KERALA FEDERATION OF OBSTETRICS AND GYNAECOLOGY Vol: 4 No: 3

CONTENTS

President
Dr.Narayanan.T
Secretary General
Dr .Jayandhi Raghavan T
Immediate Past President
Dr. Sreedevi.N.S
President Elect
Prof. V. P. Paily
Vice President
Dr. Vinayachandran. S
Vice President Elect
Dr.Neena Thomas
Joint Secretary
Dr. Sangeetha Menon
Treasurer
Dr.Rajalakshmi Janardhanan
Journal Editor
Dr. Fessy Louis .T
Chair, Maternal & Foetal Medicine Committee
Prof. V. P. Paily
Chair, Academic Committee
Dr. V. Rajasekharan Nair.V
Chair, Adoloscent Committee
Dr.V.K.Chellamma
Chair, Reproductive Health Committee
Dr .K .K . Gopinathan
Chair,Oncology Committee
Dr.Sumangala Devi
Chair, Research Committee
Dr. P.K.Sekharan
INTRAUTERINE DEATH MANAGEMENT
Dr. N.S. Sreedevi
PRECOCIOUS PUBERTY
Dr. Ashwini Bhalerao-Gandhi
PREECLAMPSIA AND ECLAMPSIA:
Dr Girija Wagh
USE OF PROSTAGLANDINS IN LABOUR
Prof. Dr. Kanan Yelikar

02
04
07
13

Address of Correspondence

Dr. Fessy Louis T.

Editor KFOG Journal
CIMAR COCHIN, Tipusulthan Road, Cheranalloor,
Edappally, Kochi -682 034, Kerala, INDIA
Mob: 09846055224 E-mail: fessylouis@gmail.com
Design : smritidesign.in Printing : Anaswara, Kochi

February 2011

Dear colleagues and friends,

We wish all of you a very warm, fruitful and enchanting 2011!
The year 2010 had its magical spin very swiftly amongst the varied activities
of KFOG and our own personal, busy schedules and engagements. Hope to have
an ACTIVE 2011 too!
We the KFOG team were fortunate to present a gratifying show through out
the year. Thanks to the untiring efforts and supports by our esteemed members from
Thiruvanthapuram to Kasargode. We could effectively persue the CRMD activities
and it is heartening to note that few southern states have expressed their desire to
emulate us.
The proposed ten sessions under the CHC Upgradation programme to train
the Medical officers and nurses could be completed and this successful venture was
acknowledged and applauded by NRHM and Kerala Health services Officials and
authorities. A plan to train nursing assistants in the same pattern is also started and
one meeting on Trainers training has already over.
We conducted secession on Research methodology at Thiruvananthapuram
for the benefit of PG Students, which was a new venture. It was KFOGs pride to
associate with FOGSI in conducting a National conference on High Risk Pregnancy
and Labour at Kozhikode under the chairmanship of P.K.Sekharan, Vice president
FOGSI- a thumping success in all dimensions.
Contd Page-2

Dear Colleagues
Rapid progress is taking place in the field of Medicine. The
knowledge in this field has to be updated frequently to keep up
with the progress and give maximum benefit to the patients. One
of the best ways to keep up with this new knowledge is to get updated through
scientific articles and journals.
I sincerely thank once again for all those who have contributed to all the issues of
KFOG Journal . All the previous issues are updated in the journal page of our
website www.kfogkerala.org.
Wishing you all a happy reading and prosperous 2011,
Dr.Fessy Louis T.

w w w. k f o g k e r a l a . o r g

INTRAUTERINE DEATH
MANAGEMENT
Dr. N.S. Sreedevi, MD; DGO; FICOG
Chief Consultant in Obstetrics & Gynaecology BMH, Calicut.

Intrauterine fetal death is defined by World Health Organisation

(WHO) in 1950 and revised by the working group formed by
the American Academy of Pediatrics and the American College
of Obstetricians and Gynecologists in 1988, is death prior to
the complete expulsion or extraction from its mother of a
human conception irrespective of the duration of pregnancy
and which is not an induced termination of pregnancy.
A variety of definitions are used in different parts of the world.
For statistical purposes however it is recommended by the
WHO that intrauterine fetal death occurring after 20 weeks or
fetal weight >500gms when gestational age is not known. This
is further divided into early (20-27 wks) and late (> 28 wks)
fetal death.
Incidence
The incidence of intrauterine fetal death varies according to
the definition used for reporting fetal deaths.
1950 : 20/1000 births
2002 : 6.4/1000 births
2004 : 6.2/1000 births
Early still birth (20-27 wks) remain static since 1999, but late
still births (> 28 wks) has down from 4.3 to 3.1/1000 births.
Risk factors for intrauterine fetal death
Fetal (25-40%)
Chromosomal anomalies
Nonchromosomal birth defects
Nonimune hydrops
Infections viruses, bacteria, protozoa

Placental (25-35%)
Abruption
Fetal-maternal hemorrhage
Cord accident
Placental insufficiency
Intrapartum asphyxia
Previa
Twin-to-twin transfusion
Chorioamnionitis
Maternal (5-10%)
Antiphospholipid antibodies
Diabetes
Hypertensive disorders
Trauma
Abnormal labor
Sepsis
Acidosis
Hypoxia
Uterine rupture
Postterm pregnancy
Drugs
Unxplained (25-35%)
Diagnosis
Intrauterine fetal death is suspected when the mother reports
with loss of fetal movements or the fundal height on palpation
is found to be less for the gestational age. Absence of fetal
heart sounds on auscultation or Doppler adds to clinical
suspicion. It should be confirmed on ultrasonography by
absence of fetal heart activity.

Contd from Page-1

KFOG

As you are aware, 33rd AKCOG will be held at Kanhangad under the joint auspices of KFOG and Kasargode society, which we hope and
pray, should be a mammoth success. This being the last bulletin of the present team headed by us let us take this opportunity to cordially thank
all those who rallied behind KFOG in all its activities.
Our special thanks to Dr.V.P Paily, Chairman, Maternal and Foetal Medicine committee and president elect KFOG, Dr.V.Rajasekharan
Nair, Chairman Academic committee and important LAISON at the capital, Dr.N.S.Sreedevi, immediate past president for their timely help,
coordination, guidance , co-operation and selfless involvement.
Hats off to Dr.Fessy Louis and his team for the wonderful work behind the KFOG journal.
Wishing all of you a happy reading and once again a successful NEW YEAR of prosperity and vigorous activities.
Dr.T.Narayanan
President

Dr.T.Jayandhi Raghavan
Secretary General

Evaluation of Fetal Death

Inspect fetus and placenta:
Weight, head circumference and length of fetus
Weight of placenta
Photographs of fetus and placenta
Frontal and profile photographs of whole body, face,
extremities, palms and any abnormalities
Document finding and abnormalities
Obtain consent from parents for cytologic specimens :
Obtain cytologic specimens with sterile techniques and
instruments
Acceptable cytologic specimens (at least one)
- Amniotic fluid obtained by amniocentesis at time of
prenatal diagnosis of demise : particularly valuable if
delivery is not
expected imminently
- Placental block ?(1 x 1cm) taken from below the cord
insertion site on the unfixed placenta
- Umbilical cord segment (1.5 cm)
- Internal fetal tissue specimen, such as costochondral
junction of patella; skin is not recommended
Place specimens in a sterile tissue culture medium of
lactated Ringers solution and keep at room
temperature when transported to cytologic lab oratory
Obtain parental consent for fetal autopsy
Foetal autopsy and placental If no consent is given for
pathology (may include fetal autopsy, send placenta
alone for pathology
whole-body X-ray)
Management of Subsequent Pregnancy After still birth
Preconception for or initial prenatal visit
Detailed medical and obstetric history
Evaluation and workup of previous stillbirth
Determination of recurrence risk
Smoking cessation
Weight loss in obese women (preconception only)
Genetic counseling if family genetic condition exists
Diabetes screen
Thrombophilia workup: antiphospholipid antibodies (only
if specifically indicated)
First trimester
Dating ultrasonography First trimester screen: pregnancyassociated plasma protein A, human chorionic gonadotropin,
and nuchal translucency.
Second trimester
Fetal ultrasonographic anatomic survey at 18-20 weeks of
gestation Maternal serum screening (Quadruple) or single
marker alpha fetoprotein
Third trimester
Ultrasonographic screening for fetal growth restriction after
28 weeks of gestation Kick counts starting at 28 weeks of
gestation Antepartum fetal surveillance starting at 32 weeks
of gestation or 1-2 weeks earlier than prior stillbirth
Delivery
Elective induction at 39 weeks of gestation
Delivery before 39 weeks of gestation only if indicate.

KFOG

Once the diagnosis is confirmed, proper counseling, regarding

the probable cause, need for evaluation of mother and fetus
including fetal autopsy, must be done. Health care providers
should emphasize that results of evaluation may be useful to
the patient and her family in planning future pregnancies.
Induction of labour
If the family objects to a standard autopsy, that should be
informed of the potential value of less invasive methods of
evaluation, including the use of photographs, x-ray imaging,
ultrasonography magnetic resonance imaging, and tissue
sampling. She should be given time to reconcile and decide
whether immediate termination is desired or not.
Spontaneous labour usually ensures in 80-90% women within
2 weeks. The risk of consumptive coagulopathy occurs only
after 3-4 wks of retention of the dead fetus. Labour will need to
be induced in the large majority of patients due to psychological
and social pressures.
Induction of labour
The different methods of induction of labour must be discussed
and more important the expected induction delivery interval.
Methods
Oxytocin
Prostaglandins
PGE2
PGE1 analogue (Misoprostol)
Mifepristone (RU486)
Prostaglandins are generally more effective than oxytocin
alone. Although misoprostol is not licensed in most counties
for use in pregnancy, it is increasingly becoming popular as
an agent for induction of labour. Mifepristone combined with
misoprostol increases the efficacy and reduces the induction
delivery interval significantly. Mifepristone 200mg orally
followed by misoprostol 400g vaginal followed by 400 g
orally 4 hourly for 4 doses is one the regimes. In third trimester
of pregnancy dose of misoprostol could be reduced to 50 g.
In low resource settings labour can be induced with insertion
of a Foleys catheter and extraamniotic infusion of saline.
Maternal evaluation
A thorough maternal history should be taken looking for known
condition. In addition obstetric history, a family history should
be reviewed, relevant original medical records and
documentation should be obtained.
Infections, abruptions and umbilical cord abnormality should
be considered. Maternal testing for lupus anticoagulant,
anticardiolipin antibodies, human parvovirus B19
immunoglobulin G and immunoglobulin M antibodies and
thyroid stimulating hormone may provide information that could
affect future pregnancy management. In cases with severe
placental pathology, significant growth restriction or in the
setting of a family history or personal history of thrombosis
factor V Leiden mutation, prothrombin mutation, antithrombin
III level, MTHFR gene mutation, protein C activity and protein
S activity may provide information.

PRECOCIOUS PUBERTY
Dr. Ashwini Bhalerao-Gandhi
MD, DGO, DFP, FCPS, DNB, FICOG
Ex.Associate Professor of Obst & Gynaec,T.N. Medical College & B.Y.L. Nair Hospital, Mumbai.
P.D. Hinduja National Hospital & Medical Research Centre, Mahim, Mumbai

KFOG

Puberty is the transition period between childhood & adulthood

during which secondary sexual characteristics start
developing, menstruation begins & psychosexual outlook of
the individual changes.
Puberty: is the rendering of the Latin word Pubertas meaning,
Grown Up.
The Oxford Dictionary defines puberty as - the state of being
functionally capable of procreation. Puberty is the stage of
physical maturation in which an individual becomes
physiologically capable of sexual reproduction and is defined
by WHO as the age between 10 and 19 years. Normal puberty
starts at 8 to 12 years in Indian girls & it takes 3-4 yrs for the
completion of the secondary sexual characteristics. Disorder
of pubertal development may occur at any stage of the
maturational process leading to either precocious or delayed
puberty.
Factors affecting the onset of puberty:
a) Genetic, a major influence,
b) Nutritional state,
c) General health,
d) Geographic location,
e) Environmental influence (Exposure to light, geographic
location)
f) Psychological state.
g) Ethinicity
h) Level of activity
Menstruation usually commences after the maximum
growth spurt (6-11 cm per year). There is also a relationship
between skeletal maturity and onset of menstruation; it is
unusual for menstruation to begin before bone age of 12.5
years or after 14.5 years (Sheil & Turner 1997). Typically
the age of menarche is earlier in girls with moderate obesity
(upto 30% above ideal body weight), while it is delayed in
those with severe malnutrition2. However, the increase in
body fat to 23.5% from pre-pubertal 16% is thought to be
an important factor influenced by nutrition (Sternleib &
Munan 1972). High levels of Leptin, a peptide secreted in
adipose tissue that circulates in blood and acts on the CNS
regulatory neurons that regulate eating behaviour and
energy balance is associated with earlier age of menarche
(Matkovic et al, 1997). Evidence also suggests that,
pubertal growth acceleration is due to estrogen and

concomitant increases in growth hormone production and

secondary stimulation of insulin-like growth factor-I levels.
Table I

Pubertal Events (Chamberlain 1995, Shah & Turner 1997)

Physical feature
Age range (yrs)
Thelarche
8-13
Adrenarche
9-13
Axillary Hair
10-14
Peak height
10-14
Menarche
11-15 (mean 12.9)
Mature sexual hair and breasts
14-15
Precocious Puberty:
If one accepts the mean +/-2.5 standard deviations as
encompassing the normal range, then pubertal changes
before the age of 8 are regarded as precocious. Increased
growth is often the first change in precocious puberty.
Occasionally, adrenarche, thelarche, and linear growth occur
simultaneously and sometimes menarche may be the first sign.
The occurrence of menarche is considered precocious when
it occurs prior to 10 years of age.
Precocious puberty can be divided into two classifications:
1. Gonadotropin-Dependent Precocious Puberty (GDPP) /
Isosexual/ Central (CPP) or true precocious puberty: This
refers to premature awakening and early activation of the
hypothalamic-pituitary-gonadal axis.
2. Gonadotropin-Independent Precocious Puberty (GIPP) /
Heterosexual/ Peripheral or Pseudoprecocious puberty:
Sexual maturation and development of secondary sexual
characteristics without maturation of the HPG axis, under
the influence of sex steroids, secreted either from the gonads
or adrenals and sometimes exogenous steroid ingestion.
3. Intermediate type of precocious puberty: Includes tumors
that secrete gonadotropin-like substances (HCG), e.g. from
dysgerminomas, teratomas, hepatoblastomas, etc. and do
not cause activation of HPG axis.
Precocity occurs 5 times more frequently in girls than boys,
and almost three-quarters (80%) of these are idiopathic or
constitutional precocity (true sexual precocity), this must be a
diagnosis by exclusion with prolonged follow-up in an effort to
detect slowly developing lesions of the brain, ovary or adrenal
gland. 15% girls and 50% boys with CPP have a lesion of CNS.

Etiological factors:
I) Gonadotropin- dependent precocious puberty:
a. Idiopathic or constitutional
i. Familial ii. Sporadic
b. CNS Lesions
i. Hypothalamic tumors-hamartomas, astrocytomas,
ependymomas, gliomas, neuroblastomas,
craniopharyngioma
ii. Infection- encephalitis, brain abscess, meningitis,
tuberculous or pyogenic
iii. Head trauma- at birth or accidental
iv. Congenital defects- hydrocephalus, craniostenosis,
third ventricular cysts
v. Irradiation
II) Gonadotropin-independent precocious puberty
a. Gonadal tumors or cysts
b. Adrenal tumors
c. Endocrinopathies- congenital adrenal hyperplasia (CAH),
primary hypothyroidism
d. McCune-Albright syndrome (MAS)
e. Accidental ingestion of oral or topical oestrogen creams,
oestrogen containing cosmetics, anabolic drugs, sex
steroids
f. Aromatase excess syndrome
g. Peutz-Jeghers syndrome
III) Intermediate type of precocious puberty

Gonadotropin-secreting tumors- teratomas, hepatoblastomas,

dysgerminomas, ovarian-granulosa cell tumor,
arrhenoblastoma, lipid cell tumor, thecoma etc.
Diagnosis:
A careful history and thorough physical examination is
mandatory, along with the required laboratory work-up which
will aid in arriving at a proper diagnosis.
History should include the chronology of pubertal events,
associated behavioural changes, drug usage or incidental
drug ingestion, symptoms suggestive of or past history of
intracranial lesions and symptoms of hypothyroidism. The
growth velocity should be plotted on appropriate growth charts
(cm/yr) to determine growth spurt. A complete systematic
examination including palpation for abdominal masses,
neurological and endocrinological examination, estimation
of visual fields and optic fundi would help in diagnosis of the
cause. The clinical stage and type of pubertal development by
Tanners method, the height of the patient, buccal smear
(pyknotic nuclei), karyotyping and bone age are the basic
investigations. Serum levels of FSH, LH, Oestradiol,
Testosterone, TSH, Thyroxine will distinguish complete and
incomplete types. High resolution USG of the ovaries and
computed tomographic images of the adrenal glands, will be
required if peripheral cause is suspected. In CNS disease,
MRI of the brain for imaging the hypothalamo-hypophyseal
area is indicated.

History, Physical examination, Height

Abnormal

Normal
Bone age

Hypothyroidism

Bone age=
Chronological age

Bone age<
Chronological age

Bone age>
Chronological age

E2, DHEAS

Hypothyroidism
T3, T4, TSH

E2, LH response to
GnRH

Ectopic source look for ovarian/

adrenal Pathology

Normal
Premature
Thelarche,
Pubarche
Adrenarche

No response: Ovarian
neoplasm, Cyst, McCuneAlbright syndrome

17 OHP
Congenital
Adrenal Hyperplasia
Controversy related to age:
Girls and boys entering puberty before 8 and 9 years of
age respectively need evaluation.
According to Lawson Williams Peadiatric
Endocrinological society, the limit for investigations of girls
and boys should be lowered to 7 and 8 years.
American Association of Pediatric recommends that the
girls with either breast development or pubic hair should

Pubertal pattern
Central precocious puberty
CT/MRI

be evaluated if occurring before 7 years in white girls and

6 years in African-American girls.
It is less common for white girls, to begin pubic hair growth,
before breast development.
A multi variate analysis confirms that, obesity as measured
by BMI is significantly associated with early puberty in
white girls and is associated with early puberty in black
girls as well, but to a lesser extent.
Management:
Treatment depends on the underlying cause. Objectives for
management include:

KFOG

Abnormal

Tumor: pelvic, adrenal

1. To identify a correctable cause, CNS or otherwise and

offer its specific management.
2. To arrest pubertal development.
3. To suppress linear growth and further acceleration of
skeletal maturation.
4. To prevent sexual abuse and pregnancy.
5. To offer multidisciplinary care for associated conditions like
behavioural problems, obesity, hyperandrogenism, etc.
6. Reassurance and counseling to the parents
Gonadal, adrenal, liver or CNS tumors require surgery and /or
subsequent chemo/radiotherapy.
For congenital adrenal hyperplasia (CAH), glucocorticoid
replacement will suppress production leading to precocity.
Thyroid replacement therapy will suppress precocity by
suppressing HPG axis in cases of primary hypothyroidism.
McCune-Albright syndrome is independent of gonadotropins
and does not respond to GnRH therapy. The syndrome may
be associated with hyperthyroidism or Cushings syndrome.
Treatment includes medical - administration of testolactone
(40 mg/kg/day) to suppress conversion of testosterone to
estrogen and Orthopaedic management.
Central precocious puberty is gonadotropin dependent and
therapy is directed to suppress its secretion. Treatment
includes, giving Medroxyprogesterone acetate (Provera) in
doses of 100-200 mg i.m. every 2-4 weeks. Alternatively,
Cyproterone acetate, a drug with antiandrogenic and
antigonadotropic properties is also used and appears superior
to MPA in the treartment of precocious puberty. However,
nowadays the mainstay of treatment is the use of LHRH
analogues. These are administered 0.2-0.3 mg/kg (max 7.5
mg) i.m. every 4 weeks. They down regulate receptors, causes
regression of secondary sexual characteristics, cessation of
menses, delay short stature by delaying the closure of epiphyses
and normalize growth. Dosage given is Triptorelin i.m. every
28 days or Buserelin with cyproterone acetate to improve height.
Table II
Indications for GnRH analog treatment in CPP:
1. Onset less than 6 years
2. Onset of puberty between 6-8 years
a. Bone age is more than chronological age by more
than 2 years.
b. Projected height is less than 2 SD from target height
c. Rapid progression of puberty.

KFOG

Table III
Advantages of GnRH analogue Therapy:
Preserves height potential especially in younger patients
Improves final adult height
Complete recovery of H-P-O axis after Rx
Good safety profile
Minimal adverse effects
No severe long-term consequences
Combining somatropin (growth hormone) with GnRH
analogues
Introduction of GnRH antagonists as an option

Recent Advances & Controversies:

Lawson Wilkins Pediatric Endocrino Society suggested that
the limit for investigations of girls and boys should be
lowered to 7 & 8 years respectively. Girls with either breast
development or pubic hair should be evaluated if this occurs
before age 7 in white girls and before age 6 in AfricanAmerican girls.
Girls with premature adrenarche / pubarche are at risk for
PCOS and its long-term sequelae. The prevalence of
overweight and obesity in children in the United States has
dramatically increased during the past 20 years and there
has been a rise in the incidence of type 2 diabetes in youth
and higher degree of insulin resistance seen in AfricanAmerican than in whites contributing to early puberty.
Girls with premature pubarche are more likely to develop
functional ovarian and adrenal hyperandrogenism.
Long acting GnRh therapy is effective in improving the
auxological outcome of patients with CIPP. Maximum
benefit is observed in girls with greater bone age
advancement treated at a younger age and for a longer
duration of treatment.
35 patients (30 girls, 5 boys with CIPP were treated with a
long acting GnRH analogue triptorelin by Anurag Bajpai,
Jyoti Sharma et al of AIIMS, New Delhi Triptorelin at a
dose of 3.75mg depot administered deep intramuscularly
every 28 days. Final height outcomes and factors affecting
treatment were analyzed. Treatment was started at the
chronological age of 6.5 1.8years in girls and 4.4 1.5
years in boys and continued for a period of 3.7 1.8 years
in girls and 6 1.8 years in boys. Follow-up period after
discontinuation of treatment was 2.2 0.5 years in girls
and 2.6 0.3 years in boys. Long acting GnRH therapy is
effective in improving the auxological outcome of patients
with CIPP, maximum benefit is observed in girls with greater
bone age advancement treated at a younger age and for a
longer duration of treatment. These girls have lower bone
age advance at discontinuation of treatment.
Very long-term follow up of girls with early and late menarche
done by Johansson Ritzen EM revealed that at age 15-16,
girls with menarche before age 11 (early) were more normbreaking, including being delinquents. In addition, they had
earlier advanced sexual experiences. Regarding somatic
development, at age 43, women with early menarche were
shorter & heavier, had worse physical fitness.

Preeclampsia and eclampsia:

a challenge in its truest sense:
bursting the challenge
Dr Girija Wagh
MD FICOG Dip in Endoscopy
Professor and Head ,OBGYN,Bharati Vidyapeeth University Medical College ,Pune
Assistant Coordinator National Eclampsia Registry

By definition Eclampsia is defined as the occurrence of

one or more convulsions superimposed on preeclampsia.

Preeclampsia is pregnancy-induced hypertension in

association with proteinuria (> 0.3 g in 24 hours) edema
and virtually any organ system may be affected
We also know that there are four major types of hypertensive
disorders during pregnancy . And we need to classify them .It is
important that we do so as that helps in better prognostication
and treatment planning.
1. Chronic hypertension
2. Preeclampsia eclampsia syndrome
3. Superimposed preeclampsia
4. Gestational hypertension
Attempts should be made to establish these diagnoses
antenatally, intranatally, postnatally and in subsequent
pregnancy
Optimum antenatal care is a must :
Early and adequate prenatal care cannot me more
emphasized ! Although the diagnostic criteria for preeclampsia
have been widely established persistent BP elevation above
140/90mmHg and proteinuria exceeding 300mg over a 24hr
collection period- the condition does not always play by the
rules. With close monitoring of weight, urine protein, and BP,
the clinician can identify and follow the patient and detect a
condition much early
Risk Factors for Preeclampsia:
Chronic hypertension
Chronic renal disease
Connective tissue disease
Current foetal growth restriction
Gestational hypertension in the current pregnancy
History of prior preeclampsia
Insulin dependent diabetes

KFOG

Introduction: As a country the biggest challenge faced today

by us obstetricians is the maternal mortality and morbidity .
Also what we encounter as the most challenging disorder is
preeclampsia and eclampsia . As said when we do not know
the makers of PIH what can we know about the markers ? .
Truly we donot know why PIH occurs and lifetimes have gone
by in bursting this mystery .
Preeclampsia and eclampsia are obstetric diseases, and
obstetricians are the group best equipped to diagnose,
evaluate and manage them. Today as a clinician however
we need to tackle what we have from the experiences gathered
and try to deliver the best to our patients .We should not falter
there and should try to deliver the best .From making the
diagnosis to treating atypical eclampsia, management of
preeclampsia involves serious , often unpredictable
challenges . In this article, we highlight several challenges
that obstetricians face when managing preeclampsia and
eclampsia, and offer useful strategies to help minimize
morbidity and mortality in both mother and infant.
Although severe preeclampsia represents only a fraction of
those amounts, and eclampsia an even lower percentage,
they are potentially catastrophic complications of pregnancy
and one of the leading causes of maternal death. They also
are responsible for a large percentage of infants born
prematurely as a result of a worsening maternal or fetal
condition.
The National Eclampsia Registry interim statistics reveals
that the incidence of hypertensive diseases during pregnancy
to be quite high with quite a substantial incidence of
eclampsia . These are actually cases reported by the FOGSI
members . There can be quite some more which are being
treated by peripheral health workers and the incidence can
actually be higher .What we know for sure is 1in 10
pregnancies are complicated by PIH and therefore we need
to have a high index of suspicion .

Inauguration of the CME at Alapuzha

Dr.Nirmala giving lecture during CME at Trivandrum society

Inauguration Of Workshop on reducing caesarian section at Kottayam

Health checkup at old age home by Calicut Society seen are

Dr.Sreedevi, Dr.Narayanan, Dr.Pushparani

Health awareness programme conducted by Kannur society at higher

secondory school Chakarakal

CME at Angamaly Club

KFOG

Cochin Society receiving 4 FOGSI awards Best activities in Reproductive health

care, Population stabilization, Adolescent health care and FOGSI girl child day from
President Sanjay Gupte during AICOG 2011 at Hyderabad

Trichur members during their tribal visit to Vettilapara

Hon.Chief Justice inaugurating the South Zone Yuva FOGSI conference

at Cochin

KFOG

Inaugral ceremony of National Conference on High Risk Pregnancy and

Labour at Kadavu Resorts, Calicut by Dr Sanjay Gupte
( FOGSI President 2010)

Multiple gestation
Nulliparity
Obesity
Thrombophilia.
It is important to diagnose it early :
Early identification of preeclampsia may allow for interventions,
including delivery, that will lessen the risk of progression to
severe preeclampsia and eclampsia and reduce foetal and
maternal morbidity and mortality. It is, therefore, essential for
the clinician to ask specifically about signs and symptoms of
preeclampsia and to listen carefully to the answers.

Signs and symptoms may sometimes be typical:

Weight gain
Increasing edema
Persistent headache
Blurred vision
Malaise
Nausea
Epigastric discomfort
Right upper quadrant discomfort.
Although a number of tests have been proposed to predict who
may be at greatest risk for preeclampsia, none have risen to
the level that they can be recommended for general population
screening.

KFOG

10

Diagnostic criteria:
The diagnosis of preeclampsia is based on persistent BP
elevation above 140/90mmHg and proteinuria exceeding
300mg over a 24-hour collection period. Other criteria have
been applied, such as rise in systolic or diastolic BP above
baseline and urine dipstick criteria for proteinuria, but BP above
140/90mmHg and proteinuria above 300mg are most frequently
used in medical centres Gestational hypertension and chronic
hypertension do sometimes coexist with superimposed
preeclampsia, but should not be confused with preeclampsia
or lead to management decisions that should apply only to
patients with preeclampsia.
Before severe preeclampsia can be diagnosed, the initial
criteria for preeclampsia should have been fulfilled, along with
one or more of the findings listed below:
Persistent blood pressure above 160/110mmHg
Protienuria
Refractory oliguria (<500cc over 24 hours)
Renal failure (minimal criterion would be a rise in
serum creatinine of 1mg/dl above baseline)
Persistent right upper quadrant or epigastric pain or
both
Persistent headache
Scotomata/blurred vision
Shortness of breath with reduced oxygen saturation
or pulmonary edema
Thrombocytopenia (platelets <100,000/cu.mm)
Hemolysis (based on peripheral smear analysis or
increased Bilirubin)
Impaired liver function of unclear etiology

Eclampsia
Estimated foetal weight below 5 th percentile for
gestational age
Prediction:
Attempts to predict preeclampsia have met with poor results.
Measurement of the ratio of uterine artery systolic to diastolic
flow has not been informative in the general healthy population
of pregnant women. Nor has uric acid determination been
useful; it generally has very poor predictive value and should
be interpreted with caution.
When to hospitalize?
Mild preeclampsia can be managed expectantly until foetal
maturity or 37weeks of gestation.But hospitalization can be
offered in the Indian context . This offers an opportunity to
investigate the patient properly ,monitor the urine output ,BP
and the fetal condition through USG and Doppler if necessary
.Also the patient can be offered dietary advice and the correct
categorization after her BP has been monitored round the
clock.But any serious presentations such as severe edema ,
ascites , high BP ,severe proteinuria ,headache , pain ,sever
IUGR ,convulsions etc demand a hospital care.
Assessment:
Initial evaluation consists of:
Foetal non stress testing
Amniotic fluid index
Serial BP determination
24-hour urine collection(if dipstick proteinuria is negative)
Initial laboratory evaluation comprising of a complete
blood count with platelets and aspartate amino
transferase(AST), alanine amino transferase(ALT), and
creatinine levels.and LDH levels
The tests should be directed to assess the maternal conditions
as Preeclampsia is a multisystemic disorder . Constant
vigilance should be undertaken to prevent eclampsia as far
as is possible and to diagnose HELLP early . There is a
tendency to prolong the pregnancy as much as possible to be
able to achieve salvagibility in the fetus .But one needs to
weigh the risk to the mothers system such a prolongation
could cause .Also LDH levels above 600 have proved to be a
better parameter to guide a clinician regarding the presence
of hemolysis . This can help one guide regarding the
intervention and rising LDH levels would help this decision
.While interpreting renal parameters in Pregnancy one should
muster care as these parameters are already reduced in a
normal pregnancy due to increased GFR and hemodilution
Additional tests may be ordered as indicated but are of limited
value in making management decisions. If foetal and maternal
evaluations are reassuring, and if the patient has remained
stable, then outpatient management may be considered. In
general, if proteinuria exceeds one gram in 24 hours, inhospital management is recommended, regardless of other
parameters.

Drug
Labetalol

Dosage
10-20mgIV

Nifedipine

10mg

Directions
push repeat every 1020mins, doubling the
dosage each time until a
maximum total cumulative
dosage of 300mg has been
given.
repeat in 20mins for four
doses (maximum 40mg);
then give 10- 20mg orally
(never sublingually)every
4-6h to achieve a stable
BP of 140-150/90-100mmHg.

Preventing seizures:
Magnesium sulfate is the drug of choice to prevent both initial
and recurrent eclamptic seizures. Two large clinical trials
ended any doubts about its efficacy, demonstrating its
superiority over both phenytoin and diazepam in the settings
of preeclampsia and eclampsia.
Magnesium sulfate is best administered intravenously(iv) via
continuous infusion pump. An initial bolus of 4-6gm is given
over 15-30mins; this amount does not need be adjusted to the
patients level of renal function. A continuous infusion of
magnesium sulfate is usually initiated at a rate of 2gm/hour. It
is this infusion dosage that may need to be altered, based on
the patients urine output and renal function.
Evidence of magnesium toxicity includes:
Loss of deep tendon reflexes
Respiratory depression
Blurred vision

Cardiotoxicity
Each of these toxicities can occur at ostensible therapeutic
levels of serum magnesium, so there can be no substitute for
the regular (atleast every 2hours) clinical assessment of the
patient who is receiving a continuous infusion of magnesium
sulfate.
There is no debate about the utility of magnesium sulfate in
severe preeclampsia, but when it comes to intrapartum
management of mild preeclampsia or cases in which
preeclampsia first manifests in the post partum period, data
are not so clear. This debate will not be resolved to anyones
satisfaction in the course of this article. Historically, the practice
has been to use magnesium in these circumstances, but the
pendulum has begun to shift based on the few arguments:
Eclampsia is a rare event (about 1 case for every 300
to 1000 deliveries)
Most cases occur outside of the hospital
Some women experience seizures before
preeclampsia has been diagnosed
Some patients experience seizures while taking
magnesium sulfate.
One might argue that number of potentially preventable cases
of eclampsia is lower-perhaps in the range of one in every
3000 to 10,000 deliveries-and that this low rate does not justify
routine use of the drug.
Regardless of ones position on this debate, there is broad
consensus that regular careful clinical assessment of the
patient who has preeclampsia is essential to minimize the
morbidity and mortality. This disease can progress from mild
to severe rapidly. Only thorough regular careful assessment
can a physician observe this change soon enough to alter
management as necessary.
Treatment of magnesium toxicity:
10% calcium gluconate(1g) is administered IV to reverse
the effects of suspected magnesium toxicity.
In addition, because magnesium freely crosses the placenta,
it is recommended that a new born resuscitation team be
present at all deliveries during the mother was receiving
magnesium sulfate because neonatal respiratory and cardiac
depression have been reported in this setting.
Delivering the patient:
Preeclampsia, severe preeclampsia, and eclampsia present
a dilemma for the managing clinician: subject her to the rigors
of labor, or to the heightened risk of cesarean delivery? Overall,
a properly vaginal delivery is less hemodynamically stressful
than cesarean delivery for the mother. To accomplish vaginal
delivery, it is necessary to provide optimal anesthesia and
analgesia.
Risks of regional anesthesia:
Women who have preeclampsia are volume depleted. As such,
they are prone to hypertension after administration of regional
anesthesia if the block sets up too rapidly. For this reason,

11

KFOG

Controlling blood pressure: Why? and How ?

Cerebrovascular accident(stroke) is the leading cause of
maternal mortality from preeclampsia. Not all cases can be
prevented, but one suggested preventive strategies is adequate
BP control. Some cases of stroke in the setting of preeclampsia
will occur despite systemic BP reading that are not considered
to be in a dangerous range. One reason may be an over ride of
normal cerebral blood flow auto regulation mechanisms,
resulting in increased cerebral blood flow, rising cerebral
perfusion pressures, and vessel rupture. Such occurrences
may sometimes, but not always, be related to coagulopathy.
When a patient has elevated BP, generally defined as persistent
systolic pressures above 160 to 170mmHg and persistent
diastolic pressures above 105 to 110mmHg, antihypertensive
therapy is indicated and should be administered in a timely
fashion.
Labetalol, nifedipine have been used effectively in such acute
settings, when administered parenterally (except nifedipine,
which can be given orally and should never be given
sublingually) and when given in proper dosage.
Pharmacotherapy of acute hypertension:

epidural anesthesia or some of the newer combined

techniques offer optimal analgesia by allowing for slower
implementation of the regional block.
Women who have preeclampsia, especially severe
preeclampsia, are usually candidates for regional analgesia
and anesthesia. Some requisites for regional anesthesia under
these conditions include the following:
The patient can tolerate preblock hydration
She has adequate IV access
There is reproducible means of determining BP
The patient has a normal coagulation profile. (a
normal platelet count with normal transaminase
should be sufficient to confirm this; women who have
preeclampsia are not at increased risk of having
altered prothrombin time, partial thromboplastin
time, or fibrinogen levels, provided there are no other
mitigating clinician circumstances).
The anesthesiology team is skilled in the
administration of regional anesthesia.
If eclampsia occurs:
Do not proceed to emergent cesaerean section. Rather,
stabilize the mother, protect her from injury during the seizure,
protect her airway, and allow the seizure to take its course.
Begin magnesium at once. If it was being infused before the
seizure, consider giving an additional 2g bolus over several
minutes. As the mother stabilizes, the foetal heart rate will
recover and she can be reassessed to determine optimal
timing and route of delivery.
In case of fetal compromise cesarean section may be a better
choice than a vaginal delivery
Practice AMTSL
Whether a vaginal delivery or a CS active management with

KFOG

12

oxytocis should be practiced to prevent PPH .It is safe to use

Oxytocin 5 U bolus equally diluted over 2-3 minutes or
Prostaglandin injections .PG can be used also as misoprostol
sublingually or transvaginally .due to hemoconcentration even
average loss maynot be well tolersated by these patients .Also
hyopertension , use of magnesium sulpahte and endpthelis
dysfunction can contribute to more blood loss which maynot
be well compensated and tolerated by these patients . All
attempts to reduce blood loss should be undertaken .The fluids
used should be liberal but judicious .recommendation is 80
ml /kg/hr as over infusion can cause pulmonary edema very
fast in these women .
Post delivery management
It involves close vigilance for eclampsia , PPH , HELLP
,Pulmonary edema and thromboembolic complications
.Delivery of the baby is the treatment but the 72 hours post
delivery are an important period when hemodynamic transition
is occurring in the mother which need close observation and
early detection of eclampsia .The NER data has shown a high
index of postpartum eclampsia and it has to be remembered
that such a occurrence leading to morbidity has to be avoided
by all means
Post partum care
Every patient of preeclampsia should be monitored closely for
6 weeks with proper advice regarding the use of
antihypertensives and should report at regular intervals .they
should be guided and encouraged to use contraception atleast
for a period of 2-3 years. The preferred method would be an
IUCD . They should be counseled regarding the importance
of prenatal checkup counseling and the necessary care
periconceptionally in the subsequent pregnancy .

The name of all the continents ends with the same letter that they start with.
Venus is the only planet that rotates clockwise.
The Guinness Book of Records holds the record for being the book most often stolen
from public libraries.
Because metal was scarce, the Oscars given out during World War II were made of
wood.
111,111,111 x 111,111,111 = 12,345,678,987,654,321
Letters a, b, c d do not appear anywhere in the spellings of 1 to 99. The letter d
comes for the first time in Hundred.
Letters a, b c do not appear anywhere in the spellings of 1 to 999. The letter a
comes for the first time in Thousand

Use of Prostaglandins in Labour

Prof. Dr. Kanan Yelikar
Professor and Head of Department
Govt. Medical College, Aurangabad

Table 1. Prostaglandins and their indications

Brand Name
Prostaglandins Indications
1.Carboprost Injection
Postpartum haemorrhage
Prostodin
Management of III stage,
II Trimester Foetal Demise,
II Trimester MTP
2. Dinoprostone Tab
Labour Induction
Primiprost
Labour Augmentation
3. Dinoprostone Gel
Cervical Ripening
Cerviprime
4. Meteneprost Gel
Pre-operative Cervical
Cervidil
Dilation
Meta analysis have shown that there are advantages to the
use of PGS for ripening of the cervix and induction of labour,
compared with oxytocin alone. (Decreased need for analgesia
in labour, fewer cases undelivered within 12 and 24 hours and
decreased operative delivery).
PGE2 both orally and locally have been shown to decrease
the mechanical stiffness of the cervix. Topical PGE2 has been
shown to double the collagenase activity in a term cervix. PGS

leads to the degradation of collagen and glycoproteins and

increase in the cervical water content and glycosaminoglycans.
Prostaglandins
BREAKDOWN OF PHOSPHOLIPIDS
PHOSPHOLIPASE A2
ARACHIDONIC ACID
LIPO OXYGENASE
LEUKOTRINES

CYCLO OXYGENASE
CYCLIC ENDO PEROXIDES
1. Prostaglandin Synthetase
PGH2 - PGD2 - PGE - PGF
2. Thromboxane Synthetase
TXA2 (Thromboxane)
3. Prostacyclin synthetase
PGI2 (Prostacyclin)

Intracervical dinoprostone gel 0.5mg per 3 gm of gel brings

changes in the cervix within 6 to 12 hours.
Personal Experience with Cervical Ripening (PGE2, Gel)
Results : Improvement in Bishops Score on a Selected
group 35

Duration
0 hr.
6 hrs.
12 hrs.
IDI

Primi
2.08+1.50
5.50+2.07
7.14+2.69
Primi=14.50+6.65 hrs.
Multi=11.36+6.11 hrs.

Multi
2.16+1.12
5.80+2.34
8.20+2.89

Conclusion: Intracervical PGE2 gel instillation prior to oxytocin infusion

decreases; induction delivery interval and contraction delivery interval
significantly. PGE2 gel can be used safely and effectively for preinduction cervical ripening.

B. Induction of Labour
About 20% of pregnant women will have labour induced for a
variety of reasons. Inductions do not usually involve just a
single intervention but is a complex set of interventions and as
such presents challenges for both clinicians and mothers.
An intervention designed artificially to initiate uterine
contractions leading to progressive dilatation and effacement
of the cervix and birth of the baby. The term is usually restricted
to pregnancies at gestations greater than the legal definition
of fetal viability.

13

KFOG

Labour is a series of complex biochemical, physiological and

physical process that result in delivery of foetus. These events
are modulated by humoral transmission, neuroendocrine
steroids and local hormones.
Prostaglandins (PGs) are said to be ultimate uterine stimulant.
It acts as the final link between complex neuroendocrine
pathway and their action on uterus.
PGs are extremely prevalent (ubiquitous) and are released as
a response to diverse stimuli. They have a broad-spectrum
biological effect. The PGS are very peculiar, in that they are
synthesized, released at the site of demand and inactivated
instantaneously.
Clinical use of prostaglandins
PGs have been successfully used in many instances as,
Pre induction cervical ripening agent
Induction of Labour
Enhancement / Augmentation of Labour
Prevention and control of Postpartum haemorrhage
A. Pre induction cervical ripening agent
The favorability of the cervix is of critical importance
and should be as assessed prior to induction by means of the
Bishops score, (Bishop 1964) or one of its modifications.

KFOG

14

INDICAT IONS
Post-term pregnancy (41 completed weeks gestation)
Prerequisites-confirmed GA (early USG),AFI,NST
Cx FAV-high dose oxytocin protocol
Cx UNFAV-ripen with pge2 gel, review after 6-8 hrs.
W/w, repeat pge2 OR augmentation with oxy
Pregnancy induced hypertension/toxaemia of
pregnancy
Chronic hypertension
Oligohydramnios
Intrauterine growth retardation
Diabetes mellitus
Reduced foetal movements
Suspected placental insufficiency
Bad obstetric history
The uterotonic action of PGE2 is more physiological than
oxytocin.
The RCOG guidelines state that PGS should be used in
preference to oxytocin when induction of labour is undertaken
in either nulliparous or multiparous women with intact
membranes, regardless of their cervical favorability.
With PGE2 although the uterine contractions increase in terms
of intensity, frequency and duration, the uterine tone is not
elevated, hence the uterine blood flow is thus preserved during
the relaxation phase. Once the labour is established the
progress is smooth and uninterrupted. PGE2 also helps is
softening the cervix, allowing rapid effacement and dilatation.
Mode of administrations / dosage / side effects
PGE2 is administered by the oral, vaginal, extra-amniotic and
endocervical routes. PGE2 , gel and PGE2 oral tablets are
currently marketed in India for pre-induction cervical ripening
and induction of labour respectively.
Method used : PGE2 tablets oral.0.5 mg tablets every one hour,
such 4 tablets.
After 4 hours 2 tablets every hour, such 6 tablets.Maximum 10
tablets. If labour was set in dose was reduced. If no labour at
the end of 5 hrs, it was labeled as failure of induction.Difference
is statistically not significant.

There was no added advantage of PGE2 over Pitocin.

Minor side effects like nausea / vomiting / diarrhea were

common, but manageable.

However oral PGE2 was convenient, acceptable and

appealing to the patient.
Cochrane Review 4 : 2001, states that oral prostaglandins
consistently resulted in more frequent gastro intestinal side
effects, in particular vomiting compared with the other
treatments, included in this review. There were no clear
advantage to oral PGS, over the other methods of Induction of
Labour.
Intravaginal PGE2, tabs can also be used. Dose of 3 mg,
which is quite high as compared to oral dose 3 mg to be
inserted in post fornix. The labour starts within 6 to 8 hrs, and
completed by 12 hrs. Maximum total dose required is 6 mg.
Extra amniotic PGS have largely been replaced by other
methods of PGS administration.
Complications
Nausea, vomiting and diarrhea seen is 0.2% to 5% cases.

(Can be prevented by giving antiemetic and antidiarrhoeal

agents) Uterine hypertonous seen is 5% of cases. Should
be treated with subcutaneous terbutaline (0.25 mg
RCOG guidelines)
Personal experience with PGE2 oral tablets, for
induction of labour
Observations IDI (Induction Delivery Interval)
PGE2 Tablet
Pitocin
Primi11.12 hrs
Multi7.55
Primi11.32 hrs
Multi8.05 hrs.

Other commonly used tocolytic agent is nitroglycerine.

100ug, given in 1ml doses. Preparation of the solution 1
ampoule of NTG (10 ml containing 5 mg/ml) into 500 ml
of solutions. Withdraw and give 1 ml aliquots (100 ug)
Genital tract trauma perineal lacerations and cervical
tears are common specially if precipitate labour occurs.
Foetal distress Specially when labour is induced in high
risk cases like foetal growth restriction and chronic
placental insufficiency:
Monitoring Continuous CTG monitoring is
recommended by RCOG guidelines. Any FHR abnormality
the tabs should be removed from vagina if possible.
Contraindications
History of hypersensitivity
History of Bronchial asthma
High Parity (relative contraindication)
Previous caesarean section
The RCOG guideline Development Group formed one review
of observational data focused on safety issues. The authors
concluded that the rate of vaginal delivery was similar to that
quoted for spontaneous labour after a previous caesarean
section, about as 75%. The rate of uterine rupture from the
largest series was 0.2%
Relative contraindications are : pregnancy complicated by
diabetes and multifoetal pregnancy, suspected foetal
growth compromise and macrosomic foetus.
Renal impairment, cardiovascular disease, hepatic disease.
Misoprostol
Synthetic PGE1 analogue.
15-deoxy-16-hydroxy-16-methyl PGE1.
Uterotonic and cervical priming action.
Commonly used for medical abortion, cervical priming,
m/m of miscarriage, IOL and m/m of PPH.
Cheap , Effective , Stable, Easy storage.
Can be used in asthma, heart disease.
PHARMACOKINETICS
Route
Onset of
Peak conc
Duration of
action
action
Oral
8 min
30 min
2h*
Sublingual
11 min
30 min
3h
Buccal
15 min
75 min
4h
Vaginal
20 min
70-80 min
4h
Rectal
100 min
20-65 min
4h
Misoprostol in Induction
Induction of labour with a viable fetus ;
Shorter induction to delivery interval by 4 6 hrs and a
lower LSCS rate.

In a Cochrane review, ( Alfizevic et al ), oral misoprostol

was found to reduce the need of oxytocin infusion.
FOR INDUCTION OF LABOR WITH A LIVE FETUS
RECOMMENDED DOSAGES :
25 mcg p.v. 4 hrly (max. 6).Oral misoprostol 50 mcg p.o. 4
hrly (max. 6).
Oral misoprostol solution 20 mcg p.o. 2 hrly (max. x 12)
MISOPROSTOL FOR INTRAUTERINE FETAL DEATH
RECOMMENDED DOSAGES :
13-17 weeks : vaginal misoprostol 200 mcg 6-12 hourly (x4)
18-26 weeks : vaginal misoprostol 100 mcg 6-12 hourly (x4)
27-43 weeks : vaginal misprostol 25-50 mcg 4 hourly (x6)
Contraindicated in cases with previous LSCS
Sublingual versus Oral Route
50 g of sublingual misoprostol given 4 hrly was found
to have similar efficacy and safety profile to 100 g oral
misoprostol
However, oral misoprostol was found to be more
acceptable to the women.
Oral ( % )
Vaginal ( % )
Successful Induction
39.7
50
LSCS rate
16.7
21.7
Uterine hyperstimulation
8.5
7.4
with FHR changes

Vaginal Misoprostol In the Cochrane review ;

Vaginal misoprostol was found to be associated with
increased cervical ripening and IOL
Reduced failure to achieve vaginal delivery within 24 hrs.
Uterine hyperstimulation without FHR changes was
increased.
less Requirement of oxytocin augmentation .
Meconium stained liquor more common.
Guidelines for minimising risk when using
misoprostol for IOL
Obtain and document informed consent from the patient.
Use a standardized institutional based protocol.
Misoprostol should not be used for the patients with uterine
scar. An evidence based dosing regimen ACOG committee
opinion recommanded 25 g of vaginal misoprostol
administered not more frequently than every 6 hrs.
A minimum 6 hr waiting period between the last
misoprostol dose and the initiation of oxytocin.
Continuous FHR and uterine contractility monitoring.
Management options for uterine hyperstimulation and FHR
abnormalities.
In the presence of abnormal FHR patterns and uterine
hypercontractility , give 0.25 mg of subcutaneous terbutaline
and deliver the baby at the earliest, if necessary by cesarean
section.

Consider AFI. Cervical status, expected fetal weight. Fetal heart status
Oligohydramnios

Normal
Bishops < 4

PGE2 gel Amniotomy and

Oxytocin

Mechanical dilators PGE2 gel

Low dose oxytocin infusion

Delivery

Unfavourable Cx. even after

hrs of foleys

Normal NST Consider Bishops

Non reactive
Recurrent decelerations

Bishops >9

Bishops < 4

LSCS

PGE2 gel Amniotomy and

Oxytocin

Mechanical dilators PGE2 gel

Low dose oxytocin infusion

Delivery

Consider NST

Unfavourable Cx. even after hrs of foleys

Normal

- 6 hrs of PGE2 gel

Repeat induction the next day

Consider NST

6 hrs of PGE2 gel

C. Labour Augmentation
Labour may be augmented when labour is progressing slowly
after checking, and there is no obvious reason for the slow
progress. The role of amniotomy has been proved to be
effective in enhancing labour. By the intake of intravaginal
PGE2 tabs every hour the desired contractions are achieved.
D. Prevention and control of post partum Haemorrhage
(PPH)
Prostodin is a synthetic analogue of naturally occurring
Prostaglandin F2 (PGF2 ). The high prevalence of PPH a
cause of maternal mortality (16%) and underlying amemia
are cited as the leading cause of maternal morbidity and
mortality in India.
Active management of the third stage of labour, results in
significant reduction of PPH and reduced postpartum anemia.
One hundred and twenty five microgram of PGE2 is given IM
at the birth of the anterior shoulder. PGF2 (Prostodin) 250 ug

Normal
Repeat induction with PGE2|

IM, are also effective in the control of PPH, especially when

refractory to other oxytocics.
Summary use of PGs Optimising labour protocol.
PGE2 gel as a cervical ripening agent.
PGE2 tabs orally / vaginally for inducing and enhancing
uterine contractions.
Inj. Prostodin 125ug in active management of third stage of
labour.
Conclusions:
Judicous use of PGs shortens the duration of labour
Facilitates cervical dilation.
Reduces the incidence of cervical dystocia.
Improves maternal and neonatal outcome.

15

KFOG

Bishops >9