BLEEDING IN LATE PREGNANCY-

 Placenta previa
 Abruptio placenta

Submitted to Submitted By:

Mrs. Ancy Mathew Mrs. Divya Devakumar

Asso. Profesor 2nd year M.Sc nursing

Govt. College Of Nursing Govt. College Of Nursing

Kottayam Kottayam
Introduction:

During my clinical posting through ward. 27 I came across a patient, mrs.

Sheeja 27 yrs old, she is G4P0L0A2IUD1. Her G1 and G2 were spontaneous abortions
and G3 was an IUD in diabetes complicating pregnancy. Her gestational age is 34
weeks now. She has been admitted in our hospital for the last one month. This
time in USG she is diagnosed to have placenta previa. What is placenta previa? Is
there any complication associated with it? Moreover, is there an chance of her
getting the baby alive?

Placenta previa and a closely resembling condition, abruptio placenta are

the two main causes of antepartum hemorrhage. Let us discuss in detail regarding
these conditions.

ANTEPARTUM HEMORRHAGE:

Definition: Antepartum hemorrhage is defined as bleeding from or into the genital

tract after the 28th week of pregnancy, but before the birth of the baby.( the first
and second stage of labour thus included).

Incidence of antepartum hemorrhage:

Causes:

 placental bleeding (70%).

 Unexplained (25%).
 Extra placental causes (5%).

placental bleeding is mainly due to placenta previa and abruptio placenta .

. Causes of Pregnancy-Related Deaths Due to

Hemorrhage
 Causes of Hemorrhage (%)
placental abruption (19)
Laceration/uterine rupture (16)
Uterine atony (15)
Coagulopathies (14)
placenta previa (7)
Uterine bleeding (6)
placenta accreta/increta/percreta (6)
Retained placenta (4)

PLACENTA PREVIA:

Definition:

When the placenta is implanted partially or completely over the lower

uterine segment, it is called placenta previa.

Incidence:

About one-third cases of ante partum hemorrhage belong to placenta previa.

The incidence ranges from 0.5-1% (1 in every 100- 200 deliveries). As shown in
the table, about 7% of maternal deaths occurring due to haemorrhage occur
due to placenta previa.
 Types of placenta previa:

Grade- I. Total placenta internal cervical os is covered completely by

previa. placenta

Grade- II. Partial placenta The internal os is partially covered by

previa. placenta.

Grade- III. Marginal The edge of the placenta is at the margin of

placenta previa the internal os.

Grade- IV. . Low-lying. The placenta is implanted in the lower uterine

segment such that the edge actually does not
reach the internal os but is in close proximity
to it.

A clinical grading is

 Mild degree- type- I and II anterior.

 Major degree- type- II posterior, III and IV

Dangerous placenta previa is the name given to type- II posterior.

i. Because of the curved birth canal, major thickness of the placenta overlies
the sacral promontory, thereby diminishing the antero-posterior diameter of
the inlet and prevents engagement of the presenting part. This hinders
effective compression of the separated placenta to stop bleeding.
ii. Placenta is more likely to be compressed if vaginal delivery is allowed.

iii. More chance of cord compression or cord prolapse.

The degree of placenta previa depends in large measure on the cervical

dilatation at the time of examination. For example, a low-lying placenta at
 2-cm dilatation may become a partial placenta previa at 8-cm dilatation
because the dilating cervix has uncovered placenta .Conversely, a placenta
previa that appears to be total before cervical dilatation may become partial
at 4-cm dilatation because the cervix dilates beyond the edge of placenta.
Digital palpation to try to ascertain these changing relations between the
edge of the placenta and the internal os as the cervix dilates can incite
severe hemorrhage

Etiology:

The exact cause is unknown.

The following theories are postulated.

 Dropping down theory: the fertilized ovum drops down and is implanted in
the lower segment of the uterus. This may be due to poor decidual reaction
in the upper uterine segment and delayed disappearance of zona pellucida.
 Persistence of chorionic activity: decidua capsularis develop into capsular
placenta and comes in contact with decidua vera.

 Defective decidua resulting in the spread of villi to a large area in the

endometrium for nourishnment leading to placenta accreta, increta or
percreta.

 Big surface area of the placenta.

Predisposing factors:

a. Advancing maternal age increases the risk of placenta previa. At the extremes,
it is 1 in 1500 for women 19 years of age or younger, and it is 1 in 100 for
women older than 35 years of age.
b. Multiparity is associated with previa. In a study of 314 women who were para 5
or greater.

c. Ananth and associates (2003a) found that the rate of placenta previa was 40
percent higher in multifetal gestations compared with that of singletons.
d. History of any previous caesarean section or any other scar in the uterus. Miller
and associates (1996) cited a threefold increase of previa in women with prior
caesarean delivery in over 150,000 deliveries

e. Placental size and abnormality (usually succenturiate lobes).

f. Smoking cause placental hypertrophy to compensate CO induced hypoxemia.

Williams and colleagues (1991) found the relative risk of placenta previa to be
increased twofold related to smoking. Related, defective decidual
vascularisation, the possible result of inflammatory or atrophic changes, is
implicated in the development of previa.

Pathological anatomy:

placenta- placenta may be large and thin. There is often a tongue shaped
extension from the main placental mass. Extensive areas with degeneration and
calcification may be evident. Placenta will be morbidly adherent.

Umbilical cord: the insertion of the cord may be on the margin or near the internal
os. Vasa previa (fetal vessels running across the internal os) may rupture along
with rupture of membranes.

Lower uterine segment: due to increased vascularity, lower uterine segment and
the cervix becomes soft and friable.

Causes of bleeding: as the placental growth slows down in later months and the
lower segment progressively dilates, the inelastic placenta is sheared off the wall
of the lower segment. This leads to opening up of utero placental vessels and lead
to an episode of bleeding. The blood is almost always maternal, although fetal
blood may escape from the villi especially when the placenta is separated during
the trauma.

The mechanisms of spontaneous control of bleeding are:

1) Thrombosis of the open sinuses.

2) Mechanical pressure by the presenting part.
 3) placental infarction.

Clinical features:

Symptoms:

The most characteristic event in placenta previa is painless hemorrhage,

which usually does not appear until near the end of the second trimester or after.
Frequently, bleeding from placenta previa has sudden onset without warning,
presenting without pain in a woman who has had an uneventful prenatal course,
apparently causeless and recurrent. In some women, particularly those with a
placenta implanted near but not over the cervical os, bleeding does not appear
until the onset of labor, when it may vary from slight to profuse hemorrhage and
clinically may mimic placental abruption.

The cause of hemorrhage is reemphasized: When the placenta is located

over the internal os, the formation of the lower uterine segment and the dilatation
of the internal os result inevitably in tearing of placental attachments. The
bleeding is augmented by the inherent inability of the myometrial fibres of the
lower uterine segment to contract and thereby constrict the torn vessels.

Hemorrhage from the placental implantation site in the lower uterine

segment may continue after delivery of the placenta, because the lower uterine
segment contracts poorly compared with the uterine body. Bleeding may also
result from lacerations in the friable cervix and lower uterine segment, especially
following manual removal of a somewhat adherent placenta.

Signs :

 General condition and anemia proportionate to visible blood loss.

 Abdominal examination:

 Size of uterus is proportionate to period of gestation.

 The uterus feels relaxed, soft, and elastic without any localized areas
of tenderness.
  Persistence of malpresentation like breech and increased frequency of
twin pregnancy.

 The head is floating irrespective of the period of gestation. Head

cannot be pushed into the pelvis.

 Slowing of the foetal heart rate on pressing down the fetal head down
into the pelvis which soon recovers as the pressure is released is
suggestive of the presence of low lying placenta especially of posterior
type. (stall worthy sign).

 Vulval inspection: Whether the bleeding is still there or not, character of the
blood (bright red or dark colored), amount of blood loss- to be assessed from
blood stained clothing. In placenta previa, the blood is bright red as the
bleeding occurs from the separated utero- placental sinuses close to the
cervical opening and escapes out immediately.

 Vaginal examination must not be done.

Clinical presentation:

 The most common symptom is the painless vaginal bleeding in the third
trimester of pregnancy. According to Crenshaw et.al., approximately one-third
of patients with placenta previa have their first bleeding episode before 30
weeks, a third from 30-35 weeks, and a third after 36 or more weeks. The
earlier in pregnancy the bleeding occurs, the worse is the outcome of
pregnancy.
 Fetal distress is unusual if there is no severe hemorrhage.

 Uterine contractions usually occur associated with episodes of bleeding and

aggravate the bleeding tendency.

Clinical diagnosis:

Placenta previa or abruption should always be suspected in women with

uterine bleeding during the latter half of pregnancy. The possibility of placenta
previa should not be dismissed until appropriate evaluation, including
sonography, has clearly proved its absence. The diagnosis of placenta previa can
seldom be established firmly by clinical examination unless a finger is passed
through the cervix and the placenta is palpated. Such examination of the cervix is
never permissible unless the woman is in an operating room with all the
preparations for immediate CS.

Localisation by sonography- placentography:

The simplest, most precise, and safest method of placental localization is

provided by transabdominal sonography, which is used to locate the placenta with
considerable accuracy.

 It can also precisely determine the extent of placental margin in relation to

internal os.
 It is helpful in assessing the fetal size and status, and provides information
pertaining to maturity and wellbeing of the fetus for guiding the
management.

Transabdominal scan:

According to Laing (1996), the average accuracy is about 96 percent after

30th week of gestation, and rates as high as 98 percent have been obtained. False-
positive results are often a result of bladder distention. Therefore, ultrasonic scans
in apparently positive cases should be repeated after emptying the bladder. An
uncommon source of error has been identification of abundant placenta
implanted in the uterine fundus but failure to appreciate that the placenta was
large and extended downward all the way to the internal os of the cervix.

An anatomical landmark of arbitrary distance of 5 cm from the internal os is

considered lower segment. As such, cases detected as placenta previa should be
subjected to repeat scan at 34 weeks or earlier for detection of placental
migration.

Placental migration:
 USG at 17 wks of gestation reveals placenta covering the internal os in
about 10% of cases. Repeat USG at 37 weeks show no placenta in the lower
uterine segment in more than 90% of cases.

Since the report by King (1973), the apparent peripatetic nature of the
placenta has been well established. Sanderson and Milton (1991) found that 12
percent of placentas were "low lying" in 4300 women at 18 to 20 weeks. Of those
not covering the internal os, previa did not persist and hemorrhage was not
encountered. Conversely, of those covering the os at mid pregnancy, about 40
percent persisted as a previa. Thus, placentas that lie close to the internal os, but
not over it, during the second trimester, or even early in the third trimester, are
unlikely to persist as previas by term.

The mechanism of apparent placental movement is not completely

understood. The term migration is clearly a misnomer, however, because invasion
of chorionic villi into the decidua on either side of the cervical os persists. The
apparent movement of the low-lying placenta relative to the internal os probably
results from inability to precisely define this relationship in a three-dimensional
manner using two-dimensional sonography in early pregnancy. This difficulty is
coupled with differential growth of lower and upper myometrial segments as
pregnancy progresses. Thus, those placentas that "migrate" most likely never had
actual circumferential villus invasion that reached the internal cervical os in the
first place.

Transvaginal scan: Transducer is inserted into the vagina without touching the
cervix. This is safe and avoids the discomfort of a full bladder. It also gives
accurate results.

Colour Doppler flow study: Prominent venous flow in the hyper echoic areas near
the cervix is consistent with the diagnosis of placenta previa.

MRI: It is non-invasive method without any risk of ionising radiation.

Clinical confirmation:
  Double set-up examination- this is a type of vaginal examination.
Indications are:

a. Inconclusive USG report.

b. USG reveals type I placenta.

c. USG facilities not available.

It is done in the operation theatre under anaesthesia keeping everything

ready for a CS.

Palpation of placenta in the lower segment not only confirms the diagnosis
but also identifies the degree.

 Visualisation of the placental implantation on the lower segment during CS.

 Examination of the placenta following vaginal delivery reveals

a. A tongue shaped comparatively thin segment of placental tissue

projecting beyond the placental mass.

b. Rent on the membranes is situated on the margin of the placenta.

c. Abnormal attachment of the cord.

Differential diagnosis:

 Abruptio placenta.
 Vasa previa- bleeding will be fetal with detection of fetal blood cells in the
blood.

 Local cervical lesions- differentiated by speculum examination.

 Circumvallate placenta- bleeding will be slight and the diagnosis is made

after examining the placenta following delivery.

Perinatal Morbidity and Mortality:

 Preterm delivery is a major cause of perinatal death even with expectant
management of placenta previa. Salihu and associates (2003) found that the
neonatal mortality rate was threefold higher in pregnancies complicated by
placenta previa primarily because of increased preterm birth. Ananth and
associates (2003) reported a comparably increased risk of neonatal death even
for those foetuses delivered at term. Some of this risk appears related to fetal
growth restriction and limited prenatal care.
 Brar and colleagues (1988) reported that the incidence of associated fetal
growth restriction with a previa was nearly 20 percent. Ananth and associates
(2001a) examined the relationship between placenta previa, fetal growth
restriction, and preterm delivery in a large population-based cohort of more
than 500,000 singleton births. They found that most of the association between
placenta previa and low birth weight is due primarily to preterm birth and, to a
lesser extent, growth impairment.

Complications:

MATERNAL:

 During pregnancy:

 Antepartum hemorrhage with varying degrees of shock.

 Malpresentations. ( breech, transverse lie and unstable lie).

 Preterm labour.

 During labour:

 Early rupture of membranes.

 Cord prolapse due to abnormal attachment of the cord.

 Slow dilatation of the cervix, due to attachment of placenta to the lower

segment.
  Intrapartum hemorrhage due to further separation of the placenta with the
cervical dilation.

 Postpartum hemorrhage due to improper retraction of the lower segment of

the uterus, abnormally large placenta, adherent placenta or trauma to the
cervix.

 Retained placenta due to increased surface area and morbid adhesion.

 Peurperium: sepsis, sub involution and embolism.

FETAL:

 Low birth weight- as bouts of hemorrhage causes chronic insufficiency of

placenta.
 Asphyxia – due to early separation of the placenta, compression of the
placenta or the cord.

 Intrauterine death – due to severe degrees of separation of the placenta, with

hypovolemia and maternal shock.

 Birth injuries due to increased operative interference.

 Congenital malformations.

Prognosis:

A marked reduction in maternal mortality from placenta previa has been

achieved, a trend that began in 1927 when Bill advocated adequate transfusion
and cesarean delivery. Since 1945, when Macafee and Johnson independently
suggested expectant therapy for patients remote from term, a similar trend has
been evident in perinatal loss. Although half of women are near term when
bleeding first develops, preterm delivery still poses a formidable problem for the
remainder, because not all women with placenta previa and a preterm fetus can
be treated expectantly. Interestingly, Butler and co-workers (2001) found that
women with placenta previa who also had maternal serum alpha-fetoprotein levels
at least 2.0 multiples of the median (MOM) were at increased risk of bleeding early
in the third trimester. The morbidity is somewhat raised due to hemorrhage and
operative interference.

There is a reduction in the fetal mortality, principally due ot judicious

extension of the expectant treatment thereby reducing the loss from prematurity.
Liberal use of caesarean section has reduced loss due to asphyxia. The causes are
prematurity, asphyxia and congenital abnormalities.

Management:

Prevention:

 Adequate antenatal care to improve health status of women and prevention

of anaemia.
 Antenatal diagnosis of low- lying placenta at 20 weeks of pregnancy with
routine ultrasound, needs repeat ultrasound examination at 34 weeks of
pregnancy to confirm the diagnosis.

 Significance of warning hemorrhage should not be ignored or

underestimated.

 Family planning and limitation of births reduce the incidence of placenta

previa.

At home:

1. The patient is immediately put to bed.

2. To assess blood loss by examining the clothes and noting pulse and pallor.

3. Quick but gentle abdominal examination to note the fundal height and
auscultate FHS to assess the well being of the fetus.

4. Vaginal examination must not be done.

Transfer to hospital:
 Transported by flying squad service, with an intravenous dextrose saline
drip on flow.

Admission to hospital:

All the cases of APH must be considered as placenta previa and admitted to
hospital.

Treatment:

Immediate attention:

Overall assessment for

 Amount of blood loss.

 Blood samples for group and cross- matching, estimation of haemoglobin.

 Start infusion of normal saline.

 Gentle abdominal palpation to determine uterine tenderness and

auscultation to note fetal heart rate.

 Inspection of the vulva to note the presence of any active bleeding.

Confirmation of diagnosis is done by physical examination and sonographic

evidence.

Three fundamental areas of concern must be evaluated quickly and

efficiently when dealing with a patient with bleeding of placenta previa.

a) The mother’s condition as primarily evidenced by the degree of

obstetric hemorrhage.
b) The fetal condition including the gestational age estimation.

c) The ability of the neonatal unit to handle an infant of that gestational

age.
 Line of management:

A. Expectant treatment:
The policy had been advocated by Macafee and Johnson (1945), in an
attempt to improve the fetal salvage without increasing undue maternal
hazards. The aim is to continue pregnancy for fetal maturity without
compromising the maternal health.
Vital prerequisites:

1) Availability of blood for transfusion whenever required.

2) Facilities for caesarean section should be available throughout 24
hours.

Selection of cases:

Suitable cases for expectant management are: (1) Mother is in good health
status (Haemoglobin > 10 gm%; haematocrit > 30%). (2) Duration of
pregnancy is less than 37 weeks. (3) Active vaginal bleeding is absent (4)
Fetal well being is assured (USG).

Conduct of expectant treatment:

(1) Bedrest with bathroom privileges.

(2) Investigations — like haemoglobin estimation, blood grouping and
urine for protein are done.
(3) Periodic inspection of the vulval pads and fetal surveillance with USG at
interval of 2-3 weeks
(4) Supplementary Haematinics should be given and the blood loss is
replaced by adequate cross matched blood transfusion, if the patient is
anaemic.
(5) When the patient is allowed out of the bed <2-3 days after the bleeding
stops), a gentle speculum (Cusco's) examination is made to exclude local
cervical and vaginal lesions for bleeding. However, their presence does
not negate placenta praevia.
(6) Use of tocolytics and cervical circlage are not helpful.
Termination of the expectant treatment: The expectant treatment Is
carried upto 37 weeks of pregnancy.
 However, premature termination may have to be done in conditions, such
as: (1) Recurrence of brisk haemorrhage and which is continuing. (2) The fetus
is dead. (3) The fetus is found congenitally malformed on investigation.

Steroid therapy is indicated if the duration of pregnancy is less than 34

weeks. Betamethasone reduces the risk of respiratory distress of the new bom
when preterm delivery is considered.

B. Active interference:
The indications of active treatment are: (1) Bleeding occurs at or after 37
weeks of pregnancy. (2) Patient is in labour. (3) Patient is in exsanguinated state
on admission. (4) Bleeding is continuing and of moderate degree. (5) Baby is
dead or known to be congenitally deformed.

These are also the contraindications for putting the patients to expectant regime.
Depending upon the urgency of the situation, definitive treatment should be
instituted as soon as possible.
C. Definitive Treatment
Definitive treatment whether instituted soon following
hospitalisation or following expectant treatment resolves into:
I. Vaginal examination in operation theatre followed by: (a) Low
rupture of the membranes or (b) Caesarean section.
II. Caesarean section without internal examination.

I. VAGINAL EXAMINATION: Double set up examination should be done in the

operation theatre keeping everything ready for caesarean section.

Contra-indications of vaginal examination are: (1) Patient in exsanguinated

state. (2) Diagnosed cases of major degree of placenta praevia confirmed by
ultrasonography (previously mentioned). (3) Associated complicating factors such
as malpresentation, elderly primigravidae, pregnancy with history of previous
caesarean section, contracted pelvis etc which themselves are indications for
caesarean section.
 a) Low rupture of the membranes: to induce labour by LROM using long

kocher’s forceps in lesser degrees of placenta previa. The finger is inserted

to exclude cord prolapse. Amniotomy encourages descent of head and
presses the separated placenta and helps to control the bleeding. Oxytocin
drip may be started. If bleeding does not stop CS can be done.
Precautions during vaginal delivery:
a. all possible steps should be taken to restore lost blood volume.
b. Methergin 0.2 mg IM following delivery of anterior shoulder.
c. Proper examination of cervix for any tear.
b) Caesarean section: to reduce maternal risk and fetal salvage.
The indications are:
1. Severe degree of placenta previa.
2. Lesser degrees where amniotomy fails to stop bleeding.
3. Complicating factors associated with lesser degrees where vaginal
delivery is unsafe.

II. Caesarean section without internal examination: CS is done after

determining the placental location by sonar.

Abruptio placenta:

The Latin abruptio placentae, which means "rending asunder of the

placenta" denotes a sudden accident, a clinical characteristic of most cases of this

complication. This condition is also called accidental haemorrhage or premature

separation of placenta. The term accidental haemorrhage was coined by Rigby in

1976

The separation of the placenta from its site of implantation before delivery
has been variously called placental abruption, abruptio placentae, or accidental
hemorrhage. The term premature separation of the normally implanted placenta is
most descriptive because it differentiates the placenta that separates prematurely
but that is implanted some distance beyond the cervical internal os from one that
is implanted over the cervical internal os—that is, placenta previa.

Frequency and Significance

 The frequency with which placental abruption is diagnosed varies because of
different criteria. The intensity of the abruption often varies depending on how
quickly the woman seeks and receives care following the onset of symptoms. With
delay, the likelihood of extensive separation causing death of the fetus is increased
remarkably.

The reported frequency for placental abruption averages about 1 in 200

deliveries. Both incidence and severity have decreased over time. the incidence
was 1 in 420 deliveries from 1956 through 1967 (Pritchard and Brekken, 1967).
As the number of high-parity women cared for decreased, and community-wide
availability of prenatal care as well as emergency transportation improved, the
frequency of abruption causing fetal death dropped to about 1 in 830 deliveries
from 1974 through 1989 (Pritchard and colleagues, 1991). Between 1996 and
2003, it decreased to about 1 in 1600.

Etiology and risk factors:

The primary cause of placental abruption is unknown, but there are several
associated conditions.

Risk Factor Relative Risk

Increased age and parity 1.3–1.5
Preeclampsia 2.1–4.0
Chronic hypertension 1.8–3.0
Preterm ruptured membranes 2.4–4.9
Multifetal gestation 2.1
Hydramnios 2.0
Cigarette smoking 1.4–1.9
Thrombophilias 3–7
Cocaine use NA
Prior abruption 10–25
Risk Factor Relative Risk
Uterine leiomyoma NA

 Preeclampsia, gestational hypertension, and chronic hypertension. Morgan and

colleagues (1994) found that hypertensive women were more likely to suffer a
more severe abruption. From the Maternal–Fetal Medicine Units Network, Sibai
and co-workers (1998) reported that 1.5 percent of women with chronic
hypertension suffered placental abruption. Ananth and associates (1999a)
reported a threefold increased incidence of abruption with chronic hypertension
and fourfold with severe preeclampsia.
 There is an increased incidence of abruption with preterm prematurely ruptured
membranes. Major and colleagues (1995) described an incidence of 5 percent in
756 women with ruptured membranes between 20 and 36 weeks. Kramer and
co-workers (1997) found an incidence of 3.1 percent in all patients if
membranes were ruptured for longer than 24 hours.

 Cigarette smoking was linked to an increased risk for In a meta-analysis of 1.6

million pregnancies, Ananth and colleagues (1999a, 1999b) found a twofold risk
for abruption in smokers. Similar findings have been reported by Odendaal and
associates (2001) and Mortensen and colleagues (2001).

 Cocaine abuse has been associated with an alarming frequency of placental

abruption. Addis and associates (2001) systematically reviewed 15 studies of
cocaine-using women, all of which showed that placental abruption was more
common than in controls.

 Trauma as in attempted cephalic version, RTA, needle puncture etc.

 Short cord.

 Sick placenta.

 Folic acid deficiency.

  Torsion of the uterus.

 Thrombophilas.

Varities:

1) Revealed: the blood insinuates between the membranes and the decidua.
Ultimately the blood comes out of cervix to become visible. This is the
commonest type.
2) Concealed: the blood collects behind the separated placenta or collected
between the membranes and the decidua. The collected blood is prevented
from coming out by the presenting part which presses on the lower segment.
This type is rare.

3) Mixed: some part of the blood is collected inside and some part is expelled
out. Usually one variety predominates over the other.

Clinical Classification: Depending upon the degree of placental abruption and

its clinical effects, the cases are graded as:
 Grade-0: Clinical feature may be absent. The diagnosis is made after inspection of
placenta following delivers
 Grade-1: External bleeding is slight, (ii) Uterus—irritable, tenderness may or
may not be present, (iii) Shock is absent, (iv) FHS is good.
 Grade 2- external bleeding is mild to moderate, uterine tenderness and feta
distress may occur. Shock is not present.
 Grade 3- bleeding is moderate to severe. Uterine tenderness is marked shock is
pronounced and foetal death is the rule.

Recurrent Abruption

Pritchard and co-workers (1970) identified a recurrence rate of severe

abruption in 1 in 8 pregnancies. Importantly, of the 14 recurrent placental
abruptions, eight caused fetal death for a second time. Furuhashi and colleagues
(2002) analyzed subsequent pregnancy outcomes from 27 women who had a prior
placental abruption. Of the six (22 percent) recurrences, four were at a gestational
age 1 to 3 weeks earlier than the first abruption. Management of the subsequent
pregnancy is made difficult in that placental separation may suddenly occur at
any time, even remote from term. In the majority of cases, moreover, fetal well-
being is normal beforehand, and thus currently available methods of fetal
evaluation are usually not predictive (Toivonen and colleagues, 2002). In an
extreme example, Seski and Compton (1976) documented both a normal nonstress
test and a normal contraction stress test performed four hours before the onset of
placental abruption that promptly killed the fetus.

Pathology: Placental abruption is initiated by hemorrhage into the decidua

basalis. The decidua then splits, leaving a thin layer adherent to the myometrium.
Consequently, the process in its earliest stages consists of the development of a
decidual hematoma that leads to separation, compression, and the ultimate
destruction of the Placenta adjacent to it.

In its early stage, there may be no clinical symptoms. The condition is

discovered only on examination of the freshly delivered organ, which has a
circumscribed depression measuring a few centimeters in diameter on its maternal
surface, and is covered by dark, clotted blood.

In some instances, a decidual spiral artery ruptures to cause a

retroplacental hematoma, which as it expands disrupts more vessels to separate
more placenta. The area of separation rapidly becomes more extensive and reaches
the margin of the placenta. Because the uterus is still distended by the products of
conception, it is unable to contract sufficiently to compress the torn vessels that
supply the placental site. The escaping blood may dissect the membranes from the
uterine wall and eventually appear externally or may be completely retained within
the uterus.

Signs and Symptoms Determined Prospectively in 59 Women with Abruptio Placentae

Sign or Symptom Frequency (%)
Vaginal bleeding 78
Uterine tenderness or back pain 66
Fetal distress 60
Sign or Symptom Frequency (%)
a
Preterm labor 22
High-frequency contractions 17
Hypertonus 17
Dead fetus 15

Complications:

 Intravascular coagulopathy:

One of the most common causes of clinically significant consumptive

coagulopathy in obstetrics is placental abruption. Overt hypofibrinogenemia (less
than 150 mg/dL of plasma) along with elevated levels of fibrinogen–fibrin
degradation products, D-dimers, and variable decreases in other coagulation
factors are found in about 30 percent of women with placental abruption severe
enough to kill the fetus. The major mechanism is almost certainly the induction of
coagulation intravascularly and, to a lesser degree, retroplacentally.

An important consequence of intravascular coagulation is the activation of

plasminogen to plasmin, which lyses fibrin microemboli, thereby maintaining
patency of the microcirculation. In every instance of placental abruption severe
enough to kill the fetus, we have identified clearly pathological levels of fibrinogen–
fibrin degradation products in maternal serum. At the outset, severe
hypofibrinogenemia may or may not be accompanied by overt thrombocytopenia.
After repeated blood transfusions, however, thrombocytopenia is common.

 Renal Failure

Acute renal failure may be seen in severe forms of placental abruption. This
includes those in which treatment of hypovolemia is delayed or incomplete. Of 72
pregnant women with acute renal failure described by Drakeley and colleagues
(2002), 32 percent had placental abruption. Fortunately, reversible acute tubular
necrosis accounts for 75 percent of cases of renal failure (Turney and colleagues,
1989). According to Lindheimer and associates (2000), acute cortical necrosis in
pregnancy is usually caused by abruptio placentae.
 Seriously impaired renal perfusion is the consequence of massive
hemorrhage. Because preeclampsia frequently coexists with placental abruption,
renal vasospasm is likely intensified (Hauth and Cunningham, 1999). Even when
placental abruption is complicated by severe intravascular coagulation, prompt
and vigorous treatment of hemorrhage with blood and crystalloid solution often
prevents clinically significant renal dysfunction.

Kidneys may show acute cortical necrosis or acute tubular necrosis. The
precise mechanism is not clear but may be due to intrarenal vasospasm as a
consequence of massive haemorrhage. Shock proteinuria is probably due to renal
anoxia which usually disappears two days after delivery, whereas, proteinuria due
to preeclampsia tends to last.

 Couvelaire Uterus

There may be widespread extravasation of blood into the uterine

musculature and beneath the uterine serosa. This so-called uteroplacental
apoplexy, first described by Couvelaire in the early 1900s, is now frequently called
Couvelaire uterus. Such effusions of blood are also occasionally seen beneath the
tubal serosa, in the connective tissue of the broad ligaments, and in the substance
of the ovaries, as well as free in the peritoneal cavity. Its precise incidence is
unknown because it can be demonstrated conclusively only at laparotomy. These
myometrial hemorrhages seldom interfere with uterine contractions sufficiently to
produce severe postpartum hemorrhage and are not an indication for
hysterectomy.

Naked eye features: Uterus is dark port wine colour (patchy or diffuse) occurring
initially in cornua, more in placental site.

Microscopic appearance: the uterine muscles over the area are necrosed and there
is infiltration of blood and fluid in between the muscle layers. The serosa may
split on occasions to allow blood to enter the peritoneal cavity. The blood vessels
show acute degenerative changes with thrombosis.
 CHANGES IN OTHER ORGANS: In the liver, apart from the changes found in
pre-eclampsia, presence of fibrin knots in the hepatic sinusoids is an important
finding.

Clinical manifestations

Symptoms:

 Severe and constant abdominal pain.(more on concealed type)

 Bleeding (in revealed and mixed types).

Signs:

Pallor (usually out of proportion to the extent of bleeding).

 Hypertension (if there is associated pre-eclampsia).
The uterus will be larger than expected for the period of amenorrhea.
 Uterus may be tense, tender and even rigid (woody hard).
 Difficulty in palpating the underlying fetal parts easily.
 Fetal distress or absent fetal heart sounds.
Vaginal examination:
The patient will be in labour, with a fixed presenting part and on ARM, the
liquour appears blood-stained.

Differentiate between placenta previa and abruptio placenta:

placenta previa abruptio placenta

CLINICAL FEATURES

Nature of bleeding Painless, apparently Painful, often attributed to

causeless and recurrent. pre- eclampsia or trauma.

Character of blood Bright red Dark coloured

General condition and Proportionate to visible Out of proportion to

anaemia blood loss. bleeding in concealed and
mixed variety.
Features of pre- Not relevant Present in one-third cases.
eclampsia
ABDOMINAL EXAMINATION

Height of uterus Proportionate height Disproportionately

enlarged in concealed type.

Feel pf uterus Soft and relaxed May be tense, tender and

rigid.

Malpresentations Common, head is high Unrelated.

floating

FHS Usually present Usually absent specially in

concealed type

placentography Placenta in lower Placenta in upper segment.

segment

Vaginal examination Placena is felt on the Not felt on lower segment.

lower segment
Management
Treatment for placental abruption varies depending on gestational age and
the status of the mother and fetus. With a live and mature fetus, and if vaginal
delivery is not imminent, then emergency cesarean delivery is chosen by most
clinicians. Hypovolemic Shock, with massive external bleeding, intensive
resuscitation with blood plus crystalloid and prompt delivery to control the
hemorrhage are lifesaving for the mother and, it is hoped, for the fetus. If the
diagnosis is uncertain and the fetus is alive but without evidence of fetal
compromise, very close observation, with facilities for immediate intervention, can
be practiced.

Prognosis: the prognosis depends on clinical types, degree of placental separation,

the interval between placental separation and delivery of the baby, and efficacy of
treatment. Bleeding in placental abruption is almost always maternal.

In revealed type- depends on maternal blood loss.

In concealed variety- poor when associated with occurance of

 Hemorrhage
 Shock

 Blood coagulation disorders.

 Oliguria and anuria.

 Postpartum hemorrhage.

 Puerperal sepsis.

The occurances of these complicating factors vary from 2-8%.

Foetal prognosis: In revealed type, foetal death range from 25-30%.

In concealed type, foetal death is appreciably high. ( 50-100% ).

 Management:

Prevention:

Aims are:

1) Elimination of possible risk factors.

2) Correction of anemia during antenatal period.

3) Prompt detection and institution of therapy to avoid grave complications.

Guidelines:

 Prevention, early detection and prompt treatment of hypertensive disorders

during pregnancy.
 Needle puncture during amniocentesis under USG guidance.

 Avoidance of trauma- especially forceful cephalic version under anaesthesia.

 Avoid sudden decompression of the uterus.

 Avoid supine hypotension.

 Routine administration of folic acid.

Treatment:

At home: shift the patient to an equipped maternity unit as early as possible.

In the hospital:

Revealed type: assessment for amount of blood loss, maturity of fetus, whether
the patient is in labour, or not.

Preliminaries-

 Blood is sent for haemoglobin and hematocrit estimation, coagulation profile,

prothrombin time, ABO and Rh grouping and urine for detection of protein.
 RL drip is started.

 Close monitoring of maternal and fetal condition is done.

Definitive treatment:

Patient in labour: labour is accelerated by LROM. Rupture will also enhance

uterine tone which causes the bleeding sinuses to be compressed in the uterine
bulk, oxytocin drip may be started to accelerate labour.

 Patient not in labour:

 Pregnancy > 37 weeks : induction by LROM with or without oxytocin.

Indications for caesarean section:

a) Appearance of fetal distress.

b) Amniotomy not done or amniotomy fails to control bleeding.

c) Associated complicating factors.

 Pregnancy < 37 weeks:

Indications for CS:

1) Bleeding- moderate to severe or continuing.

2) Bleeding slight or has stopped.

Mixed or concealed type:

Principles:

1) To correct hypovolemia- start NS infusion.

2) To bring about effective uterine contractions.

3) To observe blood coagulation profiles at 2 hrly interval.

4) Close monitoring of maternal and fetal conditions.

Definitive treatment:

 Collect blood sample.

 To correct hypovolemia – NS infusion through a wide bore cannula,
arrangement for urgent blood transfusion ( this prevents ischaemic rena
damage, prevents blood coagulation disorders and ensures the patient to be
in a better position to withstand PPH.)

 Monitoring of CVP.

 AROM +/- oxytocin drip.

 Vaginal delivery: following LROM, labour is often completed quickly within 6

hrs. Placenta with varying degrees of retroplacental clots is expelled. Inj.
Methergin 0.2 mg is administered IM with delivery of anterior shoulder.
Liberal oxytocin should be used alog with blood transfusion.

 Caesarean section:

 Early CS is indicated in unfavourable cervix where speedy delivery is

not possible.

 Late CS if, inn spite of amniotomy and oxytocin, the labour is delayed
for more than 6-8 hrs and instead the general condition deteriorates
with appearance of complicating factors or there is evidence of fetal
distress.

 Blood coagulation disorders are not a specific contraindication for

normal vaginal delivery, but before CS measures should be taken to
improve the level upto atleast 150 mg%.
Nursing management:

Assessment:

 History on parity, gravida, live children, BOH etc.

 H/O previous CS, any bleeding or coagulation disorders etc.

 Any associated complications or risk factors.

 Fetal status- gestational age, maturity etc.

Evaluating severity of bleeding:

Criteria I II III IV

Blood loss < 750 ml 750-1500 ml 1500-2000 ml >2000 ml

Pulse rate (bpm) <100 100-120 120-140 >140

Blood pressure Normal Decreased Decreased Decreased

Respiratory rate 14-20 20-30 30-40 >40

Urine output( ml/hr) >30 20-30 5-15 negligible

CNS symptoms Normal Anxious Confused Lethargic

 Management of patients with severe bleeding:

 Intensive observation and monitoring- vital signs, fluid intake and output,
blood studies.
 IV fluids.

 Transfusion therapy- usually PRC.

 Assessment of renal function

 CVP monitoring.

 Fetal status evaluation.

Management of patients with moderate bleeding:

 Monitor for fetal lung maturity

 Prepare for labour.

 Monitor for complications.

Management of patients with moderate bleeding:

 Patient selection
 Hospitalisation

 Prevention of labour

 Acceleration of fetal lung maturation.

Nursing diagnoses:

1. Decreased cardiac output related to excessive blood loss.

2. Fluid volume deficit related to excessive blood loss.

3. Altered peripheral tissue perfusion related to hypovolemia.

 4. Risk for fetal injury related to placental perfusion.

5. Anxiety and fear related to maternal and fetal outcome.

6. Knowledge deficit related to hospitalisation.

7. Altered family process related to hospitalisation of mother.

8. Anticipatory grieving related to potential pregnancy loss.

Research based evidence:

1. Recent advances in the management of placenta previa

Bhide, Amar; Thilaganathan, Basky

Current Opinion in Obstetrics & Gynecology: Women's health

December 2004 - Volume 16 - Issue 6 - pp 447-451

Purpose of review: The purpose of this review is to present the current evidence
supporting the screening, diagnosis and management of placenta previa.

Recent findings: The prevalence of placenta previa is significantly overestimated

due to the practice of routine mid-pregnancy scan, and many women currently
undergo a repeat scan in late pregnancy for placental localization. Recent reports
support limiting third-trimester scans to only those cases where the placental edge
either reaches or overlaps the internal cervical os at 20-23 weeks of pregnancy. In
some cases of mid-trimester placenta previa, the placental edge is more likely to
'migrate' than others, and it appears that ultrasound may be useful to predict this
process. At term, women with placental edge within 2 cm of the internal cervical
os require a Caesarean section for delivery, whereas an attempt at vaginal birth is
appropriate if this distance is more that 2 cm.

Summary: This review addresses screening for placenta previa. A simple and
pragmatic ultrasound classification of placenta previa and low-lying placenta is
proposed. Caesarean section is recommended for delivery in cases of placenta
previa.
 2. Association of caesarean delivery for first birth with placenta praevia
and placental abruption in second pregnancy, Q Yang, SW Wen
BJOG: An International Journal of Obstetrics & Gynaecology
Volume 114, Issue 5, pages 609–613, May 2007

Objective  To quantify the risk of placenta praevia and placental abruption in

singleton, second pregnancies after a caesarean delivery of the first pregnancy.
Design  Retrospective cohort study.
Setting  Linked birth and infant mortality database of the USA between 1995
and 2000.
Population  A total of 5 146 742 singleton second pregnancies were available for
the final analysis after excluding missing information.
Methods  Multiple logistic regressions were used to describe the relationship
between caesarean section at first birth and placenta praevia and placental
abruption in second-birth singletons.
Main outcome measures  Placenta praevia and placental abruption.
Results  Placenta praevia was recorded in 4.4 per 1000 second-birth singletons
whose first births delivered by caesarean section and 2.7 per 1000 second-birth
singletons whose first births delivered vaginally. About 6.8 per 1000 births were
complicated with placental abruption in second-birth singletons whose first births
delivered by caesarean section and 4.8 per 1000 birth in second-birth singletons
whose first births delivered vaginally. The adjusted odds ratio (95% CIs) of
previous caesarean section for placenta praevia in following second pregnancies
was 1.47 (1.41, 1.52) after controlling for maternal age, race, education, marital
status, maternal drinking and smoking during pregnancy, adequacy of prenatal
care, and fetal gender. The corresponding figure for placental abruption was 1.40
(1.36, 1.45).
Conclusion  Caesarean section for first live birth is associated with a 47%
increased risk of placenta praevia and 40% increased risk of placental abruption
in second pregnancy with a singleton.

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