OBSTETRICS HEMORRHAGE

KHADER MOHIDEEN, MOHAMMED UMAR

 CONTENTS
• MECHANISM OF NORMAL HEMOSTASIS
• TIMING
• RISKS
• BLOOD LOSS ESTIMATION
• ANTEPARTUM HEMORRHAGE
– PLACENTA ABRUPTIO
– PLACENTA PREVIA
– PLACENTA ACCRETA
• POSTPARTUM HEMORRHAGE
– UTERINE ATONY
– UTERINE INVERSION
– INJURIES TO THE BIRTH CANAL
– UTERINE RUPTURE
– PUERPERAL HEMATOMAS
• MANAGEMENT OF HEMORRHAGE
• CASE 17
• OBSTETRICAL HEMORRHAGE along with
hypertension and infections comprises the
infamous “triad” of causes of maternal death
in both developed and underdeveloped
countries.
 MECHANISM OF NORMAL HEMOSTASIS
●
Increased blood flow If, after delivery, the
●
At least 600 mL/min flows through the intervillous
myometrium contracts
At term ●
space which circulate through 120 spiral arteries
Has low pressure system due to absence of
muscularis layer after endotrophoblastic
remodeling
vigorously, fatal
hemorrhage from the
placental implantation
site is unlikely.

An intact coagulation
system is not necessary
for postpartum
hemostasis unless there
After ●

●
Blood vessels are avulsed
Hemostasis
are lacerations in the
uterus, birth
Placental ●

●
-Myometrial contraction
-Clotting canal, or perineum.
separation ●
-Obliteration of the lumen
 TIMING
ANTEPARTUM HEMORRHAGE POSTPARTUM HEMORRHAGE
• Bleeding during various • loss of ≥500 mL of blood after
completion of the third stage of labor.
times in gestation
Early postpartum hemorrhage
• Bleeding within 1st 24 hours
postpartum
Late postpartum hemorrhage
• Bleeding after the 1st 24 hours
postpartum
• Seen in up to 1% of women
 RISKS
Hemorrhage can manifest at any time
throughout pregnancy,delivery, and the
puerperium.
BLOOD LOSS ESTIMATION
 BLOOD LOSS ESTIMATION

• Estimated blood loss – like beauty – is in the eye of the beholder

• A treacherous feature of postpartum hemorrhage is the failure of the pulse
and blood pressure to undergo more than moderate alterations until large
amounts of blood have been lost.
Special considerations
• Conditions when pregnant women are susceptible to hemorrhage
– Small women
– Preeclampsia/ Eclampsia
– Chronic renal insufficiency – when excessive hemorrhage is suspected in these
patients, crystalloid and blood are promptly administered for suspected hypovolemia
 ANTEPARTUM HEMORRHAGE
• Slight vaginal bleeding is common during active labor
• Bloody show – a consequence of effacement and dilation
of the cervix with tearing of small vessels
• Vasa Previa – placental vessels may overlie the cervix due to
velamentous insertion of the umbilical cord
• Any pregnancy with antepartum bleeding remains at higher
risk for an adverse outcome even though bleeding has
stopped and placenta previa has been excluded
 PLACENTAL ABRUPTIO

• Either partially or totally separation of the placenta from its

implantation site before delivery
• “Rending asunder of the placenta”
• Premature separation of the normally implanted placenta
• Initiated by hemorrhage into the decidua basalis then splits,
leaving a thin layer adhered to the myometrium
• Process begins as decidual hematoma expands to cause
separation and compression of the adjacent placenta
• Most blood in the retroplacental hematoma in a nontraumatic
placental abruption is maternal because hemorrhage derives from
separation within the maternal decidua and placental villi are
usually initially intact.
• Seen on a freshly delivered placenta as a circumscribed depression
on the maternal surface
• The diagnosis is typically reserved for pregnancies over 20 weeks
AOG
• - If <20 weeks AOG, the diagnosis is Abortion
MAJOR CLINICAL FINDINGS
• Vaginal bleeding
• Abdominal pain
• Hypertonic uterine contractions/Uterine tenderness
• Non-reassuring fetal heart rate – late or fetal
bradycardia
 TYPES:
• REVEALED – blood tracts down between
the membranes and decidua and
escapes to the cervix into the vagina
• Manifestation: moderate to profuse
vaginal bleeding

• CONCEALED – blood accumulates

behind the placenta with no obvious
external bleeding
• Manifestation: Hypertonus or
abdominal pain
 CLINICAL CLASSIFICATION:
1. SEVERE ABRUPTIO PLACENTA
• Whether the mother is unstable (significant coagulopathy, hypotension and/or
ongoing major blood loss)
• FHR is non-assuring (persistent fetal bradycardia, late decelerations, loss of
variability, or sinusoidal FHR pattern, or a non-assuring BPP score)
2. NON-SEVERE ABRUPTIO PLACENTA
• Where the FHR pattern is reassuring, maternal vital signs are normal, lab tests are
normal, mild to moderate bleeding
3. MINOR ABRUPTIO PLACENTA
• Minimal signs and symptoms where the mother is stable, fetal status is reassuring,
lab tests are normal and active bleeding has stopped
• Rupture of maternal vessels in the decidua basalis where it interfaces
with anchoring villi of the placenta
• The accumulating blood splits the decidua separating a thin layer of
decidua with its placental attachment from the uterus

• Bleeding may continue to dissect through the placentaldecidual interface

• Complete or near complete placental separation

• Unable to exchange gas and nutrients

• Fetal compromise
Decidua basalis is the problem in Abruptio Placenta
• It may be due to acute process resulting from:
• Shearing forces resulting from trauma (“Nagpahilot” or
accident)
• Sudden uterine decompression resulting from membrane
rupture with hydramnios
• Cocaine usage leading to acute vasoconstriction with
resultant placental separation
THROMBIN
2 Pathways:
• 1. Decidual bleeding leads to release of tissue factor
(thromboplastin) from decidual cells which generate thrombin.
• 2. Decidual hypoxia induces production of VEGF which acts
directly on the decidual endothelial cells to induce aberrant
expression of tissue factor which then generates thrombin.
The production of thrombin leads to the following clinical sequelae:
• Uterine hypertonus and contractions
• Enhanced expression of matrix metalloproteinases – production of
cytokine from membrane rupture that cause infection – there is a
sudden decompression
• Triggering of coagulation
• Functional progesterone withdrawal
PREDISPOSING FACTORS
Demographic Factors
• Advancing maternal age: 2.3x in women >40 y/o
• Multiparity
• Race (Black and white women)
• Familial association
PREDISPOSING FACTORS
Pregnancy-Associated Hypertension
• Gestational hypertension
• Preeclampsia
• Chronic hypertension
• Combination thereof
• HYPERTENSION AND PREECLAMPSIA – the most frequent
condition associated with abruption placenta
PREDISPOSING FACTORS
Preterm Prematurely Ruptured Membranes (PPROM)
– Incidence of 3.1% if membranes were ruptured for >24 weeks
– 3-fold risk if with infection
 Prior Abruption
– a 6. 5-fold higher risk for recurrence of a "mild" abruption
– and 11.5-fold risk for a "severe" abruption.
– For women who had two severe abruptions, the risk for a third was increased 50-fold.
 Other associations
– Cigarette smoking
• 2-fold risk in smokers
• 5 to 8-fold risk in smokers with chronic hypertension, preeclampsia, or both
– Cocaine abuse
– Uterine leiomyomas – especially if located near the mucosal surface behind the placental implantation site
– Isolated single umbilical artery – 3.4 fold increased risk
DIAGNOSIS
Clinical
• Presence of retroplacental clots/bleeding (77.1%)
• Vaginal bleeding with uterine hypertonicity (27.2%)
• Vaginal bleeding with NRFS (16.1%)
• Fetal Demise (>50% placental separation)
DIAGNOSTICS
• EFM
• Hemoglobin/Hematocrit
• PT/PTT – DIC
• Fibrinogen/FDPs: best
correlation with severity of
bleeding
• Kleihauer-Betke Electrophoresis
– assess volume of anemia
• Ultrasound
Sonographic Features
• 1) Retroplacental hematoma
(hyperechoic, isoechoic, hypoechoic)
– “classic ultrasound finding”
• 2) Pre-placental hematoma – jiggling
appearance with a shimmering effect
of the chorionic plate with fetal
movement
• 3) Increase placental thickness and
echogenecity
• 4) Subchorionic or marginal collection
DIFFERENTIAL DIAGNOSIS
• Negative findings with sonographic
examination do not exclude placental
abruption.
• Abruption is the most common cause of
clinically profound consumptive coagulopathy
DIFFERENTIAL DIAGNOSIS
• Hypovolemic Shock
– Complicated by massive and sometimes torrential
hemorrhage
– Blood loss - atleast half of the pregnant blood volume.
– Massive blood loss and shock can develop with a
concealed abruption
• Consumptive Coagulopathy (Consumptive coagulopathy or
Disseminated intravascular coagulation)
– Abruption is the most common cause of clinically
profound consumptive coagulopathy
– Defibrination Syndrome – mainly placental abruption
and amnionic fluid embolism
– intravascular activation of clotting
– An important consequence of intravascular coagulation is
the activation of plasminogen to plasmin, which lyses
fibrin microemboli to maintain microcirculatory patency
– more likely with a concealed abruption because
intrauterine pressure is higher.
• Couvelaire Uterus (Uteroplacental apoplexy)
– widespread extravasation of blood into the uterine
musculature and between the serosa.
– 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
• End-Organ Injury
• Acute Kidney Injury
- Delayed or incomplete treatment of hypovolemia with
severe placental abruption
- Preeclampsia
- Reversible and not so severe as to require dialysis
- Long-term outcomes are good
• Acute Cortical Necrosis – irreversible
• Sheehan Syndrome – pituitary failure, follows severe
intrapartum or early postpartum hemorrhage
MANAGEMENT
• Initial management:
– Immediate continuous fetal monitoring
– Secure IV access (Closely monitor
mother’s hemodynamic status)
– Keep maternal O2 saturation >95%
– Estimate the extent of blood loss – secure
blood products
• Confirm Placenta Abruptio,
• Ex. Patient abdominal pain with minimal bleeding
• Amniotomy – artificial rupture of bag of water
– diagnostic – bloody amniotic fluid - and
– therapeutic – prevents the release of thromboplastin
through the maternal circulation that can cause DIC)
Management approach for specific AOG and mother’s condition
• Expectant management is appropriate for non-severe and minor abruptio as
long as the mother is stable and tests for fetal well-being are reassuring.
Pregnancies <34 weeks Pregnancies at 34-36 weeks
• Expectant management is reasonable if mother is stable • Conservative management is reasonable if the
and tests for fetal well-being are reassuring.
mother is stable, fetal status is reassuring, laboratory
• NST, BPP weekly
tests are normal, active bleeding has stopped.
• Serial sonographic estimation of fetal weight to assess IUGR
• But since these patients remain at risk of developing
• Corticosteroids to promote fetal lung maturity
a sudden severe abruption, we tend to deliver.
• No compelling data to guide the length of hospital stay as
long as the mother is monitored in the hospital until the • Delivery before 37 weeks AOG is indicated if
bleeding has subsided at least 48 hours, FHR and UTZ are additional complications arises (IUGR, Preeclampsia,
reassuring, and patient is asymptomatic. PPROM, NRFS, recurrent abruption with maternal
• Schedule delivery at 37-38 weeks instability).
Cesarean Delivery
• The compromised fetus is usually best served
by cesarean delivery and the speed of
response is an important factor in perinatal
outcomes.
• Major hazard is imposed by clinically
significant consumptive coagulopathy.
• - Preparations include plans for blood and
component replacement and assessment of
coagulation – especially fibrinogen levels.
• Fetus dead, cervix closed, with severe
abdominal pain, 37 weeks – Cesarean Delivery
Vaginal Delivery
• If the fetus has died, vaginal delivery is
usually preferred.
• After vaginal delivery, uterotonic agents and
uterine massage are used to stimulate
myometrial contractions.
• Uterine muscle fibers compress placental site
vessels and prompt hemostasis even if
coagulation is defective.
• Exceptions: If there is a brisk hemorrhage
that it cannot be successfully managed even
by vigorous blood replacement.
Expectant Management with a Preterm Fetus
• Tocolytics- To delay delivery
• Terbutaline
• Magnesium sulphate
 PLACENTA PREVIA

• PREVIA means going before

• Describes a placental that is implanted
somewhere in the lower uterine segment,
either over or very near the internal cervical
os
 PLACENTA PREVIA

PLACENTAL MIGRATION
• Apparent movement of the low-lying placenta relative to the internal os
• Differential growth of the lower and upper uterine segments as
pregnancy progresses
• With greater upper uterine blood flow, placental growth more likely will
be toward the fundus (Trophotropism)
• Placentas that migrate most likely never were circumferentially implanted
with true villous invasion that reached the internal cervical os.
PLACENTA PREVIA

• A low-lying placenta is less

likely to migrate within a
uterus with a prior CS scar.
• Placentas that lie close to
but not over the internal
os up to the early third
trimester are unlikely to
persist as a previa by term
 PLACENTA PREVIA

Classification

• implantation in the • fetal vessels course

• Placenta was at the • The internal os is covered partially or
lower uterine segment. through membranes and
completely by placenta
• the placental edge does edge of the internal present at the cervical os
not cover the internal os os but did not Digital palpation in an attempt to ascertain
these changing relations
but lies within a 2-cm overlie it
wide perimeter around between the placental edge and internal os as the cervix dilates
the os usually causes severe hemorrhage!
 PLACENTA PREVIA

PATHOPHYSIOLOGY
• Placental bleeding – partial detachment
– gradual changes in the cervix and
– lower uterine segment apply shearing forces to the inelastic placental attachment site
PATHOGENESIS
• Presence of suboptimal endometrium in the upper cavity
due to previous surgery or pregnancies
• Implantation of thromboplastin or unidirectional growth of trophoblast toward the lower
uterine cavity
the most virgin site of uterine cavity is the lower uterine segment
• Large placental area
(multiple gestation or in response to reduced uteroplacental perfusion increases the likelihood that placenta
will cover or encroach upon the cervical os)
 PLACENTA PREVIA
RISK FACTORS:
• Advanced maternal age
• Multiparity
• Prior CS
• Cigarette smoking – related
to decidual coagulopathy
• Uterine Leiomyomas
CLINICAL FACTORS
• Women with one or more prior
cesarean deliveries
• Women with a prior uterine
incision and placenta previa
• Abnormally elevated Maternal
serum alpha-fetoprotein (MSAFP)
levels
• Assisted reproductive technology
(ART)
 PLACENTA PREVIA

CLINICAL PRESENTATION
• In the second half of pregnancy, the characteristic clinical presentation is
“painless vaginal bleeding” which occurs in 70-80% of cases.
• The uterine body remodels to form the lower uterine segment – 24 to 28 weeks
AOG (sentinel bleeding)
• The internal os dilates and some of the implanted placenta inevitably separates.
• Bleeding that ensues is augmented by the inherent inability of the myometrial
fibers in the lower uterine segment to contract and thereby constrict avulsed
vessels – lesser myometrial fibers in the lower uterine segment; greater in
fundus
 PLACENTA PREVIA

PREDICTIVE FACTORS OF HEMORRHAGE

• Placentas that cover the os bleed earlier and more than
placentas that are proximate to the os – Complete Placenta
Previa or Placenta Previa Totalis
• Placentas near the os have a greater risk of bleeding if the
placental edge is thick (>1cm) – Marginalis
• Identification of an echo-free space in the placental edge
covering the internal os or cervical length <3cm – Low-lying
 PLACENTA PREVIA

• DIAGNOSIS
• Previa should not be excluded until sonographic
evaluation has clearly proved its absence
• Double set-up technique is used if sonography is
not readily available
• A cervical digital examination is done with the
woman in an operating room and with
preparations for immediate cesarean delivery.
Even the gentlest examination can cause
torrential hemorrhage.
Transabdominal sonography
• Most accurate method of assessment
• Safe even when there is bleeding
• if the placenta clearly overlies the cervix or if it lies
away from the lower uterine segment, the
examination has excellent sensitivity and negative-
predictive value
• Restriction of activity is not necessary unless a
previa persists beyond 28 weeks or if clinical
findings such as bleeding or contractions develop
before this time.
A. In this transvaginal image at 34 weeks' gestation, the anterior placenta
• Follow-up TVS at 36 weeks
completely covers the internal cervical os outlined by arrows
B. This transvaginal image a t 34 weeks' gestation depicts a posterior
placenta (arrow) that just reaches the level of the internal cervical os.
 PLACENTA PREVIA

MANAGEMENT
• 3 Prominent Factors: Fetal Age and Maturity, Labor and Bleeding severity
• WHEN SHOULD PLACENTAL LOCALIZATION BE DONE?
• Routine ultrasound at 20 weeks AOG
• Follow-up ultrasound between 28-32 weeks if in the initial ultrasound revealed from
the placenta was found to cover the os.
• If at 32 weeks the placental edge is still <2cms from the internal os, or covering the
cervical os
HOW PLACENTA PREVIA IS BEST MANAGED?
• The primary goal therapy is to observe mother and fetus closely so that urgent
intervention can be arranged I deterioration occurs
 PLACENTA PREVIA

EXPECTANT MANAGEMENT
• Bed rest
• Symptomatic women often remain hospitalized from their initial or second significant bleeding episode until
delivery
• For asymptomatic women with 24-34 weeks AOG, they should receive corticosteroid to hasten fetal lung
maturity
ROUTE OF DELIVERY:
• In general, any degree of overlap after 35 weeks AOG is an indication for cesarean section as the route of
delivery.
• Elective CS: Asymptomatic – 38 weeks,
• For asymptomatic cases at term and in labor with marginal/low-lying placenta, labor may be allowed to
continue with careful monitoring and consultation in a double set-up situation (Both vaginal and cesarean
delivery).
 PLACENTA PREVIA

ROUTE OF DELIVERY:
• In general, any degree of overlap after 35 weeks AOG is an indication for cesarean section as the route of
delivery.
• Elective CS: Asymptomatic – 38 weeks,
• For asymptomatic cases at term and in labor with marginal/low-lying placenta, labor may be allowed to
continue with careful monitoring and consultation in a double set-up situation (Both vaginal and cesarean
delivery).
WHEN SHOULD DELIVERY BE SCHEDULED FOR TERM ASYMPTOMATIC PLACENTA PREVIA?
• ELECTIVE DELIVERY by CESAREAN SECTION in asymptomatic women is recommended at 38 weeks AOG
• Symptomatic – earlier – 37 weeks
Hysterectomy – necessary if these more conservative methods fail and bleeding is brisk
• For women whose placenta previa is implanted anteriorly at the site of a prior uterine incision, the likelihood of
an associated morbidly adherent placenta and need for hysterectomy is increased.
 PLACENTAL ACCRETA

• Morbidly Adherent Placenta –

– abnormally implanted, invasive or adhered placenta – collectively known as Accrete
Syndromes
• Abnormal placental adherence to the myometrium stems in part from partial
or total absence of the decidua basalis and imperfect development of the
fibrinoid or Nitabuch layer
• Decidual deficiency prevents normal placental separation after delivery
• One of the most common indications for emergency hysterectomy.
• Multidisciplinary team approach to reduce maternal morbidity and mortality.
 PLACENTAL ACCRETA

CLASSIFICATION

Chorionic villi are Chorionic villi Chorionic villi penetrate

DEPTH OF attached to the invade deeper through the entire
TROPHOBLASTIC myometrium but into the uterine wall or beyond
GROWTH not the muscle myometrium but the serosa and extend
not the serosa to adjacent structures
like bladder and bowel
 PLACENTAL ACCRETA
EFFECT ON THE MOTHER
• Risk of spontaneous rupture
• Profuse vaginal bleeding (1st trimester)
• Increased risk of massive hemorrhage
• Risks of hysterectomy, ARDS, renal failure, DIC, multiorgan failure, death
EFFECT ON THE FETUS
• Growth restriction
• Prematurity
 PLACENTAL ACCRETA
• WHO SHOULD BE SCREENED FOR PLACENTA
ACCRETA?
• *Continuous causing decidual damage and
deficiency
• Previous cesarean section – the placenta may
implant on the incision site
• Placenta previa – abnormal implantation
• Asherman’s Syndrome – intrauterine adhesion
–history of previous abortion (D&C) -
endometrial
• Previous uterine surgery
• Advanced maternal age
• Multiparity
 PLACENTAL ACCRETA
WHY SHOULD WE SCREEN FOR PLACENTA ACCRETA?
• Early detection of placenta accreta will allow the OB to plan the appropriate
management and address potential complications.
HOW IS SCREENING FOR PLACENTA ACCRETA DONE?
• Early sonographic markers suspicious for placenta accreta
• Low implanted gestational sac – near the lower uterine segment
• GS attached to the anterior myometrium
• Thin myometrium in the area of the cesarean section scar where the GS is attached
• Placental lakes and abnormal endomyometrial interface
 PLACENTAL ACCRETA
DIAGNOSIS
• Diagnosis of placenta accrete can be established antenatally using grayscale ultrasound combined with
Color Doppler. This can be complemented by MRI.
• TVS, TAB, TPS are complementary techniques and should be used as necessary.
• GRAYSCALE SONOGRAPHIC SIGNS OF PLACENTA ACCRETA
• Loss of normally visible retroplacental “clear space” or hypoechoic zone
• Progressive thinning of the retroplacental hypoechoic zone <2mm on serial exams
• Presence of multiple irregular placental lacunae (“swiss cheese appearance”) – most predictive
sonographic sign
• Thinning of focal disruption of the uterine serosa-bladder wall complex – PLACENTA PERCRETA
• Focal mass elevation of tissue with the same echogenecity as the placenta goes beyond the uterine
serosa.
 PLACENTAL ACCRETA
COLOR DOPPLER
• Dilated vascular channels with diffuse lacunar flow pattern
• Vascular lakes with turbulent lacunar flow
• Hypervascularity of serosa-bladder interface
• Markedly dilated peripheral subplacental vascular channels
• Poor vascularity at sites of loss hypoechoic zone
• Diagnosis is confirmed intraoperatively by the appearance of the
placental site and by careful observation for placental separation.
 PLACENTAL ACCRETA
INTRAOPERATIVE FINDINGS:
• Bulbous and distended lower uterine segment
• Extremely thinned out uterine wall – invaded the myometrium – leads to uterine rupture if there’s invasion of serosa
• Visible placental tissue or hemorrhages beneath the visceral peritoneum
• Numerous dilated and tortuous abnormal vessels
• Failure of the placenta to separate spontaneously or during a controlled traction
• Failure to find a cleavage plane between the placenta and myometrial wall when manual delivery is attempted.
• Profuse hemorrhage after placental separation.

• WHEN SHOULD IMAGING TO ESTABLISH THE DIAGNOSIS BE DONE?

• Women with previous cesarean section whose placenta lies anteriorly and reaches the cervical os should have further
imaging at 32 weeks to establish the diagnosis and allow planning for third trimester management and delivery.
• Sonography – used for antepartum identification of abnormally placental ingrowth
 PLACENTAL ACCRETA
• Preoperative assessment ideally begins once a possible accrete syndrome is recognized
antenally.
• A major decision concerns the timing of and the ideal facility for delivery.

HOW SHOULD WOMEN AT RISK OF PLACENTA ACCRETA BE COUNSELED ANTENATALLY?

• Women suspected of placenta accreta should be counseled about the need for early delivery,
need for hysterectomy, massive hemorrhage, transfusion reaction, injury to other organs,
severe morbidity and possibility of maternal death.
• Discussion of a management plan by the 32nd week should be made in consultation with the
woman and her family.
• Most affected organs are bladder and bowel.
 PLACENTAL ACCRETA
WHEN SHOULD DELIVERY BE SCHEDULED FOR TERM ASYMPTOMATIC PLACENTA PREVIA?
• Elective delivery by cesarean section in asymptomatic women is recommended at 38 weeks AOG
• Antenatal corticosteroids should be administered between 24-34 weeks AOG for pregnancies at
increased risk of delivery within 7 days.
• Tocolytic treatment in symptomatic women decreases the amount of uterine contractions, thus
decreases the risk of bleeding without increasing morbidity and mortality.
• Regardless of AOG, delivery with possible cesarean hysterectomy is warranted if significant bleeding is
present in patients suspected of or at risk of placenta accreta.
• In asymptomatic women, a planned late preterm delivery should be scheduled at 36-37 weeks after
giving corticosteroid to diminish the risk of prematurity and to ensure availability of necessary
personnel, facilities and blood products.
• Symptomatic: earlier 36 weeks
 PLACENTAL ACCRETA
• WHAT ARE THE MANAGEMENT OPTIONS FOR PLACENTA ACCRETA?
• A planned cesarean section hysterectomy with the placenta left “in situ” is
strongly considered among women suspected of placenta accreta
undesirous of future pregnancy
• Desirous: Give Methotrexate
• Conservative management with leaving the placenta in situ can be an option
in carefully selected cases when fertility is desired or when the conditions
for extirpative surgery is not optimum
• Confirmation of a pecreta or increta almost always mandates hysterectomy.
 Postpartum Hemorrhage
• Traditionally, defined as the loss of >500ml of blood after
completion of the third stage of labor
• American College of Obstetricians and Gynecologists definition:
o Cumulative blood loss of >1000mL accompanied by signs and
symptoms of Hypovolemia
• Frequent causes:
– Uterine Atony with Placental site bleeding
– Genital Tract Trauma
– Both
 Postpartum Hemorrhage
• Initial Examination – attempts to differentiate Uterine atony from Genital Tract
laceration
• Risk Factors
• Lower Genital Tract examination
• Uterine Tone assessmen
Uterine Atony Genital Tract Laceration
identified by a boggy, soft uterus during bimanual Persistent bleeding despite a firm, well-contracted
examination and by expression uterus.
of clots and hemorrhage during uterine massage. To confirm that lacerations are a source of
bleeding, careful inspection of the vagina, cervix,
and uterus is essential.

• Sometimes bleeding may be caused by both atony and trauma, especially after
 Blood Loss Estimation
• Visual estimates – inaccurate
• Postpartum bleeding – frequently steady (instead of sudden massive
hemorrhage)
• A treacherous feature of postpartum hemorrhage is the failure of the
pulse and blood pressure to undergo more than moderate alterations
until large amounts of blood have been lost.
• Susceptible to hemorrhage:
– Small women
– Patients with severe eclampsia/preeclampsia
– Patients with Chronic renal insufficiency
Causes of Postpartum Hemorrhage
 Uterine Atony

• most frequent cause of obstetrical hemorrhage

• failure of the uterus to contract sufficiently after delivery and to arrest bleeding from
vessels at the placental implantation site
Third-Stage Labor Management

• some bleeding is inevitable during third-stage labor as the placenta begins to separate.
• 2 mechanisms of placental separation:
– Duncan mechanism – blood from implantation site may escape into the vagina
immediately (“Dirty Placenta”)
– Schultze mechanism – blood remains concealed behind the placenta and membranes
until the placenta is delivered (“Shiny Placenta”)
• Separation and delivery of the placenta by cord traction (atonic uterus)  uterine inversion
 Third-Stage Labor Management
• If heavy bleeding persists after delivery of the newborn
and while the placenta remains partially or totally
attached, then manual placental removal is indicated
• The fundus is always palpated following placental
delivery to confirm that the uterus is well contracted.
• If it is not firm:
– Do vigorous fundal massage and
– Give 20 units of oxytocin in 1000 mL of crystalloid solution given intravenously at 10 mL/min for a dose of 200 mU/min.

• Oxytocin is never given as an undiluted bolus dose

because serious hypotension or cardiac arrhythmias
can develop.
Risk Factors
 Evaluation and Management

• Careful inspection is done to exclude birth canal laceration.

• Inspection of the placenta after delivery should be routine - bleeding can be caused by
retained placental fragments
• If a defect is seen, the uterus should be manually explored and the fragment removed
• Occasionally, retention of a succenturiate lobe may cause postpartum hemorrhage
• During examination, the uterus is massaged and uterotonic agents are administered.
 Uterotonic Agents

OXYTOCIN
• 20 units of oxytocin in 1000 mL of crystalloid solution given intravenously at 10 mL/min

ERGOT ALKALOIDS – 2nd line

• Methylergonovine (Methergine) and ergonovine
• Given parenterally
• Rapidly stimulate tetanic uterine contractions and act for approximately 45 minutes
• 0.2 mg of either drug given intramuscularly.
• Methergine can be repeated at 2- to 4-hour intervals as needed
• may cause dangerous hypertension, especially in women with preeclampsia
 Uterotonic Agents

Carboprost tromethamine (Hemabate)

• 15-methyl derivative of prostaglandin F2α
• dose of 250 μg (0.25 mg) given intramuscularly
• side effects: 20 % of women: diarrhea, hypertension, vomiting, fever, flushing, and tachycardia
• pulmonary airway and vascular constriction  not for asthmatic women with suspected amnionic fluid
embolism
• Relative contraindications: renal, liver, and cardiac disease
 Uterotonic Agents

DINOPROSTONE
• prostaglandin E2
• Given as a 20-mg suppository per rectum or per vagina every 2 hours
• causes diarrhea, vigorous vaginal bleeding may preclude its use per vagina
• Contraindication: Hypotension

SULPROSTONE
• Intravenous prostaglandin E2

MISOPROSTOL (CYTOTEC)
• synthetic prostaglandin E1 analogue
• dose of 600 to 1000 μg rectally, orally, or sublingually
 Bleeding unresponsive to uterotonic agents

Management Steps:
1.Begin bimanual uterine compression
2.Immediately mobilize team to the delivery room and secure blood (WB or packed RBC)
3.Request urgent help from the anesthesia team
4.Secure at least 2 large-bore IV catheters and insert an indwelling Foley catheter for UO
monitoring
5.Begin volume resuscitation with rapid IV infusion of crystalloid
6.Manually explore the uterine cavity
7.Thoroughly inspect the cervix and vagina again
8.If the woman still unstable or persistent hemorrhage, blood transfusions are given
 Bleeding unresponsive to uterotonic agents

• Bimanual compression for the uterine atony.

• The posterior uterine wall is massaged by one
hand on the abdomen, while the other hand
is made into fist and placed into the vagina.
• This fist kneads the anterior uterine wall
through the anterior vaginal wall and the
uterus is also compressed between the two
hands.
 Balloon Tamponade

• Uterine packing
• 24F to 30F Foley catheter with a 30-mL balloon
is guided into the uterine cavity and filled with
60 to 80 mL of saline
• The open tip permits continuous drainage of
blood
• removed after 12 to 24 hours if bleeding
subsides
• Bakri postpartum balloon or BT cath  300 –
500 ml
Surgical Procedures

UTERINE COMPRESSION
SUTURES
• This surgical technique uses
a no. 2 chromic suture to
compress the anterior and
posterior uterine walls
together
• Because they give the
appearance of suspenders,
they are also called braces
 Surgical Procedures

UTERINE ARTERY LIGATION

• used primarily for lacerations at the lateral
part of a hysterotomy incision
• less helpful for hemorrhage from uterine
atony
 Surgical Procedures

INTERNAL ILIAC ARTERY LIGATION

• ligation of one or both internal iliac arteries has been used to
reduce pelvic hemorrhage.
• Drawbacks are that the procedure may be technically difficult
and is only successful half of the time
• It is not particularly helpful for abating hemorrhage with
postpartum atony
• Most important MOA: 85% reduction in pulse pressure in
those arteries distal to the ligation
• This creates vesselsmore amenable to hemostasis via
pressure and clot formation.
 Surgical Procedures
ANGIOGRAPHIC EMBOLIZATION
• This modality is now used for many causes of intractable hemorrhage when surgical access is difficult.
• In more than 500 women reported, embolization was 90-percent effective (Grönvall, 2014; Lee, 2012;
Poujade, 2012; Zhang, 2015).
• Rouse (2013) concluded that embolization can be used to arrest refractory postpartum hemorrhage.

HYSTERECTOMY
• completely or partially remove the uterus
• most commonly performed to arrest or prevent hemorrhage from intractable uterine atony or
abnormal placentation
• It is more often completed during or after cesarean delivery but may be needed following vaginal
birth.
 Uterine Inversion

• Associated bleeding is often massive

• Most common cause: traction applied to umbilical cord while uterus is relaxed
• Risk factors:
• fundal placental implantation
• uterine atony
• cord traction applied before placental separation
• abnormally adhered placentation (accrete syndromes)
 Uterine Inversion
• Classification according to occurrence after delivery
• Acute (MC)-immediately or w/in 24 hours after delivery
• Subacute- after 1st 24 hours and within 4 weeks
• Chronic- after more than 4 weeks
• Classification according to anatomical severity
• 1st stage- uterine base in uterine cavity, do not cross cervix
• 2nd stage- uterine base crossed cervix and passed through vagina
• 3rd stage- visualization of uterine bases at vulva
• 4th stage- vaginal walls participate with inversion
 Uterine Inversion

• Incomplete inversion
• uterine fundus has inverted and lies within the
endometrial cavity without extending beyond
the external os
• Complete inversion
• fundus is inverted and extends beyond the
external os
 Uterine Inversion

• Incidence: 1 in 2000 to 1 in 20,000 vaginal deliveries

• Recognition and management
– Immediate recognition improves the chances of a quick resolution and good
outcome
– Bimanual examination
– Mistaken for myoma, resolved by sonography
– Associated with life threatening hemorrhage
 Uterine Inversion
MANAGEMENT
– Immediate assistance
– Secure blood products
– Patient evaluated for emergency general anesthesia. Large-bore intravenous
infusion systems are secured to begin rapid crystalloid infusion to treat
hypovolemia while awaiting arrival of blood for transfusion
– Replace uterus by pushing the inverted fundus with the palm of hand and fingers
in the direction of long axis of vagina
– If placenta still attached,
• intravenously administered tocolytic drug (terbutaline, magnesium sulfate,
or nitroglycerin) for uterine relaxation and repositioning
• Fails: a rapidly acting halogenated inhalational agent
 Uterine Inversion
Management
– After placental removal, steady pressure with the fist, palm, or fingers is applied to the
inverted fundus in an attempt to push it up into and through the dilated cervix.
– Uterus restored to normal position, stop tocolysis, infuse oxytocin
– Bimanual compression until the uterus is well contracted
– Monitor for subsequent inversion
 Uterine Inversion
Surgical intervention
– Laparotomy
– Huntington procedure: application of atraumatic
clamps to each round ligament and upward
traction
– Haultain incision: longitudinal surgical cut
posteriorly through the ring to expose the fundus
and permit reinversion

Hysterectomy is the last resort

Antibiotic prophylaxis is advisable
– - Single dose of ampicillin 2gms/IV or Cefazolin 1
gm/IV plus Metronidazole
Injuries to the Birth Canal
 Injuries to the Birth Canal
• Vulvovaginal laceration
• Common at anterior vaginal wall near urethra
• Levator sling injuries
• Involve in deep vaginal vault laceration
• Sustain stretch injuries (overdistension)
• Pubococcygeus  urinary incontinence
• Cervical laceration
• not problematic unless hemorrhage or extend to upper 3rd of vagina
• Colphorrhexis – rare injury, cervix is entirely or patially avulsed from the
vagina in the anterior, posterior or lateral fornices
• Annular or circular detachment – rare injury, entire vaginal portion of the
cervix is avulsed
 Injuries to the Birth Canal
MANAGEMENT
• 1-2cm laceration are not
repaired unless bleeding
• Surgical repair is done for
bleeding and deep cervical
lacerations
• Angiographic embolization
for high cervical tear with
failed surgical intervention
PREVENTION
• Restricting the use of
episiotomy
• If indicated, mediolateral
episiotomy reduce 3rd and
4th degree lacerations while
median episiotomy reduces
perineal bruising
• vacuum extraction
 Uterine Rupture
COMPLETE
• Involves the full thickness of the uterine
wall, with or without expulsion of the fetus
and/or placenta and include rupture of
membranes at the site of rupture

INCOMPLETE/UTERINE DEHISCENCE
• When the uterine wall ruptures but the
visceral peritoneum remains intact
• It is usually asymptomatic and the diagnosis
is made incidentally at the time of CS.
 Uterine Rupture
• PRIMARY – occurring in a previously intact or unscarred uterus
• SECONDARY – associated with a preexisting incision, injury or anomaly of the myometrium
 Uterine Rupture
Pathogenesis:
• Rupture of previously intact uterus during labor most often involves the thinned out lower
uterine segment.
• Tears develop primarily in the lower uterine segment, they can extend upward into the active
segment or downward through the cervix and into the vagina.
• In some cases, the bladder may also be lacerated.
• If the rupture is of sufficient size, the uterine contents will usually escape into the peritoneal
cavity
 Uterine Rupture

Management
• Hysterectomy should be considered the treatment of choice when intractable uterine
bleeding occurs or when the uterine rupture sites are multiple, longitudinal, or low-lying
• Rupture of previous CS scar often can be managed by revision of the edges of the prior
incision followed by primary closure.
 Puerperal Hematomas
• Associated with laceration, episiotomy and operative vaginal delivery
• Vulvar hematomas – involve vestibular bulb or branches of the pudendal
artery, which are the inferior rectal, perineal and clitoral arteries.
• Paravaginal hematomas – involve the descending branch of the uterine artery
• Continued bleeding may dissect retroperitoneally to form a mass palpable above the inguinal
ligament
 Puerperal Hematomas

DIAGNOSIS
• Severe excruciating perineal pain (not relieved by pain relievers)
• Tense, fluctuant and tender vulvar swelling of varied sizes covered with discolored skin
• Pelvic pressure, pain and inability to void and discovery of a round fluctuant mass encroaching
the vaginal lumen  paravaginal hematoma
• Supralevator extension  hematoma extends to the paravaginal space and broad ligament -
Causes hypovolemic shock and death
• CT scan or sonography
 Puerperal Hematomas
MANAGEMENT
• Vulvovaginal hematomas are managed according to their size, location, duration since delivery and
expansion
• If bleeding ceases, small to moderate hematomas may be treated expectantly until absorbed
• If the hematoma continues to enlarge, surgical exploration is preferable.
• Angiographic embolization for supralevator or retroperitoneal hematomas.
• Bakri balloon for paracervical hematoma
 Retained Placenta
• placenta has not been delivered within one hour after the birth of the baby
• Signs of placental separation
• Sudden gush of blood
• Calkin’s sign (uterus is firm and globular)
• Lengthening of cord
• Uterine fundus rises in the abdomen
• MANAGEMENT
• Umbilical vein injection of oxytocin solution- inexpensive and simple
intervention that could be performed while placenta delivery is awaited
• manual extraction of the placenta (definitive plan)
 Coagulation Defects
• Coagulation defects can cause hemorrhage.
• These defects should be suspected in patients who have not
responded to the usual measures to treat postpartum hemorrhage
or who are oozing from puncture sites.
• Potential causes: Platelet dysfunction, Inherited coagulopathy,
Disseminated intravascular coagulation
• Evaluation should include a platelet count and measurement of
prothrombin time, partial thromboplastin time, fibrinogen level
and quantitative D-dimer assay.
MANAGEMENT OF HEMORRHAGE

• HYPOVOLEMIC SHOCK is managed with

immediate resuscitation with crystalloids and
blood (for Hgb ≤7g/dL or Hct <25%)
• One unit raises the hematocrit by 3 to 4
volume percent.
Case 17
 Case 17
• Name : S.M
• Age : 35
• DOB : June 03 1985
• Address : Caritan sur, Tuguegarao city
• Marital status : Married
• Occupation : Housewife
• Religion : Roman Catholic
 Case 17
• Chief complaint
– Profuse vaginal bleeding
HPI
• 2 Days PTA
– patient experienced occasional uterine contractions.
– No consultation
• Few hoursPTA
– Profuse vaginal bleeding soaking 2 adult diapers
PMI
• Childhood Illness: None
• Adult Illness: None
• Immunizations: Unrecalled
• Allergies: No allergies to food and
medication
Family History
• Youngest of two siblings
• No known history of hypertension, diabetes,
asthma, TB, thyroid disease, seizure, stroke,
bleeding disorder, cancer, renal disease
• Personal and Social History
– High School Graduate
– Unemployed
– Non - smoker
– Non - alcoholic beverage drinker
– Denies use of illicit drugs
•
Menstrual History
• Menarche:12 years old
• SMP: Occur at monthly regular interval
lasting 3-4 days
2 pads per day, moderately soaked
• LMP: may 05, 2020
• AOG 37 weeks AOG
Sexual History
• Coitarche: 19 years old
• With 1 sexual partner
• No history of STI
Obstetric History
• G5P4(4004)
– G1 – 2010, Term, NSD, CVMC, Living
– G2 – 2012, Term, NSD, CVMC, Living
– G3 - 2015, Term, NSD. CVMC, Living
– G4 - 2018, Pre term, CS ,Placenta abruptio, CVMC, living
– G5 - Present pregnancy
• AOG 37 WEEKS
ROS
• General: (-) fever, (-) decrease appetite, (-) easy fatigability, (-) weight loss
• Integumentary: (-) pruritus, (-) change in skin and nail color, (-) rashes
• Respiratory: (-) cough, (-) hemoptysis, (-) dyspnea
• Cardiovascular: (-) chest pain, (-) palpitations, (-) orthopnea
• Gastrointestinal: (-) vomiting, (-) constipation, (-) diarrhea
• Genitourinary: (-) hematuria, (-) nocturia, (-) dysuria
• Musculoskeletal: (-) muscular weakness, (-) joint pain, (-) stiffness, (-) leg cramps,
(-) fasciculations or tremors
• Hematologic: (-) easy bruising
PE
• General Survey :
– She is conscious, coherent and in cardiorespiratory distress.
• Vital signs
– Temperature: 36 C (Axillary; L)
– Respiratory rate: 23 cycles per minute
– Heart rate: 105 beats per minute
– Blood pressure: 80/50 mmHg (supine)
• Skin: Warm to touch, No rashes. No lesions. Nails without clubbing (+) pallor
• Neck: Trachea midline, no cervical lymphadenopathy, no palpable neck mass
• HEENT: Normocephalic, atraumatic. Pinkish conjunctiva, anicteric sclera,
pupils equally reactive to light. No hearing impairment. No nasal discharge.
Mucosa is pale, tongue is in midline.
• Chest and Lungs: Symmetrical chest expansion, no chest retractions, clear
breath sounds
• Heart: Adynamic precordium, regular rhythm, PMI in the 5th ICS at left MCL,
no heart murmur
• Abdomen: Globular, FH:27cm,EFW: 2480g, FHT: 120 bpm
– LM1: Irregular nodular mass
– LM2: Linear, convex, bony ridge on the left
– numerous nodulations on the right
– LM3: Round, ballotable mass
– LM4: Cephalic prominence is on the same side with fetal back
• Genitalia: Grossly female
– IE: cervix closed,profuse vaginal bleeding
• EXTREMITIES: No edema. Full and equal pulse. No gross deformities
• NEUROLOGIC: Oriented to person, place, and time
– Sensory: Intact
– Motor: Good muscle bulk and tone. Strength 5/5
– Cranial nerves: Intact
SALIENT FEATURES
• 35 year old, G5P4, 37 weeks AOG
• History of previous CS due to placental abrution, 2018, CVMC
• Uterine contractions
• Gross palor
• Tachypneic
• Tarchycardic
• Hypotensive
• Profuse vaginal bleeding
 ddx
Placenta abruptio
Rule in Rule out
Age
G5P4
Previous cs with abruptio
Uterine contractions
Gross pallor
Hypovolemia
Cardiorespiratory distress
IE:Profuse vaginal bleeding
• Uterine rupture
Rule in Rule out
Age (-) Palpable fetal parts
G5P4 (-) lacerations in IE
Previous cs
Gross pallor
IE:Profuse vaginal bleeding
• Placenta previa
Rule In Rule out
Age IE: (-)Placenta
G5P4
Previous cs
Gross pallor
Hypovolemia
IE: Profuse vaginal bleeding
• Preterm labor
Rule in Rule out
37 weeks AOG (-) cervical dilation
Uterine contractions
Vaginal bleeding
Impression
• G5P4(4004), Pregnancy uterine, 37 weeks
AOG by LMP, cephalic, t/c severe placenta
abruptio, hypovolemic shock secondary,
anemia severe secondary, previous CS
(PRETERM)due to placenta abruptio(2018,
CVMC)
PLAN:
• Admit the patient • Blood products
• Secure consent for admission and
management • Secure consent for CS
• TPR qshift and record and counsel for
• Double IVF PLRS
• Diagnostics
hysterectomy
–
–
CBC with PC
Blood typing with cross matching • Inform relatives
– PT,PTT
– Urinalysis
• TAS
• Hook to EFM, monitor FHT
• Monitor vital signs and UO every 1 hr
• Insert IFC aseptically and connect to urine bag
 Quiz by doc CJ MAXIMO
• 1-4 common causes of PPH
• 1. Tone- chorioamnionitis, overdustended
uterus, grand multiPARITY, fibroids
• 2. Tissue- placental abnormality (accreta,
percreta, increta), uterine surgery, manual
placental removal
• 3. Trauma- lacerations, large episiotomy,
vacuum/forceps delivery
• 4. Thrombin- previous history of pospartum
hemorrhage, anticoagulants, coagulopathy.
• 5. Early pph- blood loss within 24h of
delivery. Late pph- blood loss after 24h but
less than 12 weeks after delivery
• 6. risk factors of placenta abruption:Prior
abruption, preeclampsia/hypertension,
chorioamnionitis, prom, smoking, coccaine
use, hydramnios, increased age and parity,
trauma, mutifetal gestation, myoma
• 7.NON surgical management of PPH: Uterine
massage, bimanual uterine conpression,
uteritonics, uterine balloon tamponade
• 8. surgical management fo PPH:Uterine
artery ligation, hypogastric artery ligation, B
lynch compression, uterine artery
embolization, hysterectomy
• 9. diagnostic for placenta previa:
Transabdominal/transvaginal sonography
-Answers were sent by doc cj