Obsterics & Gyneacology Prep Manual For Undergraduates - E-Book

Obstetrics & Gynaecology
Prep Manual for Undergraduates
Muralidhar V Pai, MBBS, DGO, MD,

FICOG
Professor and Head, Department of Obstetrics and Gynaecology, Kasturba
Medical College, Manipal, Manipal University
Former Head of the Department of Obstetrics and Gynaecology, Melaka
Manipal Medical College, Melaka, Malaysia
Former National Corresponding Editor of Indian Journal of Obstetrics and
Gynaecology
Former Chairman of FOGSI Public Awareness Committee
Shripad Hebbar, MBBS, MD

Professor and Unit Head, Department of Obstetrics and Gynaecology,
Kasturba Medical College, Manipal, Manipal University
Table of Contents
Cover image
Title page
Copyright
Preface
1. Obstetrics
2. Basics in Obstetrics
1. Reproductive anatomy, physiology, endocrinology and

immunology
Anatomy
Physiology
Endocrinology
Immunology
2. Placenta, fetal membranes and amniotic fluid
3. The fetus
4. Maternal physiological changes in pregnancy
5. Imaging in obstetrics
3. Normal Obstetrics
6. Diagnosis of pregnancy, prenatal care and high-risk pregnancy

Diagnosis of pregnancy
Prenatal care
High-risk pregnancy
7. Genetics, prenatal diagnosis and congenital malformations

(anomalies)
Genetics
Prenatal diagnosis
Congenital (malformations) anomalies
8. Identification of fetus at risk, antenatal and intranatal assessment of

fetal well-being
9. Obstetric management – decision-making. Induction of labour

Induction of labour
10. Fetopelvic relationship, mechanism of labour, normal labour,

conduct of normal labour and partogram
11. Normal puerperium

4. Abnormal Obstetric
12. Abnormal labour – prolonged labour and abnormal uterine action,
obstructed labour, rupture uterus and other soft-tissue injuries
Prolonged labour
Abnormal uterine action
Obstructed labour
Rupture uterus and other soft-tissue injuries
13. Contracted pelvis and cephalopelvic disproportion. Fetal

malposition and malpresentation
Contracted pelvis and cephalopelvic disproportion (CPD)
Fetal malposition and malpresentation
14. Postpartum haemorrhage, retained placenta and inversion

Postpartum haemorrhage
Retained placenta
Inversion of uterus
15. Puerperal complications
16. Antepartum haemorrhage, placenta praevia and abruption

Placenta praevia
Abruption
17. PROM and preterm labour

PROM
Preterm labour
18. Multifetal pregnancy
5. Other Obstetric Complications
19. Rh isoimmunization
20. Fetal growth restriction and amniotic fluid abnormalities

Amniotic fluid abnormalities
21. Special cases – pregnancy in teen, elderly and obese and grand
multi
22. Miscarriage (abortion), intrauterine fetal death (IUFD) and bad

obstetric history (BOH)
Miscarriage (abortion)
Intrauterine fetal death (IUFD)
Bad obstetric history (BOH)
23. Postcaesarean pregnancy
24. Shock in obstetrics including amniotic fluid embolism
25. Renal failure in obstetrics
26. Coagulation disorders and disseminated intravascular

coagulopathy in obstetrics
6. Medical and Surgical Disorders
27. Common medical problems (urinary infections, malaria, dengue,
asthma and tuberculosis)
Urinary infections in pregnancy
Malaria in pregnancy
Dengue fever complicating pregnancy
Asthma in pregnancy
Tuberculosis in pregnancy
28. Anaemia and other haematological disorders
29. Hypertensive disorders of pregnancy
30. Diabetes in pregnancy
31. Heart disease complicating pregnancy
32. Other system disorders (epilepsy, thyroid and hepatic disorders)

Epilepsy in pregnancy
Thyroid disorders
Hepatic disorders
33. Prenatal and perinatal infections

HIV infection complicating pregnancy
Perinatal infectious diseases
34. Surgical problems in pregnancy

35. Gynaecological problems in pregnancy
7. Neonatal Care and Complications
36. Neonatal resuscitation
37. Care of the newborn
38. Low-birth weight infant
39. Neonatal complications
40. Birth injuries, neurological problems and infections in the newborn

Neurological problems
Infections in the newborn
8. Operative Obstetrics
41. Manual vacuum aspiration (MVA) and episiotomy

Manual vacuum aspiration
Episiotomy
42. External cephalic version
43. Forceps and vacuum

Forceps
Vacuum
44. Caesarean delivery
9. Contraception and Family Planning
45. Natural and conventional (barrier) methods of contraception
46. Hormonal contraceptives
47. Intrauterine contraceptive devices (IUCD)
48. Surgical methods of contraception
49. Medical termination of pregnancy

10. Safe Motherhood and Health Care
Programmes
50. Safe motherhood initiative
51. Indicators of maternity care (maternal mortality and perinatal

mortality)
52. Reproductive and child health programmes in India
53. Sustainable development goals

11. Aids to Viva Voce
54. Instruments
55. Obstetric specimens
56. Drugs commonly used in obstetrics
57. Obstetric examination, pelvis and fetal skull

Obstetric examination
Pelvis
Fetal skull
12. Gynaecology
13. Basics in Gynaecology
58. Reproductive anatomy
59. Physiology of menstruation and ovulation
60. Puberty and menopause
61. Imaging in gynaecology
62. Endoscopy in gynaecology

Laparoscopy
Hysteroscopy
Colposcopy
14. Common Gynaecological Problems

63. Making diagnosis in gynaecology
64. Dysmenorrhoea
65. Abnormal uterine bleeding
66. Vaginal discharge
67. Pelvic pain
68. Diseases of vulva
69. Diseases of vagina
70. Pelvic inflammatory disease
71. Sexually transmitted diseases
72. Tuberculosis of genital tract
73. Diseases of urinary tract
74. Injuries of female genital tract

15. Benign Gynaecological Conditions
75. Benign lesions of the cervix

76. Benign neoplasms of the uterus
77. Benign cysts of the ovary
78. Diseases of broad ligament, fallopian tube and parametrium
79. Adenomyosis
80. Endometriosis
81. Genital prolapse
82. Urogynaecology
16. Others
83. Primary and secondary amenorrhea
84. Infertility
85. Ectopic pregnancy
86. Trophoblastic diseases
87. Malformations of female genital tract
88. Disorders of sexual differentiation and development (intersex)

Components contributing to determination of sex
17. Gynaecological Malignancies
89. Cervical intra-epitheleal neoplasia (CIN) and carcinoma of cervix
90. Carcinoma of endometrium
91. Benign and malignant tumours of the ovary

Part 1 Benign tumours
Part 2 Malignant tumours
92. Carcinoma of vulva
93. Choriocarcinoma
18. Operative Gynaecology
94. Abdominal hysterectomy
95. Vaginal hysterectomy
96. Dilatation and curettage (including fractional curettage)
97. Endoscopic surgeries

19. Aids to Viva Voce
98. Gynaecology specimens

99. Drugs in gynaecology
Index
Copyright
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Obstetrics & Gynaecology: Prep Manual for Undergraduates, 1st
Edition, Muralidhar V. Pai and Shripad Hebbar
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Preface
Muralidhar V Pai, Shripad Hebbar
It gives us a feeling of immense pleasure and satisfaction to present

the first edition of this book. Even though it is advisable to read the
standard/full length text books during the course of study to
understand the concepts and principles of any given subject, near the
exam time one would like to go through the notes prepared while
studying the reference books. This prep manual should be viewed as
notes of reference books.
One would also like to prepare the answers to previous year
questions papers during exam time. Hence the subject matter is
presented in question and answer form. Yet, content of this book is
comprehensive. Care has been taken to provide up-to-date
information. Illustrations, tables and flowcharts have been inserted for
quick and better understanding.
During undergraduate studies it is always better to stick to one
book per subject and the prep manual should not deviate from the one
which has been read through out. Keeping this thought in mind the
references for this book are drawn from “Holland and Brews Manual
of Obstetrics 4th edition” and “Shaws Text Book of Gynecology 16th
edition”, both are published by Elsevier.
Ready answers are provided to most frequently asked and
important questions. However, as far as less frequently asked
questions, students have been requested to refer to the appropriate
chapters in the reference books.
Prep manual should also address the practical exams and viva voce.
This requirement has been fulfilled by adding chapters on ‘History
taking and Examination, Specimens and Instruments.
One of the common requirements of students is to test their
understanding and knowledge of the subject after reading the book.
One of the ways to do that is to practice Multiple Choice Questions
(MCQs). Keeping this in mind, each chapter has been supplemented
with online MCQs, which have been painstakingly developed
especially for students. The symbol in the contents list will

help students to identify the online resources. Besides these, reader
will get access to the complimentary e-book also.
This is a handy book that combines both Obstetrics & Gynaecology
with in one cover and students need to just look upto this “ONE
BOOK” during exams, having read and understood the subject from
standard reference books.
PA R T A
Obstetrics
SECTION I
Basics in Obstetrics
OUTLINE
1. Reproductive anatomy, physiology,

endocrinology and immunology
2. Placenta, fetal membranes and amniotic fluid
3. The fetus
4. Maternal physiological changes in pregnancy
5. Imaging in obstetrics
CHAPTER 1
Reproductive anatomy,
physiology, endocrinology and
immunology
Anatomy
(For details of descriptive anatomy please refer to Chapter 58.)
Describe perineum, perineal body and their obstetric-

applied aspects.
Applied aspects of different anatomical structures of female genital
tract are as follows:
Perineum
The perineum is a diamond-shaped space that lies below the pelvic
floor. It is bounded by the following:
■ Superiorly – The pelvic floor
■ Laterally – The pelvic outlet consisting of the subpubic angle,

ischiopubic rami, ischial tuberosities, sacrotuberous ligaments and
coccyx
■ Inferiorly – Skin and fascia
This area is divided into two triangles: (i) anteriorly, the urogenital
triangle, and (ii) posteriorly, the anal triangle. These triangles are
separated by the transverse muscles of the perineum and the base of
the urogenital diaphragm (Fig. 1.1.).
Urogenital triangle–The boundaries of this triangle are as follows:
■ Anteriorly – Subpubic angle
■ Laterally – Ischiopubic rami and ischial

tuberosities
■ Posteriorly – Transverse perineal muscles and
base of the urogenital diaphragm
Anal triangle – The boundaries of this triangle are as follows:
■ Anteriorly – Transverse perineal muscles and

base of the urogenital diaphragm
■ Laterally – Ischial tuberosities and

sacrotuberous ligaments
■ Posteriorly – The coccyx
FIGURE 1.1 Perineum viewed from below.

Perineal body
The central point of the perineum lies between the posterior angle of
the vagina in front and the anus in the rear. The muscles contributing
to its formation are fibres from the external anal sphincter, the
laevator ani muscles from either side, the transverse muscles of the
perineum and the bulbocavernosus from either side.
■ Blood supply – Pudendal arteries
■ Venous drainage – Pudendal veins
■ Lymphatic drainage – Inguinal nodes
■ Nerve supply – Pudendal nerves
Applied aspects
■ Perineum is incised during episiotomy to enlarge the introitus
during childbirth.
■ Perineal body gets stretched during the delivery of the fetal head,
especially in face to pubis delivery by broader biparietal diameter,
when it can be damaged or badly torn. This can also happen during
the instrumental delivery.
■ Perineal support is important to prevent perineal tears
Write about the obstetric-applied aspects of anatomical

parts of uterus.
Please refer to Chapter 1 of Holland and Brews Manual of Obstetrics for
answer.
Physiology
(Please refer to Chapter 59 for details of normal menstruation and
hormones involved.)
Describe briefly oogenesis, fertilization and

implantation.
Ovulation, fertilization and implantation are summarized in Fig. 1.2.
FIGURE 1.2 Hormonal control of ovulation, fertilization and embedding
of the blastocyst into the uterine endometrium.
Oogenesis
Oocyte is a unique and extremely specialized cell. During the process
of oocyte maturation, meiosis ensures genetic variability of the
species. It further develops the ability to facilitate fertilization and
provide for sustenance of the early embryo.
The primordial germ cell embryos logically develop from the
endoderm in the wall of the yolk sac. They migrate along the dorsal
mesentery of the hindgut to reach the gonadal ridge. Their numbers
progressively reduce from millions in fetal life to about 400,000 at
menarche. Around the 20th week of intrauterine life, the oocytes enter
the process of meiosis, progress up to the prophase of the first meiotic
division and enter an arrest period lasting many years. After puberty,
a few oocytes are recruited for maturation in each ovulatory cycle.
Maturation now further progresses to second meiotic metaphase,
when once again meiosis is arrested until the oocyte is activated by
fertilization.
Fertilization
Fertilization occurs in the ampullary part of the fallopian tube when
the mature ovum fuses with the spermatozoon to produce the
fertilized single mononucleated cell called the zygote. The process
involves completion of the second meiotic division of the oocyte, each
with a haploid number of chromosomes (23 X). The larger one is
called the female pronucleus and the smaller one is called the second
polar body which is extruded into the perivitelline space. The
spermatozoon enters the cytoplasm of the female pronucleus; the
head and neck form the male pronucleus with haploid number of
chromosomes (23 X or 23 Y). The male and female pronuclei unite at
the centre with restoration of the diploid number of chromosomes (46
XY or 46 XX) which is constant for the species.
Zygote and cellular division

The zygote undergoes mitotic division producing two blastomeres in
about 30 h after fertilization. The blastomeres continue to divide in a
binary division to form a cluster of cells called the morula. The morula
is transported along the tube for the next 3 days and eventually enters
the uterine cavity on the 4th day at the 12–16 cell stage.
Blastocyst
For the next 2 days, the morula remains free in the uterine cavity and
is covered by endometrial fluid and mucus. The cells of the outer mass
form the primitive ectoderm or trophoblast which embeds into the
maternal endometrium and thus causes the attachment of the
blastocyst. The outer cell mass is the precursor of the placenta and
forms the protective fetal membranes. The inner cell mass goes to
form the embryo.
Implantation (nidation)
Implantation occurs about the 6th day after fertilization (or
approximately the 20th day of a regular menstrual cycle). As the zona
pellucida surrounding the blastocyst disappears, there is increased
adhesiveness of the trophoblastic cells to the endometrium. There is
marked cellular oedema and hyperaemia at the site of contact. The
trophoblastic cells invade the stromal cells lying between the secretory
endometrial glands by histolytic action of the blastocyst, bringing
about deeper penetration into the stratum compactum of the decidua.
Vacuoles appear in the advancing trophoblastic syncytial cells, which
coalesce to form lacunae and labyrinthine passages. The syncytial cells
ultimately penetrate the endothelial coat of the maternal decidual
capillary establishing communication with the syncytial lacunar
system.
Endocrinology
Write a short note on human chorionic gonadotrophin.
Human chorionic gonadotrophin (hCG)

Chemical nature
hCG is a glycoprotein with a molecular weight of 36,000–40,000 Da. It
is composed of two side chains designated α (alpha) and β (beta)
subunits. The α side chain is similar to the α subunits of other
glycoprotein hormones such as Luteinising Hormone (LH), follicle-
stimulating hormone (FSH) and thyroid-stimulating hormone (TSH).
It has biological activity similar to LH. hCG is an exclusive product of
trophoblast. It is produced by normal placenta, multiple placentae
(twins), gestational trophoblastic neoplasm (vesicular mole) and
ectopic pregnancy. Low levels are synthesized in the fetal kidney.
Laboratory determination
The presence of hCG can be demonstrated by biological (Aschheim–
Zondek test – not done any more) and immunological assays. There
are several immunoassays, such as:
■ Agglutination or latex particle fixation test
■ Radioimmunoassay is a blood test employing antibodies to the β-

subunit of hCG
■ Radioreceptor assay is not as specific as radioimmunoassay, not

commonly used
Levels in normal pregnancy

hCG appears in detectable amount in the maternal circulation by the
8th postconceptional day and rises rapidly, doubling every 1.5–2 days
to reach peak values of 100,000 mIU/mL between the 60 and 80 days
of pregnancy. Thereafter, concentration falls slowly to reach a level of
1,000–2,000 mIU/mL by around 120 days; then it remains constant
except for a small secondary peak at 32 weeks.
Clinical implications/significance/biological functions of hCG
■ The important role of hCG is to rescue and maintain the corpus

luteum (CL) function, that is continued production of progesterone.
■ In the fetus, hCG stimulates Leydig cells of male fetus to produce

testosterone in conjunction with fetal pituitary gonadotrophins,
thus helping in the differentiation of male external genitalia. In the
female fetus, hCG induces an FSH surge late in the second
trimester, which promotes ovarian development.
■ It possesses some TSH-like activities. The maternal thyroid gland is

also stimulated by large quantities of hCG as seen in gestational
trophoblastic disease.
■ It is also used for diagnosing normal pregnancy (urine pregnancy

test), ectopic pregnancy (hCG doubling time), molar pregnancy
(very high levels of hCG) and as marker for detection of trisomy (in
dual, triple and quadruple tests).
■ hCG is used to induce ovulation in the treatment of anovulation.
Abnormally high levels of hCG are found in the following:
■ Multifetal pregnancy
■ Vesicular mole (very high levels are seen in

choriocarcinoma)
■ Erythroblastosis fetal is associated with fetal

haemolytic anaemia
■ Down syndrome
Low levels of hCG are seen in the following:
■ Early pregnancy loss
■ Ectopic pregnancy
Write a short note on human placental lactogen.
Human placental lactogen (hPL)

Chemical nature – It is a protein hormone with effects like growth
hormone and prolactin. It has a molecular weight of 22,000.
Source – Placenta
Laboratory assay – hPL is determined by radioimmunoassay.
Levels in normal pregnancy – It appears around 6th postconceptional

week and rises steadily in the first and second trimesters; it
disappears rapidly after delivery. hPL levels vary directly according
to placental mass, therefore hPL levels are higher in twins.
Clinical implication/action – hPL has the following growth hormone-

like effects:
■ It induces lipolysis, elevating levels of free fatty

acids, thus providing source for maternal
energy.
■ It inhibits glucose uptake and gluconeogenesis
in the mother.
■ hPL helps to provide the glucose necessary for

fetal growth.
■ It is insulinogenic, elevating plasma levels of

insulin, which favours protein synthesis and
provides a source of amino acids for the fetus.
■ hPL estimations were used to determine

efficacy of placental function, but now have
been replaced by more accurate and simple
biophysical tests.
Write a short note on prolactin.
Prolactin
Chemical nature– It is a protein hormone with a molecular weight of
22,000.
Source – Maternal pituitary, fetal pituitary and decidual tissue lining

the uterus.
Laboratory assay– Normal blood levels range from 5 to 25 ng/mL.

Prolactin levels are elevated by ingestion of drugs, for example
phenothiazines, in hypothyroid state, or the presence of pituitary
adenomas and sometimes in hypothalamic disorders. During
pregnancy, prolactin values rise to about 100 ng/mL due to
maternal pituitary activity.
Clinical implication – It helps in fetal lung maturity.
Immunology
Write briefly about immunology of normal pregnancy.
Pregnancy is a unique immunological phenomenon, in which the
normal immune rejection of foreign tissues does not occur. The fetal
tissue that invades maternal territory is characterized as being poorly
immunogenic. The trophoblast hardly expresses the molecules of the
main histocompatibility complex (MHC) or the human leukocyte
antigen (HLA), which contribute variability within the same species.
This and other immunoregulatory mechanisms endeavour to avoid
fetal cells from being innately rejected upon their arrival.
■ Before implantation –Immunological changes begin in the secretory

phase of the female menstrual cycle and they adapt to the immune
response from a preconceptional stage. Uterine natural killer (uNK)
cells in the maternofetal interphase intervene in the extensive
haemodynamic remodelling that the pregnant uterus undergoes.
■ Implantation and maternal immunological response on the

maternofetal surface – During human placentation, three main
changes take place in the pregnant uterus.
■ The endometrium is differentiated as the

decidua
■ Decidua and the underlying myometrium are

invaded by trophoblastic cells.
■ Extravillous cytotrophoblast (EVT), penetrates

maternal vessels, which alters and replaces the
endothelium and part of the muscle layer.
Alteration due to excessive/deficient placentation

leads to pathological pregnancy.
■ Trophoblast invasion regulation – Specific trophoblast recognition
is carried out by uNK cells. It has been demonstrated that
extravillous trophoblast cells express maternal and paternal HLA-C.
The interaction between the trophoblast HLA molecules and the
killer-cell immunoglobulin-like receptor (KIR) of the uNK cells of
the maternal endometrium inhibits cytotoxic activity and modulates
cytokine production and growth factors by uNK cells to favour
trophoblast growth, endometrium invasion and vascular
remodelling.
Write briefly about immunology of pathological

pregnancy.
answer.
CHAPTER 2
Placenta, fetal membranes and
amniotic fluid
Write about development and morphology of placenta.
Early development
The placenta develops from the apposition or fusion of the fetal
component, the chorion frondosum and the maternal component, the
decidua basalis.
On completion of the implantation of the blastocyst, it is
surrounded on all sides by the syncytial layer. When tips of the
cytotrophoblastic columns reach uterine decidua, they spread
tangentially to meet and fuse with similar expansions from adjacent
villous stems and form a layer around the conceptus, the
cytotrophoblastic shell. This firmly attaches the conceptus with the
decidua. The cytotrophoblastic shell is pierced by maternal sinusoids
and the intervillous space becomes filled with maternal blood.
The primary chorionic villi are invaded by a mesodermal core
which converts them into secondary chorionic villi. The mesodermal
invasion does not reach the cytotrophoblastic shell and thus the
anchoring villi are devoid of any mesoderm. Blood vessels develop
into the mesodermal core of the secondary villi converting them into
tertiary chorionic villi.
Simultaneously, the lacunar spaces in the syncytial layer become
confluent; the syncytium pushes aside the decidual glands and opens
into the maternal decidual blood vessels to form a haemachorial
circulation of the future intervillous space (Fig. 2.1).
FIGURE 2.1 (A) Choriodecidual circulation – vascular circulation in
chorionic villi. (B) Choriodecidual circulation – maternal blood flow
around chorionic villi.
Growth of the placenta

This results from multiplication and branching of the chorionic villi.
At about the end of the 4th month of pregnancy, the placenta occupies
about one-half of the uterine cavity, but with increasing gestational
maturity, the relative size of the placenta diminishes rapidly until at
term it occupies one-quarter to one-sixth of the surface of the uterine
wall.
The mature placenta is a fleshy, discoid organ weighing about 500
g, usually weighing about one-sixth of the fetal weight. It is about 20–
25 cm in diameter and about 2.5 cm thick. It has two following
surfaces:
■ The fetal surface – It is covered by the thin glistening amnion over

lying the chorion from which it can be easily peeled.
■ The maternal surface – It is rough, shaggy and fleshy in

appearance. It is divided by sulci into 15–20 lobules (cotyledons).
The umbilical cord is inserted on the fetal surface of the placenta, at

or near its centre. It is usually about 35–50 cm long and 1.5–2.0 cm in
diameter. It contains the two umbilical arteries, which are the
continuation of the hypogastric arteries and one umbilical vein. The
vessels are spirally twisted from left to right. The cord is ensheathed
by amnion. The main substance of the cord is composed of a mucoid
connective tissue called Wharton jelly. The cord contains the remains
of the vitelline duct and occasionally a patent allantois may be found.
Structure of a term placenta

Basal plate – This forms the floor of the placenta. From outside
inwards, it consists of (i) part of the compact and spongy layer of
decidua basalis, (ii) layer of Nitabuch, (iii) cytotrophoblastic shell
and (iv) syncytiotrophoblast. The basal plate is perforated by the
spiral branches of uterine vessels for the entry of maternal blood
into the intervillous space. Placental septa are found projecting from
the basal plate into the intervillous space. The areas between the
septa are called cotyledons.
Chorionic plate – This forms the roof of the placenta. From outside
inwards, it consists of (i) primitive mesenchymal tissue with
branches of umbilical vessels, (ii) cytotrophoblast and (iii)
syncytiotrophoblast. The stem villi actually arise from this plate.
Intervillous space – Numerous branch villi arising from the stem villi
project into this space and constitute the main content of the
choriodecidual intervillous space.
What are the functions of placenta?

The functions of the placenta are the following:
■ Respiratory function
■ Nutritive function
■ Excretory function
■ Endocrine function
■ Placental synthesis
■ Barrier function
■ Immunological function
■ Other functions
Respiratory function – Oxygen and carbon dioxide exchange occur

across the fetal membranes by simple diffusion.
Nutritive function – The fetus obtains its nutrients through the

maternal circulation. Glucose is the principal source of energy and
is transferred by facilitated diffusion. Lipids for fetal growth and
development are transferred across fetal membranes, stored in the
placenta or synthesized in the fetus. Amino acids are actively
transported through enzymatic process. Water and electrolytes,
sodium, potassium and chlorides cross the fetal membranes by
simple diffusion, whilst calcium, phosphorus and iron cross over by
active transfer; water-soluble vitamins cross over by active transfer,
but fat-soluble vitamins are transferred slowly after dissolving in
lipid.
Excretory function – Fetal metabolic wastes such as urea, uric acid

and creatinine are transferred to maternal blood by simple
diffusion. Fetal metabolism is mainly anabolic where the excretory
products are not much.
Endocrine function – Insulin, adrenal steroids, thyroxine, hPL and

hCG cross the placenta slowly. The placenta is a rich source of
steroid hormones, namely, oestrogen and progesterone.
Placental synthesis – Placenta is known to produce enzymes such as

diamine oxidase which inactivates press or amines, oxytocinase
which inactivates oxytocin and phospholipase A2 which influences
the synthesis of arachidonic acid, the precursor of prostaglandins. It
also produces heat-stable alkaline phosphatase which retains its
activity after heating at 56°C for 30 min.
Barrier function – Most drugs can cross the placental barrier; hence, it
is most important to consider the possible teratogenic effect of a
drug on the fetus before prescribing it in first trimester. Drugs of
large molecular size such as insulin or having a negative charge
such as heparin are transferred minimally. The placenta acts as a
lipoidal resistance.
Immunological function – Although the exact protective mechanism

is as yet speculative, the following mechanisms may be playing a
role:
■ Fibrinoid and sialomucin coating the

trophoblastic cells may suppress trophoblastic
antigenicity.
■ Production of mucoproteins and
mucopolysaccharides by the decidual cell.
■ Weak immunosuppressive effects of placental

hCG and steroids.
■ Nitabuch membrane between decidua basalis

and the trophoblast.
Other functions:
■ Fetal heat loss is dependent on umbilical blood

flow through the placenta.
■ The placenta possibly plays an important role to

control the duration of gestation.
■ It is also an anchoring device.

Describe briefly the abnormalities of the placenta,
umbilical cord and their clinical significance.
answer.
Describe the fetal membranes.

Fetal membranes consist of two layers: (i) the outer chorion and (ii)
the inner amnion:
Chorion – It represents the chorion laeve and ends at the placental

margin. It is relatively thicker than amnion, shaggy in appearance
and loosely attached to the amnion by primitive mesenchyme and
loose areolar tissue on the inside and to vestiges of trophoblastic
cells and decidual tissue derived from the fused decidua capsularis
and decidua parietalis.
Amnion – It is the inner layer of the fetal membranes and its inner
surface is smooth and shiny. It lines the amniotic cavity containing
amniotic fluid; it is covered on its outside beyond the placental edge
by the chorion. The amnion arises from the dorsal amniotic cavity of
the embryonic disc. Later, as a result of the folding of the embryo, it
comes to surround the embryo, merging all around except at its
attachment to the body stalk. It contains amniotic fluid. The amnion
has no blood supply, lymphatic drainage or nerve supply.
Describe the origin, normal volume, composition,

appearance and functions of amniotic fluid.
Origin
It is possibly the result of contributions from both the mother and the
fetus. The following mechanisms have been suggested:
■ Transudate from maternal circulation across placental surface and

fetal membranes.
■ Active secretion from amniotic epithelium.
■ Transudate across surface of umbilical cord and fetal placental

circulation.
■ Contribution from fetal urine.
■ Tracheobronchial secretion and transfer across fetal skin prior to its

keratinization at 20 weeks of gestation.
Volume
The volume of amniotic fluid varies according to gestational maturity.
It measures about 50 mL at 12 weeks, 400 mL at 20 weeks and peaks to
about 800 mL to 1.0 L at 36–38 weeks; thereafter, it reduces to some
extent. In postdated pregnancies, the amount of amniotic fluid may be
substantially reduced.
Practically, the adequacy of liquor is inferred either clinically by
palpation or by amniotic fluid index (AFI) ultrasonically. AFI is
calculated by measuring the vertical height of liquor pockets in four
quadrants of the abdomen using ultrasound. AFI is interpreted as
follows:
■ Normal – between 8 and 25
■ Low normal – between 5 and 8
■ Low (oligohydramnios) – less than 5
■ High (polyhydramnios) – more than 25
Composition
In the first half of pregnancy, the composition of amniotic fluid is the
same as maternal plasma except for a much lower concentration of
protein. It does not contain any particulate matter, but as pregnancy
advances the composition and volume of the liquor amnii change. The
fetus becomes capable of modifying the composition and volume of
liquor amnii by urinating in the amniotic sac and swallowing
progressively larger amounts of fluid. At the same time, the fetal
respiratory tract also takes part in the exchange of amniotic fluid and
causes further modification in its composition. At term, amniotic fluid
consists of 98–99% water and 1–2% solid constituents. It also contains
hormones, enzymes, inorganic constituents such as sodium, chloride
and potassium and suspended particles such asepithelial cells, vernix
caseosa, exfoliated amniotic epithelial cells and exfoliated cells from
the tracheobronchial tree, vagina and bladder of the fetus.
Physical properties
The fluid is pale straw coloured or faintly turbid, mildly alkaline,
having a low specific gravity of 1010. It is highly hypotonic to
maternal serum having an osmolality of 250 mmol/L around term.
Abnormal appearance
■ Greenish, due to the presence of meconium, indicative of past or
present fetal distress in presentations other than breech or
transverse lie.
■ Golden yellow, due to the presence of bilirubin, resulting from fetal

cell haemolysis due to Rh incompatibility.
■ Greenish-yellow, in postmaturity.
■ Dark maroon, due to altered blood in accidental haemorrhage.
■ Prune juice, observed in the presence of a retained dead fetus.
■ Bloodstained, freshly blood stained and bright red in vasapraevia or

low-lying placenta.
Functions
Amniotic fluid is essential for the continued well-being of the fetus
and has the following functions:
■ As a fluid medium of even temperature, permitting free movement

of the fetus.
■ Shock absorber preventing hazardous pressure on the fetal parts.
■ Prevents adhesion formation between fetal parts and amnion.
■ Provides adequate expansion of uterine cavity to prevent excessive

retraction and ensuring satisfactory placental and fetal circulation.
■ Swallowed liquor may have some nutritive value.

■ Swallowed liquor may provide gamma globulin and antibodies
providing passive immunity.
■ During labour, the amniotic fluid and fetal membranes constitute

the water bag containing the fore waters, which acts as a fluid
wedge, providing the best natural dilator of the cervix.
■ Provides the pool in which the fetus excretes urine.
■ Protects the fetus from ascending infections by its bactericidal

action.
CHAPTER 3
The fetus
Describe the stages of fetal development and growth
patterns. Enumerate the factors affecting the fetal
growth.
Development of the fetus can be divided into three phases:
1. The ovular period or germinal period lasts from the stage of

fertilization up to 2 weeks after ovulation when it is designated as the
ovum.
2. The embryonic period lasts from the 3rd week after ovulation up to
the 8th week postovulation or 10th week after the last menstrual
period (LMP). This is the period of cell division and differentiation.
3. The fetal period lasts from the 10th week after the onset of the LMP
until term. During this period less tissue differentiation occurs, but
growth and maturation of tissues formed during the embryonic
period are the hallmark. Chronology in the fetal period is henceforth
expressed in terms of menstrual age.
Normal fetal growth patterns undergo three major stages as

follows:
Stage 1: 4–20 weeks – characterized by cell hyperplasia and rapid

mitosis
Stage 2: 20–28 weeks – characterized by cell hyperplasia and

hypertrophy with declining mitosis and an increase in cell size
Stage 3: 28–40 weeks – characterized by rapid increase in cell size and

accumulation of fat muscle and connective tissue
Any growth inhibition during stage 1 will produce a fetus with
fewer cells but normal cell sizes, thus, presenting as symmetrical fetal
growth restriction (FGR).
Growth inhibition during stages 2 and 3 will cause a decrease in cell
size and a reduction in fetal weight. This presents as asymmetrical
FGR or combined type of FGR.
Factors affecting fetal growth

■ Race – Babies belonging to European race weigh more than Indian
race.
■ Genetic – Predominant control is genetic. Chromosomal/single gene

defects and inborn errors of metabolism affect the growth from
early fetal life and result in symmetrical FGR.
■ Fetal sex – A male fetus weighs 100–200 g more than a female at

term.
■ Maternal age – Mothers over 35 years of age tend to have smaller

babies. Incidence of congenital anomaly, aneuploidy are also higher.
■ Socioeconomic and nutritional – Average weight of babies born to

lower social class tends to be lower.
■ Birth order – Fetal weight rises in the first to second pregnancies by

100–200 g, with a smaller rise in the third pregnancy.
■ Smoking/substance abuse – Smoking/substance abuse in pregnancy

reduces mean birth weight by 200–400 g.
■ Maternal diseases – Anaemia, hypertension, diabetes, heart/renal

diseases or any chronic illness gives rise to asymmetrical FGR.
Describe fetal circulation.
Fetal circulation (fig. 3.1)

Well-oxygenated blood, laden with nutrients and from which
metabolic wastes such as CO2 and catabolites have been removed, is
carried by the umbilical vein. After giving a branch to the liver, the
umbilical vein proceeds as the ductus venosus to join the inferior vena
cava carrying blood from the lower limbs and trunk to the right
atrium. A large part of the oxygenated blood is diverted by the margin
of the crista dividens through the foramen ovale to the left atrium. A
small portion of the blood from the inferior vena cava, together with
deoxygenated blood returning from the head and upper extremities
via the superior vena cava and the blood returning from the coronary
sinus pass through the tricuspid valve into the right ventricle and
from then onwards to the pulmonary trunk.
FIGURE 3.1 Diagrammatic representation of the fetal circulation. The

arrows show the course taken by the blood.
The bulk of the oxygen-saturated blood diverted through the

foramen ovale, admixed with a small quantity of blood returned by
the pulmonary veins, passes through the mitral valve into the left
ventricle and is preferentially distributed to the coronary circulation
and on to the aorta for distribution through the relatively big carotid
arteries to the cerebral circulation.
The relatively deoxygenated blood entering the pulmonary trunk is
partially distributed to the collapsed lungs, but the major blood flow
is diverted to the descending aorta by the ductus arteriosus below the
exit of the carotid arteries. Thus, mixed blood is distributed to the
viscera and lower extremities and returned through the umbilical
arteries to the placenta.
At birth two events take place which alter the fetal haemodynamics:
(i) Clamping of the umbilical cord causes a rapid rise in arterial

pressure.
(ii) A rise in plasma CO2 and fall in PO2 help to initiate respiration.
The intrathoracic pressure of the newborn remains low in the first

few breaths, but as the airways and alveolar spaces fill out, the
intrathoracic pressures become similar to the adult type.
As a result of the aforementioned changes, the high vascular
resistance of the pulmonary bed is drastically (70–80%) reduced, the
pressure in the pulmonary artery falls by half and the left atrial
pressure doubles. During fetal life, the high pressure in the
pulmonary trunk diverts the bloodstream via the ductus arteriosus
into the descending aorta, but at birth with the expansion of the lungs
and rapid opening of the pulmonary circulation, the blood from the
right ventricle is carried by the pulmonary trunk and the pulmonary
arteries to the lungs instead of the ductus arteriosus. Simultaneously,
the increasing pressure in the left atrium and descending aorta
favours reversal of flow through the ductus arteriosus. The higher
oxygen tension in the reversed blood flow interacting with
prostaglandins favours closure of the ductus arteriosus and its
obliteration in early postnatal period.
The increased pressure in the left atrium after birth would normally
lead to a back flow into the right side of the heart through a patent
foramen ovale; however, its anatomic configuration is such that the
increased pressure causes a closure of the valve-like foramen, and its
fusion with the interatrial septum is completed in 6–8 weeks.
Thus, during transition from fetal to neonatal life, the following
changes occur:
■ Closure of foramen ovale
■ Closure of ductus arteriosus
■ Obliterated ductus venosus becomes ligamentum venosum
■ Obliterated umbilical vein becomes ligamentum teres of the liver
■ Obliterated umbilical arteries become the obliterated hypogastric

arteries
The adult circulation differs from the fetal circulation in the

following ways:
■ Venous and arterial blood no longer mixes in the atria.
■ The vena cava carry only deoxygenated blood to the right atrium,
from where it goes to the right ventricle to be pumped into the
pulmonary circulation for oxygenation.
■ The aorta carries only oxygenated blood from the left side of the
heart for distribution to the rest of the body.
CHAPTER 4
Maternal physiological changes
in pregnancy
Describe the physiological changes in urinary system
during pregnancy.
Physiological changes in urinary system during pregnancy are as
follows:
■ The kidneys enlarge in size approximately 1 cm.
■ The pelvicalyceal system undergoes relaxation and dilatation due to

the effect of maternal progesterone.
■ Ureter increases from 15 to 75 mL.
■ The tone of the ureters and bladder is reduced; thus, stasis of urine
is common, predisposing the gravid woman to urinary tract
infection and bacteriuria.
■ Renal perfusion is increased by 75%.
■ Glomerular filtration increases by 50%.
■ There is a lowering of the renal threshold for glucose and protein;

hence, ‘physiologic’ glucosuria may occur in euglycaemic women
and proteinuria of greater than 300 mg/day is considered as
significant as against 150 mg/day in nonpregnant status.
■ There is a decreased sensitivity to the pressure effect of angiotensin

during pregnancy and there is sodium retention.
■ The urinary bladder shows marked congestion and hypertrophy of

muscles of the bladder wall.
■ Frequency of micturition is high during the first 12 weeks as the

enlarging uterus in the pelvis rests on the bladder. It may also occur
at the end of the third trimester during engagement of the
presenting part of the fetus.
■ Stress incontinence may occur, causing discomfort to the patient. It

disappears spontaneously after the delivery.
■ Night diuresis is common due to mobilization of fluid accumulated

during daytime in the form of pedal oedema, when the pregnant
women assume recumbent position.
Describe the physiological changes in respiratory

system during pregnancy.
Physiological changes in respiratory system during pregnancy are as
follows:
■ The lower ribs flare out resulting in the increase in subcostal angle
and there is also an increase in the transverse diameter of the chest
by about 2 cm. The diaphragm is raised by about 4 cm still
diaphragmatic excursion is greater in pregnant than in nonpregnant
women.
The functional changes are as follows:
■ Upper respiratory tract is prone to hyperaemia and congestion,

predisposing to phlegm, sinusitis and epistaxis.
■ Lung compliance is unaffected by pregnancy. There is a marginal

increase in respiratory rate.
■ The ‘tidal volume’ and ‘minute ventilation’ increase by 30–40%.
■ Airway conductance is increased and total pulmonary resistance is

reduced, possibly as a result of progesterone.
■ Functional residual capacity (FRC) decreases by 20–30%.
■ Expiratory reserve volume decreases by 15–20%.
■ Residual volume decreases by 20%.
■ Inspiratory capacity, the maximum volume that can be inhaled from

FRC, increases by 5–10%.
■ Total lung capacity (TLC) – The combination of FRC and inspiratory

capacity – is unchanged or decreases by less than 5% at term.
■ Peak expiratory flow rates increase progressively as gestation

advances. The maximum breathing capacity and forced or timed
vital capacity are not altered appreciably.
■ Alteration in blood gases is a common observation, pO2 increases

above 100 mm Hg, pCO2 decreases to 27–32 mm Hg and pH
remains normal with increased renal bicarbonate excretion.
■ Dyspnoea is a common symptom during pregnancy, 60–70% of

women experience it to a varying degree.
■ Maternal hyperventilation is probably due to the action of

progesterone on the respiratory centre.
■ Maternal arteriovenous oxygen difference is decreased.
■ Oxygen consumption is increased by 20% in singleton and 30% in

multifetal gestation during pregnancy and 40–60% in labour.
Describe the physiological changes in cardiovascular

Physiological changes in cardiovascular system during pregnancy
are as follows:
■ The total amount of circulating blood volume increases by 30–40%

during pregnancy, peaking at about 32–34 weeks. The circulatory
load increases soon after delivery of the baby and placenta as extra
500 mL of blood from the uterus enters the circulation. At caesarean
section, unlike in a normal delivery, the uteroplacental circulation
ends abruptly, causing sudden rise in cardiac load, which may lead
to sudden cardiac failure.
■ Increase in cardiac output, increases further during labour.
■ Marginal rise in the heart rate (10 beats/min).
■ The increase in cardiac output is not accompanied by a rise in blood

pressure, because this is offset by the lowering of the peripheral
resistance as a result of the relaxing effect of progesterone on
vascular smooth muscle.
■ Aortocaval compression by the gravid uterus in the latter part of the

pregnancy can interfere with venous return to the heart and can
cause hypotension. This effect is mostly pronounced in the supine
position.
■ Blood pressure registers a modest fall of about 10 mm Hg during the

mid-trimester, followed by a gradual return to normal at term.
■ Increased venous pressure in the lower limbs during pregnancy

caused by prolonged standing or sitting can lead to varicose veins,
haemorrhoids and dependent oedema of the feet.
■ Some symptoms that mimic heart disease appear during pregnancy.

These include breathlessness, palpitation, fatigue and swelling of
the feet.
■ Examination of the cardiovascular system reveals lateral

displacement of the apex beat, loud S1 and S2 sounds, split first
sound, loud third sound and a short/ejection systolic murmur in
many women.
■ Radiography of the chest may show a straightened left border,

elevated diaphragm, increased heart size and increased pulmonary
vascularity.
■ ECG reveals left axis deviation, ST-T wave changes, increased

frequency and occasional atrial extrasystole. These changes are
often mistaken for left ventricular hypertrophy.
■ Central venous pressure (CVP) recordings register a rise by about 5–

10 cm H2O. During labour, the valsalva manoeuvre leads to
increased CVP.
■ Delivery and expulsion of the placenta end the low resistance

uteroplacental circulation.
Describe the physiological changes in haematological

Physiological changes in haematological system during pregnancy
are as follows:
■ Increase in the circulatory plasma volume by 40–50% commencing

from the end of the first trimester up to about 34 weeks, when it
tends to plateau out.
■ Slower increase in the total circulating RBCs mass by about 30–40%;

hence, haemodilution occurs leading to a fall in haematocrit values
and a drop in haemoglobin termed physiological anaemia of
pregnancy.
■ Haemodilution lowers the viscosity of the maternal blood to ensure

adequate gaseous exchange between the maternal and fetal blood. It
also protects the mother against the adverse effects of blood loss
during the delivery.
■ Iron absorption doubles in pregnancy to meet the demands of
growing maternal blood volumes, tissue mass and fetal needs.
■ There is a normal increase in the WBC counts from 9000 to about

12,000 mm3 and a further increase to 15,000 mm3 during labour. A
leukocytosis of 15,000–18,000 mm3 is commonly observed in the
postpartum period.
■ Changes in coagulation profile are remarkable during pregnancy.

The platelet count is generally normal; however, the platelet
survival time gets shortened.
■ Factors I, VII, VIII, IX and X increase, whereas factors II, V and XII
remain unchanged. Factor XI decreases slightly towards the end of
pregnancy and factor XIII (fibrin stabilizing factor) is appreciably
reduced, almost up to 50% at term.
■ Plasminogen levels increase concomitantly with fibrinogen levels,

causing an equilibration between clotting and lysing activity.
■ Hypercoagulability of pregnancy is caused by venous stasis in the

pelvis and lower limbs. Vascular injury associated with delivery,
especially the caesarean section and high levels of circulatory
fibrinogen may predispose to pelvic vein thrombosis.
Describe the physiological changes in endocrine system

during pregnancy.
Physiological changes in endocrine system during pregnancy are as
follows:
■ The thyroid gland enlarges in size; thyrotropin-releasing hormone

(TRH) levels are not increased during normal pregnancy and hence
no increase in thyroid stimulating hormone (TSH). There is an
increase in thyroxine-binding globulin (TBG) as a result of high
oestrogen levels and increased iodine excretion. There is also
increase in production of thyroid hormones by 40–100%. Total T4
rises, but the levels of free T3 and T4 are unaffected; thus, the
euthyroid state is maintained. Increase in pulse rate, warm skin and
increased hair loss, which are normal findings during pregnancy,
mimic altered thyroid function.
■ Suprarenals – There is an increase in the levels of corticosteroid-

binding globulin (CBG) and also total and free cortisol.
■ Pancreas – The increased maternal and fetal metabolic needs create

a demand for fuel, causing a state of accelerated starvation.
Exaggerated fasting hypoglycaemia and starvation ketosis are
common. To overcome symptomatic hypoglycaemia, the pregnant
woman is advised to consume small frequent meals. Insulin
resistance increases with advancing pregnancy mainly due to
insulin antagonism by human placental lactogen.
■ Maternal plasma prolactin levels increase up to 10 folds during

normal pregnancy. The principal function of maternal prolactin is to
ensure lactation.
Describe the metabolic changes during pregnancy.

answer.
Describe the physiological changes in breast and skin

during pregnancy.
answer.
Write a short note on hyperemesis gravidarum.

Definitions: Vomiting sufficiently pernicious to produce weight loss,
dehydration, acidosis and hypokalaemia.
Incidence – 1 in 1000 pregnancies

Associations
■ Positive family history
■ Common in first pregnancy and limited to first trimester
■ More in molar and multiple pregnancies
Aetiological factors
■ Excessive ß hCG, oestrogen, progesterone
■ Dietetic deficiency such as low carbohydrate reserve, vitamin B1, B6

deficiency
■ Allergy/immunological disturbances
■ Psychological and emotional stress
Pathology
Liver shows centrilobular fatty infiltration without necrosis; kidneys
have fatty changes. There will be subendocardial haemorrhage as well
as haemorrhage in the brain.
Clinical course/clinical features:
■ Early (mild) – without dehydration/ketosis
■ Late (moderate to severe) – with

dehydration/ketosis
Late symptoms include increased amount and frequency with mixing
of blood, epigastric pain, oliguria and constipation.
Late signs are progressive emaciation, anxious look, sunken eye,

inelastic skin, dry coated/red-raw tongue, teeth covered with
sordes, acetone breath, rapid thready pulse, low blood pressure,
raised temperature, jaundice and neurological signs.
Maternal complications include the following:
■ Wernicke encephalopathy (restlessness,

convulsion and coma)
■ Korsakoff psychosis (confusion and loss of

memory)
■ Eye complications (diplopia,

dimness/blindness)
■ Features of peripheral neuritis

Fetal complications include the following:
■ Prematurity
■ Fetal growth restriction (FGR)
■ Central nervous system malformations

Investigations
■ CBC (specially haematocrit which is high)
■ Routine urinalysis (specially chlorides which are low, and ketones

which are high)
■ Serum electrolytes
■ Hepatorenal profile
■ Blood sugars
■ Ultrasound (to exclude twins/molar pregnancy)
Management
■ It is advisable to admit the patient to correct dehydration and
electrolyte imbalance
■ Patient kept nil per oral (NPO) for 24–48 h. Intravenous

administration of 10% glucose saline, Hartman solution and 25 mEq
of potassium chloride, if indicated
■ Maintain an intake and output chart, monitor vital parameters
■ Test urine periodically for ketone bodies
■ Drug treatment consists of the following:
■ Antiemetics – Doxylamine, metoclopramide,

odansetron
■ Antihistamines – Promethazine
■ Vitamin – B1 (100 mg), B6 (25 mg t.i.d.), B

complex and C (100 mg)
■ In very rare cases, hyperalimentation may be required
■ Once patient tolerates orals – Neutral fluids and small, bland, dry,
carbohydrate diet in frequent intervals
■ In case of a molar pregnancy, an early evacuation is recommended
■ Indications for medical termination of pregnancy (MTP) are as

follows:
■ Steady deterioration despite of therapy
■ Pulse greater than 100, temperature greater than

380˚C
■ Oliguria, proteinuria
■ Presence of jaundice
■ Appearance of neurological signs

CHAPTER 5
Imaging in obstetrics
Describe the levels of ultrasonography in obstetrics.
The levels of ultrasonography are described below.
Basic ultrasonographic examination (level I)

The American College of Obstetricians and Gynecologists (ACOG)
guidelines for a Level-I scan includes the following parameters:
■ Fetal number (single or multiple pregnancy)
■ Fetal presentation
■ Documentation of fetal life
■ Placental localization
■ Amniotic fluid volume
■ Pregnancy dating and assessment of gestational maturity
■ Detection and evaluation of maternal pelvic masses (ovarian cyst

and myomas)
■ Detection of an IUD (Cu-T being the most common) with

pregnancy, failure of contraception
■ Pregnancy with Mullerian anomalies – pregnancy in one horn of

bicornuate uterus
■ Survey of fetal anatomy for anomalies in the second and third

trimesters.
■ Condition of the internal os (second and third trimester), cervical
length and calibre
Targeted ultrasonographic examination (level II)

This examination is undertaken by an expert, well versed in scanning
for anomalies. It is done routinely now a days but should be specially
recommended to the patients at a high risk of carrying a
physiologically or anatomically abnormal fetus, if suspected from her
history (diabetes, elderly age, family history of birth defects, previous
malformation, exposure to X-rays or teratogens, rubella during
pregnancy, etc.), clinical examination (placenta praevia, hydramnios
or oligohydramnios, malpresentations, etc.) or a suspicious previous
sonographic scan.
What is the schedule of ultrasound examination in

pregnancy?
Ultrasonographic evaluation has become an integral part of the
antenatal care. In current practice, the schedule of ultrasound
evaluation is as follows:
5–6 Confirmation of pregnancy and ruling out of multiple pregnancy and abnormal pregnancy (ectopic and molar)
weeks
8–10 Dating scan
weeks
11–14 Genetic scan (Nuchal Translucency [NT] scan and for other soft markers)
weeks
14–18 Early anomaly scan (combined with triple/quadruple test), uterine artery Doppler. Cervical length in high-risk cases
weeks
18–20 Targeted scan with fetal echo
weeks
20–36 Serial scans in cases suspected with growth restriction and macrosomia. Follow-up of some anomalies, confirmation of
weeks placenta praevia at 28 weeks, detection of hydrops fetalis, Doppler studies for fetal well-being and detection of fetal
anaemia in Rh isoimmunization
36–42 Growth scan, fetal weight estimation, placental location and maturity, amniotic fluid index, biophysical profile scoring,
weeks scar evaluation, presentation and position of the fetus
What are the advantages/uses of ultrasound in

obstetrics?
The advantages/uses of ultrasound in obstetrics are as follows:
First trimester
■ Confirmation of intrauterine pregnancy; the chronology of
appearance of different markers of pregnancy is as follows:
■ 35 days – Gestational sac (GC) is seen as an

echo-free area surrounded by thick echogenic
rim (30 + GC size in mm = days of period of
gestation [POG])
■ 37 days – Yolk sac and ring in a gestational sac
■ 40 days – Fetal pole
■ 42 days – Cardiac pulsations

■ Estimation of gestational age is most accurate ±5 days, provided the
crown-rump length (CRL) is measured between 8 and 10 weeks by
transvaginal sonography
■ Ruling out abnormal pregnancies such as ectopic and molar

pregnancy
■ Diagnosing missed abortion
■ Diagnosing multifetal pregnancy and determining chorionicity and

amnionicity
■ Predicting health of pregnancy
■ Evaluating threatened abortion
■ Evaluation of any adnexal pathology is the easiest at this stage of

pregnancy
■ Diagnosis of Mullerian anomalies
■ Diagnosis of anencephaly. In fact this is the only anomaly that can

be diagnosed in the first trimester
■ To perform chorionic villus sampling in indicated cases on medical

grounds
Second and third trimesters

■ NT/genetic scan to diagnose trisomy along with dual test
■ Evaluation of cervix, length and any funnelling suggestive of

incompetent os
■ To diagnose fetal anomalies
■ To diagnose and follow-up fetal growth restriction (FGR)
■ To estimate fetal size, note presentation and attitude
■ To evaluate placental location and complications
■ Amniotic fluid assessment
■ Biophysical profile scoring Doppler studies to assess fetal well-being
■ Plan mode of delivery in twins
■ Assess the uterine scar

SECTION II
Normal Obstetrics
OUTLINE
6. Diagnosis of pregnancy, prenatal care and

high-risk pregnancy
7. Genetics, prenatal diagnosis and congenital

malformations (anomalies)
8. Identification of fetus at risk, antenatal and

intranatal assessment of fetal well-being
9. Obstetric management – decision-making.

Induction of labour
10. Fetopelvic relationship, mechanism of

labour, normal labour, conduct of normal labour
and partogram
11. Normal puerperium

CHAPTER 6
Diagnosis of pregnancy, prenatal
care and high-risk pregnancy
Diagnosis of pregnancy
Write about the methods of diagnosing (confirming)
pregnancy.
Even though pregnancy is suspected on the basis of a number of
presumptive/subjective symptoms and probable signs, the
confirmation/diagnosis of pregnancy is done by one of the following
three methods:
1. Detection of hCG in either serum or urine: Serum hCG is not

estimated routinely except after assisted reproductive techniques.
Urine pregnancy test (UPT) can diagnose pregnancy as early as 5
weeks (35 days from LMP). Most of the urinary pregnancy kits need a
minimum of 25 IU/L of beta-hCG to diagnose pregnancy. However,
by UPT one cannot say whether it is intrauterine or extrauterine,
singleton or multifetal, normal or abnormal (vesicular mole)
pregnancy.
2. Detection of gestational sac by transvaginal sonography:

Gestational sac is an echo-free area surrounded by a thick echogenic
rim (due to choriodecidual reaction) seen as early as 5 weeks (35 days
from LMP). It is better to see a yolk sac (sac within gestational sac seen
by 37–40 days) and a fetal pole with pulsation (seen by 40–45 days).
Transvaginal sonography can not only confirm the pregnancy but also
locate the site, number of fetuses and the abnormality of pregnancy.
3. Clinical examination: It needs experience to diagnose pregnancy

clinically by bimanual examination. The earliest one can diagnose
pregnancy clinically and unequivocally is 8 weeks, when in the
backdrop of presumptive symptoms and probable signs (explained
subsequently), the uterus is uniformly enlarged and soft and internal
ballottement is present.
Write about the symptoms and clinical signs of

pregnancy in different trimesters.
answer.
Describe different methods of estimation of date of

delivery.
answer.
Prenatal care
What are the goals of prenatal care?
The goals of prenatal care may be stated as follows:
■ Prevention of adverse maternal/perinatal outcome
■ Early identification and treatment of emerging problems
■ Advising routine prenatal laboratory investigations
■ Discussing the do’s and don’ts during pregnancy
■ Advice on diet, exercise, travel, sexual activity, lifestyle changes,

works, etc.
■ Ordering special tests whenever indicated (Pap smear, genetic

screen)
■ Provide adequate psychosocial counselling
■ Advice regarding medication, immunization and family planning
■ Timely consultations with other specialists (physicians,

cardiologists, diabetologists, dieticians, etc.)
■ Discussion on progress of pregnancy at every visit
■ Patient education, such as mothercraft and childcare
■ Plans for delivery
■ Encouraging the patient to discuss her fears, apprehensions,

expectations and perceived problems – opportunity to allay
anxieties and emphasize cooperation
■ Contraceptive options
What constitutes ideal prenatal (antenatal) visits?

Describe the ideal prenatal schedule and the protocol to
be followed in each visit.
Ideal prenatal visits are as follows:
■ Up to 28 weeks – Once in 4 weeks
■ 28–36 weeks – Once in 2 weeks
■ 36–40 weeks – Every week
The ideal prenatal schedule and protocol are given in Table 6.1.
Table 6.1
Ideal Antenatal Visit Schedule and Suggested Protocol
Visit Week of
Things to do
no. visit
1 5–6 • Confirmation of pregnancy by UPT/USG
• If patient has symptoms, rule out threatened abortion/ectopic/vesicular mole by USG
• History, baseline clinical data and examination; clinical examination is performed in every visit
• Routine prenatal investigations, ICT (if mother is Rh –ve)
• Start/continue folic acid (to be continued throughout pregnancy)
2 8–10 Dating scan
3 12–14 • NT/genetic scan, dual test, if needed chorionic villus sampling
• Start iron and calcium (to be continued throughout pregnancy)
• First dose of tetanus toxoid
4 16–18 • Triple/quadruple test (if dual test was not done earlier)
• Consider amniocentesis as per report
• Early anomaly scan, cervical length by USG in high-risk cases
• Second dose of tetanus toxoid
5 18–20 • Targeted imaging for fetal anomalies (anomaly scan), fetal echo, uterine artery Doppler
• Urine culture sensitivity
6 24 • Repeat HB, urine albumin (this is performed in every visit henceforth), glucose challenge test, if
positive GTT
7 28 • Ultrasound to diagnose placenta praevia fetal weight
• Steroid prophylaxis (especially in high-risk pregnancy)
8 30 • Repeat Hb, GCT (if it was normal earlier)
• Look for FGR, preeclampsia, anaemia, GDM
9 32 • May start fetal well-being studies in high-risk pregnancies
• May consider admission in Grade 2–3 heart disease
10 34 • Fetal lung maturity is assumed
• May start weekly NST/AFI even in normal pregnancy
11 36 • USG for fetal growth, lie, presentation, placenta, AFI, BPP
• May consider external cephalic version in breech
12 37 • Pelvic and cephalopelvic assessment in primi
• Plan the time, place and mode of delivery
• If vaginal delivery is contemplated, induction is considered
13 38 • Induction is considered in GDM
14 39 • May consider admission even in normal pregnancy
• Monitor fetomaternal well-being
15 40 • All complicated pregnancies should be delivered
What are the routine prenatal investigations performed?

Following are the routine prenatal investigations performed:
Blood
■ Blood group and Rh typing indirect Coombs test (ICT) if mother is

negative and husband is positive (if ICT is negative then repeated
every month)
■ Haemoglobin and packed cell volume (PCV) (repeated in second

and third trimester)
■ VDRL, HIV, HBsAg
■ FBS/RBS/HbA1c (first trimester); if abnormal, GTT should be

performed
■ Glucose challenge test (50 g 1 h/75 g 2 h at 24–28 weeks; if normal to

be repeated at 32–36 weeks; if positive, GTT should be performed
■ Dual test (12–14 weeks)/triple test (15–16 weeks)/quadruple test (16–

18 weeks) is offered to all women routinely in many centres
Urine
■ Albumin, sugar and microscopy (preferably during every visit after

second trimester)
■ Culture and sensitivity (to rule out asymptomatic bacteriuria at 20–

24 weeks)
Ultrasound
■ Scan to confirm pregnancy, its normality (5–8 weeks)
■ Dating scan (at 8–10 weeks)
■ NT/genetic scanning (12–14 weeks) along with dual test
■ Targeted imaging for fetal anomalies or anomaly scan (at 18–20

weeks)
■ Scan for fetal growth, lie, presentation, placental location, liquor (at
36–38 weeks)
What is the routine prenatal advice given?

answer.
High-risk pregnancy
What is high-risk pregnancy? What are the high-risk
factors?
High-risk pregnancy is defined as one which is complicated by factors
that adversely affect the pregnancy outcome – maternal or perinatal or
both.
It is also considered as a condition where the mother, fetus and
newborn are at or may possibly be at increased risk of mortality or
morbidity due to problems and complications before, during or after
delivery. Actually all pregnancies are potentially at risk.
Risk factor is defined as ‘any ascertainable characteristics of a
person or group of persons associated with an abnormal risk of
developing or being adversely affected by a morbid disease’. Risk
factors may be present prenatally or develop in pregnancy. Risk
factors may be grouped as follows.
General risk factors

These are the factors based on patient’s age, parity, etc. and can be
easily recognized by a woman herself or her relatives. They are as
follows:
■ Maternal age (<19 or >35 years)
■ Parity (primigravida or grand multigravida)
■ Prepregnancy weight (<40 kg or >90 kg)
■ Height: short stature (<145 cm)
■ Social class (low socioeconomic status)
Risk factors based on previous reproductive history

■ Prolonged period of infertility
■ Recurrent abortions
■ Bad obstetric history (intrauterine/neonatal death in the past)
■ Congenital anomalies
■ Premature labour
■ Difficult delivery/instrumental delivery
■ Caesarean section
■ Third-stage complications
■ Preeclampsia/eclampsia/GDM
■ Birth weight of previous baby (<2.5 kg or >4 kg)
■ Rh isoimmunization or ABO incompatibility
■ Genetic, autoimmune and medical disorders such as thyroid, heart,

blood, lung, liver, renal, neurological diseases
Risk factors in present pregnancy

■ History of pain/bleeding any time (suggests imminent abortion,
ectopic pregnancy or preterm labour)
■ Poor/excessive weight gain (suggests FGR or diabetes)
■ Medical diseases such as hypertension, diabetes,

heart/respiratory/renal/hepatic diseases, anaemia, fever due to any
cause (will have severe consequences on maternal and fetal health)
■ Multiple pregnancy – twins/triplets (most of the complications seen

in a pregnancy may occur in multiple pregnancy)
■ Intrauterine growth restriction/big baby (both run the risk of sudden
intrauterine death and postnatal complications)
■ Prelabour rupture of membranes/preterm labour
■ Antepartum haemorrhage due to either abruption or placenta

praevia
■ Placenta praevia – Low lying placenta after 7 months (will have

repeated bouts of small quantity of bleeding and may be dangerous
to mother and fetus if it is heavy)
■ Oligo-/polyhydramnios
■ Malpresentation – Breech/transverse lie (difficulty at delivery is

anticipated)
■ Suspicion of cephalopelvic disproportion/abnormal pelvis
■ Prolonged pregnancy
Risk factors due to previous surgeries

Any surgery in the past, namely previous caesarean section,
myomectomy, laparotomy for any reason, surgery for prolapse uterus,
vesicovaginal fistula, complete perineal tear and stress incontinence.
Risk factors due to complications during labour in the

past
Certain potentially risky situations that develop only during the
course of labour, such as:
■ Prelabour rupture of membrane
■ Cord prolapse
■ Prolonged labour
■ Meconium-stained liquor
■ Retained placenta
■ PPH
■ Acute inversion
■ Injury to genital tract
■ Ruptured uterus
Risk factors due to fetal/neonatal complications in the

past
Even after a normal pregnancy and uneventful delivery, antenatal
complication may turn it into the high-risk group. Complications in
fetus/neonate are the following:
■ Multiple gestations
■ Congenital abnormalities
■ Fetal growth restriction and macrosomia
■ Low Apgar score
■ Asphyxia/respiratory distress syndrome
■ Neonatal jaundice
■ Early neonatal death
Other risk factors

Following factors not only adversely affect the maternal health but
they also have a negative effect on the growing fetus:
■ Smoking/tobacco chewing
■ Alcohol/drugs
■ Sedentary lifestyle
■ Heavy work/travelling
■ Neoplasms and malignancies
What are the danger signals during pregnancy and

labour (which a health worker should know)?
Danger signals during pregnancy

These signals should be noted by either the pregnant lady herself or
the primary health worker. If any of the following are present, the
pregnant lady should immediately consult an obstetrician:
■ Pain in abdomen
■ Bleeding/leaking/discharge per vagina
■ Maternal weight gain – static/excess
■ Uterine height – less/more
■ Raised blood pressure (>140/90 mm Hg)
■ Swelling of legs even after lying down, swelling of hands,

infraorbital area
■ Headache
■ Blurring of vision
■ Jaundice
■ Decreased urine output

■ Anaemia (pale nails, conjunctiva and tongue)
■ Palpitation/murmurs on auscultation
■ Difficulty in breathing
■ Decreased fetal movements
■ Short stature (height less than 4 ft 10 in)
■ Mobile head at term
■ Malpresentation (baby presenting with breech or transverse lie)
■ Prolonged pregnancy (going beyond the expected date of delivery)
Danger signals in labour

If any of the following are present, the doctor at primary care centre
should immediately transfer the mother to a higher centre:
■ Preterm labour
■ Malpresentation or position in labour
■ Compound presentation (head and hand, head and cord)
■ Multiple pregnancy in labour
■ Prolonged labour
■ First stage – cervix should dilate 1 cm/h in primi, 1.5 cm in

multipregnancy
■ Second stage – duration exceeding 1 h in primi, ½ h in

multipregnancy
■ Bleeding per vagina

■ Excessive fetal movements
■ Decreased/irregular fetal heart rate
■ Meconium-stained liquor
■ Bandle ring (deep mark between upper and lower segments of the
uterus suggesting obstructed labour)
■ Cord prolapse
■ Retained placenta (placenta not delivered beyond half hour)
■ Postpartum haemorrhage (excess bleeding after delivery of the

baby)
CHAPTER 7
Genetics, prenatal diagnosis and
congenital malformations
(anomalies)
Genetics
Classify and briefly describe chromosomal
abnormalities.
Chromosomal abnormalities may be numerical or structural.
Numerical abnormality
In this abnormality, chromosomes may be missing or present in excess
of the normal pairs. They are most easily recognized abnormalities. It
may involve autosomes (chromosomes 1–22) or sex chromosomes (X
and Y).
■ Aneuploidy – Chromosomal complement not involving a multiple

of the haploid number 23 is called aneuploidy.
■ Trisomy – Inheritance of an extra chromosome

(risk increases after 35 years)
■ Monosomy – Inheritance of loss of a

chromosome monosomy
■ Polyploidy – Chromosomal complement involving an entire
haploid set of 23 (e.g. triploidy 69 chromosomes or tetraploidy 92
chromosomes) is called polyploidy.
Some well-known trisomies are as follows:
■ Trisomy-21 (Down syndrome) (for details see the short note on

Down syndrome, under Prenatal Diagnosis section of this Chapter)
■ Trisomy-18 (Edward syndrome) – This is characterized by heart

defects (ventricular septal defects in 95% of cases), cerebellar
vermian agenesis, enlarged cisterna magna, myelomeningocele,
diaphragmatic hernia, omphalocele, imperforate anus and renal
anomalies such as horseshoe kidney.
■ Trisomy-13 (Patau syndrome) – This is associated with

abnormalities of virtually every organ system. Characteristic defect
is holoprosencephaly, others being heart defects, neural tubal
defects, cleft lip and palate, cystic kidney and polydactyly and
rocker bottom feet.
Well-known sex chromosome abnormalities are as follows:
■ 45,X Turner syndrome – Abnormalities include cardiac

malformation, renal anomalies and hypothyroidism. Other features
include short stature, broad chest with widely spaced nipples,
congenital lymphoedema and webbed posterior neck.
■ 47,XXX – They are tall without major anomalies.
■ 47,XXY Klinefelter syndrome – This is the most common sex

chromosome abnormality in males. They are phenotypically normal
without major anomalies. They may have gonadal dysgenesis and
gynaecomastia.
Structural abnormality
In this abnormality, there is rearrangement or balanced rearrangement
of chromosomes:
■ Rearrangement of chromosomes that may or may not produce

phenotypic abnormality, depending on whether genetic information
is missing or is excessive. Structural abnormalities can be of various
types, for example translocation, deletion, inversion, insertion or
ring chromosome. Such abnormalities can produce an abnormal
gamete responsible for recurrent pregnancy wastage or a congenital
malformation.
■ Balanced rearrangements yield phenotypically normal individuals
who are prone to produce abnormal gametes which predispose to
pregnancy wastage or birth of an abnormal child.
Write a short note on single-gene disorders.

answer.
Write a short note on teratogens.

answer.
Prenatal diagnosis
What are the indications for prenatal diagnostic tests?
The indications for prenatal diagnostic tests are as follows:
■ Advanced maternal age (>35 years)
■ Previous child with chromosomal abnormality/structural

abnormality
■ Parents with chromosomal abnormality/carrier of autosomal

recessive disorder
■ Mother carrying X-linked disorder/thyroid autoantibodies
■ Medical history, history of drugs and physical examination
■ Family history of congenital defects, metabolic defects, hereditary

disorders, mental retardation
■ History of recurrent pregnancy losses, neonatal deaths
Write briefly about biochemical prenatal screening tests.

Different biochemical screening tests performed are as follows:
Dual screening: Performed between 12 and 13.6 weeks. In this,

PAAP-A and free hCG are estimated along with NT scan. In Down
syndrome, PAAP-A is decreased and hCG is increased. Detection
rate is 60% with a false-positive rate of 5%.
Triple screening: Performed between 15 and 16 weeks. In this, AFP,

unconjugated estriol and free hCG are estimated along with early
anomaly scan. In Down syndrome, AFP and estriol are decreased
and hCG is increased.
Quadruple screening: Performed between 14 and 20 weeks. Usually
in women who present late without dual or triple screening. In this,
AFP, unconjugated estriol, free hCG and inhibin A are estimated
along with anomaly scan. In Down syndrome, AFP and estriol are
decreased and hCG and inhibin A are increased.
Combined test:
■ Dual test + NT – Detection rate 90%, false +ve

5%
■ Dual test + nasal bone – Detection rate 95%,

false +ve 5%
Integrated test: First trimester screening (NT + dual test) + quadruple
test
Maternal serum α-fetoprotein

AFP is elevated in the following:
■ Open NTDs (meningomyelocele and anencephaly)
■ Fetal nephrosis and cystic hygroma
■ Fetal GI obstruction, omphalocele and gastroschisis
■ Prematurity and FGR
■ Abdominal pregnancy
■ Multiple fetuses
AFP is decreased in the following:
■ Overestimated gestational age

■ Missed abortions
■ Molar pregnancies
■ Chromosomal abnormalities (including Down syndrome)
What are the prenatal diagnostic (PND) procedures?

Various PND procedures and their timing are as follows:
■ Nuchal translucency (NT), nuchal thickness and soft markers: 11–20

weeks
■ Chorionic villus sampling: 10–12 weeks
■ Amniocentesis: After 15 weeks
■ Cordocentesis: After 20 weeks
Other PND procedures not routinely performed are as follows:
■ Fetal skin sampling
■ Fetal muscle sampling
■ Fetal liver biopsy
■ Embryo/fetoscopy
■ Intact fetal cells or cell-free DNA in maternal blood
Write a short note on nuchal translucency.
Nuchal translucency
■ It is a component of first-trimester aneuploidy screening.
■ Performed between 11 and 13.6 weeks or when CRL is between 45

and 84 mm.
■ It is due to physiologic collection of fluid underneath the nuchal

skin.
■ Chromosomal anomaly detection rate is 70%.
■ Along with age and dual test, the detection rate reaches 90%.
Guidelines for NT measurement:
■ Strict sagittal section to be taken
■ Fetal head in neutral position (Fig. 7.1)
■ Image should occupy more than 70% of screen
■ Margins of NT should be clear
■ Away from amnion (amnion should be seen separately)
■ Caliper should be perpendicular to long axis of fetus
■ Inner to inner measurement of widest space is taken

FIGURE 7.1 Nuchal translucency (NT). Small line represents nuchal
translucency, arrow is pointing amnion. Note that its sagittal section is
occupying 70% of screen with head in neutral position and NT away
from amnion.
Increased NT is seen in the following:
■ Chromosomal abnormalities (60–70%)
■ Cardiac abnormalities (5–10%)
■ Structural abnormalities
■ Genetic syndromes
■ Skeletal dysplasias
■ Fetal infection
■ Twin to twin transfusion syndrome (TTTS) – four times high higher

risk
If NT is more than 3 mm, one can directly offer karyotype by

amniocentesis.
NT more than 3.5 mm is an indication for fetal echo.
What are the ultrasound soft markers of chromosomal

anomalies?
answer.
Write a short note on chorionic villous sampling (CVS).

answer.
Write a short note on amniocentesis.

Amniocentesis is a transabdominal procedure, in which, after
cleansing the lower abdomen and painting the part with antiseptic,
sterile isolation towels are placed to expose only the hypogastric
region. A fine needle is introduced under ultrasound guidance into
the amniotic cavity to draw off a sample of amniotic fluid. This
procedure is commonly performed at about 16 weeks of gestation.
During the procedure, care should be taken to avoid injecting into the
placental site. This fluid is used for prenatal genetic disorders such as
karyotyping to exclude Down syndrome and chromosomal anomalies,
to test for inherited metabolic disorders and to assess α-fetoprotein
(AFP) levels as a test to detect an open NTD (Fig. 7.2).
FIGURE 7.2 Amniocentesis.
Amniocentesis may be performed later in pregnancy for other

indications such as assessment of fetal pulmonary maturity.
Potential complications
■ Premature rupture of membranes in 1–2% of patients
■ Fetal bleeding from trauma to the fetus, placenta or umbilical cord
■ Direct fetal or maternal injury from trauma to epigastric or uterine

vessels
■ Fetal–maternal bleeding resulting in isoimmunization
■ All Rh-negative women should be protected with prophylactic

injection of anti-D
■ Preterm labour/miscarriage in less than 1% cases
■ Abruptio placentae
■ Infection risks are low, if proper aseptic precautions are observed

Write a short note on cordocentesis.
answer.
Write a short note on Down syndrome.

Down syndrome is also known as trisomy-21. In 95% of cases it is due
to nondisjunction (sporadic) and in 5% it is due to translocation
(familial).
It is the most common aneuploidy, hence becomes the focus for
screening. The incidence of Down syndrome at different ages of
mother is as follows: 25 years – 1/1352, 30 years – 1/900, 35 years –
1/356, 40 years – 1/80, 45 years – 1/18.
Screening is done by performing NT + dual test in the first trimester
or triple test in the second trimester. Confirmation is done by
amniocentesis after 15 weeks of pregnancy.
Ultrasound features:
■ Choroid plexus cyst
■ Congenital heart defects
■ Ventriculomegaly
■ Duodenal atresia
■ Hyperechogenic bowel
■ Shortened long bones
■ Nuchal fold thickness: >3 mm before 15 weeks, >5 mm during 15–18

weeks and ≥ 6 mm during 18–20 weeks
The typical physical features are brachycephaly, epicanthal folds

and upslanting palpebral fissures, a flat nasal bridge, hypotonia,
tongue protrusion, short stubby fingers, single palmar crease, saddle
toe gap.
There may be cardiac and gastrointestinal defects. Affected children
are mentally retarded and may have childhood leukaemia.
Congenital (malformations) anomalies
What is malformation and what is deformation? Classify
congenital malformations.
Congenital malformation is a structural abnormality which is present
at birth. This is a morphologic defect of an organ, part of an organ or a
larger area of the body resulting from an intrinsically abnormal
development process. It may be easily recognizable at birth, for
example spina bifida, or may not be revealed until symptoms and
signs indicate its presence, for example duodenal atresia.
Congenital deformation refers to an abnormal form, shape or
position of the part of the body caused by mechanical
force/interference, for example club foot, which in turn can be due to
intrinsic (lack of movement due to neural tubal defect) or extrinsic
(oligohydramnios) causes.
Malformations are classified below.
Major malformations
These have medical–surgical or cosmetic importance with impact on
morbidity and mortality. Some examples are as follows:
■ CNS – Hydrocephalus, anencephaly, microcephaly, meningocele,

encephalocele
■ Craniofacial – Cleft lip and cleft palate, cystic hygroma
■ Eye – Cataract and anophthalmos
■ GIT – Pyloric/intestinal atresia, imperforate anus, omphalocele,

gastroschisis
■ Heart – ASD, VSD, tetralogy of fallout, atrioventricular defects,

univentricular heart, Ebstein anomaly, pulmonary stenosis, aortic
stenosis, cardiomyopathies
■ Genital tract – Hypospadisis cryptorchidism, unicornuate uterus,
Mullerian agenesis
■ Kidney – Hydronephrosis, horseshoe kidney, renal agenesis,

posterior urethral valve, PUJ obstruction
■ Musculoskeletal – Absent radius, CDH, scoliosis and kyphosis, short

limbs, absent pubic rami
■ Hand and foot – Polydactyly, syndactyly, short hands, absence of

thumbs, calcaniovalgus, club foot
Minor malformations
These do not have serious medical–surgical or cosmetic importance.
Lethal malformations
■ CNS – Anencephaly, acrania, alobar holoprosencephaly,
inencephaly
■ Abdomen – Body stalk anomaly
What are the indications for high-resolution ultrasound

and what are the indicators of malformations on
ultrasound?
answer.
Write about management principles of congenital

malformations and write the examination/evaluation of
an anomalous fetus.
answer.
Write a short note on anencephaly.

Anencephaly is multifactorial in origin. It is a condition, in which
there is a rudimentary brain with absent cerebral hemispheres and an
absence of cranium and posterior skull bones. Skull base and orbits
are covered only by angiomatous stroma. It is the most severe form of
NTD.
It is the only anomaly diagnosed in the first trimester by absence of
BPD. In the second trimester, ultrasound scan shows absence of bony
skull vault and cerebral hemispheres. There is increased maternal
serum AFP (MSAFP) in the second trimester.
They are commonly associated with other anomalies such as spina
bifida and cardiac anomalies.
Antenatal complications are polyhydramnios, FGR, past dates and
malpresentations (breech and face). Polyhydramnios is usually
attributed to the poor swallowing, increased diuresis and CSF leak.
Anencephalous infants do not survive. These women are offered the
option of MTP, if diagnosed before 20 weeks. After that it is better to
wait for spontaneous delivery. Artificial rupture of membranes is
avoided as the bag of membrane helps in effacement and dilatation of
the cervix by exerting uniform pressure in the absence of skull vault.
Caesarean delivery should be avoided.
Shoulder dystocia is common but this is easier to manage with
simple manoeuvres such as McRoberts coupled with suprapubic
pressure and gentle traction.
Write a short note on spina bifida.

Spina bifida presents a defect due to failure of closure of neural tube,
midline defect of the posterior part of the spine, exposing the contents
of neural channel.
Types of spina bifida:
■ Spina bifida occulta – Covered with skin
■ Spina bifida cystica – Covering skin is defective, swelling is seen

over defect
■ Meningocele – Spinal cord is not involved in the defect (<10%)

■ Meningomyeloceles – Defect has little or no covering, spinal cord is
involved (Fig. 7.3)
FIGURE 7.3 Types of spina bifida.
The meningeal defect in the occipital bone of the skull is termed

occipital meningocele, and if brain tissue is involved it is termed
cephaloencephalocele. The most common site is lumbosacral region of
the spine.
Aetiology
■ Multifactorial in origin
■ Drugs such as sodium valproic acid
■ Maternal diabetes
■ Folic acid deficiency
■ Trisomy-18 and trisomy-13
Ultrasound signs
■ There is absence of posterior lamina, and lateral vertebral processes
are set apart
■ Lemon sign due to scalloping of frontal bone (Fig. 7.4)
■ Banana sign due to curved shape of cerebellar hemispheres (Fig. 7.5)
FIGURE 7.4 Lemon sign.

FIGURE 7.5 Banana sign.
Effects of spina bifida

Usually, there is caudal displacement of the medulla and cerebellum
resulting in obstruction of foramen magnum and hydrocephalus. The
local effects of spina bifida depend on the spinal level and the number
of segments involved (paralysis of both lower limbs, urinary or faecal
incontinence).
Complications
The immediate sequelae of severe (lumbar) meningomyelocele:
■ Muscle paralysis of lower limbs
■ Urinary incontinence and anal sphincter paralysis
■ Orthopaedic deformities of the feet
■ Dislocation of hips
■ Hydrocephalus later in most cases

Later problems include the following:
■ Urinary tract infection leading to renal failure
■ Retarded intellectual development
■ Scoliosis
Treatment and prognosis

There are two possible approaches:
1. One view is that irrespective of severity, all affected babies should

have an immediate closure of the defect. With this policy about 60%
will survive, of whom one-third may have very severe mental and
physical handicaps.
2. The other view is that it is wrong to promote the survival of babies

with such severe lifelong handicaps and that it is justifiable to select
cases for operation at birth. If only the less severely affected patients
are selected for operation, the overall survival rate will be reduced but
the quality of life will be better as most of the survivors will have only
mild to moderate handicaps.
Screening and prevention

The screening test is based on the measurement of serum AFP in the
maternal serum at 16–18 weeks gestation (elevated if abnormal) or by
ultrasonography. Depending on the size and site of lesion, MTP is
offered in many countries. Prevention of many cases is feasible now
with periconceptional administration of folic acid, particularly 3
months before and for several months after conception.
CHAPTER 8
Identification of fetus at risk,
antenatal and intranatal
assessment of fetal well-being
What are the risk factors contributing to perinatal death?

The risk factors contributing to perinatal death are as follows:
1. Hypoxia/asphyxia
a. Previous stillbirth or neonatal death
b. Maternal severe anaemia, diabetes,

hypertension, chronic renal disease
c. FGR
d. Postmaturity
2. Prematurity
a. Previous history of preterm birth
b. Maternal age (< 19 and > 40 years)
c. Low weight (40 kg) and short stature (< 145

cm)
d. Low socioeconomic background and poor

educational status
e. Cardiac disease, thyrotoxicosis, diabetes and

hypertension
f. Malformation of uterus (bicornuate and

subseptate, insufficient cervical os)
g. Multifetal pregnancy, polyhydramnios
h. Malpresentation
i. Antepartum haemorrhage (placenta praevia

and abruptio placentae)
j. Acute medical illnesses (pyelonephritis,

hepatitis and malaria)
3. Birth injuries
a. Prolonged labour
b. Obstructed labour due to cephalopelvic

disproportion
c. Traumatic vaginal instrumental deliveries
d. Abnormal presentations such as breech and

transverse lie
e. Shoulder dystocia in fetal macrosomia
f. Premature baby
4. Infections
a. Prematurity
b. Prolonged labour
c. Poor aseptic techniques during labour
d. Meconium aspiration
e. Operative delivery
f. Vigorous and unhygienic neonatal

resuscitative measures
What are the antenatal fetal assessment tests and the
indications for them?
Antenatal fetal assessment tests may be grouped as follows:
Clinical assessment (mostly indirect)
■ Monitoring maternal weight gain
■ Fundal height assessment
■ Clinical estimation of liquor
■ Fetal movement count and fetal heart auscultation
■ Clinical estimation of fetal weight
Biochemical (not done these days as they are indirect

and difficult to interpret)
■ Estimation of maternal serum oestriol, hPL and heat-stable alkaline
phosphatase (totally given up now)
■ Maternal serum α-fetoprotein is a screening test for open neural

tube defects
■ Dual (PAPP-A and hCG), triple (oestriol, hCG and α-fetoprotein)

and quadruple (oestriol, hCG, α-fetoprotein and inhibin A) tests are
performed as screening tests for trisomy.
Ultrasonographic evaluation/assessment
■ NT and genetic scan (12–14 weeks)
■ Targeted anomaly scan with fetal echo (18–20 weeks)
■ Serial scans to look for FGR and macrosomia
■ Growth scan and amniotic fluid assessment
■ Doppler studies
■ Uterine artery Doppler screening (to predict
FGR – 18–24 weeks)
■ Umbilical and middle cerebral artery Doppler

screening (third trimester)
■ Ductus venosus Doppler technique

Biophysical tests
■ Daily fetal movement/kick counts
■ Cardiff kick count – Time taken for 10

movements noted at a particular time
■ Sadowsky kick count – Number of movements

appreciated during 1 h each in the morning,
afternoon and night (all postmeal) is noted.
■ Nonstress test
■ Biophysical profile scoring
Invasive procedures
■ Amniocentesis for collection of amniotic fluid to estimate bilirubin
(not done now) and L/S ratio (hardly done)
■ Cordocentesis for collection of fetal blood to determine fetal blood

group type, Hb, haematocrit, bilirubin
Indications for fetal well-being tests
■ Patients at high risk
■ Diabetes mellitus, hypertension, preeclampsia and renal disease
■ Previous stillbirth
■ Suspicion of FGR
■ PROM
■ Pregnancy after 40 completed weeks
■ Multifetal pregnancy
■ Previous caesarean section
■ Induced labour
Write a short note on nonstress test.
Nonstress test
This test is based on the observation that in a healthy fetus with an
intact central nervous system and responsive autonomic system
(sympathetic and parasympathetic), gross fetal movements are
associated with fetal cardiac acceleration. This is somewhat like
increase in our heart rate when we walk or run. This response is
blunted by hypoxia, acidosis, drugs (sedatives, narcotics and β-
blockers), fetal sleep, congenital fetal anomalies and fetal compromise
from any cause.
The test is best performed in a quiet environment, the patient in
semi-Fowler or left lateral recumbent position. Most important point
to be noted is that whilst performing NST, uterus is relaxed (nonstress
= no stress of labour).
External fetal heart rate and tocodynamometer monitoring leads are
applied. A continuous fetal heart rate tracing is obtained. Whenever
the patient perceives any fetal movement, she presses on a button
which prints a mark on the tracing at that moment of time. The test is
continued until the criteria for reactivity are satisfied or the time limit
of 40 min has been reached.
The NST is interpreted as ‘reactive’ (negative test, i.e. negative for
hypoxia), if at least two accelerations of 15 bpm are observed, lasting
for at least 15 s in any 20-min period. It is indicative of a healthy fetus
(Fig. 8.1).
FIGURE 8.1 Reactive NST (accelerations corresponding to the fetal

movements).
A ‘nonreactive test’ (positive test, i.e. positive for hypoxia) (Fig. 8.2)
calls for further evaluation.
FIGURE 8.2 Nonreactive NST (no accelerations corresponding to fetal
movements).
However, positive predictive value of NST is very poor (20%);

hence, decision to deliveries not based on NST alone. The best strategy
would be to do NST for a longer time or to repeat NST at a later time
(to avoid sleep cycle of the fetus), preferably after mother takes some
food. Vibration acoustic stimulation test (VAST) may be performed. It
is also advisable to perform a full biophysical profile scoring and
Doppler studies before decision is taken to deliver.
NST has a very good negative predictive value (100%); hence, if
reactive, one is reassured of good fetal oxygenation.
All NST tests should be reviewed for the following information:
■ Baseline heart rate (110–160 bpm)
■ Beat-to-beat variability (5–25 bpm)
■ Correlation of FHR accelerations with fetal movements
The advantages of the NST test are its simplicity, suitability to an

OPD setting, rapidity, low cost and that it is free from
contraindications.
Write a short note on biophysical profile scoring.
Fetal biophysical profile (manning score)

A method of biophysical scoring system based on multiple parameters
determined at real-time ultrasound scanning forms the basis of the
test. It has been of great help in the management of high-risk
pregnancies including FGR cases in determining the timing and mode
of pregnancy termination whenever the fetus seems to be in imminent
jeopardy.
The parameters that constitute the BPP include (i) NST, (ii) fetal
breathing, (iii) fetal tone, (iv) gross body movement and (v) volume of
amniotic fluid present (AFI).
The use of several variables adds to the predictive value of the test.
Each parameter is given a score of 2 points. A score of 8–10 correlates
well with a good pregnancy outcome provided the liquor is good. A
score of less than 6 should be viewed with caution. If the gestational
age is more than 34 weeks, lung maturity is presumed to have taken
place. The test should be repeated within 24–48 h. If score persists or
deteriorates, delivery by caesarean section is conducted in centres
where good NICU facilities are available. Otherwise, timely transfer to
a tertiary care unit is advisable. If gestational age is less than 34 weeks,
steroids should be given for lung maturity and delivery is considered
after 48 h. A score of less than 2 is associated with poor fetal outcome
and delivery should be considered irrespective of gestational age with
or without steroids.
Technique of the BPP scoring – First NST is performed using
cardiotocography (CTG) machine. Then the fetus is observed for
about 20 min using real-time ultrasonography to evaluate and score
using the criteria depicted in Table 8.1.
Table 8.1
Biophysical Profile Scoring
Variable Score 2 (normal) Score 0 (abnormal)

NST Reactive Nonreactive
Fetal breathing Presence of at least 30 s of sustained FBM in 30 min No or < 30 s of FBM in 30 min
movement (FBM)
Fetal movements Three or more gross body movements in 30 min Two or less gross body movements during 30 min
Fetal tone At least one episode of a limb motion from flexion to Fetus in position of semi or full extension with no
extension and rapid return to flexion return to flexion with movement
AFI Normal AFI < 5 or SVP <1 cm
The important principle in any antepartum biophysical monitoring

testing protocol is to fully comprehend that a ‘normal test’ can be
considered a reliable evidence of fetal well-being. However, the
diagnosis based on a single absent or abnormal biophysical event may
be misleading and false positive. The positive predictive value of BPP
total score is 80–90% (much better than individual parameters).
Another important concept to know is that biophysical parameters
follow the phenomenon of hypoxia cascade which is based on the fact
that the centre governing a biophysical activity that appears first in
intrauterine life gets affected last by the hypoxia. Accordingly, NST is
the first to become abnormal with hypoxia. Breathing and gross
movements are affected next. Fetal tone is the last to disappear with
hypoxia.
Write a short note on cardiotocography (CTG) in labour.

CTG is a method of monitoring of the fetal heart and uterine
contractions using a CTG machine which has a Doppler device to pick
up the fetal heart sounds and a device to monitor the uterine
contractions. These can be recorded on a paper or digitally and
correlated to detect fetal distress.
Uterine contractions diminish placental perfusion; hence, there can
be FHR decelerations in consonance with uterine hypertonus induced
by the uterine contraction. There are three types of decelerations:
Early decelerations – These are due to the head compression, where

the nadir of the deceleration corresponds to peak of contraction and
FHR reverts back to normal, once the contractions are over (Fig.
8.3).
Variable decelerations – Due to cord compression and have variable

patterns (Fig. 8.4).
Late decelerations – In situations of uteroplacental insufficiency, the
uterine contractions may decrease the placental perfusion
sufficiently to cause fetal hypoxia which outlasts the duration of the
contraction. The FHR tracing showing decelerations which begin
with the peak of the uterine contractions and persisting even after
the conclusion of the contraction is termed late deceleration
(Fig.8.5). These are indicative of fetal distress.
FIGURE 8.3 Early decelerations.

FIGURE 8.4 Variable deceleration.
FIGURE 8.5 Late deceleration.
Causes of fetal tachycardia in CTG:
■ Maternal fever
■ Anaemia
■ Infection (chorioamnionitis)
■ Anxiety
■ Hypoxia
Causes of fetal bradycardia in CTG:
■ Maternal – medication, hypotension/shock, convulsions,

hypothermia, abruption
■ Cord compression
■ Hyperstimulation
■ Postmaturity
Causes of decreased variability:
■ Medications – anaesthetics, tranquilizers, narcotics and barbiturates
■ Marked prematurity
■ Fetal sleep
■ Chronic hypoxia
■ Brain damage
■ Fetal arrhythmias, tachycardia, with late decelerations
■ Hydrops fetalis
Causes of increased variability:
■ Medications
■ Increased fetal activity
■ Cord compression
■ Increased contractions
■ Postdates
Interpretation of CTG in labour is based on following components:
■ Fetal basal heart rate
■ Beat to beat variability
■ Decelerations
The interpretation is shown in the Table 8.2.
Table 8.2
Categories and Interpretation of CTG in Labour, Suggested
Interventions (FIGO 2015)
CHAPTER 9
Obstetric management – decision-
making. Induction of labour
Briefly describe the components of obstetric
management and decision-making.
Obstetric management is more or less similar no matter what the
disorder is and the decision-making involves essentially following
four components/questions:
1. When to deliver?
2. How to deliver?
3. Whether to wait for spontaneous onset of labour or induce?
4. How to induce?
1. When to deliver?
Of the four questions, this is the first and the most

important question. Delivery is the definitive
treatment for most of the complications in
pregnancy, but timely delivery is the key to
achieve good fetomaternal outcome. It is
usually preferred to deliver after 37 completed
weeks. However, one may deliver earlier if
there are signs for suggestive of fetomaternal
compromise.
Examples:
In cases of severe preeclampsia, it is better to

deliver earlier for mother’s sake to prevent
eclampsia/other complications and also for
baby’s sake to avoid intrauterine
death/neonatal complications.
In cases of abruption, due to any reason,

immediate delivery irrespective of gestational
age is advised.
If there are no indications to deliver before 37

completed weeks and if there are no signs of
fetomaternal compromise, one may wait up to
40 weeks and 6 days, with close monitoring of
maternal and fetal condition. However,
delivery should be contemplated between 41
and 42 weeks. It is not advisable to wait beyond
42 weeks.
2. How to deliver?
This question refers to the route of delivery. The

answer depends on the urgency to deliver,
feasibility of vaginal delivery and risk of
developing fetal distress or birth injuries during
labour and vaginal delivery.
Examples:
In the presence of cephalo or fetopelvic

disproportion, malpresentation, major degree
placenta praevia or tumours in the region of
lower segment, where vaginal delivery is not
feasible, caesarean delivery is the mode of
delivery.
If there is an urgency to deliver as in cases of

abruption with fetal distress or for that matter
fetal distress, due to any reason and if mother is
not in labour, caesarean delivery is the route of
choice. In situations where one anticipates fetal
distress during labour such as severe fetal
growth restriction (FGR), severe
oligohydramnios or anticipates intracranial
haemorrhage as in early preterm
deliveries/fetuses weighing less than 1500 g,
caesarean delivery is preferred.
3. Whether to wait for spontaneous onset of labour or induce?
If there are no fetomaternal complications, one
can wait for spontaneous onset of labour.
However, it is not prudent to wait beyond full
term (40 weeks and 6 days) for spontaneous
onset of labour.
In cases complicated with medical disorders,

where some amount of fetal compromise is
anticipated, it is advisable to induce, once fetal
maturity is deemed to have achieved (38 weeks
and 6 days). (For other indications for induction
see below.)
Examples:
Cases of preeclampsia, gestational diabetes are

usually induced between 37 weeks and 38
weeks +6 days, as waiting beyond that may be
risky for both mother and baby. All cases that
need delivery before term and considered for
vaginal delivery are induced. Caution – One
must rule out the contraindications for
induction before inducing.
4. How to induce?
Answer depends on the status of cervix as noted

by Bishop score and relative contraindications if
any.
Examples:
If Bishop score is poor, one may ripen the cervix

using PGE2 gel before inducing with artificial
rupture of membranes (ARM) and oxytocin
(relatively contraindicated in heart disease). If
cervix is favourable, however, one may proceed
directly with ARM followed by oxytocin
infusion. ARM is usually performed in cases of
abruption that are planned for vaginal delivery.
Vaginal misoprostol, 25 mg, may also be used
except in cases of previous caesarean section.
Induction of labour
What are the indications for induction of labour?
Maternal indications
In the conditions where continuation of the pregnancy may adversely
affect the maternal well-being, induction of labour is indicated:
■ Malformation of the fetus incompatible with life (anencephaly,

hydrocephaly)
■ Intrauterine death of the fetus (relative indication)
■ Polyhydramnios at term – If it causes dyspnoea and discomfort
■ Uncontrolled chorea gravidarum
Fetal indications
In these conditions, continuation of the pregnancy may affect the well-
being of the fetus:
■ Prolonged pregnancy – The perinatal mortality progressively

increases after the 41st week (>287 days) of pregnancy due to
placental insufficiency, asphyxia, increased risk of meconium
staining and increasing mechanical difficulties.
■ FGR – severe FGR with raised umbilical artery Doppler

indices/absent end diastolic flow.
■ Severe oligohydramnios due to any reason.
■ Rhesus isoimmunization – Premature induction is indicated when

the previous baby was affected, when the maternal antibodies rise
rapidly and if repeated intrauterine transfusions are already
performed in current pregnancy.
■ Unexplained IUD in prior pregnancy – Usually labour is induced 1

week prior to the previous unexplained IUD provided there are no
complications/contraindications.
■ Diabetes mellitus – If conditions are favourable and the diabetes

well-controlled, labour is induced at 38 weeks.
■ Other indications – Placental insufficiency, elderly primigravida.
Combined indications
This group includes conditions which may adversely affect both the
maternal and fetal health if the pregnancy is allowed to continue:
■ Preeclampsia – In mild cases at 37 completed weeks. In severe case

whenever there is fetomaternal compromise.
■ Eclampsia – Induction is carried out as soon as possible after control

of fits.
■ Chronic renal disease and essential hypertension – These conditions

are usually associated with placental insufficiency and FGR.
■ Preterm PROM with evidence of chorioamnionitis.
■ Term PROM – Usually induced after 4 h of rupture of membranes.
■ Bad obstetric history.
■ Abruption.
What are the contraindications for induction of labour?
Absolute contraindications
■ Major degree of cephalopelvic disproportion
■ Transverse lie
■ Pregnancy following a classical caesarean section
■ Major degree placenta praevia
■ Vasa praevia
■ Cord presentation
■ Pregnancy following repair of a vesicovaginal fistula
■ Carcinoma cervix
■ Pelvic tumours
■ Presence of active herpetic genital lesions/HIV
Relative contraindications
■ Heart disease complicating
■ Breech
■ Multifetal gestation (twins)
■ Polyhydramnios
■ Grand multipara
■ Unstable lie
■ Presenting part above pelvic brim
What are the predictors of successful induction? Write a

short note on bishop score.
The predictors of successful induction are:
■ Bishop score (higher the better)
■ Gestational age (higher the better)
■ Presence of infection (poorer outcome in frank chorioamnionitis)
■ Fetal fibronectin (positive test – reduced induction delivery interval)
■ USG assessment of cervix (<2.5 cm – reduced induction delivery

interval)
Bishop score
In Bishop score, the state of the cervix and the station of the presenting
are assessed which serve as a prognostic index for the success of
induction. Table 9.1 gives original Bishop scores.
Table 9.1
Original Bishop Score
A score of 9 indicates bright chances of successful induction. The

lower the score, the higher the chances of failed induction.
Modified bishop score

In the original scoring, the cervical effacement is in percentage which
is difficult to assess and there will be a wide variation between the
assessors. Also to simplify the scoring system, the following
modifications (Table 9.2) are made and the total score is 10 (in tune
with many scores in obstetrics). Score greater than 6 has better success
rates with induction and score less than 6 has more failures.
Table 9.2
Modified Bishop Score
What is cervical ripening? Write briefly on methods of

cervical ripening.
answer.
Write about prerequisites for induction of labour and

briefly describe different methods of induction.
Prerequisites for induction

■ Informed consent (success rates, possibility of fetal distress, need of
repeat induction and emergency LSCS should be explained)
■ Facility for emergency LSCS and NICU should be available
■ Preinduction assessment of liquor, presentation and cervical status

by ultrasound
■ Preinduction CTG and continuous fetal monitoring

■ Induction should be undertaken in secondary or tertiary care
hospitals
Different methods of induction are discussed in below subheads.
Mechanical methods
Similar mechanical methods used for cervical ripening such as:
(i). Stretching/sweeping the membranes.
(ii). Transcervical Foley catheterization with or without ethacridine,

in situations where prostaglandins/oxytocin are contraindicated, may
induce labour as they stimulate the production of prostaglandins from
decidua.
Medical methods
■ Oral prostaglandins:
■ Prostaglandin analogue PGE2 is used as tablets

containing 0.5 mg of PGE2, given at 30 min to 1
h intervals. The dose may be doubled and a
maximum of 30 mg may be used.
■ Misoprostol, a PGE1 analogue, is given in dose

of 25 mcg orally every 2 h up to 5 doses.
■ Vaginal prostaglandins:
■ PGE2 gel containing 0.5–2 mg of PGE2

(dinoprostonegel) not only ripens the cervix but
also induces labour in many. The gel is
administered in the endocervical
canal/posterior vaginal fornix and on the cervix,
taking care that the membranes remain intact
and the application is never extraamniotic. The
application, 0.5 mg, can be repeated in 6 h, and
should not exceed three doses in 24 h. Oxytocin
should NOT be started until 6 h after the last
dose.
■ PGE2 vaginal pessaries – A 10 mg vaginal insert

which is placed in the posterior fornix of the
vagina. This formulation allows the controlled
release of dinoprostone over 12 h, after which it
is removed. Like gel, pessary not only ripens
the cervix but also induces labour.
■ Misoprostol a synthetic PGE1 analogue – Doses

of 25 mcg administered vaginally are effective
in inducing cervical ripening and labour. They
are introduced at an interval of 4 h, and should
not exceed 5 doses in 24 h. There have been
incidences of uterine scar rupture, hence are
better avoided for induction in scarred uterus.
■ Extra/intraamniotic or intramuscular/intravenous prostaglandins –
NOT used for induction of labour at term currently.
■ Mifepristone (RU 486) – This antiprogesterone is not used alone for

the induction of labour. A single oral tablet of 200 mcg is used 24 h
prior to using PGE2 gel/PGE1 (misoprostol). It is recommended
especially in intrauterine death.
■ Oxytocin – It has been universally used for induction of labour. It is

best administered by intravenous infusion for this purpose. Buccal,
intramuscular and transnasal routes of administration are no longer
in use for induction of labour. It is not a good cervical ripening
agent. Current recommendation is to start oxytocin infusion only
after the rupture of membranes. The infusion may be started as
soon as the membranes are ruptured or after 2–4 h:
■ Advantages of oxytocin:
- The infusion can be stopped immediately if there

is an evidence of uterine hyperstimulation or
fetal distress and its actions cease.
- The dose can be accurately titrated depending

on the response.
■ Dose – The infusion is usually started with a

minimum physiological dose of 2 mIU/min.
This is achieved by adding 2 IU of oxytocin in
500 mL of Ringer’s lactate (4 mIU in 1 mL).
Infusion is started with 8 drops/min (2
mIU/min). Dose is increased at intervals of 15
min depending upon the response. Drops per
minute are increased in multiples of 8 as 16
drops/min, then to 24 drops/min to a maximum
of 32 drops/min (8 mIU/min). Oxytocin is best
infused with an infusion pump to adjust the
exact drops per minute.
■ Oxytocin should not be used concurrently with

prostaglandins (PGE2 gel/PGE1 tablet). It is
better started 6 h after the use of PGs.
■ Dangers of oxytocin:
- Incoordinate uterine action, especially uterine

hyperstimulation.
- Fetal hypoxia and distress.
- Uterine rupture in a multipara.
- Water intoxication.
■ Contraindications:
- Disproportion and malpresentation are obvious

contraindications.
- Hypertonic incoordinate uterineaction.
Surgical methods
■ Amniotomy (ARM): This widely used method of low rupture of
membranes is simple to perform. No anaesthesia or analgesia is
needed. It acts by releasing prostaglandins. It is also performed to
augment the labour:
■ Technique – With the usual aseptic care, the

index or the middle finger is inserted through
the cervical os. The membranes are stripped off
the lower uterine segment digitally and the bag
of membranes is ruptured by a sharp pointed
instrument (Kocher’s forceps). Liquor starts
draining as the forewaters rupture. The colour
is observed (clear or meconium stained).
■ Advantages:
- Relatively easy when the cervix is ripe.
- Effective, especially when combined with

oxytocin infusion. In fact, WHO
recommendation is to start oxytocin after ARM.
■ Disadvantages:
- Difficult in ‘unripe’ cervix with a closed cervical
os.
- It has unpredictable action.
- Risk of cord prolapse if the head is high.
- Intrauterine infection and chorioamnionitis.
■ Special indications for ARM:
- Abruption.
- Preeclampsia.
- Postdated pregnancy (to note the colour of the

liquor).
- Chronic ployhydramnios (controlled ARM).
■ Contraindications for ARM:
- CPD/mobile head (for risk of cord prolapse).
- Intrauterine death (for risk of infection).
- Anencephaly (bag of membranes will act like

head).
- Cardiac disease (for risk of infection).

CHAPTER 10
Fetopelvic relationship,
mechanism of labour, normal
labour, conduct of normal labour
and partogram
Describe fetopelvic relationships.

answer.
Describe the mechanism of labour in vertex

presentation.
Definition – The series of changes in position and attitude that the
presenting part has to make during its passage through the pelvis and
the pelvic floor during the course of labour is known as the
mechanism of labour. The fetal head which enters the pelvis in the
transverse or one of the oblique diameters undergoes rotation and
change in its attitude.
The different steps involved in the mechanism of labour are as
follows (Fig. 10.1):
■ Engagement
■ Descent (descent occurs throughout)
■ Flexion
■ Internal rotation of the head
■ Extension
■ Restitution
■ External rotation of head (corresponds to internal rotation of

shoulder)
FIGURE 10.1 Summary illustration of mechanism of labour.
Engagement
The fetal head is said to have engaged when the maximum transverse
(biparietal, 9.5 cm) and anteroposterior (which varies with the degree
of flexion or extension of the head) diameters have crossed the plane
of the pelvic brim.
Descent
Descent is almost a continuous movement throughout the first and
second stages of labour. The gradual descent of the presenting part
takes place because of uterine contraction and retraction. In the
second stage, the bearing-down pains hasten the process resulting in
complete expulsion.
Flexion
The fetal head is already flexed before the onset of labour in vertex
presentation. Further, flexion occurs in the first stage when the head
meets the resistance of the birth canal (pelvic floor to be precise
consisting of levator ani muscle and other soft tissues) during descent.
Internal rotation
Internal rotation takes place when the head reaches the pelvic floor
and meets with resistance. The disposition of the pelvic floor tends to
rotate the leading part forward by causing torsion of the fetal neck.
This movement carries the engaging diameter of the head into the
anteroposterior diameter, which is the largest diameter of the pelvic
outlet.
Extension
In the second stage of labour, two forces act on the head. Uterine
contractions and the abdominal muscles push it downwards, while
the pelvic floor muscles press it upwards and forwards. The
downward and upward pressures counterbalance each other and the
resultant force pushes the head forward. It cannot go forward as the
nape of the neck is fixed against the symphysis pubis; the head
therefore follows the curve of the birth canal by a process of extension.
Restitution
The fetal shoulder enters the pelvis in the left oblique diameter if the
head descends with its suboccipitobregmatic diameter in the right
oblique diameter. As the internal rotation takes place, the head is
completely delivered and is free outside; it resumes its normal
position with regard to the shoulders, turning the occiput towards the
mother’s left thigh. This movement is called restitution, because by it
the neck becomes untwisted and the head restores its natural relation
to the shoulders.
External rotation
The shoulder now descends and the anterior shoulder being lower
meets the resistance of the pelvic floor and so rotates forward, as did
the occiput. The shoulders now occupy the anteroposterior diameter
of the pelvis and as they rotate the head rotates with them. The
occiput thus makes a further movement of one-eighth of a circle in the
opposite direction of its internal rotation. The shoulders are then
delivered, the anterior shoulder escaping under the pubic arch, while
the posterior slides over the perineum.
The rest of the body is then expelled without difficulty as it is
smaller than either the head or the shoulders.
Describe the conditions to be fulfilled to define normal

labour.
In current practice, labour is considered normal if it meets following
criteria: Pregnancy is singleton and has reached term. The fetus
presents by vertex and labour starts spontaneously. Baby delivers
vaginally without undue delay with or without minimal assistance
(episiotomy/outlet forceps/vacuum). Mother and baby are healthy
after the delivery.
Describe the physiological events and theories of onset

of normal labour.
answer.
Describe true and false labour pains.

True labour pain is intermittent and regular. It increases in frequency,
duration and intensity over time. Pain is felt both in the back and in
the front of the abdomen. It is associated with uterine contractions,
progressive descent of the head, cervical effacement and dilatation. It
is not relieved by enema, sedation or rest.
False labour pain is more common in the primigravida and is
characterized by irregular uterine contractions of short duration with
pain confined mostly to the lower abdomen, often relieved by
sedatives. There is no dilatation of the cervical os. They are sometimes
brought on by a digestive upset and are relieved by laxative.
Describe the stages of labour.
First stage
The first stage of labour is considered as the stage of cervical
dilatation, during which effacement and dilatation of the cervix are
initiated and completed. The end of the first stage is signalled by the
full dilatation of the cervix (10 cm).
The first stage is generally divided into two phases (Fig. 10.2).
■ Latent phase: It is a variable but substantial period when little

appears to be happening. In this period, the pains are not very
distressing to the patient. The cervical dilatation progresses rather
slowly. This lasts about 6–8 h.
■ Active phase: The pain becomes distressing to the patient. The

contractions become more frequent, occurring every 3–5 min. They
last longer, 45–60 s and the intensity is increased. The dilatation of
the cervix reaches 4 cm and it undergoes important alterations that
make it more responsive and dilatation proceeds rapidly. In
primigravida the rate of dilatation is 1 cm per hour and in
multigravida it is 1.5 cm per hour. The active stage lasts about 6 h in
primigravida and 4 h in multigravida.
FIGURE 10.2 Phases of the first stage.
The active phase is sometimes further divided as the acceleration

phase, the phase with the maximum slope of the curve and the
deceleration phase.
Second stage
The second stage is considered as the stage of delivery of the fetus
during which the fetus is forced through the birth canal into the
outside world. It lasts from full dilatation of the cervix to the final
birth of the baby. The uterine contractions last 60–90 s and occur every
2–3 min.
■ Bearing-down pain – These occur due to voluntary expulsive efforts

by the patient, probably because of nerve reflexes being initiated by
the stretching of the vaginal wall by the presenting part. The main
expulsive effort is from the abdominal muscles and the diaphragm.
They contract during the uterine contractions to push the baby
down against the perineum.
■ Descent – The patient feels considerable pressure on her rectum and

sometimes the pain radiates down her legs due to pressure on the
sacral plexus and obturator nerve by the head, which descends into
the hollow of the sacrum. A little later, the rectum dilates exposing
its anterior wall. The head can now be seen advancing with each
contraction, and although it retreats in between the contractions
some advance is made with every contraction.
■ Crowning – Soon the perineum is stretched and the anus flattened

by the head and with each contraction a larger segment of the head
is visible. The head is said to be ‘crowned’ when its maximum
diameter stretches the vulval outlet and does not recede in between
contractions. With some extra effort the baby is now born.
The average duration of the second stage in a primigravida is 1–2 h

and ½–1 h in a multigravida. The second stage of labour is further
divided into following:
■ Pelvic phase, when internal rotation takes place
■ Perineal phase, when the baby delivers by extension
Third stage
The third stage is considered as the stage of delivery of placenta and
membranes and it starts at the birth of the baby and ends with the
complete expulsion of the placenta and membranes. As there is
retraction of the uterus after the baby is born, the placental bed is
reduced to one-third of its size in pregnancy. The placenta itself
remains unchanged and, therefore, the shearing effect starts
separating the placenta and causes retroplacental bleeding from the
torn blood vessels in the intervillous spaces which separate the
placenta further, the plane of separation being the deep spongy layer
of the decidua basalis. Usually, the whole process takes no longer than
5–15 min. However, one may wait up to 30 min, in the presence of
uterine contraction and retraction, before branding it as retained
placenta.
Phases of placental separation (as studied by ultrasonography) are
the following:
■ Latent phase – placenta-free wall contracts
■ Contraction phase – thickening of wall at placental site
■ Detachment phase – actual separation of placenta from the adjacent

uterine wall
■ Expulsion phase – sliding out of the uterine cavity
Methods of placental separation

Traditionally two methods have been described:
■ Mathew Duncan – marginal separation
■ Scultze – central separation
The signs of separation of the placenta are the following:
■ A fresh gush of blood, which occurs when the retroplacental blood

finds its way to the vagina separating the membranes.
■ An apparent lengthening of the cord as the placenta after separation

drops to the lower segment.
■ A suprapubic bulge, which occurs as the placenta, fills up the

collapsed lower segment and stretches it. The contracted upper
segment then rides over it.
Once these signs appear the placenta is usually delivered by

controlled cord traction to prevent the inversion of the uterus.
Fourth stage
The fourth stage is considered as the stage of permanent retraction of
the uterus. Some consider it as ‘golden hour’ when the obstetrician
should be highly vigilant following the completion of the third stage
of labour. This is necessary to avoid the development of complications
during the phase. One must monitor the following:
■ The fundal height and uterine consistency to ensure that the uterus
is well contracted, retracted and not relaxing
■ Vaginal bleeding – need not wait for 500 mL of blood loss to

administer uterotonins
■ Maternal vital signs – pulse and blood pressure should be recorded

every 15 min till stable
■ Urine out especially, if the patient is catheterized or having any

complications such as preeclampsia and abruption
Duration of labour
Normal duration of labour varies a great deal from one patient to the
other. The average duration of labour in primigravida and in
multigravida is given in Table 10.1.
Table 10.1
Duration of Labour
Primigravida (h) Multigravida (h)

First stage – latent phase 6–8 4–6
First stage – active phase 6 4
Second stage 1–2 ½–1
Third stage ¼–½ ¼–½
Total 10–12 8–10
Write the management/conduct of first and second stage

of labour.
answer.
Write the active management of 3rd stage of labour.
Management of the third stage of labour

Though the third stage of labour is a natural process, it is advisable to
follow principles of active management of the third stage of
labour/prevention of postpartum haemorrhage which involves the
following:
1. Administration of 10 units of oxytocin IM (oxytocin should NOT be

given as IV bolus to avoid hypotension) either at the time of delivery
of anterior shoulder (as mentioned in management of the second stage
of labour) or within 1 min of the delivery of the fetus (NOT placenta).
2. Controlled cord traction (Brandt–Andrews Method) to deliver the

placenta and membranes. It is better to wait for the signs of separation
of placenta (Fig. 10.3).
3. Massaging the uterus: This need not be done routinely according to

recent guidelines. However, as part of the protocol of prevention of
postpartum haemorrhage, it is better to massage the uterus if it is
taking time to contract and retract.
FIGURE 10.3 Brandt–Andrews method of delivering the placenta
during the third stage.
Examination of the placenta and membranes

The maternal surface is first inspected by holding the placenta on the
cup formed by palmar surface (some advocate dome formed by dorsal
surface) of the hands. The membranes, the chorion and the amnion are
now checked for completeness by holding the umbilical cord and
allowing the membranes to hang from the placenta like an inverted
umbrella. Usually the rent in the membrane is away from the
placental margins, if it is closer then placenta praevia is reconfirmed,
additional rents and abnormal vessels running across the membrane,
may indicate the presence of a succenturiate lobe of the placenta.
Suturing of episiotomy is performed (see Chapter 41 for details).
What is partogram? Describe the modified who

partogram and the method of using the same.
Partogram is a graphical representation of the first-stage events in a
single preprinted format. All events are pictorially represented on the
time axis. It mainly focuses on cervical dilatation and fetal head
descent. Progress of labour can be assessed at a glance. This record
can be easily analysed and provides a basis for early recognition of
any deviation from the normal.
Modified Who partogram (fig. 10.4)

In 2000, WHO made following changes to Philpott’s partogram:
■ Latent phase was removed.
■ Active phase started at 4 cm.
■ Descent of the head was recorded by abdominal examination.
■ Alert line and action line (4 h to the right) were made 4 h apart.
FIGURE 10.4 Modified WHO partogram.
Components of the partogram are as follows:
■ Patient information
■ Fetal heart rate (to be monitored every 15 min. See Table 8.2 for
details)
■ Amniotic fluid and moulding
■ Cervical dilatation and fetal head descent
■ Uterine contractions (to be checked every 10 min)

■ Oxytocic and other drugs administered
■ Maternal condition (vitals, urine output, urine protein ketones, etc.)
Amniotic fluid and moulding

Membrane status is recorded as follows:
■ I = Intact membranes

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Obstetrics & Gynaecology

Prep Manual for Undergraduates

Muralidhar V Pai, MBBS, DGO, MD,

Shripad Hebbar, MBBS, MD

1. Reproductive anatomy, physiology, endocrinology and

2. Placenta, fetal membranes and amniotic fluid

6. Diagnosis of pregnancy, prenatal care and high-risk pregnancy

7. Genetics, prenatal diagnosis and congenital malformations

Congenital (malformations) anomalies

8. Identification of fetus at risk, antenatal and intranatal assessment of

9. Obstetric management – decision-making. Induction of labour

10. Fetopelvic relationship, mechanism of labour, normal labour,

11. Normal puerperium

Abnormal uterine action

Rupture uterus and other soft-tissue injuries

13. Contracted pelvis and cephalopelvic disproportion. Fetal

Fetal malposition and malpresentation

14. Postpartum haemorrhage, retained placenta and inversion

15. Puerperal complications

16. Antepartum haemorrhage, placenta praevia and abruption

17. PROM and preterm labour

20. Fetal growth restriction and amniotic fluid abnormalities

22. Miscarriage (abortion), intrauterine fetal death (IUFD) and bad

Intrauterine fetal death (IUFD)

Bad obstetric history (BOH)

23. Postcaesarean pregnancy

24. Shock in obstetrics including amniotic fluid embolism

25. Renal failure in obstetrics

26. Coagulation disorders and disseminated intravascular

Dengue fever complicating pregnancy

28. Anaemia and other haematological disorders

29. Hypertensive disorders of pregnancy

30. Diabetes in pregnancy

31. Heart disease complicating pregnancy

32. Other system disorders (epilepsy, thyroid and hepatic disorders)

33. Prenatal and perinatal infections

Perinatal infectious diseases

34. Surgical problems in pregnancy

36. Neonatal resuscitation

37. Care of the newborn

38. Low-birth weight infant

39. Neonatal complications

40. Birth injuries, neurological problems and infections in the newborn

Infections in the newborn

41. Manual vacuum aspiration (MVA) and episiotomy

42. External cephalic version

43. Forceps and vacuum

45. Natural and conventional (barrier) methods of contraception

46. Hormonal contraceptives

47. Intrauterine contraceptive devices (IUCD)

48. Surgical methods of contraception

49. Medical termination of pregnancy

50. Safe motherhood initiative

51. Indicators of maternity care (maternal mortality and perinatal

52. Reproductive and child health programmes in India

53. Sustainable development goals

56. Drugs commonly used in obstetrics

57. Obstetric examination, pelvis and fetal skull