Premature rupture of

membranes

Dr. Fatouma Hachi Iman

MD
Consultant Obstetrician and
Gynecologist, Hargeisa University
and Hargeisa Group Hospital
Somaliland
30/05/2015
Case 1:

A 32-year-old primigravida at 32 weeks’

gestation comes to the maternity department
noting that 3 hours ago she had a gush of fluid
from her vagina without vaginal bleeding or
uterine contractions. On examination her
external genitalia appears moist. Her temperature
is 36.5, Bp is 120/70, her pulse is 76.
 Definition:

PROM: is a rupture of the fetal membranes before the

onset of labor at any stage of gestation , whether at term
or preterm, or before the onset of uterine contractions
(also known as prelabor rupture of membranes).

Preterm PROM (PPROM) refers to PROM before

370/7ths weeks of gestation. Diagnosis is clinical. Delivery
is sometimes indicated when gestational age is ≥ 34 wk
or fetal lungs are mature and is generally indicated for
infection or fetal compromise
 INCIDENCE 

 Occurs in 3% of all pregnancies and is responsible for

1/3rd causes of preterm birth
Causes significant fetal complications– sepsis,
prematurity, cord prolapse, abruptio placenta
and, fetal death.
Maternal complication – chorioamnionitis
(PROM) may occur at term (≥ 37 wk) or earlier (called
preterm PPROM if < 37 wk).
Preterm PROM predisposes to preterm delivery.
PROM at any time increases risk of infection in the woman
(chorioamnionitis), neonate (sepsis), or both, as well as risk of
abnormal fetal presentation and abruptio placentae.
Group B streptococci and Escherichia coliare common
causes of infection. Other organisms in the vagina may also cause
infection.
Prolonged preterm PROM before viability (at < 24 wk) increases
risk of limb deformities (e.g., abnormal joint positioning) and
pulmonary hypoplasia due to leakage of amniotic fluid (called
Potter sequence or syndrome).
The interval between PROM and onset of spontaneous labor
(latent period) and delivery varies inversely with gestational age.
At term, > 90% of women with PROM begin labor within 24 h;
at 32 to 34 wk, mean latency period is about 4 days.
 PATHOGENESIS OF PROM
The pathogenesis of spontaneous membrane rupture is unknown.
Ascending infection from lower genital tract is the most common
risk factor for PROM. Other risk factors are local membrane defects
and cigarette smoking.
The strength and integrity of fetal membranes derive from
extracellular membrane proteins, including collagens, fibronectin, and
laminins.
Matrix metalloproteases (MMPs) decrease membrane strength by
increasing collagen degradation.
Tissue inhibitors of MMPs (TIMMPs) bind to MMPs and shut down
proteolysis, thereby helping to maintain membrane integrity.
A variety of pathologic events can disrupt this homeostasis and
initiate a cascade of biochemical changes that culminate in PROM.
Although the pathway varies depending on the initiating event, it is
likely that all pathways lead to a final common pathway ending in
membrane rupture.
Risk Factors:
Risk factors — maternal physiologic, genetic, and environmental
factors likely predispose to development of preterm premature
rupture of membranes (PPROM) in many cases. These risk factors
are similar to those for preterm labor, but most patients have no
identifiable risk factors.
 Lower socioeconomic class
 Poor nutrition
 Prior preterm birth
 Prior PROM or PPROM
 Vaginal/Cervical Infection :
 H/O STD: Gonorrhea, Chlamydia, GBS, S. Aureus
 Multiple pregnancy
 Polyhydramnios
 Incompetent cervix
 Procedures– cervical encirclage, amniocentesis
 Antepartum bleeding (threatened abortion)
 Smoking
 Risk Factors
Previous PPROM : Women with a history of PPROM are at risk
for recurrent PPROM or preterm birth without PPROM
Genital tract infection: is the single most common identifiable
risk factor for PPROM. Many of the microorganisms that colonize
the lower genital tract have the capacity to produce
phospholipases, which can stimulate the production of
prostaglandins and thereby lead to the onset of uterine contractions
In addition, the host's immune response to bacterial invasion of the
endocervix and/or fetal membranes leads to the production of
multiple inflammatory mediators that can cause localized
weakening of the fetal membranes and result in PPROM
Antepartum bleeding  in the first trimester is associated with a
small but statistically significant increase in the risk of PPROM .
Cigarette smoking — The risk of PPROM among smokers is
increased 2 to 4-fold compared to nonsmokers. The risk persists
even after adjustment for other known risk factors for PPROM,
including infection. [
 Symptoms and Signs

The classic clinical presentation of PPROM is a sudden "gush" of

clear or pale yellow fluid from the vagina. However, many women
describe intermittent or constant leaking of small amounts of fluid
or just a sensation of wetness within the vagina or on the perineum
 Typically, unless complications occur, the only symptom is
leakage or a sudden gush of abundant fluid from the vagina.

 On external examination , clear fluid is flowing out of the

vagina.

 Fever, heavy or foul-smelling vaginal discharge, abdominal

pain, and fetal tachycardia, particularly if out of proportion
to maternal temperature, strongly suggest chorioamnionitis.

 Oligohydramnios is seen on ultrasound examination.

 Clinical course 
The majority of ♀ with PROM deliver within one week
Patients at 24 to 32 weeks with group B streptococcal (GBS)
negative managed expectantly with prophylactic antibiotics  the
median time to delivery  is 6.1 days
Cessation of fluid leakage is rare, except in women with PPROM
related to amniocentesis. Sealing of membranes is associated
with a more favorable prognosis 
Because of prematurity and chorioamnionitis the fetus and
neonate are at greater risk of PPROM-related morbidity and
mortality than the mother.
Fetal exposure to intrauterine inflammation has been associated
with an increased risk of neurodevelopmental impairment
  
Clinical course
 Approximately 1/3 of ♀ with PPROM develop potentially serious
infections, such as intraamniotic infection (chorioamnionitis),
endometritis, or septicemia.
 Endometritis is more common after cesarean than vaginal delivery.
 The incidence of infection is higher at earlier gestational ages
 Risks of abruptio placentae and prolapse of the umbilical cord is
high in PROM.
  Placental abruption occurs in 2 to 5% of pregnancies complicated
by PPROM. The risk is increased 7 to 9 -fold in PPROM
pregnancies in which intrauterine infection or oligohydramnios is
present .
 Early, severe, prolonged oligohydramnios can be associated with
pulmonary hypoplasia, facial deformation, and orthopedic
abnormalities. Especially when PROM occurs at less than 23 wks
of gestation
 DIAGNOSIS OF PROM
The diagnosis of PROM is clinical, and is generally based on
visualization of amniotic fluid in the vagina of a woman who
presents with a history of leaking fluid. Laboratory tests are used
to confirm the clinical diagnosis when it is uncertain.

Diagnosis
History
Examination
Vaginal swab
Ultrasound assessment
- amniotic fluid
- fetal assessment
 premature Rupture of the
membrane
History
Sudden gush of fluid or continued leakage of fluid, color
like urine, quantity moderate or abundant, odorless, etc.

Associated symptoms: contracting, bleeding vaginally,

has had intercourse recently, or has a fever
 physical examination
 Sterile speculum with sterile gloves: Direct observation
of amniotic fluid coming out of the cervical canal or
pooling in the vaginal fornix is pathognomonic of
PPROM. If amniotic fluid is not immediately visible, the
woman can be asked to push on her fundus, Valsalva, or
cough to provoke leakage of amniotic fluid from the
cervical os.
  Digital examination should be avoided because it may
decrease the latency period (i.e., time from rupture of
membranes to delivery) and increase the risk of
intrauterine infection
 PROM
Physical examination
PROM is diagnosed by sterile speculum examination
meeting the following criteria:
1.Pooling positive: clear watery amniotic fluid is seen in
the posterior vaginal fornix.
2 . Nitrazine test positive

3.Fern test positive

Chorioamnitis is diagnosed clinically with all the

following criteria needed:
Maternal fever and uterine tenderness in the presence of

confirmed PROM in the absence a URI or UTI

 premature Rupture of the
membrane
Diagnosis
•Laboratory confirmation of clinically suspected PPROM
•Test or investigation

1. Nitrazine test
2. Fern test
3. Nine blue test
4. Ultrasound
5. Indigo-carmine Amnioinfusion
 Nitrazine test

1. Fluid from vaginal exam placed on strip of nitrazine paper

2. Amniotic fluid usually has a pH range of 7.0 to 7.3 compared
to the normally acidic vaginal pH of 3.8 to 4.2
3. Paper turns blue in presence of alkaline (pH > 7.1) amni
otic fluid
4. Nitrazine test: the fluid turns pH-sensitive
paper blue
5. False-negative and false-positive NT results occur in up to 5 %
of cases
 Nitrazine test

1. False negative test: when leaking is intermittent or the

amniotic fluid is diluted by other vaginal fluids.
2. False positive: presence alkaline fluids in the vagina,
such as blood, seminal fluid, or soap or the pH of
urine can be elevated to near 8.0 if infected with
Proteus species.
 premature Rupture of the
membrane
Fern test

1. Fluid from vaginal exam

placed on slide and allo
wed to dry
2. Amniotic fluid narrow fer
n vs. cervical mucus bro
ad fern
 Ferning of amniotic fluid
 (A) Typical ferning pattern of dried amniotic fluid.
 (B, C) Urine and amniotic fluid can be distinguished by
microscopic examination of a droplet of the fluid spread and
dried on a microscope slide.
 The proteins in amniotic fluid give the appearance of ferning
(B) that is not observed with urine (C).
(D) Ferning pattern from amniotic fluid.
 Ferning of cervical mucus
(A) Ferning of cervical mucus.
(B) A ferning pattern of cervical mucus occurs with high
estrogen levels.
(C) Incomplete ferning during secretory phase of cycle.
 Nile blue tests
 >32 wks. Fetal fat cell can discover in amniotic fluid

 Strained with Nile blue sulphate. Become to red color

 Commercially available tests for diagnosis of
PROM.

1. AmniSure and Actim PROM 

2.  Placental alpha microglobulin-1 protein assay (PAMG-
1 [AmniSure]) and
3. insulin-like growth factor binding protein 1 (IGFBP-1
[Actim PROM])

4. (PAMG- 1 [AmniSure is more accurate than IGFBP-1

(Actim PROM) for diagnosis of ROM
 Fetal Fibronectin (AmniSure)
• Newer test
• Point of Care test
• Cost-up to $50 each
• Sensitivity-98.7-98.9%
• Specificity-87.5-100%
• Awaiting further testing prior to recommendations
• is a rapid slide test that uses immunochromatography
methods to detect trace amounts of placental alpha
microglobulin-1 protein in vaginal fluid. An advantage
of this test is that it is not affected by semen or trace
amounts of blood.
 Other tests
 Fetal fibronectin — A negative fetal fibronectin result
strongly supports absence of PROM, but a positive result only
indicates disruption of the interface between chorion and
decidua, which can occur with intact membranes .
 Alpha-fetoprotein — Alpha-fetoprotein (AFP) in vaginal
secretions suggestions the presence of amniotic fluid
Measurement of AFP is less costly than other commercially
available tests for PROM, but blood in the vagina can give
false positive results.
 PROM

1. Ultrasound
Assess amniotic fluid level and compatibility
with PROM 50—70% of women with PPROM
have low amniotic fluid volume

2. Indigo-carmine Amnioinfusion
Ultrasound guided indigo carmine dye amnio
infusion (“Blue tap”)
a) Observe for passage of blue fluid from vagin
a
 Ultrasonography and instillation of
indigo carmine 
 In equivocal cases, ultrasound can be performed to look for a
reduction in amniotic fluid volume. In addition, instillation
of indigo carmine into the amniotic cavity can be considered
and usually leads to a definitive diagnosis. Under ultrasound
guidance, 1 mL of indigo carmine in 9 mL of sterile saline is
injected transabdominally into the amniotic fluid. A tampon is
placed in the vagina. Twenty minutes later, the tampon is
removed and examined for blue staining, which indicates
leakage of amniotic fluid.
 Evaluation of pregnancies with preterm
premature rupture of membranes
Diagnostic tests :
 Nitrazine and fern

 Placental alpha microglobulin-1 protein assay (AmniSure)

Assessments to consider after confirmation of membrane

rupture:
 Complete blood count
 Test for fetal lung maturity
 culture for group B streptococcus
 Ultrasound examination for fetal growth, position, residual amniotic
fluid volume, fetal anatomy, and biophysical profile
 Cardiotocography to monitor fetal heart rate and frequency of uterine
contractions
 Nucleic acid amplification test or culture for Neisseria gonorrhea and
Chlamydia trachomatis
 Differential diagnosis

   Other causes of vaginal/perineal wetness, include

urinary incontinence, vaginal discharge, and
perspiration.
 Effect to mother and fetus
• Feto-maternal infection:Chorioamnionitis
• Placenta abruptio
• Premature infant: 30% - 40% of premature labou
r is associated with premature rupture of membra
ne
1. Cord prolapse, cord compression
2. Poor fetal lung development and fetal comp
ression syndrome: Respiratory distress
syndrome
3. Antepartum fetal death
 Pregnancy complications associated with
membranes (PPROM)
Pregnancy Potential maternal
Potential consequences for offspring
complication consequences

Neonatal sepsis
Intrauterine Postpartum
Long-term neurodevelopmental
infection endometritis
abnormalities, particularly cerebral palsy

Umbilical cord
Fetal asphyxia  
compression

Limb restriction deformities and

pulmonary hypoplasia (primarily with
severe oligohydramnios in the early to
Oligohydramnios  
mid second trimester). These
complications are rare when membrane
rupture occurs after 23 weeks.
Pregnancy complications associated with
membranes (PPROM)
Pregnancy Potential consequences for Potential maternal
complication offspring consequences
Fetal
  Cesarean delivery
Malpresentation
Umbilical cord
Fetal asphyxia Cesarean delivery
prolapse
Abruptio Cesarean delivery
Fetal asphyxia
placentae Coagulopathy
Morbidity of prematurity, including
respiratory abnormalities,
intraventricular hemorrhage,
Preterm birth
necrotizing enterocolitis, retinopathy
of prematurity, patent ductus
arteriosus
 MANAGEMENT
Initial approach — The management of PPROM is based upon
consideration of several factors, including:
Gestational age
Presence or absence of maternal/fetal infection
Presence or absence of labor
Fetal presentation
amount of amniotic fluid
Fetal well-being or fetal state
Fetal lung maturity
Cervical status (by visual inspection)
Availability of neonatal intensive care
 Gestational age
If no infection is present, management will be based on
gestational age as follows:
 Before viability < 24 weeks), outcome is dismal. Either
induced labor or manage patient with bed rest at home.
 Risk of pulmonary hypoplasia is high.

With preterm viability (24—35 weeks), conservative

management . Hospitalize the patient at bed rest, administer
IM Betamethasone to enhance FLM if < 32 weeks, obtain
cervical cultures, and start a 7- day course of prophylactic
Ampicillin and erythromycin.

At term (≥ 36 weeks), initiate prompt delivery. If vaginal

delivery is expected, use Oxytocin or prostaglandins as
indicated. Otherwise, perform cesarean delivery.
 Presence or absence of maternal/fetal infection
If chorioamnionitis is present, obtain cervical
cultures, start broad-spectrum therapeutic Iv
antibiotics, and initiate prompt delivery.

 Presence or absence of labor

If the uterine contractions occur, tocolysis is
contraindicated.
 Management of PROM
The optimal time for intervention varies among institutions
and depends on the balance between morbidity related to
prematurity and morbidity related to complications of
PPROM.
 
 (ACOG) suggests delivery for all patients ≥34 weeks of gestation

Termination of pregnancy
(1) Evidence of fetal pulmonary maturation
(2) Evidence of intrauterine infection

PROM at term:
(1)
(1 Awaiting the onset of spontaneous labor for 12-24h
(2) Termination of pregnancy after 24 hours
 Expectant therapy

Indication :
1. Evidence of fetal pulmonary immaturation

2. Without evidence of intrauterine infection

Management:
1. To enhance fetal pulmonary maturation

2. Antibiotic

3. Tocolysis
 Management: Rationale
1. Antibiotics
a. Prolong latency period
b. Prophylaxis of GBS infection in neonate
c. Prevention of maternal chorioamnionitis and neonatal
sepsis
d.  antibiotics is given for 7 days to pregnancies <34 wks of
gestation at the time of membrane rupture.
2. Corticosteroids
a. Enhance fetal lung maturity
b. Decrease risk of RDS, IVH, and necrotizing enterocolit
is
3. Tocolytics
a. Delay delivery to allow administration of corticosteroid
s
b. Controversial, randomized trials have shown no pregn
 Expectant management
Antibiotic therapy -- Ampicillin with Metronidazole

Corticosteroid therapy-
 A course of corticosteroids should be given to pregnancies
between 23 and 34 weeks of gestation
 to accelerate lung maturity

 Betamethasone 12mg I/M 24hrs apart –2 doses

 Dexamethasone 5mg 12 hrly - 4 doses

Tocolytics- to delay onset of labour

 Drug regimen

 A regimen is unclear.
 7-day course of antibiotic prophylaxis is recommended to all women
with PPROM who are managed expectantly.
 Ampicillin is the first choice -2 g IV every 6 hours for 48 hours,
followed by amoxicillin (500 mg orally three times daily or 875 mg
orally twice daily) for an additional five days. Or
 one dose of azithromycin (1 gr orally) upon admission.
 Ampicillin specifically targets group B streptococcus, many aerobic
gram-negative bacilli, and some anaerobes. Azithromycin specifically
targets genital Mycoplasma, which can be important causes of
chorioamnionitis in this setting, and also provides coverage
of Chlamydia trachomatis , which is an important cause of neonatal
conjunctivitis and pneumonitis.
  NICHD and MFMU Protocol of PROM
 IV Ampicillin 2 g every 6 hrs and erythromycin250
mg every 6 hours for 48 hours followed by
oral amoxicillin250 mg every 8 hrs and erythromycin
333 mg every 8 hrs for five days

  azithromycin in lieu of a multiple-day course of

erythromycin because of its ease of administration,
improved gastrointestinal tolerance, favorable cost
profile, and similar efficacy.
 Women with penicillin allergy
1. Cefazolin 1 gr IV every 8 hrs for 48 hrs, followed
by cephalexin 500 mg orally 4 times daily for 5 days. These
drugs provide coverage for both GBS and E Coli, the two
major causes of neonatal infection. Or a single oral dose
of azithromycin1 g.
2. Clindamycin 900 mg IV every 8 hrs for 48 hours
plus gentamicin 7 mg/kg ideal body weight for 2 doses 24
hrs apart, followed by oral Clindamycin 300 mg every 8 hrs
for 5 days. OR a single dose of azithromycin1 g.
 Tocolysis
  The principal indication for tocolysis in the setting of PPROM is
to delay delivery for 48 hours to allow administration of
corticosteroids. As a general rule, tocolytics should not be
administered:
1. for more than 48 hours. 
2. to patients who are in advanced labor (>4 cm dilation)
3. chorioamnionitis.
4. nonreassuring fetal testing,
5. abruptio placentae, and significant risk of
6. cord prolapse (e.g., dilated cervix and fetal
malpresentation). 
 Management: Surveillance
Risks
1.Maternal risks– infection
2.Fetal risks– pulmonary hypoplasia, limb
abnormalities, infection

Maternal: Monitor for signs of infection

Temperature
Maternal heart rate
Fetal heart rate
Uterine tenderness
Contractions
 Management: Surveillance

Fetal: Monitor for fetal well-being

 Kick counts
 Nonstress tests (NST’s)
 Biophysical profile (BPP)

Immediate Delivery
 Intrauterine infection
 Abruptio placenta
 Repetitive fetal heart rate decelerations
 Cord prolapse.
 premature Rupture of the
membrane
Summary of treatment
History, examination, USG

24 – 31 wks 32 – 33 wks 34 – 36 wks

Bed rest Bed rest Antibiotics

Antibiotics Antibiotics Deliver
Steroids Steroids
Deliver 34 wks Deliver 34 wks
premature Rupture of the
membrane
Algorithm for management of patients with
PPROM at 23 to 34 weeks of gestation
 preterm labor
and
Birth
21/06/15
 Case 1

 A healthy 20-year-old G1P0 woman at 30 weeks’

gestation complains of intermittent abdominal pain.
Her vital sign are normal. The fetal heart rate tracing
reveals a baseline heart rate of 120 bpm and is
reactive. Uterine contractions are noted every 3 to 5
minutes. Her cervix is 3 cm dilated. 90% effaced, and
the fetal vertex is presenting at -2 station.
 Case 2

 A 26-year-old woman, G3P1, at 29 weeks’ gestation by

dates comes to the maternity unit complaining of
irregular contractions every 6-9 minutes. She is a smoker
with chronic hypertension. She has had no prenatal care.
On examination her fundal height is 30 cm. her previous
pregnancy ended spontaneous vaginal delivery at 30
weeks’ gestation.
 INTRODUCTION 
 Preterm birth refers to a delivery that occurs before
370/7ths weeks of gestation. It may or may not be preceded
by preterm labor. Although term pregnancy has been
defined as 370/7ths to 416/7ths weeks of gestation, the period
370/7ths to 386/7ths weeks should be considered ‘early term’
because neonates born in this gestational age range have
higher neonatal morbidity and mortality than infants born
at ‘full term’ from 390/7ths to 406/7ths weeks.
 Preterm is characterized by cervical effacement and/or
dilatation and increased uterine irritability that occurs
before 37 weeks of gestation. Woman with a history of
previous preterm delivery carry the highest risk of
recurrence, estimated to be between 17 and 37 %.
Definition
 Cervical change associated with uterine contractions prior
to 37 completed weeks and after 20 weeks gestation.
In a nulliparous woman, uterine contractions and a single
cervical examination revealing 2-cm dilation and 80%
effacement or greater is sufficient to make the diagnosis.

 Preterm delivery is the most common cause of perinatal

morbidity and mortality. Overall, 8—10% of pregnancies
deliver prematurely. Many patients will have preterm
contractions but not be in preterm labor.
Definition
 Prematurity is the state of an infant born at a gestational
age of less than 37 weeks. It manifested by low birth
weight (500—2499gr, physical signs of immaturity and
multisystem disorders.
 Infants who are low birth weight but physical mature
(e.g., growth retarded infant) and infants who are larger
birth weight but immature(e.g., infants of diabetic
mothers) are considered premature.
 Three criteria need to be met

1. Gestational age – pregnancy duration ≥ 20 weeks, but

< 37 weeks.
2. Uterine contractions — at least three contractions in
30 minutes
3. Cervical change — serial examinations show change in
dilation or effacement, or a single examination shows
cervical dilation of ≥ 2cm.
Classification
 Subtypes of preterm birth are variably defined.
1. By gestational age
2. By birth weight
3. By etiology
4. Using a combination of factors
Classification
1. By gestational age:

 World Health Organization:

a. Moderate to late preterm: 32 to <37 weeks
b. Very preterm: 28 to <32 weeks
c. Extremely preterm: <28 weeks

 Centers for Disease Control and Prevention

a. Preterm: <37 weeks
b. Late preterm: 34 to 36 weeks
c. Early preterm: <34 week
2. By birth weight
a. Low birth weight (LBW): <2500 grams
b. Very low birth weight (VLBW): <1500 grams
c. Extremely low birth weight (ELBW): <1000 grams

3. By etiology:
Spontaneous: ~70 to 80% of PBs and are related to PL, which
accounts for 40 to 50% of PBs, or (PPROM), which accounts
for 20 to 30% of preterm births.
Medical or provider-initiated : The remaining 20 to 30 % of
PBs medically indicated because of maternal or fetal issues
(e.g., preeclampsia, placenta previa, abruptio placenta, fetal
growth restriction, multiple gestation).

N.B: Complications of pregnancy can lead to both spontaneous

and provider-initiated preterm births.
4. Using a combination of factors:
 The Global Alliance to Prevent Prematurity and Stillbirth has

recently proposed an alternative classification system . Under

this system, preterm birth is categorized according to the
clinical phenotype consisting of:
1. One or more conditions of the mother, placenta or fetus
2. Presence or absence of signs of parturition
3. Pathway to delivery (spontaneous or caregiver
initiated). 
 Significance
  PTB is the leading direct cause of perinatal morbidity and
mortality
 It usually results in preterm birth, a complication that affects 8—
10% of birth.
 It is responsible for 27% of neonatal deaths worldwide (neonatal
death: death in the first 28 days of life), comprising over one
million deaths annually.
 The risk of neonatal mortality decreases as gestational age at birth
increases, but the relationship is nonlinear.
 preterm birth is the second most common cause of-death (after
pneumonia) in children younger than 5 years.
Epidemiology
 Prevalence — Few countries have reliable national
PTB prevalence data.
 Worldwide, the preterm birth rate is estimated to be
about 11 % (range 5% parts of Europe to 18 %t parts of
Africa]), and about 15 million children are born preterm
each year (range 12 to 18 million) .
 Of these preterm births:
 84 % occurred at 32 to 36 weeks
 10% occurred at 28 to <32 weeks, and
 5 % occurred at <28 weeks.
Risk factors for preterm birth
 Most common risk factors for preterm delivery are:
1. Previous preterm birth faces 20—30% risk of recurrence in
the next pregnancy.
2. Multiple gestation
3. Polyhydramnios
4. Uterine cause: Uterine anomalies including
 Exposure to diethylstilbestrol-induced changes in uterus
 uterine septum
 bicornuate uterus
 cervical incompetence and
 leiomyomas especial submucosal or subplacental or
 excessive uterine contractility
5. PROM
 Other risk factors are:
1. Low socioeconomic status including:
 low income
 low level of education and
 poor nutrition such as Anemia (hemoglobin <10 g/dL) and
 low body mass index
2. Race (African-American race) non- white race.
3. Maternal complications
 age (<18 or >40)
 Smoking
 Substance abuse and
 Alcohol abuse
 Inadequate or lack of prenatal care
 Life events (no partner, divorce, separation, death)
4. Abdominal surgery during pregnancy and/or history of
abdominal-pelvic and cervical surgery
5. Infectious causes:
 Chorioamnionitis
 Sexually transmitted infections
 bacterial vaginosis
 Asymptomatic bacteriuria
 Periodontal disease
 Systemic infection, acute pyelonephritis, appendicitis, pneumonia
 Cervical vaginal colonization
6. Abnormal placentation
 Placenta previa
 Placental abruption
7. Fetal cause:
 Fetal anomaly or malformation
 fetal growth restriction
 Intrauterine fetal death
8. Occupational issues:
 upright posture
 use of industrial machines
 physical exertion or heavy physical labor
 mental or environmental stress related to work or working
conditions
 Anxiety and depression
9. Environmental factors (e.g., heat, air pollution)
10. Vaginal bleeding ,especially history of one and more
spontaneous second trimester abortions
11. Premature cervical dilatation or effacement (short cervical
length)
 Ultrasound cervical length <25mm.
12. Maternal first degree family history of spontaneous preterm
birth, especially if the pregnant woman herself was born
preterm
 Etiology

1. Idiopathic: represents the larger group

2. Infection
3. Over- distension
4. Vascular
5. Intercurrent illness
6. Cervical weakness
 Etiology
2. Infection:
 intrauterine infection rarely cause PTL but subclinical
infection of choriodecidual space and amniotic fluid is the
most widely studied etiology of PTL.
 The vagina bacteria are thought to ascend from the
vaginal specially bacterial vaginosis.
 Complications:
 Neonatal sepsis
 Postpartum endometritis and
 Chorioamnionitis.

3. Over- distension (two main causes are: polyhydramnios

and multiple pregnancy)
 Etiology
4. Vascular:
 Antepartum hemorrhage and abruptio placenta known
that blood irritate the myometrium and weaken the
membranes.

5. Intercurrent illness:
 Serious infective illness such as :
 Pyelonephritis or UTI appendicitis pneumonia
 Pathogenesis
 there are four discrete mechanisms for the pathogenesis
of preterm birth:
1. Premature activation of the maternal or fetal hypothalamic-
pituitary-adrenal axis
2. Exaggerated inflammatory response/infection
3. Decidual hemorrhage
4. Pathological uterine distention
 Clinical manifestations
The clinical manifestations of true labor, contractions and
cervical change, are the same whether labor occurs preterm or at
term. The following are early signs and symptoms of labor;
however, they are non-specific and can be present for several
hours in women who do not exhibit cervical change especially in
primgravidas.
 Lower abdominal pain or menstrual-like cramping

 Pressure sensation in the vagina

 Mild, irregular contractions

 Lower back pain

 Increased vaginal discharge of mucus, which may be clear,

pink, or slightly bloody (i.e., mucus plug, bloody show)

 Diagnostic evaluation
History and initial examinations  — includes:
1. Review of the patient’s past and present obstetrical and medical
history, and assessment of gestational age.
2. Evaluation of signs and symptoms of preterm labor check clinical
findings and risk factors for preterm birth.
3. Maternal vital signs (temperature, blood pressure, heart rate,
respiratory rate).
4. Review of the fetal heart rate pattern.
5. Assessment of contraction frequency, duration, and intensity.
6. Examination of the uterus to assess firmness, tenderness, fetal size,
and fetal position.
 Diagnostic evaluation
2. Speculum examination —  perform a wet non-lubricated
speculum. Lubricants may interfere with tests on vaginal
samples. The goals of this examination are to:
1. Estimate cervical dilation. Cervical dilation >3 cm supports

the diagnosis of preterm labor.

2. Assess the presence and amount of uterine bleeding. Bleeding
from abruptio placenta or placenta previa can trigger preterm
labor.
3. Evaluate fetal membrane status (intact or ruptured) by
standard methods.
4. Obtain a cervico-vaginal fluid specimen in case fetal

fibronectin (fFN) testing is desired after transabdominal

ultrasound examination.
 Diagnostic evaluation
4. Cervical examination — cervical dilation and effacement by digital
examination after speculum examination and after placenta previa and
rupture of membranes have been excluded by history and physical,
laboratory, and ultrasound examinations, as appropriate.
5. Laboratory evaluation 
 Rectovaginal group B streptococcal culture if not done within the previous
5 wks; antibiotic prophylaxis depends on the results.
 Urine culture, since asymptomatic bacteriuria is associated with an
increased risk of preterm labor and birth.
 Drug testing in patients with risk factors for substance abuse, given the
link between cocaine use and placental abruption.
 Fetal fibronectin (fFN) in women <34 weeks of gestation with cervical
dilation <3 cm and cervical length 20 to 30 mm on transvaginal ultrasound
examination.
 Fetal fibronectin 
 Fetal fibronectin (fFN) is an extracellular matrix protein
present at the decidual-chorionic interface. Disruption of this
interface due to subclinical infection or inflammation,
abruption or uterine contractions releases fFN into
cervicovaginal secretions, which is the basis for its use as a
marker for predicting spontaneous preterm birth. A positive
fFN test (fFN concentration ≥50 ng/mL in cervicovaginal fluid
between 220/7ths and 346/7ths weeks of gestation) in women with
intact membranes, cervical dilation <3 cm, and no gross
vaginal bleeding correlates with an increased risk of preterm
delivery within seven days.
 Diagnostic evaluation
7. Cervical length with ultrasound
 Cervical length <20 mm: Symptomatic women with
cervical length <20 mm are at high risk (>25 % of delivery
within seven days.  

 Cervical length >30 mm: Symptomatic women with

cervical length >30 mm are at low risk (<5 percent) of
delivery within seven days 
 MANAGEMENT
1. Initial assessment to determine whether patient is experiencing preterm
labor
A. assess for the following
 Uterine activity
 Rupture of the membrane
 Vaginal bleeding
 Presentation
 Cervical dilatation and effacement
 Station
B. Reassess for the estimated gestational age
2. Search for precipitating cause/factor
3. Consider specific management strategies
1. Intravenous tocolytics therapy (decision depend on GA, cause of PTL and
contraindications)
2. Corticosteroid therapy
3. Antibiotic therapy if specific infectious agent is identified or PROM
 Management
1 Confirm the diagnosis of PTB 20—37 wks’ gestation
Determine the presence of :
 Regular uterine contractions

 Rupture of membranes

 Cervical change

 Dilatation more than 2cm

 Effacement ≥ 80%

 If the diagnosis of preterm labor is suspected, but not

confirmed, it is crucial a vaginal fetal fibronectin (FFN)
sample before pelvic cervical examination.
 Management
2. Evaluate cervix
Rule out PROM
Culture GBS, gonorrhea, and Chlamydia
Document position, dilatation, effacement and station.
Evaluate urinary tract to rule out infection and calculi
Rule out early abruptio placentae

3. Start endovenous line and hydrate with one liter of normal saline
or ringer

4. Document a fetal well being

Perform a nonstress test or stress test.
If regular contractions are present

5. Ultrasound
 Management
5. Ultrasound
Estimate GA and fetal weight.
Rule out intrauterine restriction
Rule out fetal anomalies, hydramnios or multiple gestation
Rule out abruptio placentae or placenta previa
Perform biophysical profile
Consider amniocentesis for lung maturity

6. Tocolysis subcutaneous or oral

Response: consider ambulatory follow-up
NO response initiate IV tocolysis and corticosteroids if the
gestational age is at 24—34 weeks.
 Management
 Treatment of women <34 weeks with suspected PTL:
hospitalization and initiate the following treatments:
 A course of betamethasone to reduce neonatal morbidity and
mortality associated with preterm birth
 Tocolytic drugs for up to 48 hours to delay delivery so
that betamethasone given to the mother can achieve its maximum
fetal effect
 Antibiotics for GBS chemoprophylaxis
 Magnesium sulfate for pregnancies at 24 to 32 weeks of gestation.
It provides neuroprotection against cerebral palsy and other types
of severe motor dysfunction in offspring born preterm.
 Tocolytic Agents
Definition:
 Tocolytics (also called anti-contraction medications or labor repressants) are medications used to

suppress premature labor.
 Tocolytic is indicated for regular uterine contractions and cervical change (effacement and

dilatation)
 Oral tocolytic agents are no more effective than placebo.

 Parenteral agents may prolong pregnancy but for no more than 72h. This provides a

window of time for

1. Administration of maternal IM betamethasone, a glucocorticoid drug to enhance fetal
pulmonary surfactant (lung maturity), but takes one to two days to work.
2. Transportation of pregnant ♀ to a facility with neonatal intensive care.

 The suppression of contractions is often only partial and tocolytics can only be relied on to
delay birth for several days. Depending on the tocolytic used the mother or fetus may
require monitoring, as for instance blood pressure monitoring when nifedipine is used as it
reduces blood pressure. In any case the risk of preterm labor alone justifies hospitalization.
 Tocolytic Agents
1. β-Adrenergic agonists also known as β2-adrenergic receptor
agonists, include terbutaline and ritodrine.
2. In the past, beta-mimetic agents, were the agents of choice, but in
recent years their use has been significantly curtailed due to maternal
and fetal side effects, such as maternal tachycardia, hyperglycemia, and
palpitations. The use of these agents can lead to pulmonary edema,
myocardial ischemia, and cardiac arrhythmia.
 Mechanism of action: are a class of drugs that act on the beta2-
adrenergic receptor. Like other beta-adrenergic agonists, they
cause smooth muscle relaxation, such as:
 dilatation bronchial passages
 vasodilatation in muscle and liver

 Relaxation of uterine muscle, and

 Release of insulin.

They are primarily used to treat asthma and other pulmonary disorders.

1.
 Tocolytic Agents
1. β-Adrenergic agonists maternal side effects:
 Cardiovascular side effects hypotension, tachycardia are from β1-
adrenergic cardiovascular activity. other side effects are insomnia, anxiety,
and tremor, hyperglycemia hypokalemia and death from cardiopulmonary
arrhythmias, pulmonary edema, myocardial ischemia.

 β-Adrenergic agonists fetal side effects

 Fetal tachycardia
 Hyperinsulinemia
 Hypoglycemia
 Myocardial and septal hypertrophy
 Myocardial ischemia
 Tocolytic Agents
 Contraindications:

Drug names Dose Contraindications:

Terbutaline 0.25—0.5Mg Cardiac arrhythmias

(Brethine) every 3—4h diabetes

Ritodrine (Yutopar) 0.05—0.35 Mg Poorly controlled thyroid

per Minuit disease and diabetes

Fenoterol diabetes

Salbutamol diabetes
 Tocolytic Agents
 The most common tocolytic agents used for the treatment of
preterm labor are:
1. Magnesium sulfate (MgSO4)
2. Indomethacin, and
3. Nifedipine.

For ♀ 24 to 32 weeks of gestation  indomethacin is first-line

therapy for labor inhibition.
For ♀ 32 to 34 weeks of gestation,  nifedipine is the first
choice for initial treatment of preterm labor, because of adverse
fetal effects with indomethacin use at this gestational age.
 Tocolytic Agents
2. Magnesium sulfate (MgSO4)
Mechanism of action — unknown.
 MgSo4 is a competitive inhibitor of calcium. Means intracellular calcium antagonism
 It probably competes with calcium at the level of the plasma membrane voltage-
gated channels.
 It hyperpolarizes the plasma membrane and inhibits myosin light-chain kinase activity
by competing with intracellular calcium at this site. Interference with the activity of
myosin light-chain kinase reduces myometria
 Neuroprotective effects — Predelivery administration of Mg2d on So4 is
neuroprotective for the neonate 
 Monitoring: clinical monitoring is base on decreasing but maintaining detectable deep
tendon reflexes. 
 Tocolytic Agents
2. Magnesium sulfate (MgSO4)
Side effects: muscle weakness, respiratory depression, and
pulmonary edema. Magnesium overdose is treated with IV
calcium gluconate.  

Contraindications: Magnesium is eliminated by the kidneys. Thus,

women with impaired renal function will have an exaggerated
rise in serum magnesium and may develop magnesium toxicity at
the usual doses of administration. There for, it is contraindicated
♀with renal insufficiency and myasthenia .
 Symptoms of hypermagnesemia
1. Neuromuscular toxicity is the most common. Symptoms range
from diminished deep tendon reflexes when the plasma magnesium
concentration reaches 4 to 6 meq/L (4.8 to 7.2 mg/dL or 2 to
3 mmol/L) to somnolence, loss of deep tendon reflexes, and muscle
paralysis.
2. Bradycardia and hypotension may occur at a plasma magnesium
concentration above 4 to 5 meq/L (4.8 to 6 mg/dL or 2 to 2.5 mmol/L)
3. Observed electrocardiogram changes include prolongation of the
P-R interval, an increase in QRS duration, and an increase in Q-T
interval. Complete heart block and cardiac arrest may occur at a
plasma magnesium concentration above 15 meq/L (18 mg/dL or
7.5 mmol/L).
4. It may inhibit the secretion of (PTH), causing transient
hypocalcaemia.
5. Hypermagnesemia may also cause nonspecific symptoms such as
nausea, vomiting, and flushing
 Cyclooxygenase inhibitors
 Mechanism of action — Cyclooxygenase (COX, or
prostaglandin [PGH] synthase) is the enzyme responsible for
conversion of arachidonic acid to prostaglandins, which are
critical in parturition. Prostaglandins enhance the formation of
myometrial gap junctions and increase available intracellular
calcium by raising transmembrane influx and sarcolemmal
release of calcium. Cyclooxygenase exists in two isoforms,
COX 1 and COX 2. COX 1 is synthesized is dramatically
increasing in the decidua and myometrium during term and
preterm labor. (Cyclooxygenase inhibitors decrease
prostaglandin production by either general inhibition of
cyclooxygenase or specific inhibition of COX 2, depending
upon the agent
Prostaglandin and thromboxane synthesis
  Indomethacin
 Indomethacin , a nonspecific COX inhibitor, is the most commonly
used tocolytic of this class.

 Dose: 50—100 rectal suppository, then 25 to 50 Mg orally every 6h

 Maternal side effects — including, nausea, esophageal reflux,

gastritis, and emesis, are seen ~4% of patients treated with
indomethacin for PTL. Hepatitis and renal failure. Platelet
dysfunction may occur.

 The primary fetal concerns with use of indomethacin and other

COX inhibitors are constriction of the ductus arteriosus and
oligohydramnios.
 Calcium channel blockers
Nifedipine
Mechanism of action 
 Calcium channel blockers directly block the influx of calcium

ions through the cell membrane. They also inhibit release of

intracellular calcium from the sarcoplasmic reticulum and
increase calcium efflux from the cell. The resulting decrease in
intracellular free calcium leads to inhibition of calcium-
dependent myosin light-chain kinase phosphorylation and
results in myometrial relaxation
 The relative safety, maternal tolerance, ease of administration,

and reduction in adverse neonatal outcomes support use

of nifedipine rather than beta agonists for inhibition of acute
preterm labor. 
 Calcium channel blockers
Nifedipine
Dose:
 An initial loading dose of 20 mg orally, followed by an

additional 20 mg orally in 90 minutes. If contractions persist,

20 mg can be given orally every 3 to 8 hours for up to 72
hours, with a maximum dose of 180 mg/day. The (ACOG)
suggests a 30 mg loading dose and then 10 to 20 mg every
four to six hours.

 5—10Mg every 15 to 20minuts up to 4times, then 10 t0 20 Mg

orally every 4—6h
 Calcium channel blockers
Nifedipine
Maternal side effects 
 transient hypotension
 Nifedipine: is a peripheral vasodilator, thus it may cause
symptoms such as nausea, flushing, headache, dizziness, and
palpitations. Arterial relaxation results in decreased total vascular
resistance, which is accompanied by a compensatory rise in
cardiac output (reflex increase in heart rate and increased stroke
volume). These compensatory changes generally maintain blood
pressure in women who have no underlying myocardial
dysfunction.
 Calcium channel blockers
Nifedipine
Fetal side effects 
 Fetal side effects — In animal studies, CB administration
decreased uterine blood flow and fetal oxygen saturation;
however, this has not been confirmed in humans and Doppler
studies of human fetal systemic, umbilical, and uteroplacental
blood flow have been reassuring.
 Contraindications — Calcium channel blockers are contraindicated
in women with known hypersensitivity to the drug, hypotension,
or cardiac problem
 The concomitant use of a calcium-channel blocker and magnesium
sulfate could act synergistically to suppress muscular contractility,
which could result in respiratory depression.
 Postterm Pregnancy /
Postdate Pregnancy /
Prolonged Pregnancy
22/06/15
 Case 1
 A 21-year-old primigravida at 42 weeks’ gestation by
dates comes to the outpatient prenatal clinic. She has
been seen for prenatal care since 12 weeks’ gestation,
confirmed by an early sonogram. She states that fetal
movements have been decreasing. Fundal height
measurement is 42 cm. her cervix is long, closed,
posterior, and firm. Nonstress test (NST) is reactive,
but amniotic fluid index (AFI) is 4 cm.
 Postterm pregnancy
Definition:
 Postterm: describe any pregnancy that exceeds 42 completed
weeks (294 days) or more from the first day of the last
menstrual period.
 Postmaturity: refers to condition of the infant and has
characteristic features.
Dry ,peeling and cracked skin particularly on the hands and feet.
 Absence on vernix caseosa and Lanugo (fine hair)

 Loss of subcutaneous fat

 Meconium staining of the skin

 complications
 Increased prenatal mortality

 Intrapartum fetal distress

 Increased operative delivery rate

 Meconium aspiration.
 Postterm pregnancy
 These are all indicators of intrauterine malnutrition and may
occur at any stage of pregnancy if there is placenta
dysfunction.
 Postmaturity is often associated with
 Oligohydramnios
 An increased incidence of meconium in the amniotic fluid and
 An increased risk intrauterine aspiration of meconium stained fluid
into the fetal lungs.

Statistics: Generally
 50% of patients delivery by 40 weeks

 75% by 41 weeks, and

 90% by 42 weeks.

 Because up to half of these patients had cycles linger than

28 days
 Postterm pregnancy
Incidence
 41  27%

 42 4-14%

 43 2-7%

 The incidence is decreasing

Dating of pregnancy
 Accurate dating of pregnancy is essential to avoid unnecessary
intervention
 U/S scan prior to 20 wks gestation is an excellent method of
establishing or confirming true gestational age
 Routine U/S scanning   rate of IOL for post-term
 INCIDENCE
 BY LMP : 7.5 %
 BY USG : 2.6 %
 BY LMP + USG : 1.1 %
 Previous 1 Postterm : 27 %
 Previous 2 Postterm : 39 %
 Etiology
 The most common cause of true postdates are idiopathic which
occurs more commonly in young primgravidas. However, the
condition may be familial.
 Wrong dates
 Biological-previous prolonged pregnancy.
 Irregular ovulation
 Decreased fetal estrogen production
 Placental sulfatase deficiency

 Anencephaly (pregnancies with anencephaly fetuses are

the longest pregnancies reported)

 Fetal adrenal hypoplasia

 Extrauterine pregnancy (v.v. rare)

 Risk factors 
 Nulliparity or Primigravidity
 Male fetus
 Maternal obesity
 Older maternal age
 Maternal or paternal personal history of Postterm birth
 Maternal race/ethnicity (African-American women, Latina,
and Asian women are at lower risk than Caucasians)
 Genetic predisposition as concordance for postterm pregnancy
is higher in monozygotic than dizygotic twin mothers
 Specific conditions in the offspring associated with prolonged
gestation include adrenal gland hypoplasia and congenital
adrenal hyperplasia due to 21-hydroxylase deficiency.
Placental sulfatase deficiency also is a rare cause of postterm
pregnancy.
Significance
 Perinatal mortality is increased 2 to 3 fold. This is a direct result of
changes on placental function over time.

 CLINICAL MANIFESTATIONS
The clinical presentation of postterm infants is based primarily on fetal
growth. In most cases, continued fetal growth results in higher birth
weights in the postterm than term infant, with an increased likelihood of
macrosomia. However, fetal growth restriction occurs in some postterm
infants, most likely caused by a poorly functioning placenta that is
unable to provide adequate nutrition. This results in the birth of a small
for gestational age (SGA) infant, who usually appears malnourished.
 CLINICAL MANIFESTATIONS
Macrosomia syndrome:
 Infant size and birth weight are affected by extended gestational

length. Most postterm infants are larger than term infants, as both
fetal birth weight and head circumference measurements continue
to increase from 39 to 43 weeks gestation, due to placental function
continues providing nutritional substrates and gas exchange to the
fetus, resulting, in a healthy but large fetus.
 These infants appear normal at birth, apart from their large size.

They often have accentuated physiologic desquamation of the skin.

 Postterm macrosomic infants are at risk for birth injury due to

prolonged labor, cephalopelvic disproportion, and shoulder

dystocia which is more common with risk of fetal hypoxemia and
brachial plexus injury.
 Cesarean rate is increased owing to prolonged or arrested labor.
 CLINICAL MANIFESTATIONS
Dysmaturity syndrome or:
 In a minority of patients , placental function declines as infraction

and aging lead to placental scarring and loss of subcutaneous tissue.

This reduction of metabolic and respiratory support to the fetus can
lead to asphyxia that is responsible for increased perinatal morbidity
and mortality.
 Cesarean rate increased owing to nonreassuring FHR patterns.

 Oligohydramnios results in umbilical cord compression.

 Hypoxia results in acidosis and in utero meconium passage.

N.B: Fetal growth restriction in postterm pregnancy results in a long,

thin, SGA malnourished infant with meconium staining, and dry and
parchment-like peeling skin, referred to as dysmaturity syndrome
 ADVERSE PERINATAL OUTCOME ASSOCIATED
WITH POST-TERM PREGNANCY
 PERINATAL MORTALITY — Perinatal mortality (i.e., stillbirths plus early
neonatal deaths) increases as the pregnancy extends beyond 40 weeks gestation

  Risk of perinatal death (Antepartum, Intrapartum, postpartum) due to 

anomalies e.g.. Anencephaly
intrauterine infections
asphyxia with or without meconium

  Risk of neonatal morbidity 

- macrosomia - endotracheal intubation
- shoulder dystocia - respiratory distress
- meconium aspiration - persistent fetal circulation
- admission to NICU - pneumonia
- Rx with +ve pressure oxygen - seizures

 Risk of  IOL, fetal distress in labor, meconium, & operative deliveries

  Risk of post-term adverse outcome  in women with

HPT, PET,DM , abruptio placenta, & IUGR
 NEONATAL COMPLICATIONS 
 The risk of neonatal complications depend on how fetal growth
has been affected.
 Fetal macrosomia is associated with prolonged labor,
cephalopelvic disproportion, and shoulder dystocia resulting in an
increased risk of orthopedic (e.g., clavicular fractures) or
neurologic birth injury (e.g., brachial plexus palsy).

Dysmaturity infants are at increased risk of:

 perinatal depression or asphyxia
 Oligohydramnios may predispose to umbilical cord compression.

 hypoglycemia and polycythemia.

 MANAGEMENT
Management is based on two factors:
1. Confidence in dates: identify how much confidence can be
placed on the GA being truly > 42 weeks.

2. Favorableness of the cervix: assess the likelihood of successful

induction of labor by assessing cervical dilation, effacement ,
position, consistency, and station.
 Favorable cervix is dilated, effaced, soft, and anterior to mid position.
 Unfavorable cervix is closed, not effaced, long, firm, and posterior
 pat
 MANAGEMENT
1-Establishing gestational age
 HX ( in the 1st visit )

LMP
 regularity & length of the cycle
 OCP in the last 3 cycle before conception
 Exam.  Size of the uterus corresponding to dates or not

 U/S  to confirm or establish gestational age

especially if  LMP uncertain

 if the cycles were irregular
 if there is Hx of OCP use
 if size of the uterus inconsistent with GA
 The earlier the U/S the more accurate it is for GA determination

 U/S at 16-20 wks appropriate to assess other parameters of the

fetus & placenta
 MANAGEMENT
2-Management 39-40 6/7 wks

 In uncomplicated pregnancies there is no evidence to support

IOL nor fetal surveillance

 If there are other risk factors including HPT, DM, IUGR,

macrosomia, multiple pregnancy, or hydramnios  IOL or
serial fetal surveillance is indicated
 3-Management 41-42 wks

A-IOL or CS if vaginal delivery is contraindicated

 Studies have shown that IOL at 41 or> wks

 CS rate compared to expectant management
 rate of non-reassuring fetal heart changes
 meconium staining of the amniotic fluid
 macrosomia >4000 gms
 rate of fetal or neonatal death
( mostly  stillbirth due to  asphyxia
& meconium aspiration )
3-Management 41-42 wks

B-Expectant management with fetal surveillance

 There are exceptions to the above recommendations (3A) 

if the mother refuses IOL despite full explanation of the risks

Fetal surveillance
 Minimally fetal surveillance should include twice weekly
amniotic fluid volume estimation by U/S
 Fetal movement, NST, BPP, doppler

 Monitoring should be at frequent intervals

 All of the tests have false +ve & false –ve

IOL
 INTRODUCTION
DEFINITION Artificial initiation of labor before its spontaneous
onset for the purpose of delivery of the fetoplacental unit

INDICATIONS
 Post-term pregnancy  most common

 PROM

 IUGR

 Non-reassuring fetal surveillance

 Maternal medical conditions  DM, renal disease, HPT,

gestational HPT, significant pulmonary disease,
antiphospholipid syndrome
 Chorioamnionitis

 Abruption

 Fetal death
RISKS of IOL
  rate of operative vaginal deliveries
  rate of CS
 Excessive uterine activity
 Abnormal fetal heart rate patterns
 Uterine rupture
 Maternal water intoxication
 Delivery of preterm infant due to incorrect estimation
of GA
 Cord prolapse with ARM
CONTRAINDICATIONS
(Contraindications to labor or vaginal delivery)
 Previous myomectomy entering the cavity

 Previous uterine rupture

 Fetal transverse lie

 Placenta previa

 Vasa previa

 Invasive Cx Ca

 Active genital herpes

 Previous classical or inverted T uterine incision

 2 or more CS
PREREQUISITES
To assess the following
 Indication / any contraindications

 GA

 Cx favourability (Bishop score)

 Pelvis, fetal size & presentation

 Membranes status

 Fetal heart rate monitoring prior to IOL

 Elective induction should be avoided due the

potential complications
 Cx ripening prior to IOL
Mechanical methods

Foley Catheter
 It is introduced into the cervical canal past the internal os, the
bulb is inflated with 30-60 cc of water
 It is left for up to 24 hrs or until it falls out

 Contraindications Low laying placenta, antepartum Hg,

ROM, or cervicitis
 No difference in operative delivery rate, or maternal or
neonatal morbidity compared to PG gel

Hydroscopic dilators (E.g., .Laminaria tents)

 Higher rate of infections
 IOL
1-Oxytocin with Amniotomy
 IV

 Half life 5-12 min

 A steady state uterine response occurs in 30 min or >

 Fetal heart rate & uterine contractions must be monitored

 If there is hyperstimulation or nonreassuring fetal heart rate

pattern  D/C infusion

 Women who receive oxytocin were more likely to be delivered in

12-24 hrs than those who had amniotomy alone
& less likely to have operative delivery
 IOL
2-PGE2
 For women with favorable Cx  PGE2  the rate of
operative delivery & failed IOL when compared to Oxytocin
 PGE2   GIT side-effects, pyrexia & uterine hyperactivity

3-Sweeping of the membranes

 Vaginally the examining finger is placed through the os of the
Cx & swept around to separate the membranes from the lower
uterine segment
  local PGF2 α production & release from decidua &
membranes  onset of labor
  the rate of delivery in 2-7 days

  the rate of post-term

  the use of formal induction methods

 If there is urgent indication for IOL sweeping is not the

method of choice
 Specific circumstances or indications
Prelabor SROM at term
 6-19%

 IOL with oxytocin  risk of maternal infections

(chorioamnionitis& endometritis) & neonatal

infections
 PG also maternal infections & neonatal NICU

admissions
IOL after CS
 PG should not be used as it can result in rupture

uterus
 Oxytocin or foley catheter may be used