Late pregnancy bleeding

KAREEM AYMAN SULTAN

200008
 Objectives

 1. Identify major causes of vaginal bleeding

in the second half of pregnancy.
 2. Describe a systematic approach to
identifying the cause of bleeding.
 3. Describe specific treatment options based
on diagnosis.
 Case

 A 30 year old G1P0 is undergoing oxytocin

augmentation at 36 weeks for preeclampsia. Her
blood pressure has been as high as 170/110 and she is
receiving an intravenous infusion of magnesium
sulfate. Her cervix has been 6 cm dilated for one hour
and she has begun to complain of pain between
contractions. A large amount of vaginal bleeding
follows her next cervical check.
 Introduction

 Obstetrical hemorrhage is one of the

leading causes of maternal morbidity and
mortality throughout the world.
 it is responsible for 17% to 25% of all
pregnancy-related deaths
 PREGNANCY-RELATED
HEMODYNAMIC CHANGES
4 significant hemodynamic changes:
 1- Plasma volume: 40% to 50% increase in plasma volume by the
30th week of gestation.
Increase in red blood cell mass: increase 20% to 30% by the end of
pregnancy
 2- Maternal cardiac output rises: the average rise is 30% to 50%
above nonpregnant levels.
 3- Systemic vascular resistance falls.
 4- fibrinogen and the majority of procoagulant blood factors (II,
VII, VIII, IX, and X) increase during pregnancy.
 PHYSIOLOGIC ADAPTATION
TO HEMORRHAGE
 When 10% of the circulatory blood volume is lost, vasoconstriction occurs in both the arterial
and venous compartments.
 As blood loss reaches 20% or more of the total blood volume, increases in systemic vascular
resistance can no longer compensate for the lost intravascular volume and blood pressure
decreases. Cardiac output falls in parallel because of a loss in preload, resulting in poor end-
organ perfusion. If the intravascular volume is not appropriately replaced, cardiogenic shock
will ensue.
 In severe preeclampsia:
 1- plasma volume expansion is 9% lower in preeclamptic patients.
 2- Blood loss may be underestimated because blood pressure is often maintained in the
normotensive range despite significant hemorrhage.
 3- Oliguria may not be as reliable an indicator of poor end-organ perfusion
HEMORRHAGE CLASSIFICATION AND
PHYSIOLOGIC RESPONSE
 Antepartum Hemorrhage
(APH)
 Antepartum hemorrhage (APH) is defined as
bleeding from or into the genital tract after 20
weeks’ gestation (period of fetal viability) and
prior to delivery of the baby.
 Itis also referred to as bleeding in the second half
of pregnancy or late pregnancy bleeding
Causes of Antepartum
hemorrhage (APH)
Placental Abruption
 Placental Abruption
 Occurs in 1-2% of pregnancies.
 About one third of all antepartum bleeding can be attributed to
placental abruption.
 Placental abruption, or abruptio placenta, refers to the premature
separation of a normally implanted placenta from the uterus.
 Rupture of a maternal artery or vein caused by trauma or other
underlying mechanism results in bleeding into the decidual-placental
interface
 Placental Abruption

 Partial or complete
 “Marginal sinus separation” or “marginal sinus
rupture”
Bleeding, but abnormal implantation or abruption
never established.
 This process may be acute or chronic.
Classification system of
placental abruption
 Classification by site of
bleeding
 A, Retroplacental abruption: the bright red area represents
a blood collection behind the placenta (dark red).
 B, Subchorionic abruption: the bright red area represents
subchorionic bleeding, which is observed to dissect along
the chorion.
 C, Preplacental abruption: the bright red area represents a
blood collection anterior to the placenta within the amnion
and chorion (subamniotic)
Classification system of
placental abruption
 Types of placental abruption
 Clinical classification by presence or absence of vaginal
bleeding
 Revealed abruption
active vaginal bleeding
blood passes through cervix and vagina
accounts for 65%-80% of cases
 When >50% of the placenta separates, fetal death results.
 Fetal heart trace may reveal variable or late decelerations,
prolonged bradycardia, poor variability, or a sinusoidal pattern
 Types of placental abruption
 Concealed abruption
no vaginal bleeding
blood accumulates behind placenta with no external
bleeding
Theuterus is overdistended when the blood collects
behind the placenta and membranes, or enters the
amniotic cavity
“uteroplacental apoplexy” or “Couvelaire” uterus
accounts for 20%-35% of cases
Types of placental abruption
Couvelaire uterus. Blood has seeped
into the myometrium and the uterus
appears bluish black.
 Specimen of placenta shows
retroplacental clots formed in concealed
hemorrhage
Chronic placental abruption

 Chronic placental abruption is usually due

to chronic placental ischemia and presents
with recurrent episodes of bleeding.
 It results in growth restriction and
oligohydramnios.
 Coagulation abnormalities do not occur.
 Sher’s Classification -
Abruption
 Grade I Mild, often identified at delivery with
retroplacental clot

 Grade II Symptomatic, tender abdomen and live fetus

 Grade III Severe, with fetal demise:

 III A - without coagulopathy (2/3)
- with coagulopathy (1/3)
 Risk Factors
 Increasing parity and/or maternal  Inherited or acquired
age thrombophilia
 Smoking or substance abuse (e.g.  Uterine malformations or
cocaine) fibroids
 Trauma  Placental abnormalities or
 Maternal hypertension ischemia
 Preterm premature rupture of  Prior abruption
membranes  Male fetus
 Rapid uterine decompression  Unexplained elevation of
associated with multiple gestation MSAFP
and polyhydramnios
 Clinical features of acute
placental abruption
 Vaginal bleeding  Maternal
Mild/profuse Hypotension
 Abdominal pain Tachycardia
Mild/severe/persistent Decreased urine output
Signs of DIC
 Backache
 Fetal heart rate abnormalities
 Uterine tenderness Variable/late decelerations
 Uterine tetany Poor variability
 Uterine contractions Prolonged bradycardia
Sinusoidal pattern
 Overdistended uterus
 Diagnostic criteria for
placental abruption
 intra-amniotic hematoma
 subchorionic hematoma
 marginal hematoma
 increased heterogenous placental thickness (> 5 cm on perpendicular
plane)
 pre-placental collection under chorionic plate (between amniotic fluid
and placenta)
 retroplacental collection
 "jello"-like movement in chorionic plate when fetus is active
 Ultrasound may be helpful for diagnosing but not ruling out placental abruption
Ultrasound - Abruption

• Abruption is a clinical
diagnosis!
• Possible US findings
F Retroplacental
echolucency
F Abnormal thickening of
placenta
F “Torn” edge of placenta
 Management of placental abruption
depends on the severity, gestational
age, and maternal-fetal status

 Appropriate intravenous access (large-bore catheter).

 Availability of blood products.
 Continuous fetal heart rate and contraction monitoring.
 Communication with operating room and neonatal
personnel.
 Treatment – Grade II
Abruption
 Assess fetal and maternal stability
 Amniotomy
 IUPC to detect elevated uterine tone
 Expeditious operative or vaginal delivery
Decision-to-deliveryinterval > 30 min doubles
incidence of death or cerebral palsy
 Maintain urine output > 30 ml/hr, hematocrit > 30%
 Prepare for neonatal resuscitation
 Treatment – Grade III
Abruption
 Assessmother for hemodynamic and
coagulation status
 Vigorous replacement of fluid and blood
products
 Vaginal delivery preferred, unless severe
hemorrhage
Complications of placental
abruption
 Maternal
Hypovolemic shock
Renal failure
DIC
Preterm labor
Prelabor rupture of membranes
Instrumental delivery
Cesarean section
Postpartum hemorrhage
Rh sensitization
Sheehan syndrome
Maternal death
Complications of placental
abruption
 Fetal
Fetal hypoxia
Prematurity
Fetal growth restriction
Fetal death
 Pearls
 a) Mild abruption during labor should be augmented and delivery
vaginally.
 b) Moderate abruption is better delivery by c/section if advanced
cervical dilation and maternal compromise are present.
 c) Severe abruption, IUFD without DIC: artificial rupture of membranes
and induction.
 d) Severe abruption, IUFD, DIC: correction of coagulation disorder and
delivery by c/section.
 e) Severe abruption, a live fetus, mother stable, 6 cm dilated, should be
delivered vaginally.
Placenta previa
 Case

 A 22 year old G3P2 presents to labor and

delivery at 28 weeks gestation after having an
episode of vaginal bleeding. Initially she
noticed a small amount of blood-tinged mucus,
but one hour prior to admission she
experienced a gush of bright red blood. Her first
delivery was a cesarean section for failure to
progress at term, and her second was an
elective repeat cesarean at 38 weeks.
 Placenta previa

 Incidence: 4 per 1000 pregnancies and 1 in 200

births
 Complete previa placenta covers the internal os of
the cervix; accounts for approximately 30% of all
previas.
 Marginal previa <2 cm from the cervical os.
 Low-lying placenta >2 cm.
Placenta previa
Placenta previa
 Ultrasound classification

 Major previa: Grade III and IV

If the placenta lies over the internal cervical os
 Minor previa: Grade I and II
If the leading edge of the placenta is in the lower uterine
segment but not covering the cervical os (<2 cm).
 Risk Factors for Placenta
Previa
 Endometrial scarring • Increased parity
 Previous cesarean delivery • Maternal smoking
 Uterine
surgery (e.g., • Multiple gestation
myomectomy, uterine • Infertility treatments
septum resection)
•Advanced maternal
•Increased number of prior age
curettages
• Male fetal gender
 Tobacco use
 Etiology
 PP occurs in 1% of pregnancies after a single cesarean section.
The incidence after four or more cesarean sections increases to
10% and 40-fold increased risk compared with no cesarean
section.
 Two explanations for PP development:
 Endometrialscarring in the upper portion of the uterus
promotes implantation in the lower uterine segment; and
 Reduced uteroplacental oxygen exchange favors increased
placental surface area and thereby previa formation.
 Ultrasonography reveals placenta previa in a 41-
year-old asymptomatic gravida 4 para 3 at 21
weeks gestation. Appropriate management
would be:
 a. weekly speculum examinations under aseptic conditions
beginning in her third trimester to assess the risk of bleeding
 b. an MRI scan, with a repeat scan later in the pregnancy if
indicated
 c. repeat ultrasonography in her third trimester
 d. cesarean delivery at 28 weeks gestation if her L/S ratio is
favorable
 e. reassurance that US ultrasound diagnosis of placenta previa
without evidence of bleeding is no cause for concern
 Which women need further
imaging if the placenta is low at 20
weeks of gestation?
 All women require follow-up imaging if the placenta covers or
overlaps the cervical os at 20 weeks of gestation.
 Women with a previous caesarean section require a higher
index of suspicion as there are two problems
 To exclude: placenta previa and placenta accreta. If the
placenta lies anteriorly and reaches the cervical os at 20
weeks, a follow-up scan can help identify if it is implanted into
the caesarean section scar.
 What is a rising placenta?
(Placental migration)
 The phenomenon of a “rising placenta” or placental migration is due to the formation
of the lower segment from around 28th week of pregnancy which displaces the
placenta upwards.
 Thus, a low lying placenta may be diagnosed in about 5% of women at 16–18 weeks,
but placenta previa is found at delivery in only 10% of the 5% (0.05% overall) as the
placenta “rises” with the formation of the lower segment and growth of upper
segment
 Placental migration is less probable in cases of posterior placenta
 Placental migration is also less probable in cases where it existed with a previous scar.
 A mean rate of migration with anterior placenta previa is 2.6 mm per week, compared
to 1.6 mm per week in the posterior placenta previa
 Placenta accreta
spectrum (PAS)
 A general term used to describe placenta accreta, increta, and percreta. It
results from placental implantation at an area of defective decidualization
typically caused by preexisting damage to the endometrial-myometrial interface.
 DEFINITIONS
 ●Placenta accreta – anchoring placental villi attach to the myometrium (rather
than decidua) 79 % (adhere)
 ●Placenta increta – anchoring placental villi penetrate into the myometrium 14 %
(invade)
 ●Placenta percreta – anchoring placental villi penetrate through the myometrium
to the uterine serosa or adjacent organs 7 % (penetrate)
 The incidence of placenta accreta in Canada was 1 in 695 deliveries in 2009 to
2010, 1 in 731 deliveries between 2008 and 2011 in USA.
 Risk factors for Placenta
accreta spectrum
 A history of uterine surgery (eg,  cesarean scar pregnancy,
myomectomy entering the uterine  maternal age greater than 35
cavity, years,
 hysteroscopic removal of  multiparity,
intrauterine adhesions,  history of pelvic irradiation,
 cornual resection of ectopic  manual removal of the placenta,
pregnancy,  postpartum endometritis,
 dilation and curettage,  infertility and/or infertility
 endometrial ablation procedures (eg, especially
cryopreserved embryo transfer)
Morbidity with placenta
previa
 Morbidity with Placenta
accreta spectrum
 A review of 109 cases of placenta percreta
reported the following types and frequencies of
complications:
 transfusion of over 10 units (44 cases)
 infection (31 cases)
 maternal death (8 cases)
 ureteral ligation or fistula formation (5 cases each)
 spontaneous uterine rupture (3 cases)
 Management

 Patients with PP, who are bleeding, should be

hospitalized for hemodynamic stabilization and
continuous maternal and fetal monitoring.
 Specific management of PP is based on
gestational age and assessment of the maternal
and fetal status:
 Term Gestation,
Hemodynamically Stable
 Patients with complete previa at term require cesarean
section.
 Patients with partial or marginal previa at term may deliver
vaginally, with thorough consent regarding risks for blood loss
and need for transfusion.
 The staff and facilities for immediate emergent Cesarean
section must be available.
 If maternal or fetal stability is compromised at any point in
labor, urgent cesarean section is performed.
 Term Gestation,
Hemodynamic Instability
 Stabilize the mother with fluid resuscitation and
blood products
 Delivery via cesarean section is indicated for
nonreassuring fetal heart monitoring,
 Life-threatening maternal hemorrhage, or bleeding
after 34 weeks with documented fetal lung maturity.
 Preterm Gestation,
Hemodynamically Stable
 Patientsat 24 to 37 weeks' gestation with PP in
the absence of labor can be managed
expectantly until term or fetal lung maturity is
documented.
 For each bleeding episode, the following are
recommended:
 Preterm Gestation,
Hemodynamically Stable
 Hospitalization until stabilized on bed rest.
 Periodic assessment of maternal hematocrit and maintenance of an
active type and screen.
 Red blood cell transfusion as needed to maintain hematocrit above 30%
for slight but continuous bleeding.
 Corticosteroids and Rhogam as indicated.
 Fetal testing and growth ultrasounds to assess for intrauterine growth
restriction.
 Tocolysisis not warranted unless to administer a course of steroids in an
otherwise stable patient.
 Preterm Gestation,
Hemodynamic Instability
 Appropriate stabilization and
resuscitation are initiated with rapid
delivery by cesarean section.
Operative management
 Cesarean section
 Hysterectomy
 Preservation of the uterus
 Bilateral uterine artery ligation
 Internal iliac arteries ligation or embolization
B Lynch Suture
 Uterine packing
The differences between placenta
previa and placental abruption
 Non-placental causes of
antepartum haemorrhage
 Uterine rupture

 Occult dehiscence vs. symptomatic rupture

 0.03-0.08% of all women
 0.3-1.7% of women with uterine scar
 Previous cesarean incision is the most common etiology for
uterine rupture.
 Other causes : previous uterine curettage or perforation,
inappropriate oxytocin usage, and trauma.
 Risk factors for uterine
rupture
 Previous uterine surgery (e.g.  Maternal obesity
myomectomy) that involves
 Adenomyosis.
the full thickness of the
myometrium  Conditions present during
 Congenital uterine anomaly delivery that predispose to
 Uterine overdistension
uterine rupture include fetal
anomaly, vigorous uterine
 Intra-amniotic installation
pressure, difficult manual
 Gestational trophoblastic removal of the placenta, or
neoplasia abnormalities of placental
implantation
 Morbidity with Uterine
Rupture
 Maternal  Fetal
hemorrhage with respiratory distress
anemia hypoxia
bladder rupture (8.8 acidemia
percent)
neonatal death
hysterectomy (14 to 33
percent)
maternal death
 Clinical Findings – Uterine
Rupture
 Most cases (67 to 70 percent) of uterine rupture initially present with
abnormal fetal monitoring.
 Vaginal bleeding
 Pain
 Cessation of contractions
 Absence of fetal heart tones
 Loss of station, easily palpable fetal parts through the maternal abdomen
 Profound maternal tachycardia and hypotension.
 Treatment – Uterine
Rupture
 Asymptomatic scar disruption
 expectant management
 Symptomatic rupture
emergent cesarean delivery
 Vasa Previa

 Rarestcause of hemorrhage
 Associated with
In vitro fertilization
Placenta previa in 2nd or 3rd trimester
Bilobed and succenturiate lobe placentas
Velamentous insertion of the cord
Velamentous Insertion
 Vasa Previa

 Bleeding occurs with membrane rupture

 Blood loss is fetal
 56% mortality when undetected before onset
of labor
 3% mortality when detected prenatally
 Antepartum Diagnosis –
Vasa Previa
 Amnioscopy
 Ultrasound
 Vasa previa is highly associated with
placenta previa on 2nd trimester US
 Perform follow-up US with color-flow
Doppler
 Palpate vessels during vaginal
examination
 Management – Vasa
Previa
 Apt test to determine presence of fetal blood
 Based on colorimetric response of fetal hemoglobin
 Don’t delay urgent delivery for this test

 Immediate cesarean delivery if fetal heart rate non-

reassuring

 Administer normal saline 10-20 cc/kg bolus to

newborn if in shock after delivery