This document discusses antepartum hemorrhage (APH), specifically focusing on placental abruption and placenta previa. It defines APH as bleeding from or into the genital tract occurring after 24 weeks of gestation and prior to birth. Placental abruption is defined as premature separation of the placenta from the uterine wall, occurring in about 1% of pregnancies. Risk factors include increased age, previous abruption, hypertension, and trauma. Placenta previa is implantation of the placenta in the lower uterine segment, occurring in about 4-5 per 1,000 pregnancies. Risk factors include previous cesarean sections and multiparity. Both conditions require careful management to prevent

1. Dr .Prerit Devkota
2nd year GP/EM Resident
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2. Contents
 Introduction
 Classification
 Etiopathogenesis
 Placental Abruption and Placenta Previa
 Management
 Take home messeges
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3. Antepartum hemorrhage
 Bleeding from or into the genital tract, occuring after 24 weeks of
gestation and prior to birth of baby .
(RCOG 2011)
 Epidemiology:
o Affects 3-5% of all pregnancies
o 1/5th of preterm babies are in association of APH
o Occurs in 2.8/ 1000 singleton pregnancies & 3.9/1000 twin
pregnancies
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4. Definition:
 Spotting – staining, streaking or blood spotting noted on
underwear or sanitary protection
 Minor hemorrhage – blood loss < 50 ml that has settled
 Major hemorrhage – blood loss of 50–1000 ml, with no
signs of clinical shock
 Massive hemorrhage – blood loss >1000 ml and/or signs
of clinical shock.
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5. Etiology
 Placental bleeding
 Placenta previa (4-5/1000 pregnancies)
 Abruptio placenta (1% of all pregnancies)
 Unexplained/ Indeterminate (1-5% of all pregnancies )
 Local cause: cervical, vaginal or uterine pathology
 Cervical Polyps,erosions
 Infection/Inflammation
 Local trauma
 Varicose vein
 Blood stained cervical mucus
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6. Placental bleeding:
 Placenta previa:
 Separation of placenta implanted in the immediate vicinity of cervical
canal.
 Placental abruption:
 Separation of placenta located elsewhere in the uterine cavity .
 Vasa previa
 Velamentous insertion of umbilical cord and involved placental vessels may
overlie the cervix.
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8. Placental Abruption
 Premature separation of a
normally situated placenta
from the uterine wall,
resulting in haemorrhage
before the delivery of the
fetus.
 Incidence is 1 in 100
pregnancies
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9. Risk factors for Placental Abruption:
 Increased age and parity
 Abruption in previous pregnancy( recurrence:12% in subsequent
pregnancy)
 Vascular disease: hypertension in pregnancy, SLE
 Mechanical factors: Trauma, amniocentesis, sudden decompression of
uterus, poly-hydraminos, multiple pregnancy
 Drugs: Smoking, Cocaine
 Uterine factor: uterine myoma, septum, bicornuate uterus
 Thrombophilias
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10. Pathophysiology
Spasm of vessels in uteroplacental bed (decidual
spiral artery)
anoxic endothelial damage
Rupture of vessels and hemorrhage in decidua
basalis-decidua splits
Decidual hematoma(retroplacental)
Seperation and destruction of adjacent placenta
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11. Types of abruption:
• Concealed
• Mixed
• Revealed
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12. Grades of Placental Abruption:
Sher and Statland
Mild (grade 1):
 This is not recognized clinically before delivery and usually diagnosed
by the presence of a retro-placental clot.
 This is a retrospective diagnosis.
Moderate (grade 2):
 This is an intermediate grade in which the classical clinical signs of
abruption are present but the fetus is still alive.
 The frequency of fetal heart rate abnormalities is high.
Severe (grade 3):
 This is the severe grade in which the fetus is dead and coagulopathy
may be present.
 The volume of blood loss is appreciable in this condition.
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13. Investigations:
Ultrasonography:
• To exclude placenta previa
• Detects retroplacental
hematoma/fetal viability
(Negative findings does not exclude
placental abruption)
CTG:
 fetal tachycardia/ bradycardia
 Reassuring / non – reassuring
Labs:
 CBC
 Markers of consumptive coagulopathy: Platelets, BT,CT, PT-INR, APTT
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14. Complications
MATERNAL
 Hemorrhage
 Shock( out of proportion to blood
loss)
 Blood Coagulation disorders
 Renal involvement: Oligouria and
anuria
 Postpartum hemorrhage
 Puerperial sepsis
FETAL:
 Fetal death
Revealed: 25-50%
Concealed: 50-100%
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15. Management
 Treatment: Varies depending on gestational age and the status of the mother and
fetus.
 Admission
 History & examination
 Assess blood loss
 IV access, X match, DIC screen
 Assess fetal well-being
 Placental localization
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16. Contd.
Obstetric management:
 Viable fetus with no fetal compromise: Vaginal delivery
 Viable fetus with fetal compromise: Em LSCS (within 20
minutes)
 Severe abruption with fetal death: Vaginal delivery with
Amniotomy
(allow better spiral artery compression which serves decrease bleeding
and entry of thromboplastin into maternal circulation)
 Oxytocin : controversial
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17. Coagulopathy with abruption
 Occurs in 1/3rd of fetal demise
 Usually not seen with delivery of live fetus
 Etiologies: consumption, disseminated intravascular
coagulation(DIC)
 Administer platelets, fresh frozen plasma before operative
delivery.
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19. Placenta Previa
 Insertion of placenta partially/ completely in the lower segment
of uterus
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20. Risk factors for Placenta Previa
 Previous placenta praevia (OR 9.7)
 Previous caesarean sections
 1 previous CS OR 2.2 (95% CI (1.4–3.4) with a background rate of 1%)
 2 previous CS OR 4.1 (95% CI 1.9–8.8)
 3 previous caesarean sections OR 22.4 (95% CI 6.4–78.3)
 Multiparity
 Advanced maternal age (>40 years)
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21. Contd.
 Multiple pregnancy
 Smoking
 Deficient endometrium:
 uterine scar
 endometritis
 manual removal of placenta
 Assisted conception
( RCOG guidelines 2011)
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22. Types of Placenta Previa
Four types:
Type I(low lying):
 placenta encroaches lower
segment but does not reach
internal OS
Type II( Marginal)
 Reaches internal OS but does not
cover it
Type III (incomplete)
 Covers parts of internal OS
Type IV(central/total)
 Completely cover the OS
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23. Placent Accreta spectrum
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24. Pathogenesis
 Pathogenesis unknown
 Hypothesis:
 presence of areas of sub optimally vascularised decidua in
upper uterine cavity due to previous surgeries or multiple
pregnancies promote implantation of trophoblast in, or
undirectional growth toward the LUS(placental trophotropism)
 Another hypothesis:
 large placental size directly closes the Os
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25. Clinical features
 Sudden onset, painless, apparently causeless and recurrent vaginal
bleeding
 Abdominal findings:
 Uterus: soft, relaxed, non tender and proportionate to POG
 Malpresentation(breech/ transverse or unstable lie)
 Head is floating
 FHS: good
 Vulval inspection: presence of bleeding, character of blood
(PV examination is containdicated)
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26. Confirmation of diagnosis
clinical Localization of placenta
By internal examination
(double set up)
Transabdominal ultrasonography
Direct visualization during CS Transvaginal(TVS)
Examination of placenta following
delivery
Transperineal(TPS)
Colour doppler flow study
MRI
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28. Management:
 Prematurity-major complication, the main therapeutic strategy is to
prolong pregnancy until fetal lung maturity is achieved.
1. Assess general condition
2. Blood for Hb, Grouping, X-matching
3. I/V line with Crystalloid
4. Gentle abd. Examination
5. No P/V examination
6. USG for placentation, fetal maturity and viability
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29. Management:
 Active bleedng:
 If preterm, consider maternal transfer to appropriate level of care
 Antenatal corticosteroids and tocolysis
 No active bleeding :
 expectant management
 No intercourse in the third trimester
 Avoid digital examinations
 Ultrasound at 36 weeks can help determine mode of delivery
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30. Management
 Expectant management:
 No active bleeding
 Preterm<37weeks
 Normal fetus
 Normal Hb>10gm/dl
 If bleeding stops, can consider outpatient management
 Assurance of current maternal and fetal well‐being
 Patient lives in close proximity to hospital
 Immediate evaluation can occur if new bleeding episode starts or with onset of labor
 Current guidelines from the Royal College of Obstetricians and Gynecologists
(RCOG) recommend caesarean delivery for women with placental edge – internal
os distance of less than 2.0 cm.
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32. Complications:
Maternal:
During pregnancy:
 Antepartum hemorrhage and varying degree of shock
 Malpresentation
 Premature labour
During labour:
 Early rupture of membrane
 Cord prolapse
 Intrapartum hemorrhage, increased operative interference
Postpartum:
 Postpartum hemorrhage
 Puerperial sepsis
 subinvolution
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33. Fetal complications:
 Low birth weight
 Perinatal asphyxia
 Intrauterine death
 Congenital malformation
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34. Vasa previa
 Fetal blood vessels from
placenta or umbilcal cord cross
the internal OS beneath the
baby
 Rupture of membrane lead to
damage of the fetal vessels
leading to exsanguination and
death
 High fetal mortality (50-75%)
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35. Risk factors of vasa previa:
 Eccentric(velamentous cord insertion)
 Bilobed or succenturiate lobe of placenta
 Multiple gestation
 Placenta previa
 Invitro fertilization(IVF) pregnancies
 History of uterine surgery or D&C
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36.  Diagnosis:
 Moderate vaginal bleeding with fetal distress
 Vessels may be palpable through dilated cervix
 Vessels may be visible on doppler ultrasound
 CTG: Tachycardia/ bradycardia
 Management:
 Caeserean section
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37. Take Home Messeges
 Placenta previa and placental abruption are major causes of
antepartum hemorrhage
 Rapid clinical diagnosis is imperative and resuscitation is utmost
 Always remember CAB in case of APH
 No vaginal digital examination until placental location is known
 Ultrasound can help determine the cause of bleeding
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38. References
 UpToDate 2019
 Arias’ Practical Guide to High-Risk Pregnancy and
Delivery
 Royal College of Obstetricians and Gynaecologists
guidelines
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39. THANK YOU !!!!
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