‫لليان سرسم‬.‫د‬.

‫ا‬
2020-2021
ANTEPARTUM HAEMORRHAGE
Learning objectives:
At the end of this lecture, the 4th year students will be able to:
1. Define antepartum hemorrhage.
2. Identify the risk factors for placenta previa, abruptio placenta and
placenta accreta.
3. Describe the clinical features and diagnostic criteria for placenta
previa, placental abruption and placenta previa accreta.
4. Distinguish between placenta previa. abruptio placenta and other
possible causes.
5. Describe the appropriate management plan based on the cause.
Definition: This is defined as bleeding from or in to the genital tract,
occurring after 20 weeks of pregnancy and prior to the birth of the baby
Incidence: It complicates 2–5% of pregnancies.
Aetiology:
1. Placental causes: placental abruption; placenta praevia.
2. Fetal cause: vasa praevia.
3. Maternal causes: vaginal trauma; cervical ectropion; cervical
carcinoma; cervicitis and vaginal infection.

PLACENTAL ABRUPTION
Definition:
Abruptio placentae: Placental abruption is defined as premature separation
of the placenta from the uterine wall. The bleeding is from the placental bed
of a normally sited placenta.
It may occur as an antepartum or an intrapartum event.
Two principal forms:

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Concealed form (20%), the haemorrhage is confined within the uterine
cavity, detachment of the placenta may be complete, and the complications
are often severe. Approximately 10% of abruptions are associated with
clinically significant coagulopathies (disseminated intravascular coagulation.
External form (Revealed) (80%), the blood drains through the cervix,
placental detachment is more likely to be incomplete, and the complications
are fewer and less severe.
Etiology:
The exact etiology of placental abruption is unclear.
Predisposing factors:
 Previous abruption. Following one episode, the incidence of
recurrence is 10–17%. Following 2 previous episodes, the incidence
of recurrence exceeds 20%.
 Hypertention: The hypertensive states of pregnancy are associated
with 2.5–17.9% incidence of placental separation. However, in
abruptio placentae extensive enough to cause fetal death, about 50%
of cases are associated with hypertensive states of pregnancy.
Approximately half of these cases have chronic hypertension and half
pregnancy-induced hypertension.
 Poor nutrition.
 Other predisposing factors include: advanced maternal age,
multiparity, uterine distention (eg, multiple pregnancy,
polyhydramnios), vascular deficiency (eg, diabetes mellitus, collagen
diseases complicating pregnancy), uterine anomalies or tumors (eg,
leiomyoma), cigarette smoking, alcohol consumption, fetal
abnormality especially aneuploidy.
Precipitating factors:
Precipitating causes of premature separation of the placenta are rare,
included in this category are circumvallate placenta, trauma (eg, external or
internal version, abdominal trauma directly transmitted to an anterior
placenta), sudden reduction in uterine volume i.e. rapid uterine
decompression (eg, rapid amniotic fluid loss, delivery of a first twin),
abnormally short cord.

DIAGNOSIS:
The diagnosis of placental abruption is primarily a clinical one.
A. Clinical presentation
The characteristic presentation of placental abruption is that of painful
bleeding associated with a tense rigid abdomen. The absence of a tense

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abdomen does not rule out a placental abruption. Placental abruption may be
diagnosed on ultrasound but the absence of any ultrasound changes does not
rule it out and patients should be managed on the basis of their clinical
findings.
The degree of vaginal bleeding does not necessarily correlate with the
degree of abruption as abruptions may be concealed (i.e. significant
separation between placenta and uterus but blood is concealed between the
placenta and uterus so there is little vaginal bleeding seen.
Symptoms and signs are:
• Vaginal bleeding
• Abdominal pain
• Sweating
• Hypotension
• Tachycardia
• Absence or reduced fetal movements
• Tense and tender uterus
• Large for date uterus
• Hypovolaemic shock (that may be out of proportion of visible
bleeding).
• CTG may reveal evidence of fetal distress.
Warning signs: maternal collapse, feeling cold, light-headedness,
restlessness, distress and panic, painful abdomen, vaginal bleeding.
B. LABORATORY FINDINGS AND IMAGING:
1. Haemoglobin and haematocrit: The degree of anaemia will probably be
considerably less than the amount of blood loss would seem to justify,
because changes in haemoglobin and haematocrit are delayed during acute
blood loss until secondary haemodilution has occurred.
2. Peripheral blood smear: A peripheral blood smear may show a reduced
platelet count; the presence of schistocytes, suggesting intravascular
coagulation.
3. Fibrinogen and FDP: Fibrinogen depletion with release of fibrin
degredation products. If serial laboratory determinations of fibrinogen levels
are not available, the clot observation test, a simple but invaluable bedside
procedure, can be performed. A venous blood sample is drawn every hour,
placed in a clean test tube, and observed for clot formation and clot lysis.
Failure of clot formation within 5–10 minutes or dissolution of a formed clot
when the tube is gently shaken is proof of a clotting deficiency.
The following will assist in determination of coagulation status:
prothrombin time and partial thromboplastin time, platelet count,
fibrinogen, and fibrin degredation products.

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4. Ultrasonography: may be useful but is not totally reliable, because it
may not reveal the retroplacental clot in most cases.
Effects on the mother:
1. Hypovolaemic shock.
2. Disseminated intravascular coagulation (DIC): Is always a secondary
phenomenon following a trigger to generalized activation of coagulation
systems. The incidence is very variable, but serious DIC probably affects
about 0.1% of pregnancies. Laboratory investigations include measuring the
thrombin time, FDPs and platelet count. In cases of significant DIC, it is
vital to involve the haematologist in the early care of the woman.
3. Renal cortical and tubular necrosis: The possibility of renal cortical or
tubular necrosis must be considered if oliguria persists after an adequate
blood volume has been restored. An attempt should be made to improve
renal circulation and promote diuresis by increasing fluid volume (with the
aid of monitoring). If oliguria or anuria persists, renal necrosis is probable
and fluid intake and output must be carefully monitored. Continuing
impairment of renal function may require peritoneal dialysis or
haemodialysis.
4. Feto-maternal haemorrhage.
5. Maternal mortality.
6. Recurrence: 10% after a single episode of abruption, and 25% after two
episodes.
Effects on the fetus:
1.Perinatal mortality.
2.Intrauterine growth restriction.

Treatment:
A. EMERGENCY MEASURES
If the patient exhibits clinical findings that become progressively more
severe or if a major placental separation has already occurred as manifested
by haemorrhage, uterine spasm, or fetal distress, an acute emergency exists.
Blood should be drawn for laboratory studies and at least 4 units of packed
red blood cells typed and crossed. Two large-bore intravenous catheters
should be placed and crystalloid administered.
B. CONSERVATIVE ( EXPECTANT) MANAGEMENT
Expectant management is appropriate when the mother is stable, the fetus is
immature, and the fetal heart tracing is reassuring. The patient should be
observed on the labor and delivery suites for 24–48 hours to ensure that
further placental separation is not occurring. Continuous fetal and uterine

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monitoring should be maintained. Changes in fetal status may be the earliest
indication of an expanding abruption.
C. VAGINAL DELIVERY
An attempt at vaginal delivery is indicated if:
 The degree of separation appears to be limited and if the continuous
fetal heart rate tracing is reassuring.
 When placental separation is extensive but the fetus is dead or of
dubious viability.
The exception to vaginal delivery occurs when haemorrhage is
uncontrollable and operative delivery is necessary to save the life of the
fetus or mother.
Induction of labor with an oxytocin infusion should be instituted if
active labor does not begin shortly after amniotomy. In practice,
augmentation is often not needed, because usually the uterus is already
excessively irritable. If the uterus is extremely spastic, uterine contractions
cannot be clearly identified unless an internal monitor is used, and the
progress of labor must be judged by observing cervical dilatation. Progress
in labor is usually so rapid that forceps are not needed to shorten the second
stage of labor. Pudendal block anesthesia is recommended.

D. CAESAREAN SECTION
The indications for caesarean section are both fetal and maternal.
 Abdominal delivery should be selected whenever delivery is not
imminent for a fetus with a reasonable chance of survival who
exhibits persistent evidence of distress.
 Caesarean section is also indicated if the fetus is in good condition
but the situation is not favorable for rapid delivery in the face of
progressive or severe placental separation. This includes most
nulliparous patients with less than 3–4 cm of cervical dilatation.
 Maternal indications for caesarean section are: uncontrollable
haemorrhage from a contracted uterus, a rapidly expanding uterus
with concealed haemorrhage (with or without a live fetus) when
delivery is not imminent.

The mother must be continuously monitored well into the postpartum period
for evidence of a clotting deficiency. There may be depletion not only of
fibrinogen but also of platelet and of factors II, V, VIII, and X. Treatment
will depend not only on the demonstration of haematologic deficiencies but
also on the amount of active bleeding and the anticipated route of delivery.

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Cross match for blood and blood replacement. Packed red blood cells are
satisfactory for immediately replacing blood loss, but they do not contain
clotting factors.
Cryoprecipitate packs contain all the necessary labile coagulation factors.
During active bleeding, the transfusion of platelets is often the best practical
means of counteracting a clotting deficiency. Fibrinogen is rarely indicated.
The best source of fibrinogen other than fresh blood is a cryoprecipitate.
Concentrated plasma can also be used.
The prophylactic administration of heparin to block conversion of
prothrombin to thrombin (and thereby reduce the consumption of
coagulation factors) has been successfully employed in the management of
the defibrination associated with fetal death. The value of heparin in the
treatment of acute placental separation has never been established; its use
cannot be recommended because of the risks of operative and postoperative
hemorrhage if cesarean section is required.
Preparation for surgery must be completed quickly. If caesarean section is
indicated, materials to control a clotting deficiency must be on hand before
an operation is undertaken, and treatment with coagulants should be
underway if a clotting deficiency is already present.

Prognosis:
Unfavorable prognostic factors are: External or concealed bleeding,
excessive blood loss, shock, nulliparity, a closed cervix, absence of labor,
and delayed diagnosis and treatment. Maternal mortality rates ranging from
0.5% to 5% are currently reported from various parts of the world. Most
women die of haemorrhage (immediate or delayed) or cardiac or renal
failure. A high degree of suspicion, early diagnosis, and definitive therapy
should reduce the maternal mortality rate to 0.5–1%.
With severe abruption reported fetal mortality rates range from 50% to 80%.
In about 15% of cases, no fetal heartbeat can be heard on admission to the
hospital, and in another 50% fetal distress is noted early. Liveborn infants
have a high rate of morbidity resulting from predelivery hypoxia, birth
trauma, and the hazards of prematurity (40–50%).

PLACENTA PRAEVIA
Definition:
Term used when the placenta is covering or encroaching on the internal
cervical os, which may be associated with bleeding, either provoked or
spontaneous.

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The placenta is partially or wholly implanted in the lower uterine segment
within the zone of effacement and dilatation of the cervix.
Incidence:
Placenta praevia is encountered in approximately 1 in 200 births. About 90%
of patients will be parous. Among grand multiparas the incidence may be as
high as 1 in 20. Incidence of placenta previa is gestational age- dependent.
Before 20 weeks’ gestation incidence is 1-6%. After second trimester is
0.4%. Recurrence rate is 4-8%

Classification:
The classification grades of placenta praevia:
Grade 1 The placenta reaches the lower segment but not the internal os.
Grade 2 The placenta reaches the internal os but does not cover it.
Grade 3 The placenta covers the internal os before dilatation but not when
dilated.
Grade 4 The placenta completely covers the internal os of the cervix even
when dilated
Grades 1 & 2 represent a minor degree of placenta previa.
Grades 3 & 4 represent a major degree of placenta previa.

Risk factors:
1. Prior cesarean delivery.
2. Advanced maternal age.
3. Multiparity.
4. Prior uterine surgery.
5. Multiple gestation.
6. Uterine structural anomaly.
7. Assisted conception.
8. Smoking.
Association was found with fetal abnormality, IUGR, and may coexist
with placental abruption (in 10%).

Diagnosis:
A. SYMPTOMS AND SIGNS
Painless haemorrhage is the cardinal sign of placenta praevia. Although
spotting may occur during the first and second trimesters of pregnancy, the
first episode of haemorrhage usually begins at some point after the 28th
week and is characteristically described as being sudden, painless, and
profuse. With the initial bleeding episode, clothing or bedding is soaked by

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an impressive amount of bright red, clotted blood, but the blood loss usually
is not extensive, seldom produces shock, and is almost never fatal. In a small
minority of cases, bleeding will be less dramatic or will not begin until after
spontaneous rupture of the membranes or the onset of labor. A few
nulliparous patients even reach term without bleeding, possibly because the
placenta has been protected by an uneffaced cervix.
Uterus usually is soft, relaxed, and not tender. A high presenting part
cannot be pressed into the pelvic inlet. The fetus will present in an oblique
or transverse lie in about 15% of cases. No evidence of fetal distress is
likely unless there are complications such as hypovolaemic shock, abruption,
or a cord accident.
Warning signs: low-lying placenta at 20 week anomaly scan, maternal
collapse, feeling cold, light-headedness, restlessness, distress and panic,
painless vaginal bleeding.
B. ULTRASONOGRAPHY
The real-time scanner is ideal for screening purposes, because the equipment
is portable, the test is rapidly and easily performed, and the accuracy rate is
over 95%. During the middle of the second trimester, the placenta will be
observed by ultrasound to cover the internal cervical os in about 30% of
cases. With development of the lower uterine segment, most of these low
implantations will be carried to a higher station. Transvaginal ultrasound is
the diagnostic technique of choice for placenta praevia. It is safe and is more
accurate than transabdominal ultrasound in locating the placenta and in
diagnosing placenta praevia in the posterior lying placenta.
Treatment:
Placenta praevia is most dangerous for the mother. The type of treatment
given depends on the amount of uterine bleeding; the duration of pregnancy
and viability of the fetus; the degree of placenta praevia; the presentation,
position, and station of the fetus; the gravidity and parity of the patient; the
status of the cervix; and whether or not labor has begun. The patient must be
admitted to the hospital to establish the diagnosis and ideally should remain
in the hospital once the diagnosis is made. Two or more units of bank blood
should be typed, cross-matched, and ready for transfusion.
A. EXPECTANT THERAPY
( Macafee regime of expectant management )
Early in pregnancy, transfusions to replace blood loss and the use of
tocolytic agents to prevent premature labor are indicated to prolong
pregnancy to at least 36 weeks. After 36 weeks, the benefits of additional
maturity must be weighed against the risk of major haemorrhage. About

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75% of cases of placenta praevia are now terminated at between 36 and 40
weeks.
Antenatal corticosteroids should be considered if gestation is less than 35
weeks as the risk of preterm delivery is significant, a single course of
betamethasone (two doses of 12 mg intramuscularly separated by 24 hours)
should be given to promote fetal lung maturity. Clinical judgment should be
exercised as to the timing of steroid administration.
Because of the costs of hospitalization, patients with a presumptive
diagnosis of placenta praevia are sometimes sent home after their condition
has become stable under ideal, controlled circumstances. Such a policy is
always a calculated risk in view of the unpredictability of further
haemorrhage.

B. DELIVERY
1. Caesarean section—Caesarean section is the delivery method of
choice with placenta praevia. Caesarean section has proved to be the most
important factor in lowering maternal and perinatal mortality rates. If
possible, hypovolemic shock should be corrected by intravenous fluids and
blood before the operation is started.
Regarding choice of anaesthesia, a combination of rapid induction,
endotracheal intubation, succinylcholine, and nitrous oxide is a suitable way
to proceed in the presence of active bleeding.
The choice of operative technique is of importance because of the
placental location and the development of the lower uterine segment. If the
incision passes through the site of placental implantation, there is a strong
possibility that the fetus will lose a significant amount of blood. With
posterior implantation of the placenta, a low transverse incision may be best
if the lower uterine segment is well developed. Otherwise, a classic incision
may be required to secure sufficient room and to avoid incision through the
placenta.
Preparations should be made for care and resuscitation of the infant if it
becomes necessary. In addition, the possibility of blood loss should be
monitored in the newborn if the placenta has been incised. A fall in
haemoglobin to 12 g/dL within 3 hours or to 10 g/dL within 24 hours
requires urgent transfusion.
In a small percentage of cases, haemostasis in the placental bed will be
unsatisfactory, because of the poor contractility of the lower uterine
segment. Mattress sutures or packing may be required in addition to the
usual oxytocin, prostaglandins, and ergometrine. If placenta praevia increta

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is found, haemostasis may necessitate a total hysterectomy. Puerperal
infection and anaemia are the most likely postoperative complications.
2. Vaginal delivery: Vaginal delivery is usually reserved for patients
with a minor degree placenta praevia and a cephalic presentation. If vaginal
delivery is elected, the membranes should be artificially ruptured prior to
any attempt to stimulate labor (oxytocin given before amniotomy is likely to
cause further bleeding). Tamponade of the presenting part against the
placental edge usually reduces bleeding as labor progresses.
Because of the possibility of fetal hypoxia either due to placental separation
or to a cord accident, continuous fetal monitoring must be employed. If fetal
distress develops, a rapid caesarean section should be performed unless
vaginal delivery is imminent. Deliver the patient in the easiest and most
expeditious manner as soon as the cervix is fully dilated and the presenting
part is on the perineum.
Complications:
A. MATERNAL
Maternal haemorrhage, shock, and death may follow severe antepartum
bleeding resulting from placenta praevia. Death may also occur as a result of
intrapartum and postpartum bleeding, operative trauma, infection, or
embolism. Premature separation of a portion of a placenta praevia occurs in
virtually every case and causes excessive external bleeding without pain;
however, complete or wide separation of the placenta before full dilatation
of the cervix is uncommon. Placenta praevia accreta is a rare but serious
abnormality.
B. FETAL
Prematurity (< 36 weeks gestation) due to placenta praevia accounts for 60%
of perinatal deaths. The fetus may die as a result of intrauterine asphyxia or
birth injury. Fetal haemorrhage due to tearing of the placenta occurs with
vaginal manipulation and especially upon entry into the uterine cavity as
caesarean section is done for placenta praevia. About half of these caesarean
babies lose some blood. Fetal blood loss is directly proportionate to the time
that elapses between lacerating the cotyledon and clamping the cord.
Prognosis:
A. MATERNAL
With the use of caesarean section, use of banked blood, and expertly
administered anaesthesia, the overall maternal mortality has fallen to < 1%.
B. FETAL

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The perinatal mortality rate associated with placenta praevia is
approximately 10%. Although premature labor, placental separation, cord
accidents, and uncontrollable haemorrhage cannot be avoided, the mortality
rate can be greatly reduced if ideal obstetric and newborn care is given.

PLACENTA ACCRETA
Placenta accreta spectrum disorders:
Definition: Placenta accreta spectrum, formerly known as morbidly
adherent placenta, refers to the range of pathologic adherence of the placenta
including placenta accreta, increta, percreta.
Classification:
Placenta accreta—villi adhere to the superficial myometrium.
Placenta increta—villi invade the myometrium.
Placenta percreta—villi penetrate the full thickness of the myometrium.
Pathogenesis:
Both excessive penetrability of the trophoblast and defective or missing
deciduas basalis have been suggested as causes of placenta accreta.
Although the exact cause is unknown, several clinical situations are
associated with placenta accreta, such as previous caesarean section,
placenta previa, grand multiparity, previous uterine curettage, and previously
treated asherman’s syndrome..
Among women with placenta previa, the risk or accreta range from 2% in
women less than 35 years of age with no previous caesarean deliveries to
almost 39% in women with 2 or more previous caesarean deliveries and an
anterior central placenta previa.
Diagnosis:
 Adverse effects from placenta accreta in pregnancy or during the
course of labour and delivery are uncommon. Rarely, intra-abdominal
hemorrhage or placenral invasion of adjacent organs prior to labour
has occurred, with the diagnosis made at laparotomy.
 Diagnosis prior to delivery:
1. Ultrasonographic examination: Lack of the sonolucent area normally
visible retroplacentally.
2. Color Doppler imaging appear to be particularly helpful in the
diagnosis.
3. MRI has also aided in the diagnosis.

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  Most diagnosed in the third stage of labour when no plane of cleavage
is found between the placenta or parts of placenta and the
myometrium in presence of postpartum hemorrhage.
Complications:
1. Massive blood loss and hypotension.
2. Intrauterine manipulation necessary to diagnose and treat
placenta accreta may result in uterine perforation and infection.
3. Sterility may occur as a result of hysterectomy performed to
control bleeding.
4. Maternal death.
Treatment:
Successful treatment depends upon immediate blood replacement. Fluid and
blood replacement should begin as soon as excessive blood loss is
diagnosed. Conservative treatment in women of low parity, for women
who desire to preserve their fertility is increasingly attempted but successful
conservative treatment is rare but may be a reasonable option if only focal
defects are present, blood loss is not excessive, and the patient wishes to
preserve fertility.
1. The placenta (or portions of it) is left in situ to slough off later or
using methotrexate adjuvant treatment post operatively to hasten
placental resolution.
2. Internal iliac artery ligation.
3. Hydrostatic balloon.
4. Angiographic embolization.
The most generally accepted approach to placenta accreta spectrum is
cesarean hysterectomy with placenta left in situ after delivery of the fetus.
Nearly always prompt hysterectomy is needed.

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