Antepartum Hemorrhage

Antepartum hemorrhage
Objective
1.Be familiar with RCOG guide lines: APH
2.Causes(P.P, A.P, Vasaprevia, Accreta)
3.Understand the mechanism of DIC
4.Safe use of blood products
5.Be competent in Mx of APH & major obstetric Hg.
6.Have attended skills drills on obstetric collapse.
7.Be able to localize the placenta in T3 , FH activity
4% of women may develop antepartum hemorrhage( bleeding from the genital

tract from 24 weeks gestation and before the onset of labor). Is one of
commonest reasons for hospital admission in pregnancy.
Minor bleeding= bleeding less than 50 ml ,
Major bleeding= 50-1000 ml with no sign of clinical shock
Massive bleeding= more than 1000 ml with sign of clinical shock
Causes:
placenta previa (is variable depending on population and cs rate 0.4-0.8 %)
placental abruption (5%)
Uterine rupture (<1% in scarred uterus )
vasa previa (0.015-0.04%)
AP and PP account 50% of APH
Local causes( cervical infection.trauma,ectropian, tumor, varicosities)
Placental abruption Premature separation of normally implanted placentae

it occure 5% of pregnancies, some cases not visible seen only on exam of
placenta after delivery.

G0 asymptomatic retroplacental clot after delivery
G1 vaginal bleeding, uterine tenderness, visible retroplacental clot

after delivery
G2 revealed bleeding may or may not present but placental separation is
significant enough to produce evidence fetal compromise and retroplacental
clot visible after delivery
G3 revealed bleeding may or may not be seen but there are asignificant
maternal signs(uterine tetany, hypovolaemia, abdominal pain) with late stage
fetal compromise or fetal death, 30% develop DIC.
The bleeding from A.P insinuate itself between the membrane and uterus,
ultimately blood escaping through the cervix causing external bleeding, less
often doesn't escape externally, but is retained between the detached placenta
and the uterus leading to concealed hemorrhage.
Abruption placenta either total separation of placenta or partial. Concealed Hg.
Carries greater maternal and fetal risk and hazards(consumptive
coagulopathy, extent of Hg.readily appreciated, diagnosis typically delayed)
Significance
A.P severely depend on who quickly the woman is seen following
symptom onset, with delay extensive separation occurs causing fetal
death. Incidence 1/100 deliveries.
Risk factors
1. previous AP 8 times increased risk than background rate

2. family history of AP has sister history of AP double the risk
3. fetal abnormality(aneuploidy)
4. rapid uterine decompression(RM in polyhydromias)
5.chorioamnionitis/premature RM=3 fold increase

6. smoking , drug abuse(cocaine , amphetamine) 2 fold increase with smoking,
5-8 fold if smoking with chronic HT
7. abnormal placentation(circumvallate placenta)
8. pre-eclampsia, growth restriction, oligohydromias
9. underlying thrombophilia (inherited or acquired, factor V (leiden or
prothrombinogen mutation
10. trauma. Traumatic abruption like motor vehicle accident or physical
violence
11.first T bleeding especially if hematoma seen
12.low BMI, assisted reproduction, multiparous, older woman
13. Race and ethnicity A.P common in African-American and Caucasian
women(1-200), Asian (1-300), Latin American(1-450)
14. Leiomyoma specially if located behind the placental implantation site
predispose to abruption.
Pathology
Placental abruption is initiated by Hg. Into decidua basalis then decidua splits,
leaving a thin layer adhered to the myometrium.
The process in its earliest stage consist of development of decidual hematoma
that is leads to separation, compression and ultimate destruction of the
placenta adjacent to it.
Histological inflammation and infection lead to abruption
In early stage, no clinical symptom, discovered upon examination of the
freshly delivered placenta.
Concealed Hg.
1. Effusion behind the placenta but its margin remain adherent

2. Placenta completely separated but the membrane retain their attachment to
the uterine wall.
3. Blood cross the amniotic cavity after breaking through the membrane.
4. The fetal head is so closely applied the lower uterine segment that blood
cannot makes its way.

Chronic placental abruption : Hg with retro placental hematoma formation
is somehow arrested completely without delivery.
Fetomaternal Hg. Bleeding in A.P always almost maternal(separation with

in maternal decidua), non-traumatic abruption only 10 ml fetal blood while
in traumatic abruption more fetal blood because tear from placental surface
rather than separation.
Clinical diagnosis:
The diagnosis of AP is primarly clinical one, there may be no revealed

bleeding, sign and symptoms of A.P vary considerably, external bleeding can
be profuse with placenta not completely separated(no fetal compromise),
rarely no external bleeding with placenta completely separated(fetus dead)
DIC(consumptive coagulopathy)
Abdominal pain, uterine tenderness, back pain.
Preterm labor initially diagnosed, frequent uterine contraction and persistent
uterine hyper tonus.
Sonographically infrequent confirms the diagnosis of placental abruption at
least acutely because the placenta and fresh clot have similar sonographic
finding, but US used for( fetal viability, growth, liquor volume, umbilical artery
Doppler velocity, fetal normality, exclude PP)
Kleihauer testing should performed(appropriate dose of Anti D)
D.DX
Sever abruption obvious
Mild-moderate, any vaginal bleeding with a life fetus necessary to exclude P.P
and other cause of bleeding by clinical and sonographic assessment.
Painful uterine bleeding --- A.P
Painless uterine bleeding --- P.P
Labor accompany previa may cause pain suggestive placental abruption. Pain
from abruption may mimic labor, it may be painless especially with posterior
placenta, so the cause of bleeding remain obscure even after delivery.

Complication
1. Shock in A.P disproportionate to amount of Hg ., placental thromboplastin

enter maternal circulation --- intravascular coagulation, hypovolemic shock
seen in 1/2 of patient, oliguria from decrease renal perfusion which is
responsive to vigorous I.V fluid and blood infusion.
2. Consumptive coagulopathy A.P is one of the most common cause of
coagulopathy in obstetric. 1/3 of A.P that kill the baby have measurable
coagulopathy,
hypofibrinogenoemia less than 150 mg/dl, elevated FDP&D dimer,
coagulopathy higher with concealed A.P because intrauterine pressure higher
thus forcing thromboplastin into maternal venous system, procougulant also
consumed in retro placental clot.
Thrombocytopenia may or may not accompany hypofibrinogenomia, but it
is common after repeated blood transfusion.
3. renal failure acute renal failure is seen in sever A.P sp. If treat of
hypovolaemia is delayed or incomplete, most cases are reversible.
4. Sheehan syndrome sever intra partum or postpartum is rarely followed by
pituitary failure ( failure of lactation, amenorrhea , breast atrophy , loss of
pubic& axillary hair , adrenal cortical insufficiency)
5-couvelarae uterus wide spread extravasation of blood into uterine
musculature beneath uterine serosa, sometime beneath tubal serosa, broad
ligament ovaries, free in the peritoneal cavity, this myometrial Hg.
Interfere with myometrium contraction cause atonia.
6-adult respiratory distress syndrome, multiorgan failure,death
7- fetal complication (growth restriction with chronic abruption, fetal
hypoxia or asphyxia, preterm birth, perinatal mortality.
Management
Patient suspected to have A.P should have rapid initial evaluation and the
subsequent Mx. Depend on
1. Gestational age
2. Severity of A.P
3. Status of the mother and fetus
Most cases hypovolemia so
- continuous fetal monitoring

- I.V access 2 wide bore IV cannula
-pulse &BP closely monitored
-Foleys catheter, maternal UOP hourly monitored(30 ml/hr)
-CBC, blood group ,RH, PT,PTT
-blood and its product
replacement(FFP,cryoprecipitate&platelets),maintain the hematocrit above
30%(300 ml Packed RBC contain 200 ml RBC rise hematocrit 3-4% in absence
of continuous bleeding, give six unit of platelet if marked
thrombocytopenia(less 50,000/microl) with serious bleeding or planned C/S,
FFP or cryoprecipitate is indicated for fibrinogenovel less than 150.
Subsequent management
When to deliver
Fetal compromise at variable gestation should be deliverd(cs if term,near
term, late preterm, perinatal mortality 15-20%)
Very low gestatinal age vaginal delivery should be the aim, labour is often
quick although prostaglandin and oxytocin can be used. If dead fetus
vaginal delivery should be the expectation.
Live fetus near term the fetus should delivered by quickest safest mothed,
vaginal delivery is safest, C/S indicated if FH tracing is not reassuring, there is
ongoing major blood loss or other serious maternal complication, vaginal
delivery contraindicated.
Live birth remote from term FH reassuring, stable maternal condition,
delaying delivery near term, glucocorticoid
Feta death delivery mode vaginally to decrease maternal morbidity
and mortality, unless CI to vaginal delivery, or urgent delivery needed
to stabilization maternal condition

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Antepartum hemorrhage

4% of women may develop antepartum hemorrhage( bleeding from the genital

Placental abruption Premature separation of normally implanted placentae

placenta after delivery.

G1 vaginal bleeding, uterine tenderness, visible retroplacental clot

symptom onset, with delay extensive separation occurs causing fetal

death. Incidence 1/100 deliveries.

1. previous AP 8 times increased risk than background rate

5.chorioamnionitis/premature RM=3 fold increase

1. Effusion behind the placenta but its margin remain adherent

cannot makes its way.

is somehow arrested completely without delivery.

Fetomaternal Hg. Bleeding in A.P always almost maternal(separation with

The diagnosis of AP is primarly clinical one, there may be no revealed

placenta, so the cause of bleeding remain obscure even after delivery.

1. Shock in A.P disproportionate to amount of Hg ., placental thromboplastin

hypoxia or asphyxia, preterm birth, perinatal mortality.

- continuous fetal monitoring

and mortality, unless CI to vaginal delivery, or urgent delivery needed

to stabilization maternal condition

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