20 degree),if required.

8. Ensuring patent airway.

9. Baby should be shifted along with the mother if delivered already.

Referrals from outside to HDU:

Ensure attaching filled referral slips and availability of emergency medications while
transferring during referral.

Research article

Pregnancy-related emergencies: Profile and outcome

Ankita C. Nekkanti, Darpanarayan Hazra1, Reshma M. George, Sruthi Yalamanchili,

Pushpalata Kumari, Santosh T. Samuel, Kundavaram P. P. Abhilash1 Department of
Emergency Medicine, Obstetrics and Gynaecology, 3Internship Student, Christian Medical
College, Vellore, Tamil Nadu, India
Abstract: National efforts to reduce maternal mortality concerning community services have
primarily focused on upgrading transportation infrastructure and formalizing training for care
providers. There is, however, a paucity of baseline data on the profile and outcomes of
pregnant women presenting to the Emergency Department (ED) in India. Methods: This
retrospective study enrolled all pregnant women presenting to a large tertiary medical care
center in India, between November 2016 and November 2017. Results: There were 696 ED
visits by pregnant women during the study period. The mean age was 26.85 (SD: 4.88) years.
Pregnant women in the first trimester contributed to 50.8% of all visits, and 54% were
multigravida. The most common presenting complaints were bleeding/spotting per vaginum
(PV) (38.2%) and abdominal pain (37.6%) followed by fever (21.6%) and vomiting (21.5%).
Obstetric causes contributed to 53.2% of the ED visits, while nonobstetric causes amounted
to 43.2%. Over a third (39.7%) required hospital admission. Of these patients, 73% delivered
in CMC with live births amounting to 62.3% while 3.5% ended in fetal deaths. The
miscarriage rate was as high as 28%. More than half (51.1%) of the deliveries were by
normal vaginal delivery. There were no maternal deaths during the time of admission.
Conclusions: Our study sheds new light on the profile of emergency visits among pregnant
patients and their relationship to the outcome of pregnancy. First-trimester visits were most
common with complaints of bleeding PV and abdominal pain. This could explain the high
rate of miscarriages among this population.
1. Nekkanti AC, Hazra D, George RM, Yalamanchili S, Kumari P, Samuel ST, et al.
Pregnancy-related emergencies: Profile and outcome. J Fam Med Prim Care. 2020 Sep
30;9(9):4618–22.

2. Nekkanti AC, Hazra D, George RM, Yalamanchili S, Kumari P, Samuel ST, et al.
Pregnancy-related emergencies: Profile and outcome. J Fam Med Prim Care. 2020 Sep
30;9(9):4618–22.

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