Gyne Lecture Note

OBSTETRICS AND
GYNECOLOGY
FOR
Health Science Students
Lecture Note
Obstetrics and Gynecology
For
Health Science Students
Lecture Note
Samson Negussie, Assistant Professor
M.D. Obstetrician and Gynecologist
April 2006
In collaboration with The Carter Canter (EPHTI) and

The Federal Democratic Republic of Ethiopia Ministry
of Education and Ministry of Health
TABLE OF CONTENTS
Preface i
Acknowledgement ii
About the lecture note iii
Abbreviations v
SECTION ONE – BASICS

CHAPTER Reproductive anatomy, physiology and 1
1 embryology
CHAPTER Obstetric and gynecology evaluation 9

2
SECTION TWO – NORMAL AND ABNORMAL PREGNANCY

CHAPTER 3 Normal physiology and diagnosis of 17
pregnancy
CHAPTER 4 Common minor disorders of pregnancy 22
CHAPTER 5 Antenatal care 27
CHAPTER 6 Abnormal bleeding during first and 31

second trimesters of pregnancy
CHAPTER 7 Antepartum hemorrhage 44
i
CHAPTER 8 Hypertensive disorders of pregnancy 49
CHAPTER 9 Disturbances of amniotic fluid 55
CHAPTER Premature rupture of membranes and 58

10 preterm labour
CHAPTER11 Multiple pregnancy 63
CHAPTER12 Rh isoimmunization 67
CHAPTER13 Medical disorders of pregnancy 70
SECTION THREE – NORMAL AND ABNORMAL LABOUR

CHAPTER Physiology and management of normal 84
14 labour
CHAPTER Induction and augmentation of labour 92

15
CHAPTER Operative deliveries 97

16
CHAPTER Malpresentations and malpositions 105

17
CHAPTER Dystocia 115

18
CHAPTER Obstructed labour and ruptured uterus 121
ii
19
CHAPTER Fetal distress 127

20
SECTION FOUR – NORMAL AND ABNORMAL PEUPERIUM

CHAPTER Normal puerperium and its 131
21 management
CHAPTER Postpartum hemorrhage 135

22
CHAPTER Postpartum complications 141

23
SECTION FIVE – GYNECOLOGY

CHAPTER Menustral cycle and its abnormalities 147
24
CHAPTER Climacteric and related problems 158

25
CHAPTER Vaginal discharge and vulvar pruritis 161

26
CHAPTER Pelvic inflammatory disease 167

27
iii
CHAPTER Family planning 171
28
CHAPTER Infertility 179

29
CHAPTER Tumor conditions of the female genital 183

30 tract
CHAPTER Uterovaginal prolapse and urinary 193

31 incontinence
PREFACE
Ethiopia is one of the countries in the world with unacceptably
high maternal mortality rate. Various strategies are being
implemented to reduce this rate and improve the overall health
of women. One such strategy is ensuring the provision of
preventive, curative and rehabilitative health services to the
population by improving access and quality of services by
training competent midlevel and front line health workers.
Currently a number of higher learning institutions are involved in
the training of health officers. One of the objectives of health
officer training is producing competent professionals capable of
delivering comprehensive emergency obstetric care and
managing other common gynecologic problems.
One of the problems encountered during the training is
shortage of standardized training materials gauged to meet the
objective of the health officers training. Different training
institutions use different text materials and the emphasis given
iv
to different topics varies. The emphasis given to common
obstetric and gynecologic topics prevalent in resource poor
countries varies greatly.
The Ethiopian Public Health Training Initiative (EPHTI) has
recognized this critical problem and was involved in
development of standardized training materials (modules and
lecture notes) in different public health and clinical subjects.
This lecture note is prepared to help in standardizing the
training in different teaching institutions. It also aims to provide
a quick reference for students and is believed to initiate further
reading. This final version was designed and prepared to
address the needs of health officer training. It emphasizes
mainly on detection, diagnosis and management of emergency
obstetrics problems and common gynecologic diseases.
v
vi
ACKNOWLEDGEMENT
My deepest gratitude goes to The Carter Center and the

Ethiopian public health training initiative for providing technical
and financial support. Special thanks goes for Ato Aklilu
Mullugeta whose unrelenting follow up made this lecture note a
reality. The following people were involved in the development
of the first draft and need to be credited: Dr. Habtemariam
Tekle (Gondar University), Drs. Fassil Mengistu and Endris
Mohammed (Debub University), Dr Mussie Abera (Alemaya
University) and Dr. Zerai Kassaye (Jimma University).
I am highly indebted to Dr. Solomon Kumli, Dr. Yirgu G/Hiwot of

Addis Ababa University, Gynecology and Obstetric department
for their constructive comments and suggestions without which
this lecture note wouldn‘t have takes its present shape.
vii
ABOUT THE LECTURE NOTE
Organization
This lecture note is organized into five sections. The first

section deals with the basic topics needed to deal with
obstetrics and gynecology. A short summary of anatomy,
physiology and embryology of the female genital tract is
followed by an outline of obstetric/ gynecologic history and
physical examination. The second section deals with normal
changes of pregnancy, antenatal care and various antenatal
complications of pregnancy. The third section gives description
of normal and complicated (abnormal) labour along with their
management. The fourth section is entitled for puerperium and
abnormalities associated with postpartum period. The final
section deals with normal menustral cycle and different
gynecologic problems. Review questions follow each chapter.
Because of repetition of reference materials used for each
topic, the author preferred to give references for the different
topics are given at the end of each section. Malpresentations
are included in section three (normal and abnormal labour)
because of their importance in terms of maternal and neonatal
complications is related to their occurrence in labour and the
need to stress the different emergency maneuvers used in
malpresentation for a health officer student. In section five
(gynecologic section) related topics are lumped under one
viii
chapter. Tumor conditions of the female genital tract are
organized into benign and malignant conditions.
Preparation
Preparation of this lecture note was started some 18 months

back. Representatives from four different universities (Alemaya,
Jimma, Gondar and Debub now Awassa) divided the topics
among themselves and took the task of developing the first
draft. The then Debub University (now Awassa University) took
the task of compiling and editing the first draft. During this
reviewing/ editing process a number of problems were
encountered. The major one is most of the draft developed was
so detailed and did not take into consideration the level of
competence required of a health officer. The other is failure to
get the first draft from some of the universities in time. Internal
reviewing done on the available draft suggested significant
remodeling to be done on the first draft. Modification/ rewriting
of the first draft to meet the above objective could not be done
in time because of the fact that most of the professionals
involved in the development of the first draft left their respective
universities. So finalization of the lecture note was delayed.
After discussion with the responsible people in The Carter
Center, the author took the responsibility of reshaping and
rewriting the final version of this lecture note. During this
preparation the curriculum for health officer training, the first
ix
draft and different references were consulted and appropriate
modifications were made. Financial and other technical support
was provided by The Carter Center.
This final version was designed and prepared to address the

needs of health officer training. It emphasizes mainly on
detection, diagnosis and management of emergency obstetrics
problems and common gynecologic diseases. Conditions that
can not be diagnosed/ managed at a health center setting and/
or require specialist care are omitted or are briefly mentioned.
Application
This lecture note is designed to be used by a health officer

student as a guide for further reading. It can also be used as a
quick reference by other cadre of health science students
(medical students, midwives and nurses) taking obstetrics and
gynecology as part of their training. It can be used as a
reference by instructors of Obstetrics and Gynecology.
Limitations
This lecture note is by no means a replacement for standard

texts in obstetrics and gynecology. It only gives an outline of the
important aspects of the topics that are relevant for health
officer training. It omits detailed description of some aspects of
the topics involved. Some topics not included in the curriculum
are not included in this lecture note. Sophisticated and recent
x
diagnostic/ treatment modalities not applicable in the setting a
health officer works and details of pathogenesis are not given
due emphasis. The user is thus advised to use the mentioned
references for such details.
xi
ABBREVIATIONS
ACTH – Adrenocorticotrophic hormone
AFI – Amniotic fluid index
ANC – Antenatal care
ARM – Artificial rupture of membranes
APH - Antepartum hemorrhage
AUB – Abnormal uterine bleeding
BPD – Biparietal diameter
CPD – Cephalopelvic disproportion
C/S – Caesarian section
DNA – Deoxyribonucleic acid
DUB – Dysfunctional uterine bleeding
DVT – Deep vein thrombosis
E&C/ D&C – Evacuation and curettage/ dilatation and

curettage
EDD – Expected date of delivery
FHB – Fetal heart beat
GH – Growth hormone
xii
GTD – Gestational trophoblastic tumors
HCG – Human chorionic gonadotrophic hormone
HDP – Hypertensive disorders of pregnancy
HPO – Hypothalamo pitutary ovarian axis
IUCD – Intrauterine contraceptive devise
LMP/LNMP – Last menustral period/ last normal

menustral period
MSH – Melanocyte stimulating hormone
MTCT – Mother to child transmission
MVA – Manual vacuum aspiration
OCP – Oral contraceptive pills
OL – Obstructed labour
PAC – Post abortion care
PID – Pelvic inflammatory disease
PIF – Prolactin inhibitory factor
PIH – Pregnancy induced hypertension
PMI - Point of maximum impulse
PMS - Premenstrual syndrome

xiii
PPH - Post partum hemorrhage
PROM - Premature rupture of membranes
POP – Progestin only pills
RH - Rhesus factor
STD/STI – Sexually transmitted diseases/ sexually

transmitted infections
TORCH
TSH – Thyroid stimulating hormone
UTI – Urinary tract infection
VDRL – Venereal disease research laboratory
xiv
PART I: BASICS
CHAPTER 1
REPRODUCTIVE ANATOMY, PHYSIOLOGY
AND EMBRYOLOGY
By Dr. Habtemariam Tekle
Learning objective
 To know the anatomy of the female reproductive system
 To know the physiology of the female reproductive system
 To know the normal development of the female genital

tract
Introduction
It is mandatory to know the anatomy and physiology of the

female reproductive system to manage obstetric and
gynecologic problems.
1. ANATOMY OF THE FEMALE PELVIC ORGANS
1.1. External female genitalia (vulva or pudendum )
1.1.1. Anatomic landmarks
The vulva includes mons pubis, labia majora, labia minora,

clitoris, vestibule and perineum which are all visible on external
1
examination. It is bounded anteriorly by the mons pubis,

laterally by the labia majora and posteriorly by the perineum.
A. Mons Pubis
It is the pad of subcutaneous fatty tissue in front of the pubis. It

is covered by the pubic hair in inverted triangle fashion.
B. Labia majora
It is the elevation skin and subcutaneous tissue which forms the

lateral boundaries of the vulva. Posteriorly each labia majora
fuses medially to form the posterior commissure. The labia
majora contains sebaceous glands, sweat glands and hair
follicles. The dense connective tissue and adipose tissue
beneath the skin is richly supplied with venous plexus which
may produce hematoma, if injured. The labia majora are
homologous with the scrotum in the male.
C. Labia minora
These are two thick skin folds, devoid of fat, lying on either side
within the labia majora. Anteriorly they are divided to enclose
the clitoris and unite with each other in front and behind the
clitoris to form the prepuce and frenulum respectively.
Posteriorly each labia minora fuse to form a fold of skin called
fourchette. Labia minora don not contain hair follicle. It is
homologous with the ventral aspect of the penis.
2
D. Clitoris
This is a small cylindrical erectile body situated in the most

anterior part of the vulva. It consists of the glans, body and two
crura. It is analogous to the penis in the male.
E. Vestibule
It is a triangular space bounded anteriorly by the clitoris,

posteriorly by the fourchette and on either side by labia minus.
There are erectile tissues bilaterally situated beneath the mucus
membrane called the vestibular bulb. Each bulb lies anterior to
the Bartholin‘s gland and is incorporated within the
bulbocavernous muscles. They are homologous to the single
bulb of the penis and corpus spongiousum in the male.
There are four openings into the vestibule.
I. Urethral opening which is situated in the midline just

anterior to the vaginal orifice.
II. Vaginal orifice which is located posterior to the urethral

opening. In virgins and nulliparous the opening is closed
by the labia minora but in parous, it may be exposed. The
orifice is incompletely closed by a septum of mucus
membrane called hymen.
III. Bartholin’s duct opening (one on each side): The

Bartholin‘s glands are situated in the superficial perineal
3
pouch posterior to the vestibular bulb. It secretes abundant

alkaline mucus, during sexual excitement which helps in
lubrication. Each gland has got a duct which opens just
anterior to the Hymen. The Bartholin‘s gland corresponds
to the bulbourethral gland in the male.
F. Perineum (Perineal body)
This is a pyramidal shaped tissue where the pelvic floor and the
perineal muscles and fascia meet. It is located between the
vagina and the anal canal.
1.1.2. Blood supply of the Vulva
A. Arteries
Branches from the internal pudendal arteries (labial artery,

transverse perineal artery, artery to the vestibular bulb and
deep and dorsal arteries to the clitoris) and femora artery
(superficial and deep pudendal arteries) supply the different
parts of the vulva.
B. Veins
4
The veins of vulva form plexus and drain into internal pudendal
vein, vesical or vaginal venous plexus and the long saphenous
vein.
1.1.3. Nerve supply to the vulva
It is supplied by cutaneous branches from the ilioinguinal,

genital branches of genitofemoral nerve, pudendal branches
from the posterior cutaneous nerve of the thigh and labial and
perineal branches of pudendal nerve.
1.2. Internal female genital organs
The internal genital organs in female include vagina, uterus,

fallopian tubes and the ovaries. These require special
instruments for inspection.
A. Vagina
It is a fibro-musculo-membraneous canal communicating the

uterine cavity to the exterior at the vulva. It has four walls:
anterior, posterior and two lateral walls. The length of the
anterior wall measures 7 centimeters and the posterior wall is
about 9 centimeters. The projection of the cervix through the
anterior vaginal wall at the top of the vagina (vault) creates
clefts known as fornices. There are four fornices (anterior,
posterior and two lateral).
5
Its wall is composed of four layers. The four layers from within
to outwards are mucus membrane lined by stratified squamous
epithelium, sub mucous layer, muscular layer( inner circular and
outer longitudinal) and fibrous coat.
The vaginal secretion is very small but sufficient to make the

surface moist. The pH is acidic and ranges between 4.0- 5.5 in
reproductive age groups. The Doderlin‘s bacilli are responsible
for conversion of Glycogen from the exfoliated squamous cells
to lactic acid.
The vagina serves as excretory channel for menstrual blood

and uterine secretions, organ for sexual intercourse and
passage for the fetus during birth.
Blood supply
The arteries supplying the vagina are cervico vaginal branch of

the uterine artery, vaginal artery (a branch fro internal iliac
artery), and middle rectal and internal pudendal artery. These
anastomose with one another and form two azygous arteries,
one anterior the other posterior.
Veins drain into internal iliac and internal pudendal veins.
B. Uterus
6
This is a hollow pyriform muscular organ situated between

bladder and rectum. It is normally anteverted and anteflexed. It
measures 8 centimeters long, 5 centimeters wide and 1.25
centimeters thick. It has three parts.
I. Body or corpus which is the part between the isthmus

and the opening of the fallopian tubes. The part that is
above the opening of the fallopian tubes is called the
fundus.
II.Isthmus is a constricted part situated between the body

and the cervix. It measures about 0.5 centimeters.
III. Cervix is the lower most part of the uterus which is

cylindrical in shape and measures about 2.5 centimeters.
It is divided into supravaginal part (part lying above the
vagina) and portiovaginalis (which lies within the vagina).
It has two openings the internal os and the external os
with cervical canal in between.
The uterine wall consists of three layers.
I. Perimetrium is the serous coat covering the underlying

myometrium
II. Myometrium consists of thick bundles of smooth muscles

arranged in various directions.
7
III. Endometrium is the mucus lining of the endometrial

cavity. It consists of the surface epithelium and laminia
propiria.The surface epithelium is a single layer of
ciliated columnar epithelium and the lamina propria
contains stromal cells, endometrial glands, vessels and
nerves.
Blood supply
The arterial supply is mainly from the uterine artery and the
other sources are vaginal and ovarian arteries.
The venous channel corresponds to the arterial course and

drain into internal iliac veins.
C. Fallopian Tube
The uterine tubes are paired structures which are attached to

the lateral angle of uterine cavity. It has four parts intramural or
interstitial (part inside the uterine wall), the isthmus (the straight
part), ampulla (the tortuous part) and the infundibulum. The
abdominal ostium is surrounded by a number of radiating
fimbria, one of these is longer than the rest and is attached to
the outer pole of the ovary - ovarian fimbria.
D. Ovary
8
Ovaries are paired sex glands or organs. Each measures

3centimetres by 2 centimeters by 1 centimeter. Each is
attached to the uterus by the utero-ovarian ligament, to the
lateral pelvic wall by infundibulopelvic ligament and to the
posterior wall of the broad ligament by the meso-ovarium.
They are covered by a single layer of germinal epithelium. The

substance of the ovary has cortex and medulla. The cortex is
the functional layers which include primordial follicles, mature
follicles, Graffian follicles, corpus luteum and atretic follicles or
corpus albicans. Medulla consists of loose connective tissue,
muscle cells, blood vessels and nerves and hilus cells.
Blood supply
Arterial supply is from the ovarian artery, a branch of the

abdominal aorta. Venous drainage is through pampiniform
plexus to form ovarian veins which drain to inferior vena cava
on the right side and to the left renal vein on the left side.
Nerve supply
It receives sympathetic supply from T10.
2. PHYSIOLOGY OF THE FEMALE REPRODUCTIVE

ORGANS
The physiology of female reproductive system is concerned

with the functions from birth through puberty and adult hood to
9
the menopause. This is achieved through the neuroendocrine

mechanism that involves the cortico-hypothalamic-pituitary-
ovarian axis. The hypothalamo pitutary ovarian axis is a well
coordinated axis and the hormones liberated from the
hypothalamus, pituitary and the ovary are dependent on one
another.
The secretion of the hormones from these glands is modified

through feedback mechanisms operating through this axis. The
axis may also be modified by hormones liberated from the
thyroid and adrenal glands.
A. Hypothalamus
It produces specific releasing and inhibitory hormones or factors

which have effect on the production of pituitary hormones.
I. Gonadotrophic releasing hormones (GnRh) is concerned

with the synthesis storage and release of gonadotrophic
hormones, FSH and LH.
II. Prolactin inhibitory factor/ hormone (PIF) inhibits the

release of prolactin.
III. Thyrotrophin releasing hormone (TRH) stimulates the

release of TSH.
10
IV. Corticotrophin releasing hormone (CRH) stimulates

the release of ACTH.
V. Growth hormone releasing hormone stimulates the

release of growth hormone.
B. Pituitary
It has two parts, the anterior pituitary (adenohypophysis) and

the posterior pituitary (neurohypophysis).
The adenohypophysis produces
I. Gonadotrophins which include follicle stimulating hormone

(FSH) and leutinizing hormone (LH). FSH is mainly
stimulates the growth and maturation primary ooytes of
which only one develops into graffian follicle. In
conjunction with LH, it is also involved in ovulation and
steriodeogenesis. The main function of LH is
steriodeogenesis but along with FSH, it is responsible for
full maturation of the Graffian follicle and ovulation.
II. Prolactin is responsible for the production of the milk in the

breast.
III. The other hormones TSH (thyroid stimulating

hormone), ACTH (adrenocorticosteroid hormone), GH
(growth hormone) and MSH (melanocyte stimulating
hormone).
11
C. Ovary
The function of ovary is ovulation and production of ovarian

hormone. The major ovarian hormones are estrogen and
progesterone, also called the female sex hormones. The other
hormones produced by the ovary are androgens and inhibin.
Estrogen is produced by granulosa cells. Its functions include
I. Development of female secondary sexual characteristics

including deposition of fat in the breast, thighs & hips and
growth and development internal & external female genital
organs.
II. Decreases FSH and LH secretion by negative feedback

mechanism during the menstrual cycle except at mid cycle
at which time it increases LH secretion by positive
feedback mechanism.
III. In the breast it stimulates the growth of the ducts and

fat deposition.
Progesterone is secreted by the lutenized theca granulosa

cells. Its functions are
I. Increases the glandular secretions of the endometrium and

diminishes the contractility of myometrium.
II. Stimulates the growth of the acini in the breast.
III. In large doses it inhibits LH secretions.

12
IV. Increases basal body temperature.
Androgens are produced mainly by the theca interna cells. They

are source for estrogen synthesis. Inhibin and relaxin are other
hormones produced by ovary.
Hypothalamo-Pituitary-Ovarian (HPO) Axis at different

stages of life
I. Fetal life- HPO axis remains active and functional from 20

weeks of life.
II. Infancy and childhood- high level of FSH and LH at birth

gradually decline and minimum level achieved by two
years of age.
III. Prepuberity – hypothalamus is very much sensitive to

negative feedback by even a small amount of estrogens
(estrogen produced by peripheral conversion of
testosterone to estrogen). Hence, FSH and LH secretions
are inhibited.
IV. Puberty –hypothalamus become more insensitive to

estrogen to estrogen negative feedback. Hence
increasing amounts of GnRH, FSH and LH are secreted,
which in turn stimulate the ovary to secrete estrogen and
progesterone. This eventually results in thelarche,
adrenarche and menarche.
13
V. Pregnancy- the gonadotrophins level remains low.
VI. Menopause- ovarian follicles become scarce and

resistant. Hence FSH and LH levels increase while
estrogen and progesterone levels decrease.
3. EMBRYOLOGY OF THE REPRODUCTIVE ORGANS
Introduction
IN EARLY PREGNANCY, BOTH INTERNAL AND

EXTERNAL GENITAL ORGANS ARE
UNDIFFERENTIATED. DURING DEVELOPMENT,
BECAUSE OF ―X‖ AND ―Y‖ CHROMOSOMES AND OTHER
HORMONES, THE UNDIFFERENTIATED GENITALIA
DIFFERENTIATE EITHER TO MALE OR FEMALE
GENITAL ORGAN. MALE SEX IS AN INDUCED SEX
BECAUSE IT REQUIRES SPECIFIC MESSAGES TO
DEVELOP. GENITAL AND URINARY SYSTEMS ARE IN
CLOSE PROXIMITY. DURING DEVELOPMENT OF ONE
SYSTEM INDUCES THE DEVELOPMENT OF THE OTHER
SYSTEM. THIS EXPLAINS WHY CONGENITAL
MALFORMATIONS OF GENITAL SYSTEM ARE OFTEN
ASSOCIATED WITH ABNORMALITIES OF URINARY AND
MUSCULOSKELETAL SYSTEM.
Development of gonads
14
On fourth week after fertilization, primordial germ cells migrate

from yolk sac through the mesentery of the hind gut to the
posterior body wall mesenchyme at the tenth thoracic level.
Their arrival induces proliferation of adjacent mesonephros and
celomic epithelium to from the genital ridge. The celomic
epithelium forms the cortex, the mesenchyme forms the
medulla and the germ cells originate from the endoderm. This
stage of gonadal development is called the indifferent stage
(bipotential gonads).
Further development is influenced by the Y chromosome which

has the sex determining region (SRY). In its presence the
indifferent gonad develops into testis. In its absence like in XX
or XO fetus it develops into an ovary.
In further development of the ovary the medulla regresses to

form rete ovary and the cortex forms the ovarian follicles.
Between the seventh and ninth months the ovary descends to
the pelvis to be attached to the ligaments.
Development of internal female genital organs
Two major ducts give rise to the internal genital organs, namely
the Wollfian duct (male duct) and the Mullerian duct (female
duct). In the presence of testis the Wollfian duct develops
(effect of testosterone produced by Leydig cells) and the
Mullerian duct regresses (effect of Mullerian regressing factor
produced by the Sartoli cells). But, in the absence of functional
15
testis the reverse happens. The Mullerian duct is formed by

invagination of celomic epithelium. The two Mullerian ducts
grow downwards and medially. Eventually their lower ends fuse
into one. Further development results in cavitations to form
hollow organs at fifth month of gestation.
The fallopian tubes develop from upper unfused horizontal part

of the Mullerian duct. Uterus develops from intermediate
horizontal and adjoining vertical part of Mullerian duct. The
lining epithelium and glands develop from coelomic epithelium.
Myometrium and endometrial stroma arise from mesoderm.
Broad ligament is formed as a broad transverse fold as the
Mullerian ducts approach midline. It extends from lateral side of
fused duct to pelvic side wall. It has vestigial remnants like
epoophoron, paroophoron and ducts.
Vagina is formed in third month of gestation. There are two

concepts for the development of vagina. One says the whole
vagina is developed from the urogenital sinus. The other argues
that vagina is mainly developed from Mullerian duct with only
one third contributed by the urogenital sinus.
Development of External genital Organs
16
In the fifth week of embryonic life, folds of tissue form on each

side of cloacae. Development of coronal partition, called
urorectal septum, separates the endodermal cloacae into two
parts. The dorsal part, which at its lower end is covered by the
anal membrane, develops into rectum and anal canal. The
ventral part which is now called the urogenital sinus develops
into the external genital organs. It lower end is lined by the
bilaminar urogenital membrane. The site of fusion between
urorectal septum and the urogenital membrane is the primitive
perineal body.
Further development of the urogenital sinus differentiates it into

three parts. The upper or vesicourethral part forms the mucus
membrane of bladder and major part of female urethra. The
middle pelvic part receives the united caudal part the two
paramesonephric (Mullerian) ducts in the midline. It later gives
rise to the epithelium of the vagina, the Bartholin‘s gland and
the hymen. The lower phallic part is lined by the bilaminar
urogenital membrane. The phallic part has one genital tubercle,
and two genital folds and urogenital swellings (labioscrotal
folds).
Clitoris is developed from the genital tubercle. Labia minora are

developed from the genital folds. Labia majora are developed
from urogenital swellings (labioscrotal swellings). Bartholin‘s
Glands develop as out growth from the caudal part of the
17
urogenital sinus. Vestibule develops as urogenital groove from

urogenital sinus. Hymen is developed from the junction of the
sinovaginal bulbs and urogenital sinus.
Some congenital malformations
Failure of development of both mullerian ducts results in

absence fallopian tubes, uterus, and upper two thirds of vagina
(Mullerian agenesis).
Failure of development of one mullerian duct results in

unicornuate uterus with single oviduct.
Failure of recanalization of the lower part of the fused Mullarian

duct results in isolated atresia of upper vagina and cervix
causing hematometra.
Failure of fusion of mullerian duct depending on the degree

results in uterus didelphys with two cervix and vagina
canals, arcuate uterus and uterus bicornis.
Fallopian tube abnormalities are not common. Rarely

accessory ostia or diverticulum or abnormally short or long
tubes may occur.
Failure of canalization of the urogenital membrane results in

imperforate hymen. Failure of development of the external
genitalia results in ambiguous genitalia.
18
Reminants of Wollfian duct result in Gartner’s cyst found in the

upper part of the vagina.
19
CHAPTER 2
OBSTETRIC AND GYNECOLOGIC EVALUATION
By Dr. Habtemariam Tekle
Learning objective:
 To enable the student take proper history and physical

examination to reach to the diagnosis.
Introduction
To come to a clear understanding of a patient‘s problem,

detailed history and physical examination is important.
1. OBSTETRICS HISTORY & PHYSICAL

EXAMINATION
1. History
1.1. Identification
 Name
 Age – significant if less than 20 years and greater

than 35 years
 Martial status
 Address- far distance from health institution
 Religion
20
 Occupation
 Date of admission
 Ward and bed number
1.2. Chief complaints-
Patients may have come for routine antenatal care follow up or

may come with one or more specific complaints. Note the
duration of each complaint.
1.3. History of present pregnancy
Get information on the following points
 Gravidity- all forms of pregnancy whether it is term, live

births, still birth, abortion, ectopic pregnancy or molar
pregnancy.
 Parity- fetus delivered after 28 weeks of gestation for

Ethiopia and United kingdom and greater than or equal
to 20 weeks – according to WHO
 Abortion
 Last normal menstrual period (LNMP)
 Expected date of delivery (EDD) which could be

calculated by
1- Naegale‘s rule (using European calendar)
21
- LNMP- 3 months + 7 days
2- Ethiopian calendars
 NLMP+ 9 months +10 days if pagume is not

passed
 NLMP+ 9 months + 5 if pagume is passed ( 4 in

leap year )
 Calculate gestational age in completed weeks and

days
 Quickening – the first time the mother felt fetal

movement
- In primigravida it is around 18-20 weeks

and in multigravida at 16-18 weeks of
gestational age.
- Used to date pregnancy if LNMP is

unknown
 Presence of antenatal care elsewhere. place and

number of visits.
 Elaboration of chief complaints
 Danger symptoms of pregnancy (vaginal bleeding,

severe headache, blurring of vision, epigastric or
severe abdominal pain, profuse vaginal discharge,
22
absence or reduction of fetal movement, fever,

persistent vomiting)
 Common complaints in pregnancy ( like nausea and

vomiting, weakness
 Pregnancy - unplanned , unwanted and unsupported
 Ask positive and negative statement according to the

patient complaints
1.4. PAST OBSTETRIC HISTORY
The following should be asked for all previous

pregnancies in chronologic order
 Date, month and year of gestation for example first

delivery in May 2000
 Length of gestation - abortion (< 28 weeks),

preterm (<37 completed weeks), term (>37
completed to 42 completed weeks), post term
(greater than 42 completed weeks)
 Significant antenatal medical problems like

hypertension, ante partum hemorrhage, diabetes
 Onset of labor (spontaneous or induced)
 Fetal presentation
 Duration of labor
23
 Mode of delivery (spontaneous vaginal,

instrumental, caesarian section, destructive
delivery)
 Fetal outcome (alive or dead, sex of the newborn,

weight of the newborn, malformations, current
condition)
 Post partum complications postpartum hemorrhage
1.5. GYNECOLOGY HISTORY
 Family planning methods - use , type , duration

and side effects
 Sexual history- assess risk of sexually transmitted

infections and HIV/AIDS
 Gynecology operations- Female genital mutilation ,

laparatomy, dilatation and curettage ,evacuation
and curettage, manual vacuum aspiration
 Menstrual history ( age of menarche, interval of

period 21-36 days, amount of flow 10 –80 ml,
duration of flow 1-8 days, normally dark red and
non-clotting).
1.6. PAST MEDICAL AND SURGICAL HISTORY
24
 History of diabetes mellitus, hypertension, hypo or

hyper thyroidism which may the affect
pregnancy or get aggravated by pregnancy
 Blood transfusion important in hemolytic disease

of new born
 Drugs risk of teratogenicity or allergic reactions
 Maternal infection – TORCH Syndrome.
1.7. PERSONAL, FAMILY AND SOCIAL HISTORY
 Childhood development
 Educational status
 Habits like alcohol , smoking and elicit drugs
 Occupation- exposure to radiation, anesthesia-

halothane, chemical factory and others
 Income- low socio-economic status associated with

obstetric problems like preeclampsia ,preterm
labor
 Family history- diabetes mellitus, hypertension,

multiple pregnancy, genetic disorders
1.8. REVIEW OF SYSTEMS
25
 CHECK ALL SYSTEMS
2. Physical examination
Examination must be done in a private room in the presence of

a chaperone. Proper explanation must be offered to the patient
before during and after the examination. Bladder should be
emptied and the patient properly positioned on the couch.
Warm hands and instruments must be used. Adequate light,
appropriate gloves and swabs should be prepared. Always
keep eye contact throughout the examination.
2.1. GENERAL APPEARANCE
2.2. Vital signs and anthropometric measurements
 Blood pressure positions include left lateral with

300 tilt to the left to avoid supine hypotensive
syndrome or sitting position in ambulatory patient.
 Pulse rate -increases 10-15 beats/minute in

pregnancy
 Respiratory rate -increases 1-4 breath /minute in

pregnancy
 Temperature
26
 Weight – increment of more than 1kg/week is

abnormal
 Height- less than 150 centimeters could be

constitutional but may be a risk factor. Strikingly
short for every society is risk factor.
2.3. HEENT
 Emphasis on conjunctiva, sclera, teeth and buccal

mucus membrane to see pallor, jaundice, mucosal
congestion and dental carries.
2.4. Lymphoglandular System
 Thyroid gland for hyper or hypo thyroidism signs.
 Breast for nipple refraction, pigmentation, lumps,

discharge, colour change
2.5. Respiratory and cardiovascular system
Steps in examination are essentially same as non

pregnant patient. Note that the following are normal
findings in pregnancy.
 Decreased diaphragmatic excursion due to

diaphragm elevation by gravid uterus
 PMI deviation to left is possible in pregnancy
 S3 gallop may be heard

27
 Functional systolic murmur may be heard
2.6. Abdomen
2.6.1Inspection
 Linea nigra- midline hyper pigmentation due to

melanocyte stimulating hormone
 Striae gravidarum – purplish in new striae and

white in old striae. In both cases is due to
distension, which causes stretching.
 Umbilicus may be inverted, flat or everted
 Surgical or non surgical scar
 Distended veins, flank fullness, fetal movement
2.6.2. Palpation
 Superficial palpation – checks for rigidity,

tenderness, superficial mass and characterize it,
abdominal wall defects.
 Deep palpation – palpate for mass, organomegally

and characterize the mass
 Obstetric palpation or Leopold‘s maneuver
A. The first Leopold maneuver or fundal palpation
28
I. Fundal height measurement: first correct for

asymmetry before measurement. Then use one
of the following methods:
1- Finger method – one finger above

umbilicus is equal to two weeks and below
umbilicus one finger is equal to one week.
Uterus felt at symphysis corresponds to 12
weeks. At the umbilicus it is 20 weeks and
at xiphysternum it is 38 weeks.
2- Tape measurement: symphysis to funded

height in centimeter with tape meter
between 18-34 weeks is accurate to within
two weeks of actual gestational age.
II. Determine what occupies the fundus. If soft,

irregular bulky mass is found it is the breech. If
hard round ballotable mass is found, it is the
head.
B. The second Leopold maneuver or lateral

palpation
I. Determines the lie of the fetus which could be

longitudinal, transverse or oblique lie. .
II. In longitudinal lie it determines on which side

of the abdomen is the fetal back. The back of
29
the fetus is linear, rigid and smooth in outline.

The extremities are felt as small irregular and
bulky masses. The fetal heart beat is best heard
on back side.
C. The third Leopold maneuver or Pelvic

palpation
I. Determines what part of the fetus occupies

the lower uterine pole which is also called the
presentation. The possibilities are the head
(cephalic presentation), the breech (breech
presentation), and the shoulder (shoulder
presentation).
II. In cephalic presentations it determines the

descent by using rule of fifth which measures
the distance between upper border of the
symphysis to anterior shoulder.
5/5 is floating head, 4/5 is fixed head, 2/5

denotes engaged head.
III. In conjunction of the findings of the second

maneuver it determines the attitude of the fetus
(relation of head to the trunk). In extended
attitude the cephalic prominence is on the same
side of the back. In flexed attitude the cephalic
30
prominence is on the opposite side of the back.

In military attitude the cephalic prominence is felt
on both sides at the same level.
D. The fourth Leopold maneuver or Pawlik grip
It is the only maneuver that is done with one

hand. It assesses presentation of he fetus.
2.6.3. Percussion
 Shifting and flank dullness
 Fluid thrill
2.6.4. Auscultation
 Fetal heart beat is first heard in the back side at16-

18 weeks in multiparas and 18-20 weeks in
primigravida. In complete breech it is heard above
umbilicus. In cephalic presentations it is below
umbilicus .IN occipito posterior it is heard in the
flanks. .
2.7. GENITOURINARY SYSTEM
 COSTOVERTEBRAL AND SUPRAPUBIC TENDERNESS
 Pelvic examination- to be done two times in

pregnancy except in cases of complications and if
labor is suspected
31
I. First trimester (early) – To diagnose

pregnancy, for dating of the pregnancy by
measuring uterine size and to diagnose pelvic
problems
II. Late in pregnancy greater than 37 weeks
A. To diagnose contracted pelvis (refer

chapter on)
- B. To assess Bishop score- (refer to

chapter on induction)
III. In labor assess cervical dilatation and

effacement, status of the membranes and color
of liquor, presenting part, station of presenting
part and position, molding, caput, clinical
pelvimetry.
2.8. INTGUMENTARY SYSTEM
 HYPER PIGMENTATION ON BREAST, LOWER AND MID LINE

ABDOMEN GENITALIA ARE NORMALLY SEEN IN PREGNANCY
 Vascular Changes- Spider angiomata and palmar

erythema
2.9. Extremities
 Check for edema, dilated vessels and calf

tenderness.
32
Dependent edema (pretibial and pedal), seen in 80%

of normal pregnancies. Pathological edema (non
dependent) involves the face, fingers or the whole
body.
2.10. Central nervous system
 As non pregnant
2. GYNECOLOGY HISTORY AND PHYSICAL EXAMINATION
1. History
1.1. IDENTIFICATION
 AS OBSTETRIC HISTORY
1.2. Chief complaints
Patient comes with the following gynecologic

complaints. The common complaints are cessation of
menses, vaginal bleeding and discharge, lower
abdominal pain or deep pelvic pain, pain during
intercourse (dysparunia), pain during menstruation
(dysmenorrhea), protruding mass out of the introitus,
genital ulcer, urinary incontinence and others.
1.3. HISTORY OF PRESENT ILLNESS
 Gravidity, parity and abortion
33
 Detail of each complaint (localization, duration,

date and time of onset, aggravating and relieving
factors, sequence of symptoms, evolution with
time, effect on life style, relation to menstrual cycle
and others)
 LMP should be included details of menstrual

history if pertinent to the complaints
 Negative and positive statements pertinent to the

presenting complaint
 Treatment received
1.4. MENSTRUAL HISTORY
 Age of menarche
 Interval between period
 Duration of flow
 Amount & character of flow
 Dysmenorrhea , premenstrual symptoms
 Age of menopause
1.5. GYNECOLOGIC HISTORY
1.6. PAST OBSTETRIC HISTORY
34
1.7. PAST MEDICAL AND SURGICAL HISTORY
1.8. PERSONAL SOCIAL FAMILY, HISTORY
1.9. REVIEW OF SYSTEMS
 AS OBSTETRICS HISTORY
2. Physical examination
PREPARATION FOR EXAMINATION IS SIMILAR TO

OBSTETRIC EXAMINATION. IN ADDITION SLIDES,
APPLICATOR, TEST TUBE, GLOVES, SPECULUM AND
FIXATIVE ARE NEEDED.
2.1. GENERAL CONDITION
2.2. Vital signs
 Blood pressure,pulse rate, respiratory rate,

temperature
2.3. HEENT
 As nonpregnant
2.4. Lymphoglandular system
35
 Lymph nodes- to see for metastatic cancer

check mainly supraclavicular and axillary
nodes.
 Thyroid gland- hypo and hyper thyroidism

affects reproductive function
 Breast examination- inspection and palpation
2.5. Chest and cardiovascular system
 As non pregnant
2.6. ABDOMEN
 AS NON PREGNANT (INSPECTION,

AUSCULTATION, PALPATION AND
PERCUSSION)
2.7. GENITOURINARY SYSTEM
 COSTOVERTEBRAL AND SUPRAPUBIC

TENDERNESS
 PELVIC EXAMINATION
I. Examination of external genitalia
Pubic hair- diamond shaped in male and

inverted triangle in female.
Labia majora and minora – ulcer, swelling

and ` discoloration
36
Discharge from urethra and vaginal

introitus
Hymen- intact or torn
II.Speculum Examination
Vagina- note color (normally pink), vaginal

septum, rugae folds, fornices,
discharge, scar, laceration
Cervix – note color (normally pink) pink,

cervical os (pin- pointed in nulliparous
and slit-like in multiparous), dilatation,
effacement and bleeding, mass
III. Digital vaginal & bimanual pelvic examination
Vagina- mass and tenderness
Cervix- Closed normally, moves 2- 4cm

with out discomfort, smooth surface and like tip
of nose in consistency.
Uterus- normally non-tender, mobile, 9 cm

in length, pear shaped smooth and firm.
Adnexa (tubes, ovaries, parametrium and

broad ligaments): normally adenexal
structure not palpable except in thin women
with soft abdomen, description of masses.
37
IV- Rectal and recto vaginal examination
Rectal examination- In virgin and children
Rectovaginal examination- For rectovaginal

and uterosacral ligament nodularity or
malignant infiltration
To differentiate rectocele from enterocele
2.8. Intgumentary
 As non pregnant
2.9. Extremities and central nervous system
 As non pregnant
PART II
NORMAL AND COMPLICATED
PREGNANCY
38
39
CHAPTER 3
NORMAL PHYSIOLOGY & DIAGNOSIS OF

PREGNANCY
Learning Objective:
 To describe the important physiologic changes in each

organ system during pregnancy
 To describe the diagnosis of pregnancy
Introduction-
Pregnancy results in tremendous changes in the physiologic

functions of organs, systems and the body as whole. These
changes ensure that the needs of the growing fetus are met
and prepare the mother for parturition and lactation. Changes in
40
the maternal endocrine system along with hormones produced

by the placental / fetal unit are responsible for majority of the
changes. Knowledge about changes due to normal pregnancy
is important to reassure the pregnant woman and manage the
minor disorders of pregnancy. Understanding the normal
physiologic changes also gives us the basis to understand the
abnormal conditions during pregnancy.
Terminologies
Pregnancy is a maternal condition of having a developing fetus

in the body. It starts at fertilization where fusion of the ovum
(23x) and matured spermatozoa (23x or 23y) takes place in the
fallopian tubes. Zygote (46xx or 46xy) is a cell that results from
fertilization. The zygote divides and redivides forming daughter
cells named blastomeres. When the zygote reaches 16 cell
stage, it is named morula. When fluid filled cavity appears in
the morula a blastocyst is formed. The cells of a blastocyst are
arranged into layers. The outer layer is called the trophoblast
which eventually develops into the placenta. The inner layer is
called the embryoblast which later gives rise to the fetus. The
embryo is the stage after the inner layer formed two layers
(bilaminar disc). The embryonic period is a period where
major structures are formed and extends up to the end of seven
weeks after fertilization. Developing conceptus after the
41
embryonic period is called the fetus. All tissue products of

conception (embryo/ fetus, fetal membranes and placenta) are
called conceptus. On day 4 after fertilization the blastocyst
enters into the uterine cavity. By day 7, it starts embedding itself
into the prepared endometrium which is now called the
decidua. This process is called implantation.
PLACENTA AND ITS HORMONES
The placenta is formed from the trophoblast and decidua

basalis. It contains villi covered by the cytotrophoblast and
syncitiotrophoblast. The placental barrier (formed by the
syncitiotrophoblast, cytotrophoblast, the basement membrane
and the fetal vascular endothelial cells) ensures almost
complete separation of the maternal and fetal blood. For this
reason the human placenta is of hemo-chorio- endothelial type.
In a mature placenta the villi are grouped into 15- 20
cotyledons, each supplied by one to two spiral arterioles. At 20
weeks the discoid placenta reaches full development. The
placenta on average has a diameter of 18 centimeters, a
thickness of 23 millimeters, a volume of 497 milliliters, a weight
of 508 grams and villous surface area of
15 square meters. Placenta is a blue red discoid organ with

two surfaces. The maternal surface is made of the decidua
42
basalis with visible septated cotyledons. The fetal surface is

smooth and shiny and is covered by the amnion. The branching
fetal vessels are visible under the amnion.
The placenta acts to the fetus as the lung (exchange of oxygen

and carbon diaoxide), gastro intestinal tract (provision of
nutrients), kidney (excretion of hydrogen ion and urea), liver
(detoxifies drugs), immunologic system (transfer of antibodies)
and endocrine gland (production of hormones).
It is connected to the fetus by the umbilical cord or the funis. It

has an average length of 50-60 centimeters (range 30- 100)
and diameter of 0.8- 2 centimeters. It contains two umbilical
arteries and one umbilical vein. In addition to acting as conduit
for umbilical vessels, it also allows fetal mobility.
Placenta is a source of incredible amounts of protein and

steroid hormones. The major protein hormone is human
chorionic gonadotrophic hormone (HCG), also called the
pregnancy hormone. It has two subunits the alpha and the beta
subunits and is produced in increasing amount to reach a peak
between 8 -10 weeks. It maintains the function of the corpus
luteum until the placenta takes over progesterone production. It
also plays important role in male sex differentiation by
stimulating testosterone production by the fetal testis. It also
forms the basis for laboratory diagnosis of pregnancy.
43
In addition placenta produces a number of protein hormones. It

is also a source of significant amounts of progesterone and
estrogens. Since placenta lacks some of the enzymes
necessary to synthesize estrogens, it relies on provision os
substrates by the fetus and the mother (fetal-placental –
maternal unit).
Organ system changes
I. Cardiovascular system
Cardiac out put increases by 30-50%. The increase in cardiac

output is mainly distributed to the uterus (major share), kidneys,
breast and the skin. Heart rate increases by 15-20 % and stroke
volume increases by 25-38%.
Blood pressure remains largely unchanged with small drop in

diastolic pressure. This is the result of progesterone mediated
reduction in peripheral resistance. Blood pressure highest when
seated, lower when supine and lowest when ling on the side.
Near term there is a tendency to develop hypotension when
women lie on their back, a condition called supine hypotension
syndrome.
Total blood volume increases up to 45%. Plasma volume

increases 35-50% where as red blood cell volume increases by
44
20-25%. This results in hemodilution leading to a drop of

hemtocrite and is called physiologic anemia of pregnancy.
Venous pressure rises in lower extremities and central venous

pressure unchanged as the result of pressure by the gravid
uterus. This may result in leg edema and development of
varicose veins.
The point of maximum impulse is shifted to the left as the result

of elevation of the diaphragm. Splitting of the first and second
heart sounds could be found. High cardiac out put state may
result in gallop and systolic functional murmurs.
II. RESPIRATORY SYSTEM
Vasodilatations of the nasal vessels result in nasal stuffiness

and epistaxis. Diameter and circumference of chest increase.
Altered sense of smell is commonly reported. To meet the
increased oxygen consumption respiratory rate increases.
Because of elevation of the diaphragm by the gravid uterus,
diaphragmatic excuration decreases.
III. ALIMENTARY TRACT
Appetite increases but nausea and vomiting in the morning,

which typically occur in the first trimester, may reduce food
45
intake. Pica (craving for unusual food items of very low

nutritional value like clay and soap) if excessive may result in
nutritional deficiencies.
Ptyalism (inability of nauseated women to swallow normal

amount of saliva) is an early symptom of pregnancy. There is
no increased production of saliva by the salivary glands. Gums
are edematous and soft. Gum bleeding and acceleration of
dental caries from reduction in oral PH occur. Epulis
gravidarum, a tumorous gingivitis with pedunculated lesions
rarely occurs and may cause significant bleeding.
Heartburn due to relaxed esophageal sphincter is a common

complaint. Decreased gastric acid secretion and increased
gastric mucus secretion result in relief of symptoms of peptic
ulcer disease in majority of women. Delay in gastric emptying is
responsible for increased tendency of aspiration pnumonitis in
pregnant women undergoing general anesthesia.
Progesterone induced reduction in peristalsis helps in

absorption of nutrients and water from the small and large
intestines. As the result constipation is common and
hemorrhoids could occur.
IN the gall bladder residual volume increases and stasis of bile

occurs. This, along with increased biliary cholesterol saturation,
favors gall stone formation.
46
There are no significant changes in the anatomy of the liver.

Liver function tests are normal except elevation of alkaline
phosphatase, whose origin is the placenta. Spider angiomata
and palmar erythema, which are signs of chronic liver disease,
are normal findings in pregnancy.
IV. URINARY SYSTEM
THERE IS ENLARGEMENT OF THE KIDNEYS. THE

RENAL CALYCES AND URETERS SHOW DILATATION
WHICH CAUSES STASIS OF URINE. BLADDER TONE
IS ALSO REDUCED RESULTING IN INCREASED
CAPACITY AND INCOMPLETE EMPTYING AFTER
URINATION. THESE CHANGES MAKE A PREGNANT
WOMAN VULNERABLE TO URINARY TRACT
INFECTIONS.
Renal plasma flow increases by 75% and glomerular filtration

rate by 50%. Creatinine clearance is also increased. Blood urea
nitrogen, creatinine and uric acid levels decrease. Plasma
osmolality falls. There is increased glucose and amino acid
excretion. Protein loss amounts to 100-300mg/day.
V. INTGUMENTARY AND SKELETAL SYSTEM
Vascular changes include spider angiomata and palmar

erythema. Cortisol induced changes in connective tissue result
in striae gravidarum. Increased levels of melanocyte stimulating
47
hormone cause hyper pigmentation of the nipples, areola,

axilla, perineum, umbilicus and linea Alba (forms linea nigra).
The mask of pregnancy (chloasma or melasma) is seen on the
cheek bones. Increased secretion of sweat and sebum are
other features. Occasionally pigmented nevi are seen.
In an attempt to maintain the center of gravity, there is

exaggerated lordosis and drooping back of the shoulders. This
leads to common complaint of back ache. Parasthesia of the
hands may be caused if there is excessive drooping of the
shoulders, which stretch the brachial plexus.
Loosening of ligaments of symphysis pubis and sacroiliac joint

by relaxin causes is aimed to facilitate vaginal delivery. Pelvic
discomfort and gait problems may arise occasionally.
VI. Hematology
RED BLOOD CELL INDICES INCREASE. WHITE

BLOOD CELL COUNTS RISE. PLATELET COUNT
FALLS. MOST COAGULATION FACTORS INCREASE
CREATING A HYPERCOAGULABLE STATE.
VI. Endocrine & metabolic Changes.
There is massive increase in placental hormones mainly

estrogen, progesterone, human chorionic gonadotrophic
hormone and human placental lactogen.
48
Of the pitutary hormones, follicle stimulating, leutinizing and

growth hormones are reduced, while prolactin levels are high.
There is no change in thyroid stimulating and
adrenocorticotrophic hormones.
Thyroid gland shows diffuse enlargement with euthyroid state.

There is significant elevation of plasma cortisol levels.
Pregnancy has a diabetogenic effect due to peripheral insulin

resistance caused by high levels of anti insulin hormones like
human placental lactogen.
VII. Genital Systems
Uterus increases in weight from 70 gm of non pregnant state to

1000gm at term. Uterine blood flow reaches 600ml/minute with
85% supplying the placenta.
Increased vascularity gives the vagina and the cervix bluish

color. The cervix becomes soft from congestion. Increased
vaginal discharge may be noted.
Corpus luteum begins to regress at the eight week due to

negative feed back mechanism of estrogen and progesterone
on pitutary.
VII. Breast
Both acinar and ductal breast growth occur due to increased

estrogen, progesterone and prolactin levels. Erectile capacity
49
increases. But lactation is inhibited by placental progesterone

which prevents the action of prolactin on the production of
lactaalbumin.
VIII. Immune system
HCG reduces immune response of the mother. Serum IgG,

IGm and IgA decrease from tenth week to thirtieth week then
they will remain at same level.
IX. Weight gain in pregnancy
On average 12.5 kilograms is gained during pregnancy (range

9kg -15kg).The average distribution is as follow: the fetus 3300
gm, the placenta 600 gm, amniotic fluid 800 ml, uterus 900-
1000 gm, breast 400 gm, blood 1200 ml, deposition of fat
2500gm and extra cellular fluid 2600 ml.
50
Diagnosis of pregnancy
It is based on symptoms, signs and additional investigations.
I. Presumptive findings of pregnancy
 Weakness or fatigue
 Nausea and/or vomiting
 Breast swelling and tenderness
 Increased frequency of Urination
 Amenorrhea
 Discoloration of vaginal mucosa
 Increased skin pigmentation & striae
 Quickening
 Constipation, weight gain
II. Probable findings of pregnancy
 Uterine enlargement
 Change in consistency of cervix & uterus
 Ballottement rebound-16-20 weeks
 Braxton Hicks contraction
51
 Positive pregnancy test
 Symptoms as presumptive finding
III. Positive findings of pregnancy
 Fetal movement perceived by the health personnel
 Fetal heart beat heard by fetoscope (18 weeks) or

Doppler (10 weeks)
 Fetal heart beat and fetal body seen by ultrasound
PREGNANCY TESTS
ALL EMPLOY CHANGES IN THE LEVELS OF HCG

MOLECULE W HICH CAN BE DETECTED IN THE
MATERNAL SERUM AS EARLY AS NINE DAYS. TESTS
INCLUDE BIOLOGIC TESTS AND IMMUNOLOGIC
TESTS (AGGLUTINATION, RADIOIMMUNOASSAY,
RADIO RECEPTOR ASSAY AND ELISA).
Review questions
1. Describe the physiologic changes in the cardiovascular

system during pregnancy.
2. Discuss the diagnosis of pregnancy.
52
CHAPTER 4
Minor Disorders of Pregnancy
Learning Objectives
53
 To describe the minor disorders of pregnancy of

pregnancy.
 To discuss the management of the common minor

disorders of pregnancy.
Introduction
The physiologic and anatomic changes of pregnancy may result

in development of symptoms and signs that could be managed
by educating and providing explanation.
1. NAUSEA AND VOMITING (MORNING SICKNESS)
Some degree of nausea and vomiting during first trimester

especially between the first and the second missed periods is a
very common complaint. It usually continues until about the
fourteen weeks of gestation. It can appear at any time of the
day but is generally worse in the morning, thus the name
morning sickness. This condition is believed to be caused by
high or rapidly rising level of human chorionic gonadotrophic
hormone and estrogen. It is worse in
multiple pregnancy and gestational trophoblastic diseases.
Psychological problems like anxiety can aggravate the situation.
54
Eating small feedings at more frequent intervals and avoiding

food items whose smell precipitate or aggravate the symptoms
helps in relieving this problem. If persistent, anti-emetics can be
given.
2. Heartburn
Heartburn, epigastric burning sensation, is one of the most

common complaints of pregnant women especially during late
pregnancy. The symptom is usually mild. It is caused by reflux
of gastric content into the lower esophagus due to upward
displacement and compression of the stomach by the enlarging
uterus and progesterone induced relaxation of the lower
esophageal sphincter.
It is relieved by having smaller meals, avoiding bending over or

lying flat. Antacid preparation (aluminum hydroxide or
magnesium trisilicate alone orb in combination). In severe
cases H2 - blockers like cimetidine and ranitidine can be used
safely.
3. PICA
Pica, craving of pregnant woman for items of low nutritional

value like ice (pagophagia) or clay (geophagia), can occur. No
known cause has been identified but it is known to be common
55
in patients with iron deficiency anemia. In these cases, it is

relieved by correction of anemia. Some pregnant women may
have the symptom with out anemia. Educating the woman is all
that is needed.
4. PTYALISM
Ptyalism, excessive salivation, is also common. It is not related

to increased saliva production; rather it is the result of reduced
swallowing from nausea. Simple explanations will suffice.
5. CONSTIPATION
Progesterone induced relaxation of smooth muscles and

pressure by the uterus in the latter part of pregnancy result in
the common complaint of constipation. The problem is more
common with consumption of low fiber diet. This condition can
be treated with high fiber diet and increasing fluid intake.
Sometimes bulk forming laxatives may be needed.
6. HEMORRHOIDS
Hemorrhoids, varicosities of the rectal veins, may first appear

during pregnancy. More often pregnancy causes exacerbation
or recurrence of previous hemorrhoids due to increased
56
pressure in the rectal veins caused by obstruction of venous

return by the large uterus. Constipation during pregnancy also
contributes for development of hemorrhoids.
Hemorrhoids can be asymptomatic or present with rectal

bleeding, rectal pain or as a prolapsed mass through the anal
orifice. The later one can be strangulated and cause severe
pain. Thrombosis occurring in the dilated veins can also cause
severe pain.
Treatment includes topically applied anesthetic and anti-

inflammatory agents for pain and swelling, warm soaks (sitz
bath), laxatives and modification of bowel habits. Surgery is
reserved for thrombosed and strangulated hemorrhoids.
7. Urinary frequency
Increased glomerular filtration rate and in the latter part of

pregnancy pressure by the enlarging uterus explain the
common complaint of frequency of urination. Urinary tract
infection is also common as the result of incomplete emptying
of the bladder and stasis of urine. Microscopy of urine must be
done in all cases. Once UTI is ruled out simple explanation is
enough.
8. VAGINAL DISCHARGE
57
Pregnant women normally develop increased vaginal discharge

in many instances. It is clear, whitish and odorless. This is the
result of estrogen mediated increased mucus secretion by the
cervical glands. Reassurance is usually sufficient. If it is a
cause of concern vaginal douche with water mildly acidified with
vinegar can be used. Vaginal infections like trichomoniasis and
candidiasis should be ruled out in every patient with this
symptom.
Recurrent vulvo - vaginal candidiasis is common. Curd like

vaginal discharge and vulvar pruritis are major manifestations.
Identification of Candida albicans by potassium hydroxide
stains confirms the diagnosis. Treatment with antifungal vaginal
suppositories suffices. Systemic antifungals are
contraindicated.
9. Low Back and pelvic pain
Exaggerated lordosis and relaxation of the lumbar ligaments

cause the common complaint of low back pain. Minor degrees
of pain may follow excessive strain or fatigue, bending, lifting or
walking. Its severity increases with the duration of pregnancy.
58
Low back pain can be reduced by having the woman squat

rather than bending over when reaching down, providing back
support with a pillow when sitting down, and avoiding high
heeled shoes. Severe back pain with localized spinal
tenderness should not be attributed simply to pregnancy and
further evaluation is needed.
Relaxation of the joints of the pelvic girdle, cause pelvic pain

and gait abnormalities. In severe cases there may be
tenderness over the symphysis pubis which prevents mobility.
This condition is called pelvic osteoarthropathy and
necessitates admission.
10. Varicose veins
Varicose veins, dilatation of the superficial veins of the lower

extremities, could develop in predisposed women. It becomes
more prominent as pregnancy advances, weight increases, and
the length of time spent upright is prolonged. It is due to
progesterone mediated smooth muscle relaxation of the blood
vessels and increased venous pressure in the femoral veins
due to compression by the enlarging uterus.
In most, it is asymptomatic. The only concern in these women is

cosmetic. In few it causes discomfort of variable degree.
59
Treatment is periodic rest with elevation of legs and use of

elastic stocking or both. Surgical corrections like injection of
sclerosing agents, ligation and stripping are not generally
advisable during pregnancy.
11. Dependent edema
Edema of the lower extremities is common. It is as the result of

increased venous pressure of the lower extremities. It appears
near the end of the day and disappears after a period of rest.
It is important to rule out preeclampsia especially in those with

persistent dependant edema.
12. OTHER COMPLAINTS
Fatigue is the other common complaint during early pregnancy.

The woman will have a desire for excessive sleep. This
symptom remits spontaneously by the fourth month of the
pregnancy and has no special significance.
Palpitation is another common complaint. If significant, cardiac

pathologies must be ruled out.
Chloasma and striae are other sources of concern for which no

treatment is required. These often regress but may not totally
resolve after delivery.
60
Occasionally women complain about leg cramps. It is believed

to be the result of phosphorous deficiency and is relieved by
dietary adjustment.
Parasthesia of the hands which usually occurs in the morning

signify stretching of the roots of the brachial plexus by drooping
back of the shoulders in an attempt to maintain the center of
gravity.
Epistaxis and gum bleeding occur as the result of vascular

congestion and do not need special treatment. In rare cases
surgical excision is needed for tumorous condition of the gums
called Epulis gravidarum.
Hyperemesis gravidarum
Severe nausea and repeated vomiting that precludes oral

intake and leads to dehydration and ketoacidosis is termed as
hyperemesis gravidarum.
I. Pathophysiology
61
The cause is unknown but high levels of estrogen and HCG,

vitamin B 6 deficiency and psychologic factors are implicated. It
is common in molar pregnancy, multiple pregnancy and those
with family or past history of this condition.
Because of starvation ketone bodies are formed from

metabolism of fatty acid. Some of the ketone bodies appear in
the urine. In an attempt to restore the PH of the blood the
respiratory rate increases. Inadequate fluid intake results in
dehydration, weight and reduced urine output. Alkalosis from
loss of gastric hydrochloric acid in the vomitus and hypokalemia
also develop.
II. Diagnosis
Presence of exaggerated nausea, excessive vomiting, weight

loss and signs of dehydration like fatigue, dry oral mucosa,
weak pulse, low blood pressure and reduced urine are
hallmarks of this condition. Ketone in the urine confirms the
diagnosis after exclusion of other possible causes of excessive
vomiting.
III. Differential diagnosis
Gastroenteritis, cholecystitis, hepatitis, pyelonephritis, intestinal

parasitosis, peptic ulcer disease and drug induced vomiting
should be ruled out by history, physical examination and
laboratory investigations.
62
IV. Management
Once the diagnosis is confirmed the woman should be admitted

after counseling of the partners. The modalities include:
 Restricting oral intake
 Correcting dehydration and electrolyte deficit by

intravenous crystalloid solution preferably lactated ringer
solution to maintain fluid balance
 Correcting acidosis by providing calories in the form of

glucose in the intravenous fluids
 Treating underlying causes by parenteral vitamin B 6 (if

unavailable vitamin B complex)
 Parenteral antiemetics like promethazine , chlorpromazine

or metoclopramide
 Treatment of identified medical problems
 Monitor response to treatment by subjective feeling of the

patient, weight, urine out put and urine ketone
determination
With clinical response, the patient can be started on oral

feeding and antiemetics continued.
Therapeutic abortion is an option if the condition persists

despite aggressive medical treatment.
63
V. Complication
Prerenal azotemia, Mallory-Weis tears in the esophagus, in

prolonged cases Werinkes encephalopathy from thiamine
deficiency.
Review Questions
1. Describe the measures that may be taken in a pregnant

mother with nausea and vomiting.
2. Discuss the possible causes of severe nausea and

vomiting during pregnancy.
3. Describe important measures that may be taken in order to

relieve the heartburn that occurs during pregnancy in
some mothers.
64
65
66
CHAPTER 5
ANTENATAL CARE (ANC)
Learning objective
 To discuss the contents of ANC, frequency and time of

visit
 To describe the new WHO antenatal care model
 To enumerate high risk factors in pregnancy
Introduction-
Antenatal care (ANC) is a medical and general care that is

provided to pregnant woman during pregnancy. It is goal
oriented with the aim of meeting both the psychological and
medical needs of pregnant woman with in the context of health
care delivery system, culture and religion in which the woman
lives. ANC programs should be based on local situation and
should address risk assessment, health promotion and care
provision. ANC has been found to be effective in the treatment
anemia, hypertension and sexually transmitted diseases.
Frequency and timing of visit

67
Traditional or standard (Western) model recommends the

first visit to take place as early as the first missed period. This
allows accurate dating of the pregnancy and design appropriate
preventive and therapeutic interventions. Thereafter,
subsequent visits are planned every four weeks until 28 weeks,
every two weeks between 28-36 weeks and every week after
36 weeks. More frequent visits are required for high risk
patients.
The new WHO ANC model recommends a minimum of four

visits. It limits the number of visits and restricts laboratory tests
and procedures. First visit takes place at 16 weeks or before.
The second visit is planned between 24-28 weeks, the third at
32 weeks and the fourth at 36- 38 weeks. The initial visit takes
30-40 minutes and the other visits take around 20 minutes
each. Women with risk factors should not be enrolled in this
model.
Activities of the new WHO ANC model
I. First visit at 16 weeks
Major activities are diagnosis of pregnancy and determination of

the gestational age; risk assessment and determination of the
medical status of the mother; health promotion by education on
nutritional supplement, danger signs of pregnancy and finally
68
care provision like malaria prophylaxis, control MTCT of HIV,

iron supplementation and immunization with tetanus toxoid.
II. Second visit between 24- 28 weeks
Major activities are screening for hypertension, multiple

gestation, anemia, preterm labor, diabetes mellitus and RH
sensitization; further health promotion and care provision and
plan birth place.
III. Third visit at 32 weeks
Major activities are screening for hypertension, anemia, multiple

pregnancy, diabetes mellitus and RH sensitization; health
promotion and care provision and plan birth place.
IV. Fourth visit at 36 weeks
Major activities are screening for hypertension, antepartum

hemorrhage, multiple gestations; check for fetal lie,
presentation, growth and well being; health promotion and care
provision and finally up date individualized birth plan.
CONTENTS OF ANC VISIT
I. ASSESSMENT
69
Detailed history and physical examination (refer to chapter 2)

along with necessary laboratory investigations should be done
in the initial visit to assess the general medical status of the
woman and pick risk factors. For this reason the initial visit
takes 30-40 minutes. Subsequent visits look into new
developments, therefore, take much shorter time.
A. Initial visit
The pertinent elements of the history during the initial visit

include
1. History of present Pregnancy- identification (name, age,

address, marital status, occupation); pregnancy facts
(planned or unplanned pregnancy, wanted or unwanted,
supported or unsupported); gravidity , parity, abortion, LMP,
gestational age, contraceptive use prior to pregnancy,
symptoms and signs of pregnancy , danger signs and
symptoms, fetal quickening , client concern or complaints
2. Past history - antepartum and postpartum hemorrhage,

multiple pregnancy, preeclampsia, eclampsia, sepsis,
sexually transmitted infections, operative deliveries, still birth
and neonatal death, preterm delivery, low birth weight baby,
chronic medical illnesses (hypertension, diabetes, drug
allergy and cardiac diseases) and surgical problems, genital
mutilation
70
3. Others- personal, social and family history
General physical examination as described in chapter 2 should

be performed. It includes the general appearance, vital signs,
weight and height, general systemic examination including
checking for signs of anemia, physical abuse and surgical
scars. Specific obstetric examination should focus on
determining the uterine size, fetal lie and presentation, fetal
growth and well being, fetal heart beat. Pelvic assessment is
performed upon indications.
IN THE STANDARD MODEL BASELINE LABORATORY

INVESTIGATIONS ARE HEMTOCRITE, BLOOD GROUP
AND RHESUS FACTOR, URINALYSIS (PROTEIN,
KETONE AND MICROSCOPY), VDRL AND STOOL
EXAMINATION FOR OVA AND PARASITES. OTHERS
THAT COULD BE DONE UPON INDICATION OR WHEN
RESOURCES PERMIT ARE PAP SMEAR, CERVICAL
/VAGINAL SMEAR, URINE CULTURE AND SENSITIVITY,
COMPLETE BLOOD COUNT, PREGNANCY TEST,
SEROLOGY FOR HIV, HEPATITIS B VIRUS AND TORCH
SCREENING, ORAL GLUCOSE TOLERANCE TEST,
MATERNAL SERUM ALPHA FETOPROTEIN ON 16
WEEKS, AMNIOCENTESIS ,ULTRASONOGRAPHY AND
OTHERS.
71
In the new WHO model urine dip stick for bacteria and protein,
VDRL and blood group and Rhesus factor determination are
only done in the first visit. Hemtocrite is only done if there are
clinical signs of anemia.
In the new WHO model, in the initial visit women are grouped
into two using the classifying form. Women with out any risk
factor are enrolled in the basic component of the new model
that needs only three visits till delivery. Women with any
identified risk factor need special care that may need frequent
visits or even referral for specialized care.
The classifying form has 18 components that are grouped into

three:
 Obstetric history- previous stillbirth/ neonatal loss, history

of three or more consecutive abortions, birth weight of less
than 2500 or more than 400 grams, admission in the last
pregnancy for preeclampsia or hypertension, previous
uterine or cervical surgery-
 Current pregnancy - diagnosed or suspected multiple

pregnancy, age less than 16 or more than 40, RH
isoimmunization, vaginal bleeding, pelvic mass, diastolic
blood pressure of more than 90 mmhg
72
 General medical condition- insulin dependent diabetes

mellitus, renal or cardiac disease, known substance
abuse, any other severe medical illness
B. SUBSEQUENT VISITS
History focuses on new complaints and problems since the last

visit, intercurrent illnesses and medications, quickening time
and fetal movement, danger symptoms of pregnancy and any
changes in the personal history of the woman.
Physical examination focuses on the general appearance, vital

signs mainly the blood pressure, weight, checking for signs of
anemia, fundal height, fetal lie and presentation, fetal heart
beat, leg edema and other examinations based on the
complaints.
In the standard model hemtocrite is done at 24-28 and 32

weeks, antibody screening and oral glucose tolerance test at 28
weeks, ultrasound and maternal alpha feto protein at 16 weeks
and fetal survellance tests starting 32 weeks.
In the new WHO model dipstick of urine for bacteria is done in

all visits. Urine dipstick for protein is only done for nulliparous
women or for those with history of preeclampsia or
hypertension currently. Hemtocrite is done at the third visit.
II. Health promotion (advice and counseling)
73
Advice the woman about the importance of balanced diet and

avoidance of drugs, smoking and alcohol: adequate rest;
hygiene and safe sex.
Discuss about minor complaints of pregnancy and the danger

symptoms of pregnancy. Discuss about whom to contact and
where to go if these symptoms develop.
Inform the woman to record the time of quickening. Education

about labor and preparation for labor/ delivery should be done
starting from the third visit. The need for clean and safe delivery
should be stressed. Breast feeding and family planning after
delivery should be discussed.
III. Care provision (care provided)
Individualized delivery plan in should be planned starting from

the first visit and continued during subsequent visits including
arrangement of transportation in cases of emergency. Place of
birth and who attends birth should be planned.
Universal ferrous sulfate prophylaxis for nutritional anemia

should be given starting from the first visit. Tetanus toxoid
vaccination should be given according to WHO guidelines.
Appropriate prophylaxis and treatment of intestinal parasites
and malaria should be offered. Where indicated antiretroviral
therapy should be offered to HIV positive pregnant women.
74
Appropriate management of complaints and identified

problems/ complications should be done in each visit.
Timing and importance of next visit should be discussed.

Appointment should then be scheduled.
HIGH RISK FACTORS (NOT INCLUSIVE)
I. PAST OBSTETRIC HISTORY
 Ectopic pregnancy and recurrent spontaneous abortion
 Multiple pregnancy or preterm labor
 Antepartum or postpartum hemorrhage
 Malpresentation
 Intrauterine fetal death, stillbirth or early neonatal death
 Birth weight of less than 2500 or greater than 4000 grams
 Difficult operative deliveries and caesarian section
II. PRESENT OBSTETRIC HISTORY
 Short stature (height of less than 150 cm), age of less than
16 or greater than 40
 Primigravida or grandmultiparity
 Vaginal bleeding at any gestational age
 Uterine size to gestational age discrepancy (big or small

for date uterus)
75
 Multiple gestation
 Premature rupture of the membranes
 Raised blood pressure during pregnancy
 Malpresentation after 34- 36 weeks
 Unwanted pregnancy
 Extreme social disruption and deprivation
Review questions
1. Briefly describe the new WHO ANC model.
2. List the routine laboratory investigations in ANC.
3. List the high risk factors in pregnancy.
76
CHAPTER 6
Abnormal Bleeding during first and second

trimesters of pregnancy
77
Learning objectives
 To identify the common causes of abnormal bleeding

during pregnancy by trimester.
 To list the different types of abortion with their clinical

features.
 To describe the clinical feature of ectopic pregnancy.
 To describe the management the different types of

abortion and ectopic pregnancy.
 To define the spectrum of GTD
 To discuss the clinical features of GTD
 To list the main treatment modalities of GTD
 To enumerate the possible complications GTD and their

treatment
INTRODUCTION
When a woman becomes pregnant, the menstrual bleeding

stops until sometime after the end of the pregnancy. However,
abnormal bleeding from the genital tract can complicate some
pregnancies. Statistically, more than 25% of all gestations will
present to health care provider at least in early pregnancy with
vaginal bleeding and/or pelvic pain. These symptoms may
78
indicate a minor or a life threatening condition that can result in

death. Successful management of any one of these conditions
is of paramount importance and rests on timely diagnosis. This
in turn requires proper evaluation of the patient by taking the
history and doing physical examination. There may be a need
to do some laboratory studies to help the evaluation process.
The primary goal of the evaluation should focus on identifying
immediate life threatening conditions like shock. Generally,
abnormal uterine bleeding during pregnancy can result from
obstetric or non-obstetric causes. Conditions like abortion,
ectopic pregnancy, placenta abnormalities like placenta previa
and abruptio placentae, and gestational trophoblastic diseases
are some of the obstetric causes. While conditions like genital
infections, trauma to the genital organs and neoplastic changes
affecting them are some of the non-obstetric causes. Systemic
illnesses affecting blood coagulation can also result in abnormal
bleeding during pregnancy.
1. Abortion
1.1. Importance
Abortion is an important cause of bleeding during pregnancy,

as it is one of the five leading causes of maternal death in the
79
developing world. The other causes being obstructed labor,

hypertensive disorders of pregnancy, hemorrhage and infection.
1.2. Definition:
Abortion is the expulsion of the fetus from the uterus or

termination of pregnancy before fetal viability. This is usually
taken to be so if it happens before 28 completed weeks of
gestation or less than 1000g weight in Ethiopia & United
Kingdom.
1.3. Classification
1.3.1. By occurrence
Abortion could occur spontaneously or could be induced.
A. Spontaneous abortion
An abortion is said to be spontaneous if it occurs with no

intervention. The incidence of spontaneous abortion is between
10% and 20% of all pregnancies. It is most commonly due to
fetal chromosomal defects such as trisomies, monosomies and
polyploidy. This usually occurs during the first trimester.
B .Induced abortion
An abortion is said to be induced if it results from medical or

surgical intervention that can cause abortion. It could be safe or
unsafe abortion. Unsafe abortion characterized by lack or
inadequacy of skill of provider, hazardous technique and
80
unsanitary facilities or both. This is important type of abortion as

it accounts for the major proportion of abortion and is cause of
immense maternal mortality and morbidity. Moreover, it is
related to unwanted pregnancy and unawareness of the
reproductive physiology by the woman .It can largely be
prevented if there is provision of contraceptive service and
making the woman knowledgeable about her reproductive
physiology. Of the 210 million pregnancies that occur each
year, about 46 million (22 per cent) end in abortion. About 20
million of those abortions are unsafe –that is, performed by
someone without the skills or training to perform them safely, or
in a place that does not meet minimal medical standards or,
both. Every year, more than 70,000 women die as a result of
unsafe abortion; hundred of thousands more suffer from
serious, often permanent, disabilities. Everyday, 200 women die
from unsafe abortion. More than 95% of deaths and injuries
occur in developing countries. In Ethiopia maternal losses from
abortion
and its complication account for 25-50%. The majority of deaths

from abortion result from hemorrhagic shock and sepsis. Proper
management of abortion can prevent the death and the other
complications that result from it.
C.Therapeutic abortion
81
Subset of safe abortion which is performed for the purpose of

saving the life of the mother (3) or if the fetus has congenital /
chromosomal / metabolic disorders that is incompatible with life
after birth.
1.3.2. By clinical stages
Threatened abortion: is a clinical condition that is characterized

by vaginal bleeding before 28 weeks of gestation. In addition
there is crampy lower abdominal pain and the cervix remains
closed. The fetus is alive and there is a chance of continuing
the pregnancy to viability.
Inevitable abortion: is a clinical condition characterized by

vaginal bleeding of variable amount and crampy lower
abdominal pain. The cervix is open but no products of
conception have been expelled. There is no chance of
salvaging the pregnancy.
Incomplete abortion: is a clinical condition in which vaginal

bleeding continues and cervix remains open despite expulsion
of part of the products of conception.
Complete abortion: is a clinical condition in which vaginal

bleeding stops and the cervix closes following expulsion of all
products of conception. The uterus is small for the duration of
the pregnancy and it is firmer. Before 14-16 weeks it is difficult
to tell if an abortion is complete or not because to make sure it
82
is complete one has to identify the fetus and the placenta with
the membranes as fully formed structures. Before 14-16 weeks
these structures are not sufficiently well formed.
Missed abortion: is a clinical condition in which the fetus dies in

utero and is retained for at least four weeks. There is usually
history of threatened abortion preceding it. Decidual necrosis
may result in brownish vaginal discharge. Pregnancy symptoms
like morning sickness, breast tenderness and abdominal girth
increment disappear. Cessation of fetal movement is reported
by the mother if it occurs after 18 weeks. Failure of uterine
growth results in small for gestational age uterus. Pregnancy
test takes 8 weeks to become negative.
1.3.3. BY ASSOCIATED INFECTION
Septic abortion: is a clinical condition in which offensive vaginal

discharge, temperature of more than 38 o centigrade and lower
abdominal pain / tenderness accompany any of the clinical
stages of abortion. Majority follow unsafely induced abortions.
Infection starts in the uterus and if untreated spreads to
adjacent pelvic organs (pelvic peritonitis) or to the general
peritoneum (generalized peritonitis) or the blood stream
(sepsis). It eventually results in death by causing septic shock.
Postabortal sepsis: is pelvic infection after a complete abortion.
1.3.4. OTHER DEFINITIONS

83
Recurrent abortion: occurrence of three or more consecutive

spontaneous abortions. It was previously known as habitual
abortion.
1.4. INITIAL ASSESSMENT
Any woman of reproductive age experiencing at least two of the

following symptoms should be considered as a possible
abortion patient.
 Vaginal bleeding
 Cramping and/or lower abdominal pain
 A possible history of amenorrhea
Complete clinical assessment is necessary to determine all

conditions that are present in order to decide the order in which
to treat them.
1.4.1. History
 Length of amenorrhea
 Bleeding (duration, amount)
 Cramping (duration and severity)
 Abdominal or shoulder pain
 Drug allergy
 History of interference and method employed

84
 Symptoms of infection
1.4.2. Physical examination
 Check vital signs
 Note general health of the women
 General systemic examination
 Abdominal examination
Check –abdominal distension, movement with

respiration, bowel sound,
Location and severity of tenderness and

rebound tenderness,
Uterine size, masses, shifting dullness
 Pelvic examination(speculum and bimanual digital

examination)
Remove any visible products of conception from the vaginal

canal or cervical canal. Then note for the amount of
bleeding and presence of offensive discharge, the extent of
cervical dilation and presence of cervical excitation
tenderness, size and consistency of the uterus, adenexal
masse and other pelvic masses. Check for cervical
laceration
1.4.3. Laboratory examination

85
Based on clinical assessment when indicated: -
 hemoglobin / hemtocrite, blood group and rhesus factor
 white cell count, erythrocyte sedimentation rate,

urinalysis, renal function test, liver function test, platelet
count, prothrombin time, partial thromboplastin time
 Plain film of the abdomen (erect), pelvic ultrasonography
 Pregnancy test
1.5. MANAGEMENT
Life threatening conditions like shock (hypovolumic or septic),

severe anemia and sepsis should be treated aggressively prior
to instituting specific treatment. These include intravenous
fluids, parenteral antibiotics, blood transfusion and /or other
ventilatory supports. Preparations for laparatomy must be made
in cases suspected or diagnosed to have uterine perforation or
generalized peritonitis or pelvic abscess. Specific management
for each stage of abortion should be offered only after attending
to the above conditions. Appropriate and timely referrals are life
saving.
1.5.1. Threatened abortion
 Bed rest at home which could be reinforced by sedatives

like diazepam. Women who have bled much (regardless of
the gestational age) or have bad obstetric history or live far
86
away and cannot get help if bleeding becomes much

worse, especially during the night should be admitted for
observation.
 Avoid intercourse and douching
 Monitor progress by subsequent assessment. Where

available ultrasonography should be done to check for
viability.
 If there is any sign of pelvic infection evacuation of the

uterus should be performed.
1.5.2. COMPLETE ABORTION
IF COMPLETENESS IS CONFIRMED EITHER BY

EXAMINATION OF THE CONCEPTUS TISSUE OR
WHERE AVAILABLE BY ULTRASOUND
 ADMINISTER ERGOMETRINE 0.5MG
 IF JUSTIFIED PROVIDE THERAPEUTIC OR

PROPHYLACTIC ANTIBIOTICS
EVACUATION OF THE UTERUS MUST BE DONE IF

COMPLETENESS CAN NOT BE ASSURED AS IN EARLY
ABORTION OR EXPULSION OCCURRED OUT OF THE
HEALTH INSTITUTION.
1.5.3. Inevitable abortions
A. Less than 14 weeks of gestation:

87
Evacuation of the uterus is the mainline of treatment

.Evacuation can be done either by sharp metallic
curettage or by manual vacuum aspirator (MVA). MVA is
much safer and recent technology which is said to be
associated with less complications and pain, more
efficient in evacuating the uterus in less time and thus
can safely be used by lower level health professionals.
Mandatory indications for evacuation
1. Considerable bleeding
2. Bleeding which continues for more than 24 hours.
3. Patients in whom the retained products of

conception are obviously still present on vaginal
examination..
B. More than 14 weeks of gestation
In the absence of heavy bleeding evacuation of the

uterus is not advised before the expulsion of the fetus
.Management includes
 Admission and monitoring the vital signs and the

amount of bleeding
 Once the fetus / placenta are expelled completeness

should be checked .Evacuation of the uterus must be
done if incomplete or the bleeding continues.
88
 Ergometrine or oxytocin as drip should be given for

continued bleeding after expulsion or evacuation and
monitoring should continue.
 Exploration of the uterus for remnants or perforation

should be done if these measures fail and the patient
continues to bleed.
1.5.4. Incomplete abortion
Uterine evacuation should be done preferably by MVA.

Antibiotics as needed can be given.
METHODS OF UTERINE EVACUATION
Determined by uterine size
If uterine size < 14 weeks
 Manual / electrical vacuum aspiration or

evacuation and curettage(E&C)/dilatation and
curettage (D&C)if cervix is closed
If uterine size > 14 weeks
 Oxytocin infusion or evacuation and

curettage(E&C)/dilatation and curettage when
appropriate
Oxytocin administration
89
Add 10ml (ampoules) to 1000ml lactated Ringer's solution

(100mu/ml)
Start at 0.5ml/mi (50mu/mi), increase at 30 to 40min

intervals up to a maximum rate of 2mml/mi (200mu/min). If
effective contractions are not established at this infusion
rate, increase the concentration. Discard all but 500ml of
the remaining solution. Add additional 5 ampoules of
oxytocin (200mu/ml). Reduce the rate to 1ml/mi
(200mu/mi). Increase up to 2ml/mi (400mu/mi), continue at
this rate for 4-5hrs or until fetus is expelled.
1.5.5. Missed abortion
A. Expectant management up to 4 weeks
 This is based on the fact that 95% women with missed

abortion will abort spontaneously in 4 weeks time,
whatever the duration of the pregnancy. After 4 weeks
the chance of developing disseminated intravascular
coagulation or dead baby syndrome is significant.
 During this time coagulation profile is monitored weekly.

Evacuation of the uterus is done if the patient did not
expel in 4 weeks or before 4 weeks if coagulation
derangement occurs.
90
B. Aggressive management
This entails evacuation of the uterus. Methods include

dilatation and curettage (D&C) for uterine sizes up to 12
weeks or induction of labor by prostaglandins /oxytocin
infusion if uterine size is more than 12 weeks. Since
there is a risk of uterine perforation and coagulopathy
with this form of management appropriate referral to
proper health facility should be made.
1.5.6. MANAGEMENT OF COMPLICATIONS
I. Uterine perforation
The following signs seen during uterine evacuation

indicate perforation.
 An instrument (sound, cannula, and curette) extends

beyond the expected limit of the uterus.
 Fat or bowel is found in the tissue removed from the

uterus
 Severe pain and continuous bright red bleeding
 In apparent vital sign derangement (hypotension in

the absence of bleeding)
Management
91
 Stabilize the patient and do not give anything per os.
 Monitor vital signs
 Start broad spectrum antibiotics (parenteral)
 Immediate referral to a facility capable of performing

gynecologic surgeries.
If evacuation is complete
 Give ergometrine 0.5mg
 Observe her for two hours
 If patient become stable and bleeding stops,

give ergometrine and continue observation
overnight
 If the condition gets worse and the bleeding

doesn‘t stop emergency laparatomy is
performed.
IF EVACUATION IS NOT COMPLETE
 Immediate laparatomy to complete evacuation under

direct vision Depending on the findings either repair
or hysterectomy is done.
II. Intraabdominal injury
92
The following signs and symptoms indicate intra

abdominal injury
Symptoms
 Nausea, vomiting, shoulder pain,fever,abdominal pain

and cramping
Signs
 Distended abdomen, decreased bowel sound, tense

hard abdomen
 Rebound tenderness
Management
 Resuscitation, parenteral antibiotics,
 Immediate referral for laparatomy
III. Sepsis
Etiology is polymicrobial (gram positives, gram negatives

and anaerobes)
The following symptoms and signs indicate that either local

or generalized infection is likely:
Symptoms
 Chills, fever, sweating, history of interference
93
 Prolonged bleeding, general discomfort, flu like

symptoms
Signs
 Foul smelling vaginal discharge, distended abdomen
 Tenderness, low blood pressure
Assess women’s risk for developing septic shock
Low risk
 First trimester abortion, mild to moderate fever (< 38.50

c)
 Stable vital signs, no evidence of Intraabdominal injury
High risk
 second trimester abortion, high fever (> 38.50 c)
 Any evidence of intra abdominal injury, shock
Management
 Resuscitation, monitor vital signs, start broad

spectrum antibiotics intravenously
If low risk and stable
Uterine evacuation, continue antibiotics, observe for 48

hrs.
94
If high risk
 Continue antibiotics
 If there is shock ---- manage as shock
 If intra abdominal injury--- laparatomy
 If DIC present -- treat with clotting factors and fresh

blood products
IV. Other complications and their management
 Anemia - manage according to severity by either

hemathenics or blood transfusion
 Renal failure - manage accordingly
 Give tetanus toxoid as indicated and tetanus antitoxin

for non immune women
 Give anti-D for Rh negative mothers (see protocol for

management of Rh isoimmunization)
1.5.7. Post abortion family planning
All women receiving post abortion care need counseling

and information to ensure that they understand:
 They can become pregnant again before the next

menses
 There are safe methods to prevent or delay pregnancy

95
 Where and how they can obtain family planning service
1.5.8. Antibiotic choices and administration in the

management of abortion
Empiric therapy antibiotic covering wide variety of aerobic,

anaerobic, gram negative/positive organisms is used.
Regimen 1
Ampicillin or benzyl penicillin plus chloramphenicol or

clindamycin or metronidazole plus gentamycin
Regimen 2
Ceftriaxone or ciprofloxacin plus gentamycin or

metronidazole
Regimen 3
Doxycycline with metronidazole
 Once started, therapy can be continued until the patient

is afebrile at least for 24 hours, preferably 48 hours
 If there is no response in 48 hours the antibiotics should

be changed and/or complications considered
 When recovery is underway, intravenous therapy should

be followed by oral medication, for 10 to 14 days.
1.5.9. Components of Post abortion care (PAC)
96
 Emergency treatment of incomplete abortion and

potentially life threatening complications
 Post-abortion family planning counseling and services
 Links between post-abortion emergency services and

the reproductive health care system.
 Community service provider partnership
 Counseling
2. ECTOPIC PREGNANCY
2.1. Definition
Ectopic pregnancy is implantation of the fertilized ovum outside

of the uterine endometrial cavity.
2.2. Incidence and predisposing factors
Ninety–nine percent of ectopic pregnancy occurs in the

fallopian tube. The commonest site is the ampulla which
accounts for 55% of ectopics. The rest occurs in the isthmus
(25%), the fimbria (17%) and the interstitial part (2.5%). Rare
forms of ectopic pregnancy include cervical ectopic, ovarian
ectopic and abdominal pregnancy. Very rarely bilateral ectopic
or combined intrauterine and ectopic pregnancy is seen. In
97
many parts of the world one in every 50 to 200 pregnancies is

ectopic.
Any condition that alters the length, contour, peristaltic

movement or size of the tubal lumen will predispose to ectopic
gestation. Common conditions that predispose to ectopic
gestation are:
 Previous gonococcal or Chlamydia endosapingitis
 Postoperative like previous ectopic

surgery/tuboplasty or inflammatory pelvic adhesions
distorting the tubes
 Congenital abnormalities of the tubes
 Some family planning methods like progestasert and

progesterone only pills
 Medically assisted conception
2.3. Natural Coarse of tubal ectopic pregnancy
Majority of ectopic gestations end as gynecological/obstetric

emergencies in the first or early second trimester. It is a very
rare occurrence for an ectopic gestation to advance to term. As
the fertilized ovum grows, it progressively distends the tube
which leads to unilateral lower abdominal pain. Further
distension eventually leads to either rupture into the lumen
(tubal abortion) or more commonly into the peritoneal cavity
98
(tubal rupture). This results in extrusion and death of the zygote

accompanied by intraperitoneal bleeding from the edges of the
ruptured tube. For isthmic ectopic this occurs 3-4 weeks from
the LMP while in ampullary it is around 6-8 weeks and in
interstitial it is around 12 weeks. Unless surgical intervention is
undertaken majority of patients die of massive intraperitoneal
bleeding. Rarely an abdominal pregnancy results if the zygote
survives and implants in the peritoneal cavity.
Sometimes chronic ectopic gestation results if pelvic adhesions

limit the extent of the bleeding forming a pelvic mass. .
2.4. Clinical features and diagnosis
The clinical features are often atypical and diverse especially

before rupture. As it is one of the most devastating and
potentially fatal gynecologic emergencies, every clinician should
be suspicious of it all the time. The adage ‘any woman of child-
bearing age (15-50) who has abdominal pain (with or without
amenorrhea) may have an ectopic gestation unless proven
otherwise‘ is a useful one to bear in mind.
Typically women present with the three triad of symptoms –

variable period of missed menstrual period, abnormal vaginal
bleeding and lower abdominal pain. Commonly there is a short
period of missed period but in some women the vaginal
bleeding may coincide or even precede the expected time of
menses. The vaginal bleeding is often dark red and small in
99
amount with heavy bleeding being a rarity. Sometimes passage

of decidual cast may confuse the diagnosis with abortion. The
lower abdominal pain is initially unilateral and constant in nature
but after tubal rupture it becomes diffuse. Syncopal attack may
be reported at the time of rupture. With significant
hemoperitoneum shoulder pain and rectal fullness may be
reported. Presence of predisposing factors should be sought.
High grade fever is unusual.
Physical signs are also variable and largely depend on the

presence or absence of rupture. Vital signs may range from
normal to profound shock. Pallor is also variable. Peritoneal
irritation (direct tenderness/rebound tenderness/guarding) of
variable degree is always present, which could be localized to
the lower abdomen or diffuse. Shifting dullness indicates
hemoperitoneum.
The most significant findings on pelvic examination include

closed cervix with positive cervical excitation tenderness,
unilateral adenexal tenderness with or without tender mass and
tense/tender pouch of Douglas. Uterine enlargement up to 8
weeks size is a normal finding.
The most valuable bedside diagnostic procedure for ruptured

ectopic pregnancy is culdocentesis.This involves aspirating fluid
from the pouch of Douglas by passing needle through the
posterior fornix. Finding dark red non clotting blood is invariably
100
diagnostic. Negative culdocentesis does not rule out ectopic

pregnancy.
Laboratory investigations (where available) that could help in

the diagnosis of unruptured ectopic include Serum b HCG
determination in conjunction with pelvic ultrasound.
2.5. Management
The treatment can be medical or surgical depending on the type

of the ectopic pregnancy. The best management for ruptured
ectopic is emergency laparatomy to ligate the bleeding vessels
coupled with aggressive resuscitation to counteract the effects
of hypovolemia. Timely referrals to a hospital setting with
continued resuscitation along the way is life saving. Unruptured
ectopic is usually managed using drugs like methotraxate or
conservative tubal surgery.
Resuscitation
 Correcting hypovolemia with intravenous fluid
 Blood transfusion before operation; this may in fact be

undesirable if it delays very urgent surgery to stop
bleeding.
SURGICAL TREATMENT- SALPIGECTOMY

/SAPINGEO-OOPHOERCTOMY
101
Upon discharge women should be counseled about the risk of

recurrence in future pregnancy and the importance of visiting a
clinician as soon as they miss their menses.
3. GESTATIONAL TROPHOBLASTIC DISEASES

(NEOPLASMS)
3.1. DEFINITION
Pregnancy-related pathological conditions in which there is

abnormal growth and development of the trophoblast. GTDs
include the tumor spectrum of hydatidiform mole, invasive mole
or chorioadenoma destruens, and choriocarcinoma.
3.2. Classification
There are various schemes of classification, but the following is

a commonly used one:
1. Benign GTD includes hydatidiform mole (complete and

partial).
2. Malignant GTD falls into two groups:
a. Non-metastatic includes persistent hydatidiform

mole, invasive mole and choriocarcinoma which
has not metastasized.
b. Metastatic includes metastatic mole and

choriocarcinoma.
102
3.3. Unique Features
Gestational trophoblastic diseases have a number of unique

characteristics:
 They consist of tissue ―foreign‖ to the patient. They arise

from the fetal tissue in the maternal host.
 They secrete an accurate and sensitive tumor marker, the

human chorionic gonadotrophic hormone (HCG).
 They are markedly sensitive to chemotherapy so that even

advanced disease may be cured.
 Unlike other epithelial tumors malignant GTDs spread

mainly by vascular route.
 Normal pregnancies are possible following molar

pregnancy.
3.4. BENIGN GTDS (HYDATIDIFORM MOLE)
3.4.1. Types of molar pregnancy
A. Complete mole
Uterus is filled with multiple grapes like vesicles. There is

no fetus or amnion. Microscopically, there is pronounced
and generalized hydropic swelling and edema of villous
stroma, avascular villi and marked proliferation of
103
syncitiotrophoblastic and cytotrophoblastic elements

surrounding the villi. The incidence of postmolar GTD is 15
to25 % (17 % is non metastatic type).
B. Partial or Incomplete mole
An abnormal fetus or embryo is present, but it usually dies

in the first trimester. Focal vesicles are seen. Microscopic
features include localized hydropic villi and trophoblastic
proliferation along with presence of fetal tissue, and blood
vessels. Post molar GTD develop in 5 to 10 % of patients
(almost always of non metastatic type).
3.4.2. Incidence and risk factors
Hydatidiform mole (molar or vesicular pregnancy) is the most

common form of GTD. Incidence is very variable ranging from
1:200 – 1:300 in South East Asia to 1:1500-1:2000 in U.S.A.
Risk factors include:
 Age less than 20 or more than 40 years
 Genetic factors
 Low socioeconomic status
 Protein, folic acid and carotene deficiency
104
 Previous molar pregnancy (recurrence rate is

around 1:76 for the first and 1:6 for the second)
3.4.3. Clinical features
 Vaginal bleeding after a period of amenorrhea

(usually starting from the first trimester)
 Serosangineous vaginal discharge
 Passage of the ―grape-like‖ vesicles, if occurs, is

considered to be pathognomonic.
 Exaggerated symptoms and signs of pregnancy

mainly hyperemesis gravidarum
 Pre-eclampsia occurring before the gestational age of

20-24 weeks is seen in around 30% of patients
 The uterus will be big-for-date in half of patients but

small-for-date in a third and appropriate for
gestational age in the rest.
 The uterus is doughy with no fetal parts felt except in

the situation of partial mole.
 FHR tones are absent except partial mole.
 The ovaries may be palpably enlarged by the theca

lutein cysts.
105
 One may also find clinical and/or biochemical signs of

hyperthyroidism due to the elaboration of thyrotropin
by the tumor or as the effect of elevated HCG.
3.4.4. Diagnosis
.Whenever molar pregnancy is suspected on clinical grounds

the patient should be referred to an appropriately equipped
facility for confirmation of the diagnosis and management.
The most important investigations that help in the diagnosis
are determination of serum or urinary B-HCG in titer
which reveal very high values and ultrasonography which

reveal the typical snow- storm appearance without
gestational sac or fetus. Other modalities like amniography
which shows the honey comb pattern are no more used.
3.4.5. COMPLICATIONS OF MOLAR PREGNANCY
Medical complications include anemia and shock from

hemorrhage, pre-eclampsia, hyperemesis gravidarum,
hyperthyroidism and intrauterine infection with or without
sepsis. Congestive heart failure and pulmonary edema could
result from trophoblastic deportation, fluid overload during
treatment or from pre-eclampsia / severe anemia/
hyperthyroidism. Trophoblastic deportation may result in
acute respiratory distress within 6-8 hours of evacuation.
106
Post molar GTD and future recurrence other problems.

Uterine perforation could result during treatment. There may
be deposition of trophoblast in the lungs but spontaneous
regression occurs.
3.4.6. Management
Since molar pregnancy is associated with many disease and

treatment related complications, its management should be
in a facility that is capable of handling them. Furthermore
prolonged follow up is needed for early detection and
management of post molar GTD. For these reasons timely
referral from the health center is crucial.
Management in an appropriate setting includes
 Performing baseline investigations – B-HCG level, chest

X-ray, liver and renal function tests and complete blood
count.
 Treatment of medical complications
 Evacuation of the molar tissue. The method of choice is

suction curettage. Medical induction by uterotonic drugs
is not favored because it carries risk of hemorrhage and
embolization. Hysterectomy with mole in situ is the
107
preferred treatment for women having more than three

children and /or women older than 40 years. Sharp
metallic curettage is contraindicated.
 Follow up using history, physical examination and B-

HCG titer done weekly until it is negative three times
then monthly for one year. Combined oral
contraceptives are given during this period to prevent
pregnancy.
 Platueing or rising HCG levels , rising levels after

negative HCG ,HCG still high after 6 months of
evacuation and any clinical sign of metastasis are
indicative of post molar GTD and require chemotherapy.
3.5. Malignant GTDs
3.5.1. General
These are mainly invasive mole and choriocarcinoma.
A. Invasive mole makes up around 15% of GTN and is

reported in 10-15 % of patients who have had primary molar
pregnancy. It invades the myometrium and the uterine
vessels extensively; therefore, the diagnosis is usually made
from pathologic examination of hysterectomy specimens.
108
B.Choriocarcinoma is rare, making up only 2-5% of all cases

of GTD and follows 2-10% of molar pregnancy. It is an
aggressive fast-growing tumor with disordered trophoblastic
proliferation, myometrial invasion, hypervascularity, necrosis
and hemorrhage, the absence of villous structures and
metastases. 50% follow hydatidiform mole. A quarter follow
term pregnancies and another quarter follow abortion or
ectopic pregnancy. It spreads both by local invasion and via
vascular route which occurs early. Common sites of
metastasis are the lungs (80%), anterior vaginal wall (30%),
the brain (10%) and the liver (10%). All GTDs that follow
normal pregnancy are choriocarcinoma.
3.5.2. CLINICAL FEATURES
 Severe vaginal bleeding which may be absent in

some cases.
 Fulminant pre-eclampsia and hyperthyroidism
 Metastases may occur to the lungs, liver, brain,

vagina, gastrointestinal tract, and bones and may
manifest as follows:
 Pulmonary metastasis with cough, chest

pain, hemoptysis
109
 Liver secondary with abdominal pain,

hepatomegally, jaundice
 Brain metastasis with headache,

convulsion, focal neourologic deficit
 Vaginal metastasis with a bleeding blue-

purple vaginal mass
 GI metastasis with hematemesis, melena,

hematochezia
 Bone metastasis with pain, pathological

fractures
3.5.3. DIAGNOSIS
Finding elevated B- HCG levels along with pathologic

identification of typical lesions confirms the diagnosis. Chest
and bone X-rays, cerebrospinal fluid analysis and ultrasound
may help in identifying metastasis.
3.5.4. MANAGEMENT
This is best if done in specialized centers or at least in

centers where the appropriate investigations can be done
and the patient can receive the right treatment. The
management modality is single or combination
chemotherapy. Surgical removal of persistent cases is a
secondary option.
110
3.6. Long-term sequelae
The prognosis is always excellent for hydatidiform mole.

Also, almost all patients with malignant non-metastatic GTD
are cured with appropriate therapy .Recurrence, when it
occurs, is usually in the first several months of termination of
therapy but may sometimes occur as late as 3 years or more.
There is high risk of recurrence of GTD in future pregnancies.
The effect on the subsequent fertility of young patients is
insignificant. But because of the slightly increased risk of
choriocarcinoma, B-HCG should be determined at 3 week
and 3 months following delivery.
Review Questions:
1. Define unsafe abortion and recurrent abortion
2. Describe the clinical stages of abortion with respect to

bleeding, cervical status, uterine size and other signs.
3. Outline the management of incomplete abortion and septic

abortion.
4. List the methods of uterine evacuation for uterine size less

than 14 weeks.
5. Discuss the essential components of post-abortion care.

111
6. Discuss the clinical features of ectopic pregnancy.
7. Describe culdocentesis.
8. Describe the spectrum of gestational trophoblastic

diseases.
9. Discuss the most important clinical features of molar

pregnancy.
10. Describe how molar pregnancy is managed and also

discuss how post-evacuation follow-up is undertaken.
CHAPTER 7
ANTEPARTUM HEMORRHAG E
LEARNING OBJECTIVES
 To identify the major causes of ante partum hemorrhage
 To list important risk factors for ante partum hemorrhage
112
 To discuss the evaluation of a patient with antepartum

hemorrhage
 To indicate the important precautions that should be taken

in evaluating and managing mothers with antepartum
hemorrhage
 To explain the basic principles of the management of

antepartum hemorrhage
Introduction
Antepartum Hemorrhage (APH) is bleeding from the genital

tract of the pregnant mother after the fetus has reached the age
of viability (which is after 28 completed weeks or fetal weight of
1000gm or more) and before the fetus is delivered. It occurs in
2-4% of all pregnancies.
The causes could broadly be grouped into two.
 Obstetric causes which include placenta previa, abruptio

placentae, bleeding from vasa previa, ruptured uterus and
heavy show.
 Non obstetric (local or incidental causes) include
1. PLACENTA PREVIA
113
1.1. Definition and grades
Placenta previa is bleeding from a placenta implanted in the

lower uterine segment and thus lies ahead of the presenting
part.
 Grade 1 or low-lying placenta –the placenta occupies the

lower uterine segment, but does not reach the internal
cervical os.
 Grade 2 or placenta previa marginalis—the placenta

reaches the internal os but does not cover it.
 Grade 3 or placenta previa partialis—the placenta covers

the internal os but only partially, even at full dilatation
 Grade 4 or placenta previa totalis--placenta covers the

whole internal os even at full cervical dilatation.
1.2. Incidence
1 in 200 to 250 deliveries it is more common in multiparas.
1.3. Predisposing factors
The exact cause is unknown, but there are a number of

predisposing factors. These include:
 Any uterine scar secondary to previous vigorous

curettage, cesarean section, myomectomy
 multiparity
114
 Bulky placental tissue as in multiple pregnancy and

erythroblastosis fetalis
 Others include high altitude, smoking, previous history of

antepartum hemorrhage.
1.4. Pathophysiology
Bleeding usually occurs in the third trimester when progressive

formation of the lower segment results in tearing and exposure
of the blood vessels in the placental bed. The bleeding is
maternal in origin and is almost always revealed.
1.5. Clinical Features
The typical presentation is painless bright red bleeding in the

third trimester which in amount could range from spotting to
massive. It tends to come without warning but may follow
coitus or pelvic examination. It is recurrent in nature with
increasing bleeding occurring in subsequent episodes.
Changes in maternal pulse, blood pressure and the degree of

pallor are usually proportional to the external blood loss. The
usual findings on abdominal examination are non-tender,
normal-toned uterus (in labor relaxes completely between
115
contractions); high presenting part and abnormal fetal lie. Fetal

distress occurs if the mother is in shock or in labor as the
result of downward pressure on the placenta.
Since it may be attended by severe bleeding, digital or

speculum vaginal examination should never be done in any
woman with APH until placenta previa is ruled out.
1.6. Diagnosis
The diagnosis of placenta previa is strongly suggested by the

clinical features discussed above. Confirmation requires
ultrasonographic localization of the placenta. Ultrasonogrpahy
is used to diagnose placenta previa and its grade as well as to
evaluate the condition of the fetus including its gestational
age. Examination done before 30 weeks should be repeated
later as the position of the placenta may change as the lower
segment forms and increases in size.
Alternative method to diagnose placenta previa and its grade

is to do vaginal examination in the operating theatre with
everything ready for caesarian section if necessary (double-
set up examination). This procedure can cause severe
hemorrhage and thus should not be routinely recommended. It
should only be done in instances where ultrasound is not
available and termination of pregnancy is planned.
1.7. MANAGEMENT
116
All cases of suspected or proven placenta previa should be

admitted and managed in a hospital with 24 hours
comprehensive emergency obstetric service including blood
transfusion. Early referral of patients from health centers to
such facilities is crucial.
Women with life-threatening hemorrhage should receive

aggressive resuscitation which has to be started in the
referring unit and continued during transportation. Patient
should be delivered by emergency caesarian section whatever
the length of gestation or the grade of the placenta previa is.
The management of women without severe bleeding requires

admission to hospital. Further management depends on the
gestational age, condition of the fetus and extent of bleeding.
Termination of pregnancy either by induction (grade I and II
anterior placenta previa) or caesarian section (grade II
posterior and IV placenta previa) should be done if one of the
following is present:
 Gestational age of more than 37 completed weeks
 Fetal death, fetal distress or presence of

malformation incompatible with life
 Onset of active labor
117
 Continued bleeding after admission
In the absence of these conditions expectant management is

followed. This includes complete bed rest, avoidance of coitus
or vaginal manipulation, and close clinical and laboratory
monitoring. Ferrous sulphate is routinely prescribed.
2. ABRUPTIO PLACENTA (ACCIDENTAL HEMORRHAGE)
2.1. DEFINITION AND CLASSIFICATION
Abruptio placenta is premature separation of the normally

implanted placenta before the third stage of labor. The
bleeding could be concealed (internal) or revealed (external)
but in most clinically apparent cases it is a combination of
internal and external bleeding. Depending on clinical and
laboratory features, it is graded into mild (grade I), moderate
(grade II) and severe (grade III) types. Grades one and two
each account for around 40% while grade three only for 15%.
The important features of the different grades are shown in the
table below.
Gra Bleedi Contracti BP HR FHR DIC

de ng ons
118
I Minim complete Normal Norma Normal not

al relaxatio l present
n
II Mild- Incomple Postural Increa distres not

moder te hypotensi sed sed present
ate relaxatio on
n
III Moder Tetanic/ Reduced/ Fast, dead present

ate to board unrecord weak/
severe like able feeble
2.2. Incidence
It complicates 1% of all deliveries, the range being 0.3-1.6%.
2.3. Predisposing factors
The exact cause of abruptio placentae is unknown but there

are a number of well-established risk factors, including:
 Hypertensive disorders of pregnancy – single most

important factor
 Trauma such as a hard abdominal blow
119
 Sudden decrease in uterine volume, as follows rupture

of membranes in a mother with polyhydramnios and
following delivery of first twin
 Previous abruption placentae (recurrence is 10% after

one episode and increases to 25% after two)
 Others like poor socioeconomic condition and

malnutrition, smoking and short cord
An Abruptio placenta is typically an evolving process. The

bleeding begins in arterial vessels in the basal layer of the
decidua, which is split by the hemorrhage. The retro placental
hematoma expands, compressing the placental tissue. This
further separates the placenta which in turn causes more
bleeding and hematoma formation. Some of the retro placental
bleeding separates the membranes and escapes to the
external. But most remain concealed behind the placenta.
With building pressure some of it splits the myometrial cells
causing bruised appearance of the uterus, the so called
Couvelaires uterus. Occasionally blood may find its way into
the amniotic fluid resulting in bloody amniotic fluid. Damage to
the myometrium along with sequestration of clotting factors
causes disseminated intravascular coagulation. Profound
120
shock eventually ends up in acute renal failure. Rarely this

process may be self-limiting.
2.5 Clinical Features and diagnosis
This varies with the grade of abruption. Vaginal bleeding,

usually small in amount and dark red in color is present in
most. In some cases of concealed bleeding, this may be
absent. Abdominal pain of variable degree is another major
manifestation, ranging from labor like pain to unrelenting pain.
In severe cases bleeding from the other site may occur.
History of hypertension, trauma and past history should be
sought.
Vital signs derangement is indirectly proportional to the degree

of blood loss. Abdomen is almost always tender. In moderate
cases there is incomplete relaxation between contractions. In
severe cases the uterus is board like and tetanically
contracted uterus. The fetus is in distress or dead. The
presenting part is usually deeply engaged.
There are no specific diagnostic tests and therefore diagnosis

is mainly made on clinical grounds. Ultrasound is not helpful in
diagnosis.
2.6. Complications
121
Common complications are severe bleeding and shock,

consumptive coagulopathy, acute renal failure, postpartum
hemorrhage, fetal distress and intrauterine fetal death
2.7. MANAGEMENT
After admission one should secure an intravenous line,

determine hemtocrite and blood group / Rhesus factor
assessment, prepare at least two units of cross matched
blood. Crystalloids should be administered depending on the
needs. Assessment of the coagulation factors using fibrinogen
levels, prothrombin and partial thromboplastin times is not
feasible in most settings.
Simple bedside tests like whole blood clotting time and

bleeding time can be used as rough guides to the coagulation
system. Fresh frozen plasma should be given in cases of
disseminated intravascular coagulation.
Unless there are contraindications, vaginal route of delivery

preferred whether the fetus is alive or dead. Labor is usually
short and close fetal monitoring is needed to detect fetal
distress. Shortening of the second stage by instruments can
be done. Unnecessary episiotomy or laceration to the genital
tract should be avoided. Third stage should be managed
actively.
Fetal distress in the first stage mandates caesarian section.
122
3. RUPTURE OF VASA PREVIA
Vasa previa develops when the fetal blood vessels course

over the membranes and cross the internal os in conditions
such as placenta succenturiata and velamentous insertion of
the cord leading to bleeding from the fetal circulation.
It is a rare occurrence, the incidence being 1 in 5000

singletons, but much higher in multiple pregnancies. Although
a rare occurrence, it is yet very important because it leads to
fetal hemorrhage which frequently may result in fetal death
and stillbirth.
This condition may be confused with placenta previa. The

mother presents with painless bright red bleeding which
usually start after rupture of the membranes accompanied by
evidences of fetal distress.
Apt test is done to detect the presence of fetal blood in the

vaginal blood. In this test few drops of blood from the vagina
is mixed with an equal amount of 25% sodium hydroxide.
Maternal blood will turn light brown, whereas fetal blood will
not change color because of its resistance to alkali.
A LIVE VIABLE FETUS SHOULD BE DELIVERED IMMEDIATELY BY

EMERGENCY CAESARIAN SECTION AS EVEN A SMALL HEMORRHAGE MAY
BE FATAL. THE NEONAT AL HEMOGLOBIN SHOULD BE DETERMINED AFTER
BIRTH.
123
4. OTHER CAUSES
Local lesions of the cervix and vagina such as vaginitis,

cervicitis, cervical cancer or polyps, foreign bodies, etc may
cause vaginal bleeding in the antepartum period. Their
diagnosis depends on proper examination. Management
depends on the cause.
Antepartum hemorrhage could originate from the placenta.

Hemangioma of the placenta is especially important. It occurs
in approximately 1% of placentas. It sometimes may be large
enough to cause antepartum hemorrhage.
5. UNKNOWN CAUSES
These account for a significant proportion of cases of

antepartum hemorrhage. In fact, in many cases of antepartum
hemorrhage, no cause is found. And some of these are
thought to be due to abruption placentae that are so small to
be diagnosed by clinical evaluation or special investigations.
GENERAL BASIC PRINCIPLES OF THE MANAGEMENT

OF APH
124
I. Resuscitation should be started immediately, before referral

if the later is contemplated.
II. All patients with APH should be admitted to a hospital.
III. No digital vaginal examination should be performed until a

placenta previa has been ruled out except under the condition
of double-set up.
IV. Confirmation of the specific cause should be given

emphasis in order to decide on the specific management.
V. Mothers with antepartum hemorrhage, particularly abruption

placentae, are at an increased risk for postpartum
hemorrhage. Thus universal active third stage management
has to be implemented.
Review Questions
1. Describe the major causes of antepartum hemorrhage and

the clinical features that may help to distinguish between
them.
125
2. Describe the precautions that should be taken during

evaluation and management of a pregnant mother with
antepartum hemorrhage.
CHAPTER 8
HYPERTENSIVE DISORDE RS OF
PREGNANCY (HDP)
Learning objectives
 To define hypertension and significant proteinuria during

pregnancy
 To define pre-eclampsia and eclampsia
 To describe the features of severe pre-eclampsia
 To list the complications of pre-eclampsia
 To explain the basic principles of the management of

eclampsia
 To identify the indications for termination of pregnancy in

pre-eclampsia
Introduction
126
Hypertensive disorders (HDP) are one of the major causes of

maternal death both in developed and developing countries.
They are also major contributors to intrauterine growth
restriction and intrauterine fetal death. Timely diagnosis and
proper treatment can avert these major complications and
others.
1. Definitions:
HYPERTENSION DURING PREGNANCY IS DEFINED

AS SINGLE BLOOD PRESSURE MEASUREMENT OF
160/110 MM HG OR MORE OR TWO CONSECUTIVE
BLOOD PRESSURE MEASUREMENTS OF 140/90 MM
HG OR MORE MEASURED ON AT LEAST TWO
OCCASIONS 6 HOURS OR MORE APART.
SEVERE HYPERTENSION IN PREGNANCY IS

DEFINED AS SINGLE MEASUREMENT OF DIASTOLIC
BLOOD PRESSURE OF 120 MM HG OR MORE OR
DIASTOLIC BLOOD PRESSURE 110 MM HG OR MORE
ON TWO OCCASIONS MEASURED 4 HOURS OR
MORE APART.
SIGNIFICANT PROTEINURIA IN PREGNANCY IS

DEFINED AS URINARY PROTEIN EXCRETION OF 300
MG OR MORE PER 24 HOUR (QUANTITATIVE) OR 2+
OR MORE PROTEIN ON DIPSTICK OF TWO CLEAN-
127
CATCH MIDSTREAM SPECIMENS OF URINE

COLLECTED 4 HOURS OR MORE APART
(QUALITATIVE).
Pathologic edema is defined as dependent edema that

persists after nights rest OR any type of non dependent edema
that involves the face, the hands or the whole body OR
abnormal weight gain of more than 2 pounds per week.
PRE-ECLAMPSIA IS OCCURRENCE OF
HYPERTENSION, PROTEINURIA AND/ OR EDEMA
WHICH OCCURS AFTER 20 COMPLETED WEEKS OF
GESTATION AND RESOLVES WITHIN 6 WEEKS
POSTPARTUM. PREECLAMPSIA BEFORE 20 WEEKS
IS ASSOCIATED WITH MOLAR PREGNANCY. IT IS
CLASSIFIED INTO MILD AND SEVERE FORMS. THE
PRESENCE OF ANY OF THE FOLLOWING
CLASSIFIES IT AS SEVERE PREECLAMPSIA.
 severe hypertension (refer definition)
 proteinuria of 5 grams or more in 24 hours (quantitative) or

3+ or more on dipstick on two random specimens
(qualitative)
 Oliguria (urine output of less than 400 milliliters in 24

hours) with or out raised renal function tests.
128
 epigastric or right upper quadrant pain with or out elevated

liver function tests
 Thrombocytopenia
 Cerebral symptoms like persistent frontal or occipital

headache resistant to ordinary analgesics, blurring of
vision or scotoma, altered consciousness along with signs
of cerebral irritability like exaggerated deep tendon
reflexes.
 intrauterine growth restriction
 pulmonary edema
 HEELP syndrome – haemolysis, elevated liver function

test and thrombocytopenia
Chronic hypertension is hypertension that is present before

pregnancy or is first detected before 20 weeks of gestation and
persists after 6 weeks postpartum with or without long term
complications.
Gestational or transient hypertension is recurrent mild

hypertension that develops between 20 weeks of gestation and
24 hours postpartum without other signs of preeclampsia or
chronic hypertension and resolves within 10 days postpartum.
Superimposed preeclampsia is worsening of hypertension

(rise in systolic blood pressure by 30 mmhg or/and rise in
129
diastolic blood pressure by 15 mmhg from mid pregnancy

levels) and worsening or development of proteinuria with or
without pathologic edema in a woman with chronic
hypertension.
Ecclampsia is tonic clonic convulsions or coma occurring

during pregnancy, labour or within 7 days postpartum unrelated
to other cerebral conditions like epilepsy in a woman with
neglected or fulminant preeclampsia. It occurs in 50 %
antepartum, 25% intrapartum and 25% postpartum. Atypical
ecclampsia is ecclampsia occurring before 20 weeks of
gestation and after 48 hours postpartum.
2. Incidence of HDP
Hypertensive disorders of pregnancy complicate 7-10% of

pregnancies. Preecclampsia occurs in 5% of pregnancies
accounting for 70% of hypertensive disorders of pregnancy.
The incidence of ecclampsia is 0.1-0.5%.
3. Classification of HDP
Different classification schemes are used, some of which are

complicated for routine use. According to the American collage
of Obstetricians and Gynecologists (ACOG) HDP is classified
into four.
 Preeclampsia ecclampsia syndrome
130
 Chronic hypertension
 Chronic hypertension with superimposed preeclampsia

(pregnancy aggravated hypertension)
 Gestational or transient hypertension
In some cases it becomes difficult to classify hypertension into

any of the groups because of inadequate information like
unknown gestational age, hypertension that is first detected
after 20 weeks, labour or postpartum period. In these cases it is
best to manage them as having preeclampsia.
Some use the term pregnancy induced hypertension (PIH) to

describe preeclampsia/ecclampsia and gestational
hypertension.
4. Etiology of pre-eclampsia
The exact cause of pre-eclampsia is unknown. A number of

theories are forwarded, so preeclampsia is said to be a disease
of theories.
5. Risk factors for preeclampsia
Risk factors associated with pure preeclampsia are
 nulliparity especially at extremes of reproductive age

(less than 20 and greater than 35 years)
131
 conditions with hyperplacentosis (multiple pregnancy,

RH isoimmunization, non immune hydrops fetalis)
 molar pregnancy
 family history of pre-eclampsia in mother or sister
 new paternity
 black race and low socioeconomic status
Risk factors associated with superimposed preeclampsia are
 chronic hypertension before pregnancy
 strong family history of hypertension
 chronic renal disease
 diabetes mellitus
 connective tissue disorders
6. Pathophysiology of pre-eclampsia and eclampsia
The hallmark in the pathophysiology of preeclampsia is

widespread vasoconstriction which results in marked increase
in peripheral resistance. This process starts 3-4 months prior to
the development of hypertension. The subsequent effects of
this change are:
 Development of arterial hypertension which is proportional

to the increase in peripheral resistance. In severe cases
132
decrease in venous return may lead to normotensive

preeclampsia.
 Decreased blood volume from reduced vascular space.

Preeclamptic women, therefore, can not tolerate blood loss
at any time during pregnancy and delivery.
 Decreased tissue perfusion resulting in capillary

endothelial damage in various organs. In the kidneys it is
called glomeruloendotheliosis and manifests with
proteinuria (albuminuria).
 Increased capillary permeability results in increase in

interstitial fluid resulting in edema formation and
concomitant reduction in intravascular volume which
results in hemoconcentration.
 Capillary endothelial damage results in the formation of

micro thrombi in different organs mainly liver, kidneys,
brain. This results in reduction in platelet count and other
clotting factors.
7. Complications of preeclampsia
Preeclampsia, if untreated, is associated with high maternal

and perinatal mortality and morbidity. The common
complications are eclampsia, abruptio placenta, acute renal
failure, hepatic failure and rupture of subcapsular hematoma,
HEELP syndrome and disseminated intravascular
133
coagulation, cerebral hemorrhage and pulmonary edema and

heart failure. Intrauterine growth restriction and death are
fetal complications.
8. Diagnosis and clinical evaluation
The diagnosis of hypertensive disorders of pregnancy is

straight forward. The major task is to differentiate between
different types of HDP (mild and severe preeclampsia,
chronic hypertension, superimposed preeclampsia) and
identify presence of complications. To achieve this complete
history, physical examination and necessary investigations
should be carried out.
Important points that should be included in the history are:
 Gravidity, parity, gestational age and marital history for

new paternity
 Symptoms related to pathologic edema: leg swelling that

persists after rest, tightness of the rings, puffiness of the
face,
 Symptoms related to severe preeclampsia: decrease in

urine output, fetal movement,
 Symptoms of imminent eclampsia: severe and persistent

global or occipital headache, blurring of vision, epigastric
or right upper quadrant pain
134
 Presence of convulsions
 Symptoms of long term complications of chronic

hypertension: visual symptoms, neurologic symptoms,
cardiac symptoms
 Past or family history of hypertension and drugs used in

treatment
 History of renal disease and other medical illnesses
 Treatment received so far
Important areas to emphasize in the physical examination

are:
 Blood pressure and weight
 Fundal height and fetal heart beat
 Dependant and non dependent edema: pitting pedal and

pretibial edema, abdominal wall edema, periorbital edema,
ascitis
 Cardiac vascular examination: cardiomegally, murmurs,

peripheral pulses and renal artery bruit
 Deep tendon reflexes, fundoscopy, sensory and motor

functions
Depending on the availability the laboratory investigations

include:
135
 Urine protein: mid stream urine for dipstick (more

applicable) and 24 hour urine protein
 Complete blood count: hemtocrite, platelet count
 Blood chemistry: renal and liver function tests, uric acid
 Ultrasonography : gestational age, biophysical profile
9. MANAGEMENT
I. Preeclampsia
Termination of pregnancy is the definitive and curative

treatment for preeclampsia resulting in resolution of the
condition within 48 hours. It is the most appropriate treatment
for the mother. Any management short of this is palliative and
should have the objective of reducing the perinatal mortality
associated with preterm birth.
The factors that determine whether to embark on aggressive

(delivery) or conservative management are the gestational
age, the severity of the disease, the fetal maturity and fetal
condition.
A. Aggressive management
Indications for aggressive management are gestational age of

37 weeks or more, mature fetus as evidenced by lung maturity
tests, severe preeclampsia, worsening preeclampsia despite
conservative management, imminent ecclampsia, ecclampsia,
136
HEELP syndrome and fetal compromise (fetal distress,

abnormal fetal wellbeing tests or fetal growth restriction).
Important components are
 Administer short acting antihypertensive drugs like

hydralazine (5 mg IV stat followed by 5 mg in 10 minutes,
then 5-10 mg every 20 minutes to a maximum of 60 mg)or
nifedipine(10 mg sublingual to be repeated after 30
minutes) intermittently when the diastolic blood pressure is
110mmhg or more. Excessive lowering of the blood
pressure compromises placental perfusion and should be
avoided.
 Start infusion of parenteral anticonvulsants using

diazepam (10-20 mg by slow IV bolus over 2-3 minutes
followed by slow IV infusion of 30-40 mg in 1000 ml of 5%
dextrose in water over 24 hours. 10 mg IV bolus can be
repeated if convulsions recur) or magnesium sulphate
 Depending on the prevailing conditions, decide on the

mode of delivery (either by induction or caesarian section).
Since these women are anesthetic risks, caesarian section
is reserved for those with contraindication for induction.
(Refer to chapters 15 and 16).
137
 Monitor frequently blood pressure, deep tendon reflexes,

urine output, level of consciousness and if being induced
monitor induction according to the protocol hourly,
 For vaginal delivery, shorten the second stage by

instrumental delivery
 In the third stage, do not give ergometrine
 Continue monitoring the blood pressure, the level of

consciousness, the deep tendon reflexes, the urine out put
 Continue antihypertensive. Continue anticonvulsant

infusion for at least 24- 48 hours postpartum.
B. Conservative management
Based on the above considerations, if termination is not

indicated and the decision is to postpone delivery, then
Admit all cases to a hospital setting capable of managing

complications
Perform base line history, physical examination and

investigations as described in subtopic 8.
 Order bed rest in left lateral position, with necessary

mobility permissions. Do not restrict salt intake. Restrict
visitors.
138
 Take daily history of headache, blurring of vision, right

upper quadrant pain, urine output, fetal movement (kick
chart), extent of edema
 Measure blood pressure frequently (every 15 minutes to

every 6 hours, depending on severity)
 Record weight, edema, deep tendon reflexes, fetal heart

beat and urine out put daily,
 Monitor fetal growth by fundal height or ultrasound weekly
 Monitor fetal well being two or more times a week
 Monitor urine albumin daily
 Monitor uric acid, renal and liver function tests, platelet and
hemtocrite weekly
 Start medium acting antihypertensive like alpha methyl

dopa (250-500 mg 6-hourly) only if the diastolic blood
pressure is 100mmhg or above. Diuretics and angiotensin
converting enzyme inhibitors are contraindicated.
 Once the condition of the patient is stabilized, she may be

discharged and followed as an outpatient provided that
blood pressures is between 140-160/90-100 mm hg,
proteinuria is 1+ or less by dipstick or less than 500 mg in
24 hrs, there is no fetal jeopardy and the patient is
compliant.
139
Outpatient management consists of frequent ANC follow

up with blood pressure and random urine protein
measurements at least twice per week and daily fetal
movement counting by the mother. The mother should be
educated about the imminent symptoms and signs and
warned of the need to report immediately if she has any of
them at any time.
II. Eclampsia
This is an acute obstetric emergency which if not managed

appropriately results in the death of the mother and the fetus.
 Start the ABC of resuscitation (clear the airway by

suction, start an intravenous line, position the woman in
lateral position to prevent aspiration, administer oxygen
nasally and if in respiratory arrest assist ventilation
artificially)
 Prevent trauma to the tongue by inserting a mouth gag

and fall accidents by bed rails
 Catheterize the bladder by an indwelling folley catheter
 Order necessary investigations
 Start short acting antihypertensive as described above
140
 Start anticonvulsants as described in aggressive

management
 Terminate the pregnancy as described in aggressive

management. Unfavorable cervix is usually an indication
for caesarian section.
 Monitor the patient as described in aggressive

management but more aggressively (vital signs including
respiratory rate, pulse rate and temperature every half to
1 hour)
 Continue monitoring for 24 -48 hours after delivery. If the

patient convulses later than 48 hours after delivery, other
possible causes should be entertained.
Review Questions:
1. Define the following: Hypertension during pregnancy:

Significant proteinuria during pregnancy and Pre-
eclampsia and eclampsia
2. List the risk factors and complications of pre-eclampsia.
3. List the features of severe pre-eclampsia
4. Outline the management of pre-eclampsia and eclampsia
141
142
CHAPTER 9
Disturbances of Amniotic Fluid
Volume
LEARNING OBJECTIVES
 TO D I S C U S S T H E M E C H A N I S M
OF PRODUCTION AN D
AB S O R P TI O N OF AM N I O T I C
FLUID
 TO LIST THE I M P O R T AN T
F U N C TI O N S OF AM N I O TI C
FLUID
 TO L I S T T H E C AU S E S AND
C O M P L I C AT I O N S OF
P O L Y H Y D R AM N I O S
 TO L I S T T H E C AU S E S AND
C O M P L I C AT I O N S OF
P O L Y H Y D R AM N I O S
143
1. INTRODUCTION
Amniotic fluid invests and protects the fetus during its
intrauterine life, growth and development. Its volume has an
average value in normal pregnancy but there may be
abnormalities of this volume (excess or reduction) which
indicate the presence of an underlying problem in the fetus and
which also may result in certain complications.
Abnormally small volume of amniotic fluid is especially more

associated with serious problems in the fetus compared to
excess.
1.1. PRODUCTION AND ABSORPTION OF THE

AMNIOTIC FLUID
In the first trimester amniotic fluid is produced as the feto-

maternal serum dialysate or ultra filtrate. In the second and third
trimester its source is mainly fetal urination. Secretions by the
pulmonary epithelium and amnion cells also have some
contributions.
Fetal swallowing is the major mode of absorption of amniotic

fluid. Some is absorbed by the pulmonary epithelium.
THE NORMAL VOLUME AT TERM IS 500 TO 1200 ML,

THE AVERAGE BEING 800 ML.
144
1.2. Functions of amniotic fluid
 It acts as a cushion against trauma
 It also acts as a constant temperature buffer
 It functions as a waste deposit area
 It plays important role in the development of the

renal, gastrointestinal and pulmonary systems and
the development of fetal musculature
 It forms a reservoir for proteins, minerals and fluid.
 It prevents the skin and eye from drying.
2. POLYHYDRAMNIOS (HYDRAMNIOS)
2.1. Definition
Polyhydramnios refers to term amniotic fluid volume of more

than 2000 ml. But this is usually not practical and the diagnosis
is based on clinical evaluation and ultrasound assessment of
the volume of the amniotic fluid. At term amniotic fluid pool of
more than or equal to 8 centimeters and /or an amniotic fluid
index (AFI) of more than or equal to 20-25 cm are suggestive.
145
Hydramnios may be acute or chronic. The acute form tends to

develop rapidly in the third trimester and usually causes greater
discomfort to the mother.
2. 2. ETIOLOGY
Majority of polyhydramios is idiopathic (>60 %). The rest arise

either from conditions that increase the surface area of the
placenta and amnion or disrupt the integument of the fetus or
hamper the normal swallowing process of the fetus. Diabetes
mellitus, placental tumors, fetal anomalies like esophageal
atresia, tracheoesophageal fistula, spina bifida and
anencephaly, RH isoimmunization, nonimmune hydrops and
multiple gestations are clinical conditions associated with
polyhydraminos
2.3. CLINICAL FEATURES AND DIAGNOSIS
Symptoms are purely mechanical, arising from pressure within

or around the distended uterus. Abdominopelvic discomfort,
shortness of breath, edema of the lower limbs and lower
abdomen and in severe cases decreased urine output could be
reported by the patient. These could be exaggerated in acute
cases.
146
The finding of big-for-date uterus, difficulty to feel fetal parts,

easy ballotment of the fetus and distant or faded fetal heart
tones should arouse suspicion.
Ultrasound is the method of confirming the diagnosis.
2.4. COMPLICATIONS
Premature rupture of the membranes, preterm labor,

malposition and malpresentation, abruption placentae and
postpartum hemorrhage should be anticipated. Increased rate
of operative deliveries also occurs.
2.5. Management
Management is best done in well equipped settings capable of

handling the complications. Termination of pregnancy is the
management of choice for polyhydramnios caused by
malformations incompatible with life. In the absence of this
termination should be delayed as much as possible until fetal
maturity. Bed rest along with serial therapeutic amniocentesis is
the modalities of treatment. Non steroidal anti-inflammatory
drugs like indomethacin can be given.
3. OLIGOHYDRAMNIOS
3.1. DEFINITION
147
Oligohydramnios is term used when amniotic fluid volume of

less than 500 milliliters. The ultrasound criterion for diagnosis is
amniotic fluid pool of less than 1-2 centimeters and/or an AFI of
less than 5-7 centimeters.
3.2. Etiology
Prolonged rupture of membranes is the most common cause.

Others are postdate pregnancy, intrauterine growth retardation
or death, congenital anomalies especially renal agenesis and
drugs such as angiotensin converting enzyme inhibitors.
3.3. CLINICAL FEATURES
Symptoms, if present, reflect the underlying condition. The

common sign is small-for-date uterus.
3.4. Complications
Pulmonary hypoplasia, cord compression and amniotic band

syndrome are known complications of prolonged
148
oligohydramnios. Intrauterine fetal death and variable

decelerations in labor are others.
3.5. MANAGEMENT
Treatment is directed against the cause. Immediate delivery is

the best management for an alive fetus nearing maturity.
Continuous intrapartum monitoring is needed to detect
deceleration from cord compression. Aminioinfusion, where
practiced, can be used in pregnancies remote from term.
Termination of pregnancy should be considered if congenital
malformation is the cause.
Review Questions
1. Discuss the production and absorption of amniotic fluid.
2. Describe the clinical features and complications of

polyhydramnios.
3. Describe the complications of oligohydramnios.
149
150
CHAPTER 10
PREMATURE RUPTURE OF MEMBRANES (PROM)
AND PRETERM LABOR
Learning Objectives
 To define premature rupture of membranes and preterm

labor
151
 To list the risk factors for premature rupture of

membranes
 To list the risk factors for preterm labor
 To describe the diagnosis of PROM
 To list the complications of premature rupture of

membranes
 To outline the management of PROM
 To discuss the contraindications for suppression of labor

in a mother with premature labor
1. PREMATURE RUPTURE OF
MEMBRANES (PROM)
1.1. Definition
Premature rupture of membranes is rupture of membranes at

least one hour before the onset of labor, regardless of the
gestational age. It is further subdivided into preterm PROM and
term PROM depending on whether the rupture of membranes
occurred before or after 37 completed weeks of gestation.
Latency period is defined as the period between the time of

rupture of membranes and the onset of true labor. If the latency
152
period extends more than 24 hours it is called prolonged

premature rupture of membranes.
1.2. Incidence
It varies widely ranging between 6-12%. Majority occur at term.
1.3. Etiology
In most no apparent cause is found, but a number of conditions

that either increase intrauterine pressure or reduce the strength
of the membranes are implicated. Chorioamnionitis,
polyhydramnios, multiple pregnancies, cervical incompetence,
trauma and a variety of lower genital tract infection are clinical
conditions that in one way or another associated with PROM.
History gives unequivocal diagnosis in most cases. In typical

cases the patient gives history of sudden gush of clear fluid per
vagina followed by persistent uncontrolled leakage. In less
typical cases one may get small intermittent leakage of clear
fluid.
Physical examination in typical cases will reveal moist perineum

with amniotic fluid seen flowing from the vagina. Digital pelvic
examination should not be done in a patient suspected of
having PROM unless delivery is planned in 24 hours. Instead,
sterile speculum examination is done to confirm the diagnosis.
153
During the speculum examination, finding a pool of amniotic

fluid in the posterior fornix and observing amniotic fluid trickling
from the cervical opening clinches the diagnosis. Performing
Valselva maneuver of application of fundal pressure may help.
If in doubt, additional tests can be done to confirm the

diagnosis. These include tests that rely on amniotic fluid
characteristics. Nitrazine paper test (changes from yellow to
deep blue) and litmus test (changes from red to blue) is based
on the alkaline nature of the amniotic fluid. Ferning test (air
drying a drop of the fluid on a slide and examine for arborization
under light microscopy) is positive.
Other tests like dye instillation tests are not routinely done.
Ultrasound is not helpful but may give indirect evidence if one
finds oligohydramnios.
1.5. Complications
PROM is associated with increased maternal and perinatal

morbidity and mortality.
 Intrauterine infection (chorioamnionitis)
 Umbilical cord prolapse and compression
 Malpresentation
 Preterm labour and its complications
154
 Oligohydramnios, if prolonged causes pulmonary

hypoplasia and compression deformities
 Abruptio placenta
 Neonatal complications mainly congenital pneumonia

and sepsis and the effects of prematurity
1.6. Management
The management depends on the presence or absence of

chorioamnionitis, fetal distress or death or established labour. In
the absence of these management depends on the gestational
age.
I. Complicated PROM
Delivery should be accomplished in the presence of the

following. Depending on the existing conditions, the route of
delivery can either be vaginal or abdominal.
A. Chorioamnionitis
Diagnostic features are fever with chills, abdominal pain,

offensive amniotic fluid, tachycardia, uterine tenderness and
fetal tachycardia. Leukocytosis with left shift is often found.
Diagnosis is confirmed by finding microorganisms in amniotic
fluid sample.
The complications are sepsis, septic shock and neonatal

sepsis.
155
Management is administration of broad spectrum antibiotics

(ampicillin and gentamycin) and termination of pregnancy
preferably by induction. Antibiotics should be continued after
delivery. The neonate should be treated by combination
ampicillin gentamycin intramuscularly.
B. Fetal distress
C. Fetal death
D. Established labour
II. Uncomplicated PROM
Management depends on the gestational age.
A. Gestational age of 34 weeks or more
The risk of intrauterine infection is higher than the risk of

prematurity. Therefore, delivery of the fetus by induction or
caesarian section should be done. Some wait for 12-24 hours in
hope of spontaneous onset of labour.
B. Gestational age of less than 34 weeks
The risk of prematurity is higher than the risk of intrauterine

infection. Therefore, postponement of delivery till fetal maturity
(or 34 weeks) while closely monitoring for complications is the
management of choice.
 Admit the woman.
156
 Monitor the vital signs every 6 hours.
 Monitor for uterine contraction, uterine tenderness and

fetal well being (fetal heart beat and kick chart) on daily
basis (or more frequently).
 Monitor the white cell count daily.
 Monitor fetal growth by fundal height or by ultrasound

every week. Check for lung maturity
Prophylactic antibiotics and tocolytics are not generally advised.
2. PRETERM LABOR
2.1. Definition
Preterm labor is the onset of regular uterine contractions and

progressive cervical dilatation and effacement occurring
between 28 and 37 completed weeks of gestation resulting in
the birth of a physically immature neonate with birth weight
between 1000 and 2499 grams.
It is classified as spontaneous and induced preterm labour.
2.2. Incidence and importance
Preterm labour complicates 5-15% of all deliveries. Its

importance lies on its effect on the perinatal outcome. It
accounts for up to 80% of neonatal deaths in some institutions.
157
Mortality is mainly related to gestational age at birth. Four of the

six major causes of neonatal deaths are associated with
preterm labour. Survivors have increased risk of cerebral palsy
and mental retardation. The cost of caring the preterm neonate
is very high.
2.3. Etiology and risk factors of spontaneous preterm

labour
The exact cause is unknown. Risk factors are identified in only

50 % of the cases. These risk factors are
 Past obstetric and gynecologic factors: uterine anomaly

(like unicornuate and bicornuate uterus), submucosal
myomas, cervical incompetence, previous preterm labour
 Current pregnancy complications: PROM, polyhydramnios,

multiple gestation, amniotic fluid infection syndrome,
 Surgical/ medical complications: acute febrile illnesses,

abdominal surgery especially on appendix and adenexa,
penetrating abdominal trauma, asymptomatic bacteruria
 Demographic factors: non white race, low socioeconomic

status, maternal age of lees than 18 and greater than 40,
smoking, alcohol abuse, exhausting work
2.4. Diagnosis
Diagnosis is based on the following findings

158
 Gestational age between 28 and 3 completed weeks plus
 Regular uterine contractions occurring 5- 8 minutes apart

or closer (others use 4 contractions in 20 minutes or 8 in
60 minutes) each with duration of more than 30 seconds
plus
 Any one of the following with or without ruptured

membranes ( cervical effacement of more than 80 or
dilatation of the cervix of 3 cms and more or progressive
change in the cervix over time by digital examination or
ultrasound)
2.5. Prevention
A variety of regimens have been used to reduce the occurrence

of spontaneous preterm labour in those with risk factors but all
with limited success. These include
 Intensive patient education programs with weekly pelvic

examination or serial ultrasound
 Limiting activity to bed rest in late second and early third

trimester
 Adequate hydration
 Treating treatable medical conditions like febrile illnesses,

asymptomatic bacteruria and vaginal infections
159
 Others like prophylactic tocolysis and cerclage
In induced preterm labour iatrogenic immaturity should be

prevented as much as possible. This is done by ensuring the
gestational age and performing fetal lung maturity test.
2.6. Management:
Labour is allowed to continue in the following conditions.

Preparations must be made to manage/prevent complications in
the newborn.
 Fetal: fetal death, major malformation, fetal distress,

multiple gestation, intrauterine growth restriction,
gestational age of more than 34 weeks
 Maternal: APH, severe preeclampsia, cardiac disease and

others
 Others: PROM, chorioamnionitis, advanced labour (cervix

greater than 3 cm)
In the absence of the above factors conservative management

can be instituted. For the interest of the newborn such
management should be given in a setting with intensive
neonatal care unit (referral to such setting is essential). These
include
 Non specific measures with bed rest, rapid hydration and

sedation
160
 In the absence of contraindications, suppression of labour

by using B mimetic drugs (like ritodrine or terbutaline) or
magnesium sulphate
 Acceleration of fetal lung maturity by corticosteroids like

betamethasone or dexamethasone given at least 24 hours
before delivery.
2.7. Intrapartum Management]
This is generally similar to the management of labor at term

except that certain precautions are necessary in order to
prevent complication in the neonate. Among these is the
prevention of intracranial hemorrhage during labor.
Intraventricular hemorrhage affects 30-60% of all very low birth
weight babies, the majority of whom are preterm. Measures that
can be taken to minimize this risk are:
 Prevention of intrapartum hypoxia
 Perform controlled delivery of the fetus. Forceps delivery is

usually recommended for the same reason as an
episiotomy; but it may prove harmful in some cases
 Elective cesarean section is a preterm baby is growth-

retarded and also with a breech between 1000 and 1500
grams
2. 7. Neonatal complications
161
Respiratory distress syndrome (hyaline membrane disease),

intraventricular hemorrhage, hypothermia, hypoglycemia,
cerebral palsy, congenital malformations and mental retardation
are some of the major complications that contribute to mortality
and morbidity of theses newborns.
For these reasons all preterm neonates require close medical

care after delivery.
2.8. Contraindications for suppression of labor
 Fetal: intrauterine fetal death, congenital abnormalities

incompatible with life, pregnancy of gestational age more
than 34 weeks or proven lung maturity, fetal distress,
intrauterine growth restriction, PROM, multiple gesation
 Maternal: intrauterine infection

(chorioamnionitis),complications that necessitate delivery
like severe preeclampsia, APH,
 Conditions that contraindicate the administration of

tocolytics like cardiac diseases, uncontrolled diabetes,
thyrotoxicosis
Review Questions
162
1. Define premature rupture of membranes and preterm labor
2. Describe the diagnoses of premature rupture of

membranes and preterm labor.
3. List the complications of premature rupture of membranes.
4. Describe the risk factors for preterm labour.
5. Discuss the management of premature rupture of

membranes.
163
CHAPTER 11
164
Multiple Pregnancy
LEARNING OBJECTIVES
 TO D I S C U S S T H E DIFFEREN T
TYPES OF M U L TI P L E
P R E G N AN C Y
 TO DESCRIBE TH E RISK
F AC T O R S FOR M U L TI P L E
P R E G N AN C Y
 TO L I S T T H E M AT E R N AL AN D
P E R I N AT AL C O M P L I C AT I O N S
O F M U L TI P L E P R E G N AN C Y
 TO DISCUSS THE C L I N I C AL
F E AT U R E S AN D T H E D I A G N O S I S
O F TW I N P R E G N AN C Y
 TO DESCRIBE THE
AN T E P AR T U M , I N T R AP AR T U M
AN D P O S T P AR T U M
M AN AG E M E N T OF TW I N
P R E G N AN C Y
1. INTRODUCTION
165
M U L TI P L E P R E G N AN C Y ( AL S O
C AL L E D M U L TI P L E G E S T AT I O N ) I S
A P R E G N AN C Y W I T H M O R E T H AN
ONE FETUS. IT IS A HIGH-RISK
P R E G N AN C Y AS S O C I AT E D W I T H
S I G N I F I C AN T L Y H I G H E R R AT E S O F
M AT E R N AL AN D P E R I N AT AL
MORBIDITY AN D M O R T AL I T Y .
THEREFORE, MOTHERS WITH
M U L TI P L E P R E G N AN C Y WILL
NEED S P E C I AL AN T E P AR T U M ,
I N TR AP AR T U M AN D P O S T P AR T U M
C AR E W H I C H I D E A L L Y S H O U L D B E
PROVIDED IN S P E C I AL I Z E D
CENTERS ( AT L E AS T IN A
H O S P I T AL ) .
M U L TI P L E P R E G N AN C I E S I N C L U D E
TW I N S , TRIPLETS, AN D
Q U AD R U P L E T S AN D HIGH ER
O R D E R P R E G N AN C I E S , B U T T H E
M O S T C O M M O N O F TH E S E I S TW I N
P R E G N AN C Y AN D T H E F O L L O W I N G
DISCUSSION WILL FOCU S ON
TW I N P R E G N AN C Y .
2. Types and incidence of twin pregnancy
166
Depending on the number of ova involved, twin pregnancy is

divided into two types.
Dizygotic twins (fraternal twins) result from fertilization of two

separate ova by two spermatozoa. They are always diamniotic
– dichorionic and usually have separate placenta. Their sex
may or may not be the same. Their genetic content is different.
It accounts for two-thirds of twin pregnancy. The incidence

varies, ranging between 1.3 and 49 per 1000 pregnancies. A
traditional method of approximation (Hellin‘s rule) is used to
estimate the incidence of multiples roughly:
Incidence=1:80n-1 where n is the number of fetuses.
There are several factors that increase the incidence of

dizygotic twins. These are
 Race (more in blacks than whites)
 Family history of twinning especially on the maternal side
 Increasing maternal age (the peak maternal age for

dizygotic twinning is 35-40years)
 Previous history of twin pregnancy
 Pregnancy soon after stopping oral contraceptives (greater

rebound gonadotrophin secretion)
167
 Ovulation induction using human pituitary gonadotrophins

or clomiphene citrate (this may also increase the incidence
of monozygotic twinning) and
 Assisted reproductive technology.
Monozygotic twins (identical twins) result from division of a

single zygote. They have identical genetic material and are
always of same sex. They have one placenta but other features
depend on the time of division of the fertilized ova.
 If division occurs before 72 hours of fertilization a

diamniotic-dichorionic placenta with two fetuses result
accounting for 30% of monozygotic twins.
 If division occurs between the third and eights day of

fertilization, a diamniotic-monochorionic placenta with
two fetuses result which makes up 69% monozygotic
twins.
 If division occurs between eight and thirteen days a

monoamniotic-monochorionic placenta with two
fetuses result making up <1% of monozygotic twins.
 If division occurs after day 13 conjoined twins/ Siamese

twins result. These could be pygopagus (sacro-coccyx),
thoracopagus (thoracic cage), omphalopagus (area
between the umbilicus and the xiphysternum), thoraco-
168
omphalopagus (a combination of the above two) and

craniopagus (cranium).
 Further postponement of division after day 16 results in

incomplete twinning producing, for example, twins with two
heads but a single body (dicephalus).
Monozygotic twins account for around a third of twins. The

incidence is random and constant throughout, ranging between
2.3 and 4 per 1000 pregnancies. Unlike dizygotic twins, there
are no known risk factors.
3. Determination of zygocity
Following delivery one can determine the zygocity in the

following manner. First look at the sex of the twins. If they are
different then the zygocity is dizygotic. If the sex is the same
proceed further to examine the placenta and the membranes.
Presence of only one placenta without dividing membranes or
dividing membrane with only two layers confirms monozygotic
twins. Presence of one placenta with four layered dividing
membrane or presence of two placentas can exist in both
monozygotic and dizygotic twins. For these cases further
evaluation is needed like determining the blood group of the
neonates or DNA fingerprinting.
Antenatal determination of zygocity is possible by

ultrasonography.
169
4. Diagnosis
Early diagnosis is important for successful outcome. The

diagnosis of multiple pregnancy needs a high degree of
suspicion.
Suggestive symptoms are exaggerated pregnancy symptoms

like excessive vomiting, abnormally fast increase in abdominal
girth and excessive fetal movement. Risk factors like family and
personal history of twinning may be present.
Physical findings include large-for-date uterus, feeling of

multiple fetal parts with three poles identified and auscultation
of two or more distinctly different fetal heart beats with
difference of at least 10 beats/ minute. Abnormal increase in
weight, anemia and preeclampsia are common.
Confirmation of the diagnosis needs performing ultrasound or

plain abdominal X-ray. Ultrasound is the best method because
besides confirming the diagnosis it also checks for the
gestational age, malformation, placental localization and
zygocity.
5. COMPLICATIONS
GENERALLY PERINATAL MORBIDITY AND

MORTALITY IS INCREASED IN MULTIPLE
PREGNANCY AS COMPARED TO SINGLETONS. THIS
IS MORE SO WITH MONOZYGOTIC TWINS
170
ESPECIALLY IF THEY ARE OF MONOAMNIOTIC TYPE.

THE SECOND TWIN IS USUALLY THE SMALLER AND
WILL SUFFER MORE FROM THE EFFECTS OF
ABRUPTION PLACENTAE, HYPOXIA, CONSTRICTION
RING DYSTOCIA, OPERATIVE MANIPULATION AND
PROLONGED ANESTHESIA. MATERNAL MORBIDITY
IS ALSO INCREASED BY 3- 7 TIMES.
Multiple pregnancy is associated with almost all known

complications of pregnancy, childbirth and postpartum period.
 Antepartum complications include spontaneous

abortion, congenital malformations, hyperemesis
gravidarum, preeclampsia/ ecclampsia, antepartum
hemorrhage, PROM and preterm labor, intrauterine growth
restriction, malpresentations, polyhydramnios, anemia and
cord accidents (compression, entanglement and prolapse).
 Intrapartum complications include uterine dysfunction,

malpresentation in labour (40% are vertex-vertex, 35% are
vertex-breech or vise versa, 10% are breech-breech, 10%
are transverse with breech or vertex and rarely both may
be transverse), increased operative delivery especially
caesarian section, cord prolapse and retained second twin.
 Postpartum complications include postpartum

hemorrhage and puerperal sepsis.
171
 Complications unique to multiple pregnancy include

discordant twins, intrauterine fetal death of one twin, twin
to twin transfusion and conjoined twins.
6. DIFFERENTIAL DIAGNOSIS OF BIG FOR DATE UTERUS
These are wrong date, macrosomic fetus, polyhydramnios,

molar gestation, abdominal tumor with the pregnancy such as
fibroids or ovarian masses and in early pregnancy full bladder.
7. MANAGEMENT
7.1. ANTE PARTUM MANAGEMENT
SINCE MULTIPLE PREGNANCY IS A HIGH-RISK

PREGNANCY REQUIRING SPECIALIZED CARE,
DIAGNOSING THE PREGNANCY AS EARLY AS
POSSIBLE IS ESSENTIAL. THESE MOTHERS ARE
FOLLOWED AS HIGH-RISK WITH MORE FREQUENT
ANTENATAL VISITS. TASKS TO BE PERFORMED
DURING THE ANTENATAL PERIOD ARE
 Dietary advice on the need to take more calories, proteins

and vitamins
 Supplementation with iron and folic acid
 Frequent and careful fetal monitoring using fundal height,

kick chart and where available serial ultrasound and fetal
wellbeing tests
172
 Provision of adequate rest especially after the 24th week
 Prevention, if possible, and/or early detection and

treatment of complications (including referrals) associated
with multiple pregnancies.
 Education on the need for hospital delivery
 Decision on the mode of delivery, which in the absence of

other complications, is determined by the number of
fetuses, the presentation of the first twin and the presence
of conjoining. Caesarian section is indicated in triplets and
above, if the first twin is non vertex and in conjoined twin.
7.2. Intrapartum management
Ideally, labour should be attended in a hospital setting with

personnel skilled in intrauterine manipulation and neonatal
resuscitation and with capacity to monitor both fetuses and with
set up to perform emergency caesarian section and blood
transfusion and with set up for intensive neonatal care. At least
delivery should be in a hospital with facilities for caesarian
section.
In the first stage, admit the patient in early labor, secure an

intravenous line and start infusion of crystalloids. A minimum of
two units of blood should be cross matched. Close monitoring
of the vital signs, uterine contractions and fetal heart beat of
both fetuses should be done. Monitor progress of labour by
173
periodic cervical examination. If labour is prolonged caesarian

section must be done. Augmentation is contraindicated.
In the second stage, deliver the first twin. Clamp and cut the
cord. Immediately following this perform abdominal palpation to
determine the lie of the second twin and auscultate for its fetal
heart beat. Assess also the degree of vaginal bleeding.
 Await spontaneous delivery if the lie is longitudinal and

there is no fetal distress or excessive vaginal bleeding.
Augment with oxytocin If uterine contractions are not
adequate.
 If the lie is transverse one should attempt external cephalic

version. If successful proceed as above. If this fails either
perform internal podalic version followed by total breech
extraction. This should only be done by persons with
considerable expertise in an operating theatre. If this can
not be done the second twin should be delivered by
caesarian section.
 In the presence of fetal distress or excessive vaginal

bleeding deliver the second twin fast by instrumental
delivery (if vertex) or by total breech extraction (if breech)
or by internal podalic version and breech extraction (if
transverse) or by caesarian section (if the above
procedures are contraindicated or have failed).
174
Third stage is managed actively. The placenta and the

membranes are delivered with care for subsequent
examination.
Review Questions
1. Describe the two types of twin pregnancy.
2. List the factors that increase the risk of dizygotic twinning.
3. List the complications of multiple gestation in the antenatal

period.
4. Discuss the diagnosis of multiple gestation.
5. Outline the intrapartum management of twin pregnancy.
175
CHAPTER 12
RH ISOIMMUNIZATION
LEARNING OBJECTIVES
 To define Rh isoimmunization and hemolytic disease of the

newborn
 To describe the pathogenesis of Rh isoimmunization
 To describe the effects of Rh isoimmunization on the fetus-

newborn
 To outline the management of Rh negative unsensitized

pregnancy.
1. Introduction
Many different antigens are found on the surfaces of red blood

cells and they may cause important isoimmunization in
obstetrics. The most important of these is the Rh group.
176
Next to the ABO system, the Rh system is the second most

important blood group system. The Rh antigens are found on
red blood cell membrane protein. Although more than 40
different antigens in the Rh system have been described, five
determinants account for the vast majority of phenotypes. One
of the systems used to designate Rh antigens is the Fishers
CDE system. Inheritance of Rh antigens follows Mendellian
law, which is an individual is either homozygous or
heterozygous for each antigen.
The D antigen, also called the Rh factor is the most powerful

and important of the Rh antigens. An individual who possess it
is labeled as Rh positive and who lack it as Rh negative.
Some people react weakly to anti D antibody and are labeled
as Du positive. The incidence of Rh negative people varies
from population to population (15% in Caucasians and 4% in
African blacks). Exposure of these Rh-negative people to even
small amounts of Rh-positive cells, by either transfusion or
pregnancy, can result in the production of anti-D alloantibody, a
condition called Rh sensitization or isoimmunization.
2. Definitions
I. Rh incompatibility is the presence of different Rh types in a

woman and her partner. In obstetrics, the significant
incompatibility is when the woman is Rh negative and the
partner is Rh positive.
177
II. Rh isoimmunization (Rh sensitization) is production of

antibody against the Rh factor by an Rh negative woman
following exposure to Rh-positive cells.
III. Erythroblastosis fetalis is the condition in which large

numbers of nucleated red cells are seen in the fetal circulation,
occurring in response to excessive destruction of fetal red blood
cells.
.IV. Hydrops fetalis is generalized edema in the fetus and

collection of serous fluid in body cavities of the fetus resulting
from a variety of pathologic conditions (immune hydrops and
non immune hydrops).
V. Hemolytic disease of the newborn is occurrence of

progressive anemia and hyperbilirubinemia in a newborn
caused by haemolysis of red blood cells, in most cases
antibody mediated.
3. Pathogenesis
FOR RH ISOIMMUNIZATION TO OCCUR, THE

FOLLOWING PREREQUISITES MUST BE FULFILLED:
I. Rh negative mother carrying Rh positive fetus
The chance of having Rh positive fetus from Rh positive father

ranges from 50% (if the father is heterozygous) to 100% (if the
178
father is homozygous). Non paternity explains the development

of hemolytic disease of the newborn.
II. Entry of the fetal Rh positive red blood cells into

maternal circulation
This occurs following transfusion of incompatible blood (rare

nowadays because of screening before transfusion) or more
commonly following fetomaternal hemorrhage (through leaks
in the placenta).
Fetal red blood cells are detected in maternal circulation in 6%

in the first trimester, 15% in the second trimester and 30% in
the third trimester. It may be silent or may follow obstetric
complication. Fetomaternal hemorrhage occurs in more than
50% during delivery especially in the third stage. Conditions
that aggravate fetomaternal hemorrhage are spontaneous or
induced abortion, ectopic gestation, antepartum hemorrhage
especially abruptio placenta, amniocentesis, abdominal trauma,
and external cephalic version. Conditions that worsen
fetomaternal bleeding during labour are manual removal of
placenta, twin delivery and caesarian section.
III. Development of Rh antibodies by the mother
179
The maternal immune system responds by producing

antibodies which are initially of Igm type (big immunoglobulin
that can not pass the placental barrier). Fetomaternal bleeding
in the subsequent pregnancies results in the anamenstic
reaction producing an Igg type of antibody (small antibody that
can pass the placental barrier).
Factors that affect this maternal response are inborn

responsiveness of the mother (30% are non responders),
volume and rate of hemorrhage (as little as 0.1 ml is enough),
and presence of ABO incompatibility (reduces risk by 50 -75%).
The overall risk of isoimmunization of an Rh positive ABO

compatible fetus is 16%. Antibodies can be detected before the
delivery of the first Rh positive fetus in 1% and in another 8% it
will be detected within 6 months of delivery and in another 8%
the level is so low that it cannot be detected until the early part
of the second pregnancy.
In addition, for hemolytic disease of the newborn and hydrops

fetalis to develop transfer of the Igg type antibody and antibody
mediated destruction of fetal red blood cells must occur. The
first neonate is usually spared but subsequent Rh positive
fetuses are affected, extent worsening with each pregnancy.
4. Effects on the fetus and the newborn
180
Hemolytic anemia develops, the extent of which depends on the

amount of antibody. To compensate for the ensuing anemia the
fetal bone marrow and later the extramedullary sites that
produce RBC (liver, spleen and placenta) are called to produce
red blood cells at fast rate. This results in the appearance of
young nucleated cells in the blood stream.
In severe cases even extramedullary hematopoiesis can not

cope with the degree of destruction. This results in progressive
anemia which eventually leads to congestive heart failure and
tissue hypoxia. The liver parenchyma is replaced by
hematopoeitic tissue. Serum albumin falls as the result. Portal
hypertension develops from obstruction of the portal veins. The
combination of these causes generalized edema of the fetus
called hydrops fetalis. Eventually fetal death occurs.
Before delivery the bilirubin, mainly of unconjugated type is

cleared by the placenta. Following the delivery of the fetus,
increasing amounts of unconjugated bilirubin accumulate in the
neonatal circulation (because the limited capacity of the liver to
clear). The unconjugated bilirubin crosses the blood brain
barrier and damages the basal ganglia to cause kernicterus.
The neonate may die of severe anemia or kernicterus.
5. Management of Rh negative unsensitized pregnancy
I. Identification of pregnancies at risk at the initial ANC visit
181
 Determine blood group & Rh factor and indirect coombs

test for antibody screening for all pregnant mothers. The
possible outcomes are
a. Rh positive with negative antibody screen – no further

testing needed
b. Rh positive with positive antibody screen – consider

atypical antibodies
c. Rh negative with positive antibody screen – manage as

sensitized pregnancy
d. Rh negative with negative antibody screen – manage as

unsensitized pregnancy
II. Management of unsensitized pregnancy
 Determine the blood group and Rh factor of the partner
 Repeat indirect coombs test at 28 weeks and at 36 weeks.

If negative consider antepartum prophylaxis with 300
micrograms of anti D gamma globulin at 28 weeks. If
positive manage as sensitized pregnancy.
 Provide anti D prophylaxis in cases with amniocentesis,

APH, external cephalic version.
 Following delivery determine blood group of the newborn

and antibody screening. If the newborn is Rh negative no
further treatment is needed. If antibody screen is positive
182
monitor the newborn for haemolysis and manage next

pregnancy as sensitized. If newborn is Rh negative and
antibody screen is negative, provide anti D gamma
globulin within 72 hours. The usual dose is 300
micrograms but ideally should be determined by the extent
of fetomaternal hemorrhage. This is done by performing
Kleihauer Betke test (acid elusion test). For abortion of
less than 12 weeks gestation the dose is 50 micrograms.
6. Management of sensitized mother
These women need specialized care with measurement of

antibody levels in titers at regular intervals, amniocentesis for
bilirubin levels, serial ultrasound for detection of hydrops and
management of neonatal anemia and hyperbilirubinemia.
Therefore, referral of these women is the correct approach at
health center level.
Important points about ABO hemolytic disease
 It occurs when the mother has group O blood (with anti-A

and anti-B antibodies in her serum) and fetus is group A, B
or AB.
 Unlike Rh isoimmunization, 40-50% of ABO

incompatibilities occur in the first-born infant.
 ABO hemolytic disease is primarily manifest following birth,

when the infant becomes jaundiced within the first 24 hours
183
with a variable amount of anemia and hyperbilirubinemia

which is usually mild. Serious complications almost never
occur.
 The management consists of measurement of bilirubin

serially and provision of phototherapy to the newborn.
Review Questions
1. Discuss the pathogenesis of Rh isoimmunization.
2. Outline the management of unsensitized Rh negative

pregnancy.
3. Describe the important features of ABO hemolytic disease.
CHAPTER 13
COMMON MEDICAL DISOR DERS IN
PREGNANCY
Learning objectives
 To enumerate the common medical disorders in

pregnancy.
 To describe the clinical features of each of the common

medical disorders in pregnancy and their causes.
184
 To outline the management of each of the common

medical disorders in pregnancy.
 To describe the effect of each of the common medical

disorders on the pregnant woman and her child with their
implications.
1. ANEMIA IN PREGNANCY
1.1. Definition:
Anemia during pregnancy is defined as a hemoglobin level of

11 g/dl or less (hemtocrite of < 33%) except during the second
semester, when the cut-off point is reduced to 10.5 g/dl. It is
said to be severe if the hemoglobin is less than 8gm/dl.
1.2. Incidence and causes
It affects approximately 5- 50% of pregnant women in tropics

and < 2% of in developed countries. It is ore severe in tropics. It
is the leading cause of indirect maternal mortality and morbidity.
It is the most common hematological abnormality during
pregnancy.
Majority are nutritional anemias. Iron deficiency anemia account

for 80-95 % of nutritional anemias during pregnancy.
Megaloblastic anemias from folate and vitamin b 12 deficiency
185
account for only 3-4% of nutritional anemias. Other causes of

anemia (hemoglobinopathies, leukemia, hemolytic anemias
anemia of chronic illness and the like) are not common during
pregnancy.
1.3. Pathophysiology of nutritional anemia
The requirement of iron during pregnancy is around 1000mg.

(450mg for red blood cells and uterine muscle, 270 mg for fetal
iron, 170-200 mg for daily loss and 90 mg for placenta). There
are additional needs for blood loss during delivery (190 mg) and
lactation (1mg/day). Assuming the stores are adequate a
pregnant woman average daily dietary requirement is 3.5
mg/day. Failure to meet this demand eventually ends up in
anemia. The sequence of events in the development of frank
anemia is depletion of the stores followed by deficient
hematopoiesis (microcytic and hypochromic RBC with abnormal
RBC indices) and finally reduction in RBC production results in
evidences of frank anemia (decreased hemtocrite and pallor).
The predisposing factors for iron deficiency anemia are
 Inadequate intake of iron: food taboos, poor dietary habit,

low socioeconomic state
 Low store at the beginning of pregnancy: short interval

between pregnancies, excess menustral flow, hookworm
infestation
186
 Blood loss during pregnancy: early and late pregnancy

bleeding, hookworm
 Increased demand: multiple pregnancy, chronic infections
1.4. Complications
Anemia is associated with adverse pregnancy outcome.
 Fetal: spontaneous abortion, preterm delivery, low birth

weight, intrauterine growth restriction, stillbirth,
 Maternal: congestive heart failure and pulmonary edema

especially in labour and postpartum period, postpartum
hemorrhage, puerperal sepsis, delayed wound healing,
apathy, increased risk of other infections like tuberculosis
 Neonatal: anemia of infancy
1.5. Treatment
It depends on the cause, severity and the gestational age.
I. Iron deficiency anemia
 Ferrous sulfate 300mg containing 60 mg elemental iron of

which 10%is absorbed, three times per day,
orally. Continue treatment for 3 months after
the hemoglobin concentration returned to normal.
Alternatives are ferrous fumarate and ferrous gluconate.
187
Follow up with weekly hemoglobin and reticulocyte

determination should be done.
 Parenteral route of treatment in cases of intolerance of oral

route or refractory to treatment by oral route, and for very
severe anemia.
 Indications for blood transfusion are presence of

congestive heart failure, severe anemia with hemoglobin
of<4.4 gm/dl, anemia with sepsis and renal failure, anemic
patient with hemoglobin of <6-7gm/dl seen for the first time
in labour, abortion or in the last 4 weeks of pregnancy.
Packed RBC should be used.
 Underlying causes, if any (like hook worm, malaria and

chronic illnesses), other than nutritional deficiency, should
be treated also.
II. Megaloblastic anemia
 Folic acid 5 mg three times / day and continued at a dose

of 5 mg / day for the rest of pregnancy.
1.6. Prevention of anemia
 improve diet and dietary habit, socioeconomic status
 Prevent and treat hookworm (deworming) and malaria
 Child spacing by family planning
188
 Universal supplementation of iron and folic acid to all

pregnant women throughout pregnancy
 iron fortification of staple diet
2. CARDIAC DISEASE IN PREGNANCY
2.1. Introduction
A woman with a known cardiac illness can become pregnant or

a healthy pregnant woman can develop cardiac illness while
pregnant. In a woman with a preexisting cardiac illness, the
increased homodynamic burden of pregnancy, labor and
delivery can aggravate the symptoms of the illness and/or
precipitate complications. The risk of congestive heart failure is
the highest around 24 weeks of gestation, labour and the
immediate postpartum period. During each uterine contraction
in labor about 200-300 ml blood is squeezed from the
contracting uterine muscles, increasing the cardiac output by
about 20%.
2.2. Significance
Cardiovascular diseases are the most important non-obstetric

cause of disability and death of pregnant women, occurring in
0.4-4% of pregnancies. The most common cardiovascular
189
disease that complicates pregnancy is rheumatic heart disease.

The reported maternal mortality rate ranges from 0.4% in
patients with New York heart association classifications I and II
to 68%or higher among patients with class III and IV severity.
Patients with valvular heart disease may develop subacute
infectious endocarditis. It is also associated with adverse fetal
outcome like spontaneous abortion, preterm labour, low birth
weight, and intrauterine fetal death.
2.3. Classification
The degree of functional disability due to cardiac disease is

graded according to the New York Heart Association
classification as follows:
 Class I: No symptoms limiting ordinary physical activity.
 Class II : Slight limitation with mild to moderate activity

with no symptoms at rest
 Class III: Marked limitation with less than ordinary

activity; dyspnea or pain on minimal activity.
 Class IV: Symptoms at rest or with minimal activity and

symptoms of frank congestive heart failure.
Note: With rare exceptions, women in class I and most in class

II go through pregnancy without morbidity. As much as possible
patients in classes III and IV should avoid pregnancy.
190
Therapeutic abortion is an option in early pregnancy. If the

pregnancy is continued, prolonged hospitalization or bed rest
will often be necessary. These women tolerate major surgical
procedures poorly.
2.4. Management
Once diagnosed, these patients should be referred for

specialized care by obstetrician, internist and neonatologist.
The general principles in the management are:
I. Antepartum
 Bed rest
 Moderate dietary restriction
 Provision of diuretics (chlorothiazides are accepted) with

potassium supplementation
 Prophylactic digitalization
 Frequent ANC for maternal and fetal monitoring
II. Intrapartum
 Unless contraindicated vaginal route of delivery is

preferred
 Conduct labour and delivery in lateral decubitus position
 Provide adequate pain relief
191
 Restrict intravenous fluids
 Provide oxygen with breathing mask along with continuous

pulse oxymetery
 Provide prophylaxis for SBE for those with structural

lesions
 Shorten the second stage by instrumental delivery
 Do not use ergometrine in the third stage
 Prevent postpartum pulmonary edema by keeping the

woman in sitting position
 Provide thrombus prophylaxis by early ambulation and/ or

low dose aspirin
Note: A patient with a known heart disease should consult her

physician before becoming pregnant in order to determine the
advisability and optimum timing for pregnancy. In a pregnant
woman with a cardiac disease:
 Recognize the presence of preexisting cardiac diseases.
 Assess the degree of disability
 Understand the impact of the added homodynamic

changes of pregnancy.
 Anticipate, prevent, diagnose and treat complications such

as arrhythmia, congestive heart failure when they arise.
192
 Advise the patient regarding discontinuation or

continuation of the pregnancy and risk of future
pregnancies.
3. INFECTIOUS DISEASES IN PREGNANCY
3.1. Tuberculosis in pregnancy
It is a commonly encountered medical problem in pregnancy. Its

effects on pregnancy include preterm delivery, intrauterine
growth restriction and low birth weight which increase the
perinatal mortality by 6 fold.
Adverse outcome on pregnancy correlate with late diagnosis,

incomplete or irregular treatment and advanced disease.
Diagnosis and management is similar to nonpregnants. With

the exception of streptomycin and pyrazinamide, all the first-line
antituberculous drugs are safe to be used during pregnancy.
Streptomycin causes congenital deafness in the new born. The
safety of the use of pyrazinamide during pregnancy is not
ascertained. Therefore, drugs used for treatment of tuberculosis
include: isoniazid (INH), rifampicin and ethambutol. However,
pyrazinamide can be included into the regimen if there is drug
resistance. (Refer to the module on tuberculosis for further
detail).
193
Neonatal Tuberculosis
Neonates, though rare, can get tuberculosis infection in utero if

the mother is suffering from active tuberculosis. The incidence
of congenital infection increases if the mother is HIV positive.
The tuberculous lesions in the new born are usually found in the
liver. This can be prevented if the mother is properly treated
while pregnant.
3.2. Malaria in pregnancy
Types
Stable malaria occurs in endemic areas where there is repeated

infection since childhood. Community immunity is well
developed and epidemics do not occur. During pregnancy
immunity slackens resulting in increased parasitemia and
relapse rate of dormant exoerythrocytic stages. Episodes of
malarial infection increase by three to four folds during the latter
two trimesters of pregnancy and two months postpartum.
Severity of falicparum malaria is increased.
Unstable malaria occurs in areas with intermittent transmission.

Community immunity is poorly developed and epidemics occur.
Malarial attacks are severe and cerebral malaria is common
especially in nulliparous women.
194
Effects
They are related to pyrexia, haemolysis, placental parasitization

(in immune) and transplacental infection (in nonimmune).
Maternal: increased number of attacks, anemia from folic acid

deficiency induced by haemolysis, cerebral malaria, puerperal
pyrexia
Fetal: spontaneous abortion, preterm labour and prematurity,

intrauterine growth restriction, intrauterine fetal death (stillbirth),
congenital malaria in nonimmune in few days after delivery
Diagnosis
In immune women constitutional symptoms are subtle. Non

immune women present with constitutional symptoms with fever
and chills. Blood film identifying the plasmodium parasite
confirms the diagnosis.
Treatment
Once diagnosed, malaria should be treated aggressively.

Severe forms need inpatient treatment with parentral
antimalarials. Drug of choice depends on the type of
plasmodium parasite and the degree of resistance in the
community. Chloroquine, sulfadoxine-pyrimethamine,
195
mefloquine and quinine are safe to be used in pregnancy. For

details refer to modules on malaria.
Prophylaxis
This is given for nonimmune people traveling to endemic areas.

The drug should be taken 1-2 weeks before travel and
continued for4 weeks after return. Depending on the pattern of
resistance, drugs like chloroquine, mefloquine or sulfadoxine-
pyrimethamine can be used.
3.3. HIV infection and pregnancy
I. Epidemiology
Since its discovery in 1981, HIV/AIDS has become a serious

health problem worldwide. The problem is most prevalent in
developing countries. 80% of HIV-infected women are of
childbearing age.
The prevalence of HIV infection among pregnant women

attending antenatal care services in East and Central Africa
ranges from 20% to 30%. In Ethiopia it is 10% to 20%.
HIV/AIDS is now a common cause of death among young
women, most importantly pregnant women. AIDS related
maternal deaths are increasing dramatically and are displacing
common obstetric causes. It also increases childhood mortality
196
directly as the result of childhood AIDS or indirectly from

neglect off orphans.
II. Effects of HIV on pregnancy
HIV infection is associated with increased adverse obstetric

outcomes like spontaneous abortion, preterm delivery, low birth
weight and stillbirth. Another significant effect is mother to child
transmission of infection (MTCT), which is by far the largest
source of HIV infection in children. There is also increased
maternal morbidity and mortality from intrapartum and
postpartum infection.
III. Effects of pregnancy on HIV
Pregnancy induced immune suppression accelerates the

progress of HIV infection only in women in late stages of the
disease but not in asymptomatic HIV positive women. When
comparing changes in CD4 count/percentage over time, there is
no difference between HIV-positive pregnant and non-pregnant
women, suggesting that pregnancy does not accelerate decline
in CD4 cells in asymptomatic carriers.
IV. Mother to Child Transmission (MTCT)
MTCT of HIV infection occurs during pregnancy (5-10%),

delivery (10-20%) and through breast feeding (10-20%). The
197
overall rate of HIV transmission from an HIV positive mother to

her child is 25-50% In developed countries 15-25%). Factors
affecting MTCT of HIV are
 General factors: maternal viral load and CD4 counts

(more in advanced disease and recent infections), type of
virus (HIV2 has 20 times risk than HIV1), treatment with
antiretroviral drugs (reduces MTCT by 50%)
 Antenatal factors: prematurity, obstetric procedures

(amniocentesis and external cephalic version), obstetric
complications (abruptio placenta and placenta previa),
infections (malaria and STI), vitamin A deficiency and
smoking
 Intrapartum factors: prolonged labour, chorioamnionitis,

prolonged rupture of membranes (risk increases by 2%
every hour after 4 hours) invasive procedures (internal
monitoring, scalp sampling, operative vaginal delivery and
episiotomy)
Note: elective caesarian section reduces risk but caesarian

section done after labor has started especially in the
presence of rupture of membranes or prolonged labor
increases risk. Another problem with caesarian section is
increased risk of postpartum infection by 5-7 times.
198
 Breast feeding factors: cracked nipples, acute mastitis,

neonatal oral thrush and other gastrointestinal lesions,
mixed feeding, duration of breast feeding of ore than 14-
16 weeks
V. Prevention of MTCT (PMTCT)
For effective PMTCT, a four pronged approach has been

developed by WHO. These basic components of
comprehensive PMTCT are
I. Primary prevention of HIV in women:
 Provision of VCCT for all women
 Helping HIV negative women to remain HIV seronegative

through risk reduction behaviors (abstinence, limiting
partners and safe se by use of condoms)
II. Prevention of unwanted pregnancy in HIV positive

women:
 Counseling about the effects of HIV on pregnancy, health

of the mother, long-term health of the mother and child and
risk of transmission to the newborn
 Provision of family planning services
III. Prevention/ reduction of transmission of HIV virus

during pregnancy, childbirth and breast feeding:
199
A. Antepartum:
 Universal VCCT service for all pregnant women
 Reduce viral load by short coarse antiretroviral therapy

(niverapine 200 mg at the start of labour to be repeated if
not delivered in 48 hours and single dose 2 mg/ kg for the
neonate within 72 hours of delivery. If delivery occurs less
than 1 hour after the maternal dose two doses are given
for the neonate one as soon after delivery as possible and
the second dose after 48-72 hours of the first dose). Other
regimens include zidovudine, lamivudine, combination of
zidovudine and niverapine/ lamivudine and finally highly
active antiretroviral therapy (see below).
 Additional measures: risk reduction behaviors including

safe sex, treatment of nutritional deficiencies and
concomitant STI, prophylaxis for malaria and avoidance of
smoking
Note: There may be no need to increase the number of

visits unless there evidences of obstetric complications
and signs/symptoms of advanced infection (opportunistic
infection and other AIDS indicator illnesses).
B. Intrapartum
Improving obstetric practices to prevent avoidable exposure to

the virus at birth
200
 Avoid prolonged rupture of membranes and prolonged

labour by proper use of partograph
 Avoid artificial rupture of membranes as long as labour is

progressing well. If it is done delivery has to occur within 4
hours. Some use anti septic preparation of the vagina
when rupture of membranes is more than 4 hours.
 Avoid repeated pelvic examinations, internal monitoring of

the fetus and fetal scalp blood sampling
 Treat chorioamnionitis aggressively
 As much as possible avoid caesarian section after rupture

of membranes. Provide prophylactic antibiotics to the
mother.
 Avoid routine pubic hair shaving, unnecessary episiotomy

or instrumental delivery
 Prevent tears by controlled delivery of the fetus
 Clamp the cord immediately after delivery. Cut the cord

after pulsation stopped under light gauze. Do not milk the
cord towards the newborn
 Avoid/ reduce suction by nasogastric tube. If needed do it

gently. Provide universal neonatal care to the neonate.
 Apply universal precautions throughout
201
 Educate about the infectiousness of the lochia and how to

handle sanitary napkins.
C. Breast feeding
Modify infant feeding practices. Depending on the resources,

two options: exclusive replacement feeding and exclusive
breast feeding for 6 months followed by abrupt weaning.
Ideally decision should be made during pregnancy and
necessary preparations made. Mixed feeding should be
avoided.
IV. Care and support of the mother (PMTCT Plus):
 Continued care of the mother after delivery by provision of

antiretroviral drugs, treatment of opportunistic infections
 Social and economic support
Other drug regimens in PMTCT
I. Zidovudine: Antepartum: treatment is initiated at14-34

weeks and continued throughout pregnancy, being
administered 2-5 times per day, depending on the dose.
Intrapartum: zidovudine is given IV over 1 hour followed by
continuous infusion until delivery. Postpartum: zidovudine is
given orally to the newborn for the first 6 weeks of life,
beginning at 8-12 hours after birth.
202
II. Zidovudine/Lamivudine: Antepartum: Zidovudine and

lamivudine given orally at the onset of labor followed by
Zidovudine orally every 3 hour until delivery with lamivudine
orally every 12 hours. Postpartum: Zidovudine orally every 12
hours with lamivudine orally every 12 hours for 7 days
III. Zidovudine/Nevirapine: Intrapartum: Zidovudine IV bolus

followed by continuous infusion until delivery with nevirapine
single oral dose at the onset of labor. Postpartum:
Zidovudine orally every 6 hours for 6 weeks with nevirapine
single oral dose at age 48-72 hours
3.4. URINARY PROBLEMS IN PREGNANCY
I. Asymptomatic bacteruria
Definition and incidence
It is defined as presence of greater than 105 colony forming

units (CFU) of bacteria of single pathogen per ml of clean-catch
midstream urine sample with no clinical symptoms of urinary
tract disease.
Asymptomatic bacteruria occurs in 7% of pregnant women

(ranging from 2%-12%). The predisposing conditions are
reduced peristalsis and dilatation of the ureters and the bladder
causing incomplete emptying and stasis of urine and pregnancy
induced glycosuria.
203
Significance
If untreated, about 25%-30% of patients with asymptomatic

bacteruria will later develop acute pyelonephritis as compared
to only 2%-3% of patients who have been treated. It is also
associated with preterm labour and postpartum endometritis.
Acute pyelonephritis is one cause preterm birth and perinatal
death.
Etiology
In 80 to 90% of cases the etiology is E coli, the other causes

are Klebsiella, Proteus, Pseudomonas, S saprophyticus and C
trachomatis.
Diagnosis and management
Sine it has no symptoms and is associated with adverse

obstetric outcome, routine urine culture for all women is
recommended in ANC. Once diagnosed al women with
asymptomatic bacteruria should be treated with appropriate
antibiotics. Urine culture should be repeated to confirm cure.
Empirical treatment with antibiotics should be started until

culture and sensitivity result is ready. Commonly used
antibiotics (since the most common pathogen is E coli) are:
amoxicillin, amoxicillin/clavulanate potassium, cephalexin,
nitrofurantoin, trimethoprim- sulfamethoxazole or one of the
third generation cephalosporins. The antibiotic should be safe
204
to be used during pregnancy and given for duration of 10-14

days. Culture of urine should be done 1-2 weeks after therapy
is begun and monthly for the remainder of pregnancy.
Treatment failure can be due to resistance and patient non
compliance.
II. Acute cystitis
It is the inflammation of the bladder in this case due to infection.

The predisposing factors and etiologic agents are similar with
that of asymptomatic bacteruria.
Clinical features are urinary frequency, urgency, dysuria,

suprapubic discomfort or pain, and suprapubic tenderness. The
urine may be cloudy and malodorous. Systemic symptoms like
nausea, vomiting, fever and chills are unusual.
Diagnosis is made by microscopic examination of urine (shows

bacteria, leukocytes and red blood ells) and urine culture.
Treatment: similar with that of asymptomatic bacteruria.
III. Acute pyelonephritis
Acute pyelonephritis is the infection of the renal pelvis and the

kidneys. The single most important predisposing factor for
acute pyelonephritis during pregnancy is asymptomatic
bacteruria. The etiologic agents are similar with those of
205
asymptomatic bacteruria and acute cystitis. Acute

pyelonephritis affects 1% - 2% of all pregnant women.
Clinical features generally develop rapidly over a few hours or

a day. Symptoms include fever (usually > 390C), shaking chills,
nausea, vomiting, bilateral flank pain and possibly diarrhea.
Symptoms of cystitis may or may not be there. In some
hematuria may be evident. On physical examination, there is
pyrexia and tachycardia along with costovertebral angle
tenderness on one or both sides.
Diagnosis is made by urine microscopy showing pyuria (in

centrifuged urine >10 WBC per high power field), bacteruria,
hematuria (1-2 RBC in centrifuged urine or ≥5 RBC in
uncentrifuged urine per high power field) and leukocyte casts,
leukocytosis (WBC >15,000/mm 3) with left shift and positive
urine/blood cultures.
Complications are septic shock, acute renal failure, preterm

labour and low birth weight baby.
Management: Admit for parentral antibiotics. Start high dose

parentral antibiotic until the patient is afebrile for 24-48 hours
(usually 3-5 days) then continue orally for 7- 10 days.
Antibiotics are initially started empirically but later can be
adjusted according to culture results. (Examples: ampicillin 1
gm four times plus gentamycin 80mg three times a day or
ceftriaxone 1-2g daily).
206
Supportive care includes correction of dehydration, antipyretic

agents as required for control of fever and monitoring vital signs
and urinary output.
4. DIABETES MELLITUS IN PREGNANCY
4.1. Definition
Diabetes mellitus is a chronic disorder of metabolism affecting

carbohydrates, proteins, and fats. It is characterized by an
absolute or relative lack of insulin, hyperglycemia and
glycosuria. The worldwide incidence of diabetes mellitus during
pregnancy is 1-4%.
4.2. Classification
I. Pregestational (overt) diabetes: This is diabetes existing

before pregnancy. It is further classified into:
Type I diabetes: It is also known as juvenile or insulin

dependent diabetes mellitus. There is autoimmune destruction
of β-cells of the pancreas resulting in absolute lack of insulin in
the body. Patients require exogenous insulin for treatment and
to prevent ketoacidosis.
Type II diabetes: It is also known as maturity-onset or non-

insulin dependent diabetes mellitus. In this type there is
207
abnormal insulin secretion and insulin resistance in target

tissues. It is hereditary. Most patients are obese.
II. Gestational diabetes (GDM or Type III diabetes): This is

defined as carbohydrate intolerance of variable severity with
onset or first recognition during pregnancy. This definition
applies regardless of whether or not insulin is used for
treatment. ―Gestational‖ diabetes implies that this disorder is
induced by pregnancy, perhaps due to exaggerated physiologic
changes in glucose metabolism. An alternative explanation is
that gestational diabetes is maturity-onset or type II unmasked
or discovered during pregnancy. Actually, some women with
gestational diabetes have previously unrecognized overt
diabetes.
4.3. Diagnosis
I. Overt diabetes
Previous history of diabetes along with symptoms of polyuria

polydypsia polyphagia and weight loss and in long standing
cases finding of signs of organ damage (retinopathy
nephropathy and atherosclerosis) suggest the diagnosis. It is
confirmed by finding high plasma glucose levels and / or
glycosuria
II. Gestational diabetes mellitus
208
The process of diagnosis of gestational diabetes involves a two-

step screening and diagnostic glucose tests on patients with
risk factors for gestational diabetes. Since 35-50 % of women
with gestational diabetes have no risk factors, it is wise to adopt
universal screening of all pregnant women.
A. Risk factors
 Maternal age greater than 35 years
 Bad obstetric history: recurrent abortion, previous

unexplained stillbirth, previous macrosomic (>4000g)
infant, history of congenital malformed fetus, previous
unexplained neonatal death, history of polyhydramnios or
PIH in multipara
 History of pregnancy with GDM
 Family history of diabetes mellitus in first degree relative
 Obesity (>90 kg)
 Recurrent urinary tract infection or vulvovaginal

candidiasis
 Persistent glycosuria.
B. Screening for GDM
Screening for GDM should be performed between 24 and 28

weeks by giving 50 gm glucose orally and determining plasma
209
glucose after 1 hour. Plasma glucose level of > 140 (135) mg/dl
is abnormal and mandates oral glucose tolerance test. If it is <
140 (135) mg/dl no further test is needed.
C. Diagnostic test
Oral glucose tolerance test (OGTT) performed by administering

100gm of glucose after 8-14hrs overnight fast and 3 days
carbohydrate loading. Blood glucose is determined every hour
for three hours. It is abnormal if two or more of the following are
found: (FBS > 95 mg/dl, 1 hour plasma glucose > 180 mg/dl,
2hour plasma glucose > 155mg/dl, 3 hr plasma glucose > 140
mg/dl).
4.4. Complications
Unlike GDM, over diabetes has significant impact on

pregnancy outcome. The adverse outcome depends on the
degree of glucose control and to the intensity of the long term
effect of the diabetes on the mother‘s health. Some of the
effects are:
 Fetal: spontaneous abortion, congenital malformation,

intrauterine growth retardation, polyhydramnios/
oligohydramnios, prematurity, macrosomia, sudden
intrauterine fetal death
 Maternal: preeclampsia, recurrent vulvovaginal

candidiasis, urinary tract infection, operative deliveries,
210
worsening nephropathy and retinopathy, increased dose of

insulin
 Neonatal: hypoglycemia, hyaline membrane disease,

hypocalcaemia, hyperbilirubinemia, traumatic delivery of
macrosomic neonate
Depending on the degree of hyperglycemia, the following are

some of the adverse effects of GDM.
 Fetal: macrosomia, polyhydramnios, unexplained

intrauterine fetal death, congenital malformations
 Maternal: preeclampsia, operative deliveries, Urinary tract

infection, candidiasis, postpartum endometritis,
4.5. Management
I. Overt diabetes
Preconception: Counseling on the complications of diabetes,

evaluation of the diabetic status, achieving adequate glycemic
control.
Pregnancy: Target glucose levels to be achieved during

pregnancy are fasting glucose of 105 g/ dl (60-90mg/dl
preferable), postprandial glucose <130mg/dl at 1 hr or 120mg/dl
at 2hrs without development of significant hypoglycemia
(plasma glucose <70mg/dL) during the hours of sleep.
211
This is achieved by multiple insulin injection adjusted to bring

glycemic control, dietary adjustment and/ or exercises.
Optimum glucose monitoring assured by repeated self glucose
determination. Insulin requirement increases during pregnancy
to reach maximum at 16-18 weeks. Fetal growth and well being
is followed by fundal height, kick chart, ultrasound and other
fetal wellbeing tests.
Delivery: If the glucose control is optimal and the fetal condition

is reassuring, delivery can be accomplished near term. In the
presence of arrested fetal growth, intrauterine growth
restriction, abnormal fetal well being tests, maternal
complications like severe preeclampsia and mature fetus
delivery should be accomplished either by induction or
caesarian section.
Intrapartum glycemic control is achieved by regular insulin and

hourly monitoring of the blood glucose levels.
Postpartum: Insulin requirements drop drastically. Prevent

neonatal complications like hypoglycemia (early feeding).
II. Gestational diabetes
Glycemic control is achieved in most cases by dietary

adjustment. If this fails insulin in low doses is used. Insulin is
indicated when FBS>95mg/dL and 1 hr postprandial glucose
concentration > 120mg/dL on two or more occasions within a
212
two weeks interval despite attempted dietary control. Fetal

growth and well being monitoring is conducted as for overt
diabetes.
Note: Oral hypoglycemic agents are contraindicated during

pregnancy.
4.6. Postpartum consequence of GDM
There is a 50% likelihood of women with GDM of developing

overt diabetes within 20 years of delivery. If fasting
hyperglycemia develops during pregnancy, diabetes is more
likely to persist postpartum. Therefore, it is recommended that
women diagnosed to have GDM undergo evaluation with 75-g
oral glucose tolerance test after 6 to 12 weeks after delivery.
Fasting blood sugar ≥140 mg/dl and 2 hr plasma glucose level ≥
200mg/dl in this 75-g oral glucose tolerance test indicate overt
diabetes.
Review Questions
1. Discuss the causes and consequences of anemia during

pregnancy.
2. Describe classification and general management principles of

cardiac disease in pregnancy.
213
3. Discuss the measures taken to prevent MTCT.
4. Discuss the diagnosis and complications of asymptomatic

bacteruria.
5. Discuss the risk factors and screening methods of GDM.
214
215
References
1. DeCherney AH, Pernoll ML Current. Obstetrics and

Gynecologic diagnosis and treatment, 8th edition, 1994.
2. Lawson J. B, Stewart D. B, Obstetrics and Gynecology in the

Tropics and developing countries
3. Scott JR., DiSaia PJ, Hammond CB, Spellacy WN: Danforth‘s

obstetrics and Gynecology, 8th edition, 1999.
4. Novak‘s text of Obstetrics & Gynecology, 10th edition, 1981.
216
5. Addis Ababa University faculty of medicine department of

Obstetrics and Gynecology: Guideline for management of
obstetric and gynecologic problems, 1st edition, 2003.
6. Bennett V.Ruth and Brown Linda K.: MYLES text book for
mid wives, 13th edition
7. Llewellyn Jones D, Fundamentals of Obstetrics and

Gynecology, Volume 1, Fifth edition, 1990
8. Kenneth R. Niswander, Manual of Obstetrics, diagnosis and

therapy, 1st edition, 1982
9. John Cook, Surgery at district hospital, Obstetrics and

Gynecology 1991
10. Dreissen F, Obstetric problems, A practical manual, 1991
11. WHO, Department of reproductive health and research,

integrated management of pregnancy and childbirth. Managing
complications in pregnancy and childbirth. A guide for midwives
and doctors, 8.
12. MOH/ FHD, Technical Guidelines in managing maternal and

new born care
13 Cunningham F. Gary et. al, Williams Obstetrics,20th edition,

1993
14. King M, Bews P, Karins, Thornton J: Primary surgery,

Volume 1 (Non trauma); Oxford medical publication, 1990
217
15. WHO, Safe Abortion: Technical and Policy Guidance for

Health Systems, 2003.
16. WHO, Clinical Management of Abortion Complications: A

Practical Guide., 1994.
17. Addis Ababa University, Faculty of Medicine, Department of

Obstetrics and Gynecology, The Management of Abortion and
Post Abortion Care. September 2001.
218
PART II
NORMAL AND ABNORMAL LABOUR
219
220
CHAPTER 14
PHYSIOLOGY AND MANAGEMENT OF NORMAL LABOUR
Learning objectives
 To define true labour and describe its difference from false

labour
 To describe the stages of labour
 To describe cardinal movements in the mechanism of

labour
 To discuss the management of normal labour
 To list the types and complications of episiotomy
I. Definitions
True labour (parturition) is a continuous process in which

progressive regular uterine contractions result in the expulsion
of the products of conception from the uterus through the birth
canal after progressive effacement and dilatation of the cervix.
221
Labour can be preterm (if it starts before 37 completed weeks)

or term (if it starts between 37- 42 weeks) or post term (if it
starts after 42 weeks). It can be spontaneous or induced.
Labour is said to be normal only if the following are met. These

are:
 It starts spontaneously
 It starts at term (37- 42 completed weeks)
 The fetus presents by vertex
 Delivery is effected vaginally spontaneously
 It ends in a birth of healthy newborn with minimal morbidity
False labour is a painless irregular uterine contraction

occurring in the last 4-8 weeks of gestation and which doesn't
result in cervical dilatation and effacement.
DIFFERENCES BETWEEN TRUE LABOUR AND FALSE

LABOUR
false labour true labour
contractions occur at irregular contractions occur at regular

intervals intervals
222
with time contractions remain with time contractions

the same or decreases in increase in intensity,
intensity, frequency frequency and duration
contractions disappear with contractions persist despite

analgesics analgesics
lower abdominal and back only lower abdominal

pain present discomfort present
can occur in the last trimester occurs when labour

commences
there is no cervical there is progressive cervical

effacement and dilatation dilatation and effacement
occurs at night occurs at any time
Braxton-hicks contraction is an irregular painless contraction

which occurs in the last trimester of pregnancy with no effect on
the cervix.
Lightening is a sensation (the fetus falling down into the pelvis

and emptiness in the upper abdomen) felt by most
primigravidas in the last weeks of pregnancy prior to the onset
of labour. It denotes engagement of the fetal head.
223
II. Stages of Labour
Even though labour is a continuous process, for the sake of

management, it is classified into the following four stages.
1. First stage of labour
It extends from the onset of regular uterine contractions

to full cervical dilatation. It is further subdivided into two phases
the latent phase and the active phase. The latent phase
extends from the onset of labour to three to four centimeters of
cervical dilatation. The active phase extends from three
centimeters to full cervical dilatation (10 centimeters). The
active phase has acceleration phase, phase of maximal
slope (average rate of cervical dilatation is greater than 1.2
cm/hr for primigravida and 1.5 cm/hr for multigravida)
and deceleration phase.
2. Second stage of labour
It extends from full cervical dilatation to delivery of the

fetus. It is characterized by more frequent and strong
contractions. In addition to uterine contractions maternal
voluntary efforts play major role. Descent is more during this
stage.
3. Third stage of labour
224
It extends from the delivery of the fetus to the delivery of

the placenta and membranes. Its duration is equal in
multiparas and primiparas. In majority it lasts 15 minutes.
4. Fourth stage of labour
It extends from the delivery of the placenta and

membranes to one hour postpartum.
Mean duration of primigravida and multigravida
Stage of Primigrav Multigravid Factors

labour ida a
Latent first 8 hours 4-6 hours parity, uterine

stage contraction, ability of
the cervix to dilate, feto
Active first 6- 8 4-6 hours
pelvic diameter,
stage hours
presentation, position
Second 1 hour 20-30 parity, contraction, soft

stage minutes tissue resistance, feto
pelvic diameter,
presentation, position,
maternal effort
225
Third stage 15-30 15-30 speed of separation of

minute minutes placenta
Rate of 1.2 cm/ 1.5 cm/ hr -

cervical hr
dilatation
Rate of 1 cm/ hr 2 cm/ hr -

descent
III. Theories for initiation of labour (parturition)
Many theories have been proposed over the years to explain

labour and delivery. The physiological processes in human
pregnancy that results in initiation of labour and onset of labor
are not defined. The mother, fetus and placenta contribute to
the initiation of labour.
IV. The mechanism of labour
226
The mechanism of labour refers to the changes in the positions

of the presenting part during its passage in the birth canal. It is
a process of adaptation in which the smallest diameter of the
presenting part is presented to the various portions of the
pelvis. The major force for these changes comes from uterine
contractions.
There are seven cardinal movements in the mechanism of

labour.
1. Engagement: is said to occur when the largest diameter of

the presenting part passes the plane of the pelvic inlet. For
occiput presentation the largest diameter is the biparital
diameter (BPD). In nulliparous engagement occurs in the last
weeks of pregnancy and is experienced as lightening by the
mother. But in multiparous this usually occurs at the onset of
labour. Engagement occurs in occiput transverse or oblique
position.
2. Descent: occurs in discontinuous manner. In women with

engaged head descent starts in late first stage or in the second
stage. In others it starts with engagement with the greatest rate
occurring in the deceleration phase.
3 Flexion occurs as a passive movement resulting from the

resistance of the soft tissues of the pelvis. Flexion ensures
presentation of smaller diameter of the fetus to birth canal. It is
important for both engagement and descent.
227
4. Internal Rotation occurs at the pelvic floor at the level of the

ischial spines. The sagittal suture rotates 450 (in left or right
occipito anterior position) or 900 (in left or right occipito
transverse positions) so that the sagittal suture lies in the
anteroposterior diameter. It occurs because of the force exerted
by the uterine contraction and resistance created by the v-
shaped levator ani muscles. This helps the head to pass the
ischial spines.
5. Extension: After further descent and flexion the head

reaches the introitus. Delivery of the head is then achieved by
extension where the lower border of the symphysis acts as the
fulcrum for the occiput and the fetal face sweeps the perineum
to be delivered. Following delivery of the head, the head
restitutes to the oblique lateral position.
6. External rotation is evidenced when the face starts to look

to the side. This indicates internal rotation of the shoulders.
7. Lateral flexion of the body or expulsion results in the

delivery of the anterior shoulder under the symphysis to be
followed by the posterior.
One can remember the cardinal movements by the mnemonic

Every Decent Family In Europe Eats Eggs.
V. Physiologic changes in labour
228
Contractions increase in intensity and frequecy as labour

progresses. With contractions, the uterus differentiates into an
active upper segment (which gets progressively thicker) and a
passive lower segment (which gets progressively thinner).
In response to the increased hydrostatic pressure of the

amniotic fluid and direct pressure of the fetus, the cervix initially
undergoes effacement (taking up of the cervix into the lower
segment so that 3 centimeters long cervix becomes a circular
orifice with paper thin edges) and later dilatation (from closed
state to 10 centimeters).
The fetal head descends in the birth canal dictated by the

mechanisms of labour. Pressure over the leading part of the
head results in edematous swelling, called caput succedaneum.
Overlapping of the fetal skull bones called molding may
accompany the caput.
In the second stage, uterine contractions are intense and

frequent. At this time most will have the urge to defecate and
vomiting along with appearance of beads of sweat on the face.
During this stage the most important force to expel the fetus is
maternal voluntary expulsive force.
In the third stage, sudden reduction in uterine cavity results in

decrease in the surface area of the placental attachment. The
placenta becomes thicker and eventually gives way at the
decidua spogiosa. Separation proceeds through this layer until
229
it is complete. Then, the placenta is delivered by the help of

uterine contraction and maternal effort. There are two
mechanisms of separation: Schueltz method (central separation
with clot behind so that the placenta is delivered by the fetal
side like an inverted umbrella) and Mathew-Dunken
method (peripheral separation with blood escaping ahead of the
placenta so that the placenta is delivered sideways by the
maternal side).
VI. Diagnosis of labour
Labour can be diagnosed if three of the following present:
 Presence of regular painful contractions at least 2 in 10

minutes
 Bloody show which is expulsion of the cervical mucus plug

of pregnancy along with some blood
 Cervical dilatation of 3 cm. or more which is progressive
 Cervical effacement of 80% or more
VII. Management of normal labour
1. Major objectives
 Prevention minimize infection which could be intrinsic or

extrinsic
 Prevent dehydration and ketosis
230
 Prevent or minimize trauma to the fetus and the mother
 Provide pain relief
 Avoid asphyxia to the newborn
 Prevent postpartum hemorrhage
2. Initial assessment
Its objective is to diagnose labour and its stage and identify

significant problems. This is done by brief history and physical
examination and appropriate investigations (mainly hemtocrite
and urine protein). If available, antenatal data should be
reviewed.
In the history one should get information on time of onset of

contractions, status of fetal membranes and time of rupture,
presence/absence of vaginal bleeding and show, presence and
quality of fetal movement, symptoms of severe preeclampsia
(head ache, blurring of vision, epigastric pain), presence of
fever, history of allergy, time and content of last ingestion of
food or fluid and use of any medications. Information should
also be gathered on the presence of ANC and significant
problems during pregnancy. Review of past obstetric medical,
surgical, personal, social and family history must be made.
(Refer to chapter 2)
231
In the physical examination, special attention should be given to

vital signs, weight, signs of anemia and dehydration, fetal
position and presentation (proper Leopold‘s maneuver), fetal
heart rate and its pattern, frequency, duration and quality of
uterine contractions and estimation of fetal weight. If there is no
contraindication digital pelvic examination must be done to
assess degree of cervical effacement and dilatation, status of
membrane and the color of the liquor, the presenting part , its
position and station, in cephalic presentation degree of caput
and molding and when indicated clinical pelvimetry (pelvic inlet,
mid pelvis, pelvic outlet).
Correct diagnosis and identification of high risk patient is made

for adequate surveillance through out labour and delivery.
3. Subsequent management
This depends on the stage of labour and identified problems.
3.1. First stage of labour
The woman is admitted to the delivery ward. Ambulation can be

allowed except in those with ruptured membranes or having
vaginal bleeding or are sedated. Left lateral position should be
adopted while lying in bed. She should be allowed to take sips
of fluid, but not solid diet. Parenteral fluids are reserved for
those with vomiting or have prolonged labour of more than 12
232
hours. Routine use of cleansing enema and pubic hair shaving

are not recommended.
Monitoring of labour has the following components (refer to

annex 2 for partograph).
 Monitoring the fetal condition by auscultation of the fetal

heart beat every 30 minutes (for high risk every 15
minutes) for 1 minute after the end of contraction
 Monitoring the maternal condition by taking the vital signs

every 1-2 hours (more frequent in high risk woman) and
measuring the urine output
 Monitoring the progress of labour by assessing uterine

contraction for 10 minutes every 30 minutes and cervical
dilatation (and decent of the presenting part) every 4
hours. Vaginal examination is made every 4 hours to
assess cervical dilatation, station, degree of caput and
molding and status and color of liquor. Vaginal
examination has to be done at any time following rupture
of the membranes or if there is unexplained fetal distress
or if second stage is suspected.
3. 2. Second stage of labour
 Position the woman in lateral recumbent or lithotomy

position with the knees supported
233
 Monitor vital signs more frequently ( every 30 minutes to

1 hour)
 Fetal heart rate is checked every 15 minutes (if high risk

every 5 minutes) looking for late decelerations which is
common (strong contractions, premature separation,
tightening of loops of cord)
 Vaginal examination is performed frequently. Prepare for

delivery when the head crowns and perineum bulges.
If needed, perform episiotomy.
 Clean any feces that soil the perineum with sponges

soaked with dilute soap solution
 Deliver the fetus in controlled way. Deliver the head

slowly. This is facilitated by using modified Ritegen‘s
maneuver (gentle upward pressure at the chin thigh the
perineum just in front of the coccyx). Check for nuchal
cord. If present slip it over the head or cut it after double
clamping. Suction any fluid from the nose and mouth by
soft rubber suction bulb or catheter. After external
rotation, apply gentle downward traction by holding to
the sides of the head to deliver the anterior shoulder. As
soon as the anterior shoulder slips under the symphysis
apply upward traction to deliver the posterior shoulder.
234
 Provide immediate neonatal care. Clamp the cord after

15- 20 seconds by two clamps placed 4-5 centimeters
from the fetal abdomen and cut the cord using sterile
scissors. Later tie the cord tightly. Airway cleared of
blood and amniotic fluid by soft suction bulb or catheter.
Dry the baby, wrap with blanket and put under radiant
heat. Examine for gross malformations and take Apgar
score.
3. 3. Third stage of labour
A. Expectant or traditional method: controlled cord traction
 Determine the height and consistency of the uterus and

assess the degree of bleeding. Until the signs of placental
separation are observed, frequently assess the tone but do
not massage
 When the signs of placental separation (gush of blood from

the vagina, lengthening of the cord, uterus becomes globular
and rises in the abdomen) are observed, deliver the placenta
by controlled cord traction using either
1. Pastore technique: Stand on the patient‘s left. Hold the

fundus by the right hand and put the left hand superior to
the symphysis to prevent the uterus coming down. If signs of
placental separation noticed, massage the fundus gently to
let the placenta into the vaginal canal.
235
2. Modified Brandt-Andrews technique: This controlled

cord traction with the left hand superior to the symphysis to
support the uterus.
Credes manuvoere of delivering the placenta (traction of

the cord with concomitant fundal pressure) is an abandoned
technique that predisposes to uterine inversion.
 After delivery of the placenta give uterotonic drugs as

described below
B. Active third stage management
It is universally recommended method of management of the

third stage for all women. Its components are:
 Secure an intravenous line; get blood for hemtocrite and

blood group and cross match.
 Depending on the presenting part and twin (in vertex: after

the delivery of the anterior shoulder, in breech immediately
after delivery of the fetus, in twins after the delivery of both
fetuses) give uterotonic as below:
1. Oxytocin: 10 IU intramuscular or 10-20 IU added in

1000 ml of IV fluids to run over 1 hour or
2. Ergometrine 0.2-0.5 mg intravenous slowly if not

contraindicated.
236
 Apply controlled cord traction without waiting for signs of

placental separation. If the placenta is not delivered within
6-10 minutes perform manual removal of the placenta.
C. Subsequent management
 Examine the placenta, cord and the membranes for

completeness and abnormalities. If incomplete or if
excessive bleeding occurs perform intrauterine
exploration
 Examine the genital tract for laceration
 If performed, repair episiotomy
3.4. Fourth Stage of labour:
It is a critical stage of labour where most maternal deaths occur.
 Monitoring of maternal vital signs at least every 30

minutes (blood pressure must be more than 90/60 mmhg
and pulse rate must be less than 90/ minute)
 Examination of the uterus for its tone and size (it should
be firmly contracted and at the level of the umbilicus)
 Inspect the vulva for bleeding and hematoma
237
EPISIOTOMY
Episiotomy (periniotomy) is an intentional incision made into the

perineum with an objective of widening the vulva to allow easy
passage of the fetus. The common types of episiotomy are
midline (median) and mediolateral, each with its own
advantages and disadvantages (see table below).
 Median episiotomy is an incision made vertically in the

midline of perineum over the perineal raphae starting at
the posterior fourchette and ends just anterior to the anal
sphincter.
 Mediolateral episiotomy is an incision made at an angle

of 450 from the midline beginning at the midpoint on the
posterior fourchette.
Medial Mediolateral
Technically easier to make and relatively

repair difficult
Healing better Less
Blood loss less more
Dysparunia less more
Anatomic end Better Less
238
result satisfactory
Extension into the relatively more rare

rectum common
risk of rectovaginal higher lower

fistula
Routine use of episiotomy is not advisable. Episiotomy should

only be done in conditions where perineal tear is imminent or
likely. Such conditions include macrosomia, tight perineum,
breech delivery, shoulder dystocia, instrumental deliveries
especially forceps delivery and destructive deliveries.
PROCEDURE
I. INCISION OF EPISIOTOMY
INFILTRATE 5 - 10 ML OF LOCAL ANESTHETIC

AGENT SUCH AS 1% LIDOCAINE INTO THE
INTENDED SITE OF EPISIOTOMY. INSERT THE
NEEDLE AT POSTERIOR FOURCHETTE AND GIVE
THE LOCAL ANESTHETIC IN FAN MANNER.
PERFORM THE INCISION, PREFERABLY WHEN THE
PERINEUM IS THINNED OUT AND THE PRESENTING
239
PART HAS CROWNED, BY SHARP TISSUE SCISSORS

IN ONE GO.
II. REPAIR OF EPISIOTOMY
After the delivery of the placenta, insert a rolled vaginal pad and
inspect the episiotomy site for extension. Identify the apex. Start
suturing 0.5-1 centimeters above the apex using chromic 2/0
catgut. Suture the vaginal mucosa continuously upto the
hymen, the perineal muscles by 2-3 interrupted sutures and the
perineal skin by interrupted sutures. Perform rectal examination
to check for any sutures that may have passed (If found remove
the suture). Remove any vaginal pad.
Proper anatomic approximation of tissues, careful handling of

tissues and proper hemostasis are essential for success of the
repair.
SUBSEQUENT CARE
The episiotomy wound should be cleaned with plain water and

soap at least once or twice a day and after voiding or
defecation. Cool sitz bath can be used for relief of the pain.
Simple analgesics like parcetamol relieve the pain. Increasing
swelling, persistent/ increasing pain and offensive discharge
call for inspection of the episiotomy.
COMPLICATIONS
240
 Extensions to upper vagina and even the cervix causing

PPH
 Extensions to the anal sphincter and rectum
 Episiotomy site hematoma manifests with increasing

swelling and pain in the first 48 hours. The site must be
opened, bleeding points identified and ligated and
wound is then resutured.
 Episiotomy site infection manifests with increasing pain

and swelling along with offensive discharge usually
occurring after the third day. Management includes
removal of sutures and drainage, wound cleaning and
debridement and later secondary closure. Antibiotics are
needed only if there are signs of systemic infection.
 Episiotomy breakdown/ dehiscence
 Rectovaginal fistula and anal incontinence
 Dysparunia from vulvar stenosis
 Gaping vulva
REVIEW QUESTIONS
1. Define episiotomy
241
2. Discuss the types of episiotomy with their advantages and

disadvantages
3. List the steps of making an episiotomy and repairing it
4. List the complications of episiotomy and their management
242
CHAPTER 15
INDUCTION / AUGUMENTATION OF LABOR
Learning Objectives
 To define induction and augmentation of labor
 To list indications for induction of labor
 To list contraindications for induction of labor
 To out line the steps in induction of labor
1. DEFINITION
Induction of labor is initiation (stimulation) of uterine

contraction artificially for the purpose of delivering the fetus
after the fetus has reached viability (after the 28th week of
gestation). It can be elective (planned) or emergency.
AUGMENTATION OF LABOR IS ENHANCING

UTERINE CONTRACTIONS THAT ARE INADEQUATE
TO ALLOW NORMAL PROGRESS OF LABOUR.
2. Indications
243
The decision to induce labor is largely governed by the

assessment of obstetric balance. The three factors that should
be considered are
 The risk if the pregnancy continues
 The risk if the pregnancy is interrupted and
 The hazards of induced labour
Because of associated risks, induction of labour should be

performed only upon specific maternal or fetal indications. The
following are common indications for induction of labor (not
inclusive):
 Hypertensive disorders of pregnancy
 Antepartum hemorrhage from abruptio placenta and some

types of placenta previa
 Post term pregnancy
 Intrauterine fetal death and intrauterine growth restriction
 Premature rupture of membranes
 Polyhydramnios and oligohydramnios
 Gross congenital malformations incompatible with life
 Recurrent intrauterine fetal death at term
 Rh isoimmunization
244
 Medical disorders like diabetes mellitus, chronic

hypertension, cardiac diseases
3. Contraindications
I. Absolute contra indications
 Cephalopelvic disproportion more than border line

(macrosomia or contracted pelvis)
 Transverse or oblique lie, footling breech
 Previous history of uterine surgery like classical caesarian

section, two or lower segment caesarian section,
myomectomy entering the endometrial cavity
 Diagnosed major placenta previa
 Extensive vaginal plastic operations like repaired fistulas

or pelvic tumors obstructing delivery like cervical cancer
and tumor previa
 Cord presentation
 Abnormal fetal heart rate pattern
 Absence of caesarian section facility
II. Relative contraindications
 Elderly primigravida or grand multiparity or

245
 Uterine over distention from polyhydramnios or multiple

pregnancy
 One lower segment caesarian section
 Frank breech
These conditions require internal or external continuous

monitoring of uterine contractions and the fetal heart beat. In
the absence of such monitoring, they become absolute
contraindications.
Unfavorable cervix is another relative contraindication

especially for elective induction. Favorability of the cervix for
induction is evaluated by pelvic examination to assess the
Bishop score. Bishop score of more than eight is taken as
favorable for elective induction. Cervix is said to be
unfavorable if the score is lees than five. The chance of
vaginal delivery is guarded in unfavorable cervix.
The Bishop Score
Rating
Factor
0 1 2 3
Dilation Closed 1-2 3-4 >5
246
(cm)
Effacement 0-30 40-50 60-70 >80

(%)
Station -3 -2 -1,0 +1,+2
Cervical Firm Medium Soft -

consistently
Position of Posterior Midposition Anterior -

cervix
4. Prerequisites
 Presence of clear indication
 No contraindication
 Presence of caesarian section facility
 For elective induction screening for iatrogenic

prematurity
 Ripening of the cervix using prostaglandins or folley

catheter.
247
5. Methods of induction
5.1. Medical induction – Intravenous oxytocin

administration
The goal of oxytocin induction is to get sufficient (adequate)

contractions without causing hyperstimulation and fetal
distress.
The principles of oxytocin induction are
 Use oxytocin diluted in balanced salt solution or 5%

dextrose in water as continuous intravenous infusion
 It has to be started from the minimum dose capable of

causing contractions and increased every 30- 40
minutes until adequate contraction is achieved or
hyperstimulation and fetal distress occurs or maximum
dose is reached.
 Continuous bed side attendance by a trained health

professional should be provided
 Close monitoring of uterine contractions and fetal heart

beat (intermittently or continuously) should be done
 If hyperstimulation or fetal distress occurs discontinue

the infusion
Complications of intravenous oxytocin are uterine

hyperstimulation (more than 5 contractions in 10 minutes or
248
contractions that last more than 1 minute) and fetal distress,

uterine rupture, water intoxication from antidiuretic effect of
oxytocin if high dose is used for prolonged periods,
congestive heart failure from fluid overload and atonic PPH.
Different protocols to administer oxytocin are in use.

Depending on the available resources, some use high dose
regimen while others use low dose. In our country the low
dose regimen is used.
Add 5 IU (for primigravida) or 2 IU (for multiparas) of

pitocin in 1000 cc of 5% dextrose in water. Start with 10
drops/ minute and double the drop rate every 20 minutes until
3-4 contractions each lasting 40- 60 seconds is achieved.
Rate in Pitocin in milli

drops/min units/minute
Primipara Multipara
10 2.5 1
20 5 2
40 10 4
80 20 8
249
If adequate contraction is not achieved, add another 5 IU

(for primigravida) or 2 IU (for multipara) of pitocin into the
same bag of intravenous fluid. Start with 40 drops/ minute
and proceed as above.
Rate in Pitocin in milli

drops/min units/minute
Primipara Multipara
40 20 8
80 40 16
If adequate contraction is not achieved, add 5 IU ( for

primigravida) or 2 IU (for multipara) of pitocin for multipara
into the same bag. Start with 40 drops/ minute and proceed as
above.
Rate in Pitocin in milli units/min

drops/min
Primipara Multipara
40 40 16
60 60 24
250
80 80 80
Maintain the drop rate that brought adequate contractions

till delivery and continue for one hour after delivery.
Note: For augmentation the same regimen using half the

dose of the pitocin used for induction.
5.2. Surgical induction - Artificial rupture of the

membranes (ARM)
ARM stimulates labour mainly by initiating by release of

prostaglandins from the membranes.
Contraindications for ARM are high (floating) presenting part,

abnormal lie and presentation, cord presentation, intrauterine
fetal death, active genital herpes, maternal HIV infection and
history of unidentified APH.
Complications of ARM are umbilical cord prolapse and

compression, chorioamnionitis, abruptio placenta, adverse
changes in fetal position and transmission of infection to the
fetus (HIV and genital herpes). Rare complications are
amniotic fluid embolism and rupture of vasa previa.
251
Procedure can be done either before or sometime after

starting medical induction.
 Discuss the procedure to the mother.
 Check fetal heart rate pattern,
 Wear sterile gloves and clean the vulva with antiseptic

solution.
 Perform pelvic examination and check the presenting

part, the station of the head and for cord.
 Introduce one or two fingers through the cervix and pass

Kocher forceps along side the fingers towards the fore
waters.
 Hook or scratch the membranes and gently turn it to

rupture the membranes. Allow the liquor to drain slowly
so that the head settles down.
 Check thoroughly for the cord and note the color of the
liquor.
 Remove the fingers from the vagina and check the fetal
heart for any variability.
 If there is no adequate contraction in 1- 2 hours start

oxytocin.
 Give prophylactic antibiotics if not delivered in 12 hours.

252
5.3. Stripping of the membranes
6. Conduct of induction
 Document the indication
 Obtain informed consent after discussing about the

indication, the methods, and risks including the possibility
of caesarian section
 Thorough evaluation of the mother (to exclude

contraindications and detect medical problems).
 For elective induction, if there is unfavorable cervix, use

cervical ripening drugs the day before. Start induction early
in the morning. Emergency induction should be started at
any time of the day.
 Start induction using either medical or surgical method or

combination of these methods as described above.
 Monitor induction by following dose of oxytocin, vital signs

every 1 hour, uterine contractions every 30 minutes, fetal
heart beat every 20- 30 minutes, pelvic examination for
cervical dilatation and station every 4 hours, input output
chart and urine output.
253
 If labour starts follow with partograph. If the patient

develops tetanic type of contraction, stop the pitocin drip,
sedate the patient and consider cesarean section. If the
patient is not in established labour after 6 hours of
maximum dose of pitocin, the induction is said to have
failed.
 Antibiotics cover when membranes are ruptured for more

than 12 hours. Continue pitocin drip until 1 hour after
delivery.
7. COMPLICATIONS
Besides the complications of oxytocin and ARM, failure of

induction and prematurity (known or missed) are other
complications.
Review questions
1. Define induction of labor
2. Outline the steps in ARM
3. List the maternal and fetal contraindications for induction

of labor
254
4. List the maternal and fetal complications of induction of

labor
255
CHAPTER 16
OPERATIVE DELIVERIES
Learning Objectives
 To describe the parts of the obstetrics forceps and

vacuum extractor
256
 To describe the classification of forceps delivery
 To list the indications, prerequisites and complications

of instrumental deliveries.
 To name the types, prerequisites and complications of

destructive deliveries
 To describe the major types of caesarian section with

their advantages and disadvantages
 To list the major complications of caesarian section
INSTRUMENTAL DELIVERY
Forceps delivery and vacuum delivery constitute instrumental

deliveries. These are techniques used to assist a laboring
mother mostly in the second stage of labour. Except for some
variations the indications, prerequisites and complications of
these procedures are similar. They are entirely different in the
type of instruments and the technique used to apply the
instruments.
1. Forceps delivery
Forceps delivery is a means of extracting the fetus with the aid

of paired metallic instrument called obstetric forceps.
1.1. Description of obstetric forceps
257
The obstetric forceps consists of two matched parts that

articulate or "lock". It is designed to fit to the sides of the fetal
head with primary functions of traction, compression and in
some cases rotation of the fetal head. Each part of the
obstetric forceps is composed of a blade, shank, lock and the
handle.
The blade, which may be fenestrated or solid, possesses two

curves: the cephalic curve, which permits the instrument to fit
accurately to the sides of the fetal head and the pelvic curve,
which fits the curved axis of the maternal pelvis. The blades are
referred to as left blade and right blade according to the side of
mother's pelvis on which they lie after application. After
articulation the left blade is held by left hand and the right
blade is held by the right hand of the operator. The shank could
be short or long depending on the type of forceps. The shanks
are either overlapping or separate. The two blades articulate at
the lock. Most obstetric forceps possess a fixed type of lock
(either English type or French type) where as very few like the
Kielland forceps possess sliding type lock. The lock leads to
the most proximal parts of the forceps which are the shoulder
and the handle where the hand of the operator rests to apply
traction.
1.2. Classification of Forceps Delivery
258
Based on the station and the degree of rotation of the head,

forceps delivery is classified as
 Outlet forceps: head has reached the pelvic floor and is

visible at the vulva with the sagittal suture in
anteroposterior or one of the oblique diameters
 Low forceps: head at station +2 cm or lower but has not

reached pelvic floor
 Mid forceps: head is engaged but station is above +2. It

should be done as a trial of forceps in an operating
theatre.
 High forceps: head is above station 0 and is not engaged.

It is obsolete in modern obstetrics.
1.3. Indications
 Fetal distress in the second stage of labor
 Prolonged second stage of labor: inefficient uterine

contraction or maternal exhaustion or malpositions.
 Maternal conditions which need shortening of the second

stage of labor, where pushing is contraindicated like
cardiac disease, hypertensive disorders of pregnancy and
previous cesarean section
 After coming head of breech
259
1.4. Prerequisites (for outlet and low forceps)
 Well documented indication should be present
 Cervix must be fully dilated
 Membranes must be ruptured
 Presenting part must be either vertex, mento anterior face

presentation or after coming head of breech
 Head must be engaged and station should be below +2
 Exact position of the head should be determined
 No gross cephalopelvic disproportion (contracted pelvis or

macrosomia)
 Maternal bladder should be empty
 Appropriate anesthesia should be given and prophylactic

episiotomy done
 Adequate skill and experience
1.5. Technique of out let forceps delivery
 Check the indication and the prerequisites
 Put the mother in lithotomy position at the edge of the

delivery coach. Clean and drape the vulva.
260
 Empty the bladder and insure adequate anesthesia

(pudendal, local infiltration) Select the appropriate forceps.
Articulate the forceps in front of the vulva (phantoms
application) in the direction of fetal position.
 Lubricate the blades with antiseptic solution
 Hold the left blade with the left hand and insert 2-3 fingers
of the right hand into the left side of the vagina. Slide the
left blade gently between the head and the fingers in an
arc to put it on the side of the fetal head. Initially hold it
vertically then bring it to the horizontal position through a
smooth arc.
 Repeat the same step for the right blade holding it in right
hand and fingers of the left hand in the vagina
 Depress the handles and lock the forceps. If difficulty is

encountered, remove the blades and recheck the position
of the fetal head.
 After locking, check for proper application. (I. Posterior

fontanel should be located midway between the sides of
the blades with lambdoid suture equal distance from the
blades and one finger breadth above the plane of the
shank II. Fenestration of the blades should be barely felt
and the amount of fenestration should be equal (in solid
blade no more than a fingertip should be able to be
261
inserted between the blade and the head). III. Sagittal

suture must be perpendicular to the plane of the shanks
throughout its length.)
 Apply traction along the axis of the pelvis using no more

force than a force exerted by flexed forearms. Traction
should be applied gradually and sustained at its maximum
intensity for not more than 30 seconds. Then relieve for
15-20 seconds.
 As head crowns make adequate episiotomy
 After the head is delivered unlock and remove the forceps
 Following the delivery of the placenta, inspect the lower

genital tract for tear and episiotomy for extension. Repair
episiotomy and any tear.
 Provide care for the neonate and check for complications

on the neonate.
 Document your findings
1.6. Complications of forceps delivery
The fetal/ newborn complications are laceration of face and

scalp, cephalhematoma, subgaleal bleeding, facial nerve injury,
fracture of face and skull, intra cranial bleeding and increased
risk of mother to child transmission of HIV.
262
The maternal complications include tears of genital tract

(perineal, vaginal, and cervical), episiotomy extension and
uterine rupture with or without bladder rupture.
2. Vacuum (vantous) delivery
The vacuum extractor is a traction instrument used as an

alternative to the obstetric forceps. It is designed to deliver the
fetal head by drawing the scalp into the cup forming an artificial
caput called the chignon.
The vacuum extractor has the following advantages over

obstetric forceps
 The vacuum cup does not take up room in the often limited
space in the birth canal
 The vacuum extractor brings about ―autorotation‖ of the fetal

head at the level of the pelvis where this is best, rather than
where the person using forceps choose to rotate the fetal head
 Generally anesthesia is not required and the mother shares

in the delivery and helps to push
 Episiotomy is not always necessary
2.1. Description of the vacuum extractor
263
The vacuum extractor has the cup, hoses that connect the cup
to the trap bottle and the pump, trap bottle with manometer
and a pump which is either manual or electrical.. There are
various types of cups made either from metals or plastics like
silastic. The Malmstrom cup is a metallic cup of three different
sizes (40 mm. 50mm, 60mm) with narrow rim. It has a hole at
the center of the cup through which the chain passes. The
chain passes through a hose and gets attached to the metal
cross bar. Threading the chain attaching it to the metal bar
takes some time. For these reasons the Bird's modification of
the cup is developed It has a chain permanently attached to its
center on the back and a hole for the hose at the periphery of
the cup. This modification eliminates the need to thread the
chain through the hose. Later silastic cups were developed.
These are soft, easy to manipulate and vacuum is attained
more quickly.
2.2. Indications
The indications are similar to forceps delivery except after

coming head of breech.
2.3. Prerequisites
The prerequisites are similar to forceps but need modifications

in the following.
264
 Cervix need not be fully dilated. Vacuum can be applied if

cervix is more than 8 centimeters dilated.
 Presenting part must be vertex
 Position need not be known
 It can be applied for higher stations. Head must be engaged

station 0 or below (descent of less than 2/5)
 Live fetus at term
 Need for anesthesia is less and routine prophylactic

episiotomy is not a must
2.4. Procedure
 Check the indication and the prerequisites
 Put the mother in lithotomy position at the edge of the

delivery coach. Clean and drape the vulva.
 Empty the bladder and insure adequate anesthesia

(pudendal, local infiltration) Select the largest cup that can
easily be introduced.
 Introduce the cup unto the vagina and position it over the
sagittal suture about 3 centimeters in front of the posterior
fontanel.
 Check the full circumference of the cup for entrapped

maternal tissue
265
 Create a vacuum of 0.6- 0.8 kg/ cm3. For silastic cups it

can be done rapidly over 1 minute where as for metallic
cups gradual increment of 0.2 kg/ cm 3 every 2 minutes
allows adequate caput formation.
 Check again for tissue entrapment before traction.
 Apply perpendicular traction using two handed technique

(fingers of one hand placed at the rim of the cup and the
other hand grasps the traction bar). Sustained traction in
the direction of the pelvic curve should be applied
coincident with uterine contractions and maternal pushing.
 As soon as the head is delivered release the cup and

complete the delivery of the fetus and the placenta.
 Following the delivery of the placenta, inspect the lower

genital tract for tear and episiotomy for extension. Repair
episiotomy and any tear.
 Provide care for the neonate and check for complications

on the neonate.
 Document your findings
2.5. Complications
The fetal and maternal complications are similar to forceps

delivery but generally occur at reduced incidence. Localized
scalp edema which disappears in few hours, scalp abrasions
266
and lacerations and necrosis of scalp from prolonged

application of the cup is usual.
DESTRUCTIVE DELIVERY
Destructive delivery is vaginal operative delivery that

accomplishes delivery of the fetus by reducing its size in a
woman with obstructed labour with dead fetus. The advantages
of destructive delivery over caesarian section for a woman with
obstructed labour and fetal death are
 The uterus will remain intact, thus avoids the risk of

rupture of the uterus in the subsequent pregnancies.
 Peritoneal contamination by infected uterine contents is

avoided
 Risks of anesthesia and prolonged postoperative stay in

bed are avoided
267
1. Types of destructive delivery
I. Craniotomy is destructive delivery done on the head. It

involves reducing the size of the head by removing the brain
tissue through an opening made in the skull of the fetus.
Depending on the presentation the brain tissue can be
approached through the suture lines and fontanel or the palate
or the foramen magnum.
II. Decapitation is destructive delivery for impacted shoulder

presentation with hand prolapse. It involves severing the neck
of the fetus allowing the delivery of the rest of the body and
later the head.
III. Evisceration is also a destructive operation for impacted

shoulder presentation with hand prolapse. It involves removing
the abdominal and thoracic viscera through an opening made in
wall of the thorax or abdomen.
IV. Clediotomy is a destructive operation for shoulder dystocia.

It is reduction of the biacromial diameter by cutting the clavicles.
Note: Destructive operations should ideally be performed in an

operating theatre under general ansthesia with at least two
units of cross matched blood available.
2. Prerequisites
268
 Clear indication- obstructed labour (gross CPD, impacted

shoulder presentation, shoulder presentation)
 Fully dilated cervix
 Dead fetus (need to be confirmed by ultrasound or

auscultation by three people
 Accessible presenting part for the type of procedure

selected ( head with decent of less than 2/5 for
craniotomy, neck for decapitation, axilla or abdomen for
evisceration)
 Imminent rupture or rupture of the uterus ruled out
 Access for immediate laparatomy and blood transfusion
 Adequate skill and ansthesia
3. Complications
Major complications are rupture of the uterus, genital tract

lacerations (perineal, vaginal and cervical), bladder and rectal
damage.
269
CAESARIAN SECTION (C/S)
Caesarian section is delivery of fetus or fetuses along with the

placenta and membranes by an incision made through the
abdominal and uterine wall after the fetus has reached viability.
The correct terminology for the surgical delivery of a previable
fetus is hysterotomy. Caesarian section is classified as
elective (caesarian section that is performed before the onset
of labor or before the appearance of any complication that
mandates an urgent delivery) and emergency (caesarian
section that is performed after the onset of labor or appearance
of a complication that mandates urgent delivery). Primary
caesarian section is one that is done for the first time while
repeat caesarian section is the one that is done for more than
one time.
1. Types of caesarian section incision
I. Lower segment transverse (Kerr) caesarian section
In this type the lower segment is incised transversely after

incising and reflecting the vesico uterine fold of peritoneum.
270
This is the most commonly done type of cesarean section and

has long been the standard operation because it has the
following advantages
 Less blood loss, easy to repair
 Good wound healing therefore less risk of future rupture
 Less risk of adhesion formation because of its peritoneal

coverage.
The major disadvantages are:
 Lateral extension with damage to uterine vessels and

ureters
 Bladder injury especially in repeat cases.
II. Classic (Sanger) caesarian section
In this type uterine incision is made vertically through the

corpora uteri (upper segment). It is simple and fast to perform
but is associated with a number of disadvantages
 More blood loss and difficult to close
 Poor healing of the incision, therefore high chance of

future rupture
 Risk of adhesion formation with bowel and omentum
271
Therefore it is not a routine method of caesarian section and is

only done upon specific indications.
 Inaccessible lower segment because of dense adhesions

from previous caesarian section
 Large myoma over the lower segment
 Highly vascular lower segment from anterior placenta

previa
 Fetal malformations like conjoined twin and transverse lie

with back down
III. Less common types
 Lower segment vertical (Sellheim) caesarian section
 Delee incision – J-
shaped extension of the lower segment transverse
incision
 Inverted T incision lower segment incision
2. Indications
272
Caesarian section is done in cases in which vaginal delivery

either is not possible or would impose undue risks to mother or
baby or both. Some of the indications are clear and absolute
while others are relative. Common indications for caesarian
section include
 Cephalopelvic disproportion
 Mal presentations (transverse lie, breech, persistent brow)
 Cord presentation and prolapse
 Fetal distress in the first stage of labor
 Failed induction/ augmentation and instrumental delivery
 Ante partum hemorrhage (placenta previa, abruption

placenta)
 Conditions with unripe cervix where rapid delivery is

needed like preeclampsia, ecclampsia,
 Previous caesarian section after failed trial of scar or

electively
 Carcinoma of the cervix
 The X-factor relative indications, which considered

separately, might not warrant caesarian section but when
taken together constitute a valid indication. Example is
273
post term plus elderly primigravida or prior infertility

problem.
3. Procedure and patient care
Informed consent should be obtained. An intravenous line is

opened and crystalloids started. Hemtocrite and blood group
should be determined. Blood should be cross matched and be
readily available. Self or catheter assisted bladder emptying is
done. Prophylactic antibiotics, if indicated, are given. Non
particulate antacids with gastric decompression by nasogastric
tube should be done in emergency cases.
Both inhalational (general) and regional (spinal, epidural)

ansthesia can be used. Proper preparation of the operative site
is done.
Abdomen is opened by midline, paramedian or pfannenstein

(transverse suprapubic) incisions. The abdomen is then opened
in layers. The vesicouterine fold of peritoneum is opened
transversely and bladder reflected down. The lower uterine
segment is opened transversely and the fetus extracted. The
cord is clamped and cut. The placenta is delivered. The
endometrial cavity is mopped of any reminants by sterile moist
pack. The edges of the uterine incision are caught by
Greenarmytage forceps. Uterine incision closed in one or two
274
layers by chromic 0 or 1. Hemostasis secured. Bladder

peritoneum closed by continuous chromic 2/ 0. Abdominal wall
closed in layers.
Postoperatively the level of consciousness, vital signs and

degree of vaginal bleeding should be monitored frequently.
Intravenous fluids are continued until the woman is taking fluids.
Do not give anything orally until bowel sound returns. Antibiotics
and transfusion are given if indicated. Encourage early
ambulation.
Upon discharge ensure that she is taking regular diet, wound is

clean, dry
and not infected and there is no fever. Counsel on future risks

and need to
have hospital delivery in future pregnancies.
4. Complications
275
Complications occur during the operation or in the post

operative period. Intraoperative complications include bladder
laceration especially in repeat cases, ureteral injury,
hemorrhage from damaged uterine vessels, anesthetic
complications like Mendelsons syndrome, fetal blood loss from
incision through placenta or laceration at the time of incision,
trauma at time of extraction and fetal hypoxia from venacaval
compression and anesthetic drugs.
Postoperative complications include hemorrhage from atonia or

incision site, pelvic hematoma, endomyometritis, wound site
infection, deep vein thrombosis and future risk of rupture of the
scar in subsequent pregnancies. Other post operative
complications seen in any surgical patient can be encountered.
5. Vaginal birth after caesarian (VBAC)
In the absence of absolute contraindications a woman with

caesarian section scar can be given the chance to deliver
vaginally. These contraindications which mandate elective
caesarian section are
 Classic or inverted T or low vertical incision with extension

to the corpus
 Two or lower segment incisions or the type of incision is

unknown
276
 Gross CPD from macrosomia (estimated weight of more

than 3500 grams) or any degree of pelvic contracture
 Multiple pregnancies
 Malpresentation
 Conditions that preclude vaginal delivery or need induction
REVIEW QUESTIONS
1. List the indications of forceps and vacuum delivery.
2. List the prerequisites to forceps and vacuum delivery.
3. List the complications of forceps and vacuum delivery.
4. Name the types of destructive deliveries.
5. List the prerequisites and complications of destructive

delivery.
6. Describe the major types of caesarian section with their

advantages and disadvantages.
7. List the complications of caesarian section.
277
CHAPTER 17
MALPRESENTATIONS AND MALPOSITIONS
Learning Objectives
 To list the types of mal presentations and mal

positions with their predisposing factors.
 To define breech presentation and describe the

varieties of breech presentations with there
diagnostic approaches.
278
 To describe the maternal and fetal risks associated

with vaginal breech delivery.
 To describe the techniques of conducting vaginal

breech delivery.
 To know how to diagnose and manage the other mal

presentations.
 To describe the options of management for persistent

occipito posterior positions.
INTRODUCTION
Malpresentation and malpositions are essentially abnormalities

of fetal position, presentation, attitude or lie. They collectively
constitute the most common cause of fetal dystocia occurring in
approximately 5% of all labors.
Breech presentation is the commonest malpresentation. The

other malpresentations are face presentation, brow
presentation, shoulder presentation, and compound
presentation.
The malpositions include occipito posterior position and

persistent occipito transverse positions.
279
Often no cause is identified but any condition that changes the

proportional volume of the fetus and amniotic fluid resulting in
increased or decreased mobility of the fetus predisposes to
malpresentations. These conditions are well known and fall into
three major groups.
 Fetal factors: fetal anomalies like e.g. hydrocephalus,

multiple gestation, prematurity, polyhydramnios and
oligohydramnios.
 Maternal factors: uterine anomalies like septate and

bicornuate uterus, contracted pelvis, submucus myoma,
grand multiparity and past history of malpresentations.
 Placental factors: placenta previa.
1. BREECH PRESENTATION
Breech presentation is a fetal presentation where the fetus lies

longitudinally and the buttocks or the fetal lower extremities
occupy the pelvic inlet with the cephalic pole occupying the
fundus.
1.1. Types and incidence
There are four types of breech presentation
280
Frank breech presentation: fetal with flexed hips and

extended knees so that the thighs are apposed to the
abdomen and the lower legs to the chest. The presenting part is
the buttocks. It accounts for 60% - 65%of all breech
presentations at term and 40% before term.
Footling breech presentation (single or double): fetus with

one or both hips and knees extended so that the feet become
the presenting part. It accounts for 25%-35% of breech
presentations at term and 50%before term.
Complete breech presentation: fetus with flexed hips and

knees so that the buttocks and the feet become the presenting
part. it accounts for 10% of all breech presentations at any
gestational age.
Knee presentation is a rare form seen in a fetus with extended

thighs and flexed knees.
Incidence depends on the gestational age and the fetal weight.

Breech presentation accounts for 3-4% of all births but occurs
in 15% of low birth weight (<2500gm) infants. Its incidence in
premature fetuses is high and decreases as gestational age
increases.
1.2. Diagnosis
There are no specific symptoms but occasional tightness or

discomfort in the upper abdomen may be reported.
281
Leopold‘s maneuver reveals round, globular, smooth head

occupying the fundus, which will be ballotable if adequate
amniotic fluid is there and narrow and softer breech occupies
the lower pole of the uterus. Fetal heartbeat will be heard more
easily at or above the umbilicus.
Pelvic examination in labour identifies the soft irregular mass

with anal orifice, the ischial tuberosities, genital groove and
external genitalia. In footling and complete breech presentation
one or both feet are felt.
The important differential diagnosis at this point is face

presentation which should be differentiated by the presence of
the hard maxilla and if the fetus is alive the presence of
suckling.
Ultrasonography and plain film of the abdomen can be done to

confirm the diagnosis.
1.3. Mechanism of labour (frank breech in left

sacrotransverse position)
The denominator of breech presentation is the sacrum and the

diameter is bitrochanteric diameter. The eight possible positions
are recognized: sacrum anterior (SA), sacrum posterior (SP),
left sacrum transverse (LST), right sacrum transverse (LST), left
sacrum anterior (LSA), left sacrum posterior (LSP), right sacrum
anterior (RSA) and right sacrum posterior (RSP).
282
In labour the breech engages as the bitrochanteric diameter

passes the plane of the pelvic inlet, usually in one of oblique
diameters. Decent occurs with further flexion. Internal rotation
ordinarily takes place when breech reaches levator musculature
which brings the bitrochanteric diameter to anteroposterior
position. Further decent with flexion brings the pelvic outlet.
Delivery of the buttocks, first the anterior to be followed by the
posterior, occurs by lateral flexion.
As the trunk is delivered the shoulders enter the pelvic inlet in

the transverse diameter causing rotation of the trunk so that the
back faces up. The shoulders descend in the birth canal and at
the level of the pelvic floor internal rotation occur causing
external rotation of the body. At this point the back is directed to
the left side of the mother, which indicates readiness for the
delivery of the shoulders. The shoulders are then delivered by
lateral flexion, anterior followed by posterior.
At the time the shoulders rotate internally the head engages in

the transverse diameter of the inlet. The head, after decent
rotates internally at the pelvic floor. This causes rotation of the
rest of the body so that the back faces up. Further decent
results in the delivery of the head by flexion (the face sweeps
the perineum).
1.4. Management
I. Antepartum management
283
Breech presentation diagnosed before 32 weeks of

gestation should be managed expectantly with frequent follow
up. Spontaneous version to cephalic presentation at the latter
weeks of gestation is likely.
After 36 weeks the chance of spontaneous version is less

likely. If the there are no contraindications external cephalic
version should be performed. This requires expertise and
facilities for emergency caesarian section. If external cephalic
version is contraindicated a decision on the mode of delivery
(vaginal breech delivery or elective caesarian section) has to be
made before labour starts. For these reasons pregnant
women with breech after 36 weeks have to referred for
hospital management.
II. Intra partum management – vaginal breech delivery
All breech deliveries should ideally be conducted in a set

up with caesarian section facility. In the absence of such
facility laboring mothers with breech presentation in whom
delivery is not imminent (cervical dilatation of less than 8 cm)
should be referred. Women in whom delivery is imminent
should be attended in the same health facility. This justifies
why all health workers dealing with laboring women need to
be skilled in conducting vaginal breech delivery.
Vaginal breech delivery trial should be allowed in:
284
 Estimated fetal weight of less than 3500gms
 Frank or complete breech with flexed head
 Pelvis should be judged to be adequate with

favorable shape
 Live fetus with normal heart rate pattern or gross

malformation or dead fetus
 No other obstetric factor (X factor)
Evaluation at admission is like any laboring mother (refer to).

This confirms the diagnosis and identifies parameters for
allowing vaginal breech delivery. Artificial rupture of
membranes should not be done.
First stage of labor should be followed as described in chapter

14. Vaginal examination should be done and fetal heart
beat checked following spontaneous rupture of membrane to
rule out cord prolapse. Progress of labor in breech presentation
is not remarkably different from vertex presentation. The
occurrence of in coordinate uterine action, uterine inertia, arrest
or delay in cervical dilatation or failure of descent of breech
warrants urgent caesarian section. There is no place for
augmentation of breech presentation with poor progress of
285
labour. The mother should be instructed not to push till full

cervical dilatation is achieved.
In the second stage of labour, before conducting delivery, pelvic

examination should be done to confirm full cervical dilatation.
Bladder must be emptied and the mothered positioned into
lithotomy position. There are three types of vaginal breech
delivery.
1. Spontaneous vaginal breech delivery where the infant is

expelled entirely spontaneously with out any help other than
support. This occurs rarely except for premature babies in a
multipara. It is associated with higher perinatal mortality.
2. Assisted vaginal breech delivery (Partial breech

extraction) where the fetus is delivered upto the level of the
umbilicus spontaneously and the rest of the body is delivered
with the assistance of the health professional using special
maneuvers.
3. Total breech extraction where the entire fetus is delivered

from the birth canal by the assistance of the health professional.
It is associated with significant maternal and fetal risks. This
procedure is only performed for the delivery of the second twin.
Third stage is managed actively and the genital tract explored

for tears.
286
III. Techniques of assisted breech delivery
A. Delivery of the buttocks and legs
Instruct the mother to bear down with every contraction. Do

episiotomy when the fetal anus is visible and perineum
distended. Allow the breech to be delivered with out
intervention up to the level of the umbilicus. After the delivery
of the buttocks, supporting the baby around the hips without
pulling and keeping it below the horizontal is all that is
needed. The baby should be grasped with clean towel
moistened with warm water. Holding the baby around the
hips avoids fetal visceral damage. Ensure the anterior
position of the sacrum and the back until the lower border of
the scapula is visible.
In frank breech, if the legs can not be delivered

spontaneously, it can be assisted by splinting the medial
thigh of the fetus with the position parallel to the femur and
exerting pressure laterally so as to sweep the legs away from
the midline (Pinnard maneuver).
Apply gentle and steady down word traction until the lower
halves of the scapula are delivered.
B. DELIVERY OF THE ARMS AND SHOULDERS
AFTER THE LOWER BORDER OF THE SCAPULA IS

VISIBLE PULL A LENGTH OF UMBILICAL CORD.
287
ENSURE THE BACK IS FACING TO THE RIGHT OR LEFT

SIDE BEFORE DELIVERING THE ARMS. INTRODUCE
TWO FINGERS INTO THE VAGINA OVER THE CHEST OF
THE FETUS AND FEEL FOR BOTH ARMS. IF THE
ARMS ARE NOT FELT IT INDICATES EXTENDED OR
NUCHAL ARM. IF THE ARMS CAN‘T BE DELIVERED
SPONTANEOUSLY, DELIVER THE ARMS IN ONE OF
THE FOLLOWING WAYS:
I. Lovset maneuver
Holding the baby‘s hip rotate the fetus by half a circle

(1800) keeping the back uppermost and applying
downward traction at the same time. This delivers the
posterior arm, which now becomes the anterior arm,
beneath the pubic arch. This may be assisted by placing
one or two fingers on the upper part of the arm flexing it,
which sweeps the arm over the chest. Then reverse the
rotation (half a circle (1800) keeping the back upper most to
deliver the remaining arm beneath the symphysis.
II. Delivery of the posterior arm followed by anterior (or

the reverse)
Put one or two fingers into the vagina over the back of the
baby. Slip the fingers over the shoulders, place them
parallel to the humerus and apply downward pressure to
deliver the arm.
288
III. Extraction of the posterior arm
It is useful for extended arm and the Lovset maneuver is

not successful.
C. DELIVERY OF THE HEAD
Allow the baby to hang until the nape of the neck or

posterior hairline is visible. Then deliver the head in one of the
following ways:
I. Mauriceau Smellie Veit maneuver
Introduce the non-dominant hand into the vagina over the

face of the fetus which is supported by the forearm. Place
the first (index) and the third (ring) fingers on the right and left
cheek bones and place the second (middle) finger into the
baby‘s mouth. Pull the jaw down to flex the head.
At the same time introduce the dominant hand into the

vagina over the back of the fetus. Put the first and third
fingers over the shoulders and the middle finger over the
occipital prominence. Press down on the occiput to assist
in flexion of the head.
Ask an assistant to give supra pubic pressure by the base

of the hand. Pull gently to deliver the head by making an arc
following the pelvic curve.
II. Wigand maneuver
289
The procedure is like Mauriceau Smellie Veit maneuvers

but differs by
1. The dominant hand instead of being introduced into

the vagina it is put on the supra pubic area to provide
supra pubic pressure.
2. An assistant is not needed to apply supra pubic

pressure.
III. by Pipers forceps
D. Difficulties during vaginal breech delivery
I. Nuchal arms (extended arms found behind the neck of

the fetus) should be managed by Lovset maneuver or by
rotating the fetus counter clock wise to deliver the right arm
and often clock wise to dislodge and deliver the left arm.
II. Extended arm is diagnosed when the arms are not felt
on the chest. Management is like the nuchal arm.
III. Arrest of the after coming head could be caused by

incompletely dilated cervix, extended head, hydrocephalus or
cephalopelvic disproportion (contracted pelvis or big baby)
1.5. Complications
Breech presentation is associated with high perinatal morbidity

and mortality. Possible complications contributing to maternal
mortality and morbidity are obstructed labor, genital tract
290
lacerations and increased risk of operative delivery. Fetal

complications are cord prolapse, birth injury (superficial tissue
damage, edema and bruising, fractures of the humerus, clavicle
or femur, dislocation of shoulder or hip, Erb‘s palsy, trauma to
internal organs especially a ruptured liver or spleen, damage to
adrenals, spinal cord damage or fracture of the spine and
intracranial hemorrhage) and associated congenital
malformations.
2. FACE PRESENTATION
Face presentation is a kind of cephalic presentation where the

neck of the fetus is fully extended so that the occiput lies on the
back and the face (area of the fetal face between the orbital
ridges and the chin.
It is a rare condition occurring in 1 in 550 births.
291
2.1. DIAGNOSIS
Antenatal diagnosis is often difficult. Diagnosis is usually made

in labour by vaginal examination. Diagnosis by Leopold
maneuver is based on finding long ovoid uterus with no bulges
in the flanks, S shaped ill defined fetal back with marked
depression between the occiput and the back, and palpation of
the cephalic prominence on the same side as the fetal back.
Fetal heart beat is heard on the side of the feet in mento
transverse and difficult to identify in mento posterior.
On vaginal examination, with sufficiently dilated cervix, feeling

the orbital ridges, eyes, nose and mouth clinches the diagnosis.
Confusion may arise with breech presentation in prolonged
labor with edema of the presenting part. The mouth may be
open and the hard gums are diagnostic and the fetus may suck
the examining finger.
2.2. MECHANISM OF LABOUR
The denominator is the mentum (chin). The presenting diameter

is submento- bragmatic which is 9.5 centimeters. Eight possible
positions exist depending on the relation of the chin to the
various positions of the pelvis.
Engagement occurs when the submento-bragmatic diameter

passes the pelvic inlet. Decent with extension of the head
occurs. At the pelvic floor internal rotation occurs. In most
rotation of the chin occurs anteriorly so that the fetus assumes
292
mento anterior position. In few the chin rotates towards the

sacrum assuming persistent mentoposterior position.
For mento anterior further decent with extension occurs till it

reaches the perineum. Delivery occurs by flexion so that the
sinciput, vertex and the occiput sweep the perineum.
Restitution, external rotation and delivery of the shoulders by
lateral flexion occur in the same manner as vertex presentation.
For persistent mento posterior there is no further mechanism of

labour. Unless relieved, further impaction results in obstructed
labour.
2.3. Management of labour
Caesarian section is indicated in the presence of big baby,

contracted pelvis, previous uterine scar like previous caesarian
section and elderly primi or woman with bad obstetric history. In
labour persistent mentoposterior position, poor progress of
labour and fetal distress are indications for caesarian section.
Appropriate evaluation before or at the start of labour and
proper follow up of labour is, therefore, essential.
Follow up in the first stage of labour is like in vertex.

Labour may be slow but as long as it is progressing nothing has
to be done. The old saying "if a face is progressing leave it
alone‖ is still valid. Augmentation of labour is generally
contraindicated.
293
Low forceps may be needed for mentoanterior position in

prolonged second stage.
2.4. Complications
These include cord prolapse, facial bruising and swelling which

disappear in one week and 1-2 days respectively, cerebral
hemorrhage, extensive perineal lacerations, increased
operative delivery and obstructed labour.
3. BROW PRESENTATION
Brow presentation is a kind of cephalic presentation in which

there is partial extension of the fetal head so that the brow (area
between the anterior fontanel and the orbital ridges) becomes
the presenting part.
It occurs in 0.06 % of deliveries.
3.1. Diagnosis
Diagnosis by abdominal palpation is possible but unusual.

Usually diagnosis is made in late labour. Finding the frontal
suture, anterior fontanel, the orbital ridges and the base of the
nose on vaginal examination with dilated cervix clinches the
diagnosis.
3.2. Mechanism of labour
294
The denominator is the anterior fontanel or the frontal bone.

The presenting diameter is mentovertical diameter which is 13
centimeters. Engagement does not occur as this diameter is
larger than the diameters of the pelvic inlet. Unless it reverts to
either face or vertex presentation, there is no mechanism of
labour for brow presentation. Spontaneous delivery of a term
brow is unlikely. If no intervention is made the end result is
obstructed labor.
3.4. Management
In the absence of other conditions that mandate caesarian

section, determination of the pelvic capacity and fetal size must
be made. Emergency caesarian section is indicated for
macrosomia and contracted pelvis.
In early labour, in the absence of such conditions, management

is expectant. This is based on the assumption that a brow may
spontaneously revert to face or vertex, which occurs in 30 % of
the cases. If it persists, the fetus has to be delivered by
caesarian section. Augmentation of labour for arrested labour is
not recommended.
4. COMPOUND PRESENTATION
295
Compound presentation is a presentation in which an extremity

(hand or foot) prolapses or descends along side the presenting
part. The most common type is upper extremity prolapsing with
vertex. Other varieties are upper extremity with breech or rarely
lower extremity with vertex.
Incidence is 1 in 1000 pregnancies.
Diagnosis is made on vaginal examination in labour by

palpating fetal extremity adjacent to the presenting part. If
diagnosis is suspected but uncertain, ultrasound or X-ray can
be used to locate the position of the extremities and search for
mal formations.
Management depends on gestational age, type of presentation

and whether the hand or foot is prolapsing. Viability of the fetus
should be documented prior to delivery since compound
presentation is associated with prematurity. Labour should be
allowed and delivery anticipated, if the fetus is non-viable (<28
weeks according to our country's protocol) or has gross
congenital malformation or is dead.
For viable fetus, hand prolapsing with vertex labour could be

allowed to continue with the hope of spontaneous retraction of
the hand as labour progresses. Any attempt to reduce the
extremity by digital manipulation is contraindicated. Persistent
cases should under go caesarian section.
296
Vertex with foot and breech with hand are indications for
caesarian section.
5. SHOULDER PRESENTATION (TRANSVRESE LIE)
Shoulder presentation is a presentation in which the long axis of

the fetus is at right angles to the axis of the uterus so that the
presenting part becomes the shoulder. It is the most dangerous
of the fetal presentations. Occasionally the lie is oblique but this
does not persist as the uterine contractions during labour make
it longitudinal or transverse.
Incidence is 1:300 deliveries at term but is higher in preterm.
5.1. Diagnosis
Diagnosis is easy but can be overlooked. On abdominal

examination, the uterus is transversely oval with the fundus
scarcely above the umbilicus. The fundal height is less than
expected for the period of gestation. There is no fetal pole in the
fundus and the pelvic inlet. The fetus lies crosswise with head
in one side of the abdomen. These findings may be obscured
after membrane rupture in late labour A very high and
unreachable presenting part on vaginal examination highly
suggests transverse lie. Ultrasound confirms the diagnosis and
identifies the possible causes.
297
In labour vaginal examination identifies the shoulders and/ or

the ribs or in neglected cases the hand prolapsing through the
vulva.
5.2. Mechanism of labour
There is no mechanism of labour for an average sized fetus. If

labour is allowed to continue obstructed labour develops.
In women with capacious pelvis and premature fetus, delivery

could occur by doubling up or spontaneous version.
5.3. Management
 If transverse lie is diagnosed antenatal, refer the patient to

hospital as term approaches.
 If shoulder presentation is diagnosed during labour, refer

the patient immediately to hospital.
 Shoulder presentation diagnosed before term should be

managed expectantly since there is a chance of
spontaneous version.
 Shoulder presentation reaching term can be managed by

external cephalic version.
7.6. Complications
 Cord prolapse
298
 Uterine rupture with possible maternal death. This is

especially true in neglected shoulder presentation.
6. UMBILICAL CORD PRESENTATION AND PROLAPSE
It is decent of the umbilical cord into the lower uterine segment.

Intermittent or continuous compression by the presenting part
compromises the fetal circulation causing fetal hypoxia and
eventually death. It may take the following forms:
Overt cord prolapse: presentation of the cord beyond the

cervix after rupture of the membranes, so that loop of cod is
palpable or visible during examination.
Occult cord prolapse: with ruptured membranes the cord has

prolapsed along side the presenting part but not in front of it.
This is not palpable during vaginal examination
Cord presentation: the cord is in front of the presenting part

with intact membranes so that it is felt through the membranes
during vaginal examination.
Incidence varies with the type of presentation. For overt cord

prolapse it is 0.5% in cephalic, 0.5% in frank breech, 5 % in
complete breech, 15 % in footling breech and 20% in
transverse lie.
299
Any condition that provides space between the presenting part

and the pelvic inlet predisposes to cord presentation and
prolapse.
 Maternal factors are contracted pelvic inlet, multi parity,

tumor previa
 Fetal factors are malpresentation, long umbilical cord, low

lying placenta, prematurity, multiple gestation, conditions
that cause rupture of membranes before engagement of
the presenting part like in PROM and polyhydraminos
 Iatrogenic factors are artificial rupture membrane done for

fetus at high station
Diagnosis of overt cord prolapse is done by finding loops of

cord in the vagina or cervix. Feeling loops of cord through the
membrane ahead of the presenting part diagnoses cord
presentation. Diagnosis of occult cord prolapse is suspected by
finding variable deceleration following rupture of the
membranes.
Management
I. Cord presentation- emergency caesarian section if the fetus is

mature or is nearing maturity.
II. Occult cord prolapse – perform pelvic examination to rule out

overt prolapse. Put in a position that corrects the fetal
300
decelerations. If this does not correct it and the deceleration

persists deliver the fetus by the fastest route (instrumental
delivery or caesarian section.
III. Overt cord prolapse – depends on presence of cord

pulsation and cervical dilatation.
 If there is no pulsation await spontaneous delivery with or

without destructive delivery.
 If pulsations are felt deliver by the fastest route (caesarian

section if cervix is not fully dilated, instrumental delivery if
cephalic and cervix is fully dilated, total breech extraction if
breech and cervix is fully dilated).
Note: If fetus is viable (FHB positive and cord pulsating) until

the patient is ready for caesarian section put the patient in
knee-chest position, apply continuous up ward pressure
against presenting part , put the cord inside the vagina and
give oxygen to the mother
Complications are maternal (complications of operative

deliveries) and neonatal (prognosis depends on the degree and
duration of umbilical cord compression occurring before the
diagnosis is made and neonatal resuscitation is begun. If the
duration of complete cord occlusion is less than 5 minutes, the
prognosis is good).
Prevention and early detection

301
 Artificial rupture of membrane should be avoided until the

presenting part is well applied to the cervix.
 After spontaneous or artificial rupture of membrane,

careful and prompt pelvic examination should be done to
rule out cord prolapse.
 Before doing ARM, check for the presence of cord.
7. MALPOSITIONS (VERTEX-MALPOSITION)
Occipito posterior (OP) may be normal in early labor. Most

change by spontaneous rotation to occipitoanterior position.
Progress of labor is not different from that of occipitoanterior
position. But slow progress is common as the result of minor
degrees of disproportion and the long rotation of the fetal head.
In 10% it persists in occipito posterior position.
Mechanism of labor in right occipito posterior position (long

rotation) is the same as that of occipito anterior position except
that it undergoes long rotation. In some cases the occiput takes
short rotation to assume persistent occipitoposterior position
and is delivered with face to pubis.
Diagnosis is easily made by manual vaginal examination when

one finds the posterior fontanel directed towards the
302
sacrum. Women may

complain of continuous and severe backache worsening with co
ntractions.
Management of persistent occipitoposterior position is similar to

that of occipitoanterior position. One should anticipate
prolonged labour from abnormal shape of the pelvis and the
long rotation of the head. In the absence of CPD, augmentation
of labour is possible for hypotonic uterine action.
Possibilities for vaginal delivery in persistent occipitoposterior

position include spontaneous vaginal delivery with generous
episiotomy, forceps delivery with or without rotation, vacuum
delivery and caesarian section for CPD.
Review questions
1. Describe the general causes of malpresentation
2. Describe the techniques used in assisted breech delivery.
3. Describe the mechanism of labour in face presentation.
4. Discuss the diagnostic features of transverse lie.
5. Describe the management of overt cord prolapse.
303
CHAPTER 18
DYSTOCIA
304
Learning Objectives
 To define dystocia and list its main causes.
 To discuss the difference between hypo and hyperactive

uterine dysfunction.
 To list the major causes and complications of

macrosomia.
 To define shoulder dystocia and enumerate the steps in

the management.
 To discuss the clinical features and management of

hydrocephalus.
 To describe ideal obstetric pelvis and list the indications

for pelvic assessment.
 To define and classify contracted pelvis.
Dystocia is difficult labor, which is characterized by abnormally

slow progress of labor. It is the most common indication for
primary caesarian section. Dystocia is a consequence of faults
in the five P‘s operating alone or in combination.
 Power (uterine contraction and voluntary muscular

efforts)
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 Passage (bony pelvis and soft tissues of the birth

canal)
 Passenger (the fetus)
 Psyche and physician
1. Faults in the power (Inefficient uterine contraction or

uterine dysfunction)
Myometrial contractions in normal labor start from one of the

pacemakers located in the uterine cornu. These contractions
are characterized by triple descending gradient, which
constitutes
 Propagation of contraction which is downward from the

fundus to the cervix.
 Intensity of contraction that is stronger in the upper part

of the uterus.
 Duration of contraction that is longer in the upper part.
 Peak of uterine contraction which occurs

simultaneously in all parts.
The net result of this is to provide effective uterine contraction,

which pushes the fetus downwards, thus dilating the cervix. In
306
normal labor effective uterine contraction should fulfill the

following.
 Frequency of 3-4 contractions per 10 minutes
 Duration of 45-60 seconds during each contraction
 Intensity of 20-60 mm Hg with resting tone of 10-15

mm Hg (fundus of the uterus can not be indented at
the height of contraction)
Any deviation from this pattern results in uterine dysfunction.

In majority of uterine dysfunctions the cause is unknown. In the
rest the following are implicated:
 Minor to moderate degrees of CPD, which result in

poor application of the presenting part to the cervix.
 Uterine overdistension as in polyhydramnios or

multiple pregnancy.
 Anxiety and emotions (psychological factors), which

depress release of oxytocin from the posterior
pituitary.
Uterine Dysfunction is common in primigravida than in

multiparas (4% vs. 2%). It leads to prolonged labor which intern
results in maternal exhaustion, increased risk of intrapartum
and postpartum infection of the mother and fetus, fetal distress
and operative deliveries.
307
There are two types of uterine dysfunction
a. Hypotonic uterine dysfunction (uterine inertia)
b. Hypertonic uterine dysfunction (in coordinate

uterine action)
Hypotonic UD Hypertonic UD
Resting tone decreased Resting tone increased
Normal gradient pattern with Distorted gradient pattern

fundal dominance present lower segment
dominance or complete
assynchronism of
electrical impulses.
Contractions are decreased Contractions are

in intensity with slight rise in increased in but are
pressure therefore, less disorganized ,therefore,
pain and uterus is contractions more
indentable at the height of painful leading to ketosis
the contraction
Responds favorably to gets accentuated by

oxytocin oxytocin
308
2. Faults in the passenger
The fetus may be the cause of dystocia if the presentation is

abnormal, if it is big sized or if it is grossly malformed.
I- Malpresentation
In the absence of contracted pelvis or/and big sized fetus most

malpresentations and malpositions do not cause dystocia.
Significant dystocia is a rule in shoulder presentation, persistent
brow presentation, persistent mentoposterior presentation and
breech with extended head, nuchal arm and hydrocephalus.
II- Macrosomia
Macrosomia is defined as fetal weight exceeding 4000 grams.

The general rule is, the larger the size of the fetus the higher
the chance of dystocia. There is no clear cut fetal weight limit
implicated in causing dystocia. In a woman with normal sized
pelvis dystocia is unusual if fetal weight is less than 3500
grams.
The causes of macrosomia are maternal diabetes mellitus

especially of gestational type and post date pregnancy.
Increasing parity, increasing age and size of the mother are
associated with macrosomia.
309
Macrosomia should be suspected in a woman with big

abdomen, fundal height of the uterus bigger than the calculated
gestational age from the LMP, fetus seems large with minimum
amount of amniotic fluid and non-engagement of fetal head at
term. Fetal weight can be estimated by Johnson‘s formula
and ultrasound.
Fetal weight in gram= fundal height in

centimeters –n * 155
n= 12 if the vertex is above the ischial

spine
n= 11 if the vertex is below the ischial

spine
The anticipated complications of macrosomia are deep

transverse arrest, shoulder dystocia, post partum hemorrhage
from uterine atonia or genital tract tears and obstructed labor
and its complications.
III. Shoulder dystocia
Shoulder dystocia is an acute obstetric emergency in which

following the delivery of the head the shoulders of the fetus can
not be delivered despite the performance of routine obstetric
maneuvers. It results from impaction of the anterior shoulder
above the symphysis pubis in an anteroposterior diameter.
310
Risk factors for shoulder dystocia, which are identified in only

less than 50%, include fetal macrosomia, maternal obesity;
prolonged labor especially prolonged second stage of labor,
previous history of shoulder dystocia and difficult operative
vaginal deliveries.
Diagnostic features include
 Turtle sign – following the delivery of the head the

neck is retracted and the head recoils against the
perineum with the chin pressed against the maternal
thigh.
 Spontaneous restitution doesn‘t occur and the face

becomes plethoric.
 Failure to deliver the shoulders with maternal

expulsive effort and gentle down ward traction on the
fetal head.
Complications of shoulder dystocia are post partum

hemorrhage from genital tract tears and uterine rupture, birth
injuries (fractures, brachial plexus injury) and fetal asphyxia and
death.
Shoulder dystocia requires prompt and skillful management.

The following steps are useful.
311
Step1- Stop maternal expulsive efforts. Stop desperate pulling

on the fetal head. Call for help.
Step2- Disimpact the anterior shoulder by one or combination of

the following maneuvers.
 McRoberts maneuver (hyper flexion of both legs

on the maternal abdomen)
 Rubins maneuver (application of suprapubic

pressure in lateral direction on the posterior aspect
of the anterior shoulder)
Step 3- Rotational maneuvers (effective anesthesia needed)
 Wood screws maneuver – rotating the posterior

shoulder backward through 1800(half circle).
 Rubin rotational maneuver-Rotating the posterior

shoulder forward through 1800.
Step 4- Extraction of posterior arm
Step 5- if the above fail perform symphysiotomy and clediotomy
IV- Congenital malformations
1. Hydrocephalus
Hydrocephalus is progressive enlargement of the cranium

resulting from excess accumulation of cerebrospinal fluid in
the ventricles of the brain. It accounts for 12% of
312
malformations at birth and occurs in 1:1000 deliveries. In one

third associated defects like spina bifida are found. Breech
presentation is found in one third of cases. Significant
dystocia from gross CPD is a rule.
Clinical features, which may head in diagnosis, are broad

firm mass above symphysis in cephalic presentation and in
labour finding on vaginal examination of tense large fontanel,
widened suture line and indentable thin cranial bones
Definite diagnosis requires ultrasound examination, which

shows dilated ventricles. Plain x-ray of abdomen may show
large globular head with small face and thin cranial bones.
The management of diagnosed hydrocephalus is drainage of

excess cerebrospinal fluid by cephalocentesis
(ventriculocentesis). This procedure involves passing long
needle through the dilated suture lines into the ventricles. It
can be done vaginally (after 3-4 cm cervical dilation in
cephalic presentation or after the body and shoulders are
delivered in breech presentation) or transabdominally before
the onset of labor.
2. Others
Malformations that may cause dystocia include congenital

goiter and other neck swellings, abdominal masses including
313
ascitis, distended fetal bladder, enlargement of liver, kidneys

and spleen and conjoined twins.
Diagnosis is often difficult and should be suspected if

dystocia arises after delivery of the head .Often stillbirth is
the end result.
3. Faults in the passage
3.1. Bony dystocia
The true pelvis has an inlet, mid-cavity and outlet. An ideal

obstetric pelvis fulfills the following:
 Round or transversely oval pelvic brim (inlet)

without undue projection of the sacral promontory.
The inclination of the brim should be less than 550
below the horizontal, obstetric conjugate
(anteroposterior diameter) of 12 cm and available
transverse diameter of 12.5cm.
 The cavity should be shallow with straight sidewalls

from which the ischial spines do not project unduly
and large sciatic notches with sacrospinous ligament
accommodating two fingers (3.5cm).
314
 Outlet with rounded sub pubic angle of 850 or more

(two fingers) with inter tuberous distance of at least
10cm (4 knuckles).
CONTRACTED PELVIS results if one or more of the critical

internal diameters of the pelvis are shortened by 2cm or
more. It is classified into:
I. Generally contracted pelvis-involves contracture of the

inlet, midcavity and outlet.
II Inlet contracture – anteroposterior diameter of less

than 10 cm OR transverse diameter of less than 12 cm.
III. Midcavity contracture – anteroposterior diameter of

less than 11.5cm or transverse diameter of less than
9.5cm.
IV. Outlet contracture- intertuberous diameter of less than

8cm
The causes of contracted pelvis are classified as follows.
I. Normal development of the pelvic bones but with

abnormal shape: android type pelvis (triangular brim) and
platypelloid type pelvis (flat oval brim which is more
common in women with short stature).
II. Nutritional deficiency from rickets (Vitamin D deficiency)

in child hood and osteomalacia in adult.
315
III. Diseases or injury in the spines (kyphosis, scoliosis),

pelvis (pelvic tumors, fractures) and the limbs
(poliomyelitis in childhood)
IV. Congenital disorders of spines (spondtlolistesis, high

assimilation pelvis), pelvis (Naegels pelvis and Roberts‘s
pelvis) and the limbs (congenital dislocation of hips)
Pelvic assessment
The capacity of the pelvis can be assessed by clinical and

X-ray pelvimetry. Pelvic assessment is indicated in:
 Primigravida at term with unengaged head.
 Primigravida with height less than 1.5 meters or age

less than 18 years.
 Multipara with history of prolonged labor, stillbirth,

early neonatal death or severe neonatal injury.
 Women to be induced or augmented.
 Before trial of scar in lady with previous caesarian

section.
 Women with abnormal presentation (face, breech and

brow).
316
Clinical pelvic assessment should be done after emptying

the bladder and putting the woman in lithotomy position.
Then one should assess the following:
 Reachability of sacrum promontory. If reachable

measure the diagonal conjugate.
 Smoothness and concavity of sacrum.
 Straightness of the sidewall and projection of the

ischial spine.
 Size of sub pubic angle and intertuberous distance.
 Soft tissue masses and strechability of the perineum.
Management
The management of contracted pelvis depends on the

degree of contracture and presence of other obstetric
complications notably malpositions, malpresentations and
macrosomia. Regardless of other obstetric complications,
grossly contracted pelvis should be managed by
caesarian section preferably electively.
The management of borderline contracted pelvis

depends on the presence of other obstetric complications.
Caesarian section should be done in the presence of
macrosomic fetus, malpresentation in a normal sized fetus
and conditions which need induction/ augmentation. In the
317
absence of these a trial of labor should be given before a

decision of caesarian section.
3.2. Soft tissue dystocia
Cause Management
A. Cervical Dystocia
318
Rigid cervix from stenosis digital dilation, cervical

incision
Conglutination of the cervix digital dilation, cervical

incision
Cervical cancer with caesarian section

infiltration
B. Vagina
Septum(transverse or Incision or caesarian section

longitudinal)
Incomplete atresia caesarian section
Annular stricture manual dilatation, incision or

caesarian section
Extensive scarring manual dilatation, incision or

caesarian section
Gartner duct cyst Aspirate aseptically
Tetanic contraction of anesthesia

levator ani
Vulvar scar generous episiotomy
319
C. Pelvic masses
Myoma, ovarian cyst caesarian section
Review Questions
1. Enumerate the causes of dystocia.
2. Discuss the difference between hypotonic and hypertonic

uterine dysfunction.
3. Discuss the management of shoulder dystocia.
4. Discuss the classification and causes of contracted pelvis.
5. List the indications for pelvic assessment.
320
CHAPTER 19
OBSTRUCTED LABOR AND RUPTURED UTERUS
Learning Objectives
 To define obstructed labor and uterine rupture.
 To list the important causes of obstructed labor and uterine

rupture.
 To enumerate the immediate and late complications of the

obstructed labor.
 To discuss the clinical features obstructed labor and

uterine rupture.
 To outline the management of obstructed labor and uterine

rupture.
 To discuss the prevention of obstructed labor.
321
1. OBSTRUCTED LABOR
1.1. Definition-
Obstructed labor (OL) is failure of descent of the fetus in the

birth canal for mechanical reasons arising from either the
passage or passenger in spite of adequate uterine contraction.
It is an absolute condition, which should be applied only when
further progress is impossible without assistance.
1.2. Importance
OL is one of the major causes of maternal mortality in

developing countries. Its incidence is mainly related to the
availability, accessibility and quality of antepartum and
intrapartum services in the community and to a lesser extent to
the incidence of fetopelvic disproportion in the community. OL
should never occur in communities where obstetric care is
optimal even if disproportion is prevalent. Therefore, OL is
considered as a sign of major failure in obstetric care.
1.3. Causes
Cephalopelvic disproportion (CPD) remains to be the

commonest cause of OL. Contracted pelvis (which is prevalent
in developing countries where childhood malnutrition and early
marriage are common)is responsible for most of the CPD.
322
Macrosomic babies and fetal malformations account for the

minor proportion of CPD.
Malpresentation is the other major cause of OL. Included in

here are neglected shoulder presentation, impacted big breech,
and arrested aftercoming head in breech, persistent brow and
mentoposterior presentations. In the presence of borderline
contracted pelvis mentoanterior and persistent occipitoposterior
positions may cause OL.
Other rare causes of OL include deep transverse arrest,

shoulder dystocia and soft tissue obstruction.
1.4. Complications
The immediate and late complications of OL are responsible for

the high maternal mortality, stillbirth and early neonatal death
associated with this condition. In those who survive significant
maternal and neonatal morbidity results in short and long term
debility. The impact of these complications is immense in
developing countries where health service coverage is low and
resources are scarce.
The immediate complications include
 Atonic postpartum hemorrhage
 Uterine rupture (rare in primigravidas)
323
 Intra and post partum infection leading to peritonitis, sepsis

and septic shock
 Maternal tetanus
 Fetal cerebral birth trauma
 Fetal distress
 Fetal and early neonatal infection and sepsis
The late complications include
 Fistulas(vesico-vaginal fistula and recto-vaginal fistula)
 Vaginal stenosis and stricture
 Foot drop(sciatic and common peroneal nerve injury)
 Contracture of joints and ostitis pubis
 Perinatal asphyxia & mental retardation
1.5. Clinical features
Women with obstructed labour invariably give history of

prolonged labor with early rupture of membranes. Usually these
women did not receive ANC during pregnancy.
On examination they are exhausted, anxious and weak.

Invariably there are signs of dehydration and intrapartum
infection. In multipara three tumors abdomen is seen prior to
rupture (bladder, lower segment and thick upper segment with
324
the Bandls ring in between).Uterus may be hypotonic or may

show strong contractions especially in multipara. Bladder is
edematous and distended with very little urine in it. Bowels are
usually distended from acidosis induced hypokalemia. Fetus
may be in distress or dead. Evidence of gross CPD (caput and
significant molding) or malpresentation is found on pelvic
examination.
1.6. Management
The principles in the management of OL are
 Obstruction must be relieved without delay. Before doing

so, one should rectify the effects of prolonged labor
(dehydration, acidosis and intrapartum infection) partially
or fully.
 Some form of operative delivery is always needed to

relieve the obstruction (vaginal or abdominal).
 Non-operative methods like oxytocin have no place in the

management of OL.
I. Resuscitation
It should be started as soon as the diagnosis is made using

the available facilities and resources. In referral cases, this
has to be started at the peripheral clinic and continued during
transportation. The components are:
325
A .Fluid and electrolyte replacement to tackle dehydration

and acidosis
 Open an intravenous line preferably with a wide bore

indwelling cannula
 Infuse crystalloids fast.(for example 5%dextrose in saline

with 50% glucose added )
 Monitor urine output by inserting indwelling plastic catheter

(Catheterization may be difficult if the presenting part is
impacted and may require digital dislodgement .Never use
metallic catheter as this causes urethral injury.)
B. Control infection
In all cases infection must be assumed and intravenous

broad spectrum antibiotics should be commenced
prophylactically. The chosen antibiotics should cover gram
positive, gram negative and anaerobic bacteria. Initial loading
dose followed by maintenance dose should be given.
II. Preintervention preparation
 Catheterize the bladder as described above.
 Empty the stomach by nasogastric tube.
 Determine hemtocrite and blood group. Cross match at

least 1 unit of blood
326
 Give antacids orally
III. Relief of obstruction
One should decide on the best method of delivery because it

has an impact on the survival of the mother. Unless there are
contraindications vaginal route is preferred route of delivery.
The risks associated with abdominal delivery are
 Peritonitis from peritoneal contamination by infected

uterine contents
 Anesthetic risks like aspiration pnumonitis
 Bladder and ureteral damage
 Bleeding from extension of the incision
 Scar on the uterus with risk of future rupture in a mother

who may not return next time
Abdominal delivery (caesarian section or laparatomy for

uterine rupture) is indicated in the following conditions
 Alive fetus with incomplete cervical dilatation or

preconditions for instrumental delivery not fulfilled
 Imminent or definite uterine rupture even if the fetus is

dead
 Dead fetus when criteria for destructive delivery are not

met
327
The modes in vaginal delivery include
 Generous episiotomy if the cause is tight perineum or

scarring from genital mutilation
 Vacuum is of limited value except as an adjunct to

symphysiotomy
 Forceps is limited value except in deep transverse arrest
 Symphysiotomy –limited experience
 Destructive delivery (embryotomy)
Vaginal route of delivery is contraindicated in the following

conditions
 Ruptured uterus (manipulation may extend the tear or

removes the tamponade effect )
 Imminent uterine rupture (manipulation may complete the

rupture)
 Alive fetus with high station or incomplete dilatation of the

cervix
 Dead fetus where the criteria for embryotomy are not

fulfilled
IV. Post intervention care
 Increase intake (parenteral or oral) to reverse dehydration
328
 Continue antibiotics (initially parenteral later oral) to

complete full coarse
 Institute continuous bladder drainage by indwelling

catheter for 5-7 days
1.7. Prevention
Even with aggressive management OL is associated with high

mortality and morbidity both to the mother and the fetus.
Therefore, health programs should focus on prevention of OL,
which is considered to be a largely preventable condition. As a
general rule, OL should never occur in a patient who has
received optimal antenatal and intrapartum care. This can be
achieved by non-sophisticated and non-expensive methods
tailored to the immediate resources of the community. Where
feasible, hospital care for all is ideal.
The measures that should be undertaken to prevent OL include
 Provision of accessible family planning methods
 Provision of universal quality ANC to all pregnant women

to identify risk factors
 Provision of intrapartum care (includes use of partograph)

by skilled personnel who can identify intrapartum risk
factors and provide appropriate management (ranges from
early referral to provision of treatment).
329
 Provision of a well-organized and fully functional unit

(hospital or health center) for delivery of comprehensive
emergency obstetric care. This includes availability of
functional operation theatre and blood transfusion
services.
 Provision of a good referral system for immediate transfer

of mothers.
 Community education on:
 Harmful traditional practices (early marriage, female

genital mutilation, harmful maneuvers in labor).
 Importance of good nutrition in childhood and

pregnancy
 Empowering women.
 Importance of ANC and supervision of labor by skilled

personnel.
2. UTERINE RUPTURE
2.1. Definition and types
Ruptured uterus is defined as a tear in the wall of the uterus

which commonly occurs in the lower segment of the uterus. The
tear could be anterior, posterior, lateral or combination of these.
330
It could be transverse, vertical or combination of these

configurations. In most, it occurs in the intrapartum period but
antepartum rupture can occur especially in women with classic
caesarian section scar or scars related to other gynecologic
surgeries like myomectomy.
Rupture of the uterus is classified into two categories.
 Complete (true) - the tear extends through the whole

thickness of the uterus including the myometrium and the
peritoneum so that there is free communication with the
peritoneal cavity.
 Incomplete (occult) - the tear extends through the

myometrium but not through the overlying peritoneum so
that there is no free communication with the general
peritoneal cavity.
2.2. Causes
By far the commonest cause of uterine rupture is neglected

obstructed labor especially in multipara. The next common
cause is rupture or dehiscence of a previous caesarian section
scar. Other causes include
 Oxytocin or prostaglandin administration
 Difficult instrumental delivery like high or mid forceps
 Difficult destructive delivery
331
 Internal podalic version and breech extraction
 Difficult manual removal of placenta
 Other surgical scars on the uterus(repaired ruptured

uterus, myomectomy)
 Vigorous fundal pressure and sharp penetrating trauma
Diagnosis of uterine rupture is usually reached using clinical

symptoms and signs. But at times it is difficult especially in
those with scar on the uterus and those under regional
anesthesia. Diagnosis in these cases often needs manual
exploration of the uterus and even exploratory laparatomy.
Clinical features are variable and are largely dependant on the

time elapsed after the rupture, the site and extent of the rupture,
the degree of fetal and placental extrusion(the degree of
intraperitoneal spill)and the tamponade effect offered by the
fetus. Therefore, a high index of suspicion is needed for
diagnosis for those not presenting classically.
The usual symptoms of impending (imminent) uterine rupture

are
 Worsening abdominal pain especially suprapubic

persisting between contraction
 Strange feeling of the fetus moving upwards

332
The usual symptoms in uterine rupture include
 Sudden cessation of contraction and fetal movement often

following a sharp tearing pain at the height of the
contraction
 Temporary relief of pain followed by diffuse, continuous

abdominal pain
 Variable degree of vaginal bleeding depending on the

degree of fetal impaction
 Gross hematuria in anterior wall rupture with bladder

rupture
The clinical signs are also variable and include
 Normal vital signs to profound shock (tamponade effect

and involved blood vessels)
 Variable pallor
 Variable abdominal tenderness and distension
 Absent uterine contraction and fetal heart beat
 In anterior rupture, defect in the uterine wall and easily

palpable fetal parts
 Variable shifting dullness
 Presenting part may be jammed or retracted with variable

vaginal bleeding
333
Feeling a defect on vaginal examination or seeing the defect at

laparatomy makes definitive diagnosis of uterine rupture.
2.4. Management
The life of the patient depends on the speed and efficacy with
which hypovolemia is corrected, hemorrage is controlled and
infection is treated. In places where surgical intervention cannot
be provided, early referral should be undertaken only after
resuscitative measures are initiated.
A. Supportive management
This has the objective of initiation of treatment for impending or

full blown shock, intrapartum infection and preparing the woman
for laparatomy. Components include
 Opening intravenous line with wide bore cannula.
 Vigorous infusion of crystalloids.
 Initiation of parenteral antibiotics covering the mixed

organisms like obstructed labour.
 Performing laboratory tests for hemoglobin and blood

group/RH status.
 Preparing at least two units of cross matched blood.
 Inserting naso-gastric tube and folley catheter.
334
B. Definitive management
Immediate laparatomy should be performed .The surgical

options include
 total abdominal hysterectomy
 subtotal abdominal hysterectomy
 repair of the rupture with bilateral tubal ligation
Review Questions
1. Define obstructed labor and list the important causes.
2. Describe the complications of obstructed labor.
3. Discuss the management and prevention of obstructed labor.
4. Discuss the clinical features and management of ruptured

uterus.
335
336
CHAPTER 20
FETAL DISTRESS
Learning Objectives
 To define fetal distress and describe its pathophysiologic

basis
 To list the etiology of fetal distress with emphasis to

iatrogenic causes
 To discuss the diagnostic features of fetal distress
 To describe the management of fetal distress
Fetal Distress is the sign of inability to withstand the stress of

labor leading to asphyxia, which if prolonged, places the fetus
at risk of permanent neurologic injury, multiple organ failure and
eventually death .There is no single indicator that definitely
337
diagnoses fetal distress but abnormal fetal heart rate patterns

and fetal scalp PH determination (where available) are usually
used in the diagnosis.
1. Pathophysiology
A normally grown fetus has stored reserves of glycogen and fat

to be used at times of stress like labor. In labor temporary
cessation of placental transfer of oxygen and nutrients occur
during uterine contraction. This results in anaerobic metabolism
with accumulation of lactic acid and carbon dioxide that
increases as labor progresses. This is normally corrected
between each contraction provided there is adequate oxygen
carrying capacity of the mother, adequate perfusion of the
placenta, adequate relaxation period between contractions
(resting tonus), good umbilical blood flow (patent vessels) and
adequate fetal energy reserve.
Failure to correct this mild form from pathological conditions

results in progressive accumulation of lactic acid and carbon
dioxide. This results in acidosis and reduction of oxygen ending
up in asphyxia .The net effect is change in fetal heart beat,
which forms the basis fir diagnosis and in extreme cases
passage of muconium.
2. Etiology
338
In general all forms of fetal distress originate from deficient

delivery of oxygen to the fetus. Some occur as the result of
sudden catastrophic events like massive abruptio placenta and
cord prolapse. Some are iatrogenic in origin.
I. Uterine and placental factors
 Increased tone and frequency of contraction from oxytocin

induction and augmentation and precipitate labor
 Decreased placental surface area from abruptio placenta
 Uteroplacental insufficiency from post term pregnancy and

hypertensive disorders of pregnancy
II. Umbilical cord
 Cord prolapse either iatrogenic or spontaneous
 Cord compression from oligohydramnios and

entanglement and knot
III. Fetal factors
 Limited or exhausted reserve like in intrauterine growth

restriction, prolonged labor and fetal anemia (example
isoimmunization)
IV. Maternal factors
 Decreased oxygenation from cardiac and respiratory

diseases, severe anemia, smoking
339
 Decreased blood pressure from sudden maternal shock

(example APH), supine hypotension syndrome and
conduction anesthesia
3. Diagnosis
The diagnosis of FD is usually based on
I. Abnormal fetal heart rate patterns
An abnormal FHR pattern is associated with high false positive

rate; therefore, it should be used as a screening method for
which additional methods (scalp PH) are needed for
confirmation. In the absence of confirmatory tests combination
of abnormal patterns should be used to increase the sensitivity.
.The abnormal patterns include
 Baseline bradycardia is classified as moderate (fetal heart

beat of 80-100/min for >3 min) and severe (fetal heart beat
of <80 /min for > 3 min)
 Baseline tachycardia is classified as mild (fetal heart beat

of 161-180 /min for >15 min) and severe (fetal heart beat
of > 180 / min for > 15 min)
 Repeated late deceleration
 Severe recurrent variable deceleration (drop of FHB to <

70/ min with duration of > 60 sec)
 Reduced beat to beat variability

340
II. Fetal scalp blood PH and gas analysis
Currently, it is the best method to assess the acid base status

of the fetus. It needs special gas analyzer and is not available in
all settings.
4. Management
The management of fetal distress has two components
I. Correction of the potential insults (intrauterine resuscitation)
 Put the mother in left lateral position
 Start intravenous infusion of fluids(dextrose in saline with

40 %glucose)
 Give oxygen by mask at the rate of 8-10 liters/minute
 Discontinue oxytocin
 Correction of hypotension of regional anesthesia
 For cord prolapse put in knee chest position and disimpact

the presenting part
 Others- amnioinfusion for cord compression
-acute tocolysis with terbutaline till delivery
II. Remove the fetus from the hostile environment
Deliver the fetus by the most expeditious route. This is

accomplished by caesarian section (if in the first stage or if
341
prerequisites for instrumental delivery are not met in the second

stage) or by instrumental delivery (if in the second stage).
Review questions
1. Describe the pathophysiology of fetal distress.
2. Enumerate the causes of fetal distress.
3. Discuss the management of fetal distress.
References



342

7. Llewellyn Jones D, Fundamentals of Obstetrics and

Gynecology, Volume 1, Fifth edition, 1990
8. Kenneth R. Niswander, Manual of Obstetrics, diagnosis and

therapy, 1st edtion, 1982
9. John Cook, Surgery at district hospital, Obstetrics and

Gynecology 1991
10. Dreissen F, Obstetric problems, A practical manual, 1991
11. WHO, Department of reproductive health and research,

integrated management of pregnancy and childbirth. Managing
complications in pregnancy and childbirth. A guide for midwives
and doctors, 8.
12. MOH/ FHD, Technical Guidelines in managing maternal and

new born care
13 Cunningham F. Gary et. al, Williams Obstetrics,20th edition,

1993
343
14. King M, Bews P, Karins , Thornton J: Primary surgery,

Volume 1 (Non trauma); Oxford medical publication, 1990
344
PART IV
NORMAL AND ABNORMAL
PEURPERIUM
345
346
CHAPTER 21
NORMAL PUERPERIUM AND ITS MANAGEMENT
Learning objectives
 To describe the normal changes of puerperium
 To know the conduct of normal puerperium
 To detect and manage abnormal puerperium
Introduction:
347
Puerperium is the period of adjustment following pregnancy

and delivery when anatomic and physiologic changes of
pregnancy are reversed and the body returns to non pregnant
state. This period of adjustment traditionally extends to six
weeks postpartum. It is classified into three phases
 Immediate extends from delivery to 24 hours postpartum
 Early extends from 24 hours to the end of the first week
 Late extends from the end of the first week to complete

involution of the generative organs which is traditionally 6
weeks
Physiologic changes of puerperium
1. Involution
This is a process by which the reproductive organs return to the

pre-gravid state.
The uterus from a size of 20 weeks (at or just below the

umbilicus) just after delivery reduces in size at a rate of one
finger per day. By the end of the first week it is 12 weeks, by 10
-14 days it becomes impalpable per abdomen and reaches non
gravid state by 6 weeks. Its weight reduces from 1000 grams at
the end of delivery to 50- 100 grams by 6 weeks.
In the first 2- 3 days after delivery the uterus contracts strongly

causing lower abdominal discomfort and pain. This is called the
348
after pain and is commonly seen in multiparas. It is worse after

suckling.
The endometrium, besides the placental site, differentiates into

superficial and basal layers in 2-3 days. The superficial layer
gets necrotic and is cast off as lochia. Regeneration of the
basal layer is completed in 10- 16 days. The placental site is
reduced by 50% following delivery. Regeneration starts by day
7 and is completed between 3-6 weeks.
Lochia is an alkaline discharge of variable amount from the

uterus during puerperium. Depending on the color, it is
classified as
 Lochia rubra reddish discharge from day 1- 4 which rapidly

becomes reddish brown and mainly contain blood.
 Lochia serosa pink colored discharge from day 5-9
 Lochia Alba thick yellowish whitish discharge starting from

day 10 and extends for variable period. It mainly contains
white blood cells and degenerated decidual cells
The cervix becomes a little more than one centimeter dilated at

the end of the first week, and then closes slowly. For those that
have delivered vaginally, the external os changes to transverse
slit. Complete healing and re epithialization of laceration takes
6-12 weeks.
349
Vagina, perineum and abdominal wall regain their tone but

some degree of laxity remains. The torn hymen forms
carenculae myrtiformis. Traumatic lesions of the vagina and the
vulva heal in 5-7 days.
2. Systemic changes
Enlargement of the kidneys persist for moths. Glomerular

filtration rate returns to normal in 8 weeks. Ureteric dilatation
persists for 12 weeks. Urinary ladder capacity is increased with
little increase in intravesical pressure. Incomplete emptying
results in more residual urine. Diuresis of the excess extra
cellular fluid starts between days2-5 and causes weight loss of
4 kilograms.
There is rapid consumption of clotting factors in the first few

hours after delivery. But after the first day, there is rapid crease
in clotting factors which reaches maximum y days 3- 5 and
maintained for 2 weeks.
Leukocytosis of upto 25000 per mm 3 is common.
Blood volume returns to normal in third week. Blood pressure

tends to increase is the first 5 days owing to the increase in
peripheral resistance. Cardiac output takes moths to return to
normal.
3. Endocrine changes
350
Most protein placental hormones, like human placental

lactogen, become undetectable within one day. HCG levels
gradually decline and disappear by 11-16 days. Estrogen and
progesterone levels also decline to reach their lowest between
3-7 days.
The pitutary gland, which has increased in size by 30- 100%

during pregnancy, starts to regress after the first week. In non
lactating mother, prolactin level returns to non pregnant level by
2 weeks. In lactating mother, it remains above the non pregnant
level with dramatic increase during suckling. Depending o the
frequency of feeding, this response gradually declines over a
period of 6- 12 months.
With the disappearance of human placental lactogen, relative

hyperinsulinemia develops resulting in lower fasting ad
postprandial glucose levels. In diabetic women insulin
requirements fall.
4. Return of fertility and menustration
Follicular phase level of estrogen is reached in 19- 21 days in

non lactating, in 60 – 80 days in lactating and menstruating
women vagina up to 180 days lactating amenorrhic women.
FSH ad LH levels are very low in the first 10- 12 days in all
women Levels then reach follicular phase levels at the end of
second and third weeks.
351
Menustration resumes in six weeks in 30% and in 12 weeks in

70% of non lactating women. In lactating women the range for
resumption of menustration is 2-18 months, with 70 % starting
to have ovulation by 36 weeks.
In non lactating women, ovulation resumes as early as 33 days.

In lactating women this is highly variable and is largely
dependent on the strength of suckling (frequency and duration
of each feeding and weaning). The earliest time of ovulation in
lactating women is 10 weeks, with only 20 % ovulating in six
months.
5. Initiation and maintenance of lactation
Two events needed for the initiation of lactation are drop in

placental hormones mainly progesterone and estrogen and
release of oxytocin and prolactin by suckling reflex (letdown
reflex). This reflex is a neuroendocrine reflex. The first milk
(colostrum) has high fat and antibody content with little casein.
Advantages of breast feeding includes acceleration of uterine

involution, provides postpartum contraception, provides
nutrients and antibodies to the neonate, it is ideal food at right
temperature and is sterile, does not need preparation and
enhances mother to child bonding.
Risks are mother to child transmission of HIV in HIV positive

mother, development of cracked nipples and mastitis.
352
Lactation suppression can be achieved by tight fitting brassiere,

giving estrogen alone or combined with testosterone and
bromocryptine.
Conduct of normal puerperium (Post partum care)
Depending on the practices in different settings, women with

uncomplicated labour and delivery can be discharged in 6 to 24
hours. Adequate patient support at home is essential.
 Adequate rest during the day and a good night sleep is

essential. Insomnia, which is a common during early
puerperium, should be treated with sedatives.
 Early ambulation as of the second day. This will accelerate

involution, helps in drainage of lochia, and reduces deep
vein thrombosis and constipation. Usual household
activities should be started after three weeks including
postpartum exercises.
 The importance of nourishing diet with high calorie and

high fluid intake should be stressed.
 Bathing can be take as soon as the woman is ambulatory.

Vaginal douching should be avoided in early puerperium.
Perineal hygiene using clean soap and water should be do
353
e twice a day. Perineal pads are used as needed and

should be properly disposed.
 Encourage periodic voluntary micturition every four hours

to prevent acute urinary retention.
 Sexual intercourse may resume when bright bleeding

ceases, the vulvar lacerations have healed and the woman
is physically comfortable and emotionally ready. Physical
readiness usually takes three weeks.
 Care of the baby which includes breast feeding,

immunization, weaning practice and hygiene.
 Breast care
 Contraception: Risks of pregnancy with or without breast

feeding should e discussed. Family planning methods
should be started as early as possible (2-3 weeks)
depending on free informed choice of the mother.
Abstinence till the postpartum visit is one option. Natural
methods can be used in highly motivated couples. But it
needs the resumption of normal menstrual cycle. Barrier
methods such as condoms and spermicidals can be used
except the cervical cup and diaphragm. Hormonal
contraceptives mainly progesterone only pills, injectables
and implants can be used safely. Intrauterine device can
be inserted after 6 weeks. Permanent methods of
354
contraception mainly tubal ligation can be done

immediately (within 72 hours) or after 6 weeks.
 Danger symptoms that include persistent bloody lochia,

offensive lochia, severe perineal pain or swelling, fever,
unilateral painful swelling of the legs and playful swollen
breast.
 Provision of medications: analgesics for afterpain and

perineal pain, sedatives for insomnia, sitz bath for
episiotomy and perineal lacerations, hemathenics for
anemia, anti D gamma globulin for RH negative
unsensitized women with RH positive neonate, antibiotics
if indicated
 Postnatal follow up: It is usually conducted after 6 weeks.
Review questions
1. Define puerperium.
2. Describe the physiologic changes of puerperium.
3. Discuss the management of normal puerperium.
355
356
CHAPTER 22
POSTPARTUM HEMORRHAGE (PPH)
Learning objectives
 To define PPH and describe the important causes of PPH
 To identify high risk factors for PPH.
 To outline the management of PPH. .
 To describe the techniques of manual removal of placenta.
 To describe the diagnosis and management of uterine

inversion.
357
Introduction
Postpartum hemorrhage (PPH) accounts for 25% of direct

maternal deaths and affects 5.8% of vaginal deliveries. PPH is
a description of an event not a diagnosis; therefore, one should
identify the cause before giving specific treatment. It is the
second commonest cause of maternal death in Ethiopia. In
developed countries, better obstetric care and use of oxytocic
drugs has reduced the incidence of primary PPH from over 15%
to fewer than 4% of all deliveries.
1. Definition and classification
Post partum hemorrhage is defined as blood loss of more than

500ml following vaginal delivery of the fetus and 1000 ml
following delivery of the fetus by caesarian section or a fall in
hemtocrite of more than 10% from predelivery values or
bleeding following delivery causing change in the vital signs.
Depending on when it occurs, it is classified into three.
Third stage hemorrhage is PPH that occurs between the

delivery of the fetus and the delivery of the placenta.
Primary PPH is PPH that occurs within the first 24 hours of the
delivery of the fetus.
358
Secondary PPH is PPH that occurs between 24 hours of the

delivery of the fetus and 6 weeks postpartum.
2. Primary PPH
2.1. Causes and predisposing factors
There are four major causes of primary PPH.
I. Uterine atonia
This account for 50% of primary PPH. Predisposing factors

include
 Over distended uterus from multiple pregnancy,

polyhydramnios and macrosomia.
 Exhausted or weak myometrium from

prolonged/obstructed labor, chorioamnionitis,
induction/augmentation of labor using oxytocin, anesthesia
with halothane, precipitate labour and conditions which
decrease nutrient supply to the uterus ( anemia and
hypotension of any cause).
 Previous history of uterine atony
 Others; - full bladder, grandmultiparity (more than five

children), uterine liomyoma and APH (ante partum
hemorrhage from placenta previa and abruptio placenta).
359
II. Genital tract trauma (lacerations)
This causes 20% of primary PPH and includes bleeding from

perineal tears, episiotomy extensions, vaginal tears, cervical
tears and ruptured uterus. It also includes pelvic hematoma.
The risk factors are precipitate labour, difficult instrumental and
destructive deliveries, macrosomia, shoulder dystocia,
caesarian section and difficult manual removal of the placenta.
III. Retained placenta cotyledons and membrane
This mainly results from the mismanagement of the third stage

of labour (controlled cord traction before the signs of separation
of the placenta and failure to properly examine the placenta
following its delivery).
IV. Coagulation and bleeding disorders
The risk factors include severe preeclampsia/ ecclampsia,

severe abruptio placenta, prolonged intrauterine fetal death,
amniotic fluid embolism, anticoagulant treatment and bleeding
disorder before pregnancy.
2.2. Management
Call for help! Effective management of primary PPH

requires team work. One group is involved in resuscitation
and at the same time another group has the task of
identifying and treating the cause of the bleeding.
360
I. Resuscitation
 Establish an intravenous line. Take blood for hemoglobin,

blood group and Rh factor determination and cross
matching.
 Start infusing intravenous fluids fast. Rate depends on the

extent of bleeding and vital sign derangement.
 Insert an indwelling bladder catheter and record urine

output.
 Take vital signs frequently.
II. Identify the cause and institute appropriate treatment.
Step1. First assess the tone of the uterus per abdomen .If
the uterus is firmly contracted; uterine atony is unlikely and
proceed to step 2. If the uterus is flabby and soft institute the
following management for uterine atony.
 Make sure that the bladder is empty.
 Initiate uterine contraction by either rubbing up the uterus

and by giving oxytocic drugs like pitocin or ergometrine or
prostaglandins. Oxytocin can be given as an infusion of 20
I.U. in 1000 ml dextrose in saline initially run fast until the
uterus contracts well then at the rate of 40 drops/min. The
dose of ergometrine is 0.25 – 0.5mg intramuscular or
intravenous which can be repeated every 5 minutes to
361
maximum of 1.25 mg. Hypertension and cardiac diseases

are a relative contraindication for ergometrine use. It may
inhibit subsequent uterine exploration because of titanic
uterine contraction. If no intravenous access oxytocin 10
IU intramuscular or intramyometrial can be given.
 If bleeding continues despite the above measures one

should perform bimanual compression of the uterus.
This is a life saving obstetric procedure which must be
performed by all health professionals attending deliveries.
The first part of the procedure involves grasping the
posterior aspect of uterine fundus and pushing it down to
the symphysis by the nondominant hand per abdomen.
The second part of the procedure involves inserting sterile
gloved other hand into the vagina and placing the first and
second fingers on either side of the cervix in the anterior
fornix and push it up and anteriorly. Then massage the
uterus with both hands while compression of the uterus is
maintained. The pressure should be applied continuously
for 5 minutes.
 If the bleeding continues surgical intervention should be

taken without delay. The options range from conservative
surgery of uterine or internal iliac artery ligation to radical
surgery of hysterectomy (subtotal or total). Manual
compression of the aorta can be done while preparing for
362
surgery or during referrals. This method can be kept for

hours.
Step2. Inspect of the perineum, the vagina and the cervix

under good light for laceration or tears. Inspection of the
vagina is done with the help of vaginal specula and all the
walls are inspected. Inspection of the cervix requires
placement of two oval forceps on the lips of the cervix which
are rotated alternatively to cover the whole circumference of
the cervix.
Management of genital tears is repair of the tears.
Step3. If no tear is found then perform manual exploration

of the uterus under aseptic conditions for reminants of the
placenta and to detect uterine rupture.
 For reminants the management is manual curettage or

postpartum curettage by manual vacuum aspiration or
postpartum curret, which must be done under the cover of
oxytocin.
 For uterine rupture laparatomy must be done.
Step4. If no reminants or uterine rupture is found on manual

exploration then consider coagulopathy as a cause of
primary PPH.
363
The management is treating the underlying cause and

replacing clotting factors by fresh whole blood or fresh frozen
plasma.
2.3. Prevention
The most important preventive measure for uterine atony is

universal application of active third stage management.
Prevention of risk factors during ANC (like anemia) and
intrapartum period (like prolonged labour) is also equally
important.
Provision of controlled delivery of the fetus and adhering to the

principles of instrumental and other operative deliveries reduces
genital tract trauma.
Proper third stage management prevents PPH from reminants.
3. Secondary PPH
3.1. Causes
 Retained placental pieces or blood clot or membrane
 Sub involution of the uterus
 Endomyometritis
 Undiagnosed genital tract tear
364
 Uncommon: Necrotic fibroid, choriocarcinoma,

chronic inversion
3.2. Management
I. GENERAL
a. Treatment of shock
b. Start antibiotics
c. Investigations- hemoglobin, white blood cell count,

ultrasound for reminants, HCG in titer and others
II. Specific
a. Evacuate the uterus under oxytocin. oral ergometrine

may be continued for 3-5 days.
b. Sitting or semi-sitting position assists in gravitational

drainage.
c. Treat anemia
d. Rarely hysterectomy and exploration may be required.
3.3. Prevention
 Proper examination of the placenta and membranes.
 Clean delivery.
 Prophylactic antibiotics when there are any of the

predisposing factors.
365
4. Retained Placenta
Retained placenta is the term used when the placenta is

retained with no part of it extracted or delivered after 30 minutes
of the delivery of the fetus. Retained placenta causes third
stage hemorrhage and if this does not occur it predisposes to
puerperal sepsis.
The possible causes are uterine inertia, constriction ring,

retracted cervix, pathological adherence of the placenta
(placenta accreta) and mismanagement of third stage.
The management of retained placenta is removal of the

placenta. Before removal is attempted, an intravenous line
should be opened and blood for hemtocrite, blood grouping and
cross matching should be taken.
To determine the method of removal of the placenta, first

assess the size and tone of the uterus abdominally and perform
vaginal examination to assess the degree of cervical dilatation
and the presence of placental tissue in the cervix or vagina.
Depending on the degree of placental separation and cervical
dilatation the retained placenta can be delivered by one of the
following methods.
 Controlled cord traction as described in chapter
366
 Manual removal of placenta
 Postpartum curette in pieces
Manual removal of the placenta is a basic life saving obstetric

procedure. It is indicated in third stage hemorrhage, retained
placenta of more than 1 hour and in active third stage
management when the cord is severed or if the placenta is not
delivered by controlled cord traction in 5 minutes.
The potential complications are cervical tear, uterine rupture,

PPH secondary to remnants of the placenta and puerperal
sepsis.
Technique
Manual removal has to be done after catheterizing the bladder

and opening an intravenous line. Some sort of analgesia/
ansthesia has to be used like pethidine 25-50mg and diazepam
10-20 mg intravenous or ketamine. Lithotomy position is
adopted. Remove the placenta as follows,
 The vulva and protruding cord are cleaned with antiseptic

solution.
 Controlled cord traction is tried for last time.
 Stop oxytocin drip just before manual removal to allow the

cervix to relax, so that the fingers pass through it.
367
 Hold the cord with the left hand. The right hand traces the
course of the umbilical cord through the vagina and cervix
into the uterus to palpate the edges of the placenta.
 Identify the physiologic line of separation by gentle

pressure using the ulnar border of the hand. Failure to
identify this line suggests adherent placenta and further
attempt to separate the placenta should be abandoned at
once.
 Once the physiologic line of separation is identified, gently

separate the placenta from the wall of the uterus with a
slow sawing movement with the ulnar border of your hand.
After full separation of the placenta, remove it by holding it
in the palm of the hands. Inspect the placenta for
completeness. Reintroduce the hand to explore the uterus
for any pieces that may have been left behind and for
intactness of the uterus.
Following successful removal, give ergometrine 0.25 – 0.5 mg

intravenous or intramuscular and continue oxytocin drip. Assess
the tone of the uterus. Inspect the lower genital tract for tears.
Give prophylactic antibiotics. Monitor the vital signs and
observe for vaginal bleeding.
5. Uterine inversion
368
Uterine inversion is the prolapse of the fundus to or through the

cervix so that the uterus is in effect turned inside out. It could be
incomplete (fundus is inverted but does not protrude through
the cervix) or complete (the fundus has prolapsed through the
cervix and may even be visible at the vulva)
Depending on the duration it is classified into three.
 Acute inversion is that occurs immediately after delivery

or within 24 hours post delivery (before the cervix retracts).
 Sub acute inversion is that occurs between 24 hours and

before 4 weeks after delivery (the cervix already retracted).
 Chronic inversion is that occurs after 4 weeks following

delivery.
Acute uterine inversion
Acute uterine inversion is an acute obstetric emergency which

occurs 1 in 2000-2500 deliveries. The exact etiology is
unknown. For acute inversion to occur the following conditions
must be fulfilled.
 The cervix must be dilated,
 The placenta must be fundally attached,
369
 The fundus must be relaxed (from congenital weakness or

prolonged labour or magnesium sulphate induced) and
 A force pushing down the fundus (strong traction on the

cord before placental separation without controlled cord
traction or vigorous fundal pressure)
The predisposing factors are mismanagement of third stage

(pulling on the cord before separation and failure to do
controlled cord traction), fundal pressure in a relaxed uterus like
Crede maneuver, adherent placenta, vigorous manual removal
of placenta and previous history of uterine inversion.
Clinical features
The patient typically presents with severe or dull aching pain in

the lower abdomen (from stretching of the ovaries). Vaginal
bleeding is variable and largely depends on the degree of
placental separation.
Shock, which is out of proportion of the degree of vaginal

bleeding, in the third stage or soon after should arouse the
possibility of acute uterine inversion (mainly of neurogenic
origin). Failure to palpate the uterus and feeling of cup like
depression instead on abdominal palpation and feeling of the
fundus as a dark red-blue mass in the vagina or the cervix on
vaginal examination confirms the diagnosis. The placenta may
or may not be attached.
370
Prevention
 Proper third stage management (wait for signs of placental

separation before cord traction and apply counter
pressure).
 Avoid excessive traction on the cord
 Avoid excessive fundal pressure.
 Avoid excessively vigorous manual removal of the

placenta.
Management
Resuscitation which includes aggressive and prompt treatment

of shock by two intravenous lines (crystalloids and later blood
are used).
Specific treatment is immediate replacement of the uterus by

manual repositioning of the uterus. Where available, hydrostatic
repositioning of the uterus can be done. If these fail immediate
referral for surgical repositioning of the uterus must be done.
Review Questions
1. Describe the causes and predisposing factors of primary

PPH.
2. Describe the management of primary PPH.

371
3. Describe the techniques of the following life saving

procedures.
A. Bimanual compression of the uterus
B. Manual removal of placenta
C. Inspection of the cervix and repair of cervical tear
4. Describe the diagnostic features and the management of

acute uterine inversion
372
CHAPTER 23
POSTPARTAL COMPLICATIONS
Learning Objectives:
 To define puerperal sepsis and list the predisposing

factors
 To describe the causes and the management of puerperal

sepsis
 To describe the clinical characteristics and management of

breast engorgement and acute mastitis
 To list the clinical features of deep vein thrombosis
 To describe the psychosocial complications that can occur

during post partum period.
373
1. PUERPERAL SEPSIS
1. Definition and etiology
Puerperal sepsis is a temperature elevation of 380c (100.40F) or

more occurring at least twice after the first 24 hours and before
the tenth postpartum day and ascribed to genital origin. It is a
general term which describes any infection of the genital tract
after delivery.
WHO defines it as infection of the genital tract occurring at any

time between the onset of rupture of membranes or labour and
42nd postpartum day in which 2 or more of the following are
present: pelvic pain, oral temperature of 38.50c or more at any
one occasion, abnormal vaginal discharge or pus, delay in
involution of the uterus (<2 cm/day) and abnormal odor of the
discharge.
In majority, it is an ascending infection caused by the normal

polymicrobial flora of the vagina and the gastrointestinal tract.
These include aerobes, facultative anaerobes and anaerobes of
both gram positive and gram negative types. Rarely exogenous
microorganisms may cause puerperal sepsis like Clostridial and
Staphylococcal infections. This occurs by using contaminated
instruments and hands or by inserting foreign objects into the
vagina.
2. Incidence and risk factors
374
It is one of the most common complications of puerperium

occurring in 1-3 % o vaginal deliveries and 25- 50 % of
caesarian deliveries. It is still a significant cause of maternal
deaths in developing countries.
The risk factors could be local or systemic. They include
 Route of delivery- the single and most important actor (risk

is 5-8 times higher after caesarian section as compared to
vaginal delivery)
 Prolonged rupture of membranes of > 12 hours
 Prolonged labour of > 12 hours
 Multiple pelvic examinations
 Chorioamnionitis
 Intrauterine manipulations like manual removal of placenta
 Reminants of placenta and genital lacerations
 Systemic factors like immunosuppressive conditions

(diabetes and HIV/AIDS), anemia,
 Use of prophylactic antibiotics
3. Differential diagnosis
375
The following extragenital infections may cause fever in the

postpartum period. These must be ruled out by history,
physical examination and appropriate investigations. These
conditions are urinary tract infection (cystitis and pyelonephritis
mainly caused by E. coli), acute mastitis, breast engorgement,
thrombophlebitis, acute febrile illnesses (malaria, relapsing
fever and others) and other less common causes of fever like
pneumonia.
4. Types of puerperal sepsis
4.1. Endomyometritis
It is infection of the endometrium and myometrium. It is the

commonest form of puerperal sepsis. It usually starts from
the placental site and adjacent endomyometrium. If untreated
it progresses to pelvic cellulitis, pelvic peritonitis and
generalized peritonitis, pelvic abscess, septicemia/ septic
shock and pelvic thrombophlebitis.
Symptoms are fever o variable degree which often starts on

the 3rd post partum day, profuse and malodorous lochia
(absent in Group B streptococcal infection), lower abdominal
pain initially central and later on as the disease progresses
may involve the lower quadrants and the rest o the abdomen
and constitutional symptoms like malaise.
376
The physical findings are temperature of >38.80c,

tachycardia, tachypnea in advanced cases, lower abdominal
tenderness and uterine tenderness with sub involution. Signs
of pelvic and generalized peritonitis indicate complicated
endomyometritis. Evidence of septic shock may be found.
Laboratory investigations reveal leukocytosis with let shift

and positive blood culture in some cases.
Complications include pelvic peritonitis and generalized

peritonitis, pelvic abscess, pelvic thrombophlebitis, septic
shock and as late complication infertility and ectopic
pregnancy.
Management, therefore, should be aggressive. All cases

should be admitted.
 Specific measure is initiating multiple broad spectrum

parenteral antibiotics covering the causative organisms
(gram positives, gram negatives and anaerobes) and
continued until the patient is fever free for 24- 48 hours. In
our setting the antibiotic regimen uses ampicillin, an
aminoglycoside and metronidazole. If reminants is
suspected or diagnosed evacuation of the uterus under the
cover of oxytocin infusion should be done.
 General measures like resuscitation with intravenous

fluids; maintenance of electrolytes and bowel
377
decompression if paralytic ileus occurs, antipyretics and

bed rest in the semi- fowler position should be started.
Monitoring for progress can be done by measuring the vital
signs four times a day, performing abdominal examination
daily and checking white cell count on daily basis.
NOTE. If fever is still present 72 hours after initiation of

treatment or if the condition of the patient worsens or if
abdominal tenderness increases reevaluate the patient
and revise the diagnosis (consider peritonitis, pelvic
abscess, pelvic thrombophlebitis, other febrile illnesses
and drug resistance).
Prevention is by following aseptic technique during labor,

avoiding traumatic delivery, avoiding repeated pelvic
examinations, preventing prolonged labour by using
partograph, using prophylactic antibiotics when needed,
proper third stage management to prevent remnant and
treating systemic illnesses and nutritional deficiency.
4.2. Wound infections
It includes episiotomy site infections, infections of lower genital

tract tears, and abdominal wound infections after caesarian
section or laparatomy.
Episiotomy site infection presents with persistent pain and

offensive discharge from the site. Fever is variable. Finding a
378
tender, indurated, swollen and reddened wound edges with or

with out discharge clinches the diagnosis.
Signs of abdominal wound infection include persistent pain over

the wound and tender, indurated, swollen, and reddened wound
edges. Fever with no apparent cause which persists to the fifth
postoperative day should arouse suspicion of postoperative
wound infection.
Management is removal of sutures and drain abscess if any

and provision of local wound care with antiseptic solutions.
Antibiotics indicated only if there are systemic signs of
infections. Secondary closure may be needed after signs of
infection have cleared.
2. BREAST COMPLICATIONS
1. Breast engorgement
It results from lymphatic and venous congestion (not from over

distension of the breast with milk). It often occurs within 48
hours of delivery. Most often both breasts are swollen, tender,
tense, and warm. Temperature may be mildly elevated but
doesn‘t exceed 380c.
Management includes expression of milk by hand or with a

pump or by breast feeding the neonate. If sever and persistent
379
suppression of lactation may be needed. Supporting the breast

with a binder or brassiere and applying cold compress to the
breast helps.
2. ACUTE POSTPARTUM MASTITIS
IT IS AN INFECTIONS CONDITION OF THE BREAST CAUSED BY

STAPHYLOCOCCUS AUREUS. IT USUALLY PRESENTS NEAR THE END OF THE
FIRST WEEK POST PARTUM AND OFTEN INVOLVES ONE OF THE BREASTS
(UNILATERAL). IF NOT TREATED IT MAY END UP IN BREAST ABSCESS.
PRESENTING COMPLAINTS INCLUDE FEVER, CHILLS, AND PAINFUL
SWELLING OF THE BREAST. PATIENT HAS TACHYCARDIA WITH
0
TEMPERATURE OF GREATER THAN 38 C. THE INVOLVED BREAST IS HOT,
TENDER AND SWOLLEN. IN CASE OF ABSCESS FORMATION THERE WILL BE
TENDER FLUCTUANT MASS.
MANAGEMENT IS CLOXACILLIN 500 MG ORALLY EVERY SIX HOURS FOR 7

DAYS, ANTIPYRETICS AND SUPPORT OF BREAST WITH BRA AND COLD
COMPRESS. BREAST FEEDING CAN BE CONTINUED. IF ABSCESS IS
DIAGNOSED IT MUST BE DRAINED.
2. DEEP VEIN THROMBOSIS (DVT)
Pregnant women are at increased risk of DVT because of

hypercoagulable state o the blood and prolonged immobilization
that commonly occurs in the immediate postpartum period. It is
an emergency condition that should be treated promptly and
aggressively.
380
Symptoms are painful swelling of one of the legs (rarely

bilateral) which is occasionally associated with fever.
Signs are swollen and tender thighs and calves positive

‗Homan‘s sign‘ (pain on dorsiflexion of the foot).
The feared complication is pulmonary thromboembolism and

subsequent death.
Management includes immobilization o the leg and immediate

referral of the patient to a setting where anticoagulant therapy
can be initiated and monitored.
3. PSYCHOSOCIAL COMPLICATIONS
Three different types of postpartum psychosocial disorders

have been described.
1. Postpartum blues
It is characterized by mild mood disturbances, marked by

emotional instability (crying spells apparently with no cause,
insomnia, exaggerated cheerfulness, anxiety, tension,
headache, irritability, etc). Usually the complaints develop with
in the first postpartum week and continue for several hours to a
maximum of ten days and then disappear spontaneously.
381
The management is for one of the medical or nursing staff to

talk with the women, explaining what is occurring, and
restricting visitors.
2. Postpartum depression
It is a more protracted depressive mood with complaints of

affective nature; the woman is gloomy, depressed, irritable, sad,
insomniac, anorexic, poor concentration, and loss of libido.
The management is support and encouragement,

psychotherapy and use of antidepressants.
3. Puerperal psychosis
Symptoms usually start at the end of the first week, sometimes

in the second week, seldom later and tend to recur in the next
pregnancy. The woman is anxious, restless, and sometimes
manic with paranoid thoughts or delusions. She reacts
abnormally towards her family members.
Management includes psychotherapy, antipsychotic treatment

and isolation of the neonate from the mother.
Review Questions
1. Define puerperal sepsis.
2. List the risk factors for puerperal sepsis.
382
3. Describe the complications and the management o

endomyometritis.
4. List the risk factors for DVT.
383
References




384
385
PART V
GYNECOLOGY
386
387
CHAPTER 24
THE MENSTRUAL CYCLE AND ITS ABNORMALITIES
Learning Objective:
 To characterize the normal menstrual cycle including the

phases of endometrial and ovarian cycle
 To know the changes observed during climacteric.
 To know the clinical importance of menstrual cycle
 To describe the different abnormalities of menustration
 To discuss the approach in the management of

abnormalities of menustration
A. THE MENUSTRAL CYCLE
1. Introduction
There are periodic physiologic changes in women in

reproductive age group. For these changes to occur there
should be a well controlled coordination between
hypothalamus, pituitary, ovary and end organs to result in
menstruation. Cessation of these physiologic changes after
388
reproductive age results in atrophy of reproductive organs,

vasomotor symptoms and other health hazards.
Menustration is orderly, periodic sloughing of progestational

endometrium accompanied by blood. The first menses is called
menarche and the last one is called menopause.
Characteristics of normal menstrual cycle are:
 Duration of flow is on average 5 days( range1-8 days)
 Average cycle length is 28 days (range 21 to 35 days)
 Amount of flow on average is 30 ml (range10-80ml)
 Menustral blood is dark red and non clotting
2. Hypothalamo pitutary ovarian cycle
At the beginning of each cycle the hypothalamus secretes

increasing amount of GNRH which in turn stimulate the
anterior pitutary to secrete increasing amount of FSH
(increases from basal level of 5-20 MIU/ml at the beginning
of the cycle to reach peak of 12-30 MIU/ml at mid cycle). LH
secretion in early part of the cycle also increases but at a
much lower level.
FSH stimulates the growth of a cohort of primary follicles in

the ovary out of which only one becomes the dominant
follicle (Graffian follicle). As the follicles grow increasing
389
amount of estrogen is produced. Estrogen exerts negative

feedback effect on the hypothalamus and pitutary, mainly on
the secretion of FSH.
At around midcycle there is a surge in the production of

estrogen (from basal level of 20-60 pg/ml to more than
200pg/ml at the surge) which positive feedbacks the
hypothalamus and the pitutary. As the result, there is an
increased production of gonadotrophins, mainly LH (the LH
surge- from basal level of 5-25 MIU/L to peak of 25-100
MIU/L).
LH finalizes the maturation of the Graffian follicle, which is

culminated by ovulation some 24 hours after the surge.
Under the effect of LH it is changed into corpus luteum. The
corpus luteum starts secreting increasing levels of
progesterone (from follicular phase of less than 2 ng/ml to
luteal phase levels of 2-20 ng/ml) and to a lesser extent
estrogen. Because of the increasing negative feedback,
levels of FSH and LH decline. Starting day 20 the corpus
luteum regresses and eventually dies. Estrogen and
progesterone production declines, thus, lifting the negative
feedback on the hypothalamus. Increased secretion of
GNRH then starts another cycle.
In summary, the ovarian cycle has three phases that are of

clinical importance. These are:
390
I. Follicular phase (estrogenic phase) which is of variable

length
II. Ovulation transient period which occurs at mid cycle
III. Luteal phase (progestational phase) which is always 14

days in length.
3. Endometrial cycle
Because of the systemic effects of estrogen and

progesterone, the endometrium undergoes histologic cyclic
changes that culminate in menustration. There are three
phases in this cycle.
I. Menustral phase starts from day 1 and usually lasts 3 to 5

days. During this phase there is irregular sloughing of the
superficial two thirds of endometrium (decidua functionalis)
accompanied by blood. This combination forms a coagulum
in the endometrial cavity, which under normal circumstances
undergoes lysis before expulsion from the uterus. Expulsion
is aided by uterine contraction.
II. Proliferative phase starts near the end of the menustral

phase. During this phase the basal layer of the endometrium
(decidua basalis), under the influence of estrogen,
proliferates to regenerate the superficial layer that is shaded
391
during menses. This involves both the stromal cells and the
endometrial glands. Histologically, the glands are straight
without secretory activity and the stromal cells are compact.
III. Secretory phase extends from ovulation to the onset of

the next menustration. During this phase the proliferative
endometrium, under the influence of progesterone, is
changed to secretory type. Glands become tortuous and
exhibit secretory activity. Stromal cells are separated by
interstitial edema. These changes are maximal between days
20 to 22, after which regressive changes are seen in
preparation for menses.
4. Mechanism of menustration
In the absence of pregnancy, decreasing levels of

progesterone from the dying corpus luteum, result in
dehydration of the stroma. As the result there is increased
coiling of the spiral arteries, which supply the superficial layer
of the endometrium. There is also spasm of these arteries.
The resulting ischemia from these mechanisms is followed by
necrosis and sloughing of the superficial layer in haphazard
manner, which is shaded as menustration. Prostaglandins
initiate uterine contraction.
392
B. ABNORMALTIES OF MENSTRUATION
1. Abnormal uterine bleeding (AUB)
This is defined as bleeding from the female genital tract that

is abnormal in amount, duration, frequency or any
combination of these.
1.1. Patterns of AUB
 POLYMENORRHEA IS MENSES
OCCURRING R E G U L AR L Y AT
I N TE R V AL O F L E S S T H AN 2 1
D AY S ( F R E Q U E N T M E N S E S )
 OLIGOMENORRHEA IS MENSES
OCCURRING R E G U L AR L Y AT
393
I N TE R V AL S O F M O R E TH AN 3 5
D AY S
 HYPERMENORRHEA
(MENORRHAGIA) IS EXCESSIVE
BLEEDING DURING A MENSES
WITH R E G U L AR INTERVALS.
THIS COULD OCCUR WITHIN
T H E N O R M AL F L O W TI M E O R
M AY M AN I F E S T AS P R O L O N G E D
F L O W TI M E .
 HYPOMENORRHEA IS
U N U S U AL L Y S M AL L
M E N U S T R AL B L E E D I N G D U R I N G
A MENSES WITH REGULAR
I N TE R V AL S .
 METRORRHAGIA
(INTERMENUSTRAL BLEE DING)
IS BLEEDING OCCURRING AT
AN Y TI M E B E TW E E N
M E N S T R U AL C Y C L E S .
 MENOMETRORRHAGIA IS
U T E R I N E B L E E D I N G , U S U AL L Y
E X C E S S I V E AN D P R O L O N G E D ,
394
OCCURRING AT I R R E G U L AR ,
F R E Q U E N T I N T E R V AL S
 CONTACT BLEEDING: (POST
COITAL BLEEDING): IS SELF –
E X P L AN AT O R Y B U T M U S T B E
CONSIDERED A SIGN OF
C E R V I C AL C AN C E R UNTI L
P R O V E D O TH E R W I S E .
1.2. CAUSES OF AUB

D E P E N D I N G O N T H E AG E O F T H E
P ATI E N T O N E O R M O R E O F T H E
FOLLOWING C L I N I C AL
C O N D I TI O N S C O U L D B E C AU S E
AU B .
Early pregnancy complications like abortion, ectopic
pregnancy and hydatidiform mole are the commonest causes of
AUB in women during reproductive age.
Genital tract infections like vaginitis, cervicitis, endometritis

and rarely salphigo oophoritis could be causes of AUB in
sexually active women.
Tumor conditions of the genital tract (anatomic causes) are

usual causes of AUB in women nearing menopause. Malignant
tumors often cause AUB in perimenopausal and
395
postmenopausal women. Tumors arise from any part of the

genital tract but with differing prevalence.
 UTERINE: E N D O M E T R I AL
POLYP, E N D O M E T R I AL
H Y P E R P L AS I A, L I O M Y O M A,
AD E N O M Y O S I S , E N D O M E T R I AL
C AN C E R AN D S AR C O M A O F T H E
UTERUS.
 CERVIX: ECTROPION, EROSION,
C E R V I C AL P O L Y P , C E R V I C AL
C AN C E R
 V AG I N A AN D V U L V A:
V AR I C O S I T I E S , C O N D Y L O M AS ,
C AN C E R O U S C O N D I TI O N S
( R AR E )
 F A L L O P I A N T U B E : R AR E
 O V A R I E S : F U N C TI O N AL C Y S T S ,
P O L Y C Y S TI C O V AR I E S ,
E N D O M E T R I O S I S , B E N I G N AN D
M AL I G N AN T T U M O R S
S Y S T E MI C D I S E A S E S : E N D O C R I N E
D I S O R D E R S ( TH Y R O I D , AD R E N A L ,
AN T E R I O R P I T U T A R Y ) , L I V E R AN D
396
R E N AL D I S E AS E S , BLEE DING
DISORDERS, H Y P O T H AL A M I C
D I S E AS E S LIKE AN O R E X I A
NERVOSA
MEDICATION RELATED:
H O R M O N AL C O N T R AC E P TI V E S ,
I N TR AU T E R I N E C O N T R AC E P TI V E
DEVICES, AN TI C O AG U L A N T
T R E ATM E N T
TRAUMA RELATED: S E X U AL
I N TE R C O U R S E , F O R E I G N B O D I E S
E X T R A G E N I T A L C A U S E S : U R I N AR Y
T R AC T ( H E M O R R H AG I C C Y S T I TI S )
AN D AN AL C AN AL
(HEMORRHOIDS, FISSURE)
LESIONS AR E NOT AC T U AL L Y
C AU S E S O F AU B , B U T S H O U L D B E
R U L E D O U T TO AV O I D W R O N G
D I AG N O S I S
Dysfunctional uterine Bleeding is a diagnosis by exclusion
1.3. Approach to a woman with AUB
397
Appropriate history and physical examination as described in

chapter 2 supplemented by necessary laboratory investigation
will identify the cause of AUB.
In the history, emphasis should be given to the age of the

patient, parity, the last menustral period (LMP), duration and
extent of the complaint (amount and length of menstrual flow,
cycle interval, intermenustral bleeding, if sexually active post
coital bleeding and associated pain), age at menarche and
where applicable age at menopause, vaginal discharge history,
multiple sexual partners and history of sexually transmitted
infections, past and present medical illness and medication,
urinary and rectal symptoms
Physical examination should focus on vital signs and signs of

anemia, secondary sexual characteristics, abdominal and
inguinal masses, thorough pelvic examination (inspection of the
vagina, vulva and cervix, digital palpation for the size,
consistency and surface of the cervix and uterus, Palpation of
the adnexa and pouch for mass). In addition signs for endocrine
and other medical illnesses should be looked for.
Depending on the findings appropriate investigations should be

ordered. These include complete blood count, serum or urine
for HCG, cytologic examination (Pap smear), pathologic
examination of endometrium after endometrial biopsy or
curettage using manual vacuum aspiration or dilatation and
398
curettage, ultrasonography, hysterosalpingography, fractional

curettage (curettage of the endocervix followed by dilatation of
the cervix and curettage of the endometrium) and others.
1.4. Management of AUB
This depends on the specific etiology of AUB. Refer to the

different chapters that deal with each cause.
2. Dysfunctional uterine bleeding (DUB)
Exclusion of pathologic causes of abnormal bleeding

establishes the diagnosis of dysfunctional uterine bleeding.
Virtually, all variations of DUB can be related to disruption in
normal ovarian function. Greater than 80% of DUB is
anovulatory and the remaining 20% is due to dysfunction of
corpus luteum or endometrial abnormalities.
DUB most commonly occurs at the extremes of reproductive

age (20% of cases occur in adolescence and 40% in patients
over age 40).
In anovulatory conditions there is continued estrogen

stimulation of the endometrium. There are two mechanisms of
bleeding. One is estrogen breakthrough bleeding where the
endometrium outgrows its blood supply and will desquamate in
399
an irregular manner. The other is estrogen withdrawal bleeding

where the endometrium sheds when the estrogen levels decline
sharply. The pattern of bleeding is dependent entirely on the
duration and level of estrogen stimulation and may take any
pattern of AUB. Characteristically, anovulatory DUB is acyclic,
unpredictable as to the onset of bleeding, and variable in the
duration and amount of bleeding.
Ovulatory DUB is usually associated with premenstrual

symptoms such as breast tenderness, dysmenorrhea and
weight gain, and regular periodicity. It is a result of the
dysfunction of the corpus luteum which in most cases has short
life span.
Abnormalities in endometrial physiology involving chemicals like

prostaglandins may be a cause of DUB.
Uterine bleeding secondary to such pathologic entities as blood

dyscrasia, endocrinopathies, hepatic dysfunction, and other
iatrogenic causes with no organic pathologic factors should not
be considered as true DUB but rather as pseudo DUB.
2.2. Diagnosis
DUB is a diagnosis by exclusion (organic causes of AUB should

be ruled out
before diagnosis of DUB is entertained).
400
2.3. Treatment
Individualized treatment plan should be designed according to

the patient age,
the desire for contraception or fertility and the severity and

chronicity of the
bleeding.
The goals of treatment should be arresting the acute episode of

bleeding, preventing recurrences and inducing ovulation if
patient desires to conceive.
In adolescents pregnancy related complications should be

ruled out first. Acute bleeding episode with vital sign
derangement should be treated with intravenous fluid
resuscitation. Bleeding can be arrested either by dilatation and
curettage or suction curettage or administration of high dose
estrogen followed by medroxy progesterone acetate.
Recurrences can be prevented by 3-6 months coarse of

combined oral contraceptives or intramuscular progesterone in
oil.
Hysterectomy is rarely needed for this group of women.
In women in reproductive age group (20-40 years)

pregnancy related complications and organic lesions should be
ruled out. Management of acute episode and prevention of
401
recurrences is as for adolescents. In addition ovulation

induction can be given for those anovulating women who desire
pregnancy. For persistent cases hysterectomy can be offered
provided that the woman has no desire for future pregnancy.
In Perimenopausal women appropriate work up must be done

to rule out neoplastic conditions including Pap smear and
endometrial sampling. Management includes hormonal
treatment using progesterone derivatives or combined oral
contraceptives or surgical treatment using dilatation and
curettage or hysterectomy.
3. Premenstrual Syndrome (PMS)
This is a psychoneuroendocrine disorder with biologic,

psychologic and social manifestations. It occurs cyclically prior
to menstruation and then regress or disappears during or after
menstruation.
3. 1. Epidemiology
Premenstrual symptoms have been described to occur in 15%

to 100% of women of reproductive age, with 5% to 10%
reporting severe symptoms at some point in their lives. The
highest incidence is in the late twenties to early thirties. PMS is
rarely encountered in adolescents and there is an intercultural
variability of the type of premenstrual complaint.
402
3.2. Etiology and pathophysiology
A single cause for PMS has not been identified. Multiple factors
have been proposed of which hormonal hypothesis is widely
favored. The other presumed theories include; fluid retention
theory, hypoglycemia hypothesis, prostaglandin and
psychologic theories.
Mittlschmerz (periovulatory ovarian pain), premenstrual

molmina, bloating, breast soreness and menstrual cramps are
symptoms that usually accompany normal menustral cycle.
When these symptoms are severe, the premenstrual syndrome
(PMS) and dysmenorrhea result. They occur in the first 7 to 10
days prior to menstruation. During these days, women are more
likely than usual to absent themselves from work, to require
hospital admission, involved in accidents, to commit crimes, to
develop acute psychiatric symptoms and to commit suicide.
3.3. Clinical Features
The common symptoms associated with premenstrual

syndrome include:
403
Affective symptoms: sadness, anxiety, anger, irritability, labile

mood
Cognitive symptoms: decreased concentration, feelings of

isolation and withdrawal, indecision, paranoia, suicidal ideation
Pain: headache, breast tenderness, joint and muscle pain
Neurovegetative: insomnia, hypersomnia, libido change
Autonomic: nausea, palpitations, alteration in bowel habits
Central nervous system: clumsiness, dizziness
Fluid / Electrolyte: weight gain, edema
Dermatologic: acne, dry hair
Behavioral: decreased motivation, poor impulse control,

craving for salt and sugar
PMS is usually considered significant if the severity of the

symptoms interferes with day to day activity of the woman. This
general definition serves to differentiate premenstrual molmina
from the more severe symptoms characteristic of PMS.
3.4. Diagnosis
It relies on a patient‘s self reporting of symptoms that she feels

increase significantly during the premenstrual period and
diminish following menses.
404
A careful history and physical examination are most important

to exclude organic causes localized to the reproductive, urinary
or gastrointestinal tracts.
3.5. Treatment alternatives for PMS
There is no specific treatment for PMS but a number of

treatment modalities have been tried.
A. Non pharmacologic modalities like modification of exercise,

nutrition and stress.
B. Pharmacologic modalities, which are empiric and

controversial, include ovulation suppression (GNRH agonists,
danazol, combined oral contraceptives and progestins) and
anxiolytics/ antidepressants.
C. Surgical modality (bilateral oophorectomy) is rarely needed.
4. Dysmenorrhea
405
This signifies painful menustration which prevents normal

activity and requires medication. There are two types of
dysmenorrhea, primary and secondary.
4.1. Primary Dysmenorrhea
This is a type of dysmenorrhea in which no organic pelvic

pathology can be found. Primary dysmenorrhea generally
begins with the onset of ovulatory cycles, typically six months to
1 year after the onset of menarche.
Incidence varies from population to population.
Symptoms include a colicky abdominal pain localized to the

mid line or lower quadrants, with radiation often noted to the
lower back and legs. The pain usually starts twenty four hours
before the onset of menses, and may extend for 24 to 36 hours
after the onset of bleeding. Accompanying symptoms may
include nausea, vomiting, headaches, anxiety, fatigue, diarrhea,
syncope and abdominal bloating.
Diagnosis is by exclusion of organic pelvic pathologies causing

secondary dysmenorrhea.
Treatment options include
A. Prostaglandin synthesis inhibitors (non steroidal anti-

inflammatory drugs). Reported success rate ranges
from 70 – 80 %.
406
B. Ovulation suppression by hormones like combined oral

contraceptives.
C. Calcium channel antagonists (verapamil and

nifedipine)
D. Surgical treatment like presacral neurectomy,

uterosacral transection can be done for those who did not
respond to medical therapy.
4.2. Secondary dysmenorrhea
Dysmenorrhea that occurs in association with organic pelvic

pathology is termed as secondary dysmenorrhea.
Causes include endometriosis, uterine liomyoma, and

intrauterine contraceptive devices (IUCD), pelvic adhesions
secondary to chronic pelvic inflammatory disease and pelvic
surgery, cervical stenosis, imperforate hymen and transverse
vaginal septum.
Secondary dysmenorrhea is unusual before the age of 25. The

pain is not limited to the menses. It is less related to the first
day of flow and may be associated with other symptoms like
dysparunia, infertility and abnormal bleeding.
Management is directed against the specific cause.
407
5. Amenorrhea
5.1. Definition and classification
Amenorrhea is defined as the absence of menstruation at any

time between the usual ages of puberty and menopause. It is
classified as
 Primary amenorrhea: is the absence of spontaneous

menses by age 16 regardless of the presence of
secondary sexual characteristics or absence of both by
age 14.
 Secondary amenorrhea: is the absence of menses

for more than or equal to 6 months in a woman with
regular cycles or for a period of more than three cycle
length in women with irregular cycle.
5.2. Causes of amenorrhea
I. Physiological amenorrhea results from pregnancy, lactation,

prior or directly after menarche and after menopause. It
accounts for 90-95 % of amenorrhea. Pregnancy is the
commonest cause of physiologic amenorrhea.
II. Pathologic amenorrhea results from pathologic conditions

affecting the hypothalamus, pitutary, ovaries, uterus and the
outflow tract. It accounts for 5-10 % of amenorrhea. Depending
408
on the level of gonadotrophins, it is subdivided into

hypogonagotrophic, hypergonadotrophic and eugonadotrophic
amenorrhea.
Hypogonagotrophic amenorrhea
Hypothalamic causes are the most common causes of this type

amenorrhea. It is usually a diagnosis by exclusion. Stress
(physical, psychological), acute weight loss, anorexia nervosa
and strenuous exercise are functional causes of hypothalamic
amenorrhea. Drugs like psychotropic drugs, drug addiction and
post pill amenorrhea operate at this level. In Kallman syndrome,
a rare condition there is congenital absence of GnRH along with
anosmia.
Pituitary causes include hyperprolactinemia (amenorrhea-

galactorrhea syndrome) either drug induced or from
prolactinomas, damage to the pitutary (trauma, surgery and
irradiation), postpartum ischemic necrosis of the anterior
pitutary (Sheeans syndrome) and destruction by
craniopharyngioma.
Hypergonadotrophic amenorrhea
This results from congenital (primary) or acquired (secondary)

ovarian failure.
409
Primary ovarian failure is seen in pure gonadal dysgenesis,

Turner‘s syndrome (45, X0), and testicular regression
syndrome, resistant ovary syndrome and enzyme deficiency.
Secondary ovarian failure, also called premature ovarian failure

(amenorrhea before 35 years of age), results from surgery,
radiation, chemotherapy, autoimmune diseases, pubertal
mumps, and genetic predisposition.
Eugonadotrophic amenorrhea
Uterovaginal causes include congenital absence or acquired

destruction of the endometrium as seen in Mullerian agenesis,
Testicular feminization syndrome, isolated atresia of the uterus,
Ashermans syndrome, radiation atrophy, granulomatous
infections like tuberculosis and post hysterectomy.
Conditions that are associated with obstruction to outflow of

menustral blood are cervical and vaginal atresia, transverse
vaginal septum and imperforate hymen.
Other causes are mild hypothalamic dysfunction,

hyperandrogenism (polycystic ovary disease, androgen
producing ovarian tumors, adrenal tumors, Cushing‘s syndrome
and congenital adrenal hyperplasia) and systemic diseases
(hypothyroidism, hyperthyroidism, and chronic renal failure).
5.3. Importance
410
 Amenorrhea is important for several reasons:
 Failure to ovulate causes infertility.
 Prolonged estrogen deficiency results in health hazards
 Amenorrhea with some estrogen production can

predispose to endometrial cancer.
 Primary amenorrhea in a girl who has not already

developed secondary sexual characteristics may give rise
to major social and psycho sexual problems.
 It may be a sign of other pathologies.
5.4. Diagnosis
In majority of the cases diagnosis is reached by history,

physical examination and simple laboratory investigations. The
rest need sophisticated and expensive investigations.
I. History
Points to be included in the history are:
 For physiologic causes – age, pregnancy symptoms,

lactation
 For central causes - life style, general health condition,

abnormality with smell and vision, nipple discharge,
headache, seizure, vomiting, head injury, medication
history, history of PPH, weight changes,
411
 For ovarian causes - hot flushes, history of surgery,

chemotherapy and surgery, pubertal mumps, family
history
 For outflow causes – cyclic lower abdominal pain,

history of curettage, symptoms of tuberculosis, sexual
difficulty, abdominal surgery
 For hyperandrogenism – pattern of hair distribution,

voice changes, body habitus change, breast changes
 For medical illnesses – renal disease, symptoms of

hypo and hyperthyroidism
II. Physical examination
It must assess
 General - body build, stature, obesity, height and

weight
 HEENT - eyes, hirsutism, temporal recession of

hair
 Glands – lymphadenopathy, breasts (Tanner staging,

galactorrhea), thyroid for enlargement, inguinal mass
 Abdomen - striae, lower abdominal and flank mass
 Vaginal examination –clitoral enlargement, vagina

(patency, if not patent for bluish membrane at the vulva
412
or septum in the vagina or blind pouch), cervix

(presence, texture), uterus (presence, size), adenexa
(masses)
 Rectal examination if vagina is not patent
 Intgumentary system – hair distribution
 Central nervous system – visual field examination
III. Investigations
Pregnancy must be ruled out by urine or serum HCG

determination. Depending on the type of amenorrhea and the
clinical findings the following investigations can be ordered
 Hormone assays: prolactin, LH, FSH, thyroid hormones,
 Ultrasound, skull X-ray and other imaging techniques
 Buccal smear for sex chromatin and chromosomal

analysis
 Laparatomy/ laparoscopy
5.5. Work up of Secondary amenorrhea
I. Rule out pregnancy by history, physical examination and

urine HCG.
413
II. Perform progestin challenge test like medroxy

progesterone acetate 10mg daily for 05 days.
 Presence of withdrawal bleeding (positive test) after 2-7

days signifies normal estrogen primed endometrium,
normal outflow tract and absence of endogenous
progesterone (anovulation).
 Absence of withdrawal bleeding (negative test) signifies

absence of estrogen primed endometrium which may
result from either faults in the hypothalamus/ pitutary/
ovary/ or endometrium/outflow tract. Further test is
needed to differentiate these.
III. Perform combined estrogen- progesterone challenge test

by giving drugs like combined oral contraceptives.
 Presence of withdrawal bleeding (positive test) indicates

absence of endogenous estrogen and progesterone
arising either from ovarian failure or hypothalamo
pitutary failure. To differentiate these, determine LH/ FSH
levels. Low FSH/LH levels diagnose hypothalamo pitutary
failure. High levels diagnose ovarian failure.
 Absence of withdrawal bleeding (negative test) indicates

either obliteration of the endometrium by synechia
(Ashermans syndrome) or destruction/atrophy of
414
endometrium. To differentiate these

hysterosalpingography is needed.
5.6. Work up of primary amenorrhea
I. Check for secondary sexual characteristics
II. If secondary sexual characteristics of feminizing type are

present, check the vagina and for pelvic mass.
 If there is bluish membrane which bulges with straining

and associated pelvic mass – Imperforate hymen
 If there is a blind ending vagina with pelvic mass –

transverse vaginal septum
 If vaginal canal does not exist and there is pelvic mass –

isolated vaginal agenesis
 Normal vagina with absent cervical os and associated

pelvic mass – cervical atresia
 If there is a blind ending vagina without pelvic mass, two

possibilities exist which can be differentiated by Barr body
determination. These are testicular feminization
syndrome (Barr body negative and presence of inguinal
mass) and Mullerian agenesis (Barr body positive).
415
III. If secondary sexual characteristics of virilizing type are

present
 Consider mild form of congenital adrenal hyperplasia, post

pubertal adrenal hyperplasia and virilizing adrenal/ ovarian
tumors.
IV. If secondary sexual characteristics are absent with infantile

but normal sexual organs
 If height is less than 147 cm consider Turner syndrome

(XO) and panhypopitutarism. Check for other features of
these conditions.
 If height is greater than 147 cm consider true gonadal

dysgenesis (XX or XY) or Kallman syndrome. Refer for
karyotyping and LH/FSH levels.
 It could be an idiopathic delay
5.7. Management
The management principles of amenorrhea are:
I. Treatment of the underlying pathologic entity
 Hyperprolactinemia- Bromocryptine and or surgery/

radiation
 Craniopharyngioma – surgery
416
 Ovarian tumor – surgery followed by hormone replacement
 Systemic diseases – treatment of the underlying systemic

disorder
 Autoimmune oophoritis – corticosteroids
 Stress – life style modification (change)
 Anorexia nervosa - psychotherapy
2. Treatment of the medical needs of the amenorrhic patient
 Ovulation induction or assisted reproductive technology for

infertile couple
 Estrogen replacement for primary amenorrhea (Reduce

risk of osteoporosis, cardiovascular complications and
genital atrophy)
 Cyclic progesterone treatment for those with unopposed

estrogen action
 Plastic surgery or vaginal dilators for blind vagina
 Gonadectomy for those with dysgenetic Y gonads and

undesended testis.
 Psychotherapy
Review questions
417
1. Discuss the menustral cycle.
2. Describe the patterns of abnormal uterine bleeding.
3. Discuss the causes and the management of primary

dysmenorrhea.
4. Describe the work up of secondary amenorrhea.
418
CHAPTER 25
CLIMACTERIC AND RELATED PROBLEMS
Learning objectives
 To define climacteric and menopause
 To describe the physiologic changes of climacteric
 To discuss the health problems of climacteric
 To enumerate the causes of postmenopausal bleeding
Definitions
Climacteric is the phase of life for women that marks transition

from being able to reproduce to being non-reproductive.
Menopause is cessation of physiologic uterine bleeding (the
419
last menustration). It is diagnosed retrospectively. It is the most

visible event marking climacteric. The average age at
menopause is 51 years and is not affected by race, number of
pregnancies, contraceptive use, age at menarche and physical
characteristics. In practice these two terms are used
interchangeably. Pre-menopause is the period before
menopause during which the menstrual cycle is irregular and
climacteric symptoms are experienced. Post menopause is the
period after menopause. Perimenopause includes the
premenopause and postmenopause and extends from 40-55
years.
Pathophysiology
As menopause nears, ovarian follicles get depleted and

become resistant to gonadotrophic hormones. Estradiol
production diminishes which inturn results in elevated FSH and
later LH levels. Oligoovulation or anovulation results in
menustral irregularity and unopposed estrogen action on the
endometrium. Later there will not be any follicles to be
stimulated by high levels of gonadotrophins resulting in
significant drop in estrogen to a level that is not capable of
stimulating the endometrium causing menopause. The
hypoestrogenic state that follows menopause results in a
number of medical conditions associated with climacteric.
Changes in menopause
420
I. Hormonal changes
 Change in FSH and LH levels is the most striking

hormonal change of climacteric. Both exceed 40 IU/liter
and continue to rise for 2-3 years and thereafter remain
stable or slightly decrease. FSH levels are higher than LH
levels for the first time in the woman‘s life.
 Changes in estrogen levels are the last hormonal change

in climacteric. Estradiol levels become very low and levels
of < 20pg /liter is diagnostic of climacteric. The
predominant estrogen in climacteric is estrone, a result of
peripheral conversion of androgens.
 Progesterone levels are very low in climacteric.
 Levels of androgens like dehydroepiandrosterone sulfate,

androstendione and testosterone fall.
II. Reproductive organs
Effect depends on the level of endogenous estrogen. In typical

hypoestrogenic states of climacteric atrophic changes occur.
 Atrophy of the vagina results in thinning of the epithelium

and flattening of the rugae which gives it the appearance
of smooth, shiny pale surface.
421
 Atrophy of the cervix reduces its size creating shallow

fornices. Vaginal dryness results from decreased cervical
mucus production.
 Uterus decreases in size from reduction in myometrial

thickness. The endometrium atrophies.
 The ovaries reduce in size and are impalpable.
 Supporting structures and muscles lose their tone.
 The labia lose fat and flatten.
III. Menustral cycle
Changes in menustral cycle are the first clinical evidence of

climacteric. The usual pattern is gradual increase in cycle
length and reduction in amount and duration of flow. Heavy
bleeding and abrupt cessation are unusual.
IV. Other organs
 Bladder and urethral epithelium atrophy
 Breasts decrease in size
 Generalized thinning and loss of elasticity of the skin

results in wrinkling that is prominent on light exposed
areas (face, neck and hands).
 Accentuated bone loss
422
Problems of climacteric
These are related mainly to estrogen deficiency and rarely to

estrogen excess.
Problems of estrogen deficiency
Hot flush is the most common and characteristic subjective

symptom of climacteric. It is an episodic vasomotor disturbance
consisting of sudden flushing (feeling of heat or burning in the
face, neck and chest) immediately followed by outbreak of
sweating affecting the whole body. It is seen in 75% of women
in climacteric. In 25-50% it may persist for more than 5 years. In
severe cases it may come as frequently as 1-2 hours. These
women suffer from insomnia. For severe cases treatment with
estrogens or progestins is recommended.
Osteoporosis is the most important health hazard of

climacteric. It affects the trabecular bone. It may end up in
pathologic fracture of the spines and the other bones. Diagnosis
needs special imaging investigations. Treatment is estrogen
replacement. It is prevented by estrogen replacement.
Atherosclerotic disease of the heart
Dysparunia arises from vaginal dryness and atrophic vaginitis.

Local treatment with estrogen creams relieves this problem.
423
Psychologic problems may arise from estrogen deficiency or

from the effects of other climacteric problems (hot flush and
dysparunia). Symptoms include anxiety, insomnia, irritability,
depression, dementia and mood changes.
Postmenopausal bleeding
It is defined as vaginal bleeding after 6 months of menopause.

It is an abnormal condition that always needs proper
investigation. It could arise from benign conditions or more
seriously it may be a sign of serious malignant conditions of the
genital tract. The causes are
 Atrophic vaginitis
 Atrophic endometritis
 Cervical cancer
 Endometrial hyperplasia and polyps
 Endometrial cancer
 Sarcoma of the uterus
 Vulvar and vaginal cancer
 Estrogen producing tumors
 Exogenous estrogen therapy
424
Note: All women with postmenopausal bleeding should be

referred for identification of the cause.
Review questions
1. Define climacteric and describe the hormonal changes.
2. Describe the problems of climacteric.
3. List the causes of postmenopausal bleeding.
425
426
CHAPTER 26
ABNORMAL VAGINAL DISCHARGE
AND VULVAR PRURITIS
LEARNING OBJECTIVES
 TO UNDERSTAND PHYSIOLOGY OF
NORMAL VAGINAL DISCH ARGE
 TO LIST THE CAUSES OF LEUCORRHEA
 TO ENUMERATE THE CAUSES OF

ABNORMAL VAGINAL DISCHARGE
427
 TO DISCUSS THE CLINICAL FEATURES,

DIAGNOSIS AND MANAGEMENT OF
CANDIDIASIS
 TO DISCUSS THE CLINICAL FEATURES AND

MANAGEMENT OF TRICHOMONIASIS
 TO DISCUSS THE CLINICAL FEATURES AND

THE MANAGEMENT OF BACTERIAL
VAGINOSIS
 To describe the causes of vulvar pruritis
VAGINAL DISCHARGE
1. .DEFINITION
NORMAL VAGINAL DISCHARGE IS DEFINED AS

VAGINAL SECRETION WHICH IS SCANTY TO
MODERATE IN AMOUNT, NON OFFENSIVE, NON
PURULENT AND NON IRRITANT. BUT TO DECLARE
IT TO BE NORMAL AND NOT AN INFECTIVE ONE,
428
REQUIRES CLINICAL AND LABORATORY

INVESTIGATIONS.
ABNORMAL VAGINAL DISCHARGE IS ABNORMAL

CONDITION WHERE BY THE PATIENT COMPLAINS
OF UNUSUAL VAGINAL SECRETION EITHER IN
AMOUNT, ODOR, COLOR OR ASSOCIATED ITCHING.
2. PHYSIOLOGY OF VAGINAL DISCHARGE
THE PHYSIOLOGIC BASIS INVOLVED IN NORMAL

VAGINAL SECRETION IS DEPENDENT MAINLY ON
ENDOGENOUS ESTROGEN LEVEL AND TO A
LESSER EXTENT ON ENDOGENOUS
PROGESTERONE LEVEL. DURING FOLLICULAR
PHASE OF MENUSTRAL PERIOD, THERE IS
ABUNDANT SECRETARY ACTIVITY OF THE
ENDOCERVICAL GLANDS, WHICH SECRETE THIN
AND CLEAR MUCOID SECRETION. IN THE
PRESENCE OF PROGESTERONE IT BECOMES THICK
AND WHITE. IN THE PRESENCE OF ESTROGEN, THE
SUPERFICIAL VAGINAL EPITHELIUM BECOMES
RICH IN GLYCOGEN. FOLLOWING DESQUAM ATION
OF THESES CELLS, THE GLYCOGEN IS CHANGED
TO LACTIC ACID BY LACTOBACILLUS DEODERLI,
429
COMMONLY CALLED, THE DODERLEIN BACILLI.

THE RESULTING ACIDIC PH OF THE VAGINA
INHIBITS THE GROWTH OF MANY BACTERIA.
3. CAUSES
I. PHYSIOLOGIC VAGINAL DISCHARGE -

LEUCORRHEA
EXCESS DISCHARGE FROM THE V AGINA NOT

RELATED TO ANY PATHOLOGY COULD OCCUR IN A
VARIETY OF CONDITIONS LIKE
 SEXUAL STIMULATION WITH OR WITHOUT

COITUS
 IN THE PERIOVULATORY PERIOD
 FOLLOWING MENUSTRATION
 PREGNANCY
 CERVICAL ECTROPION
II. PATHOLOGICAL VAGINAL DISCHARGE

430
 VAGINAL AND CERVICAL INFECTIONS INCLUDE

CANDIDIASIS, TRICHOM ONIASIS, BACTERIAL
VAGINOSIS AND CERVICITIS (ACUTE OR
CHRONIC). THIS IS THE COMMONEST CAUSE
OF VAGINAL DISCHARGE.
 BENIGN AND MALIGNANT TUMORS OF THE

VULVA, VAGINA, CERVIX AND THE UTERUS
 ATROPHIC VAGINITIS IN CLIMACTERIC
 FOREIGN BODY WITH SECONDARY INFECTION
 RARELY INTESTINAL PARASITES MIGRATING

INTO THE VAGINA (ENTEROBIASIS, AMEBIASIS)
4. VAGINAL INFECTIONS
4.1. TRICHOMONAS VAGINALIS VAGINITIS

(TRICHOMONIASIS)
ETIOLOGY
431
THIS CONDITION IS CAUSED BY TRICHOMONAS

VAGINALIS, A MOTILE PROTOZOAN. IT IS
PREDOMINANTLY A SEXUALLY TRANSMITTED
ORGANISM. THE MALE H ARBORS THE INFECTION
IN THE URETHRA AND THE PROSTATE. RARELY, IT
MAY BE TRANSMITTED BY FOMITES. THE
INCUBATION PERIOD IS 3- 28 DAYS.
INCIDENCE
IT ACCOUNTS FOR APPROXIMATELY 25% OF

VULVOVAGINAL INFECTIONS. ABOUT 20 -50% ARE
ASYMPTOMATIC.
CLINICAL PRESENTATION
THE PRIMARY SYMPTOM IS PROFUSE AND

OFFENSIVE VAGINAL DISCHARGE DATING FROM
THE LAST MENSTRUATION. IT IS OFTEN YELLOW –
GREY OR GREENISH IN COLOR AND FROTHY IN
CHARACTER. VARIABLE DEGREE OF VULVAR
IRRITATION AND ITCHING IS PRESENT.
SIGNIFICANT DYSPARUNIA IS PRESENT.
432
VAGINAL EXAMINATION IS PAINFUL. EXAMINATION

WILL SHOW THIN GREENISH YELLOW AND FROTHY
OFFENSIVE DISCHARGE IN THE VAGINA. VAGINAL
WALLS ARE INFLAMED (RED). PUNCTUATE OR
STRAWBERRY SPOTS MAY BE SEEN ON THE
CERVIX AND THE VAGIN A. VARIABLE DEGREE OF
VULVAR SORENESS MAY BE SEEN. ABNORMAL
PAP SMEAR IS SEEN IN 70 % OF THE CASES.
DIAGNOSIS
THIS MADE BY IDENTIFYING THE FLAGELLATED

TRICHOMONADS ON WET MOUNT OF VAGINAL
FLUID. CULTURE IS ONLY NEEDED IN RESISTANT
CASES.
TREATMENT
METRONIDAZOLE IS THE DRUG OF CHOICE. IT CAN

BE GIVEN AS A SINGLE 2 GRAM DOSE OR CAN BE
GIVEN AS 500 MG THREE TIMES /DAY FOR 7 D AYS.
THE PARTNER SHOULD BE IDENTIFIED AND
TREATED. DURING PREGNANCY THIS DRUG
SHOULD NOT BE GIVEN IN THE FIRST TRIMESTER.
433
FOR PERSISTENT CASES HIGHER DOSES OR

PARENTERAL METRONIDAZOLE CAN BE USED.
COMPLICATIONS
IF UNTREATED IT MAY SERVE AS A VEHICLE FOR

STI AGENTS TO CAUSE PID.
4.2. CANDIDAL VULVOVAGINITIS (MONILIASIS OR

CANDIDIASIS)
ETIOLOGY
IN MORE THAN 80 % OF THE CASES, IT IS CAUSED

BY THE FUNGI CANDIDA ALBICANS. THIS IS A
DIMORPHIC FUNGUS WITH YEAST AND
FILAMENTOUS FORMS. IN 20% CANDIDA
GLABRATA IS RESPONSIBLE. THESE ORGANISMS
ARE NORMAL FLORA OF THE LOWER
GASTROINTESTINAL TRACT AND THE VAGINA IN
SOME WOMEN.
INCIDENCE AND PREDISPOSING FACTORS

434
75 % OF WOMEN DEVELOP THIS INFECTION

SOMETIME DURING THEIR LIFE TIME. IN 40% IT
RECURS. MONILIASIS IS CONSIDERED TO BE AN
OPPORTUNISTIC INFECTION THAT ARISES WHEN
THERE IS CHANGE IN THE LOCAL OR SYSTEMIC
DEFENSE MECHANISMS. THE PREDISPOSING
FACTORS FOR SUCH CHANGES ARE
 PREGNANCY
 ORAL CONTRACEPTIVES
 DIABETES MELLITUS
 BROAD SPECTRUM ANTIBIOTICS
 SUPPRESSED IMMUNE SYSTEM LIKE

HIV/AIDS OR USE OF STEROIDS
 PRESENCE OF LOCAL WARMTH AND

MOISTURE
CLINICAL FEATURES AND DIAGNOSIS
435
THE INFECTION IS ASYMPTOMATIC IN 20% OF

WOMEN. INTENSE VULVO-VAGINAL PRURITIS IS
THE PRIMARY SYMPTOM. OFTEN IT IS
ASSOCIATED WITH VAGINAL DISCHARGE.
TYPICALLY THE DISCHARGE IS VARIABLE IN
AMOUNT, THICK AND CURD LIKE CONSISTENCY,
WHITISH IN COLOR AND NON OFFENSIVE. THE
PRURITIS IS OFTEN OUT OF PROPORTION TO THE
DISCHARGE. THERE MAY BE SUPERFICIAL
DYSPARUNIA AND DYSURIA DUE TO LOCAL
SORENESS.
EXAMINATION MAY SHOW EXCORIATED VULVA. IN

SEVERE CASES IT IS SWOLLEN AND RED.
SPECULUM EXAMINATION SHOWS CURD LIKE
DISCHARGE IN FLAKES OFTEN ADHERENT TO
REDDENED VAGINAL W ALL. SCRAPING OF THESE
FROM THE VAGINAL W AL L REVEALS BLEEDING
POINTS ON THE VAGINA. VAGINAL PH IS ACIDIC,
OFTEN LESS THAN 5.2.
BALANOPOSTAITIS MAY BE PRESENT IN THE

COITAL PARTNER. THE MOST COMMON
COMPLAINTS ARE IRRITATION OF THE GLANS
436
PENIS AND PREPUCE AND ITCHING OF THE

SCROTUM.
DIAGNOSIS IS MADE BY DOING 5-10 % POTASSIUM

HYDROXIDE STAINING OR WET MOUNT OF A
SAMPLE OF VAGINAL DI SCHARGE. THIS WILL
SHOW THE YEAST OR THE HYPHAE. IN RECURRENT
CASES CULTURE MAY BE NEEDED.
TREATMENT
SYSTEMIC AND LOCAL (SUPPOSITORIES OR

CREAMS) ANTIFUNGALS ARE USED TO TREAT THIS
CONDITION. SYSTEMIC ANTIFUNGALS ARE
CONTRAINDICATED DURING PREGNANCY.
 LOCAL ANTIFUNGALS: NYSTATIN,

CLOTRIMAZOLE, MICONAZOLE, ECONAZOLE
 SYSTEMIC ANTIFUNGALS: KETOKONAZOLE

(200 MG / DAY FOR 10 DAYS), FLUCONAZOLE
(150 MG ONCE)
FOR RECURRENT CASES TREATMENT OF MALE

PARTNER, IDENTIFYING AND TREATING THE
437
PREDISPOSING FACTOR AND VAGINAL

ACIDIFICATION ARE MANAGEMENT OPTIONS.
4.3. BACTERIAL VAGINOSIS
THIS IS A CONDITION OF THE VAGINA IN WHICH

THERE IS AN OVERGROW TH OF ANAEROBES WITH
PAUCITY OF LACTOBACILLI AND FREQUENT
ABSENCE OF INFLAMMATORY CELLS. IT HAS
UNDERGONE NOMENCLATURE CHANGES OVER
THE YEARS (NONSPECIFIC VAGINITIS, ANAEROBIC
VAGINITIS).
ETIOLOGY
BACTERIAL VAGINOSIS IS CAUSED BY A VARIETY

OF FACULTATIVE ANAEROBIC ORGANISMS.
GARDNERELLA VAGINALIS IS THE MOST
FREQUENTLY ASSOCIATE D ORGANISM. OTHERS
ARE MYCOPLASMA HOMINIS, BACTEROIDES,
PEPTOSTREPTOCCUS AND PEPTOCOCCUS.
INCIDENCE
438
IT ACCOUNTS FOR 25- 30 % OF VAGINAL

DISCHARGES. IN 50% IT IS ASYMPTOMATIC.
CLINICAL FEATURES
THE MOST FREQUENT COMPLAINT IS A FOUL

SMELLING, THIN HOMOGENOUS VAGINAL
DISCHARGE WITH A FISHY SMELL. OFTEN IT IS
PROFUSE, FROTHY AND GRAYISH. PRURITIS IS
OFTEN MINIMAL.
EXAMINATION WILL SHOW NORMAL VAGINAL

MUCOSA WITH NO SIGN OF INFLAMMATION AND
THIN OFFENSIVE DISCHARGE WHICH IS EASILY
WIPED FROM THE VAGIN AL WALL.
DIAGNOSIS
A POSITIVE AMINE TEST (THE DETECTION OF

A FISHY SMELL WHEN A DROP OF 10% KOH IS
ADDED TO A DROP OF THE VAGINAL DISCHARGE
ON A MICRO SLIDE) AND FINDING OF CLUE CELLS
ON WET – MOUNT PREPARATION MADE WITH 0.9%
PHYSIOLOGIC SALINE ARE DIAGNOSTIC OF
BACTERIAL VAGINOSIS. VAGINAL PH IS ABOVE 4.5.
439
GRAM STAIN OF THE VAGINAL DISCHARGE SHOW S

ABSENT LACTOBACILLI, NUMEROUS GRAM
VARIABLE BACTERIA AND MINIMAL LEUKOCYTES.
THE DIAGNOSIS IS CONFIRMED IF 3 OF THE

FOLLOWING 4 CRITERIA ARE PRESENT:
 A GREY – WHITE VAGINAL DISCHARGE, WHICH

IS SOMETIMES FOAMY
 POSITIVE AMINE FISH TEST
 POSITIVE CLUE CELLS
 VAGINAL PH OF .4.5
TREATMENT
METRONIDAZOLE IS THE MOST EFFECTIVE

TREATMENT. THE DOSE IS SIMILAR TO THE DOSE
USED IN TREATMENT OF TRICHOMONIASIS. OTHE R
OPTIONS ARE CLINDAMYCIN AND AMPICILLIN.
ACIDIFICATION OF THE VAGINA USING ACID GE L
OR COMMERCIAL YOGURT (LYOPHILIZED
440
LACTOBACILLUS ACIDOPHILUS) IS AN OPTION IN

RECURRENT CASES.
COMPLICATIONS
IF UNTREATED IT IS ASSOCIATED WITH PID,

PRETERM LABOUR, PROM AND POSTPARTUM
ENDOMETRITIS.
4.4. GONOCOCCAL CERVICITIS
IT IS CAUSED BY NEISSERIA GONORRHEA, A

SEXUALLY TRANSMITTED ORGANISM.
IT MAY NOT CAUSE ANY SYMPTOMS. WHEN

SYMPTOMATIC IT MANIFESTS WITH
MUCOPURULENT, USUALL Y NON OFFENSIVE AND
NONPRURITIC IN NATURE. SPECULUM
EXAMINATION REVEALS INFLAMED CERVICAL OS
WITH MUCOPURULENT DISCHARGE FROM THE
INSIDE OF THE CERVIX.
DIAGNOSIS IS MADE BY FINDING GRAM NEGATIVE

INTRACELLULAR DIPLOCOCCI ON GRAM STAIN OF
VAGINAL DISCHARGE.
441
MANAGEMENT IS TREATMENT OF BOTH THE

WOMAN AND HER PARTNE R WITH CEPHTRIAXONE
250 MG INTRAMUSCULAR SINGLE DOSE OR
SPECTINOMYCIN 2 GRAM INTRAMUSCULAR SINGLE
DOSE.
IF UNTREATED IT MAY CAUSE ACUTE PID.
VULVAR PRURITIS
Vulvar pruritis is significant itching that is confined to the

vulva. It is one of the commonest presenting complaints in
gynecology. It affects around 10 % of women.
In some cases the cause is easy to diagnose but in most

arriving at the diagnosis poses considerable difficult. The
causes could be systemic illnesses or they could be local
conditions.
1. Etiology
I. Systemic causes
 Unstable diabetes
442
 Hepatobiliary diseases like biliary cirrhosis and cholestatic

jaundice
 Renal failure
 Hematological conditions like polycythemia, anemia
 Fat malabsorption
 Systemic dermatosis like psoriasis, seborrheic dermatitis
 Skin infections like scabies, pediculosis and tinia cruris
II. Local conditions
 Vaginal discharge of any cause but mainly candidiasis
 Atrophic conditions during climacteric
 Allergic conditions from soap, contraceptive creams
 Vulvar dystrophies and vulvar cancer
III. Psychosomatic
Note: Candidal vulvovaginitis is the commonest cause of vulvar

pruritis.
2. Diagnostic work up
History should identify
 The exact site of itching (vulvar, perianal or other sites in

the body)
443
 The duration
 The nature - intermittent or continuous and progress over

time
 Severity as related to lack of sleep or presence of

excoriations
 Presence of vaginal discharge
 Drugs used
 Medical illnesses and conditions causing allergy
Physical examination
 General dermatologic examination
 Inspection of the vulva and adjacent area (vagina, cervix,

perianal areas) for discharge, excoriation marks, ulcers
and masses.
Investigations
This depends on the suspected cause and include;
 Potassium hydroxide, gram stain and wet mount

examination of vaginal discharge
 Screening for diabetes, renal, biliary and hematological

diseases
 Work up of dermatologic illnesses

444
 For persistent cases referral for biopsy to rule out

dystrophies
Treatment
 Treatment of identified systemic, dermatologic and local

conditions
 Appropriate local hygiene is to be taken care of. Avoid

washing with soap or application of perfumes. Vulvo –
vaginal douching should be avoided. Use loose fitting
undergarments preferably made of cotton to keep the area
aerated.
 To prevent the vicious cycle of scratch itch scratch use

local cortisol creams and sedation at night. For atrophic
conditions use estrogen creams.
 Persistent cases should be referred.
6. VULVOVAGINITIS IN CHILDHOOD
INFLAMMATORY CONDITIONS OF THE VULVA AND

VAGINA ARE THE COMMONEST DISORDERS
DURING CHILDHOOD. DUE TO LACK OF
ESTROGEN, THE VAGINAL DEFENSE IS LOST AND
THE INFECTION OCCURS EASILY.
445
ETIOLOGY
 NON SPECIFIC VULVO VAGINITIS
 PRESENCE OF FOREIGN BODY IN THE VAGINA
 ASSOCIATED INTESTINAL INFESTATIONS,

THREAD WORM BEING THE COMMONEST
 RARELY MORE SPECIFIC INFECTION CAUSED

BY CANDIDA ALBICANS OR GONOCOCCUS MAY
BE IMPLICATED
CLINICAL FEATURES AND DIAGNOSIS
THE CHIEF COMPLAINTS ARE PRURITIS OF

VARYING DEGREE AND V AGINAL DISCHARGE.
THERE MAY BE PAINFUL MICTURITION.
INSPECTION REVEALS SORENESS OF THE VULVA.

THE LABIA MINORA MAY BE SWOLLEN AND RED.
VAGINAL DISCHARGE VARIES FROM SCANTY TO
COPIOUS, AT TIMES OFFENSIVE. IF A FOREIGN
BODY IS SUSPECTED A RECTAL EXAMINATION M AY
HELP IN DIAGNOSIS. IF IT FAILS TO DETECT,
446
EXAMINATION UNDER ANESTHESIA USING AN

AURAL OR NASAL SPECULUM IS TO BE DONE.
IN EVERY CASE, THE INVESTIGATION REGARDING

THE CAUSE IS TO BE SOUGHT FOR. THE VAGINAL
DISCHARGE IS COLLECTED WITH A PLATINUM
LOOP AND TWO SMEARS ARE TAKEN, ONE FOR
DIRECT EXAMINATION AND THE OTHER FOR GRAM
STAIN. A SMALL AMOUNT MAY BE TAKEN WITH A
PIPETTE FOR CULTURE. TO EXCLUDE INTESTINAL
INFESTATION, STOOL EXAMINATION IS OF HELP.
TREATMENT
IN MOST CASES, THE C AUSE REMAINS UNKNOWN.

SIMPLE PERINEAL HYGIENE WILL RELIEVE THE
SYMPTOMS. IN CASES OF SORENESS OR AFTER
REMOVAL OF FOREIGN BODY, ESTROGEN
OINTMENT IS TO BE APPLIED LOCALLY EVERY
NIGHT FOR 2 WEEKS. ALTERNATIVELY, HALF
TABLET OF ETHINYL ESTRADIOL 0.01 MG IS TO BE
GIVEN DAILY FOR THREE WEEKS TO IMPROVE THE
LOCAL VAGINAL DEFENSE. WHEN THE SPECIFIC
ORGANISMS ARE DETECTED, THERAPY SHOULD BE
DIRECTED TO CURE THE CONDITION.
447
REVIEW QUESTIONS
1. DESCRIBE THE CAUSES OF VAGINAL

DISCHARGE.
2. DISCUSS THE CAUSES, CLINICAL FEATURES

AND MANAGEMENT OF INFECTIOUS VAGINAL
DISCHARGE.
3. DISCUSS THE CAUSES OF VULVAR PRURITIS
448
CHAPTER 27
PELVIC INFLAMMATORY DISEASE (PID)
449
Learning objectives
 To define and classify pelvic inflammatory disease (PID)
 To discuss the pathophysiology of PID
 To discuss the diagnosis of acute PID
 To list the complications of acute PID
 To describe the management of acute PID
Pelvic inflammatory disease (PID) is a clinical syndrome used to

describe infection or inflammation of the upper female genital
tract above the level of the internal os of the cervix often
with involvement of the adjacent tissues.
This general term does not specify the site [endometrium

(endometritis), fallopian tubes (salphingitis), ovaries (oophoritis)
and parametrium (parametritis)] or the stage (acute, subacute,
recurrent and chronic) or the etiologic agent.
Besides the site and stage, PID can be classified using the
antecedent event
 Postpartum PID (follows delivery)
 Postabortal PID (follows abortion)
450
 Port IUCD or instrumentation (follows IUCD

insertion or diagnostic curettage or
hysterosalpingography)
 Post operative (follows pelvic operations mainly

after hysterectomy)
 Post STD (follows sexually transmitted infections)
 Secondary to other infections like appendicitis and

tuberculosis
ACUTE PELVIC INFLAMMTORY DISEASE
1. EPIDEMIOLOGY
Acute PID is common problem affecting 1-2 % of women

between ages 15 -35 years. Incidence is increasing because of
increasing antecedent events. Risk groups include
menstruating teenagers, those with multiple sexual partners,
those using IUCD and those with previous history of PID.
2. PHYSIOLOGICAL BARRIERS
The upper female genital tract above the level of the internal os
is sterile, despite the fact the cervical canal and the vagina are
colonized by millions of bacteria. The barriers that prevent
colonization of the upper female genital tract are
451
 Cervical canal that is normally closed and is plugged by

mucus
 Presence of lysozyme and secretory IgA in cervical

secretions
 Cyclic shedding of the endometrium
 Apposition of the chorion leave to the decidua during

pregnancy
 Downward beating of the tubal celia
 Systemic host defense
3. Pathogenesis
Microorganisms causing PID are not sufficiently mobile to reach

the upper female genital tract. Conditions that cause a breach
in the physiologic barriers like childbirth or abortion or IUCD
insertion or surgery create conducive situation for PID to occur.
But PID occurs spontaneously in a woman having none of
these conditions. Two theories are forwarded to explain this
452
 Vector transport theory – bacteria use vectors like

spermatozoa and Trichomonas vaginalis (a sexually
transmitted agent), to transport them to the upper female
genital tract
 Pressure gradient theory – negative pressure in the

uterus during orgasm sucks the bacteria into the
endometrium
Note: Coitus is a prerequisite for PID. It is rare to find PID in

virgins, if found it is almost always PID descending infection
from appendicitis or pelvic tuberculosis from haematogenous
spread. PID in an intact pregnancy is also rare.
Once bacteria are inoculated into the endometrial cavity,

bacteria proliferate and disseminate to the other parts of the
genital tract. Two routes of spread exist.
 Direct upward canalicular spread (endometrial –

endosalphingeal –peritoneal spread) most common way of
post STI (non puerperal) PID spread
 Indirect parametrial - paracervical lymphatic spread is

most common way of puerperal/ postabortal PID spread.
4. Etiology
It depends on the antecedent event.
453
 Acute PID following abortion and delivery is a

polymicrobial infection caused by organisms ascending
from the vagina. These are normal flora of the vagina
which under normal circumstances do not cause infection.
Variety gram negative and positive, aerobic and anaerobic
organisms are involved. Common aerobic organisms
include non hemolytic streptococcus, E.coli, group B
streptococcus and staphylococcus. Common anaerobic
organisms are Bacteroides fragilis and bivius,
peptostreptoccus and peptococcus.
 Acute post STI PID is primarily caused by Neisseria

gonorrhea or Chlamidia trachomatis. Secondary infection
may involve polymicrobial organisms.
 Rarely exogenous organisms like clostridia may cause

PID.
5. Clinical features and diagnosis
Clinical diagnosis of acute PID is often difficult because

presentation varies widely and symptoms are vague and non
specific. Therefore, current criteria for diagnosis use
combination of physical signs rather than symptoms.
Typical cases of acute salphingitis present with bilateral lower

abdominal pain (severe and acute in gonococcal PID and dull
and subacute in chlamydial PID) and fever with constitutional
454
symptoms like malaise, headache nausea and vomiting which

usually start in few days after menustration.
The typical physical findings are pyrexia, tachycardia, lower

abdominal direct and rebound tenderness, cervical excitation
tenderness and bilateral adenexal tenderness. These findings
are less pronounced in chlamydial PID.
Laboratory investigations reveal leukocytosis of more than

10,000/cc, an elevated ESR value of more than 15 mm per
hour and high white cell count and positive gram stain/ culture
in culdocentesis aspirate. In early uncomplicated cases
ultrasound and gram stain of vaginal discharge are of little help.
According to the Hegar criteria clinical diagnosis of acute

PID is made when all major criteria plus at least one minor
criterion are found.
I. Major criteria:
 Lower abdominal pain with direct and/ or rebound

tenderness,
 Cervical excitation tenderness,
 Adenexal tenderness
II. Minor criteria:
 Fever of >380c,
455
 WBC count of >10,000/mm3 or ESR of >20 mm/hour,
 Positive gram stain for gonorrhea or >5 WBC/ oil

immersion field from cervical discharge,
 Culdocentesis shows purulent fluid or WBC with bacteria

on gram stain
 Inflammatory mass or abscess on pelvic examination or

ultrasound
Clinically acute PID can be graded into three.
 Grade I: PID limited to the adnexa
 Grade II: PID with inflammatory mass or abscess
 Grade III: Ruptured tuboovarian abscess with generalized

peritonitis
6. Differential Diagnosis
Clinical conditions that mimic acute PID include appendicitis,

ectopic pregnancy, torsion of ovarian cyst, hemorrhage or
rupture of ovarian cyst, urinary tract infections and less
common conditions like endometriosis.
7. Complications
If early diagnosis is not made and aggressive therapy is not

given, acute PID progresses to cause serious and debilitating
456
complications including death. The immediate

complications are
 Pelvic peritonitis or even generalized peritonitis with ileus
 Septicaemia producing metastatic infections, like arthritis

and endocarditis
 Septic shock ending up in multiple organ failure
 Pelvic abscess and tuboovarian abscess
 Infectious perihepatitis (Fitz – Hugh – Curtis syndrome)
 Complications of surgical management
The late complications are
 Infertility – overall rate is 25% but risk increases with the

number of attacks.
 Ectopic pregnancy – increased by 6-10 folds
 Chronic pelvic pain with dysparunia and dysmenorrhea
 Intestinal obstruction
8. Management
The goals of therapy are controlling acute infection, preventing

long term complications and re-infection. Treatment of acute
PID can be given as outpatient or inpatient. The indications for
inpatient management are:
457
 Severe toxic: temperature of >390c with lower abdominal

tenderness/guarding
 Current pregnancy
 Patient known to have HIV/ AIDS
 Suspected or proven tuboovarian abscess
 Failure of response to outpatient treatment in 48-72 hours
 Noncompliance or non tolerance to outpatient treatment
 Uncertain diagnosis in which surgical conditions can not

be ruled out
I. Outpatient management
Apart from adequate rest and analgesic, antibiotics should be

prescribed even before the microbiological report is available.
Because the infection is poly microbial in nature, combination of
antibiotics should be prescribed.
There are many different antibiotics regimens, but the spectrum

of activity of the antimicrobial agents should cover the following
organisms: Neisseria gonorrhea, chlamydia trachomatis,
aerobic and anaerobic organisms. Follow up visit should be
arranged after 72 hours, 7days and 3 weeks.
II. Inpatient management

458
General or supportive care includes intravenous or oral

hydration, bed rest in semi fowler‘s position and administration
of analgesic/ antipyretic.
The specific treatment is administration of intravenous

combination antibiotics that cover Neisseria gonorrhea,
Chlamydia trachomatis, aerobic and anaerobic bacteria. Clinical
response is evidenced by remission of temperature,
improvement of pelvic tenderness, normal white blood cell
count and negative report on bacteriological study.
Indications for laparatomy are worsening condition of the

patient, generalized peritonitis, pelvic abscess and if other
surgical conditions (appendicitis, ectopic pregnancy) can not be
ruled out.
9. Prevention
 Early detection and treatment of STI including

asymptomatic cases like gonococcal cervicitis
 Partner identification and treatment (contact tracing)
 Safe sexual practices including condoms and avoiding

multiple partners
Review questions
1. Define and classify PID.

459
2. List the major and minor Hegar criteria.
3. Describe the management of acute PID.
4. List the complications of acute PID.
CHAPTER 28
FAMILY PLANNING
460
Learning Objectives:
 To list the different types of contraceptive methods
 To describe the natural family planning methods
 To list the different types of barrier methods
 To describe the side effects of IUCDs
 To describe the different types of hormonal methods
 To describe the surgical contraceptive methods
Introduction
The term contraception includes all measures, temporary and

permanent, designed to prevent pregnancy. On the other hand,
the term family planning (fertility control) includes both fertility
inhibition (contraception) and fertility stimulation.
Rapid population growth is a critical issue in most developing

countries. Family planning methods save women‘s lives by
preventing unintended pregnancies. Slower population growth
conserves resources, improves health and living standard.
Ideal contraceptive methods should be widely acceptable,

inexpensive, simple to use, safe, highly effective and requiring
minimal motivation, maintenance and supervision. So far there
is no universally acceptable method.
461
METHODS OF CONTRACEPTION ARE DIVIDED INTO
 Natural family planning method
 Barrier methods
 Intrauterine contraceptive device
 Hormonal contraception
 Surgical contraception
The effectiveness of contraceptive method can be measured by

the pearl index. The Pearl Index is a figure which is obtained
by using the pearl formula and it indicates the number of
pregnancies which would occur if 100 women use a specific
method for one year.
The pearl index of the pregnancy figure per 100 women

years of use =
100 (women) * 12 (ovulations per year) * number of

pregnancies / total months of use.
Failure rate is further less when methods are used correctly and
consistently.
Clients have to be counseled about all the available family

planning methods and should make their own choice. This is
called informed choice and is usually reached by the GATHER
approach.
462
 G stands for greeting
 A stands for asking the client needs
 T stands for telling the client about all the methods
 H stands for helping the client to make the choice
 E stands for explaining about the chosen method
 R stands for return visit or referral to the facility that gives

the services
A. NATURAL FAMILY PLANNING
1. Rhythm method (Periodic abstinence)
The technique used in this method is confining sexual

intercourse to the phases of menustral cycle where conception
is unlikely to occur. It needs identification of the fertile (unsafe)
and infertile (safe) phases of the menustral cycle. The fertile
(safe) period extends from 4 days before to 4 days after
ovulation. The rest of the menustral cycle is infertile (safe)
period. This is based on the fact that a human ovum can not be
fertilized no later than 48 hours after ovulation and the human
spermatozoa can not fertilize an ovum 48 hours after
ejaculation. Since there is no sign or test to tell the exact time
ovulation, various methods are used to determine the
463
approximate time of ovulation and fertile period. These methods

include.
I. The calendar method
This method requires recording the length of 12 consecutive

menustral cycles. The beginning of the fertile phase (first unsafe
day) is calculated by subtracting 18 from the shortest cycle. The
end of the fertile phase (the last fertile day) is calculated by
subtracting 11 from the longest cycle. Sexual intercourse is
abstained between these dates. User effectiveness is 20- 30 per
100 women.
II. The temperature method
This method requires measuring the basal body temperature

before rising from the bed daily staring from the first day of the
menustral cycle. Sexual intercourse is abstained from the start
of the menustral cycle to 3 days after the record of temperature
rise. User effectiveness is 20- 30 per 100 women.
III. The cervical mucus or Billings method
This method requires observing the cervical secretions daily by

wiping the introitus with white toilet tissue paper. Sexual
intercourse is abstained from the onset of menses to 4 days
after maximum secretion of the cervical mucus. User
effectiveness is 15- 20 per 100 women.
464
IV. Symptothermal method
This method is a combination calendar and temperature

methods. In this method the first day of abstinence is predicted
by using calendar method and the last day by temperature
method.
2. Coitus Interruptus (Withdrawal method)
This method requires withdrawal of the penis from the vagina

prior to ejaculation which must occur outside the vagina and
away from the immediate perivaginal area. This needs high level
of motivation and is associated with high failure rates.
3. LACTATIONAL AMENORRHEA METHOD
Prolonged and sustained breast feeding offers a natural

protection against pregnancy. This is more effective in women
who are amenorrhic that those who are menstruating. The risk
of pregnancy in the first 6 months in a woman who is fully breast
feeding and amenorrhic is less than 2 percent. Higher failure
rates are observed in women who are breast feeding and are
menstruating. Protection gradually decreases after 6months.
465
B. BARRIER AND CHEMICALS METHODS
1. CONDOMS
These are thin sheaths made of latex. The male condom is put
on a fully erect penis and removed after ejaculation before the
penis is deflated. The female condom is unrolled into the vagina
before sexual intercourse. Concomitant use of spermicidals
improves effectiveness.
Besides its contraceptive effectiveness, it also protects against

STI and HIV/AIDS. It is useful for couple with infrequent sexual
intercourse.
Disadvantages are condom breakage, condom slippage,

occasional allergy to latex and claim of dulling of sexual
sensation.
User effectiveness ranges from 6- 30/ 100 women and is mainly

from improper and inconsistent use.
2. Diaphragm
466
This is a shallow dome shaped rubber cup with flexible rim. It

has different sizes. It is designed to fit behind the pubic bones,
the lateral vaginal walls and the posterior fornix, thus covering
the external os of the cervix.
It is correctly placed in the vagina before sexual intercourse and

is removed 6-8 hours after sexual intercourse. Spermicidal jelly
is applied to the inside and outside surface before placement in
the vagina.
It is advantageous to those who practice sex infrequently. The

disadvantages are the inappropriateness of the method and the
increased incidence of urinary tract infections and vaginal
laceration.
The user effectiveness is 10- 20/ 100 women.
3. Cervical cup
This is a rubber cup with metallic rim designed to fit the cervix.
It is applied to the cervix before intercourse and provides
continuous protection for 48 hours. It is not frequently used.
4. Spermicidals
This method involves deposition of spermicidal chemical

(nanoxynol 9) into the vagina 10- 15 minutes before each
sexual act. The various preparations include aerosol foams,
creams, foaming tablets and contraceptive sponges.
467
They also offer protection against STI and HIV/AIDS. The

disadvantages are inappropriateness, allergy, and presumed
risk of congenital malformation.
The user effectiveness ranges between 2- 40/ 100 women.
C. INTRAUTERINE CONTRACEPTIVE DEVICES (IUCD)
This is a long term reversible contraceptive method involving

insertion of a specially made devise into the uterine cavity to
offer constant protection against pregnancy.
A variety of devises have been used over years. The

nonmedicated IUCDs, also called the loop, are no more used
nowadays. They have larger size and do not need regular
replacement. The medicated IUCDs contain either copper or
progesterone that increases their contraceptive effectiveness.
They are smaller in size and need regular replacement.
Currently used medicated IUCDs are copperT380A (replaced
every 8-10 years) and the progestasert (replaced every year).
The mechanism of action is not clear but is believed to be

related to the sterile inflammatory reaction in the endometrium,
asynchronous development of the endometrium and
interference of the enzymes involved in implantation. Altered
468
tubal motility, formation of thick cervical mucus and maintenance

of decidualized endometrium are additional mechanisms in
progestasert. IUCDs do not inhibit ovulation and fertilization.
The absolute contraindications are suspected or proven

pregnancy, acute PID or purulent cervicitis, unresolved
abnormal uterine bleeding, uterine anomaly or myoma and
cervical or uterine malignancy. Relative contraindications are
history of dysmenorrhea or hypermenorrhea, valvular heart
disease, bleeding disorders, impaired immunity (HIV/AIDS or
diabetes), nulliparous woman, previous ectopic pregnancy and
women with multiple sexual partners.
The side effects / complications are perforation, cramps and

syncopal attack during insertion, hypermenorrhea,
dysmenorrhea, ectopic pregnancy and PID. Spontaneous
expulsion may occur.
DEPENDING ON THE TIMING, THERE ARE THREE TYPE

OF IUCD INSERTION: INTERVAL (INSERTION MADE IN
A NON PREGNANT WOMAN OR AFTER 6 WEEKS
POSTPARTUM OR ABORTION), POSTABORTAL
(IMMEDIATELY AFTER ABORTION) AND POSTPARTUM
(IMMEDIATELY AFTER DELIVERY). INTERVAL
INSERTION CAN BE DONE AT ANY TIME OF THE
MENUSTRAL CYCLE AS LONG AS PREGNANCY IS
RULED OUT, BUT THE BEST TIME IS DURING
469
MENUSTRATION OR WITHIN 7 DAYS OF THE

MENUSTRAL CYCLE. IUCD INSERTION IS AN OUT
DOOR PROCEDURE AND CAN BE DONE EVEN BY A
TRAINED PARAMEDICAL PERSONNEL WITHOUT
ANESTHESIA.
INDICATIONS FOR REMOVAL ARE SUSPECTED

PERFORATION, PERSISTENT CRAMP AFTER
INSERTION, HYPERMENORRHEA CAUSING ANEMIA,
SEVERE DYSMENORRHEA, PID, PREGNANCY,
DISPLACEMENT OF THE IUCD, MISSING THREAD AND
CLIENT REQUEST.
User effectiveness is 1-3 %.
D. HORMONAL CONTRACEPTION
1. Combined Oral Contraceptives (The Pill or OCPs)
The combined oral steroidal contraceptive is a very effective

short term reversible method of family planning. It contains both
estrogen and progesterone derivatives in a single tablet. There
are two types of formulations. The multiphasic pills have
tablets with varying amount of estrogen and progesterone in
different rows. The monophasic pills have the amount of
estrogen and progesterone in all the tablets. Depending on the
470
amount of estrogen, the monophasic pills are further subdivided

into low dose (if the amount of ethinyl estradiol is < 0.05 mg)
and standard dose (the amount of ethinyl estradiol is 0.05 mg).
The commonly used progestins are levonorgestrel,
norethisterone and lynosterol. The estrogens are either ethinyl
estradiol or menstranol.
The mechanism of action of OCPs is mainly by inhibition of

ovulation but thickening of cervical mucus, decidualization of
the endometrium and alteration of motility of the fallopian tubes
also contribute.
The absolute contraindications are proven or suspected

pregnancy, undiagnosed abnormal uterine bleeding, coronary
artery disease, history of stroke or thromboembolism, active
liver disease, liver adenoma, estrogen dependent neoplasm,
breast cancer, and smoking over the age of 35 years. The
relative contraindications are breast feeding, migraine
headache, history of cholestasis, severe hypertension, diabetes
mellitus, varicose veins and elective operation in 4 weeks.
Epilepsy, and anti Tb treatment are relative contraindications
because of accelerated clearance of the hormones.
The side effects are nausea, vomiting, weight gain, headache,

breast soreness, acne, chloasma, and mild hirsutism, mood
changes like depression, break through bleeding, post pill
471
amenorrhea, leucorrhea, vaginal candidiasis, headache and

decreased amount of breast milk.
The complications which occur in those with risk factors are

vascular thrombosis and embolism, myocardial infarction,
stroke, hypertension, liver tumors especially hepatic adenoma
and cholelithiasis.
The danger symptoms that indicate discontinuation are severe

migraine, visual disturbance, sudden chest pain, severe cramps
and swelling of the legs, severe right upper quadrant pain or
jaundice and breast lump.
Additional indications for discontinuation are excessive weight

gain, client wish to conceive, client request and planned
elective surgery.
Non contraceptive benefits of OCPs are relief of menorrhagia,

relief of dysmenorrhea, relief of dysfunctional uterine bleeding
and premenstrual syndrome, improvement of iron deficiency
anemia and endometriosis. It is also associated with marked
reduction in the risk of pelvic inflammatory disease (protective
thick cervical mucus), benign breast disease, fibroid uterus,
carcinoma of the endometrium, carcinoma of the ovary and
osteoporosis.
2. Progestin only pill (Minipill or POP)
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These pills contain only progesterone derivatives in very low

dose. The progestins commonly used are levonorgestrel 75 g,
norethisterone 350 g, ethinodiol diacetate 500 g, desogestrel
75 g, lynosterol 500 g, or norgestrel 30 g. They have to be
taken continuously with no hormone free interval.
They are useful for women in whom estrogen containing

contraceptives are contraindicated.
The mechanism of action is mainly by cervical mucus

thickening, decidualization of the endometrium and changing
tubal motility. Ovulation suppression is partial and occurs in
only 50 %.
The advantages include elimination of side effects attributable

to estrogen like thrombosis and change in lipid profile and
absence of adverse effect on lactation and milk volume.
Because of these advantages POPs can be prescribed to
lactating women and women with hypertension, thrombosis,
diabetes and smokers.
The disadvantages are increased incidence of menustral

changes like breakthrough bleeding and in some amenorrhea,
very low dose contraceptive with increased failure rate
especially if pill is missed or taken late, increased risk of ectopic
pregnancy and ovarian cyst formation.
473
Because of the very low dose nature of these contraceptives

and the partial suppression of ovulation, patients should be
counseled about the importance of taking the pills at the same
time of the day and the dangers of missing the pill. A back up
method like barrier methods have to used in the first month, if
the menustral cycle is regular, if there is delay in taking the pill
on time or if missed and if a woman is taking drugs that
accelerate clearance of the progesterone from the body like anti
epileptics and anti TB drugs.
Failure rate is about 0.5 – 2 per 100 women years.
3. Injectables contraceptives
These are long acting reversible contraceptives containing

progesterone preparations. Preparations commonly used are
depomedroxy progesterone acetate (DMPA), also called Depo-
Provera and norethisterone enanthate (NET-EN). Both are
administered intramuscularly; DMPA in a dose of 150 mg every
three months or 300 mg every six months and NET – EN in a
dose of 200 mg given at two months intervals. They are
administered by deep intramuscular injection. The site of
injection should not be massaged. There is a grace period of 2
weeks for Depo-Provera, in which the client may be late for
injection without increased risk of pregnancy. This does not
work for NET-EN.
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The mechanism of action is mainly by inhibition of ovulation by

suppressing the mid cycle LH peak. Additional effects include
cervical mucous thickening and endometrial atrophy which
prevents blastocyst implantation.
The advantages are similar to that of the mini pills. In addition

injectable contraceptives avoid the need of daily administration
of the drugs. It causes amenorrhea thus relieves menustral
disorders like menorrhagia and dysmenorrhea. It is not affected
by gastrointestinal functions. Because it is not visible, it is
culturally acceptable in most settings. It protects against
endometrial cancer. Unlike other hormonal contraceptives, it is
devoid of drug interactions like antiepileptics.
The disadvantages are related to the side effects that it causes.

These include weight gain, headache, and back pain, loss of
hair and mood changes. There is delay in return of menses and
fertility of upto 8 months after discontinuation. The other
disadvantage is once the drug is injected it can not be retrieved,
thus side effects can not be reversed promptly.
Failure rate for DMPA is < 1% per hundred women year.
4. Implants (Norplant)
Norplant is a long term, extremely low dose reversible progestin

only contraceptive method that is effective for a period of 5
years.. It has six silastic rubber capsules each containing 36 mg
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of levonorgestrel. This hormone is released by slow diffusion

over a period of five years. It is placed sudermally in a fan like
manner into the inner aspect of the nondominant arm by sterile
minor surgical procedure.
The mechanism of action is similar to Depo-Provera. It inhibits

ovulation in 90% of the cycles for the first year. This effect
gradually wanes as the years of use increase.
The advantages are similar with Depo-Provera. Unlike Depo-

Provera, it is effects are immediately reversed upon removal.
There is no delay in return of fertility. It is suitable for women
who have completed their family but do not desire
permanent sterilisation.
The disadvantages are procedure related like the need for

professional for insertion and removal, need for minor surgical
procedure, inflamation and infection at the insertion site and
visibility of the implants. It has also higher initial cost. Failure
rate is increased in women taking anticonvulsants and anyiTB
drugs. Breakthrough bleeding may be troublesome. Other side
effects like weigh gain, mood changes ,hair loss and back pain
are common.
The indications for removal are prergnancy, client request,

infection at the site of insertion, spontanous expulsion of one or
more of the implants, after 5 years of use, and development of
476
serios side effects like migraine headache, bluuring of vision,

unilateral leg pain and swelling and chest pain.
Failure rate is 0.1 per 100 women years which increases with
years of use.
E. VOLUNTARY STERILIZATION (SURGICAL

CONTRACEPTION)
Surgical contraception is a permanent method of contraception.

The operation done on male is vasectomy and that on the
female is bilateral tubal ligation (occlusion). It is important to
explain to the clients that all operative sterilizations are intended
to be permanent. Consent for the operation should be signed
after counseling.
1. Male voluntary sterilization- Vasectomy
It is a permanent sterilization operation done in the male, where

a segment of both vas deferens is resected and the cut ends
are ligated. It is a simple outdoor minor surgical procedure
requiring minimal training.
Immediate and late complications are few. Impotence mainly of

psychological nature may develop. It does not increase the risk
477
of testicular cancer. Failure rate is 0.15% and there is a fair

chance of success of reversal anastomosis operation (50%).
The procedure is not immediately effective. It usually takes 2-3

months or about 20 ejaculations before the semen is free of
spermatozoa. Therefore, additional contraceptive protection is
needed for about 2-3 months following operations. Confirmation
by semen analysis is needed after 3 months.
2. Female voluntary sterilization- tubal ligation
Occlusion of the fallopian tubes is the most popular method of

surgical contraception, especially in areas where high parity
births prevail in a comparatively younger age group. It is also
widely accepted in the affluent countries. The procedure is
immediately effective.
Timing of operation
 Postpartum tubal ligation - If the patient is otherwise

healthy, the operation can be done 24 – 48 hours following
delivery. Its chief advantage is technical simplicity.
 Postabortal tubal ligation - Sterilization performed along

with elective abortion.
 Interval tubal ligation – The operation is done after 3

months following delivery or after 3 weeks following
478
abortion. The ideal time of operation is following the

menstrual period in the proliferative phase.
It can be done during caesarian section or by minilaparatomy

or by laparoscope. Either ligation methods or mechanical
occlusion or electro coagulation are used to occlude the tubes.
There are various techniques of ligating the tubes, the
commonest one being the Pomeroy method.
Failure Rate in tubal sterilization is about 0.7%.
F. EMERGENCY CONTRACEPTION
This is a kind of contraception that is used in the prevention of

pregnancy following an episode of unprotected intercourse
during the fertile period. It used to be called morning after pill
or post coital pill.
There are two types of emergency contraception.
I. Hormonal emergency contraception
These act by temporarily disrupting ovarian hormone production

causing absent or dysfunctional luteal phase. This results in
development of out of phase endometrium that is not suitable
for implantation.
They have to be taken within 72 hours of unprotected

intercourse. There are a variety of regimens. The commonest
479
one is Yuzepe regimen. In this method two doses of

combination of ethinyl estradiol and norgestrel is taken 12 hours
apart. The first dose should be taken as early as possible as but
no later than 72 hours after intercourse. The total dose of
ethinyl estradiol is 0.2 mg and that of norgestrel should be 2 mg
(2 tablets of standard dose pills like Ovral taken 12 hours
apart).
The side effects are nausea, vomiting, breast tenderness,

headache and menustral disturbance. Incidence of ectopic
pregnancy is increased. Therefore, women should be
counseled to report if they miss their menses and develop lower
abdominal pain.
II. Mechanical emergency contraception
This involves inserting an intrauterine devise within 5 days of

unprotected intercourse.
Review Questions
1. Describe the GATHER approach.
2. Describe the natural family planning methods.
3. Describe the different barrier methods.
480
4. List the contraindication for combined pills.
5. Describe the complications of IUCD.
6. Describe the norplant.
7. Describe the emergency contraception.
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CHAPTER 29
INFERTILITY
Learning objectives
 To define and classify infertility
 To list the causes of infertility
482
 To describe the diagnostic work up of infertile couple
 To list the management modalities of infertility
1. Definition and classification
Infertility is failure of a woman to conceive after one year of

unprotected intercourse (without contraception) if the woman is
>35 years and after two years if the woman is <35 years. There
are two types of infertility
 Primary infertility - if conception has never occurred

before.
 Secondary infertility - if there was history of pregnancy

before the current problem, irrespective of its site and
outcome.
2. Epidemiology
Incidence varies according to the socioeconomic and

geographic factors. Globally 8 - 12% couples face problem of
infertility in their life time. In sub-Saharan Africa the incidence
rises to 20 - 30% where around 8-10 million women are
estimated to be infertile. In addition to the personal
psychosocial trauma (shock, denial, depression), infertility has
an impact in the couple‘s relations that can lead to marital
disharmony and divorce.
483
3. Etiology
In 85- 90% of infertile couple a probable cause is found. In 10-

15% the infertility is unexplained. The causes of infertility could
arise either from the female or the male or both. According to
WHO, male cause accounts for 8-22%, female cause accounts
for25-37% and both partners are responsible for 21 – 38%.
Globally the most common causes are:
 Tubal factor, which accounts for 20- 30 % of infertility,

arises from congenital or acquired obstruction of the
fallopian tubes. Acute PID is the commonest cause of
tubal obstruction.
 Male factor, which accounts for 15-25% of infertility,

arises either from failure of spermatogenesis (testicular
failure) or more commonly from obstruction of the vas
deferens. Gonococcal infection is the commonest cause of
obstruction of the vas deferens.
 Ovulatory factor, which accounts for 10-15% of infertility,

arises from any condition that cause anovulation. This may
arise from disease conditions affecting the hypothalamus,
pitutary and the ovaries.
 Pelvic factor, which account for 10% of infertility, is mainly

the result of endometriosis.
484
 Cervical factor, which account for 15% of infertility, arises

from structural abnormality of the cervix (like cervical
atresia and stenosis) and functional abnormality of cervical
mucus (like cervicitis, hormone deficiency or colonization
by mycoplasma).
 Immunologic factor occurs as the result of development

of antisperm antibodies by the woman or her partner.
4. Diagnostic evaluation
The goals are detection of a possible cause, providing accurate

information about prognosis, providing guidance on treatment
options and providing continuous counseling.
The approach should ideally include both partners at the initial

assessment. Joint interview of couple should be followed by
separate private consultation. Based on the findings a variety of
investigations are ordered.
I. Evaluation of male partner
History: age, previous paternity, sexual history (technical

difficulty, history of STI, malformations of penis), medical history
(trauma, mumps, chronic medical illness, prolonged febrile
485
illness), drug history (including alcohol and smoking), surgical

history (mainly inguinal and scrotal), occupation (toxins,
prolonged heat) and review of systems (breast enlargement,
headache, exercise), previous tests and results.
Physical examination: general appearance, male habitus, hair

distribution, breast enlargement, voice, external genitalia (penis
and scrotum), rectal examination (prostate).
II. Evaluation of female partner
History: age, menustral history (including ovulatory symptoms

like mid cycle pain, dysmenorrhea, breast pain), contraceptive
history (duration, type, date of last use), obstetric history
(especially on abortion, ectopic pregnancy, post partum
hemorrhage), sexual history (frequency, regularity, timing
around mid cycle, STI, PID), surgical history (especially pelvic
operation), medical history (medical illness, breast discharge),
drug history (type, duration), review of systems (diet, weight,
exercise)
Physical examination: general appearance, thyroid, secondary

sexual characteristics, breast discharge, uterine/ adenexal
mass, uterine position and mobility, adenexal tenderness, visual
fields
III. Investigations
A. Baseline for both partners

486
Hemtocrite, white cell count, ESR, urinalysis, VDRL, fasting

blood sugar
B. Investigations for the male
Seminal analysis
This is the most important fertility evaluation for the male. A

normal test usually excludes significant male factor. An
abnormal result must be repeated after 3 months. The test is
done after 3-7 days of abstinence. Specimen should be
examined within 60 minutes of collection.
Normal parameters are volume of 2- 6 ml, total sperm count 20

– 250 million /ml, sperm motility of > 60% by subjective
methods, sperm morphology of > 50% normal and celularity
of < 10 WBC / ml without significant agglutination. Of these the
most important parameters are the sperm count and motility.
Extended tests
These are done for those with abnormal seminal analysis.

These include endocrine assay (TSH, T3 /T4, FSH, LH,
testosterone, prolactin), skull X-ray for sella turcica, sperm
antibody testing and others.
C. Investigations for female
Documentation of ovulation
487
History suggestive of ovulation is midcycle pain, premenstrual

molmina and primary dysmenorrhea. Indirect tests of ovulation
determine the presence of sufficient amount of progesterone in
the body. These tests are recording the basal body temperature
for three cycles (biphasic shift), determining midluteal phase
serum progesterone level (> 25ng//L), endometrial biopsy at
21st day of the cycle( secretary endometrium), cervical mucus
examination after expected time of ovulation ( thick, yellowish
with no ferning) and vaginal cytology for maturation index.
Hysterosalpingography (HSG)
This assesses tubal patency. It is done in the early part of the

follicular phase.
Post coital test (Sims Hunner Test)
This assesses the cervical factor. It is done by aspirating

cervical mucus from the cervical canal at the level of the
internal os 2–4 hours after sexual intercourse. A satisfactory
result is finding of >10 motile spermatozoa with good forward
movement under high power field in the presence of adequate
cervical mucus.
Other tests
These include endocrine assay for anovulatory women (TSH, T3

/ T4, FSH, LH, estradiol, prolactin levels), laparoscopy/
488
laparatomy for assessing pelvic factors), determination of

sperm antibodies and others.
5. Management
Management depends on the specific cause.
Male factor infertility
It is directed against the cause.
There is no treatment for azospermia from primary testicular

failure. Azospermia from secondary testicular failure is treated
by hormone replacement (GnRh agonists and human
menopausal gonadotrophins). Azospermia from obstruction of
the vas deferens can be treated by microsurgical vasovasotomy
or by aspiration of the sperm followed by invitro fertilization.
A number of interventions to improve the quality of the sperm

have been used in those abnormal or border line oligospermia
or asthenospermia. These include drags like clomiphene citrate
or bromocryptine, surgery for varicocele, exercise modification,
change in occupation, abstinence from alcohol and smoking
and avoiding hot baths. Treatment with testosterone has limited
value.
Other interventions include surgical correction of hypospadias

and epispadias.
Female factor infertility
489
I. Anovulation: ovulation induction by clomiphene citrate. Other

drugs like human menopausal gonadotrophins are not available
in Ethiopia. Underlying medical causes like hyperprolactinemia
and hypothyroidism have to be treated with appropriate drugs.
II. Tubal factor: surgical correction by tuboplasty
III. Cervical factor: antibiotics like erythromycin and tetracycline

for cervical infection and colonization by mycoplasma, hormonal
treatment for inadequate cervical mucus
IV. Immunologic factor: modalities of treatment that are tried

include occlusive therapy by condom for 6- 9 months, immune
suppression by steroids, suppression of spermatogenesis and
intrauterine insemination.
Other treatment options
These should be offered to couple in whom treatment for

infertility fails. They include adoption, and where feasible
assisted reproductive technology and serrogation.
Review Exercises
1. Define infertility and describe its types.
2. Discuss causes of infertility and their diagnostic methods.
490
3. Briefly describe the management modalities of infertility.
491
492
CHAPTER 30
TUMOURS CONDITIONS OF THE FEMALE GENITAL
TRACT
LEARNING OBJECTIVES
 TO KNOW THE EPIDEMIOLOGIC FEATURES OF

GENITAL TRACT TUMORS
 TO KNOW THE APPROACH TO PATIENTS WITH

GENITAL TUMORS
493
 TO UNDERSTAND THE GENERAL PRINCIPLES

AND MANAGEMENT OPTIONS GENITAL TRACT
TUMORS
Like any organ system in the body, a variety of benign and

malignant tumors develop in the female genital tract. No part of
the genital tract is immune for tumors, but the relative frequency
varies. In most the exact cause is unknown. The manifestations
are varied and range from absence of symptoms to symptoms
affecting local or distant organs. Depending on the site, the
common presenting complaints are abnormal vaginal bleeding,
postmenopausal bleeding, abnormal vaginal discharge, vulvar/
abdominal mass, pruritis and pelvic/ abdominal pain. The
diagnostic modalities include cytologic studies,
histopathological studies and other advanced investigations like
tumor markers and computerized tomography. The
management options are surgical excision, radiotherapy and
chemotherapy.
BENIGN CONDITIONS OF THE FEMALE GENITAL TRACT
1. Vulva
 White lesions include lichen sclerosis and hyperplasic

dystrophy.
494
 Hidradenoma: are lesions originating from the apocrine

sweat glands. They are seen in women in their twenties
and thirties.
 Pigmented nevus occurs on the vulva. It carries a risk of

subsequent malignant transformation due to junctional
activity. Thus, excisional biopsy should be performed on
all pigmented lesions on the vulva.
 Fibromas are uncommon and when present in the vulva

are usually fibromyomas or fibroangioma.
 Hemangioma Vulva may be
 Ulcerative lesions could arise following trauma or may be a

manifestation of STI (syphilis, chancroid, granuloma
inguinale, lymphogranuloma venereum, and genital
herpes) or may be a sign of systemic condition (Crohns
disease and Bahcets disease). Persistent ulcerative
condition of the vulva should arouse suspicion of vulvar
cancer and should be biopsied.
2. Vagina
Inclusion cyst
Gartner (mesonephric) duct cyst
Endometriosis
Adenosis
495
3. Cervical polyp
Cervical polyp is a localized overgrowth of the endocervical

glands. It manifests with abnormal vaginal discharge,
intermenustral bleeding and contact bleeding. Speculum
examination shows a polypoid soft mass protruding through the
cervical os. Management is polypectomy.
4. Endometrial polyp
Endometrial polyp is a localized growth of the endometrium

which could be sessile or pedunculated. In some cases it may
be long enough to protrude through the cervix where it may be
confused with cervical polyp. It may be asymptomatic.
Symptoms include intermenustral bleeding, menorrhagia and if
it protrudes through vaginal discharge. Physical findings are
minimal. Diagnosis is made by hysterosalpingography or
hysteroscopy. Removal by dilatation and curettage is the
treatment.
5. Uterine liomyoma (Fibroids, Myoma)
5.1. Definition and classification
Liomyoma is a benign tumor of the smooth muscle cells of any

mullerian duct organs especially the myometrium often with
some admixture of fibrous tissue. It could be single or multiple.
Size ranges from 1mm to 20 cm in diameter. Depending on the
location liomyomas are classified as
496
 Interstitial or intramural myoma is located in the

myometrium and accounts for 70 % of myomas.
 Submucus myoma is a myoma that grows into the

endometrial cavity. When a submucus myoma protrudes
into the cervical canal and the vagina it is called delivered
myoma.
 Subserous myoma is a myoma that grows to the serosal

surface, thus distorts the surface of the uterus. Sometimes
a subserous myoma gets detached from the uterus and
gets its blood supply from another intraabdominal organ
especially the omentum. This kind of myoma is called
parasitic myoma. A subserous myoma that grows
between the leaves of the broad ligament is called
intraligamentary (broad ligament) myoma.
 Cervical myoma is a myoma that grows on the cervix.
5.2. Epidemiology and etiology
It is the commonest tumor of the uterus. It is found in 20-25 %

of women in reproductive age group. It is more common in
blacks.
The etiology of myoma is unknown. But translocations and

additions of several chromosomes, mostly affecting
chromosome 12 is observed in myomatous cells. Growth of
myoma is related to the presence of estrogen. This explains
497
why myomas are rare before puberty and why they atrophy
after menopause.
5.3. Secondary changes
Myomas usually have a firm consistency and are non tender.

But with subsequent growth, they undergo secondary changes,
which give them a varied consistency.
 Hyaline degeneration gives it a soft consistency.
 Cystic degeneration gives it a cystic consistency.
 Fatty degeneration usually occurs after menopause and

is a precursor for calcareous degeneration.
 Calcareous degeneration (womb stone) occurs when

calcium is deposited in the myoma. This gives it a hard
consistency.
 Red (carneous) degeneration occurs as the result of

ischemic necrosis from obstruction of the venous return
during pregnancy. This results in tender swelling of the
myoma. It resolves in 1-2 weeks.
 Sarcomatous degeneration is a malignant transformation

of a myoma. It should be suspected when there is
significant growth of a myoma in a short period associated
with pain. It usually occurs in postmenopausal women.
The incidence is 1:1000.
498
 Suppurative (infective) degeneration usually occurs in

submucosal types.
Symptoms depend on the site of the myoma. Approximately 35-

50% of myomas are asymptomatic. Symptoms are varied and
include:
 Abnormal uterine bleeding is the commonest presenting

symptom. It usually takes the form of menorrhagia and
may cause significant anemia. Intermenustral and contact
bleeding may occur in delivered myoma.
 Pressure symptoms like frequency of urination, intermittent

overflow incontinence (urinary bladder), constipation
(rectum), pelvic pain (pelvic nerves, torsion, red
degeneration), edema of the extremity (vena cava or iliac
vein) or flank pain (hydronephrosis from ureteric
obstruction).
 Painless gradually enlarging suprapubic mass
 Abnormal vaginal discharge in submucus type
 Pelvic pain from torsion, infection, red degeneration or

pressure on pelvic nerves
 Reproductive symptoms like Infertility, recurrent abortion

and preterm labour
499
The physical findings depend on the site, size and number.

Submucosal myomas cause symmetrical enlargement of the
uterus while interstitial and subserosal ones cause asymmetric
enlargement of the uterus. The typical finding is a firm, irregular,
non tender mass attached to the uterus (moves with the cervix).
Degenerative changes may give a myoma varied consistencies.
Diagnosis is reached with history and physical examination in

95 % of cases. Additional diagnostic modalities are ultrasound,
hysterosalpingography and hysteroscopy.
5.5. Complications
Medical complications are anemia, uremia and rare reports of

hypoglycemia and polycythemia.
Gynecologic complications are torsion with gangrene,

sarcomatous change, rupture of surface vessel with
intraperitoneal bleeding, chronic inversion and infection of
delivered myoma.
Obstetric complications are infertility, recurrent abortion,

preterm labour, red degeneration, malpresentation, uterine
inertia, obstructed labour, postpartum hemorrhage and
postpartum necrosis.
5.6. Differential diagnosis
500
Pregnancy, adenomyosis, congenital malformation of the

uterus, tuboovarian inflammatory and neoplastic conditions and
conditions that cause abnormal uterine bleeding
5.7. Management
There are two types of management for myomas.
I. Conservative medical management
This is indicated for asymptomatic myomas of less than 12

weeks. Monitoring of the growth of myoma by biannual pelvic
examination and serial hemtocrite determination is done.
Where available, drugs like GnRh agonists are given to reduce
the size and amount of bleeding.
Another indication for medical management is red degeneration

during pregnancy. The treatment includes bed rest, analgesics
and/or tocolytics. Laparatomy is only done if the diagnosis is
uncertain.
II. Surgical management
The indications are AUB leading to anemia, size of more than

14 weeks, and rapid increase in size especially after
menopause, hydronephrosis from myoma, infertility and
recurrent abortion resulting from myoma, uncertain nature of
the tumor and severe pain from torsion.
501
The type of surgery is determined by the site and the desire for
future fertility. It ranges from conservative abdominal or vaginal
n\myomectomy to total abdominal hysterectomy. Hysterectomy
is the definitive treatment of myomas.
6. Ovaries
I. Functional (physiologic) cysts
 Follicular cysts result from failure of ovulation and are

usually multiple with average size of 2 cm in diameter.
Besides causing abnormal uterine bleeding (usually
Oligomenorrhea with menorrhagia), they rarely cause
symptoms. They regress within 8 weeks.
 Corpus luteum cyst is usually unilateral and rarely

exceeds 4 cms in diameter. It causes AUB in the form of
oligomenorrhea. In most they are asymptomatic.
Symptoms are related to size and complications like
hemorrhage, rupture and torsion. It resolves
spontaneously within 8 weeks.
 Theca luteum cyst is the least common functional cyst. It

occurs in women with hydatidiform mole and
choriocarcinoma. It is usually bilateral with size ranging
from microscopic size to more than 15 cm in diameter.
Symptoms are continued pregnancy symptoms and
502
occasionally pelvic and lower abdominal discomfort. It

regresses after successful treatment of the associated
conditions.
II. Inflammatory lesions
Tubo-ovarian complex or abscess and post vaginal

hysterectomy ovarian abscess often cause tender masses.
III. Hyperplasic lesions
 Polycystic ovaries are found in Stein Leventhal

syndrome (polycystic ovarian syndrome) which manifests
with obesity, oligomenorrhea /amenorrhea, hirsutism and
infertility from anovulation.
 Others include leuteoma, serous inclusion cysts and

endometrial cysts.
IV. Benign ovarian neoplasms
Depending on the histology the various types of benign ovarian

neoplasms are epithelial neoplasms, gonadal stromal tumors,
nonintrinsic connective tissue tumor and germ cell tumors.
Epithelial tumors are the commonest benign ovarian tumors.
They usually occur during the reproductive age. Thecoma and

Brenner tumors usually occur in postmenopause. Size varies
and may reach upto 30 cm in diameter in mucinous
503
cystadenoma. They usually present as pelvic or abdominal

mass. Those secreting hormones present with AUB.
Peculiar features of some benign ovarian tumors
 “Pseudo mamma bodies” which are calcified concretion

apparent on plain x-ray is seen in serous cystadenoma.
 ―Abnormal sexual development‖ is seen in

gonadoblastoma. Thus, gonadal removal after puberty is
recommended as there is a 25% risk of developing
malignancy
 “Meig’s syndrome‖, is occurrence right side pleural

effusion and ascitis with Brenner tumor.
 Cystic teratoma (dermoid cyst) – contain sebaceous

material, teeth; sweat glands, nervous tissue and skin.
 “Struma ovari‖ is a variant of cystic teratoma that has a

thyroid tissue and manifests with thyrotoxicosis
SURGICAL EMERGENCIES IN BENIGN OVARIAN

TUMORS
 Torsion of an ovarian cyst is more common in right

ovary especially in pregnant and children
 Hemorrhage into the ovarian cyst
504
 Rupture of and ovarian cyst may occur due to bleeding,

torsion or trauma
Management
Surgical removal is indicated for any of the following:
 Premenarchal or postmenopausal palpable adenexal mass

whether cystic or solid
 Solid adenexal mass during reproductive age
 Cystic adenexal mass that is more than 8 cm in diameter
 Cystic adenexal mass of < 8 cm that persists for more than

8 weeks
 Development of surgical emergencies
Observation with close follow up (clinical examination and serial

ultrasound) is indicated for cystic adenexal masses in
reproductive age with size of < 8 cm in diameter.
7. Endometriosis
7.1. Definition
It is the presence of functioning endometrial glands and stroma

outside their usual location in the uterine cavity, resulting in
pelvic adhesion. Common sites of endometriosis are ovaries,
tubes, uterosacral ligament, recto sigmoid colon, and bladder.
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7.2. Epidemiology and pathogenesis
It affects women in their reproductive age years and regresses

after menopause. The different theories in its pathogenesis are
 Retrograde menstrual flow
 Metaplasia of coelomic epithelium
 Vessel spread ( blood vessels or lymphatic

vessels)
 Genetic and immunologic influence
Symptoms are secondary dysmenorrhea, dysparunia, chronic

pelvic pain; Infertility Signs are fixed reteroverted uterus
adenexal mass and indurations of the rectovaginal septum.
Diagnosis is made by pathologic examination of biopsied tissue
obtained at laparatomy/ laparoscopy.
7.4. Management
This is dictated by age, extent of the diseases, and desire for

future fertility. The options are medical treatment (nonsteroidal
anti-inflammatory drugs, danazol, OCP, progestins and GnRH
agonists) and surgical treatment (conservative or radical
surgery).
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MALIGNANT CONDITIONS OF THE FEMALE GENITAL

TRACT
1. Vulvar cancer
It is an uncommon tumor accounting for 3- 5 % of primary

genital tract cancers. It is a disease of postmenopause with an
average age of 60-65 years. Etiology is unknown STI agents
like human papilloma and herpes simple type 2 viruses are
implicated. Conditions that cause chronic vulvar irritation like
diabetes mellitus, vulvar dystrophy and granulomatous STIs
(LGV) predispose to vulvar cancer.
More than 90% of primary vulvar cancer is squamous cell type.

Others include melanoma, basal cell carcinoma and verrucous
carcinoma. More than 65% arise from the labia majora and
minora.
Squamous cell carcinoma usually starts as dysplasia of the

vulvar skin in the third and fourth decades of life. This usually
manifests as pruritis or lump on the vulva. It spreads by direct
extension and by lymphatics to involve the inguinal, femoral and
pelvic lymph nodes.
Despite its anatomic location late diagnosis is common mainly

from reluctance of elderly patients to seek medial advice and
neglect of the health care worker to investigate vulvar pruritis
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and lesions. The main symptoms are long standing pruritis,

vulvar mass and ulcer. Diagnosis is made by biopsy.
Note: All women with grossly suspicious vulvar lesion, confluent

wart like mass, ulceration that persists for more than 1 month
should be referred for biopsy.
Surgery is the main stay of management with or with out

adjuvant radiotherapy and chemotherapy.
2. Vaginal cancer
Primary vaginal cancer is not common. The variants of primary

vaginal cancer are epidermoid (accounts for more than >75%),
clear cell adenocarcinoma, sarcoma and melanoma. It accounts
for 2 – 4% of genital canal cancer. The mean age of occurrence
is 55 years. Secondary vaginal cancer is the common form of
cancer affecting the vagina. The commonest primary site is the
cervix followed by endometrium.
Clinical features are bloody vaginal discharge, ulceration or/and

exophytic vaginal lesion, pelvic pain and edema. Diagnosis is
made by histologic examination of biopsied material from the
vaginal lesion.
Differential diagnosis includes granulomatous infections like

LGV and genital tuberculosis, chemical/ trauma induced
ulcerations and endometriosis.
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Treatment options include surgery and radiation therapy.
3. Cervical cancer
3.1. Classification and staging
70-80% of cervical cancer is squamous cell type. It almost

always (>90%) arises from the transformation zone of the
cervix at the squamocolumnar junction. It starts as dyplastic
change which eventually progresses to cervical cancer in situ
and finally to invasive cancer. This is a slow process which
takes 7-10 years.
The next common type of cervical cancer is adenocarcinoma

which arises from the endocervical glands.
Cervical cancer spreads mainly by direct extension (vagina,

uterus, parametrium, bladder and rectum) and by lymphatic
spread (pelvic lymph nodes, paraaortic nodes). Depending on
the progress it is staged clinically into four stages.
Stage O: Carcinoma in situ: Intraepithelial carcinoma
Stage I: Confined to the cervix
Stage- II: Extends beyond the cervix onto either the vagina or
parametrium but not to the lower 1/3 of the vagina and
not to the pelvic wall.
Stage III: Extension either to the lower third of the vagina or to

the pelvic wall.
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Hydronephrosis or non-functioning kidney with no

apparent cause necessitates allocation to III B.
Stage IV: Extension beyond the true pelvis or involvement of

mucosa of bladder or rectum
3.2. Premalignant lesions of the cervix (Cervical

intraepithelial neoplasia)
Squamous cell carcinoma of the cervix develops from precursor

lesions of the cervix called cervical intraepithelial neoplasia
(CIN), previously called cervical dysplasia. This is an abnormal
growth of cells in the transformation zone of the cervix that
develops from the squamocolumnar junction of the cervix.
Depending on the depth of the cervical epithelium, there are

three types of CIN namely CIN1 (mild dysplasia), CIN2
(moderate dysplasia) and CIN3 (severe dysplasia or carcinoma
in situ).
Majority of CIN1 remain static or regress with only few

progressing to CIN2. Significant proportions (20-25%) of CIN2
progress to CIN3, the rest remain static or regress. CIN3 is
universally agreed to be a true cancer precursor with 30-70 %
developing cervical cancer over 10 years time.
CIN lesions are characteristically symptomless. On naked eye

examination, the cervix is normal. Diagnosis is only made after
biopsy. Detection needs special examinations. These include
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 Pap smear (cervical exofoliative cytology), which is an

ideal screening test for cervical cancer. It should be done
periodically (every 1 to3 years depending on the risk
factors) in all sexually active women.
 Colposcopy
 If the above tests show abnormal result biopsy is

recommended.
Management includes ablation (destruction) of the

transformation zone or conization of the cervix or hysterectomy.
3.2. Etiology and risk factors
The exact cause of cervical cancer is unknown. But it is known

to be a sex associated disease, being rare in virgins. A number
of sexually associated factors were implicated. Of these, human
papilloma virus types 16, 18 and31 are strongly associated with
cervical cancer. The risk factors for development of cervical
cancer are
 Sexual intercourse at an early age
 Multiple sexual partners
 High risk male partner (promiscuous partner, contact with

cervical cancer patient)
 Immunosuppression like HIV/AIDS
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 Smoking
 Young age at first pregnancy
3.3. Epidemiology
Previously cervical cancer was the leading cancer of the genital

cancer. But now its incidence is decreasing because of early
detection of preinvasive stage of the cancer. In areas where
regular screening is not available it is still a common
gynecologic cancer. Cervical cancer is the third most-common
cancer world wide and the leading cause of death among
developing country women. An estimated 466,000 new cases of
cervical cancer occur annually among women world wide; about
80% occur in developing countries.
3.4 .Clinical features and diagnosis
In early stages, cervical cancer is usually asymptomatic

emphasizing the importance of cytological screening to detect a
cancer as early as possible.
Early symptoms include abnormal vaginal discharge which is

offensive and watery and abnormal uterine bleeding.
Intermenustral bleeding post coital and contact bleeding and
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postmenopausal bleeding are the usual forms of AUB. In

advanced cases the patient presents with pelvic and back pain
and symptoms of uremia. Some times leg edema develops.
In early stages the cervix appears normal. As the disease

advances two types of appearance may be seen depending on
whether the lesion is endophytic or exophytic. In exophytic
lesions the cervix develops an ulcer and later cauliflower like
growths into the vagina which easily bleed to touch. In
endophytic type the cervix is hard and nodular with variable
surface ulceration. In advanced cases there is infiltration of the
vagina and necrosis of the tumor on the cervix. Involvement of
the rectum and the parametrial tissues is found on rectal
examination.
Diagnosis is made by pathologic examination of the tissue

taken from the transformation zone or from grossly abnormal
sites on the cervix. Whenever a gross cervical lesion is
present, referral for a biopsy is indicated.
3.5. Complications
Uremia is the leading cause of death. Other complications are

severe bleeding, sepsis and pulmonary embolism.
3.6. Management
There are two options of management.
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 Surgical management - (total abdominal hysterectomy and

pelvic lymphadenectomy) for stages upto IIb
 Radiotherapy – for all stages
3.7. Prevention
Invasive cancer of the cervix is considered a preventable

cancer because it has a long preinvasive state, a sensitive
screening method to detect preinvasive stages and effective the
treatment for pre-invasive lesions.
Papanicoaus smear is a cervical cytology study that should be

done in all sexually active women every 1-3 years. It is an ideal
screening test for detection of precancerous stage of cervical
cancer.
4. Endometrial cancer
Endometrial cancer is an adenocarcinoma of endometrial

glands. There are different histologic variants with different
impact on the prognosis. Some of these variants are
endometriod type carcinoma, adenosquamous carcinoma, clear
cell carcinoma, papillary carcinoma and secretory
adenocarcinoma.
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It spreads mainly by direct contagious and lymphatic routes. In

late cases haematogenous spread occurs. Unlike cervical
cancer, endometrial cancer is staged surgically.
4.2. Etiology and risk factors
Most develop in hyperestrogenic states with unopposed

estrogen action without cyclic influence of progesterone.
Antecedent endometrial hyperplasia is found in most
endometrial cancers. The risk factors are
 Age of 55- 65 years (postmenopausal), rarely occurs

before 40 years
 Early menarche, delayed menopause
 Infertile or history of repeated abortions, nulliparity
 Obesity , hypertension, diabetes and middle class life style
 Hyperestrogenic states like chronic anovulation (Stein

Leventhal Syndrome), estrogen secreting tumors,
exogenous estrogen use
4.3. Epidemiology
The incidence is 12-15 /100000 women and increasing over the

years. The peak age is 60-70 years. It is mainly a disease of
post menopause which accounts for 75% of the cases. 15%
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occurs in the perimenopausal period and the rest in the

premenopausal time.
The principal symptom is abnormal uterine bleeding. It is

usually of postmenopausal type with scanty, small and
recurrent bleeding. In the premenopausal period it may take the
form of menorrhagia, polymenorrhea and intermenustral
bleeding. The second common symptom is abnormal vaginal
discharge which is usually offensive. In advanced disease
pelvic pressure from hematometra/ pyometra, weight loss and
debility occurs.
The usual finding on physical examination is moderately

enlarged uterus.
Diagnosis is reached by histopathological examination of

endometrial tissue. This can be done by simple endometrial
biopsy/ curettage/aspirate or commonly by fractional curettage
which is considered to be the gold standard for diagnosis..
Note: All women with abnormal uterine bleeding in the

perimenopausal and postmenopausal period should be
referred for diagnostic curettage and surgical staging.
4.5. Management
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The definitive management is surgery (total abdominal

hysterectomy + bilateral saphingeophorectomy + pelvic
lymphadenectomy) supplemented by radiation and/ or
chemotherapy.
4.6. Complications
These include hematometra, pyometra and perforation / rupture

of uterus.
5. Ovarian cancer
Ovarian cancer is classified by the histologic types. Epithelial

tumors are the commonest accounting for 90% of all ovarian
cancers. The remaining 10 % include germ cell, gonadal
stromal, nongonadal stromal and unclassified tumors.
Ovarian cancer spreads mainly by transperitoneal route and by

direct extension. It also uses lymphatic and in advanced cases
haematogenous routes. Staging is done surgically during
laparatomy.
5.2. Epidemiology and risk factors
Risk for epithelial cancers increases upto 80 years of age. It

accounts for 4% of cancers in women and contributes for 40%
of deaths related to gynecologic cancers. It is called the silent
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killer because of nonspecific symptoms and difficulty in

accessing the ovaries by physical examination and absence of
reliable screening test for detection of early lesions.
Some of the risk factors for epithelial ovarian cancer are high fat
diet, early age at menarche, late menopause, and history of
premenstrual syndrome, nulliparity, celibacy and repeated
abortions.
Symptoms are non specific and are usually absent in early

stages. These include nausea, vomiting, bloating abdominal
fullness constipation and flatulence. Hormone secreting tumors
are associated with AUB. Weight loss is a late manifestation.
In early stages there will not be any abnormal physical finding

but later one may find ascitis, pelvic or abdominal mass,
hepatomegally pleural effusion and lymphadenopathy (inguinal
or supraclavicular).
Definitive diagnosis is made by histopathology of a biopsy

made during laparatomy.
5.4. Management
Surgery (total abdominal hysterectomy, bilateral

saphingeophorectomy, omentectomy, appendectomy along with
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resection of grossly visible lesions) supplemented by

chemotherapy and or radiotherapy
Review questions
1. Discuss the degenerative changes and clinical features of

myoma.
2. Discuss the risk factors, complications and prevention of

cervical cancer.
3. List the indications for surgery for an adenexal mass.
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CHAPTER 31
UTEROVAGINAL PROLAPSE AND URINARY

INCONTINENCE
Learning objectives
 To discuss the anatomic supports of the uterus and vagina
 To classify uterovaginal prolapse
 To discuss the causes of uterovaginal prolapse
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 To discuss the diagnosis and management of uterovaginal

prolapse
 To list the different types of urinary incontinence and their

clinical features
 To discuss the different tests used in the diagnosis of

urinary incontinence
1. UTEROVAGINAL PROLAPSE
Anatomic supports of the uterus and vagina
A condensation of the parietal endopelvic fascia running from

the back of the symphysis pubis to the ischial spines provides
the origin of the levator ani muscle. The parietal endopelvic
fascia over the levator ani is condensed in certain areas to
forming ligaments that are very important in supporting the
uterus. Of these ligaments the cardinal ligament or
Mackenrodt’s ligament is the most important one. It runs from
the lateral sides of the cervix to the lateral pelvic wall. The
others are uterosacral ligament and pubocervical fascia.
In addition to the facial supports of the cervix, the uterus

receives from the round ligaments, which keep it anteverted
and the infundibulopelvic ligaments. Another significant aspect
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to the anatomic support of the uterus is its anteverted and

anteflexed position in relation to axis of the vagina.
The levator ani and the perineal muscles along with the
rectovaginal septum provide the most important muscular
support for the vagina.
Definition and types
Uterovaginal prolapse is the downward descent of the

uterus and the vagina from their normal pelvic positions.
Fundamentally, there are two types of genital prolapse
I. Vaginal prolapse
 Anterior vaginal wall prolapse – may exist in the form of

cystocele (herniation of the bladder base into the upper
vagina), urethrocele (herniation of the posterior wall of
urethra into the lower part of the vagina) or
cystourethrocele (herniation of the entire anterior vaginal
wall).
 Posterior vaginal wall prolapse – can present as a

rectocele (herniation of the rectum into the vagina, usually
involving the lower one half or two thirds of the posterior
vaginal wall) and/or enterocele (herniation of a peritoneal
sac of Pouch of Douglas into the upper part of the
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posterior vaginal wall that may contain loops of small

bowel).
 Vault prolapse: refers to a herniation of a peritoneal sac at

the vaginal vault after abdominal or vaginal hysterectomy
II. Uterovaginal prolapse
The uterine component of the uterovaginal prolapse is

measured in relation to the degree of prolapse of the cervix
below the level of the ischial spines (the normal station of the
cervix in the pelvis)
 First degree prolapse – refers to descent of the cervix

below the ischial spines as far as, but not beyond, the
introitus
 Second degree prolapse – descent of the cervix (but not

the entire uterus) beyond the introitus
 Third degree prolapse (procidentia) is herniation of the

entire cervix and uterus beyond the introitus.
Etiology
The causes of uterovaginal prolapse are
 Childbirth related trauma to the pelvic support and

improperly repaired genital tract tears
 Climacteric related atrophy of the pelvic supports
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 Chronic increase in intra abdominal pressure from chronic

cough and constipation
 Congenital weakness of the pelvic supports
 Neurologic problems affecting the pelvic musculature
Clinical Features
The symptoms of genital prolapse could be general or

specific. The general symptoms are
 Painless mass bulging through the introitus which is

prominent when standing or straining
 Pelvic pressure or bearing down sensation in the pelvis or

sensation of something coming down or dragging
discomfort and low back pain
The specific symptoms are
 For anterior vaginal wall prolapse: stress incontinence,

symptoms of urinary tract infection, sense of incomplete
emptying and urinary retention
 For posterior vaginal wall prolapse: constipation, rectal

fullness, difficulty in emptying the bowel, sense of
incomplete emptying which necessitates splinting or digital
removal
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 For enterocele: usually nonspecific symptoms resulting

from traction of the abdominal viscera
 For uterine prolapse: abnormal uterine bleeding, abnormal

vaginal discharge
The physical findings are
 For anterior vaginal wall prolapse: soft, reducible mass

bulging into the anterior vagina and distending the vaginal
introitus (best demonstrated by means of Sim‘s specula
with the patient in left lateral position). With straining or
coughing it bulges more and may be associated with
stress incontinence.
 For rectocele: soft, thin walled mass projecting into the

posterior vaginal wall. On rectal examination, the
rectovaginal septum projects well into the vagina and there
is anterior sacculation of the rectum into the vagina.
 For enterocele: rectovaginal examination, especially with

the patient standing, reveals a reducible thickness or
bulging of the upper recto vaginal septum. Occasionally
loops of bowel may be felt in the mass.
 For uterine prolapse: Almost always there is an associated

anterior and posterior vaginal wall prolapse. In addition,
visualization or palpation of the cervix with or without the
patient straining and palpation of the uterus grades the
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degree of uterine prolapse. In long standing cases

decubitus ulcer and thickened cervical/ vaginal epithelium
is seen.
Complications
 Keratinization of the vagina and cervix
 Decubitus ulcer on the cervix
 Urinary tract infection and urinary obstruction (angulation

of the urethra or constriction of the ureters in procidentia)
 Incarceration of the prolapse
 Sexual dysfunction
Management
I. Medical measures:
Small or moderate sized cystocele and rectocele and first

degree uterovaginal prolapse requires reassurance, explanation
and pelvic exercise (Kegel‘s exercise) for 6-12 months. Other
medical measures are vaginal pessaries, estrogens for
postmenopausal women.
Note: Kegel‘s exercise is done by repeatedly contracting the

pubococcygeus muscle as if one is trying to stop urination (150
– 200 x /day)
II. Surgical measures

526
For cystocele: anterior colporrhaphy
For rectocele: poteriorcolpoperineorraphy
For uterovaginal prolapse: The standard surgery is vaginal

hysterectomy combined with anterior colporrhaphy and
posterior colpoperineorraphy. Other options are Manchester
operation (combines anterior colporrhaphy, cervical amputation,
posterior colpoperineorraphy and suturing of cardinal ligaments
in front of the cervix) and Lefort‘s partial colpocleisis (partial
suturing of anterior and posterior vaginal walls together).
Prevention
 Encouraging postnatal perineal exercises
 Proper suturing of perineal and vaginal lacerations with

proper anatomic restoration
 Avoidance of excessive fundal pressure during delivery
 Treatment of chronic cough and constipation
2. URINARY INCONTINENCE
Definition and classification
Urinary incontinence is an involuntary leakage of urine due to

involuntary reversal of the pressure gradient between the
527
bladder and urethra. The various types of urinary incontinence

are
 Genuine stress incontinence
 Motor urge incontinence (unstable bladder)
 Sensory urge incontinence
 Overflow incontinence
 Bypass incontinence
 Psychogenic incontinence
Etiology
When the urinary tract is intact, continence is maintained as

long as the pressure closing the urethra is greater than the
intravesical pressure. When this pressure gradient is reversed,
urine passes to the urethra. This occurs in voluntary micturition
due to the urethral relaxation and detrusor muscle contraction.
Urinary incontinence may be due to any of the following, alone

or in combination
 Lowered urethral pressure (momentary or continuous)
 Detrusor contraction
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 Greater transmission of intraabdominal pressure to the

bladder than to the urethra
 Passive increase in intravesical pressure due to distension

beyond the elastic units of the bladder
 Bypassing of the continence mechanism
Tests and investigations
 Urinary stress test is done by instilling 300 ml of saline in

the bladder and the patient performs Valselva maneuver
eight to ten times while standing with feet spread as wide
as the shoulders and the perineum is inspected for
leakage of urine. It provides gross quantization of degree
of incontinence. In 20% false negative results are found.
 Pad test is done when the stress test is negative (no urine
leakage). In this procedure the patient wears preweighed
sanitary napkin, does some exercise and then the pad will
be reweighed to determine how much urine has been lost.
It is used to assess degree of incontinence.
 Cotton – tipped applicator ( Q-tip) test - assesses the

degree of bladder or urethral descent during straining by
measuring the angle formed by the applicator stick and an
imaginary line parallel to the floor while patient is in
529
lithotomy position and doing Valselva maneuver. An angle

of < 15O both during rest and the Valselva maneuver
shows good anatomic support. An angle of > 30O during
the Valselva maneuver shows poor anatomic support. An
angle of 15 – 30O is considered inconclusive.
 Bonney test- assesses support of proximal urethra. It is

performed in a woman with stress incontinence by putting
the index and middle fingers in the vagina, lifting the
bladder base towards the pubic bone and asking the
woman to strain or cough. If there is no incontinence then
the diagnosis of poor urethral support is made. If there is
incontinence then other causes of stress incontinence are
looked for.
 Dye (cotton ball) test- this is a test to detect small

vesicovaginal fistulas and differentiate vesicovaginal fistula
from other types of urinary fistulas (urethero and
ureterovaginal fistula). It is done by putting three cotton
balls into the vagina and instilling diluted methylene blue
into the urinary bladder through a bladder catheter. If the
dye stains the upper cotton balls then the diagnosis of
vesicovaginal fistula is made. If there is no staining with
the dye then consider ureterovaginal fistula as a cause.
are
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 Urine analysis and culture
 cystoscopy/ urethroscopy
1. Genuine Stress incontinence (GSI)
GSI is the involuntary loss of urine through the urethra

occurring simultaneously with an increase in intraabdominal
pressure but in the absence of detrusor muscle contraction.
Pathophysiology
Normally at rest the intraurethral pressure is greater than the

intravesical pressure. The pressure difference or urethral
closure pressure represents the margin of continence.
Therefore, if the resting intravesical pressure plus any increase
in pressure generated during stressful activities (coughing,
exercise) exceeds the intraurethral pressure at rest plus any
increase in urethral pressure generated during the activities, the
urethral closure pressure will decrease to zero, and genuine
stress incontinence will result.
Etiology
Two possible causes exist
 Anatomic descent of the proximal urethra below its normal

intraabdominal position during stressful activities, altering
531
the vesicourethral angle: This occurs in anterior vaginal

wall prolapse, especially with urethrocele.
 Failure of neuromuscular mechanisms that increase

intraurethral pressure which result in the dysfunction of
the extrinsic or intrinsic urethral sphincter.
Clinical Features and diagnosis
Classic symptom is involuntary loss of urine which occurs

simultaneously with stressful activities like coughing, sneezing
and laughing. It stops as soon as the stressful act is over.
Examination will usually show variable degree of
cystourethrocele in 75 % of the cases. In cases of anatomic
descent of the urethra, poor support of urethra can be
demonstrated by clinical tests like Q-tip test which is abnormal
in 95% of GSI.
Criteria for diagnosis of genuine stress incontinence are
 Normal neurologic examination
 Poor anatomic support (Q – tip test, X-ray or urethroscopy)
 Demonstrable leakage with stress (stress or pad test)
 Normal urine analysis, negative urine culture
 Normal cystometrogram or urethrocystometry
Management
532
I. Medical measures
For poor anatomic support: Kegel‘s exercise, estrogen for

postmenopausal
For intrinsic sphincteric defect:  adrenergic agonists
II. Surgical measures for severe cases either by abdominal or

vaginal approaches
2. Motor urge incontinence (detrusor instability, unstable

bladder)
This Is the result of involuntary uninhibited detrusor muscle

contractions in most cases idiopathic in origin. It may be
associated with cystitis. In most it is idiopathic. It is the second
most common cause of urinary incontinence. Because of its
unpredictability and loss of large volumes of urine, it has greater
detrimental effect on patients than GSI.
533
Pathophysiology
Normally increasing detrusor contractions occur when the

bladder contains more than the cystometric capacity (the
bladder volume that can be tolerated in the awake,
unanesthetized state). Micturition occurs because of the
increase in the intravesical pressure and along with
simultaneous voluntary relaxation of the external urethral
sphincter. This process can be inhibited voluntarily at any time.
In unstable bladder uninhibited detrusor contractions typically

occur spontaneously or upon provocation (as coughing,
exercise, tactile or auditory stimuli) at bladder volumes below
normal resulting in incontinence.
Symptoms are usually multiple. Patients usually have a strong

urge for urination moments before incontinence. If associated
with stressful activities, incontinence occurs seconds after the
stress has started and will continue after the stressful activity is
over, despite the patients effort to stop it. Symptoms of urinary
tract infection may be present. The physical examination may
be normal. Anatomic support of the bladder and urethra may
be good or poor. Neurologic signs are typically absent.
Diagnosis is based on finding delayed urinary leakage or

continuous heavy flow despite the patient‘s effort to stop during
534
the urinary stress test and simultaneous urethrocystometry

confirms the diagnosis.
Management
I. Medications
 Anticholinergic agents are the most effective
 Others include smooth muscle antispasmodics, calcium

channel blockers and prostaglandin synthase inhibitors
II. Behavior modification: bladder retraining and psychotherapy
III. Surgery is the last resort in the management: denervation,

cystoplasty and urinary diversion are the procedures
3. Sensory Urge Incontinence
It is leakage of urine (in association with great urgency) that

occurs in a stable bladder without excessive descent of the
urethra or bladder.
It is associated with bladder irritation as it occurs in cystitis,

bladder stone or neoplasia. Psychological factors may also play
a role. This stimulates the afferent arc of micturition reflex
resulting in strong urgency to micturate. has the ability to inhibit
detrusor contraction and does so when instructed showing that
her bladder is stable.
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Incontinence is associated with frequency, urgency, dysuria and

/or hematuria. Urine analysis and culture show urinary tract
infection. Urethroscopy and cystoscopy are important to
diagnose underlying pathologies like calculi and neoplasms.
Cystometric findings are usually normal.
Management
 Treatment of infections
 Treatment of the specific underlying cause
4. Overflow Incontinence
Etiology
Urinary retention and subsequent overflow incontinence can be

caused by
 Lower motor neuropathies and diabetes
 Obstructive causes in postoperative period or by pelvic

masses
 Pharmacologic causes: ganglionic blocking agents,

anticholinergics
Treatment
536
 Treatment of the underlying cause
 Medical management directed towards reducing urethral

closure pressure and increasing detrusor contractility
5. Bypass Incontinence
Urinary leakage occurs as a result of bypassing of the normal

anatomic urethral continence mechanism. It is characterized by
continuous leakage of urine. Commonest cause is urinary
fistula. Others are ectopic ureter (leakage starts from early age)
and urethral diverticula‘s (leakage occurs with change of
position minutes or hours after urination).
Treatment is usually surgical depending on the specific cause

and the prognosis is generally good.
6. Urinary Fistula
Definition
It is a direct communication between the urinary and genital

tracts. It could be vesicovaginal (commonest between the
vagina and the bladder), ureterovaginal (between the ureters
and r\the vagina), urethrovaginal (between the vagina and the
urethra) and vesicouterine (between the uterus and the
bladder).
537
Etiology
Obstructed labor is the commonest cause of urinary fistulas.

The other causes are advanced genital cancers (cervix, vagina,
and endometrium), trauma (rape, ghorning accident),
radiotherapy and lymphogranuloma venereum.
Clinical features
Continuous leakage of urine per vagina is the hallmark of

urinary fistulas. Speculum and digital examination may identify
hole in the anterior vaginal wall with urine coming through.
Small ones can be identified by doing dye test or cystoscopy or
intravenous pylogram.
Management
I. Fistulas following obstructed labour
Small ones may close spontaneously. In these cases,

continuous catheter drainage (bladder or ureteric) should be
tried for three weeks. If it persists then surgical closure after
three months should be planned. This will allow adequate
healing of the surrounding ischemic tissue. Ample fluid intake
during this time will prevent calculi formation at the fistula site.
Method of repair depends on position of fistula, size of the
defect and degree of fixity.
538
Note: Unless the fistula is very small, women with repaired

fistulas should be delivered by elective caesarian section.
II. Other types of fistulas
Surgical closure is the method of management. Success

depends on the cause.
7. Psychogenic Incontinence
It can take any form of the incontinences discussed above. It is

commonly diagnosed in patients with significant psychologic or
psychiatric disorders.
Review questions
1. Describe the classification, causes and diagnosis of

uterovaginal prolapse.
2. List the complications of uterovaginal prolapse.
3. List the different types of urinary incontinence.
4. Describe the different tests used in the diagnosis of urinary

incontinence.
539
540
541
References

Gynecologic diagnosis and treatment, 8th edition.
2. Larry J. Copeland, Text Book of Gynecology

4. Scott JR, Danforth‘s text book of Gynecology & Obstetrics,

1996
6. Department of Obstetric and Gynecology, The management

of infertile couple protocol. AAA, Faculty of Medicine, 2000
542
ANNEX 1
EPIDEMIOLOGY OF OBSTETRICS AND GYNECOLOGIC

PROBLEMS
1. OBSTETRIC BASIC STATISTICS
1. Birth - Complete expulsion of a fetus from the mother
2. Live birth - Any fetus that is born with any sign of life
regardless of fetal weight or gestational age.
543
3. Still birth - The birth of a fetus with no sign of life (WHO

weight greater than 500grams or greater than 20 weeks of
gestation and in Ethiopian context weight greater than or equal
to 1000 grams and greater than 28 weeks).
4. Still birth rate- Number of stillbirths /1000 live births.
5. Neonatal mortality rate - number of live born infant death

within first 28 days per 1,000 live births
 Early neonatal death – Live born infant deaths within first 7

days of life
 Late neonatal death- Live born infant deaths within first 28

days of life excluding the first 7 days of life
 Neonatal period I - From birth through 23 hours and 59

minutes.
 Neonatal period II- 24 hours through 6 days, 23 hours and

59 minutes
 Neonatal period III- from 7 days through 27 days, 23 hours

and 59 minutes
6. Perinatal mortality rate (PMR) - Number of still births and

number of neonatal death in 1st 7 days of life per 1000 live
births.
 In developing countries, 3 million neonates die in first week

after delivery and 4 million are still births.
544
 PMR in developing countries ranges from 40 to 60 /1000 live

births, but it is between 6 to 10 /1000 live births in developed
countries.
 Major causes of perinatal death are mechanical trauma

during delivery, hypertension in pregnancy, antepartum
hemorrhage, fetal malformations, low birth weight and
Infections.
7. Fertility rate - Number of live births per 1000 women

between age of 15 and 44 years of age.
8. Reproductive mortality: - Death due to direct result of

pregnancy or use of contraceptive per 1000 women
9. Maternal mortality - Death of a woman while pregnant or

within 42 days of termination of pregnancy irrespective of the
site & duration of pregnancy, from any acutely related to or
aggravated by the pregnancy or its management but not from
accidental or incidental cause.
10. Maternal mortality rate - Number of maternal deaths due

to reproductive process per100, 000 live births
 500,000 maternal deaths occur each year world wide
 99% of maternal death occurs in developing countries
 In Africa maternal death is 630/100,000 live births

545
 East Africa maternal death is 680/100,000 live births
 Lifetime risk of maternal death in Africa is 1 in 21
According to the etiology maternal deaths are subdivided into:
Direct maternal death: Maternal death is directly attributable to

obstetric causes or the quality of obstetric care.
Indirect maternal death: Maternal death is attributable to a

concomitant disease & conditions aggravated by the
pregnancy.
Non maternal death: Maternal death due to accidents & not

related to pregnancy.
MAJOR CAUSES OF MATERNAL DEATH IN THE

DEVELOPING COUNTRIES INCLUDE
 Hemorrhage 25%
 Infection (sepsis)15%
 Unsafe abortion 13%
 Hypertensive disorders 12%
 Obstructed labor 8%
 Indirect causes 19%
 Others 8%
546
2. DEMOGRAPHIC STATISTICS
1. Crude birth rate (CBR) = Number of total births per 1,000

total population per year at midyear.
2 Crude death rate (CDR) = Number of death per 1000 total

population per year at mid year.
3. Crude rate of natural increase (CRNI) = CBR-CDR

per1000 population per year
4. Population growth rate (PGR) = CRNI + the sum of the

migration of people in and out of the population.
5. Life expectancy (LE) = Average number of years of life

remaining in individual at a specific age.
Population Trend
 World population growth increase at a rate of 2% per year

and doubles every 35 years.
 World population 1980 was 4.4 billion; at 2000 it was 6.2

billion. At the time of Christ, it was about 250 million.
 If the trend continues, there may be 12 billion people in the

world by the year 2035.
547
3. HEALTH INDICATORS FOR THE STATUS OF WOMEN IN

ETHIOPIA
 Fertility rate 6.2
 Antenatal care utilization 20%
 Assisted deliveries by trained health worker 14%
 Family planning coverage less than 10%
 MMR= Average 500-700 /100,000
4. EXPOSURE & DISEASE IN GYNECOLOGY
EXPOSURE TO SOME FACTORS MAY CAUSE FEMALE

GENITAL ORGAN DISEASE.
4.1. Exposure
4.1.1. Reproductive events
Age at menarche, character of menstrual cycle, gravidity and

age of menopause have impact on endometriosis, myoma,
heart disease, and osteoporosis, cancer of breast,
endometrium and ovary.
548
4.1.2. Contraceptive and sterilization
Barrier methods are protective of pelvic inflammatory disease,

tubal infertility, ectopic pregnancy and cervical cancer.
Intrauterine devices - increases pelvic inflammatory disease,

tubal infertility and ectopic pregnancy
Oral contraceptives- increase the risk of thromboembolism,

hypertension, myocardial infarction and liver adenoma. They
are protective against benign breast disease, ovarian cancer
and pelvic inflammatory disease
Sterilization- induces early menopause and protective for

ovarian cancer.
4.1.3. Menopausal hormones
Increase endometrial cancer, protective effect on heart

disease, osteoporosis and Alzheimer disease.
4.1.4. Sexually transmitted infections
Predispose for HIV, syphilis, pelvic inflammatory disease,

chlamydia and gonorrhea.
4.1.5. Life style
Smoking – increase heart and lung disease, tubal infertility,

ectopic pregnancy, cervical cancer and early menopause.
549
Alcohol- Decrease cardiovascular disease, risk of breast

cancer increased, Increases circulating estrogen
Exercise and nutrition : lean athelets and anorexia nervosa

cause amenorrhea, obesity causes menstrual difficulty and
endometrial cancer
Talc use- increases risk for ovarian cancer
4.2. Disease
 Mortality caused by cancer in decreasing order: lung

cancer, breast, colorectal, pancreas and ovary.
 Incidence of gynecologic cancer in decreasing order:

cervical, endometrial and ovarian cancer, but mortality is
higher in ovarian tumor.
 Incidence of benign gynecologic conditions varies from

place to place: pelvic inflammatory disease, benign
ovarian cyst, endometriosis, myoma, ectopic pregnancy.
550
ANNEX 2
THE PARTOGRAPH
The partograph is a tool to assess and interpret the progress

of labour. Its central feature is graphic record of cervical
dilatation but descent of the fetal head and uterine activity are
also indicators of progress of labour. It also detects other
problems developing in the mother and the fetus.
Advantages include
 It gives comprehensive view of all major events of labour
 It allows early detection and management of abnormal

labour patterns
 It simplifies handover to other health professionals

551
 It saves time and is more efficient
 It is simple (only symbols and letters are used) and skill in

its use is quickly attained.
 It helps in research and teaching
Parts
The WHO model partograph has three parts that assess

different parameters.
I. Labor progress
 Cervicograph: Four hourly digital pelvic examination is

done and cervical dilatation is plotted by mark X on the
graph whose vertical arm shows the cervical dilatation in
centimeters and horizontal arm shows the time. The
graph has a latent phase which has 8 hours limit and an
active phase which takes the rest of the graph to the
right of the latent phase. A vertical line drawn at 8 hours
mark separates the two. A horizontal line drawn at 3
centimeters of cervical dilatation separates the latent and
active phases. On the active phase there are two parallel
diagonal lines set at four hours apart. They are named
the alert line (the one found on the left side) and the
action line. Labour is said to be progressing normally if
the cervical dilatation curve stays to the left of the alert
line. Strict observation (in a health center preparation for
552
referral) is indicated if the curve crosses the alert line.

Action in the form of augmentation or caesarian section
or referral for these measures must be done if the curve
crosses the action line.
 Descent of the fetal head is assessed by abdominal

examination in fifths and plotted on the cervicograph with
a mark 0.
 Uterine contraction is assessed by abdominal palpation

for 10 minutes every 30 minutes. The number of uterine
contractions in 10 minutes and their average duration is
then plotted on the squares provided. Corresponding
number of squares are shaded to indicate the number of
uterine contractions. The average duration of contraction
is plotted by filling the squares with different shades. If
the duration is less than 20 seconds the squares are
filled with dots. If between 20- 40 seconds fill with
striped lines. If greater than 40 seconds completely
shading of the squares is done.
II. Fetal condition
553
 Fetal heart rate is counted by intermittent auscultation

every 15 minutes. It is recorded in by writing in numbers
in the square provided.
 Molding of the fetal head is obtained during pelvic

examination. According to its degree it is given different
codes. If the bones of are separate it is recorded as 0. If
they are touching each other but not overlapping it is
recorded as +. If they are overlapping but can be
separated by digital pressure it is given ++. If they are
overlapping and can not be separated digitally it is given
+++.
 Color of the liquor is observed during pelvic

examination. The letter I is used for intact (unruptured)
membranes. The letter C is used for ruptured
membranes with clear liquor and letter M if the liquor is
muconium stained.
III. Maternal condition
 Blood pressure is measured every 4 hours or more

frequently if there is hypertension. It is on the vertical
lines using to v indicate the systolic pressure and ^ to
indicate the diastolic pressure.
554
 Pulse rate and temperature are measured every 1-2

hours and the number is entered into the square
provided.
 Urine volume, dipstick (for glucose and ketone) and

microscopy is performed and recorded in space
provided.
 Drugs given to the mother along with the doses is also

recorded.
555

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OBSTETRICS AND

Health Science Students

Health Science Students

Samson Negussie, Assistant Professor

M.D. Obstetrician and Gynecologist

In collaboration with The Carter Canter (EPHTI) and

About the lecture note iii

SECTION ONE – BASICS

CHAPTER Obstetric and gynecology evaluation 9

SECTION TWO – NORMAL AND ABNORMAL PREGNANCY

CHAPTER 4 Common minor disorders of pregnancy 22

CHAPTER 5 Antenatal care 27

CHAPTER 6 Abnormal bleeding during first and 31

CHAPTER 7 Antepartum hemorrhage 44

CHAPTER 9 Disturbances of amniotic fluid 55

CHAPTER Premature rupture of membranes and 58

CHAPTER11 Multiple pregnancy 63

CHAPTER13 Medical disorders of pregnancy 70

SECTION THREE – NORMAL AND ABNORMAL LABOUR

CHAPTER Induction and augmentation of labour 92

CHAPTER Operative deliveries 97

CHAPTER Malpresentations and malpositions 105

CHAPTER Dystocia 115

CHAPTER Obstructed labour and ruptured uterus 121

CHAPTER Fetal distress 127

SECTION FOUR – NORMAL AND ABNORMAL PEUPERIUM

CHAPTER Postpartum hemorrhage 135

CHAPTER Postpartum complications 141

SECTION FIVE – GYNECOLOGY

CHAPTER Climacteric and related problems 158

CHAPTER Vaginal discharge and vulvar pruritis 161

CHAPTER Pelvic inflammatory disease 167

CHAPTER Infertility 179

CHAPTER Tumor conditions of the female genital 183

CHAPTER Uterovaginal prolapse and urinary 193

My deepest gratitude goes to The Carter Center and the

I am highly indebted to Dr. Solomon Kumli, Dr. Yirgu G/Hiwot of

This lecture note is organized into five sections. The first

Preparation of this lecture note was started some 18 months

This final version was designed and prepared to address the

This lecture note is designed to be used by a health officer

This lecture note is by no means a replacement for standard

ACTH – Adrenocorticotrophic hormone

AFI – Amniotic fluid index

ANC – Antenatal care

ARM – Artificial rupture of membranes

APH - Antepartum hemorrhage

AUB – Abnormal uterine bleeding

BPD – Biparietal diameter

CPD – Cephalopelvic disproportion

C/S – Caesarian section

DNA – Deoxyribonucleic acid

DUB – Dysfunctional uterine bleeding

DVT – Deep vein thrombosis

E&C/ D&C – Evacuation and curettage/ dilatation and

EDD – Expected date of delivery

FHB – Fetal heart beat

HCG – Human chorionic gonadotrophic hormone

HDP – Hypertensive disorders of pregnancy

HPO – Hypothalamo pitutary ovarian axis

IUCD – Intrauterine contraceptive devise

LMP/LNMP – Last menustral period/ last normal

MSH – Melanocyte stimulating hormone

MTCT – Mother to child transmission