Obstetrical Hemorrhage

Dr Nabin Pandey
Resident , OBGYN
KUSMS
• A profuse hemorrhage occurring prior to or
shortly after the birth of the child is always
dangerous and not infrequently a fatal
complication —J. Whitridge Williams (1903)
• As in Williams’ time, obstetrical hemorrhage
continues along with hypertension and infection to
be one part of the infamous “triad” of maternal
death causes.
• Hemorrhage was a direct cause of 11.4 percent of
5367 pregnancy-related maternal deaths from 2006
to 2013 in the United States.
• In developing countries, hemorrhage’s contribution
is even more striking, and it is the single most
important cause of maternal death worldwide.
Mechanisms of Normal Hemostasis
• A major concept in understanding the pathophysiology and
management of obstetrical hemorrhage is the mechanism
by which hemostasis is achieved after normal delivery.
• Recall that near term an incredible amount of blood—at
least 600 mL/min—flows through the intervillous space .
• This prodigious flow circulates through the spiral arteries,
which average 120 in number.
• Also, recall that these vessels have no muscular layer
because of their remodeling by trophoblasts, which creates
a low-pressure system.
• With placental separation, these vessels at the
implantation site are avulsed, and hemostasis is
achieved first by myometrial contraction, which
compresses this formidable number of large vessels.
• Compression is followed by clotting and obliteration
of vessel lumens.
• If, after delivery, the myometrium contracts
vigorously, fatal hemorrhage from the placental
implantation site is unlikely.
• Importantly, an intact coagulation system is
not necessary for postpartum hemostasis
unless there are lacerations in the uterus,
birth canal, or perineum.
• At the same time, however, fatal postpartum
hemorrhage can result from uterine atony
despite normal coagulation.
• Definition:
• Traditionally, postpartum hemorrhage is
defined as the loss of ≥500 mL of blood after
completion of the third stage of labor.
• This is problematic because almost half of all
women delivered vaginally shed that amount
of blood or more when losses are carefully
measured .
• According to the American College of Obstetricians and
Gynecologists , postpartum hemorrhage is defined as
cumulative blood loss >1000 mL accompanied by signs and
symptoms of hypovolemia.
• Almost a third of women undergoing cesarean delivery
have blood loss that exceeds 1000 mL .
• Studies show that estimated blood loss is commonly only
approximately half the actual loss
• Because of this, estimated blood loss in excess of average
should alert the obstetrician to possible excessive bleeding.
• Excessive blood loss has been estimated by several
methods.
• Sosa and colleagues (2009) used specially constructed
drapes and reported that 10.8 percent of women had
hemorrhage in excess of 500 mL with vaginal delivery,
whereas 1.9 percent lost >1000 mL.
• Tita and associates (2012) used a 6-volume percent drop
in the postpartum hematocrit to define clinically
significant blood loss with vaginal delivery. This decline
easily signifies a >1000-mL blood loss in the averaged-
sized woman.
• Another marker used to estimate hemorrhage
incidence is the transfusion rate.
• In the study by Tita , more than 6 percent of women
who delivered vaginally underwent blood
transfusions.
• In a study of more than 66,000 women delivered at
Parkland Hospital, 2.3 percent overall were given
blood transfusions for hypovolemia .
• Half of these women had undergone cesarean
delivery.
• Green and coworkers (2016) reported that
the incidence of massive transfusion for
postpartum hemorrhage was 23 per 100,000
births.
 Obstetrical Hemorrhage: Causes,
Predisposing Factors, and Vulnerable Patients
• Abnormal Placentation
• Placenta previa
• Placental abruption
• Morbidly adherent placenta
• Ectopic pregnancy
• Hydatidiform mole
 Injuries to the Birth Canal

• Episiotomy and lacerations

• Forceps or vacuum delivery
• Cesarean delivery or hysterectomy
• Uterine rupture
Previously scarred uterus
High parity
Hyperstimulation
Obstructed labor
Intrauterine manipulation
Midforceps rotation
Breech extraction
 Uterine Atony
• Uterine overdistention
Large fetus
Multiple fetuses
Hydramnios
Retained clots
• Labor induction
• Anesthesia or analgesia
Halogenated agents
Conduction analgesia with hypotension
• Labor abnormalities
Rapid labor
Prolonged labor
Augmented labor
Chorioamnionitis
• Previous uterine atony
• Parity: primiparity, high parity
 Obstetrical Factors

• Previous postpartum hemorrhage

• Early preterm pregnancy
• Sepsis syndrome
• Preeclampsia/eclampsia
 Coagulation Defects—Intensify Other Causes
• Massive transfusions
• Placental abruption
• Sepsis syndrome
• Severe preeclampsia syndrome
• Acute fatty liver
• Anticoagulant treatment
• Congenital coagulopathies
• Amnionic fluid embolism
• Prolonged retention of dead fetus
• Saline-induced abortion
 Vulnerable Patients

• Chronic renal insuiciency

• Constitutionally small size
• Obstetrical hemorrhage is traditionally
classified as antepartum —such as with
placenta previa or placental abruption, or as
postpartum —commonly caused by uterine
atony or genital tract lacerations .
• In these cases, rapid assessment should
always consider the deleterious fetal effects of
maternal hemorrhage.
 PLACENTAL ABRUPTION

• Separation of the placenta—either partially or totally

—from its implantation site before delivery is
described by the Latin term abruptio placentae .
• Literally translated, this refers to “rending asunder of
the placenta,” which denotes a sudden accident that is
a clinical characteristic of most cases.
• In the purest sense, seldom used—term premature
separation of the normally implanted placenta is most
descriptive because it excludes separation of a
placenta previa.
• Abruption likely begins with rupture of a decidual
spiral artery and then an expanding retroplacental
hematoma.
• Placental abruption is initiated by hemorrhage into
the decidua basalis.
• The decidua then splits, leaving a thin layer adhered to
the myometrium.
• Consequently, the process begins as a decidual
hematoma and expands to cause separation and
compression of the adjacent placenta.
• Incidence: 0.49% - 1.8%
• Concealed : 20% - 35%
• Revealed: 65% - 80%
 Grading
• 0 Asymptomatic patient with a small retroplacental
clot

• 1 Vaginal bleeding , uterine tetany and tenderness may

be present; no signs of maternal shock or fetal compromise

• 2 External vaginal bleeding possible ; no signs of

maternal shock or fetal compromise

• 3 External bleeding possible , marked uterine tetany ,

board like consistency , persistent abdominal pain ,
maternal shock and fetal demise. ( Coagulopathy seen in
30 % cases.)
• Most blood in the retroplacental hematoma in a
nontraumatic placental abruption is maternal.
• This is because hemorrhage derives from separation
within the maternal decidua, and placental villi are
usually initially intact.
• In 78 women at Parkland Hospital with a
nontraumatic placental abruption, fetal-to-maternal
hemorrhage was documented in only 20 percent—
and all of these had <10 mL fetal blood loss .
• When clinically suspected, an abruption is seen
on a freshly delivered placenta as a circumscribed
depression on the maternal surface.
• These usually measure a few centimeters in
diameter and are covered by dark, clotted blood.
• Because several minutes are required for these
anatomical changes to materialize, a very
recently separated placenta may appear totally
normal at delivery.
• Defining severity of placental abruption is problematic.
• Ananth and coworkers (2016) have defined severe
abruption as displaying one or more of the following:
(1) maternal sequelae that include disseminated
intravascular coagulation, shock, transfusion,
hysterectomy, renal failure, or death;
(2) fetal complications such as nonreassuring fetal status,
growth restriction, or death; or
(3) neonatal outcomes that include death, preterm
delivery, or growth restriction.
Conditions associated with abruption
 Pregnancy-Associated Hypertension

• Some form of hypertension is the most frequent

condition associated with placental abruption.
• This includes gestational hypertension,
preeclampsia, chronic hypertension, or a
combination thereof.
• In a report by Pritchard and colleagues (1991) that
described 408 women with placental abruption
and fetal demise, hypertension was apparent in
half once hypovolemia was corrected.
• A causal relationship between hypertension and abruption
is not completely proven.
• Hypertension may be associated with vascular or placental
abnormalities, increased fragility of vessels, vascular
malformations, or abnormalities in placentation.
• Decreased placental blood flow and abnormal endothelial
responses to vasoactive substances may be due to the
absence of transformation from high- resistance muscular
arterioles to low-resistance dilated vessels as in normal
pregnancy, and the lack of trophoblastic invasion of
uterine vessels .
 Clinical Presentation
• The diagnosis of placental abruption is clinical,
based on characteristic signs and symptoms.
• This is then confirmed by evaluation of the
placenta after delivery on gross examination
of the placenta, which reveals a clot and/or
depression in the maternal surface.
• Clinical signs of abruption are tense, tender
and/or irritable uterus (this may be less obvious
if posterior placenta), signs of shock which are
out of proportion to estimated blood loss
(concealed abruption), frequent uterine
contractions on tocograph suggestive of uterine
irritability with or without associated fetal
heart rate abnormalities on the
cardiotocography traces.
• There is a serious risk of development of
coagulopathy in the mother due to
consumption of the clotting factors.
• The clinical signs of blood loss are more
pronounced than the amount of visible vaginal
bleeding.
• Ultrasound is an insensitive and unreliable
tool for detecting or excluding placental
abruption, as negative sonographic findings
are common with clinically significant
abruptions.
• Sensitivity: 24%
• Specificity: 96%
 Couvelaire Uterus

• At the time of cesarean delivery, it is not uncommon to find

widespread extravasation of blood into the uterine
musculature and beneath the serosa .
• It is named after Couvelaire, who in the early 1900s termed
it uteroplacental apoplexy .
• These myometrial hemorrhages seldom cause uterine
atony, and alone they are not an indication for
hysterectomy.
• Effusions of blood are also seen beneath the tubal serosa,
between the leaves of the broad ligaments, in the
substance of the ovaries, and free in the peritoneal cavity.
 Fetal risks
• The majority of fetal morbidity is due to prematurity.
• Low birth-weight, fetal growth restriction, neonatal
anaemia and hyperbilirubinaemia are significantly more
common.
• Premature separation of the placenta also leads to fetal
hypoxia.
• In cases presenting with the fetus still alive, fetal heart
rate abnormalities are common.
• A marked elevation in stillbirth rate is observed if the
separation exceeds 50% of the placental area.
 Maternal risks
• In severe abruption, complications include
large haemorrhage requiring transfusion,
disseminated intravascular coagulopathy
(DIC), infection and rarely, maternal death.
• Recurrence: 6 % - 17 % after 1 episode.
25 % after 2 episodes.
 Management
• Action should be swift and decisive once placental
abruption has been suspected, because the prognosis
for mother and fetus is worsened by delay.
• Treatment consists of initial resuscitation and
stabilization of the mother and recognition and
management of complications, as described previously.
• It is individualized based on the extent of the
abruption, maternal and fetal reaction to this insult,
and gestational age of the fetus.
For the purpose of management, Sher and
Statland classified placental abruption into
three degrees of severity:
 Placenta Previa
• Placenta praevia is defined as a placenta that lies
wholly or partly within the lower uterine segment.
• The prevalence of clinically significant placenta praevia
is estimated to be approximately 4 or 5 per 1000
pregnancies at term.
• With the rising incidence of caesarean sections
combined with increasing maternal age, the number
of cases of placenta praevia and its complications,
including placenta accrete is likely to continue to
increase.
 Classification
• Type 1 – Low-lying placenta: Where the lower placental
edge in the lower uterine segment, but does not reach
the internal os
• Type 2 – Marginal praevia: Where the lower placental
edge reaches the internal os.
• Type 3 – Incomplete central praevia: Where the placental
edge overlaps the internal os, but the placental
attachment is asymmetric across the internal os.
• Type 4 – Complete central praevia: Where the placental
edge symmetrically overlaps the internal os.
 Placental Migration
• Beginning with the use of sonography in obstetrics,
the term placental migration was coined to describe
the apparent movement of the placenta away from
the internal os .
• Obviously, the placenta does not move per se, and
the mechanism of apparent movement is not
completely understood.
• To begin with, migration is clearly a misnomer,
because decidual invasion anchors chorionic villi at
the cervical os.
• First, apparent movement of the low-lying placenta relative
to the internal os is related to the imprecision of two-
dimensional sonography.
• Second, as pregnancy progresses, growth of the lower and
upper uterine segments differs.
• With greater blood flow in the upper uterus, placental
growth is more likely directed toward the fundus—
trophotropism .
• Many of those placentas that “migrate” most likely never
were circumferentially implanted with true villous invasion
that reached the internal cervical os.
 Aetiology and Associated Factors
• Placenta praevia occurs when the blastocyst is implanted low in
the uterine cavity.
• previous placenta praevia,
• advancing maternal age,
• increasing maternal parity,
• large placental size (multiple pregnancy),
• endometrial damage (previous dilatation and curettage),
• uterine scars like previous caesarean section or myomectomy,
• pathology-like endometritis,
• placental pathology such as marginal cord insertions and
succenturiate lobes.
• Previous history of placental praevia and,
curiously, cigarette smoking increases the
chance of placenta praevia.
• 1 previous CS: 0.65%
• 2 previous CS: 1.5%
• 3 previous CS:2.2%
• 4 or more CS:10%
• Recurrence after 1 placenta previa : 4% - 8 %
 Clinical Features
• Painless bleeding is the most characteristic
event with placenta previa.
• Bleeding from a previa usually begins without
warning and without pain or contractions in a
woman who has had an uneventful prenatal
course.
• This so-called sentinel bleed is rarely so
profuse as to prove fatal.
• A specific sequence of events leads to bleeding in cases
in which the placenta is located over the internal os.
• First, the uterine body remodels to form the lower
uterine segment.
• With this, the internal os dilates, and some of the
implanted placenta inevitably separates.
• Bleeding that ensues is augmented by the inherent
inability of myometrial fibers in the lower uterine
segment to contract and thereby constrict torn vessels.
• Similarly, bleeding from this lower segment
implantation site also frequently continues
after placental delivery.
• Last, there may be lacerations in the friable
cervix and lower segment.
• These may be especially problematic following
manual removal of a somewhat adhered
placenta.
 Diagnosis
• Clinical Features
• Ultrasonography
• Double setup examination
• USG:
• 28 % low lying before 24 weeks
• 18 % by 24 weeks
• 3 % by term
 Management
• The management of placenta praevia depends
upon clinical presentation, gestational age, severity
of bleeding and the type of praevia.
• Initial haemorrhages called warning haemorrhages
are often small and tend to stop spontaneously.
• Delivery may be needed for severe, intractable or
recurrent bleeding.
• Fetal morbidity is because of iatrogenic
prematurity.
• Traditionally, caesarean section has been the
recommended mode of delivery for major placenta
praevia, whereas for minor praevia an attempt at
vaginal delivery was considered appropriate.
• It was proposed that cases with placental edge to
internal os distance of less than 2 cm be referred to
as major placenta praevia and an elective
caesarean section should be recommended.
• Vergani and colleagues reported that more than
two-thirds of women with a placental edge to
cervical os distance of 1.0 cm deliver vaginally
without increased risk of haemorrhage .
• Bronsteen and coworkers also reported that
26/34 (76.5%) of women with placental edge-
internal os distance of 1.0–2.0 cm within 4
weeks of delivery and were allowed to labour,
achieved a successful vaginal birth .
• Current guidelines from the Royal College of Obstetricians
and Gynecologists (RCOG) recommend caesarean delivery
for women with placental edge – internal os distance of
less than 2.0 cm.
• The guidelines also recommend that any women going to
the operation theatre with known major placenta praevia
should be attended by an experienced obstetrician and
anaesthetist.
• This is especially true if these women also have previous
uterine scars, an anterior placenta or are suspected to be
associated with placenta accreta.
 Complications
• Maternal:
• Antepartum hemorrhage of varying degree.
• During labor :
• Early rupture of the membranes
• Cord prolapse due to abnormal attachment of the cord.
• Slow dilatation of the cervix due to the attachment of placenta on the
lower segment.
• Intrapartum hemorrhage due to further separation of placenta with
dilatation of the cervix.
• Increased incidence of operative interference.
• Postpartum hemorrhage
• Retained placenta
• Fetal :
• Low birth weight babies and fetal growth
restriction.
• Asphyxia
• Intrauterine death
• Birth injuries
• Congenital malformation
• Maternal and fetal morbidity and mortality
Thank You
 Postpartum Hemorrhage
• According to the American College of
Obstetricians and Gynecologists , postpartum
hemorrhage is defined as cumulative blood
loss >1000 mL accompanied by signs and
symptoms of hypovolemia .
• The incidence is about 4–6% of all deliveries.
• TYPES:
Primary
Secondary
• Primary:
• Hemorrhage occurs within 24 hours following the birth
of the baby.
• In the majority, hemorrhage occurs within two hours
following delivery.

• Secondary:
• Hemorrhage occurs beyond 24 hours and within
puerperium, also called delayed or late puerperal
hemorrhage.
 CAUSES
Four basic pathologies are expressed as the four
Ts’ (RCOG):
• Tone (atonicity),
• Tissue (retained bits, blood clots),
• Trauma (genital tract injury) and
• Thrombin (coagulopathy).
 Atonicity
• Grand multipara
• Overdistension of the uterus
• Malnutrition and anemia (<9.0 g/dL)
• Antepartum hemorrhage (Both placenta previa and abruption)
• Prolonged labor
• Anesthesia
• Initiation or augmentation of delivery by oxytocin
• Malformation of the uterus
• Uterine fibroid
• Placenta
• Mismanaged third stage of labor
• Obesity (BMI > 35)
• Previous PPH
• Age (>40 yrs)
• Drugs: Use of tocolytic drugs (ritodrine),
MgSO4, Nifedipine.
 Traumatic
• Trauma involves usually the cervix, vagina,
perineum (episiotomy wound and
lacerations), paraurethral region and rarely,
rupture of the uterus occurs.
• The bleeding is usually revealed but can rarely
be concealed (vulvovaginal or broad ligament
hematoma).
 Retained tissues
• Bits of placenta, blood clots cause PPH due to
imperfect uterine retraction.
 Thrombin
• The blood coagulopathy may be due to
diminished procoagulants (washout
phenomenon) or increased fibrinolytic activity
.
• The conditions where such disorders may
occur are abruptio placentae, jaundice in
pregnancy, thrombocytopenic purpura, severe
preeclampsia, HELLP syndrome or in IUD .
• The effect of blood loss depends on—
(a) Predelivery hemoglobin level,
(b) degree of pregnancy induced hypervolemia and
(c) speed at which blood loss occurs.
• Alteration of pulse, blood pressure and pulse pressure
appears only after class 2 hemorrhage (20–25% loss of
blood volume).
• On occasion, blood loss is so rapid and brisk that death
may occur within a few minutes.
• State of uterus, as felt per abdomen, gives a
reliable clue as regards the cause of bleeding.
• In traumatic hemorrhage, the uterus is found
well contracted.
• In atonic hemorrhage, the uterus is found
flabby and becomes hard on massaging.
• However, both the atonic and traumatic cause
may coexist.
 Management
• The principles in the management are:
 To empty the uterus of its contents and to
make it contract.
 To replace the blood. On occasion, patient
may be in shock. In that case patient is
managed for shock first .
 To ensure effective hemostasis in traumatic
bleeding
PRINCIPLES: Simultaneous approach
• Communication
• Resuscitation
• Monitoring
• Arrest of bleeding

• It is essential in all cases of major PPH (blood

loss > 1000 mL or clinical shock). (RCOG - 2009).
Thank You
Obstetrics Shock
 Shock Index
• It refers to heart rate (HR) divided by systolic
blood pressure (SBP).
• The normal value is 0.5–0.7.
• Increase in the pulse rate and a fall in systolic
blood pressure that is seen with significant
haemorrhage, results in an increase in the shock
index.
• It has been reported that if it increases above
0.9–1.1, intensive resuscitation may be required.
• Recently, attempts have been made to
determine the normal and abnormal values of
an ‘Obstetric Shock Index’ (OSI).
• A preliminary pilot study has suggested that
the normal value in pregnancy is 0.7–0.8 and if
OSI > 1, then it indicated a massive blood
obstetric haemorrhage that required blood
transfusion in 80% of cases.
 Golden First hour and The Rule of 30

• Severe PPH can lead to cardiovascular

compromise, aggressive resuscitative
measures should be deployed before the
estimated blood loss is more than one-third of
the woman’s blood volume (blood volume
[mL] = weight [kg] * 90 during pregnancy) or
more than 1000 mL or a change in
haemodynamic status.
• The ‘golden first hour’ is the time at which
resuscitation must begin to achieve maximum
survival before metabolic acidosis sets in.
• This has led to the concept of rule of 30 to
recognize ongoing massive blood loss.
• Rule of 30 is used to measure severity of shock
resulting from at least the loss of 30% of blood
volume leading to moderate shock .
• It is based on the fact that when a woman
loses 30% of her blood volume, her systolic
blood pressure (SBP) is likely to fall by 30
mmHg, her heart rate (HR) is likely to increase
by 30 beats/min, her respiratory rate is likely
to be >30 breaths/min and her haemoglobin or
haematocrit is likely to drop by 30%.
• As a result of peripheral shut down, her
urinary output is likely to fall < 30 mL/hour.
• Chandraharan and Arulkumaran proposed a
management algorithm ‘HAEMOSTASIS’ to aid
systematic management of PPH and a recent
study has suggested that use of this algorithm
‘HEMOSTASIS resulted in a logical and timely
approach for the management of PPH, can
help to stop more than 90% of cases of
massive postpartum haemorrhage .
 Fluid Resuscitation
• The best replacement is blood and blood
products but until these are available, a rapid
infusion of pre-warmed crystalloids such as
Hartmann solution (2 L) and colloids (1.5 L)
should be administered.
• If fully cross matched blood is still unavailable
by the time 3.5 L of fluid resuscitation and if
bleeding continues or haemodynamic
parameters deteriorate, then uncrossmatched
group specific blood or O Rh D negative blood
can be given if clinical situation demands so .
• British Committee of Standards in Haematology
has recommended haematological parameters
to be achieved in massive blood loss .
 Transfusion Strategies
• Fluid replacement is the initial resuscitating
step of PPH to normalize blood volume and
current recommendation is to infuse
crystalloids and colloids.
• However, this significantly worsens existing
coagulopathy and enhances fibrinolysis .
• Therefore, there is a drive to rapidly correct
coagulopathy by increasing the ratio of FFP
units to red blood cell (RBC), to increase the
chances of survival.
• A retrospective study analysing patients
receiving massive blood transfusion concluded
that survival rate improved with a high platelet
to RBC ratio (> 1:2) relative to patients with
low platelet to RBC ratio(<1:2) .
• A ratio of FFP:platelets:RBC = 1:1:1 was associated
with a significant reduction in mortality (40% versus
60%) as compared to the traditional 1 unit of FFP, 1
unit of platelets for every 4 units of blood transfused
(1:1:4 ratio).
• Based on this emerging evidence, our transfusion
strategy for massive PPH is very likely to change in
the future with platelets and FFP administrated
simultaneously with every unit of packed call (RBC)
transfusion to correct ongoing coagulopathy .
 Massive Transfusion
• The morbidity and mortality associated with
massive PPH is often accompanied by a triad
of hypothermia, acidosis and coagulopathy.
• This has led to the development of predefined
protocol driven early transfusion of RBC,
platelets, FFP and crystalloid solutions which
may allow significant improvement in
outcomes .
• Compatible whole blood is ideal for treatment of
hypovolemia from catastrophic hemorrhage.
• It has a shelf life of 40 days, and 70 percent of the
transfused red cells function for at least 24 hours
following transfusion.
• One unit raises the hematocrit by 3 to 4 volume percent.
• Important for obstetrical hemorrhage, whole blood
replaces many coagulation factors in obstetrics—
especially fibrinogen— and its plasma treats
hypovolemia.
Transfusion - related acute lung injury (TRALI)

• It is the most common cause of transfusion-related

mortality.
• The syndrome is characterized by severe dyspnea, hypoxia,
and noncardiogenic pulmonary edema that develop within
6 hours of transfusion
• Although the pathogenesis is incompletely understood,
injury to the pulmonary capillaries may arise from anti-
human leukocyte antigen (HLA) and neutrophil (HNA)
antibodies in donor plasma .
• Management is supportive and may include mechanical
ventilation .
Thank You
 Amnionic Fluid Embolism

• The classic triad of abrupt hemodynamic and

respiratory compromise along with DIC
underpins its diagnosis .
• Most reports describe a frequency of 1 in
40,000 to 1 in 50,000 .
• The case-fatality rate in all of these studies
ranges from 11 to 43 percent.
• Predisposing conditions are rapid labor, meconium-
stained fluid, and tears into uterine and other large
pelvic veins that permit an exchange of fluids
between the maternal and fetal compartment .
• Other commonly cited risks include older maternal
age; postterm pregnancy; labor induction or
augmentation; eclampsia; cesarean, forceps, or
vacuum delivery; placental abruption or previa;
and hydramnios .
• The classic example is dramatic, and a woman
in the late stages of labor or immediately
postpartum begins gasping for air.
• Seizures or cardiorespiratory arrest rapidly
follows accompanied by massive hemorrhage
from consumptive coagulopathy.
• Clinical manifestations are variable.
• The mechanism of injury from amnionic fluid
embolism has evolved.
• Early theories proposed that amnionic fluid
and debris entered maternal circulation and
obstructed pulmonary artery flow, which led
to hypoxia, right heart failure, and death.
• Current explanations describe disruption of the
maternal-fetal interface, which allows material
from the fetal compartment to enter maternal
circulation.
• This leads to abnormal activation of
proinflammatory mediator systems, similar to
the systemic inflammatory response syndrome
(SIRS), and causes initial, transient pulmonary
vasoconstriction and hypertension.
• Acute right ventricular failure is then followed
by hemodynamic collapse from right
ventricular infarction coupled with
interventricular septum displacement to the
left and ultimately decreased left-sided cardiac
output.
• This right and now left ventricular dysfunction
is followed by cardiogenic pulmonary edema
and systemic hypotension.
• Concurrently in this process, acute respiratory
failure with severe hypoxemia from shunting
develops.
• Notably, the resulting multiorgan dysfunction
is an interrelated process, with both the
cardiac and pulmonary systems aecting each
other.
• Women who survive beyond these first phases
invariably have the third component of the
classic triad—a consumptive coagulopathy .
• If resuscitation is successful, hemodynamic
instability is common in survivors.
• Beginning either immediately after cardiopulmonary
collapse or during the ensuing phases of injury, a
coagulopathy develops in most cases from activation of
factor VII and X.
• This may be exacerbated by ongoing hemorrhage.
• A common source of obstetrical bleeding is uterine
atony.
• Therefore, immediate evaluation of coagulation
parameters is prudent with concurrent clinical
management of bleeding.
Thank You