Antepartum and Postpartum

Hemorrhage
FITSUM ASHEBIR
 Outlines
Introduction
Pregnancy-Related Hemodynamic Changes
 Physiologic Adaptation to Hemorrhage
 Classification of Hemorrhage
Antepartum Hemorrhage
Placental Abruption
Placenta Previa
Vasa previa
Local causes
APH of unknown cause
Introduction
Antepartum and postpartum hemorrhage remain one of the leading
causes of obstetric morbidity and mortality throughout the world.
Between 17 and 25 percent of all pregnancy-related deaths can be
directly attributed to hemorrhage.
Because of this significant contribution to maternal mortality, it is
critical for the Physician/obstetrician to have a thorough understanding
of the homodynamic changes that accompany pregnancy and the
maternal adaptations that occur with excessive blood loss.
 Pregnancy-Related
Hemodynamic Changes
1. The first of these is plasma volume expansion.
 The average singleton pregnancy has a 40 to 50% increase in plasma
volume, which occurs by the 30th week of gestation.
 With appropriate substrate availability, red blood cell mass increase 20
to 30 % by the end of pregnancy.
2. Maternal cardiac output rises with normal pregnancy owing to both
increased stroke volume and heart rate.
 Average rise in cardiac output is 30 to 50 % above nonpregnant levels, with
the peak occurring in the early third trimester.
3. Systemic vascular resistance falls in parallel with this rise in cardiac
output and blood volume expansion.
4. Finally, fibrinogen and the majority of procoagulant blood factors (I, VII,
VIII, IX, and X) increase during pregnancy.
These four physiologic changes are protective of maternal hemodynamic status and, in doing so,
allow for further physiologic adaptations that accompany obstetric hemorrhage.
 Physiologic Adaptation To
Hemorrhage
During pregnancy and the puerperium, a defined sequence of physiologic
adaptations occur with hemorrhage.
When 10 % of the circulatory blood volume is lost, vasoconstriction occurs
in both the arterial and venous compartments in order to maintain blood
pressure and preserve blood flow to essential organs.
 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 result in

└ blood pressure decreases

└Cardiac output falls in parallel due to a loss in preload, resulting in
poor end-organ perfusion
 If the intravascular volume is not appropriately replaced, cardiogenic
shock will ensue
 Exception to the Physiologic
Adaptation To Hemorrhage
In severe preeclampsia, these physiologic adaptations are altered.

The protective mechanism of blood volume expansion is diminished

with severe preeclampsia. plasma volume expansion is 9% lower in
preeclamptic patients
Because of the significant vasoconstriction accompanies preeclampsia,
blood loss in these patients may be underestimated because BP may be
maintained in the normotensive range despite significant hemorrhage.
Finally, in preeclampsia, oliguria may not be as reliable an indicator of
poor end-organ perfusion secondary to hemorrhage because reduced
urine output is often a manifestation of the severity of the hypertensive
disorder.
Physiologic Adaptation To
Hemorrhage
Classification of Hemorrhage
Classification of Hemorrhage
Classification of Hemorrhage
Class 3
 Severe Tachycardia – 120-160 beats/min
 Severe Tachypnea – 30-50 breath/min
 Overt Hypotension and
 Cold extremities

Class 4
 Absent distal pulse
 Cardiogenic shock
 Oliguria/ anuria –
 With large hemorrhage RBF decreases & blood is directed from the renal cortex to the
jaxtamedulary region where there is increased water and sodium retention resulting in
o low urinary Na,
o high Osmolality &
o low urine volume
 Urine Na <10-20 mEq/l or S/U osmolarity ratio >2 indicate significant reduction of renal
perfusion
 APH
 Definition - APH or late pregnancy bleeding is vaginal bleeding of the pregnant
mother after the fetus has reached the age of viability (which is after 28
completed weeks or fetal weight of 1000gm or more) and before the fetus is
delivered (last fetus in case of multiple pregnancies) is delivered.

Incidence - 2-4% of all pregnancies. In more than 50% of cases cause is unknown.

Precautions
No vaginal / rectal examination
Management should be at a site with operative and transfusion facility.
 Common Causes of 3rd-Trimester
Bleeding.(APH)
1. Placental causes
 Placenta previa
 Abruptio placentae
 Rare causes - Vasa previa and other placental abnormalities
2. Non placenta causes
 Bleeding disorders; - Disseminated intravascular coagulopathy (DIC)
 Genital injury; Vaginal laceration, Uterine rupture
 Bloody show (heavy show)
 Local causes;;- Pathology of cervix ,vagina and vulva such as
 Cervical cancer or dysplasia, Cervicitis ,Cervical polyps, Cervical eversion ,
vaginitis

3. Unclassified causes;- Insufficient evidence to establish a definite cause ether

retrospectively or prospectively.
 1. Placental Abruption
Definition & Pathogenesis
Placental abruption, or abruptio placenta, refers to the premature separation of a
normally implanted placenta from the uterus.
Typically, defective maternal vessels in the decidua basalis rupture and cause the
separation.
On rare occasions, the separation may be caused by a disruption of the fetal-
placental vessels.
In both ways the damaged vessels cause bleeding,
└ decidual hematoma
└ placental separation, destruction of placental tissue, and
a loss of maternal-fetal surface area for nutrient and
gas exchange.
Placental Abruption
Incidence
 Placental abruption complicates 1 in 75 to 1 in 226 deliveries.
 The range in incidence likely reflects variable criteria for
diagnosis as well as an increased recognition in recent years of
milder forms of abruption.
 Approximately 1/3 of all antepartum bleeding can be attributed
to placental abruption.
 Placental Abruption
Clinical Manifestations
 Dark, clotted, vaginal bleeding or occult uterine bleeding
 Abdominal pain
 Uterine contractions or hypertonus
 Uterine tenderness
 NRFHRP or fetal death, and DIC
 Approximately 80 percent of placental abruptions occur before the onset
of labor.
The diagnosis is confirmed with certainty by the
 Macroscopic inspection of a placenta with adherent retroplacental clot
 Depression / disruption of the underlying placental tissue
 Classification of Placental Abruption
classified into three grades that correlate with the following clinical and laboratory
findings:
 Grade 1: A mild abruption characterized by slight vaginal bleeding and minimal uterine
irritability.
 Maternal blood pressure and fibrinogen levels are unaffected, and the fetal heart
rate pattern is normal.
 Approximately 40 percent of placental abruptions are grade 1.
 Grade 2: A partial abruption with mild to moderate vaginal bleeding and significant
uterine irritability or contractions.
 Maternal blood pressure is maintained, but the pulse is often elevated and postural
blood volume deficits may be present.
 The fibrinogen level may be decreased, and the fetal heart rate often shows signs of
fetal compromise.
 Account for 45 percent of all placental abruptions.
 Grade 3: A large or complete abruption characterized by moderate to severe vaginal
bleeding or occult uterine bleeding with painful, tetanic uterine contractions.
 Maternal hypotension and coagulopathy are frequently present along with fetal
death.
 Approximately 15 percent of placental abruptions are recognized as grade 3.
Classification of Placental
Abruption
 Placental Abruption
Risk Factors - exact etiology of placental abruption is unclear, a variety of risk
factors have been identified .
Increasing parity and/or maternal age > 35 – 1%in primi and 2.5% in multi
 Damage to the endometrium that impair proper decidualization
Cigarette smoking- decidua ischemia and necrosis (40% risk of fetal death)
Cocaine abuse- Vasospasm & decidua ischemia and necrosis (10% in 3rd-trimester)
Trauma (blunt or penetrating)
Maternal hypertension- (5X)
Preterm PROM- risk increases with chorioamnitis & oligohydramnios
 Membrane rupture  cytokine & protease release  damage to decidua
vasculatures  placental abruption OR
 Hemorrhage & thrombin generation  cytokine & protease release  PROM
Multiple gestation (3X) and Polyhydramnios with rapid uterine decompression
Inherited or acquired thrombophilia
Uterine malformations or fibroids
Placental anomalies- circumvallate placenta, short cord
Hx of Previous abruption – recurrence is 5-17% after 1, 25% after 2 Hx
 Placental
Diagnosis
Abruption
 The diagnosis of placental abruption is primarily clinical, with supportive evidence from
sonographic, laboratory, and pathologic studies.
 Any vaginal bleeding in the 3rd- trimester of pregnancy should prompt an investigation to
determine its etiology.
 Although vaginal bleeding is the hallmark sign of placental abruption, 10 to 20 percent of
affected women may have an occult or concealed hemorrhage.
 Sonography
 Acute hemorrhage is typically hyperechoic or isoechoic, whereas resolving
hematomas are hypoechoic within 1 week and sonolucent within 2 weeks of the
abruption.
 Ultrasound can identify three predominant locations for placental abruption.
 Subchorionic (between the placenta and the membranes),
 Retroplacental (between the placenta and the myometrium) worst prognosis, and
 Preplacental (between the placenta and the amniotic fluid).
 Size of the hematoma also affect fetal prognosis i.e. large retroplacental clot >60 ml
are associated with 50% mortality where as small clots have 10% mortality rate.
Placental Abruption
 Placental Abruption
Laboratory Findings
 Hypofibrinogenemia and evidence of DIC are supportive of the
diagnosis; however, clinical correlation is necessary.
 Most abruptions are not accompanied by coagulopathy.
 DIC- platelet count, PT, PTT, D dimer, fibrinogen and peripheral smear
(fragmented red cells, schistocytes, helment cells)
Pathologic Studies
 Macroscopic inspection of the placenta demonstrates adherent clot and
depression of the placental surface.
 Fresh or acute placental abruptions may not have any identifiable
evidence on pathologic examination.
 Placental Abruption
 COMPLICATIONS

 Maternal  Fetal
 Hypovolemia & severe anemia  IUGR (with chronic abruption)
related to blood loss  Fetal hypoxemia or asphyxia
 DIC  Preterm birth
 PPH, couvelaire uterus  Perinatal mortality
 Renal failure
 ARDS
 Multisystem organ failure
 Death
Management of Placental Abruption
Nearly half of all placental abruptions will result in delivery at less than
37 weeks' gestation.
 Gestational age at the time of presentation is an important prognostic
factor.
In patients presenting at less than 20 weeks, 82 percent can be expected to have a
term delivery despite evidence of placental abruption.
However, if the presentation occurs after 20 weeks' gestation, only 27 percent will
deliver at term.
Management of Placental Abruption
Once the diagnosis of placental abruption has been made, precautions should
be taken to anticipate the possible life-threatening consequences for both
mother and fetus.
These precautions include;
Baseline laboratory assessment (HG, HCT, PT, PTT, platelet count, BG &
RH, fibrinogen, and coagulation studies),and follow-up investigation (HCT
and coagulation profiles)
Appropriate intravenous access (large-bore catheter), and resuscitation
if needed.
Availability of blood products for DIC
Continuous fetal heart rate and contraction monitoring,
Communication with operating room and neonatal personnel.
Management of Placental Abruption
The timing and mode of delivery dependent on the
 Severity of the maternal-fetal condition,
 The gestational age, and
 The cervical examination.

In the case of a Grade 1 abruption and pregnancy that is remote from term,
Hospitalization with expectant management may be warranted.
 Tocolysis- for preterm labour
 Corticosteroids - If maternal-fetal status is stable in near term --
- Dexamethasone
 Management of Placental Abruption
Women presenting at or near term with a placental abruption should undergo delivery
Delivery indications
37 completed weeks,
Fetal compromise,
Ongoing separation
Vaginal delivery preferred unless Contraindicated

Induction or augmentation of labor is not contraindicated in the setting of an

abruption;
If induced Continuous fetal heart rate monitoring is recommended because 60% of
fetuses may NRFHRP
Because induction may cause a raised intrauterine rest pressure  low uterine blood
flow and low fetal oxygenation
Maternal hemodynamic and clotting parameters must be followed closely in order to detect signs
of evolving coagulopathy.
Although vaginal delivery is generally preferable, operative delivery is often necessary owing to
fetal and maternal decompensation.
 Management of Placental Abruption
The management of women with severe coagulopathy and fetal demise
Requires a thorough knowledge of the natural history of severe placental abruption.
Pritchard and Brekken - clinically important and relevant observations concerning the
natural course of placental abruption
1. Approximately 40 percent of patients with grade 3 placental abruption will
demonstrate signs of DIC;
2. Within 8 hours of initial symptoms in such women, Hypofibrinogenemia will
be present;
3. Severe Hypofibrinogenemia will not recover without blood product
replacement; and
4. The time course for recovery from Hypofibrinogenemia is roughly 10 mg/dl
per hour after delivery of the fetus and placenta.
So when managing patients with severe or grade 3 placental abruptions with intrauterine
fetal demise,
 Maintenance of maternal volume status and replacement of blood products is
essential.
 Blood product replacement and delayed delivery until hematologic parameters have
improved are generally associated with good maternal outcomes.
Management of Placental
Abruption
Couvelaire uterus
 When operative delivery is necessary, a Couvelaire uterus
characterized by extravasation of blood into the
myometrium may be found in 8 percent of patients.
 This finding may be associated with significant uterine
atony.
 Administration of uterotonic therapy usually improves
the condition.
 Hysterectomy should be reserved for cases of atony and
hemorrhage unresponsive to conventional uterotonic
therapies.
Management of Placental Abruption
 Neonatal Outcome
 Women with placental abruption has
 9x risk of IUFD (20 to 30 %),
 4x risk of Preterm delivery, and
 2x risk of IUGR
 2. Placenta Previa
Definition - Placenta previa is defined as the presence of placental tissue in the LUS, over or
adjacent to the cervical os
Classification
Traditionally 3 variations of placenta previa are recognized: Complete, Partial, and Marginal.
 Complete placenta previa referred to the total coverage of the cervical os by placental tissue,
 The differences between partial (placental edge at the cervical os) and marginal (placental
edge near the cervical os) are often subtle and vary by the timing and method of diagnosis.
MOH classifies as Minor degree (Type 1,2) vs. major degree (Type,3,4 )
 Minor placenta previa
o Type 1 PP (low lying) – in the LUS but not reaching internal OS
o Type 2 PP (marginal) – the placenta reaches the internal OS but dose not cover it
 Major placenta previa
o Type 3 PP (partialis) - the placenta cover internal OS but only partially
o Type 4 PP (complete , Totalis) – the placenta cover the internal os totally
 Contemporary classification of placenta previa consists of two variations:
 Placenta previa totalis, in which the cervical os is covered by placental tissue, and
placenta previa marginalis, in which the placenta lies within 2 to 3 cm of the cervical os but
does not cover it.
 Placenta Previa
Incidence
The overall reported incidence of placenta previa at delivery is 4/1,000
deliveries.
 In the 2nd- trimester, placenta previa may be found in 4 to 6 percent of
pregnancies.
 The term placental migration has been used to explain this “resolution” of
placenta previa that is noted near term.
Two theories have been suggested to account for this phenomenon.
 As the pregnancy advances the stationary lower placental edge
relocates away from the cervical os with the development of the lower
uterine segment that grow from 0.2cm at 20 wk. to 5cm at term.
 Trophotropism, or the growth of trophoblastic tissue away from the
cervical os toward the fundus, (atrophy and hypertrophy) results in
resolution of the placenta previa
 Placenta Previa
Risk Factors
 Increasing parity- endometrial damage 5% risk, 0.2% in nulli
 Increasing maternal age, >35 – 4x and >40 – 9x
 Cigarette smoking - decreased Uteroplacental oxygenation, 3x
 Residence in higher altitude - decreased Uteroplacental oxygenation
 Multiple gestations – 8x
 Previous placenta previa
 Prior curettage - endometrial damage 1.3x
 Prior cesarean delivery - uterine damage 1.4x
 Additionally, some reports have documented a higher association of fetal
malpresentation, preterm PROM, erythroblastosis fetalis and IUFD with
placenta previa
 DM- vascular arteriosclerosis and lack of enough O2 resulting in macro
placenta
 Placenta Previa
Clinical Manifestations
 Placenta previa typically presents as painless, bright red, vaginal bleeding in
the 2nd- or 3rd-trimester.
 Occurs with out warning / causeless, mostly reccurent
 Some patients present with uterine contractions that precede a bleeding
episode.
 Nontender normal toned uterus
 P/E- pulse, BP are proportional to the blood loss
 High presenting part
 Abnormal fetal lie
 The bleeding is believed to occur from disruption of placental blood
vessels in association with the development and thinning out of the lower
uterine segment
 Placenta Previa
Diagnosis
 Painless 3rd-trimester bleeding was a common presentation for placenta previa in
the past,
 Whereas most cases of placenta previa are now detected antenatally with
ultrasound before the onset of significant bleeding.
 Sonography
 Transabdominal at least 95% and transvaginal ultrasound (100%) provide the
best means for diagnosing placenta previa.
 Typically, a combined approach can be used in which transabdominal
ultrasound is employed as the initial diagnostic modality and transvaginal
ultrasound is reserved for uncertain cases.
 If placenta previa is diagnosed before 24 weeks' gestation, repeat Sonography
should be obtained between 28 and 32 weeks' gestation.
 More than 90% of the cases of PP diagnosed in the mid 3rd trimester resolve by
term.
 Complete placenta previa diagnosed in the 2nd- trimester will persist into the
3rd- trimester in 26% of cases, whereas marginal placenta previa will persist in
only 2.5% of cases
 Placenta Previa
 COMPLICATIONS

Maternal Fetal / Neonatal

 Blood loss & shock  ↑ed PNMR from prematurity
 Adherent placenta
 ↑ed risk of fetal anomalies ( 5x)
 Transfusion risks
 Longer hospital stay  ↑ed IUGR (20% Vs. 5%)
 Surgical morbidity  Trauma ( b/c of malpresentation)
 Post partum hemorrhage
 Recurrence rate - 4 to 8%  Anemia
 Management Placenta Previa
General management principles for patients with placenta
previa in the 3rd-trimester include
Investigation and observation
 Hct, Sonography to monitor Maternal and fetal condition monitoring
and placental location
Avoid cervical exam and coitus
Resuscitation if need be
Counseling regarding labor symptoms and vaginal bleeding
Dietary/nutrient supplementation to avoid maternal anemia and early
medical attention if any vaginal bleeding
Management Placenta Previa
Outpatient Management
 Asymptomatic patients with placenta previa or patients with
a history of a small bleed that has resolved for greater than 7
days are potential candidates for outpatient management.
 Candidates for outpatient management must be
 Highly compliant,
 Live within 15 minutes from the hospital,
 Have 24-hour emergency transportation to the hospital,
and
 Verbalize a thorough understanding of the risks
associated with placenta previa and outpatient
management
 Management Placenta Previa
Expectant Management of Preterm Patients
 Patients with placenta previa who present preterm with vaginal
bleeding require hospitalization and immediate evaluation to assess
maternal-fetal stability.
 Immediate delivery can be delayed & prolongation (>2 weeks) of
pregnancy can occur even in pts. with initial bleeding episodes >500 ml.
 In order to optimize maternal - fetal outcome,
 patients should initially be managed in a labor and delivery unit
with continuous FHR and contraction monitoring.
 Large-bore intravenous access and baseline laboratory studies
(Hg, HCT, platelet count, BG & RH, and coagulation studies) should
be obtained.
 If the patient is less than 34 weeks' gestation, administration of
antenatal corticosteroids should be undertaken as well as an
assessment of the facility's emergency resources for both the mother
and the neonate.
Management Placenta Previa
Expectant Management of Preterm Patients
Tocolysis can be employed if the vaginal bleeding is preceded by
or associated with uterine contractions.
Magnesium sulfate is generally considered superior to β-mimetic
therapy, given its reduced potential for hemodynamic-related
side effects.
Once stabilized, patients can be maintained on hospitalized bed
rest and expectantly managed.
Management Placenta Previa
Expectant Management of Preterm Patients
Although some authorities have recommended prophylactic
transfusions to keep the maternal hematocrit greater than 30 percent,
alternative options to increase endogenous red blood cell formation
should be considered including
 oral iron,
 vitamin C, and folate supplementation,
 intravenous iron sucrose administration, and
 recombinant erythropoietin alpha administration.
The use of facility-based blood conservation programs can assist the
clinician in conservative options for blood product replacement.
Lastly, consideration of autologous blood donation may be appropriate
for stable patients who are candidates for this service.
Management Placenta Previa
Expectant Management of Preterm Patients
Although maternal hemorrhage is of outmost concern, fetal blood can
also be lost during the process of placental separation.
Rh-immune globulin should be given to all Rh-negative, unsensitized
women with 3rd-trimester bleeding from placenta previa.
A Kleihauer-Betke preparation of maternal blood should be
performed.
 Procedure used to determine the concentration of fetal cells in
the maternal circulation
 This test detects the occasional patient with a fetomaternal
hemorrhage of >30 ml who requires additional doses of
RhoGAM.
35% of infants whose mothers have received antepartum transfusion
will also be anemic and need a transfusion when delivered.
Management Placenta Previa
Delivery
 Cesarean delivery is indicated for all patients with sonographic evidence
of placenta previa.
 In patients with a marginal placenta previa in which the placental edge is
clearly 2 to 3 cm from the cervical os, vaginal delivery may be
considered;
 When performing cesarean delivery for placenta previa, the surgeon
should be aware of the potential for rapid blood loss during the delivery
process.
 Patients should have 2 to 4 units of packed red blood cells available at the
time of delivery..
 Ideally, the placenta should not be disrupted when entering the uterus.
 If the placenta is disrupted, expedited delivery is essential. Once the
fetus has been removed from the uterus, the cord blood should be
“milked” to the fetus in order to avoid immediate neonatal hypovolemia
and anemia.
Management Placenta Previa
Indications For Delivery
 37 completed weeks
 Severe or recurrent hemorrhage
 IUFD
 Fetal distress
 Major congenital anomalies
Mode of delivery
 Vaginal- Type1 or Type2 anterior placentae previa
 C/D - Major degree placenta previa(Type2 posterior, Type3
and Type 4)
Management Placenta Previa
Delivery
Given the potential for placenta accreta, the physician should allow
the placenta to spontaneously deliver. If accreta occur manage with
caution.
Once the placenta separates, bleeding is controlled by the contraction
of uterine myometrial fibers around the spiral arterioles. Because the
lower uterine segment often contracts poorly, significant bleeding can
occur from the placental implantation site.
Aggressive uterotonic therapy and surgical intervention should be
undertaken to rapidly control the bleeding.
Clinical Findings in Placenta
Previa and Abruptio Placenta
Associated Conditions
A. Placenta Accreta
 Definition and Pathogenesis
 Placenta accreta represents the abnormal attachment of the
placenta to the uterine lining due to an absence of the deciduas
basalis and an incomplete development of the fibrinoid layer.
 Variations of placenta accreta include placenta increta and
placenta percreta, in which the placenta extends to and through
the uterine myometrium, respectively.
Associated Conditions
Incidence and Risk Factors
The overall incidence of placenta accreta or one of its variations is 1 in
533 deliveries.
 The two most significant risk factors for placenta accreta are placenta
previa and prior cesarean delivery.
 The risk with only placenta previa is ~ 3%. This risk dramatically
increases with one or more cesarean deliveries i.e. 1 C/S is
associated with ~ 11% risk of placenta accreta.
This risk rises to 67 percent when placenta previa occurs with a history
of four or more cesarean deliveries.
Other risk factors that have been reported include increasing parity and
maternal age, prior uterine surgery, and endometrial defects.
Associated Conditions
 Associated Conditions
Clinical Manifestations - similar to those of placenta previa
Diagnosis
In the past, placenta accreta was usually diagnosed intrapartum by the difficult or
incomplete removal of the placenta and associated PPH. Today with advanced radiographic
technology, the diagnosis can be made antenatally.
Ultrasound / Color and power Doppler ultrasound is the best radiographic modality for the
diagnosis of placenta accreta. The diagnostic sensitivity and specificity approaches 85 to 90
percent with experienced sonographers.
 Findings that are suggestive of placenta accreta include
 A loss of the normal hypoechoic retroplacental-myometrial zone,
 Thinning and disruption of the uterine serosa-bladder interface,
 Focal exophytic masses within the placenta, and
 Numerous intraplacental vascular lacunae.
MRI can be used in conjunction with Sonography to assess a placenta at risk for abnormal
invasion. MRI is useful in cases with equivocal ultrasound findings or with a posterior
placental location.
Unexplained elevations in maternal serum alpha-fetoprotein have been associated with
placenta accreta.
 Associated Conditions
Management
The delivery should occur at a facility that is prepared to manage significant hemorrhage.
IV with two large-bore catheters and ample blood product availability are mandatory.
When performing the C/S for delivery , the uterus is incised above the placental
attachment site and the placenta left in situ after clamping the cord b/c disruption of the
implantation site may result in rapid blood loss.
B/c placenta accreta poses a risk for massive PPH, at least 2/3 of the patients require C/S
hysterectomy.
When future fertility is desired, a variety of uterine conservation techniques can be
considered. These techniques include
 Delayed manual removal of the placenta,
 Packing of the lower uterine segment,
 Curettage,
 aortic and/or internal iliac artery balloon occlusion catheters
 Oversewing of the placental implantation site,
 uterine artery embolization, and administration of methotrexate.
3.Vasa previa
Definition and Pathogenesis
 Defined as the velamentous insertion of fetal vessels over the cervical OS.
 Typically, the fetal vessels lack protection from Wharton's jelly and are prone to
rupture.
 When the vessels rupture, the fetus is at high risk for exsanguination B/C of
bleeding from the fetal circulation.
 The overall perinatal mortality for vasa previa is between 58 and 73% .

Incidence and Risk Factors

 The incidence of vasa previa has been reported as 1/2,000 to 5,000 deliveries.
 Risk factors for vasa previa include
 bilobed, succenturiate-lobed
 low-lying placentas;
 pregnancies resulting from in vitro fertilization;
 multiple gestations; and
 history of 2nd-trimester placenta previa.
Vasa previa
Clinical Manifestations
 Vasa previa usually presents after rupture of membranes with the
acute onset of vaginal bleeding from a lacerated fetal vessel.
 If immediate intervention is not provided, fetal bradycardia and
subsequent death occur.

Diagnosis
 In the past, vasa previa was usually detected by palpation of the fetal
vessels within the membranes during labor or with the acute onset of
vaginal bleeding and subsequent fetal bradycardia or death after
membrane rupture.
 With the use of Sonography and Doppler imaging, vasa previa is
being detected more frequently antenatally.
 Transabdominal, transvaginal, and translabial approaches have
been used.
 The diagnosis is confirmed when umbilical arterial waveforms
are documented at the same rate as the fetal heart rate.
Kleihauer-Betke Test
Is a blood test used to measure the amount of fetal hemoglobin
transferred from a fetus to the mother's bloodstream.

Used to determine the required dose of Rh immune globulin.

Used for detecting fetal-maternal hemorrhage.

Apt test
The test allows the clinician to determine whether the blood
originates from the infant or from the mother.
◦ Place 5 mL water in each of 2 test tubes
◦ To 1 test tube add 5 drops of vaginal blood
◦ To other add 5 drops of maternal (adult) blood
◦ Add 6 drops 10% NaOH to each tube
◦ Observe for 2 minutes
◦ Maternal (adult) blood turns yellow-green-brown; fetal blood stays pink.
◦ If fetal blood, deliver STAT.
Management of Vasa previa
When diagnosed antenatally, vasa previa should be managed similarly to
placenta previa. And Some authorities have recommended
 Hospitalization in the third trimester with the administration of
antenatal corticosteroids, serial antepartum testing, and cesarean
delivery at approximately 36 weeks' gestation.
If an intrapartum diagnosis of vasa previa is made,
expeditious C/D delivery is needed.
Immediate neonatal blood transfusion is often required.
 Approach to 3rd-Trimester
Bleeding
 History:  DDX based on severity of
 Detail of personal identification, abruptio placenta
obstetric, gynecologic, & medical  Mild abruption:
history  placenta previa,
 Detail characterization of bleeding:  local causes,
 Site of bleeding : urethral, vaginal,
anal, from skin (perineum)  heavy show
 Time of onset  vasa previa
 Amount, color, clots,  Severe abruption with acute abdomen
 Frequency presentation:
 Immediate event  ruptured uterus,
 Associated abdominal pain &  appendicitis,
characteristic  volvulus
 Risk assessment  Chorioamnionitis
 Physical examinations  Other rare causes:
o red degeneration,
o retroperitoneal bleeding,
o rectus muscle bleeding
 Approach to 3rd-Trimester
Bleeding
 Physical examination:
 V/s, anemia,
 Obstetric examination - 3rd Leopold carefully, avoid 4th Leopold
 P/v
 Inspect the vulva
 Avoid digital PV & PR till diagnosis
 ??Gentle PV (active labor, bearing down feeling, defecating)
 Diagnosis:
 Clinical picture and predisposing factor
 U/s
 Speculum examination to r/o local causes- 48 hr. to 10 days after
bleeding stops or r/o Placenta Previa
 Consider referral if no adequate facility or do double setup
examination if having C/S facility
Initial management of APH
Admit Kleihauer-Betke test
History Apt test
Examination CTG
NO PV Observation
Nurse on side Placental localization
IV access/ resuscitate Speculum examination when
placenta previa excluded
Clotting screen
Anti-D if Rh-negative
Cross match
Approach to 3rd-Trimester
Bleeding (DSE)
 General management of APH
 Admission Indication for delivery-
 Heavy or recurrent bleeding
 Resuscitation  Fetal distress /Demise /congenital
 Avoid vaginal and rectal examination anomaly incompatible with life
 APH at term- 37 wks.
 Monitor maternal and fetal condition
Mode of delivery
 Hct, blood group and Rh  Emergency C/D if severe
hemorrhage / FD
 Prepare at lest 2 units of blood  Double set up examination- APH
at term and mild hemorrhage-
 Anticipate PPH Decide on mode of delivery
 Decide on final mode of
management-conservative or
aggressive
General management of APH
General management of APH
DDx read
Uterine Rupture