Objectives

Our aim from this lecture be able to

- Understand the definition of prolonged
pregnancy and distinguish it from post
maturity syndrome .
- Recognize the options in the Management of
prolonged pregnancy and .
Select the patients and sent them further
investigation .
- Be able to list the risks of prolonged pregnancy
.
PROLONGED PREGNANCY

Pregnancies of 294 days duration or more are

defined as prolonged, post-date ,post –
Term. Prolonged pregnancy is associated with an
increase in perinatal mortality &morbidity in
pregnancy which appear to be otherwise low risk
.
INCIDENCE OF PP:
If we depend on LMP ,the incidence of PP is
10%.
If we depend on first trimester U/S , the
incidence will decrease to 6%.
PP is increase in first pregnancies , but it is
not related to maternal age &the median
duration of pregnancy is 2 days longer in
nulliparae compared with multiparae .
Women with body mass index of greater than
30 are at increase risk of PP.
Perinatal mortality is two to three times
higher in these prolonged gestations.
Much of the increased risk to the
fetus and neonate can be attributed
to development of the fetal
postmaturity (dysmaturity) syndrome,
which occurs when a growth restricted
fetus remains inutero beyond term.
Occurring in 20-30% of Postterm
pregnancies, this syndrome is related to
the aging and infarction of the placenta,
with resulting Placental insufficiency
The fetus with postmaturity
syndrome typically has loss of
subcutaneous fat, long fingernails,
dry, peeling skin, and abundant hair.
The 70-80% of postdate fetuses not
affected by placental insufficiency
continue to grow in utero, many to
the point of macrosomia (birth eight
greater than 4000 g). Macrosomia often
results in abnormal labor, shoulder
dystocia, birth trauma, and an increased
incidence of cesarean delivery .
ETIOLOGY
The cause of postterm pregnancy is unknown
in most
instances. Prolonged gestation is common in
associa-
tion with an anencephalic fetus. This is
probably related to the lack of a
fetal labor-initiating factor from the
fetal adrenals, which are hypoplastic
in anencephalic fetuses. Rarely,
prolonged gestation may be ssociated
with placental sulfatase deficiency and
extrauterine pregnancy. Paternal genes, as
expressed by the fetus, play a role in
the timing of birth.
DIAGNOSIS

The diagnosis of postterm

pregnancy is often difficult.
The key to appropriate
classification and subsequent
successful perinatal management
is the accurate dating of gestation.
It is estimated that uncertain
dates are present in 20-30% of all
pregnancies .
MANAGEMENT
Antepartum

The appropriate management revolves around

identifying the low percentage of fetuses with
postmaturity syndrome that are truly at risk of
intrauterine hypoxia and fetal demise.
When biophysical tests of fetal well being are
available, the timing of delivery for each
patient should be individualized. However, if
the gestational age is firmly established at 41
weeks, the fetal head is well fixed in the pelvis,
and the condition of the cervix is favorable,
labor usually should be induced.
The two clinical problems that
remain are :-
- (1) patients with good dates at
42 weeks’ gestation with an
unripe cervix .
- (2) patients with uncertain
gestational age seen for the
first time with a possible or
probable diagnosis of
prolonged pregnancy.
In the first group of patients, a
twice-weekly NST and biophysical
profile should be performed.
The AFI is an important ultrasonic
measurement that should also be
used in the management of these
patients .
Delivery is indicated if there is any
indication of oligohydramnios (AFI
< 5) or if spontaneous fetal heart
rate decelerations are found on the
NST.
At 41 weeks’ gestation with firm dates,
delivery should be initiated by the
appropriate route,
regardless of other factors, in view of
the increasing potential for perinatal
morbidity and mortality.
When the patient presents very late for
initial
assessment but the gestational age is in
question and fetal assessment is normal,
an expectant approach is often
acceptable.
Intrapartum
Continuous electronic fetal monitoring must be
employed during the induction of labor.
The patient should be encouraged to lie on her left
side to assure adequate perfusion of the uterus and
the fetal membranes should be ruptured as early as
is feasible so that an internal fetal scalp electrode
can be applied and the color of the amniotic fluid
ssessed.
Cesarean delivery is indicated for fetal distress.
It should not be delayed because of the decreased
capacity of the post term fetus to tolerate
asphyxia and the increased risk of meconium
aspiration.
If meconium is present, neonatal asphyxia should
be anticipated, and a neonatal resuscitative team
should be present at delivery.
Intrauterine Fetal Demise
Intrauterine fetal demise (IUFD) is fetal
death after
20 weeks’ gestation but before the onset
of labor. It complicates about 1% of
pregnancies.
With the development of newer
diagnostic and therapeutic modalities,
the management of IUFD has shifted
from watchful expectancy to more active
intervention.
ETIOLOGY
In more than 50% of cases, the etiology of
antepartum
fetal death is not known or cannot be
determined.
Associated causes include IUGR, hypertensive
diseases
Of pregnancy, diabetes mellitus,
erythroblastosis
fetalis, umbilical cord accidents, fetal
congenital anomalies, fetal or maternal
infections, fetomaternal
hemorrhage, antiphospholipid antibodies, and
hereditary thrombophilias.
DIAGNOSIS
Clinically, fetal death should be suspected when
the patient reports the absence of fetal
movements, particularly if the uterus is small for
dates, or if the fetal heart tones are not detected
using a Doppler device.
Because the placenta may continue to produce
hCG, a positive pregnancy test does not exclude
an IUFD.
Diagnostic confirmation has been greatly
facilitated since the advent of ultrasonography.
Real-time ultrasonography confirms the lack of
fetal movement and absence of fetal cardiac
activity.
MANAGEMENT

Fetal demise between 14 and

28 weeks allows for two
different approaches:
watchful expectancy and
induction of labor.
Watchful Expectancy
About 80% of patients experience the
spontaneous
onset of labor within 2 to 3 weeks of fetal
demise.
The patient’s feeling of personal loss and
guilt may create significant anxiety, and
this conservative
Approach may prove unacceptable.
Thus, in general, the management of
women who fail to go into labor
spontaneously is active intervention by
induction of labor or dilation and
evacuation (D&E)
Induction of Labor

Justifications for such an intervention include

the emotional burden of carrying a dead fetus
on the patient, the slight possibility of
chorioamnionitis, and the 10% risk of
disseminated intravascular coagulation when
a dead fetus is retained for more than 5
weeks in the second or third trimesters.
Vaginal suppositories of prostaglandin E2
(dinoprostone [Prostin E2]) can be used from
the 12th to the 28th week of gestation.
There have been reported cases of uterine
rupture and cervical lacerations, but with
properly selected patients, the drug is safe.
Furthermore, prostaglandins are
contraindicated in patients with a history
of bronchial asthma or active pulmonary
disease, although the E series act primarily
as bronchodilators.
Misoprostol (Cytotec, a synthetic
prostaglandin E1 analogue) vaginal tablets
have been found to be quite effective with
little or no gastrointestinal side effects, and
they are less expensive than dinoprostone.
After 28 weeks’ gestation, if
the condition of the cervix is
favorable for induction and
there are no
contraindications, Cytotec
followed by oxytocin are the
drugs of choice.
Monitoring of Coagulopathy
Regardless of the mode of therapy
chosen, weekly fibrinogen levels should
be monitored during the period of
expectant management, along with a
hematocrit and platelet count.
If there is clotting defect or if there is
evidence of bleeding, blood volume
support or use of component therapy
(fresh-frozen plasma) should be given
before any intervention.
FOLLOW-UP
A search should be undertaken to determine the
cause
Of the intrauterine death.
TORCH and parvovirus studies and cultures for
Listeria are indicated.
In addition, all women with a fetal demise
should be
tested for the presence of anticardiolipin
antibodies.
Testing for the hereditary thrombophilias
should also be considered. If congenital
abnormalities are detected, fetal chromosomal
studies and total body radiographs should be
done, in addition to a complete autopsy.
A significant number of cases of
IUFD are the result of
fetomaternal hemorrhage, which
can be detected by identifying
fetal erythrocytes in maternal
blood (Kleihauer-Betke test).
Subsequent pregnancies in a
woman with a history
Of IUFD must be managed as
high-risk cases.