ABRUPTIO PLACENTAE

(accidental haemorrhage)
Definition:

It is one form of antepartum haemorrhage where the bleeding occurs due to premature separation of normally situated placenta before delivery.

Incidence- 0.6-1% of all births.

It can occur any time after 20 wks but most common in 3 rd trimester
Incidence....
• Depending on the extent (partial or complete) and intensity of
placental separation, it is a significant cause of perinatal mortality
(15–20%) and maternal mortality (2–5%).
• ABRUPTIO placentae contribute nearly to 30% of all APH cases and
majority (60%) occur in third trimester of pregnancy.
Types
1. Revealed :
• Following separation of the placenta, the blood insinuates downwards
between the membranes and the decidua.
• Ultimately, the blood comes out of the cervical canal to be visible
externally.
• This is the most common type(80%)
• 2) Concealed :
• The blood collects behind the separated placenta or collected in
between the membranes and decidua.
• The collected blood is prevented from coming out of the cervix by the
presenting part which presses on the lower segment.
• At times, the blood may percolate into the amniotic sac after
rupturing the membranes. In any of the circumstances blood is not
visible outside.
• This type is rare(20%).
• (3) Mixed :
• In this type, some part of the blood collects inside (concealed) and a
part is expelled out (revealed).
• Usually one variety predominates over the other.
• Bleeding is almost always maternal.
Etiology
• Risk factors are : (a) high birth order pregnancies with gravida 5 and above —
three times more common than in first birth
• (b) advancing age of the mother
• (c) poor socio-economic condition
• (d) malnutrition
• (e) smoking (vasospasm).
•
• Hypertension in pregnancy is the most important predisposing factor.
• Preeclampsia, gestational hypertension and essential hypertension, all are
associated with placental abruption.
• The association of preeclampsia in abruptio placentae varies from 10% to
50%.
The mechanism of the placental separation in preeclampsia is:
• Spasm of the vessels in the utero-placental bed (decidual spiral artery)
→ anoxic endothelial damage → rupture of vessels or
extravasation of blood in the decidua basalis (retroplacental
hematoma).
• Trauma: Traumatic separation of the placenta usually leads to its
marginal separation with escape of blood outside.
• The trauma may be due to: (i) Attempted external cephalic version
specially under anesthesia using great force
(ii) Road traffic accidents or blow on the abdomen
(iii) Needle puncture at amniocentesis.
• Sudden uterine decompression: Sudden decompression of the uterus
leads to diminished surface area of the uterus adjacent to the placental
attachment and results in separation of the placenta.
• This may occur following—
(a) delivery of the first baby of twins
(b) sudden escape of liquor amnii in hydramnios and
(c) premature rupture of membranes.
• Short cord, either relative or absolute, can bring about placental
separation during labor by mechanical pull.
• Supine hypotension syndrome: In this condition which occurs in
pregnancy there is passive engorgement of the uterine and placental
vessels resulting in rupture and extravasation of the blood.
• Placental anomaly: Circumvallate placenta
• Elevated maternal serum alpha fetoprotein levels
• Sick placenta: Poor placentation, evidenced by abnormal uterine artery
Doppler waveforms is associated with placental abruption.
• Folic acid deficiency even without evidence of overt megaloblastic
erythropoiesis — this has been observed to be associated.
• Uterine factor: Placenta implanted over a septum (Septate Uterus) or a
submucous fibroid.
• Torsion of the uterus leads to increased venous pressure and rupture of
the veins with separation of the placenta.
• Cocaine abuse is associated with increased risk of transient
hypertension, vasospasm and placental abruption.
• Thrombophilias, inherited or acquired have been associated with
increased risk of placental infarcts or abruption.
• Prior abruption: Risk of recurrence for a woman with previous abruption
varies between 5% and 17%.
 Pathogenesis
Lack of trophoblastic invasion of uterine vessels result in
decreased placental blood flow and abnormal response to
vasopressor substances.
The resultant spasm of vessels supplying the placental site
results in capillary anoxia and endothelial disruption.
The damaged capillaries are unable to cope up with vascular
engorgement, results in bleeding.
Pathogenesis:

• This results in the formation of haematoma and an increase in hydrostatic

pressure leading to separation of the adjacent placenta.
• The resultant haematoma may be small and self-limited or may continue to
dissect through the decidual layer.
• In a full blown case of concealed haemorrhage, the uterine size is greater
than the period of gestation and contains a large retroplacental clot that may
track beyond the confines of the placental margin and may burst into the
amniotic sac.
• Blood may dissect into myometrium towards serosa and releases
thromboplastins and bleeding into myometrial layers (Couvelarie uterus).
 RCAS1 is the membrane protein that plays a role in the
maintainence of maternal immune tolerance during pregnancy.
This protein is shown to be potentially involved in the
mechanism of abruption.
• COUVELAIRE UTERUS (uteroplacental apoplexy)
• It is a pathological entity first described by Couvelaire and is met with
in association with severe form of concealed abruptio placentae.
• There is massive intravasation of blood into the uterine musculature
upto the serous coat.
• Hematoma freely communicates from intradecidual space into
maternal circulation releasing thromboplastins,which may result in
DIC.
• The condition can only be diagnosed on laparotomy.

• Couvelaire uterus as observed during cesarean section is not an

indication per se for hysterectomy
• The peritoneal cavity usually contains an appreciable quantity of
blood stained fluid and rarely the uterus may actually rupture with
profuse intraperitoneal haemorrhage.
• The uterine muscle fibres themselves may necrose with patchy areas.
Nevertheless, the patients who recover do not show any residual
uterine weakness.
• The kidneys are vulnerable to damage due to ischaemia, either in the
form of bilateral cortical necrosis, which is a characteristic sequel of
concealed abruption and is practically fatal, or a tubular necrosis as a
result of shock leading to acute renal failure.
• CLINICAL CLASSIFICATION:Depending upon the degree of placental
abruption and its clinical effects, the cases are graded as follows:
• Grade—0: Clinical features may be absent. The diagnosis is made
after inspection of placenta following delivery. Diagnosis is made
retrospectively.
• Grade—1 (40%)i) vaginal bleeding is slight
• (ii) uterus: irritable, tenderness may be minimal or absent
• (iii) maternal BP and fibrinogen levels unaffected
• (iv) FHS is good.
• Grade—2 (45%)(i) vaginal bleedingmild to moderate
(ii) uterine tenderness is always present
(iii) maternal pulse ↑, BP is maintained
(iv) fibrinogen level may be decreased
(v) shock is absent
(vi) fetal distress or even fetal death occurs.

Grade—3 (15%): (i) bleeding is moderate to severe or may be concealed

(ii) uterine tenderness is marked
(iii) shock is pronounced
(iv) fetal death is the rule
(v) associated coagulation defect or anuria may complicate.
Grades
CLINICAL FEATURES
• depend on: (i) degree of separation of placenta,
(ii) speed at which separation occurs and
(iii) amount of blood concealed inside the uterine cavity.
Table
Diagnosis:
• Mainly clinical,USG or MRI may be helpful.
• USG:Early haemorrhage is hyperechoic or isoechoic in comparision to
placenta.
• But as the haematoma starts resolving it becomes hyperechoic after
aweek and sonolucent after two weeks.
• Biophysical score on ultrasound also helps to determine the presence
of fetal compromise.
• Acute haemorrhage is often confused with fibroid or thick placenta.
• MRI is more accurate.
Differential diagnosis
• Placenta praevia
• Rupture uterus
 Complications
• MATERNAL:
• In revealed type—maternal risk is proportionate to the visible blood
loss and maternal death is rare.
• In concealed variety—The following complications may occur either
singly or in combination.
(1) Hemorrhage which is either totally concealed inside the uterus or
more commonly, part is revealed outside. There may be intraperitoneal
or broad ligament hematoma.
(2) Shock may be out of proportion to the blood loss. Release of
thromboplastin into the maternal circulation results in DIC or there may
be amniotic fluid embolism.
(3) Blood coagulation disorders
(4) Oliguria and anuria due to—
(a) hypovolemia
(b) serotonin liberated from the damaged uterine muscle producing
renal ischemia and
(c) acute tubular necrosis.
However, a severe case may lead to
(d) cortical necrosis and renal failure.
(5) Postpartum hemorrhage due to —
(a) atony of the uterus and
(b) increase in serum FDP
(6) Puerperal sepsis.
• Some cases who manage to survive may develop features of ischemic
pituitary necrosis. There is failure of lactation (Sheehan’s syndrome) .
FETAL:
• In revealed type, the fetal death is to the extent of 25–30%.
• In concealed type, however, the fetal death is appreciably high,
ranging from 50% to 100%.
• The deaths are due to prematurity and anoxia due to placental
separation.
• With same degree of placental separation, the fetus is put to more
risk in abruptio placentae than in placenta previa.
• This is due to the presence of preexisting placental pathology with
poor functional reserve in the former, in contrast to an almost normal
placental functions in the latter.
Management:
• Prevention
1) Elimination of the known factors likely to produce placental
separation.
(2) Correction of anemia during antenatal period so that the patient can
withstand blood loss.
(3) Prompt detection and institution of the therapy to minimize the
complications namely shock, blood coagulation disorders and renal
failure.
Treatment:
AT HOME:
• The patient is to be treated as outlined in placenta previa and
arrangement should be made to shift the patient to an equipped
maternity unit as early as possible.
IN THE HOSPITAL:
• Assessment of the case is to be done as regards:
(a) amount of blood loss
(b) maturity of the fetus and
(c) whether the patient is in labor or not (usually labor starts)
(d) presence of any complication and
(e) type and grade of placental abruption
.......
• A caeserean section is indicated in the following situations:
1. Significant abruption with baby alive and reasonable mature.
2. Maternal condition unstable and does not respond to resuscitative
measures.
3. Uncontrolled haemorrhage
4. Fetal distress
5. Failure of labour to progress
Management of complications :
• The major complications of placental abruption are:
1. Haemorrhagic shock
2. DIC
3. Renal failure
4. Uterine atony and post partum haemorrhage.
• Hypovolemia should be corrected early. Blood pressure may not be a
correct guide to assess shock, as it may be high due to severe degree
of vasospasm.
• Irrespective of the patient’s general condition, at least one liter of
blood transfusion should be the minimum when the diagnosis of
concealed accidental Hemorrhage is made.
• . The best guide to monitor the patient is the use of central venous
pressure (CVP), which is maintained at 10 cm of water.
• Hematocrit should be at least 30% and urinary output >or=30 ml/hr.
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