Antepartum hemorrhage is defined as bleeding from the genital tract after 20 weeks of gestation, categorized into minor, major, and massive hemorrhages based on blood loss. Key causes include placenta previa, abruptio placenta, and various genital tract conditions, with risk factors such as hypertension, substance use, and trauma contributing to its occurrence. Management involves early diagnosis and assessment, hospitalization, and potentially early delivery, especially in cases of severe bleeding or fetal distress.

1. Antepartum
hemorrhage
Dr Sreelatha s
Professor
Dept of OBG
ESICMC & PGIMSR
Bangalore 560010

2. Definition
• Antepartum hemorrhage is defined as bleeding from the genital tract
after 20 weeks gestation till delivery.
• Minor hemorrahge – blood loss < 50 ml that has settled(includes spotting)
• Major hemorrhage – blood loss of 50-1000 ml
• Massive hemorrhage – blood loss > 1000 ml

3. Causes of bleeding in late pregnancy
Placental
1. Placenta previa (31%)
2. Abruptio placenta (22%)
3. Vasa previa (0.5%)
4. Unclassified
Genital tract
1. Cervicitis
2. Trauma
3. Vulvovaginal varicosity
4. Genital tumor
5. Genital infection
6. Hematuria
7. Others

4. Abruptio placenta
• The premature separation of a normally implanted placenta from the
uterus prior to the delivery of the fetus.
• Latin term – rendering asunder of the placenta
• Incidence – 1 in 100 births
• 40 to 60% abruption occurs prior to 37 weeks gestation

5. 1. PRIOR H/O ABRUPTION
• Highest relative risk: 10 -18.8
• Recurrence risk after 1 abruption is 5 to 15% , after
2 abruptions is 20 to 25%.
• Risk of recurrence is greater after severe abruption
• Abruption associated with fetal demise 7%
incidence of same outcome in future gestation.
• Abruption recurred at a gestational age 1 to 3
weeks earlier than the 1st
abruption in half the
patients
2. INCREASED AGE & PARITY
• Incidence of abruption in Primigravida < 1%, in
grand multipara is 2.5%
• Causes
a) Damaged endometrium
b) Impaired decidualization
c) Aberrant vasculature
• Age – maybe because of higher parity,
hypertensive disease
RISK FACTORS FOR ABRUPTION

6. 3. MATERNAL DISEASES
a. Hypertension
• Most consistently identified risk factor for abruption
• Both chronic hypertension & pregnancy related
hypertensive disease
• 5 fold higher risk of abruption
• Severity of hypertension doesn’t corelate with
abruption incidence
• Elevated cardiovascular mortality risk in women with
prior abruption, with / without chronic hypertension
• Antihypertensive therapy doesn’t decrease risk of
abruption in chronic hypertension
• Women with preeclampsia with/without chronic
hypertension , given MgSO4 have reduced risk of
abruption – Magpie trial collaborative group
b. Subclinical hypothyroidism
c. Asthma
4. UTERINE & PLACENTAL FACTORS
i. Anomalies
ii. Synechiae
iii. Fibroids – mucosal surface behind
the placental implantation site
iv. Cesarean scar
v. Abnormal placental formation
vi. Chronic ischemia – PE & growth
restriction
• Circumvellate placneta – chronic
tissue outside tha placental margin
has the tendency to detach & bleed
Suboptimal
placental
implantation

7. 5. MATERNAL SUBSTANCE USE
a. Cigarette smoking
• Dose dependant relationship with the number of cigarettes smoked & the risk of abruption & fetal loss.
• Compared with non smokers, smokers have 40% increased risk of fetal death from abruption with each pack of cigarette
smoked. 2 fold increased risk of abruption in smokers.
• Smoking & hypertension have additive effect on likelihood of placental abruption. Risk was 5 to 8 fold if smokers had
chronic hypertension, severe PE or both.
• Antepartum Vitamin C & E – protective for abruption in smokers
• Placental hypoperfusion with resulting ischemia & necrosis. Cigarette smoking causes vasoconstriction of the placental
vessel. When the spasm pass off, vasodilatation & capillary damage lead to decidual hematoma, that separate the
placenta from its attachment
b. Cocaine abuse
• Cocaine abuse in 3rd
trimester – 10% placental abruption rate
• Cocaine induced vasospasm with subsequent decidual ischemia, reflex vasodilatation & vascular disruption within the
placental bed

8. 6. RAPID UTERINE DECOMPRESSION
• Rapid decompression of an overdistended uterus –
as in multiple gestation or with polyhydramnios.
• Twins have 3 fold higher risk of abruption
compared to singletons
7. PPROM
• Abruption occurs in 2 to 5% of PPROM
• Risk of abruption is increased with comorbid
infection
• Abruption as cause of PPROM – Hemorrhage &
associated thrombin generation may stimulate
cytokine & protease production, leading to PPROM
• PPROM as cause of abruption – cytokine damage
following ruptured membranes may cause damage
to the decidual vasculature, leading to abruption

9. 8. TRAUMA
• Trauma following External Cephalic Version
• Motor vehicle accidents & domestic abuse
• After minor trauma, risk of abruption is 7 to 9%,
• After severe injury, risk of abruption is 13%
1. Uterine stretch
2. Direct penetration
3. Placental shearing from acceleration –
deceleration forces
9. THROMBOPHILIA
• Hyperhomocysteinemia – fasting level >15µ mol/L
• Thrombophilias associated with thromboembolic
disorders but not with abruption.
• Lupus anticoagulant associated with maternal floor
infarction of the placenta but less association with
abruption

10. 10. ISOLATED SINGLE UMBILICAL ARTERY
• 3.4 fold increased risk of abruption

11. 11. FOLIC ACID DEFICIENCY
• Important role in early embryogenesis.
• Deficiency in early pregnancy may cause defective
placentation, & its separation.
• Deficiency in later half of pregnancy doesn’t cause
abruption
12. SNAKE BITE
• Abruption & coagulation failure has been reported
in these cases.

12. Pathogenesis
• Defective maternal vessels in the decidua basalis , which rupture &
cause separation.
• Rarely, the separation maybe due to disruption of fetal placental
vessels
• Commonly decidual spiral arteriole rupture
• These vessels cause bleeding, resulting in decidual hematoma that
promotes placental separation, destruction of placental tissue, and a
loss of maternal – fetal surface area for nutrient & gas exchange.

13. Chronic
Acute
(After a sudden mechanical event – blunt trauma,
sudden uterine decompression, motor vehicle accident)
Abnormal development
of the spiral arteries
• Decidual necrosis
• Inflammation
• Infarction
• Bleeding due to vascular
disruption
Decidual
hemorrhage /
hypoxia
Thrombin
release
1. Direct uterotonic
2. Enhanced action of matrix metalloproteinase
3. Upregulates apoptosis genes
4. Increased expression of inflammatory cytokines
5. Triggers coagulation cascade
6. Functional progesterone withdrawal

14. Clinical manifestations
• Temporal nature – acute / chronic
• Clinical presentation – overt / concealed
• Severity - Total / partial

15. ACUTE OVERT ABRUPTION
• Vaginal bleeding, pain abdomen, uterine
contractions (high frequency, low amplitude)
• As the separation increases – uterine tenderness,
tachysystole, FHR abnormalities consistent with
fetal hypoxia and death
• Fetal death occurs with 50% separation of placenta
CHRONIC ABRUPTION
• Insidious presentation
• Associated with ischemic placental disease
• Intermittent light vaginal bleeding, evidence of
chronic placental inflammation & dysfunction like
oligohydramnios, fetal growth restriction, preterm
labor, PPROM, pre eclampsia
• CAOS – chronic abruption oligohydramnios sequence
• Can be associated with 1st
& 2nd
trimester bleeding
• Abnormally elevated levels of AFP, placenta specific
RNA
CLINICAL MANIFESTATIONS

16. REVEALED ABRUPTION
• Bleeding insinuates between the membranes &
uterus
CONCEALED ABRUPTION
• Blood is retained between the
detached placenta & the uterus.
Expanding retroplacental clot
Increased pressure within intervillous
space
More thromboplastin release into
maternal circulation
Increased risk of consumptive
coagulopathy
Overt/ revealed abruption Concealed abruption
(10 -20%)
MIXED ABRUPTION

17. TRAUMATIC ABRUPTION
• Motor vehicle accidents or aggravated
assault
• Associated feto maternal hemorrhage is
more common because of concomitant
placental tears or fractures.
• Due to deformation of the elastic
myometrium around the relatively
inelastic placenta
• Mostly concealed, occult – no uterine
pain, tenderness or bleeding;
• Features of fetal distress present – fetal
tachycardia, sinusoidal pattern, late
decelerations, acidosis, fetal death
NON TRAUMATIC ABRUPTION
• Separation within maternal
decidua, placental villi are
usually intact
• Bleeding is maternal

18. MATERNAL SEQUELAE
1. Shock
2. Transfusion
3. Disseminated intravascular
coagulation
4. Renal failure
5. Hysterectomy
6. Death
NEONATAL OUTCOMES
1. Preterm delivery
2. Growth restriction
3. Death
SEVERE ABRUPTION
FETAL COMPLICATIONS
1. Growth restriction
2. Non reassuring fetus
3. Fetal death

19. Diagnosis
• Clinical – supported by radiographic, laboratory, pathologic studies
1. Vaginal bleeding – mild to severe
2. Uterine contractions – high frequency, low amplitude; board like
rigidity
3. Abdominal / back pain
4. Trauma

20. Grading of placental abruption
Grade Description
0 Asymptomatic patient with retroplacental clot
1 Vaginal bleeding; uterine tetany & tenderness maybe present
No signs of maternal shock or fetal distress
2 External vaginal bleeding possible, no signs of maternal shock
Signs of fetal distress
3 External bleeding possible,
Marked uterine tetany – boardlike consistency on palpation
Persistent abdominal pain
Maternal shock & fetal demise
Coagulopathy maybe there in 30%

21. Radiology
• USG – only 24% sensitivity
• Early hemorrhage – hyper or iso echoic (DD – homogenous thickened placenta or fibroid)
• Resolving hematoma – hypoechoic within 1 week, sonolucent within 2 weeks of abruption
• Intrauterine clots can be seen floating in the amniotic fluid which “jiggle” on maternal movement
or on bouncing with the transducer – JELLO SIGN
• Negative finding with USG do NOT exclude placental abruption
• If USG is equivocal MRI can be used
• Location – 3 types

22. Subchorionic
• Between placenta &
membranes
• Better prognosis
• >60 ml = 10% fetal
mortality
Retroplacental
• Between placenta &
myometrium
• Worse prognosis
• >60 ml = >50% fetal
mortality
Preplacental
• Between placenta &
amniotic fluid

23. Laboratory investigations
• Maternal coagulopathy – hypofibrinogenemia
• Elevated
1. MSAFP – maternal serum alpha feto protein
2. HCG
• Decreased
1. PAPP – A
2. Estriol
Increased risk
of subsequent
abruption, if
noted in early
pregnancy

24. HISTOPATHOLOGY
• Macroscopic – adherent clot, depression of the
placental surface (chronic abruption)
• Microscopic :
Acute – preservation of villous stroma,
eosinophilic degeneration of
syncytiotrophoblast, scattered neutrophils
with villous agglutination
Chronic – chronic deciduitis, maternal floor
decidual necrosis, villitis, decidual
vasculopathy, infarction, thrombosis, villous
maldevelopment, hemosiderin deposition
PATHOLOGIC STUDIES

25. • At Cesarean section, widespread extravasation of blood
into the uterine musculature & beneath the serosa.
• Uterus appears bruised, bluish purple in colour, with
multiple ecchymosis in its wall, more marked over the
placental location.
• Serosa maybe ruptured causing intraperitoneal
hemorrhage
• Effusions of blood also seen beneath tubal serosa,
between leaves of broad ligament, in the substance of
ovary, & free in the peritoneal cavity.
• Not an indication for hysterectomy
COUVELAIRE UTERUS / UTEROPLACENTAL APOPLEXY

26. Revealed Mixed / concealed
Symptoms Abdominal discomfort or pain followed
by vaginal bleeding(usually slight)
Acute intense abdominal pain followed by
slight vaginal bleeding
Character of bleeding Continuous dark color
(slight to moderate)
Continuous, dark color(slight) or blood
stained serous discharge
General condition Proportionate to the visible blood loss,
(shock usually absent)
Shock maybe pronounced, out of
proportion to the amount of bleeding
Pallor Related with visible blood loss Usually severe & out of proportion to
amount of bleeding
Features of pre
eclampsia
Maybe absent Frequently associated
Uterine height Proportionate to period of gestation Maybe disproportionately enlarged &
globular
Uterine feel Normal feel with localised tenderness,
contractions frequent & low amplitude
Uterus is tense, tender & rigid
Fetal parts Can be identified easily Difficult to make out
FHS Usually present Usually absent
Urine output Normal Usually diminished
CLINICAL FEATURES

27. • General examination - Pulse, BP
• Abdominal examination
 Uterine size
 Consistency
 Tenderness
 Contractions
 Palpation of fetal parts
 Presentation
 Fetal heart sounds
• Local examination
 Vaginal bleeding
 Leaking of amniotic fluid
CLINICAL EXAMINATION
• Vaginal examination
 Clots in the vagina
 Cervical effacement
 Cervical dilatation
 Presence or absence of membranes
 Presentation / station
 Blood stained amniotic fluid

28. MATERNAL - SEVERITY
• Hemorrhage – intra peritoneal or broad ligament hematoma
• Shock
• DIC
• Oliguria & anuria, renal failure
 Hypovolemia
 Serotonin liberated from the damaged muscle produces renal
ischemia
 Acute tubular necrosis
 Cortical necrosis
COMPLICATIONS
• Preterm labor
• Instrumental delivery
• Cesarean section
• Rh sensitisation
• Post partum hemorrhage – uterine atony, increase
in serum FDP
• Sheehan syndrome
• Puerperal sepsis
• Maternal death

29. FETAL – TIMING & SEVERITY
• IUGR
• Oligohydramnios
• Prematurity
• Fetal hypoxia
• Hypoxia associated periventricular leukomalacia
• Fetal death – 10 fold higher risk
• Sudden infant death syndrome
• Long term adverse neurobehavioural outcomes
• With the same degree of placental separation, the fetus is more at
risk in abruptio placenta than in placenta previa – because of pre
existing placental pathology with poor functional reserve in
abruption

30. • The decidua which is rich in thromboplastin , due to damage releases thromboplastin, which enters the maternal
circulation & consumes fibrinogen to from intravascular clotting
• Normal fibrinogen level – 450 mg/dl
• In DIC - <100 mg/ dl causes afibrinogenemia and coagulation failure
• If the woman survives, plasmin is released which dissolves the clot by lysing the fibrin microemboli– raise in fibrin
degradation products above 10 microgram /ml
• Treatment – Epsilon Amino Caproic Acid (EACA) which inhibits plasminogen activation . 5to 15 g can be given as a iv
drip over 1-2 hours
• Trasylol – inhibits plasminogen activation. 25000 units is given iv
DIC – DEFIBRINATION SYNDROME

31. • Renal failure –
o Irreversible acute cortical necrosis
o Acute tubular necrosis
o Hypovolemia – when SBP falls below 80mm Hg , glomerular filtration comes to a standstill
o Prolonged spasm of glomerular vessels due to the toxins released resulting in anoxia & death of glomeruli
o Responds to treatment combating shock
END ORGAN INJURY

32. PRINCIPLES OF MANAGEMENT
1. Early diagnosis & assessment of the severity of abruption
2. Prompt hospitalization for close surveillance
3. Maternal resuscitation
4. Assessment of fetal condition
5. Early delivery – timing & method of delivery
6. Management of complications
MANAGEMENT

33. • Blood - Hb, Hct, coagulation profile, ABO and Rh typing
• Urine for protein
• 2 wide bore iv canula to be secured – Ringer solution drip is to be started till blood is cross matched.
• Close monitoring of maternal & fetal condition
• Communication with operation theatre & neonatal personnel.
• In Rh negative women – 300 micro gram of anti D
EMERGENCY MEASURES

34. IMMEDIATE DELIVERY INDICATIONS
• Irrespective of gestational age
 Moderate – severe bleeding
 Maternal complications
 Fetal distress
• Gestational age > 34 weeks with mild bleeding
EXPECTANT MANAGEMENT INDICATIONS
• Non severe abruption at < 34 weeks
• No maternal complications
• Fetal surveillance tests are normal
TYPE OF MANAGEMENT

35. VAGINAL DELIVERY
• Fetus is alive, FHR normal & bleeding is controlled
• Fetus is dead but maternal condition is stable
CESAREAN SECTION
• Abruption is severe & bleeding is persistent
• Non reassuring fetal status
• Maternal complications - renal failure , DIC
MODE OF DELIVERY IN ABRUPTION

36. PATIENT IS IN LABOR
• Labor is accelerated by low rupture of membranes
 Initiates myometrial contractions & labor process
 Expedites delivery
 Better compression of spiral artery to arrest hemorrhage
 Reduces entry of thromboplastin into maternal circulation
 Decreases risk of renal cortical necrosis & DIC
• vaginal delivery is favoured when
1. Limited placental abruption
2. FHR is reassuring
3. Facility for continuous electronic fetal monitoring is available
4. Prospect of vaginal delivery is soon
5. Placental abruption with dead fetus
PATIENT NOT IN LABOR
1. Induction of labor by low rupture of membranes – followed
by oxytocin augmentation (misoprostol is not preferred as it is
more associated with uterine tachysystole)
2. Cesarean section – indications
• Severe abruption with live fetus
• Amniotomy couldn’t be done (unfavorable cervix)
• Prospect of immediate vaginal delivery despite amniotomy is
remote
• Amniotomy failed to control bleeding
• Amniotomy failed to arrest abruption – fundal height continues
to increase
• Appearance of adverse features – fetal distress, falling
fibrinogen level, oliguria
 Correct associated consumptive coagulopathy – otherwise
intraop uncontrollable bleeding with increased risk of
hysterectomy
DEFINITIVE TREATMENT – IMMEDIATE DELIVERY

37. IT IS AN EXCEPTION, NOT THE RULE
• Bleeding is light & stopped (grade 1)
• Fetus reactive CTG and remote from term
 Goal – prolong pregnancy with the hope of improving fetal maturity & survival
 Continuous fetal monitoring
 Patient should be observed in labor ward for 24 – 48 hours to ensure that no further separation is occurring
 Steroid is given for lung maturity in case preterm delivery has to be contemplated
 Kleihauer Betke test & administration of Anti D if Rh negative
 Counselling at the time of discharge to return to hospital immediately if - bleeding recurs, fetal movements decrease,
uterine contractions begin
 Weekly BPP and estimation of fetal growth
 Deliver if feftal growth restriction, oligohydramnios or recurrent bleeding
 Induction of labor at 37 -38 weeks by cervical ripening with prostaglandin E2, amniotomy and oxytocin
EXPECTANT MANAGEMENT

39. THANK YOU