Gynaecology Illustrated PDF

GYNAECOLOGY ILLUSTRATED
Commissioning Editor: Pauline Graham

Development Editor: Helen Leng
Project Manager: Glenys Norquay, Elouise Ball
Designer/Design Direction: Charles Gray
Illustration Manager: Gillian Richards
GYNAECOLOGY
ILLUSTRATED
Catrina M Bain MBChB MRCOG
Consultant Obstetrician and Gynaecologist
Glasgow Royal Infirmary
Glasgow, UK
Kevin Burton MD MRCOG

Consultant Gynaecological Oncologist
Glasgow Royal Infirmary
Glasgow, UK
C Jay McGavigan MD MRCOG FRANZCOG

Consultant Obstetrician
Head Fetal-Maternal Medicine
Flinders Medical Centre
South Australia
Illustrations by
Robin Callander FFPh FMAA AIMBI

Medical Illustrator, Formerly Director of Medical Illustrations, University of Glasgow,
Glasgow, UK
Ian Ramsden
Head of Medical Illustration Unit, University of Glasgow,
Glasgow, UK
SIXTH EDITION
Edinburgh London New York Oxford Philadelphia St Louis Sydney Toronto 2011
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First edition 1972
Second edition 1978
Third edition 1985
Fourth edition 1993
Fifth edition 2000
Sixth edition 2011
ISBN 9780702030673
International ISBN 9780702030772
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A catalogue record for this book is available from the British Library
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A catalogue record for this book is available from the Library of Congress
Notices
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broaden our understanding, changes in research methods, professional practices, or medical treatment
may become necessary.
Practitioners and researchers must always rely on their own experience and knowledge in evaluating
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With respect to any drug or pharmaceutical products identified, readers are advised to check the most
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Printed in China
PREFACE
This is the 6th edition of Gynaecology Illustrated, a textbook that owes its long-standing
popularity to the clarity of its line-drawn illustrations and of the accompanying text. The
latest edition has been extensively revised and updated by three new authors who have
complementary specialist interests. The structure of the text has been reorganised to place
particular emphasis upon clinical areas of clinical relevance. Despite the extensive revisions
the authors have remained true to the original objectives of their predecessors and Gynaecology
Illustrated continues to offer an up-to-date and focused visual learning experience in this
practical specialty.
Catrina Bain
Kevin Burton
Jay McGavigan
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CONTENTS
1. Embryology of the 4. Disorders of Sex Development 57

Reproductive Tract 1
Maturation of Germ Cells: Meiosis 58
Development of the Ovary 2–4 Genetic Abnormalities 59–61
Development of Uterus and Fallopian Congenital Abnormalities 62, 63
Tubes 5, 6 Abnormalities of Ovary and Tube 64
Development of External Genitalia 7, 8 Abnormalities of the Uterus 65, 66
Development of Male External Abnormalities of the Vagina 67
Genitalia 9 Abnormalities of the Vulva 68
2. Anatomy of the 5. History and Examination 69

Taking the History 70, 71
The Perineum 12 Pelvic Pain 72, 73
The Vulva 13, 14 Other Gynaecolgical Symptoms 74
Bartholin’s Gland 15 Abdominal Examination 75–77
Muscles of the Perineum 16 Examination of the Vulva 78
The Urogenital Diaphragm 17 Bimanual Pelvic Examination 79
Ischiorectal Fossa 18 Speculum Examination 80, 81
Muscles of the Pelvis 19 Examination of the Breasts 82
Pelvic Diaphragm 20 Laparoscopy 83–85
Pelvic Fascia 21
The Vagina 22–24 6. Abnormalities of Menstruation 87
Uterus 25–31
Normal and Physiological Changes in
Fallopian Tube 32
the Menstrual Cycle 88
Broad Ligament 33
Physiological Amenorrhoea 89
Ovary 34–37
Uterine and Lower Genital Tract
Changes in the Genital Tract
Disorders 90, 91
with Age 38
Ovarian Disorders 92–96
Blood Supply of the Pelvis 39–41
Pituitary Disorders 97–100
Lymphatic Drainage of the Genital
Hypothalamic Disorders 101
Tract 42
Investigation of Amenorrhoea 102–104
Nerves of the Pelvis 43
Hirsutism 105
Autonomic Nerve Supply of the
Virilisation 106
Pelvis 44
Management of Hirsutism 107, 108
Menstrual Disorder 109
3. Physiology of the
Dysfunctional Uterine Bleeding 110
Investigation of the
Ovulation 46–50 Endometrium 111, 112
Cyclical Ovarian Hormonal Changes 51 Investigations of Endometrium -
Action of Ovarian Hormones 52 Complications 113
Effects of Ovarian Hormones 53 Management of Heavy Menstrual
Puberty 54 Bleeding 114–119
The Menopause 55 Dysmenorrhoea 120, 121
CONTENTS
Adenomyosis 122 Premalignant and Malignant Cervical

Endometriosis 123–128 Disease 178
Premenstrual Syndrome 129, 130 Colposcopy 179
Treatment of Cervical Intraepithelial
7. Gynaecological Infections 131 Neoplasia 180–182
Carcinoma of the Cervix 183–185
Inflammation in the Lower
Diagnosis of Cervical Carcinoma 186
Gynaecological Tract 132
Staging of Cervical
Vulval Inflammation 133
Carcinoma 187, 188
Vaginal Discharge and Infection 134
Radiotherapy and Chemotherapy in
Complaints of Vaginal Discharge 135
Cervical Carcinoma 189
Vaginal Discharge 136–138
Surgery for Cervical Carcinoma 190–193
Vaginitis 139
Genital Herpes 140
11. Diseases of the Uterus 195
Genital Warts 141
Bacterial Infections 142 Uterine Polyps 196
Tropical Sexually Transmitted Fibroids 197–200
Infections 143 Endometrial Hyperplasia 201, 202
Gonorrhoea 144 Carcinoma of the Endometrium 203, 204
Syphilis 145–147 Staging of Endometrial Carcinoma 205
Physiological Variation of the Cervix 148 Spread of Endometrial Carcinoma 206
Pelvic Inflammatory Disease 149, 150 Aetiological Factors in Endometrial
Genital Tuberculosis 151, 152 Carcinoma 207
Human Immunodeficiency Virus 153, 154 Prognosis of Endometrial Carcinoma 208
Treatment of Endometrial Carcinoma 209
8. Diseases of the Vulva 155 Recurrence of Endometrial
Carcinoma 210
Vulval Dermatoses 156, 157
Sarcoma of the Uterus 211, 212
Benign Tumours of the Vulva 158
Vulval Intraepithelial Neoplasia 159
12. Prolapse and Urogynaecology 213
Carcinoma of the Vulva 160–164
Diseases of the Urethra 165 Retroversion of the Uterus 214, 215
Uterovaginal Prolapse 216, 217
9. Diseases of the Vagina 167 Vaginal Prolapse 218, 219
Clinical Features of Prolapse 220
Benign Vaginal Disease 168
Differential Diagnosis of Prolapse 221
Malignant and Premalignant Disease 169
Pessary Treatment 222
Carcinoma of the Vagina 170, 171
Anterior Colporrhaphy
Plastic Surgery of the Vagina 172
(and Repair of Cystocele) 223, 224
Manchester Repair 225, 226
10. Diseases of the Cervix 173
Posterior Colpoperineorrhaphy
Normal Cervical Epithelium 174 (Including Repair of Rectocele) 227
The Role of Human Papilloma Virus Repair of Enterocele 228
in Cervical Disease 175 Vaginal Hysterectomy 229, 230
Screening for Cervical Cancer 176 Urogynaecology 231, 232
Cervical Smears 177 Blood Supply of the Ureter 233
viii
CONTENTS
Physiology of Micturition 234, 235 14. Complications of

Mechanism of Voiding 236 Gynaecological Surgery 287
Detrusor Instability 237
Urinary Tract Injuries 288
Genuine Stress Incontinence 238
Injury to the Ureter 289
Other Incontinence Mechanisms 239
Management of Ureteric Injury 290, 291
The Urethral Syndrome 240
Fistula Formation 292, 293
Investigation of Incontinence 241
Lymphoedema and Lymphocyst 294
Urodynamic Investigation of Bladder
Venous Thrombosis 295–297
Function 242
Clinical Features of Deep Venous
Indications for Urodynamic
Thrombosis 298
Assessment 243
Investigations for Deep Venous
Treatment of Stress Incontinence 244
Thrombosis 299
Surgical Treatment of Stress
Methods of Thromboprophylaxis 300, 301
Incontinence 245
Pulmonary Embolism 302–304
Marshall–Marchetti–Krantz
Treatment of Pulmonary Embolus 305
Urethropexy 246
Mortality 306
Burch’s Colposuspension
Operation 247
15. Early Pregnancy 307
Sling Procedures 248
Treatment of Detrusor Instability 249 Miscarriage 308, 309
Management 310–313
13. Diseases of the Ovary and Recurrent Miscarriage 314–316
Fallopian Tube 251 Termination of Pregnancy 317–319
Ectopic Pregnancy 320
Clinical Features of Ovarian
Diagnosis of Tubal Pregnancy 321, 322
Tumours 252–254
Sites of Implantation 323
Differential Diagnosis 255–258
Treatment of Tubal Pregnancy 324
Ovarian Cyst Accidents 259–261
Gestational Trophoblastic
Benign and Malignant Ovarian
Disease 325–330
Tumours 262, 263
Risk Factors of Ovarian Cancer 264
16. Sexuality and Contraception 331
Epithelial Ovarian Tumours 265, 266
Germ Cell Ovarian Tumours 267–270 Physiology of Coitus 332, 333
Hormone-Producing Tumours 271–274 Dyspareunia 334
Other Hormone-Producing Sexual Problems Affecting the Male 335
Tumours 275 Treatment Options for Erectile
Surgical Treatment of Ovarian Dysfunction 336
Tumours 276 Medico-Legal Problems 337
Treatment of Ovarian Methods of Contraception 338, 339
Cancer 277, 278 Hormonal Contraception 340, 341
Staging of Ovarian Cancer 279, 280 Minor Side Effects of OCs 342
Principles of Chemotherapy 281 Oral Contraception: Risks 343–345
Chemotherapeutic Agents in Ovarian Intrauterine Devices (IUDs) 346, 347
Cancer 282 Complications of Intrauterine Devices 348
Broad Ligament Cysts 283, 284 Diaphragms and Caps 349
Carcinoma of Fallopian Tubes 285 Condoms 350
ix
CONTENTS
Contraception Based on Time of Assisted Conception 370

Ovulation 351 Fertility Drugs 371, 372
Postcoital Contraception 352 Tubal Surgery 373
Irreversible Methods 353, 354 Assisted Conception Techniques 374–379
Laparoscopic Sterilisation 355 Assisted Conception 380
Vasectomy 356
18. The Menopause 381
17. Infertility 357
The Menopause 382, 383
Infertility 358, 359 The Greene Climacteric Scale 384
Investigations 360 Changes in the Genital Tract 385
Evidence of Ovulation 361–363 Osteoporosis 386–388
Seminal Analysis 364 Cardiovascular Disease and the
Sperm Production Tests 365 Menopause 389, 390
Abnormalities in Sperm Production 366 Hormone Replacement Therapy 391–393
Sperm Function Tests 367
Tests of Tubal Patency 368, 369 Index 395
x
CHAPTER 1
EMBRYOLOGY OF THE
REPRODUCTIVE TRACT
Development of the Ovary 2

Development of Uterus and Fallopian Tubes 5
Development of External Genitalia 7
Development of Male External Genitalia 9
EMBRYOLOGY OF THE REPRODUCTIVE TRACT
DEVELOPMENT OF THE OVARY
The germ cells, which will eventually inhabit Allantois

the gonads, originate from the primitive
hind gut. They appear around the 25th day. Amniotic cavity
Embryo
By 30 days, the gut, complete with its

mesentery, is formed. The germ cells now Germ cells
migrate from the gut to the root of the
mesentery. Of the original 6 or 7 million,
only 1–2 million are present at birth and this
number is reduced to 300,000 at puberty. Yolk sac
A smaller number of these cells may be a
factor that leads to premature menopause.
Vitelline duct
Hind Mesonephric
gut duct and
Allantois tubules
Cloaca
Transverse Section of Embryo
Spinal cord
Notochord
Aorta
Primordial Mesonephric
Metanephros germ cells duct
Meso-
Genital nephros
ridge
At the same time, the coelomic epithelium Gut

proliferates and forms thickenings, the genital Coelomic
ridges, together with the underlying or
peritoneal
mesenchyme on either side of the mesenteric
cavity
root, near the developing kidney.
2
At this stage, the primitive gonad Mesonephric

(genital ridge) consists of a duct
mesoderm (coelomic epithelium Germ
plus mesenchyme) covered by the cells
coelomic epithelium. The germ
cells now migrate from the root of
the mesentery to the genital ridge.
Mesonephric
swelling
Genital ridge
The coelomic epithelium, growing

Coelomic epithelium
into the genital ridge, forms the
so-called sex cords, which enclose
each germ cell. Gut
Until this time, that is, around the Mesonephric

7th week, the gonad is of an indifferent tubules
type, the male being indistinguishable
from the female. Germ
cells
The germ cells and most of the sex

cord cells remain in the superficial
part, which is the future cortex of the
ovary. The cords then lose contact with
the surface epithelium and form small
Coelomic epithelium
groups of cells, each with its germ cell, a
(primitive germinal epithelium)
primitive follicle. Some of the sex cord
cells grow into the medulla. These
tend to regress and form
rudimentary tubules, the rete.
Degenerating
mesonephric
tubules
and
duct
Mesentery
As the ovary grows, it projects
of ovary
increasingly into the peritoneal
(coelomic) cavity, thus forming a
mesentery. Primitive follicles
3
Simultaneously, the ovary descends extraperitoneally within the abdominal cavity. Two
ligaments develop and these may help to control its descent, guiding it to its final position
and preventing its complete descent through the inguinal ring, in contrast to the testes.
The first structure is the suspensory ligament attached to the anterior (cephalic) pole of the
ovary which connects it with its site of origin, the genital ridge.
Suprarenal
gland Suspensory
ligament
Ovary
Kidney Mesonephric
duct
Mesonephros
Ureter
Gut
Bladder Gubernaculum
Another ligament, or gubernaculum, develops at the posterior or caudal end of the ovary. At
first attached to the genital ridge, it later becomes attached to the developing uterus and
becomes the ovarian ligament.
4
DEVELOPMENT OF UTERUS AND FALLOPIAN TUBES
When the embryo reaches a size of 10 mm at 35–36 days, a longitudinal groove appears on the
dorsal aspect of the coelomic cavity, lateral to the Wolffian (mesonephric) ridge.
Mesonephric
duct
Para-
mesonephric
groove
Primitive
gonad becomes
Kidney
Gut
Para-
mesonephric
duct
Mesonephric
This groove or fold is then sealed off to duct
form a tube, the paramesonephric or
Müllerian duct. The tube is open at its
upper end, enabling communication with Mesonephros
the future peritoneal cavity. The lower end
forms a solid tip (Müllerian tubercle), Gonad
which develops burrowing properties.
Mesonephric duct
Ureter
Cloaca
5
DEVELOPMENT OF UTERUS AND FALLOPIAN TUBES
The Müllerian ducts from either side grow in a caudal direction, extraperitoneally. They also
bend medially and anteriorly and ultimately fuse in front of the hind gut. The mesonephric
duct becomes involved in the walls of the paramesonephric ducts.
Gubernaculum of
ovary
Para- (ovarian ligament) Ovary
Mesonephric mesonephric
ducts ducts
Fallopian or Developing
uterine tube uterus
Degenerating
mesonephric Müllerian
duct (becomes tubercle
Gartner’s duct) Urogenital
sinus
At first, there is a septum that separates the lumina of the two
ducts. Later the septum disappears and a single cavity is
formed, the uterus. The upper parts of both the ducts remain
separate and form the fallopian tubes.
Uterus
While this is happening, the ovary is also

Ovary
affected. Its gubernaculum is ultimately
attached to the Müllerian duct at the
Ovarian
cornu of the developing uterus. This
Bladder gubernaculum
pulls the ovary medially such that its
attached to
long axis becomes horizontal. cornu of
uterus
Symphysis Part of it
pubis continues
The lower end of the fused Müllerian ducts, as the
beyond the uterine lumen, remains solid, round
proliferates and forms a solid cord. This cord ligament.
will canalise to form the vagina, which
opens into the urogenital sinus. Urogenital After passing
sinus through the
inguinal canal
Hymen it ends in the
At the point of entry into the urogenital
labium majus
sinus, a part of the Müllerian tubercle of the vulva.
persists and forms the hymen.
6
DEVELOPMENT OF EXTERNAL GENITALIA
At an early stage, the hind gut and A septum (urorectal) grows down
the various urogenital ducts open into between the allantois and the hind gut
a common cloaca. during the 5th week.
Allantois Hind gut
Ureter Ureter
Cloaca
Cloacal
Urorectal
membrane
septum
Eventually, this septum fuses with the cloacal membrane, dividing the cloaca into
two compartments – the rectum dorsally and the urogenital sinus ventrally. At
the same time, the developing uterus grows down and makes contact with the
urogenital sinus.
Ureter Uterus Allantois (or urachus)
Uterine body
Hind gut
Cervix
Genital Bladder
tubercle
Urogenital Developing Vagina
sinus urethra
Urogenital Urogenital
membrane sinus (or
Genital vestibule)
Anal membrane Rectum tubercle
At the end of the 7th week, the urogenital membrane breaks down and the urogenital sinus
opens on to the surface.
The developing uterus and vagina push downwards and cause an elongation and narrowing of
the upper part of the urogenital sinus. This will form the urethra. 7
DEVELOPMENT OF EXTERNAL GENITALIA
Meanwhile, on the surface of the embryo, around the urogenital sinus, five swellings appear.
At the cephalic end, a midline swelling grows, the genital tubercle, which will become the
clitoris. Posterior to the genital tubercle and on either side of the urogenital membrane a fold
is formed – urethral folds. Lateral to each of these another swelling appears – the genital or
labial swelling. These swellings approach each other at their posterior ends, fuse and form the
posterior commissure. The remaining swellings become the labia minora.
Genital
tubercle Labial Clitoris
swelling
Urogenital Labium
membrane Urethral majus
fold Vestibule
Anal
membrane Labium
minus Posterior
commisure
Anus
Certain small, but clinically important, glands are

formed in and around the urogenital sinus.
Prepuce Clitoris
In the embryo, the epithelial buds arise from the
urethra and also from the epithelium of the Urethra
urogenital sinus. In the male, these two sets
Ducts of
of buds grow together and give rise to the glands glands of
of the prostate. They remain separate in the Skene
female, with the urethral buds forming the urethral
glands and the urogenital buds giving rise to the Labium
paraurethral glands of Skene. The ducts of the minus
latter open into the vestibule, on either side of
the urethra. Vestibule
Two other small glands arise by budding from the Vagina
epithelium of the posterior part of the vestibule, one
on either side of the vaginal opening. These are the Labium majus
greater vestibular or Bartholin’s glands. Similar Greater vestibular
smaller glands also arise in the anterior portion of the (Bartholin’s) gland ducts
vestibule.
8
DEVELOPMENT OF MALE EXTERNAL GENITALIA
As in the female, a mesodermal mass, the Glans penis

urorectal septum, grows downwards and Urogenital Primitive
separates the urogenital sinus from the rectum sinus urethral
and anus. The urogenital portion of the groove
cloacal membrane disintegrates and an open
gutter is formed through which the urine Scrotal
drains. This gutter is continuous anteriorly swelling
with the primitive urethral groove on the
phallus.
The ectoderm on the under surface of the

Anal pit
phallus disappears, exposing the underlying
endodermal plate.
Ectoderm Ectoderm
Penile
urethra
Genital
raphe
Endodermal plate
Primary urthral groove
The endodermal plate then becomes hollowed

and forms the primary urethral groove. Glans penis
Urethral fold
The hollow endodermal plate is drawn back
into the body of the phallus and, in this process, Primitive
urogenital
it forms a tube. The ectodermal surface is then Phallus
orifice
restored.
Simultaneously, the urethral folds are
approximated and ultimately fuse.
Genital
The testes descend into the labio-scrotal Scrotum raphe
swellings which then become distended and
move medially to form the scrotum.
9
CHAPTER 2
ANATOMY OF THE
REPRODUCTIVE TRACT
The Perineum 12 Cavity of the Corpus 27

The Vulva 13 Cervix 27
Mons Pubis and Labia Majora 13 Relationship of Uterus
Clitoris and Labia Minora 13 and Ureter 28
Bartholin’s Gland 15 Ligaments of the Uterus 29
Histology of Bartholin’s Gland 15 Histology 31
Muscles of the Perineum 16 Fallopian Tube 32
Ischiocavernosus 16 Broad Ligament 33
Bulbospongiosus 16 Blood Vessels 33
Superficial Transverse Perineal Vestigial Structures 33
Muscle 16 Ovary 34
External Anal Sphincter 16 Histology 35
The Urogenital Diaphragm 17 Changes in the Genital Tract
The Urogenital Diaphragm with Age 38
(Triangular Ligament) 17 The Vulva 38
Ischiorectal Fossa 18 The Vagina 38
Boundaries 18 The Ovary 38
Muscles of the Pelvis 19 The Uterus 38
Pelvic Diaphragm 20 Blood Supply of the Pelvis 39
Functions of the Pelvic Diaphragm 20 Supply to Uterus, Vagina
Pelvic Fascia 21 and Bladder 39
The Pelvic Fascia 21 Collateral Blood Supply 41
The Vagina 22 Abdominal Aorta 41
Histology 24 External Iliac Artery 41
Vaginal Secretion 24 The Femoral Artery 41
The Vaginal Epithelium 24 Lymphatic Drainage of the
Uterus 25 Genital Tract 42
Corpus and Cervix 26 Nerves of the Pelvis 43
Corpus (Uterine Body) 26 Autonomic Nerve Supply of the
Cervix 26 Pelvis 44
Isthmus Uteri 26
ANATOMY OF THE REPRODUCTIVE TRACT
THE PERINEUM
THE PERINEUM (Gk. ‘around

the natal area’)
‘Urogenital
triangle’
Ischial
The anatomical or true perineum tuberosity Pubic
is the diamond-shaped outlet of arch
the pelvis and the soft tissues that
cover it.
Coccyx
Sacro- ‘Anal
tuberous triangle’
ligament
The gynaecological perineum is the

area between the posterior commissure
and the anus. This is the area referred
to in gynaecology and obstetrics as ‘the
perineum’.
The anterior or urogenital triangle of the

true perineum is covered by the external
genitalia and other structures and is called
the vulva. (L. vulva or volva: a covering.) Prepuce
of clitoris
The VULVA consists of the following:
Mons pubis
Clitoris
Urethral orifice
Vestibule
Labia majora
Labia minora
Vaginal orifice
Hymen
Subcutaneous: the bulb of the vestibule and

12 the greater vestibular (Bartholin’s) glands.
THE VULVA
MONS PUBIS AND LABIA MAJORA Mons pubis

The mons pubis is a pad of fatty tissue
overlying the symphysis pubis and
covered by skin and pubic hair. The
labia are folds of skin and fat which pass
from the mons back to the perineum.
The lateral labial surfaces are pigmented Labium
and hairy, and the inner surfaces smooth majus
and contain many sebaceous, sweat and
apocrine glands.
Pigmented
The substance of the labia consists of and hairy
vascular fatty tissue with many lateral
lymphatics, and also vestigial remnants surface
of the dartos muscle. (The labium is the
homologue of the scrotum.) Smooth
inner
surface
CLITORIS AND LABIA MINORA

Prepuce
The clitoris is the vestigial homologue of the penis
and is formed the same way from two corpora
Clitoris cavernosa and a glans of spongy erectile tissue which
Frenulum has a copious blood supply from the clitoral artery.
The clitoris is highly innervated.
The labia minora are two cutaneous folds enclosing
the urethral and vaginal orifices. Anteriorly, each
Labium divides to form a hood or prepuce, and a frenulum
minus for the clitoris. Posteriorly, they unite in a frenulum
or fourchette, which is obliterated by the delivery of
a baby. The labia minora contain no fat but many
sebaceous glands.
Fourchette
13
THE VULVA
The VESTIBULE is the area between the labia

minora. It is perforated by the urethral and vaginal
orifices and the ducts of Bartholin’s and Skene’s External
glands. The fossa navicularis between the vagina urethral
orifice Vestibule
and the fourchette is, like the fourchette,
obliterated by childbirth. The lesser vestibular
glands are mucosal glands discharging on to the
surface of the vestibule.
The EXTERNAL URETHRAL ORIFICE is, in Vagina

the healthy state, a small protuberance with a vertical
cleft. The tiny orifices of
Urethra the paraurethral (Skene’s)
Fossa
ducts lie just inside or
navicularis
outside the meatus. The
paraurethral glands are
homologues of the
prostate and form a Ducts of
system of tubular glands, Bartholin’s glands
surrounding most of the
Skene’s ducts urethra.
The VAGINAL ORIFICE is a midline aperture incompletely closed by the HYMEN. The
hymen is a thin septum of tissue lined by squamous epithelium with a small hole (sometimes
several) for the passage of menstrual blood. It is stretched or torn by coitus and more or
less obliterated by childbirth. A few tags of skin called carunculae myrtiformes are left.
Normal Hymen after

virgin coitus (or
hymen after using
tampon)
Carunculae
myrtiformes
14
BARTHOLIN’S GLAND
The BULB of the VESTIBULE consists Bulbospongiosus

of two masses of erectile tissue on either muscle (cut)
side of the vagina, lying beneath the skin
and bulbospongiosus muscle, but superficial
to the perineal membrane. They are
connected anteriorly by a narrow transverse
strip and are the homologue of the bulb of
the penis. Bulb of
BARTHOLIN’s (Greater vestibular) vestibule
glands are the homologues of the
bulbourethral (Cowper’s) glands in the male
but lie superficial instead of deep to the
perineal membrane. Each gland is partly
covered by the erectile tissue of the bulb and
drains by a duct about 2 cm long which opens
into the vaginal orifice lateral to the hymen.
Bartholin’s
Bartholin’s gland is not palpable in the healthy gland
state.
The erectile tissue of the bulb becomes tumescent during sexual excitement and the glands
secrete a mucoid discharge, which acts as a lubricant.
HISTOLOGY OF BARTHOLIN’S
GLAND Duct
The gland is formed of racemose
glands lined with columnar or
cuboid epithelium. The duct
demonstrates the very intimate
embryological connection between
genital and urinary tracts by being
lined with transitional epithelium. Gland
15
MUSCLES OF THE PERINEUM
ISCHIOCAVERNOSUS BULBOSPONGIOSUS
This muscle compresses the root of the This muscle conceals the vestibular bulb
clitoris during sexual excitement, to and Bartholin’s glands. Its function is to
produce erection by venous congestion. diminish the vaginal orifice during coitus.
Perineal
body Ischiocavernosus
Superficial
SUPERFICIAL Bulbospongiosus
transverse
TRANSVERSE perineal
PERINEAL MUSCLE muscle Urogenital
A small muscle that helps diaphragm
to fix the perineal body.
Levator ani
EXTERNAL ANAL
SPHINCTER
Normally in a state of
contraction to keep the
External
anus closed. It also helps Coccygeus
anal sphincter
to fix the perineal body.
The Perineal body is a

fibromuscular node
between the anus and
vagina with attachments to
eight muscles:
One Sphincter ani
One Bulbospongiosus
Two Transversi perinei superficiales
Two Transversi perinei profundi (deep: not shown here)
Two Levatores ani
The whole mass is what gynaecologists mean when they talk about ‘the perineum’. If it is
damaged during childbirth and not properly repaired and healed, it will not function properly
and the efficiency of the whole pelvic diaphragm may suffer, leading to urinary or faecal
incontinence.
16
THE UROGENITAL DIAPHRAGM
THE UROGENITAL DIAPHRAGM (Triangular Ligament)

This area of the perineum is more developed and surgically more important in the male. It
consists of two sheets of fascia with a layer of muscle in between. It covers the pubic arch and
is pierced by the urethra and, in the female, by the vagina.
Upper fascia of diaphragm

(same as fascia of obturator muscle)
⎧ Trans. perinei profundus

Muscle layer ⎨
⎩ Sphincter urethrae
(This space between the fasciae is
sometimes called the ‘deep perineal pouch’.)
Lower fascia of diaphragm or perineal

for vagina membrane or deep fascia of urogenital region
for urethra
Urogenital
diaphragm
Coccyx
Transversus
perinei
profundus,
superficialis Symphysis
pubis
Perineal body Sphincter Anal

Perineal
urethrae sphincter
body
All the perineal muscles lie superficial The ‘sphincter urethrae’ is the system of
to the perineal membrane, except the musculature that assists the bladder
transversus perinei profundus, which muscle in closing the urethra. It is made
helps to fix the perineal body. up of the transversus perinei, the
(See page 16 on the function of the bulbospongiosus, and the levator ani; the
sphincter.) anchoring bony points are the lower
border of the symphysis pubis and the
coccyx.
17
ISCHIORECTAL FOSSA
A wedge-shaped space between the ischial tuberosity and the anus, filled with fat and crossed
by vessels and nerves.
Piriformis
BOUNDARIES
Laterally, the obturator
fascia and ischial tuberosity.
Obturator
Posteriorly, the internus
sacrotuberous ligament.
Anteriorly, the urogenital
diaphragm.
Medially, the sphincter ani
and levator (anal) fascia.
Ischial
Sacrotuberous tuberosity
ligament
Pudendal
nerve and
vessels
Urogenital
diaphragm
Ischiorectal
The ischiorectal fat is fat
traversed by the pudendal
vessels and nerves and
some small perineal
branches of sacral nerves.
This pad of fat supports
the anal canal and pelvic
diaphragm.
Levator
ani
Gluteus
maximus
18
MUSCLES OF THE PELVIS
Obturator
Levator ani
Pelvic diaphragm fascia
Coccygeus
‘White
Obturator internus
line’
Piriformis Ischial
spine
The Levator ani arises from the
back of the pubis, the obturator
fascia (by a ‘tendinous arch’ or Coccyx
‘white line’), and the ischial spine.
Levator ani
Vagina Urethra
Anus
The fibres pass back and medially to
be inserted into the vaginal wall, the
perineal body, the anal wall, the
anococcygeal raphe and the coccyx.
Nerve supply: nerve to levator ani and

pudendal nerve (S4).
Coccyx
Levator ani
muscle
(From below)
S1
S2
The Coccygeus is a triangular Piriformis
muscle, partly replaced by the muscle S3
sacrospinous ligament. It arises
from the ischial spine and fans S4 Pudendal
out to an insertion on the sides of nerve
the sacrum and coccyx. S5
Nerve supply: S4 and anococcygeal

nerve (S5). Sacral
plexus
Coccygeus muscle
19
PELVIC DIAPHRAGM
The Obturator internus arises

Piriformis
from the anterolateral wall of the
pelvis (and obturator
membrane) and passes Origin of
backwards through the lesser levator ani
sciatic foramen to be inserted
into the trochanter of the femur
(L5, S1 and S2).
The Piriformis arises from the
front of the sacrum and passes
through the greater sciatic
foramen to be inserted into the
trochanter of the femur
(S1 and 2).
These muscles are primarily

lateral rotators of the hip and
postural muscles. Ischial
spine Obturator internus
FUNCTIONS OF THE PELVIC DIAPHRAGM

Apart from helping to fix the perineal body and assist the vaginal and anal sphincters, the main
function of the pelvic diaphragm is to support the pelvic viscera.
The muscles used to be named as follows:

pubococcygeus
¼ levator ani
iliococcygeus
ischiococcygeus ¼ coccygeus
In the lower animals, their function is to move the tail (the coccyx). In man, they have to meet
the requirements of the erect position and resist the strain imposed by any increase in intra-
abdominal pressure such as when laughing, coughing, straining at stool, etc. In addition, a
complete relaxation of the muscles should be possible during parturition so that the vaginal
foramen may enlarge almost to the size of the bony pelvic outlet.
20
PELVIC FASCIA
THE PELVIC FASCIA

Parietal Layer
The aponeuroses and fascial sheaths
of the pelvic muscles (the ‘wallpaper’
Bladder
of the pelvis).
Visceral Layer
The fascial sheaths of the organs and the
fatty tissue filling the space between Cervix
them (the ‘stuffing’ of the pelvis).
In certain areas, this stuffing is
condensed and strengthened by
plain muscle fibres and elastic
tissue to form the ligaments of Rectum
the uterus (pp. 28–31).
Uterosacral
Sacrum
ligament
Muscle Fascia
with Relations of the Fascia
nerves
The nerve trunks, which leave the pelvis,
are ‘outside’ the fascia. The vessels are
Vessels
‘inside’ and lie between the fascia and
peritoneum.
Peritoneum
Bone
These fascial prolongations on

structures leaving the pelvis Inguinal
form points at which pus may ring
track from a pelvic abscess to
a point in the buttock or groin
or above the inguinal ligament, as
Femoral
demonstrated in this image.
ring
(The greater sciatic notch is not
shown.)
Obturator
foramen
21
THE VAGINA
The vagina is a tubular structure extending from the vulva to the uterus.
Uterus
Bladder
Posterior
fornix
Anterior
Urethra Vagina Rectum Vagina fornix
Lateral view. Note the close Sagittal section. Note anterior and
relationship to urethra, bladder posterior walls normally in contact;
and rectum. also anterior and posterior fornices.
Cervix Levator
Ureter ani Vagina
Cervix
Trigone
of bladder
Obturator
internus
Vagina
Urethra Ischiorectal
fossa
Crus of
Urogenital Bulb clitoris
diaphragm
Anterior view shows the very intimate Coronal section shows the relationship
relationship with the bladder base and of vagina and pelvic floor.
ureters.
22
THE VAGINA
In the nulliparous adult, the vagina

is H-shaped in section and marked Cervix
by longitudinal furrows – the Rugae
columns of the vagina – and (transverse
numerous transverse ridges or ridges)
rugae. This configuration permits
great distension during childbirth
and is much less marked in parous
women.
Longitudinal
fold
H-shape
Vaginal fornices
These are gutters at the top of the
vagina, surrounding the cervix.
Anterior fornix – related to the

bladder base and the
uterovesical fossa.
Posterior fornix – related to the Posterior fornix

peritoneum of the Pouch Bladder
Anterior fornix
of Douglas. This fornix is deeper
than the anterior one because of the
angle the cervix makes with the
vagina.
Uterine artery
Lateral fornices – related to the

Ureter
ureters and the uterine vessels. Lateral fornix
Vagina
23
THE VAGINA
HISTOLOGY
Its length is about 9 cm along the posterior wall and 7.5 cm along the anterior. The width
gradually increases from below upwards.
Connective tissue
(contains many veins)
Plain muscle with
Strong fascial sheath elastic tissue (outer
Squamous epithelium
(part of pelvic fascia) coat longitudinal,
(no glands)
inner irregular)
The vagina pierces the urogenital diaphragm and is encircled at its lower end by the
voluntary bulbospongiosus, which has some sphincteric action, although the levator ani
muscle is more effective.
VAGINAL SECRETION
This is composed of alkaline cervical secretion, desquamated epithelial cells and bacteria.
The epithelium is rich in glycogen which is converted by Doderlein’s bacillus into lactic
acid. The vaginal pH is about 4.5 and provides a fairly effective barrier against infection.
THE VAGINAL EPITHELIUM

This is composed of several layers of
squamous cells with no keratinisation. It
develops papillae, which dip into the
fibrous corium. It is much thinner in the
child, and the rugae are absent. This
appearance recurs in old age. Cyclic
changes are discussed on page 53.
24
UTERUS
The uterus is a hollow viscus Fallopian

composed of smooth muscle, tube
whose sole function is gestation. Ovarian
ligament
It lies between the rectum and Round
the bladder and is continuous ligament
with the vagina.
Ureter
Bladder
Cervix
Rectum Urethra
Vagina
7.5 cm It is important to be familiar with

the measurements of the adult
6 cm nulliparous uterus because of the
1.2
frequent physiological or
cm
pathological variations.
Length 7.5 cm
2.5 cm Thickness 2.5 cm
Length of cavity 6 cm
Thickness of muscle wall is
about 1.2 cm
Vaginal ultrasound can be used to
measure the uterine dimensions.
25
UTERUS
CORPUS AND CERVIX

The upper two-thirds of the uterus are Fundus
called the corpus or body, and the
lower third is the cervix or neck. They
are quite distinct in function, and 5 cm
therefore in structure as well, although Corpus
the transition from muscle to fibrous
tissue is gradual.
Internal os
2.5 cm Cervix
External os
CORPUS (UTERINE BODY) CERVIX

Its function is to provide a mucous Its function is to provide an alkaline
membrane (endometrium) suitable for secretion favourable to sperm penetration,
implantation, and thereafter to contain the and once the uterus is gravid, to act as a
growing fetus until it is mature. It is sphincter. It is composed mainly of fibro-
composed mainly of smooth muscle. elastic tissue.
ISTHMUS UTERI
This name is sometimes given to the
upper few millimetres of the cervical canal
below the internal os, an area to which the
specific function of developing into the Corpus
lower segment has been ascribed. The
epithelium is intermediate between
Anatomical
corpus and cervix; but if it were not for internal os
the importance of the lower segment in
the theory of the physiology of pregnancy, Isthmus
it is unlikely that anatomists would have
provided either an identity or a name for Histological
the isthmus uteri. internal os
Cervix
26
UTERUS
CAVITY OF THE CORPUS

The anterior and posterior
walls are almost in contact, but
in coronal plane the cavity is
triangular.
The muscle wall at each cornu
is pierced by the very narrow
interstitial portion of the
fallopian tube. Interstitial
portion
CERVIX
The external os is small before
parturition and is sometimes
called the os tincae (mouth of a
small fish). After the birth of a
child, it becomes a transverse
Nulliparous os Parous os
slit – ‘the parous os’.
Supra-
vaginal
The cervical canal is portion
fusiform and marked by
curious folds called the
‘arbor vitae’.
The cervix is divided

into supra- and
infravaginal portion by
the attachments of the
vagina. Bladder Portio
vaginalis
27
UTERUS
RELATIONSHIP OF UTERUS AND URETER

The ureter is directly related to the uterine artery and the vaginal vault but is not in direct
contact with the uterus.
Fallopian
tube
Ovarian
ligament Uterus
Ureter Round
ligament
This picture shows the ureter

passing under the uterine artery
Bladder
on its course to the bladder.
Uterine
artery
Uterus
Ureter In this picture, the bladder has been

removed to show just how close the
Uterine ureter is to the cervix. It also
artery demonstrates the problems that are
likely to be encountered in
controlling haemorrhage and
Uterine avoiding damage to the ureter
vein during surgery in this area
Cervix
(see pages 288–291).
Vagina
28
UTERUS
LIGAMENTS OF THE UTERUS Round

ligament Fallopian
tube
Epoophoron
Fallopian tube
Ovarian
ligament
Uterine
artery
Round
ligament
Broad
ligament Ureter
Ovary Bladder
The broad ligament is a fold of peritoneum passing from the uterus to the side wall of the
pelvis. It contains the fallopian tube, the round and ovarian ligaments, the mesonephric
remnants, the ovario-uterine anastomosis and, in its base, the ureter.
Fallopian External
tube iliac
Ovarian vessels Infundibulopelvic ligament
ligament Ovarian vessels
Uterus
Broad ligament
Round
ligament
Ovary
Inguinal
ring
The ovarian and round ligaments The part of the broad ligament between
are the vestigial gubernaculum. The the infundibulum and pelvic wall is called
round ligament ends in the inguinal the infundibulopelvic ligament and
canal and its fibres disperse in the contains the ovarian vessels and nerves.
labium majus. Note the proximity of external iliac vessels.
29
UTERUS
LIGAMENTS OF THE UTERUS—(cont’d)

The main supports of the uterus are the fibromuscular condensations of tissue in the pelvic
fascia (page 21).
Recto-
uterine
fold
Uterosacral
ligament
The uterosacral ligaments pass from the back of the uterus to the front of the sacrum and
are easily identified by the covering recto-uterine fold of peritoneum. These ligaments
maintain the anteverted position of the uterus, and they are accompanied by uterine vessels
and nerves.
Bladder ‘pubo-
Round
cervical’
ligament
Transverse Uterus
cervical Transverse
ligament cervical
ligament
‘utero-
Rectum sacral’
The transverse cervical ligaments (Mackenrodt’s, cardinal ligaments) pass from the uterus and
vagina to a wide insertion in the lateral pelvic wall. They lie below the broad ligament and
contain vessels and nerves. The uterosacral ligament may be regarded as the posterior edge of
the transverse cervical; its anterior edge is sometimes called the pubocervical, but this is not
well defined.
30
UTERUS
HISTOLOGY Fallopian
The uterus has an incomplete tube Ovarian ligament
peritoneal coat, which is very
Peritoneum
adherent. The anterior bare area is
to allow movement of the bladder.
There is a complete fascial sheath
continuous with the vagina, and the Round Posterior
body is made of smooth muscle ligament surface
interspersed with fibro-elastic tissue.
There is a reversion of the ratio of
muscle to connective tissue as the Anterior Ureter
cervix is approached, and the cervix surface
is nearly all fibrous.
The epithelium of the cavity is called the

endometrium and consists of a single layer
of cuboid or columnar ciliated cells on a
cellular stroma. The stroma is deeply
pierced by invaginations of the epithelium
called uterine glands, which secrete a small
amount of mucus to maintain moistness.
Endometrium (low power)
For cyclical changes in the endometrium see
pages 49–51.
Uterine gland (high power)
The cervix is lined by a single layer of high

columnar ciliated epithelium, which covers
the folds of the arbor vitae (pp. 29–30) and
Cervical lines the cervical glands. The glands secrete
gland an alkaline mucus, which is favourable to the
(low power) activity of spermatozoa.
31
FALLOPIAN TUBE
The tube extends from the cornu of the uterus into the peritoneal cavity and is about 10 cm
long. The two tubes are twice the width of the pelvis, and they do more than just provide a
passage for the ovum into the uterus. They must be sufficiently mobile to assist the ovum
onwards by peristalsis; and sufficiently long to allow the ovum time for maturation after it has
been fertilised in the ampulla and before it is ready for implantation in the uterus. The tube
and ovary together are called the adnexa (‘viscera adnexa’ – organs next to) of the uterus.
Interstitial part Isthmus Ampulla Infundibulum

1 cm long and 2 cm long, straight 5 cm long, thin 2 cm long. The
very narrow and cord-like. walled and terminal expansion,
(less than 1 mm). 1 mm diameter. convoluted. with fimbrial
processes
which help
to attract
the ovum.
The tube has a lining of ciliated cells interspersed with non-ciliated secretory cells (‘peg’
cells). There is little or no submucosa. The epithelium is arranged in a complex pattern of
plications, which becomes more marked as the outer end is approached.
32
BROAD LIGAMENT
BLOOD VESSELS
Fallopian tube
There is an
anastomosis
between the uterine
and ovarian
arteries, and the
fallopian tube is
supplied by vessels
in an arcade pattern
(cf. bowel).
Anastomosis
Uterine vessels
Ovarian vessels
VESTIGIAL STRUCTURES
The epoöphoron and the paroöphoron are remnants of the mesonephros, and the duct
(Gartner’s duct) is the vestige of the mesonephric duct, which passes into the uterine muscle
about the level of the internal os and continues downwards in the vaginal wall.
Epoophoron
These structures may

give rise to cysts
(hydatids of Morgagni,
Kobelt’s tubules,
fimbrial cysts) whose
Ovary embryonic derivation is
uncertain. They are
probably mesonephric
and can be grouped
Vestigial
together as ‘vestigial
Paroophoron ducts
cysts’.
Gartner’s duct
33
OVARY
The ovary is about 3 cm long and 1.5 cm

wide, roughly the size and shape of a date.
It has its own mesentery, the mesovarium
from the posterior leaf of the broad
ligament, and is attached to the cornu of
the uterus by the ovarian ligament, which
is continuous with the round ligament, the
vestigial gubernaculum.
Ovary
Right
ovarian
Left renal
vein
vein
Ovarian The ovary is developmentally an abdominal

Abdominal
arteries organ and its blood supply is from the
aorta
abdominal aorta. The ovarian vessels lie in
Inferior the infundibulopelvic ligaments.
mesenteric
artery Note: The left ovarian vein empties into the
left renal vein.
Ovarian ligament
Mesovarium
Hilum
The free surface of the ovary has no

peritoneal covering, only a surface
epithelium. The part attached to the
mesovarium through which all vessels
and nerves pass, is called the hilum.
Free surface
of ovary
34
OVARY
HISTOLOGY Hilum Mesovarium

Cross section shows the ovary to be
roughly divided into a vascular medulla
and a cortex.
The cortex is composed of a specialised

ovarian stroma with a cuboidal surface
epithelium which, like the tubal ostium,
is intraperitoneal.
Surface
epithelium
Tunica
albuginea Medulla Cortex
Note the condensed layer of stroma under The hilum is characterised by the presence
the surface epithelium, called the tunica of paroöphoron tubules, which are of
albuginea. smooth muscle lined with ciliated
epithelium; and by vestigial remnants of
the sex cords called the rete ovarii, the
analogue of the seminiferous tubules.
These tissues are one reason for the
extraordinary variety of ovarian tumours
that can develop.
The hilum, showing cross section

Cortex in an infant Cortex in an adult of paroophoron tubules.
35
OVARY
The CORPUS LUTEUM (‘yellow body’: the high lipid content required for steroid
production gives the mature corpus luteum a yellow colour). During growth, the Graafian
follicle gradually approaches the surface of the ovary and eventually extrudes the ovum
through the stigma, into the waiting fimbriae of the tube. The follicle cells then quickly
become luteinised by the retention of fluid to form the corpus luteum whose function is to
secrete progesterone and prepare the endometrium for implantation of the fertilised ovum.
Thecal cells Lutein cells
Corpus luteum (low power)

Corpus luteum (high power)
LH
LH Theca interna The growing corpus luteum is

receptor
supplied with capillaries from the
Cholesterol ovarian stromal vessels, and both
theca and granulosa lutein cells
Testosterone Pregnenolone secrete all the hormones. Under the
3βHSD
influence of luteinising hormone
17βHSD Progesterone (LH), theca cells metabolise
cholesterol into androstenedione. The
Andro- 17-hydroxy-
stenedione granulosa cells then metabolise the
Desmolase progesterone
androstenedione produced by the
Basement
membrane theca cells into oestradiol under the
Blood control of follicle stimulating
supply hormone (FSH). Thus, both cell
17βHSD
types and both gonadotrophins are
Andro- Testosterone
crucial to oestrogen synthesis.
stenedione
Aromatase Aromatase
Oestrone Oestradiol
17βHSD
FSH
receptor
Granulosa
Follicular cells
FSH fluid
36
OVARY
Corpus albicans
As the physiological cycle proceeds, degeneration gradually occurs, and eventually the corpus
luteum is hyalinised – a corpus albicans – and is absorbed in about a year. Consequent
scarring accounts for the irregular surface of the ovary in the more mature woman.
Follicular atresia
In utero, there are 7 million ovarian follicles. Atresia of the follicles commences in utero. At
birth, the ovary contains a million follicles. There is continued loss of ovarian follicles with
advancing age. Only about 400 can ever become mature follicles, but at each cycle and
probably during childhood several follicles may start to develop and for a time produce
hormones. This abortive attempt ends in atresia and the atretic follicle is absorbed; but
the process may account for anovular cycles and for the oestrogens produced by young
pre-pubertal girls whose breasts are beginning to develop. The rate of follicular loss
appears constant until the age of 37 and thereafter the rate of loss accelerates until the
menopause.
106
Ovarian follicles
105
104
103
102
0 10 20 30 40 50
Age
37
CHANGES IN THE GENITAL TRACT WITH AGE
Apart from normal growth, the appearances of the genital tract depend entirely on the supply
of oestrogens.
THE VULVA THE VAGINA
This is only a cleft in the perineum The rugae are absent before puberty and
before puberty. Then the labia minora gradually (over several years) disappear
become more prominent and the fat of after the menopause. In old women, the
the mons and the labia majora is vagina is thin, atrophic and completely
increased. Apart from the effects of smooth.
coitus and parturition (p. 14) the most
obvious sign of ageing is the gradual THE OVARY
increase in size of the labia minora This is at its largest during the
compared with the labia majora. reproductive stage and shrinks thereafter.
All the oocytes are gone by the time of
the menopause, and the cortex consists of
fibrous tissue.
THE UTERUS
Infantile: the cervix is longer than the Pubertal: with the gradual increase in
corpus, and there is no flexion. oestrogens, the corpus grows in relation
to the cervix.
After the menopause, the uterus gradually

Adult: the corpus is now twice as long as atrophies and in an old woman, the cavity
the cervix and the normal degree of may be less than 5 cm and the cervix simply
flexion has appeared. an aperture in the senile vaginal vault.
38
BLOOD SUPPLY OF THE PELVIS
The common iliac artery Common iliac

bifurcates at the level of
the sacrovertebral junction Internal iliac
into external and internal ⎩ ⎩
iliac arteries. The internal ⎨
Iliolumbar
iliac runs for about 4 cm
⎧ ⎪⎪
⎩ ⎪
and divides into an ⎨ Lateral
⎧ sacral
⎨
anterior and a posterior Posterior
⎪⎪
trunk, which are the main trunk
pelvic supply. The ⎪ mainly
Superior ⎧
branches are subject to muscular
gluteal
great variation. Obturator
Inferior
Superior vesical gluteal
Uterine
⎧ Vaginal
⎪
Often the same ⎨ Internal
⎪ Inferior pudendal
⎩ vesical Middle rectal
Ureter
Ovary
SUPPLY TO UTERUS, VAGINA

Uterus
AND BLADDER
This picture shows an arrangement
often met with.
Bladder
39
The vessels of the uterus and vagina are

much coiled to provide extra length Uterus
during pregnancy. Note the nearness of
Ureter
the ureter.
Cervix Uterine
artery
Uterine
vein
Vagina
This picture shows the course

of the pudendal artery
Pudendal passing behind the ischial
artery spine and along the pudendal
canal to the perineum.
Ischial
spine
Pudendal canal
inside ischial tuberosity
In the ischiorectal
fossa, the pudendal artery
divides into inferior rectal
and perineal branches.
40
COLLATERAL BLOOD SUPPLY

If the internal iliac artery has to be ligated, the collateral circulation should be adequate. It
depends on anastomoses with the abdominal aorta, external iliac and femoral arteries.
ABDOMINAL AORTA
1. Ovarian artery ! uterine artery. Ovarian artery
2. Inferior mesenteric ! superior
rectal ! inferior rectal (pudendal).
3. Median sacral ! lateral sacral. Aorta Inferior mesenteric
artery
Median sacral artery

EXTERNAL ILIAC ARTERY
Inferior epigastric
artery
Transversus
abdominis
External muscle
iliac
artery
Obturator
Deep circumflex
artery
iliac artery
The inferior epigastric anastomoses with the obturator; the deep circumflex iliac with the
iliolumbar and lumbar arteries.
Circumflex
THE FEMORAL ARTERY branches of
The deep external pudendal femoral
anastomoses with the internal pudendal.
Femoral
The superior and inferior gluteal arteries
anastomose with the perforating and Deep
circumflex branches of the femoral and external
profunda femoris. (This is the ‘cruciate’ pudendal
anastomosis.) Profunda
femoris
41
LYMPHATIC DRAINAGE OF THE GENITAL TRACT
The lymphatic plexuses

accompany the blood vessels
and drain into groups of glands,
which are constant in position Presacral
and are given names. Para-aortic
It will be seen that while the Common iliac
uterus is likely to drain into the
external iliac group on the Internal
lateral wall of the pelvis, the iliac
vagina drains into the internal
iliac group and the ovary drains External
directly into the aortic glands. iliac
Uterus
Bla
dd
er
The superficial inguinal glands also receive lymph

drainage from the vulva and the lower vagina. (But
these structures may also drain via the pudendal
vessel channels into the internal iliac group.)
Because lymphatic plexuses and glands are a path of metastatic spread of cancer, treatment by
either irradiation or surgery must involve an attack on the area of lymphatic drainage of the
organs concerned. The lymphatic network is very widespread and the metastatic paths are not
always the same; it is now recognised that the chance of cure is much reduced once the spread
to the glands has occurred, whatever be the treatment given.
42
NERVES OF THE PELVIS
Lumbosacral
cord
Piriformis
Obturator
nerve
The sacral plexus lies and
on the piriformis artery
muscle beneath the
vessels.
Superior
gluteal
artery
s
Inferior
bi
Internal Vesicle
Pu
gluteal
pudendal branch
artery
artery
Pudendal
artery and Pudendal
nerve artery
Ischial Ischial
spine tuberosity
The pudendal artery and nerve pass behind The pudendal nerve crosses the
the ischial spine to gain the ischiorectal fossa. ischiorectal fossa to supply the vulva and
perineum.
43
AUTONOMIC NERVE SUPPLY OF THE PELVIS
Superior hypogastric
plexus
Ovarian artery
and nerves
Middle
hypogastric
plexus
Superior
hypogastric
plexus (pre-
sacral nerve) Nervi
erigentes
Middle
hypogastric
plexus S2
Inferior
hypogastric plexus S3
S4
Sympathetic fibres enter via the
lumbosacral chain and the mesenteric
nerves. These are called the presacral Inferior
hypogastric plexus
nerves at the bifurcation of the aorta.
They pass forward in the uterosacral
Parasympathetic nerves (nervi erigentes) join
ligaments to reach the viscera and are
the hypogastric plexuses from sacral roots 2, 3
known there as the hypogastric plexus
and 4.
or plexus of Frankenhauser.
There is an additional sympathetic supply
by the nerves accompanying the ovarian
vessels.
The function of the autonomic nerves is not understood. The cervix or vagina may be grasped
by forceps in some patients with only minimal sensation, and a uterine sound or intrauterine
contraceptive device in the uterine cavity may only cause a vague ‘visceral’ discomfort.
However, there are cases where cervical stretch at a procedure or during passage of a clot
causes vasovagal symptoms, and on occasion collapses.
44
CHAPTER 3
PHYSIOLOGY OF THE
REPRODUCTIVE TRACT
Ovulation 46
Female Reproductive Physiology 46
Hypothalamus 49
GnRH 50
FSH 50
LH 50
Ovulation 50
Cyclical Ovarian Hormonal Changes 51
Oestrogens 51
Progesterone 51
Endometrial Cycle 51
Action of Ovarian Hormones 52
Oestrogen 52
Progesterone 52
Target Tissues 52
Effects of Ovarian Hormones 53
Genital Tract 53
Breast 53
Hypothalamus 53
Cardiovascular System 53
Skeleton 53
Psychological Characteristics 53
Puberty 54
The Menopause 55
PHYSIOLOGY OF THE REPRODUCTIVE TRACT
OVULATION
FEMALE REPRODUCTIVE PHYSIOLOGY

During reproductive life, the cyclical development of ovarian follicles is the dominant process.
The associated hormonal production has significant effects on the female genital tract,
hypothalamus and pituitary.
In men, gamete production continues throughout life, whereas women develop their life
supply of gametes during intrauterine life. See Chapter 1. The numbers decline even before
birth, and there will be around 300,000 remaining at puberty.
The surface of the ovary is covered by a cuboidal ‘germinal’ epithelium. This layer is
contiguous with the peritoneum. Underneath the epithelial layer is a thin layer of fibrous
tissue, beneath which is the true cortex.
Specialised
parenchyma
Cortex
Blood vessels Primordial
and nerves follicles
Medulla
entering hilum
embedded in
supporting Germinal
fibrous tissue Cortex epithelium
Rete
ovarii
Fibrous
tissue
The cortex consists of a specialised stroma or parenchyma; the primordial follicles are
embedded in this layer.
Granulosa
Pre-granulosa cells
Nucleus
cells
Fat
Zona Zona
globules Eccentric
pellucida pellucida
nucleus of ovum
Primary oocyte
The primordial follicle consists of a primary oocyte surrounded by a single layer of flattened
cells, the pre-granulosa, said to be derived from the cells of the sex cords.
The pre-granulosa cells become cuboidal and proliferate to form a shell several layers thick. At
46 this stage, a hyaline membrane is formed immediately around the ovum – the zona pellucida.
OVULATION
The granulosa cells continue to proliferate Granulosa cells

until the follicle is approximately 200 mm in
diameter. Fluid spaces now appear between
Liquor folliculi
the granulosa cells. They coalesce to form a in antrum
cavity, the antrum, pushing the ovum to one
side. The granulosa cells immediately Corona
surrounding the ovum are now known as radiata
the corona radiata, and the whole mass of
cells in this situation is termed the cumulus
oophorus. Zona
Ovum pellucida
At the same time, the surrounding parenchymal cells arrange themselves concentrically
around the follicle. The cells opposite the ovum become smaller and more epithelial in
appearance. As the follicle increases in size, this epithelial change spreads to the parenchymal
cells around the circumference of the follicle. This band of cells constitutes the theca interna.
The cells are surrounded by sinusoidal capillaries, thus forming an endocrine gland-like
structure. External to this band, the parenchymal cells are also arranged concentrically but
retain their fusiform shape.
Theca interna Released

ovum
Theca
externa
Ruptured Ovulation
follicle
The follicle, which is called the Graafian follicle, continues to grow to a size of more than
1.0 cm. Approximately four to five follicles may attain this size and project on the surface
of one ovary. One of these follicles ruptures on the surface, releasing the ovum surrounded
by some of the granulosa cells. Ovulation is initiated by the gonadotrophin surge occurring
in response to the long loop oestradiol positive feedback. Vascular changes occur in the
follicle within minutes of the luteinising hormone (LH) surge, possibly due to release of
histamine or other kinins. Proteolytic enzymes are released and collagen disintegrates.
It is likely that insulin-like growth factors (IGFs) such as IGF-1 regulate granulosa
differentiation. It is not known whether ovarian adrenergic nerve fibres or smooth muscle cells
are involved. Prostaglandins may play a role. 47
OVULATION
From fetal life to the menopause, follicular growth is continuous. Oestrogen initiates the
process. Three phases can be distinguished:
FETAL CHILDHOOD ADULT

Primordial
follicle Placental Intra-ovarian Intra-ovarian
oestrogen oestrogen oestrogen
Growth Growth Growth

Induction Induction Induction
of FSH of FSH of FSH
receptor receptor receptor
Continued growth Continued growth Continued growth

Pituitary Pituitary
FSH FSH
Minimum
FSH.
Large
quanitities
of Cyclical
luteinising Lack of LH
HCG LH production
Limited growth Growth limited:

no ovulation
Atresia Ovulation
Atresia
HCG = Human Chorionic Gonadotrophin.

FSH = Follicle Stimulating Hormone.
LH = Luteinising Hormone.
Normally only one follicle ovulates. Cohorts of follicles enter the growth phase in succession,
and follicles of various sizes are usually found. The follicle destined to ovulate is among a
cohort stimulated to grow by follicle stimulating hormone (FSH) secreted by the pituitary
during the last few days of the cycle. Only about 400 of the original 2 million follicles will
48 reach the ovulatory stage and there is continuous wastage of follicles from fetal life onwards.
OVULATION
Ovulation is the final event in a step-wise stimulatory mechanism starting in the

hypothalamus, which contains gonadotrophin releasing cells. These produce a gonadotrophin
releasing hormone (GnRH).
HYPOTHALAMUS
Gonadtrophin releasing
Median eminence
cells
Gonadotrophin releasing
hormone
FSH LH
Anterior
pituitary
hormones
LH
FSH
Ovarian Progesterone
hormones
Oestradiol
Day
1 5 12 14 22 28
Bleeding Proliferation Secretory phase Bleeding
49
Endometrial cycle
OVULATION
GnRH
This substance begins to be secreted just before puberty in pulses every hour and continues in
this fashion for the rest of life. There is only a single releasing hormone responsible for the
production of both FSH and LH. The type of gonadotrophin secreted by the pituitary appears
to be determined by other factors related to the phase of the menstrual cycle.
FSH
FSH stimulates follicular development and production of oestrogen. A peak of FSH is reached
by the 6th day of the menstrual cycle. At this point, the rising oestrogen has a negative
feedback effect, and the FSH curve languishes for a day or two; then, it resumes its upward
trend to achieve a second peak at the time of ovulation on day 12.
Inhibin is produced by the corpus luteum and inhibits the production of FSH while
it is active. As a result, follicular growth ceases. After the 22nd day, when the corpus
luteum becomes inactive, FSH secretion and growth of follicles are resumed.
LH
Very low levels of LH are recorded in the early part of the cycle, but a sudden surge,
coinciding with the second peak of FSH, induces ovulation and formation of the corpus
luteum. Shortly thereafter, the level of LH returns to pre-ovulatory values.
OVULATION
FSH production is usually inhibited by rising oestradiol levels; however, a change occurs
as the dominant follicle develops. Changes occur in the receptors on the follicular cells
as the cycle progresses. Although the blood FSH is temporarily reduced after the 6th day,
the larger follicles have accumulated sufficient FSH to maintain growth and oestrogen
production. As the blood concentration of oestrogen continues to increase, it appears to reach
a critical level at the 12th day, and in place of its usual negative feedback effect on the
pituitary, it suddenly exerts a positive feedback effect with a consequent rise in FSH
(the second peak) and secretion of LH.
Gonadotrophin Secretion (International Units per Litre)
Menstruation Follicular Ovulation Luteal phase

phase
Mean Range Mean Range Mean Range Mean Range
FSH 10 3–13 8 3–15 20 4–32 5 2–0
LH 8 3–12 8 6–14 65 43–88 8 2–13
50
CYCLICAL OVARIAN HORMONAL CHANGES
OESTROGENS
The plasma values of the three main oestrogens, oestradiol, oestrone and oestriol, are
almost parallel throughout the cycle. The levels are low during menstruation and very
gradually increase. Significant changes are noted around the 7th–8th day of the cycle,
the levels rising to a maximum around the 12th day – ovulation peak. A fall occurs
24 h later, followed by a further increase a week later – the maximum phase of corpus
luteum activity.
PROGESTERONE
Progesterone is almost absent from the plasma in the early stages of the menstrual cycle.
At the time of ovulation, there is a steep rise, and a maximum value is achieved around the
20th–22nd day. Thereafter, a steep fall occurs.
ENDOMETRIAL CYCLE
Early Proliferative Phase
The endometrium shows proliferation of its stroma and glands, the latter elongating.
The cells lining the glands are cuboidal, with definite limiting membranes, and the stromal
cells are thin and spindly.
Late Proliferative Phase

The glands are very large and dilated – late proliferative phase. The blood vessels are also
more prominent, and capillaries are dilated.
These proliferative changes are due to the influence of oestrogen secreted by the ovary at this
time.
Secretory Phase
Following ovulation, the corpus luteum produces large quantities of progesterone, which
induce secretory changes in the glands and swelling of the stromal cells. There is a rich blood
supply, and the capillaries become sinusoidal.
Menstruation
Towards the end of the 28-day cycle, the stroma becomes even more vascular and
oedematous, small haemorrhages and thrombi appear, and the endometrium ultimately breaks
down due to withdrawal of the hormonal support. Vessel necrosis is preceded by intense
vasospasm, possibly stimulated by prostaglandin F2-a.
The superficial layers of endometrium, together with blood and leucocytes, are shed and
discharged – menstruation. Within a day or two, the raw surface is healed over by epithelium
proliferating from the basal portions of glands.
51
ACTION OF OVARIAN HORMONES
OESTROGEN PROGESTERONE
Oestrogens have multiple effects including This hormone prepares the endometrium
stimulation of growth and development of for implantation of the fertilised ovum and
secondary sex features in the female. has no homologue in the male. In a clinical
sense, it has an antioestrogen action.
TARGET TISSUES
Tissues of these structures are particularly sensitive to oestrogen
stimulation. The cytoplasm of their cells contains a specific
Hypothalamus
oestrogen receptor molecule that has an affinity for oestrogen
100,000 times greater than the carrier protein, which retains the
hormone in the bloodstream. Oestrogen also acts at the cell
Breasts
membrane, regulating ligand-gated ion channels.
Genital tract
Progesterone receptors appear in the cytoplasm only after the cell
has been primed by oestrogen.
Blood- Extracellular
stream space Cytoplasm Nucleus Nuclear
receptor
protein
Oestrogen Oestrogen
en Oestrogen
trog
Oes tor
p
rece in
Carrier r o t e
p
protein
Cell
Nuclear
membrane
membrane
Transfer of the oestrogen molecule to the cell nucleus occurs more readily during the
FSH phase of the cycle than during the LH phase, when progesterone levels are the highest.
The number of oestrogen receptors is reduced after the menopause, but they never
disappear.
The steroids, being lipids, are transported by quite separate lipophilic proteins, and the tissues
stimulated by the steroids have their receptors in the cell cytoplasm, instead of on the cell
52 surface as in the preceding steps of the ovulatory process.
EFFECTS OF OVARIAN HORMONES
GENITAL TRACT
Oestrogen stimulates growth and
vascularisation, while progesterone increases
endometrial gland secretion. In the cervix,
secretion is considerably increased by
oestrogen (to produce a favourable medium
for spermatozoa), while progesterone reduces
this. In the vagina, oestrogen causes
cornification of cells and enlargement of ‘Ferning’ pattern in vaginal smear due to
nuclei, with increased deposits of glycogen. oestrogen stimulation.
BREAST HYPOTHALAMUS
Oestrogen stimulates growth of the The hypothalamic–pituitary axis
stroma, duct system and mediates the effects of ovarian
pigmentation, while cyclical hormones and controls the menstrual
progesterone stimulates growth of cycle through FSH and LH.
gland alveoli. Secondary
sexual characteristics are controlled by
oestrogen.
CARDIOVASCULAR SYSTEM SKELETON

Oestrogen and progesterone have a Oestrogen is an antiresorptive agent
number of different effects on the that helps to retain calcium in the
vascular tree, including effects on bones; at puberty, it causes the growth
endothelial function, lipid profile and spurt and then the closure of long
clotting factors. bone epiphyses.
PSYCHOLOGICAL CHARACTERISTICS
Mood may fluctuate with the menstrual cycle. Some women experience adverse psychological
and physical symptoms premenstrually, termed premenstrual syndrome (PMS) or
premenstrual tension (PMT).
53
PUBERTY
Puberty is the period of rapid growth when the child develops the physical characteristics of
the adult. In addition to growth in stature, enlargement and changes in the function of
reproductive organs occur. The mechanisms are poorly understood, but the main feature is an
awakening of centres in the hypothalamus, with an increase in the pulsatile release of GnRH,
leading to secretion of gonadotrophins. The reason for the absence of pulsatile GnRH
secretion in infancy is not known.
Hypothalamus
Releasing hormones
stimulate the pituitary
Other endocrine organs

Gonadotrophin
stimulated
secretion Growth hormone
ACTH
FSH Skeletal growth
Retention of nitrogen. Adrenal

Altered fat and CHO
Ovary metabolism
? Pigmentation
Androgen
of vulva
secretion
Increase in number Deposition of fat on

of growing follicles shoulders, buttocks, Pubic and
thighs and pubic area axillary hair
growth
Rise in oestrogen Beginning of growth of

uterus, fallopian tubes,
Time-scale (years)
vagina, labia, breasts
and endometrium 91/2–13 Breast buds appear.
13–14 Sexual hair appears.
Secretion of Irregular anovulatory 10–14 Greatest spurt in
oestrogen irregular menstruation skeletal growth.
111/2–15 Developed feminine
contours.
13–16 LH appears in
Oestrogen output LH secretion blood → ovulation.
becomes steady and and ovulation
rises to a critical level
Adult cyclical menstruation

54
THE MENOPAUSE
Menopause is the name given to the stage in life when the woman gradually loses her cyclical
ovarian activity. In many ways, it is a reversal of the changes occurring at puberty. It usually
takes place between the ages of 47 and 52 and is termed premature if it occurs before 45.
Menstruation rarely ceases abruptly but tends to become somewhat irregular and less frequent
over a year or a little longer. The cessation does not appear to be due to a complete
disappearance of ovarian follicles. Primordial follicles have been found in the ovaries of
postmenopausal women. It would appear that there has to be a critical number of actively
growing follicles before the menstrual cycle can operate.
For details of the pathophysiology and clinical features etc. of the menopause, see Chapter 18.
55
CHAPTER 4
DISORDERS OF SEX DEVELOPMENT
Maturation of Germ Cells: Meiosis 58

Genetic Abnormalities 59
Clinical Syndromes 59
Investigations of Genetic Defects 59
Laboratory Studies 59
Turner’s Syndrome (Sex Chromosome Deletion: X) 60
Klinefelter’s Syndrome (Sex Chromosome
Acquisition: X) 61
Congenital Abnormalities 62
Complete Androgen Insensitivity (CAIS) 62
Congenital Adrenal Hyperplasia (CAH) 63
Abnormalities of Ovary and Tube 64
Abnormalities of the Ovary 64
Abnormalities of the Fallopian Tube 64
Abnormalities of the Uterus 65
Absent or Rudimentary Uterus 65
Double Uterus (Bicornuate Uterus) 65
Uterus Didelphys 65
Bicornuate Uterus or Uterus Bicornis 65
Uterus with Accessory Horn 65
Arcuate Uterus 66
Septated Uterus 66
Uterus Unicornis 66
Abnormalities of the Vagina 67
Abnormalities of the Vulva 68
Ectopia Vesicae 68
Congenital Abnormalities of Cloacal Origin 68
Genital Abnormalities 68
MATURATION OF GERM CELLS: MEIOSIS
Cells in the adult contain 46 chromosomes, two of which are sex chromosomes, XX in the
female and XY in the male. These are known as diploid cells.
Before fertilisation of the ovum can occur, the chromosomes must be reduced from 46 to 23 in
both ovum and sperm. Each gamete will contain one sex chromosome and is known as a
haploid cell.
The process of meiosis begins with a rearrangement of the genetic material within the nuclei of
the germ cells of both male and female. The reduction from diploid to haploid occurs during
fetal life in the female, but in the male it is delayed until puberty.
58
GENETIC ABNORMALITIES
CLINICAL SYNDROMES
The X chromosome favours development of female characteristics but full development is
only possible if there are two such chromosomes. Any alteration in this number leads to
abnormalities.
Development of the testis is entirely dependent on the presence of a Y chromosome. The
testis, in addition to forming testosterone, which aids the development of male characteristics,
produces a Müllerian inhibitory factor. Both male and female fetuses initially have both
Müllerian and Wolffian systems.
In the absence of a testis, the whole Müllerian tract will develop, but curiously this does not
depend on the presence of ovaries. These interrelationships result in a number of clinical
syndromes with variations in individual cases.
INVESTIGATIONS OF GENETIC DEFECTS

In all cases, it is important to obtain a family history as complete as possible. Siblings and
relatives of patients may give a history of amenorrhoea and infertility.
LABORATORY STUDIES
Chromosome Analysis
Cells are cultured, usually lymphocytes from a blood sample but other cells can also be
used. The standard technique terminates the mitotic process at metaphase using a mitotic
inhibitor such as colchicine. The resulting chromosomes are separated, counted, arranged
in their groups and studied. Some chromosomal abnormalities are not visible with routine
analysis. Fluorescence in-situ hybridisation (FISH) is a more rapid technique used to
identify specific DNA sequences.
59
TURNER’S SYNDROME (Sex Chromosome Deletion: X)
• Amenorrhoea • Infantile figure of

• Normal female phenotype
intelligence • Small stature, poor
• Webbing of neck hip development
• Coarctation of
aorta
• Streak gonad, failure
of ovarian
• Secondary sex development
characteristics
absent
• Uterus and fallopian
tubes infantile
The commonest chromosomal pattern is 45XO. Not all features of the condition are always
present. In patients who are mildly affected, there may be a partial deletion of the X
chromosome (Xx) or mosaicism (XO/XX). In such cases, normal ovaries can develop and
menstruation can occur.
In males some of the somatic stigmata of Turner’s may appear. This may be due to partial
deletion of the Y chromosome – Xy, or to mosaicism – XO/XY.
Treatment
This diagnosis should be considered early in girls with short stature as hormone replacement
therapy is required to encourage secondary sexual characteristics and skeletal development.
For young women, the combined pill is often a socially acceptable maintenance therapy that
results in a ‘menstrual cycle’.
60
KLINEFELTER’S SYNDROME (Sex Chromosome Acquisition: X)

There is a Y chromosome with an increase in the
number of X chromosomes. The commonest
abnormality is 47XXY. The phenotype is male. The
clinical features vary but the majority have
hypogonadism and infertility. Facial hair is scanty and
pubic hair has a female distribution. Gynaecomastia
can also be present. Mild developmental problems and
learning difficulties can occur but the vast majority of
individuals have normal intelligence. There is an
association between mental impairment and the
number of X chromosomes.
SUPER-FEMALE (Sex Chromosome Acquisition: X, Sometimes at Both Stages

of Meiosis)
This is a term sometimes used when the patient possesses extra X chromosomes but no Y
chromosome. The pattern may be XXX, XXXX or even XXXXX. Physically these
individuals are normal females, but the important point is that there is usually some mental
impairment and the degree of this increases with each extra X chromosome. Diagnosis is
made by chromosomal analysis.
61
CONGENITAL ABNORMALITIES
COMPLETE ANDROGEN INSENSITIVITY (CAIS)

This condition was previously known as testicular feminisation and may be mistaken for a sex
chromosome abnormality. The chromosomal pattern is 46XY; however, there is insensitivity
of the androgen receptor to respond to androgenic stimulation. As a Y chromosome is
present, the testes form normally, producing anti-Müllerian hormone (AMH) and
testosterone. AMH causes the regression of the Müllerian ducts (see Chapter 1), and the
uterus, fallopian tubes and upper part of vagina therefore do not form. As the tissues are
insensitive to androgens, the lower genital tract fails to virilise and a short vagina is formed.
The patient is phenotypically female. Usually the diagnosis is made in early adult life when the
patient complains of amenorrhoea.
• Female phenotype.
• Normal or large breasts with small nipples.
• Absent or scanty pubic hair and axillary hair.
• Female external genitalia with blind vagina.
• Absent or rudimentary internal genitalia.
• Undescended testes anywhere along course of normal
descent (20% become malignant in 4th decade).
• Testes secrete oestrogens and androgens. Probably Leydig
cells produce feminising hormones.
Patients with CAIS usually inherit it from their mother in an

X-linked pattern, but new mutations are also common.
Most carriers are unaffected, but some may show scanty pubic and
axillary hair and have delayed menarche.
Until full growth is achieved, no therapy should be attempted. After
puberty and fusion of epiphyses, the gonads should be removed
surgically. This is a precautionary measure in view of the increased
incidence of tumours in such gonads. Following this treatment, the
patient is liable to have menopausal symptoms and should be given
oestrogen replacement therapy for symptom control and for skeletal
and cardiovascular prophylaxis until age 50 years at least. As the
uterus is absent, progesterone is not required.
All of these foregoing syndromes, whether genetic or not, can pose
social, psychological and sexual problems. The patient may have to
make a great deal of mental adjustment and in such cases sensitive
counselling will be required. Karyotyping and referral for genetic
counselling should be considered.
Partial androgen insensitivity can also occur. A variety of clinical features occur, but
ambiguous genitalia is a common presentation.
62
CONGENITAL ABNORMALITIES
CONGENITAL ADRENAL 17-hydroxyprogesterone

HYPERPLASIA (CAH)
This is an abnormality of cortisol production that can affect
both male and female infants. The commonest enzyme 21-hydroxylase
deficiency is of 21-hydroxylase. The adrenals also produce
mineralocorticoids and steroid hormones, and deficiencies CORTISOL
of one pathway lead to excess production in other
pathways. The severity of the enzyme deficiency can vary
and will lead to different clinical conditions.
Adrenal dysfunction is due to congenital deficiency of the enzyme 21-hydroxylase. It should
be detected and treated at birth.
• Deficiency of 21-hydroxylase leads to low cortisol secretion.

• Low cortisol leads to high ACTH secretion.
• High ACTH secretion leads to adrenal hypertrophy.
• As the pathway to cortisol is blocked, the alternative pathway to
androgen formation is taken.
• The fetus and neonate show signs of virilisation.
• If aldosterone production is affected, the salt losing effects can be
potentially life threatening if the condition is not detected promptly.
Single Urethra Bladder

orifice
External Vagina
genitalia
of female
child with
adrenogenital
syndrome
Treatment
In female infants with virilised genitalia, chromosome analysis will reveal a 46 XX karyotype.
Addisonian crisis may develop at any time and may be fatal. The diagnosis must be recognised as soon
as possible and corticosteroid replacement therapy given immediately. This will reverse the changes
in the endocrine organs, reducing the ACTH level and ultimately the adrenal hypertrophy. Further
virilisation will be prevented but surgery may be required for female infants with virilised genitalia.
The abnormal genitalia should alert the attendant at the birth and help should be sought from
a paediatrician. Milder forms of CAH can present later in childhood and adolescence with
precocious puberty or oligoamenorrhoea.
CAH is an autosomal recessive condition and prenatal diagnosis is possible. Maternal treatment with 63
corticosteroid can potentially reduce the intrauterine virilisation, although this remains experimental.
ABNORMALITIES OF OVARY AND TUBE
Congenital abnormalities arise from the following:-
• Incomplete development of the Müllerian ducts.

• Imperfect development of the gonad.
• Imperfect development of the cloacal region.
• Sex chromosome abnormalities.
Because of the close relationship between the genital and urinary tracts, renal tract imaging
should always be carried out when a genital abnormality is found.
ABNORMALITIES OF THE OVARY

Absence of one ovary may occur in an otherwise normal woman. Before operating on one
ovary, always look at the other.
With ovarian dysgenesis, the ovaries appear
as ‘streaks’. In place of the ovary there is a
strip of whitish connective tissue continuous
with the ovarian ligament. It may contain
vestiges of a rete, and occasional cells which
may be of germ cell type, but no follicles.
These ‘streak’ ovaries are sometimes the
seat of tumour growth, such as
gonadoblastoma and dysgerminoma, and
should always be removed.
ABNORMALITIES OF THE
FALLOPIAN TUBE
Absence is rare. The tube may be
imperfectly developed.
This illustration shows a condition in
which the proximal half of the left tube
has failed to develop. The right adnexa
are normal. All of these conditions are
rare, but their importance lies in their
association with infertility.
64
ABNORMALITIES OF THE UTERUS
ABSENT OR RUDIMENTARY UTERUS

The uterus consists of two nodules connected
by a membrane (‘ribbon’ uterus). The other
structures are normal. If a cavity exists in a
nodule, cryptomenorrhoea (concealed bleeding)
and dysmenorrhoea may arise and retrograde
flow may lead to pelvic endometriosis.
This can be associated with atresia of the vagina
(Mayer–Rokitansky syndrome).
DOUBLE UTERUS (BICORNUATE

UTERUS)
One or other variant of this condition is the commonest abnormality of the genital tract. It is
due to failure of fusion of the Müllerian ducts, or failure of one to develop. There are a
number of terms that describe the abnormality.
UTERUS
DIDELPHYS BICORNUATE
Double uterus UTERUS OR
and cervix, UTERUS
usually with BICORNIS
double vagina. Note the ligament,
which may pass
Two uterine from rectum to
corpora with bladder.
two cervices. There is a cleft
Both cervices need to be sampled present at the
at cervical screening. There are fundus.
occasional reports of discrepancies
with vaginal assessment during
labour due to unrecognised double
cervices.
UTERUS WITH ACCESSORY

HORN
The accessory horn has no cervix. If it
menstruates, cryptomenorrhoea will
follow. Spermatozoa can reach the horn
by crossing the peritoneal cavity, and
pregnancy can occur within a
rudimentary horn.
65
ABNORMALITIES OF THE UTERUS
ARCUATE UTERUS
The cavity has an
indentation at the fundus.
This is probably the mildest
form of uterine abnormality.
SEPTATED UTERUS UTERUS UNICORNIS

The uterus appears normal externally, One Müllerian duct has failed to develop.
but the cavity has a septum.
All of these abnormalities may be associated with obstetric implications. These include
increased rates of infertility, miscarriage, preterm delivery and malpresentation. This, however,
depends on the extent of the abnormality, and many women will have uncomplicated
pregnancies.
66
ABNORMALITIES OF THE VAGINA
Gynatresia (occlusion of the genital canal) may be due to complete absence of the vagina, or
incomplete development. When this is associated with absence of the uterus, it is known as
Mayer–Rokitansky syndrome.
Septae can also occur. These are usually transverse septum producing the same effect as an
imperforate hymen; sometimes, they may also be a vertical septum producing a double vagina.
This often occurs in association with a double uterus.
When a transverse septum is identified, it may represent an imperforate hymen. This often
presents with a thin bluish membrane because of a haematocolpos. If the tissue is thicker, it
could represent a more extensive vaginal atresia. Where a uterus is present, dysmenorrhoea
and cryptomenorrhoea will occur.
a. Absence of the whole genital tract except

for the lower one third of the vagina. Coitus
is possible but there is no possibility of
pregnancy.
b. Complete absence of
vagina. There is a
slight depression over
the hymen. Normal
coitus is not
possible.
c. Vertical septum, double

vagina and cervices.
Normal pregnancy and delivery are possible. Vaginal abnormalities can occur alone, but are
usually associated with other abnormalities of the genital and renal tract. Imaging using
ultrasound and/or MRI should be performed. Laparoscopic inspection of the pelvis may be
required.
67
ABNORMALITIES OF THE VULVA
• Absence of the vulva or duplication of the vulva is exceedingly rare.

• There is a wide variation in the size of normal labia.
ECTOPIA VESICAE
Is an extreme defect seen in the newborn,
but one which is susceptible to surgical
treatment. There is failure of development
of the symphysis pubis, mons, lower
abdominal wall and anterior wall of the
bladder. The tissues exposed are the
posterior wall of the bladder, the ureteric
orifices and the floor of the urethra.
CONGENITAL ABNORMALITIES OF CLOACAL ORIGIN

These are due to failure of the cloacal septum to divide the cloaca perfectly into hindgut and
urogenital sinus. The less serious degrees may persist unnoticed in adults as some form of
ectopic anus.
Patients with these abnormalities can defecate through the vestibule or vagina, apparently
without suffering from incontinence.
The The vaginal

vestibular anus (very
anus rare)
In all of these vulval abnormalities, infection is a problem – of the urinary tract in ectopia
vesicae, and of the genital tract in the other two.
GENITAL ABNORMALITIES
The results of these conditions as they relate to gynaecological practice have already been
68
mentioned in the section dealing with amenorrhoea.
CHAPTER 5
HISTORY AND EXAMINATION
Taking the History 70

Parity and Obstetric History 70
Contraceptive and Fertility Requirements 70
Smear History 71
Menstrual History 71
Useful Definitions 71
Pelvic Pain 72
Other Gynaecological Symptons 74
Premenstrual Symptoms 74
Vaginal Discharge 74
Vaginal Prolapse 74
Urinary Symptoms 74
Gynaecological Examination 74
Abdominal Examination 75
Examination of the Vulva 78
Bimanual Pelvic Examination 79
Speculum Examination 80
Examination of the Breasts 82
Laparoscopy 83
Technique 83
Complications 85
Indications 85
TAKING THE HISTORY
The key to any consultation is taking an accurate and complete history. This is relevant in all
medical disciplines and particularly in gynaecology. Do not assume that the referral letter
contains all the relevant information. It is important to ask what the main problem is – it may
be hidden away among a list of relatively unimportant or misleading complaints.
Women may find discussing gynaecological symptoms difficult and require
Privacy Time Sympathy

The consultation should be held in a The patient should be The doctor’s manner must
room with adequate facilities and allowed to tell her own story be one of interest and
privacy. Permission should be sought before any attempt is made understanding
for any students who are present to elicit specific symptoms
Gynaecological history follows the standard principles of medical history taking but there are a
number of other issues that are relevant to gynaecology.
Standard history taking Additional features relevant to gynaecology

Age Parity
Presenting complaint Obstetric history
Past medical history Contraception and fertility requirements
Medication history Smear history
Allergies Menstrual history – this will often be part of the
Social history presenting complaint
Family history
Systemic enquiry
PARITY AND OBSTETRIC HISTORY

The first number refers to the number of pregnancies beyond 24 weeks. This cut off largely
relates to the gestation of potential viability although any liveborn infant before 24 weeks
would also be counted among this number. The second number refers to pregnancies of less
than 24 weeks. In practical terms, the easiest way to ask about this is to ask if the woman has
any children and then ask if she has had any other pregnancies. Pregnancies in this category
are likely to be miscarriages, terminations or ectopic pregnancies. It is important to be
sensitive about the terminology when discussing pregnancy loss. The term ‘abortion’ is out
dated and should not be used when discussing miscarriage.
Details of the mode of delivery of any children are always important in gynaecology, but other
factors such as perineal trauma and postnatal infection are also relevant.
CONTRACEPTIVE AND FERTILITY REQUIREMENTS

This information will be relevant to many gynaecological issues as potential treatments may
affect fertility, and many contraceptive treatments will have a useful effect; for example, the
combined oral contraceptive pill and menstrual loss and dysmenorrhoea. Infertility may also
be the presenting complaint.
70
TAKING THE HISTORY
SMEAR HISTORY
Women should be asked when their last cervical smear was performed and if the result was
normal. Any abnormal smears and colposcopy history should be noted. Within the UK,
routine smears are generally performed by primary care, but cervical cytology may be required
for symptomatic women.
MENSTRUAL HISTORY
At the very minimum, the last menstrual period (LMP) should be recorded. For premenopausal
women, the length of a menstrual period and frequency of period should be recorded. This
is conveniently expressed as a numerical fraction. Thus, 5/28 means the cycle lasts for 5 days
and occurs every 28 days. Make sure that you obtain the number of days from the start of one
period to the start of the next. Irregular cycle may produce fractions such as 5–10/21–35.
USEFUL DEFINITIONS
Menarche – first menstrual period.
Menopause – date of final menstrual period. This can only be defined with certainty after a year
has elapsed since the final menstrual period. It is also useful to ask about menopausal
symptoms and hormone replacement therapy (HRT) use. The classic menopausal symptom is
vasomotor flushes, but a myriad of other symptoms can also be experienced (see Chapter
18 The Menopause).
Perimenopause – the years of transition where irregular cycles occur. For most women, this lasts
for 4 years before the final menstrual period occurs.
Menorrhagia – heavy periods. This is one of the commonest reasons that women are referred
to gynaecology. You should ask for how long and how often bleeding occurs. The passage
of clots and flooding through sanitary protection are signs that the menstrual flow is excessive.
It can also be useful to ask about frequency of changing sanitary protection and whether
‘double’ protection is required, that is, having to wear a sanitary towel and tampon at the
same time.
Abnormal Bleeding
Postcoital bleeding – bleeding occurring after intercourse.
Intermenstrual bleeding – bleeding between periods.
Postmenopausal bleeding – bleeding more than one year since LMP.
Irregular Bleeding
Primary amenorrhoea – failure to menstruate by age 16.
Secondary amenorrhoea – no menstruation for 6 months after periods are established.
Oligoamenorrhoea – infrequent, erratic periods.
Remember that anovulatory cycles occur at the extremes of menstrual life. It is therefore
physiological to have erratic infrequent periods in the first few years after menarche and in the
perimenopause.
71
PELVIC PAIN
This may or may not be related to the menstrual cycle. Premenstrual pain may represent
endometriosis. Dysmenorrhoea refers to painful menses, usually of a crampy nature. This is
usually central low abdominal cramp but can be referred to the thighs and lower back.
Primary dysmenorrhoea – periods have been painful since established menstruation has
occurred.
Secondary dysmenorrhoea – periods have become painful. This is thought to be more likely to
be associated with pelvic pathology.
Mittelshmertz – mid-cycle pain related to ovulation.
There are a number of other organ systems that can be
responsible for pelvic pain. The most likely sources within the
pelvis are the gastrointestinal and urinary tracts. It is
important to ask about these systems when assessing for a
source of pain. For example, acute right iliac fossa pain could
represent an ovarian cyst accident or appendicitis among
other diagnoses. Classically, appendicitis will also present with
anorexia.
Areas of referred pain during

Renal menstruation
pain
The nature and pattern of pain will also be useful.
Bladder pain is central and low, but renal pain will
Period radiate to the loins.
pain
72
PELVIC PAIN
The severity of pain can be judged to some extent by

the patient’s behaviour. Pain that causes a woman to
take time off work or wakes her from sleep is likely to
be caused by an underlying pathology. Pain that
causes nausea and vomiting is important. Associated
symptoms such as fainting, shoulder tip or pain with
defecation imply potential intra-abdominal blood
loss, and ectopic pregnancy should be strongly Tubal pregnancy
considered.
Dyspareunia – Pain or exacerbation of underlying pain during sexual intercourse is an

important symptom. Deep dyspareunia implies pathology of the upper genital tract. Patient will
describe the pain as ‘deep inside’ during intercourse. Superficial dyspareunia is more likely to
represent a vaginal cause. Superficial causes of dyspareunia include causes such as local
infections, that is, Candida or scarring from episiotomy or vaginal tears during childbirth.
Vaginismus is also a common cause of dyspareunia, where the vaginal muscles tense during
attempted penetration. It can affect tampon insertion and smear taking and can usually be
demonstrated with vaginal examination. It may be present in women with entirely healthy
vaginal tissues, but understandably women who experience dyspareunia for any reason can
tense up because of anticipation of pain so the presence of vaginismus does not exclude pelvic
pathology. A careful one finger vaginal examination to identify if there are any specific areas of
tenderness can be useful if the patient will not tolerate a speculum or two-finger bimanual.
73
OTHER GYNAECOLGICAL SYMPTOMS
PREMENSTRUAL SYMPTOMS
Many women experience premenstrual mood disturbance. A range of other physical
symptoms occur, including breast tenderness, bloating and headaches. Ideally, women should
keep a diary of these symptoms to explore the relationship to their menstrual cycle.
VAGINAL DISCHARGE
Women who complain of a vaginal discharge should be asked about the colour, odour and any
associated vaginal irritation or systemic upset. It can also be useful to determine any
relationship to the menstrual cycle as the discharge may be physiological in nature.
VAGINAL PROLAPSE
Women with prolapse present with a sensation of something coming down within the vagina.
They may also experience backache and a dragging sensation.
URINARY SYMPTOMS
Women are frequently referred to gynaecology with the complaint of urinary incontinence.
This may or may not be associated with vaginal prolapse. Other urinary symptoms should be
considered.
Urinary incontinence can be ‘stress’ incontinence, where the woman leaks when she coughs or
exercises or it can be urge incontinence where the woman complains of a sudden sensation of
urinary urgency and is incontinent before she makes it to the toilet. The latter symptom is
often associated with urinary frequency and nocturia. In practice, many women complain of a
mixed pattern of symptoms.
GYNAECOLOGICAL EXAMINATION
General Principles
The majority of women have varying degrees of anxiety about vaginal examination.
Examination is usually more informative in a relaxed patient and a number of simple measures
can be used to make the patient feel at ease.
Women should be given an appropriate area to change in privacy. A sheet should be provided
to allow the woman to cover herself. A chaperone should be present for any intimate
examination. This should apply for both male and female practitioners. The chaperone
provides two purposes, firstly as a source of support and distraction for the patient but also to
provide evidence that no improper behaviour has taken place. Formal consent should be given
for any intimate examination by a student including under anaesthesia.
An explanation of the purpose of the examination should be given to the woman and
permission sought to perform the examination. Simple terms should be used to explain the
likely sensations experienced. The examination should be thorough but gentle. The patient
should feel confident that you will stop the examination if she wishes.
74
ABDOMINAL EXAMINATION
This must never be omitted, whatever be the patient’s complaint. Many gynaecological
tumours form large swellings, which leave the pelvis altogether, and an undisclosed pregnancy
may be present. Always examine the upper abdomen. Be certain that the bladder is empty.
Ask the patient to tell you if you are hurting her.
Ovarian cysts often have long

pedicles. This ovarian cyst is
completely abdominal, and
would not be palpable on
bimanual pelvic
examination.
The characteristic swelling

of the 16-week pregnancy
may not be seen but can
always be felt by pressing
with the flat of the hand.
The bladder must not be
full.
An enlarged uterus may be

missed if bimanual examination is
performed without an abdominal
examination.
75
All the classical techniques of

inspection, palpation, percussion Stomach
Liver
and auscultation are advised, but
the most important is gentle Spleen
palpation with the flat of the hand
Gall Kidney
to detect solid or semi-solid
bladder
tumours. Pancreas
The examiner must bear in mind Caecum Ureter
the various intra-abdominal
structures which may give rise to Sigmoid
swellings.
Rectum
Appendix Ovary
Uterus
Tube Bladder
The hypochondria should be

examined to exclude liver and
spleen enlargement or gallbladder
tenderness, before palpating the
lower abdomen.
An attempt to palpate the kidneys

should be made. Tenderness may
be elicited in the loin, suggesting
urinary tract infection.
76
Inspection may show the

characteristic shape of a large
ovarian cyst. The outline is rounded
and uniform, the skin is stretched
and a fluid thrill may be elicited.
Tympanitic
(due to
bowel gas)
If ascites is present (and this means that the cyst is

probably malignant), the outline tends to be
cylindrical, with some flattening at the top. The
Dull
Cyst umbilicus is everted, and the percussion note is dull in
the flanks but tympanitic above because of the upward
floating of the intestines.
Tympanitic If the patient is turned on her

side, and the percussion is
repeated after about 30 s, the
dull and tympanitic areas are
reversed – ‘shifting dullness’.
Cyst
Dull
Unfortunately, obesity is an
increasing problem, and abdominal
examination can be particularly
challenging. With an ‘abdominal
apron’ of fat, the symphysis pubis
may be mistaken for a hard lower
abdominal mass on palpation.
Investigation techniques can also be
technically difficult. Abdominal
ultrasound is significantly limited by
abdominal fat, but transvaginal
scanning will be useful. 77
EXAMINATION OF THE VULVA
The dorsal position is most convenient for

patient and doctor although examination in a
lateral position is useful to assess vaginal
prolapse. During palpation, visual inspection of
the labia, clitoris, anus and surrounding skin
should be performed. Raised or ulcerated areas
should raise the question of vulval malignancy.
There are specific skin conditions that affect
the vulva, including lichen sclerosus, which
often presents with itchy white patches and
labial fusion. Common benign lesions include
sebaceous cysts. Excoriation suggests an
underlying irritation.
1. A single finger presses on the perineum, 2. Urethral meatus and vestibule are
avoiding the sensitive vestibule, and exposed. Pressure from the finger will
accustoming the patient to the squeeze any pus from the peri-urethral
examiner’s touch. glands.
3. Bartholin’s gland is palpated (on both 4. If there is room, a second finger is

sides). It is difficult to feel the normal inserted and the perineal floor is
gland. palpated by stretching.
78
BIMANUAL PELVIC EXAMINATION
This technique needs practice. The external

hand is the more important and supplies more
information. It is customary to use two fingers
in the vagina, but an adequate outpatient
examination may be made with only one finger.
Very little information is gained if the patient
finds the examination painful. In a virgin or a
child, vaginal examination should not be
performed, unless there are exceptional
circumstances, and examination under
anaesthesia should be considered.
Pelvic models are available, with
interchangeable uterine and adnexal
components to simulate normal and
pathological conditions, for practice
examination.
1. The vagina and cervix are palpated and 2. The whole uterus is identified, and size,
any hardness or irregularity noted. shape, position, mobility and tenderness
are noted.
3. The lateral pelvis is palpated and any 4. Sometimes rectovaginal examination is

swelling noted. Normal adnexa are helpful, particularly if the rectovaginal
difficult to feel, unless the ovary septum is to be examined, for example, in
contains a corpus luteum. assessment of extent of malignant disease.
79
SPECULUM EXAMINATION
The bi-valve speculum is the most useful (Cusco’s pattern is shown here). It is made of either
steel or Perspex (disposable) and is designed to open after insertion so that the cervix and
vagina can be visualised. Versions with a screw or ratchet are available to hold the device open
so that cytological smear or bacteriological swab can be taken as required.
1. The speculum is applied to the vulva at 2. When fully inserted, it is gently opened
an angle of 45 from the vertical. This out and held in position with the cervix
allows the easiest insertion. between the blades. A good light is
needed for inspection. Care is required
when removing the speculum to ensure
that the blades have not caught the cervix
or vagina and that the blades have not
been held open by the ratchet or screw.
80
SPECULUM EXAMINATION
SIMS’ SPECULUM (the duckbill speculum) is designed to hold back the posterior vaginal
wall so that air enters the vagina because of negative intra-abdominal pressure, and the
anterior wall and cervix are exposed.
In this picture, the patient is in Sims’ position (semi-prone) which is useful if the anterior wall
is to be studied (e.g. if fistula is suspected).
81
EXAMINATION OF THE BREASTS
A gynaecological examination provides a

suitable opportunity for examining the
breasts. Signs of pregnancy or lactation may
be observed or a lump may be palpated. The
breast is a much commoner site of cancer
than the genital tract.
The examination should be made with the
patient seated and also lying on her back. The
breast is gently but thoroughly palpated with
the fingers, and the axilla is also palpated.
Montgomery’s tubercles,
seen in early pregnancy.
Routine X-ray mammography is offered by the NHS every 3 years between 50 and 65 years of
age. In women with a first degree relative diagnosed with breast cancer before 50 years,
mammography may be appropriate and referral to a breast cancer family history clinic is ideal.
82
LAPAROSCOPY
Inspection of the pelvic organs through an endoscope passed through the abdominal wall.
This is a common procedure, frequently performed in day surgery units, but it does carry
a small risk of visceral injury which must be taken into account.
TECHNIQUE
The patient is anaesthetised, the
bladder emptied and a bimanual
examination should be performed to
assess for pelvic masses and to assess
the direction of the uterus. A forceps is
fixed to the anterior lip of the cervix
and the uterus is cannulated. This
allows the uterus to be moved about
once the endoscope is passed, and dye
can be injected through the cannula to
test the patency of the tubes.
Cannula Blunt Trochar

CO2
Intestine
Laparoscopy can be performed by various techniques. A cut down technique can be used to
open the rectus sheath and underlying peritoneum just below the umbilicus. A blunt trocar is
then inserted, and the abdominal cavity is filled with CO2 gas to allow visualisation of pelvic
organs. The patient is tilted head down to encourage the intestines to fall away from the
pelvis. Alternatively, a Veress needle can be used to fill the abdominal cavity, and a sharp
trocar is inserted through the rectus sheath. There are also devices that allow insertion of a
trocar with direct visualisation.
83
LAPAROSCOPY
Many instruments for laparoscopy are now disposable and incorporate retractable safety
features to help avoid perforation of viscera. Any secondary ports should be inserted under
direct vision, and care taken to avoid vessels within the anterior abdominal wall, for example,
inferior epigastric artery.
The laparoscope is passed through the initial port and the inspection made of the abdomen
and pelvis. The uterus should be manipulated to allow visualisation of the adnexa and Pouch
of Douglas. A camera attached to the eyepiece of the laparoscope permits assistants and
observers to share the surgeon’s view on a video screen and permits video recording of the
findings or procedure.
Additional ports are needed to insert surgical instruments. For diagnostic laparoscopy, this is
usually simply a manipulation of the tissues to allow adequate inspection. For operative
laparoscopy, a range of standard surgical instruments, such as forceps, scissors and suture
holders, are available. There are also a number of instruments designed to apply diathermy
and other modalities. Many procedures are now performed entirely by laparoscopy or assisted
by laparoscopy.
84
LAPAROSCOPY
COMPLICATIONS
1. Perforation of a viscus, especially bowel.
Patients who are overweight or have had
previous abdominal surgery are more at
risk of this complication. There is no
primary entry technique that will remove
the risk of perforation; however, adequate
pressures of CO2 should be used for
secondary port entry to raise the
abdominal wall away from visceral
structures. Good laparoscopic technique
keeps any operating instruments in clear
view away from viscera.
2. Haemorrhage from damage to vessels, or
from a trocar puncture.
3. Infection is very rare and nearly always the
result of unnoticed bowel damage.
Complications are more frequent with
operative laparoscopy than with diagnostic
laparoscopy.
INDICATIONS
1. Diagnostic. Such conditions as salpingitis, early tubal pregnancy and ovarian
pathology can be identified or excluded. Laparoscopy is useful in the investigation
of complaints of pelvic pain.
2. Infertility investigation. Besides inspection, the patency of fallopian tubes can be
demonstrated by observing the passage of dye injected through the cervix
(hydrotubation).
3. Sterilisation. See page 353–355.
4. Other applications of laparoscopy include the following:
Division of adhesions
Oophorectomy
Ovarian cystectomy
Salpingectomy and salpingostomy
Laparoscopic hysterectomy
Colposuspension
Vaginal vault suspension for vault prolapse.
85
CHAPTER 6
ABNORMALITIES OF MENSTRUATION
Normal and Physiological Changes Estimation of Blood Loss 110
in the Menstrual Cycle 88 Investigation of the
Amenorrhoea 88 Endometrium 111
Menarche 88 Outpatient Procedures 111
Physiological Amenorrhoea 89 Investigations of Endometrium 112
Pregnancy 89 Methods of Endometrial Biopsy 112
Lactation 89 Dilatation and Curettage 112
Menopause 89 Investigations of Endometrium -
Causes of Amenorrhoea 89 Complications 113
Uterine and Lower Genital Tract Management of Heavy Menstrual
Disorders 90 Bleeding 114
Imperforate Hymen or Transverse Medical Management 114
Vaginal Septum 90 Surgical Management 115
Asherman’s Syndrome 91 Endometrial Ablation Techniques 115
Müllerian Agenesis 91 Dysmenorrhoea 120
Congenital Androgen Nature of the Pain 120
Insensitivity 91 Aetiology 120
Ovarian Disorders 92 Clinical Features of Primary
Gonadal Dysgenesis 92 Dysmenorrhoea 121
Premature Ovarian Failure 93 Management 121
Resistant Ovary Syndrome 93 Drug Treatment 121
Polycystic Ovarian Syndrome 94 Adenomyosis 122
Pituitary Disorders 97 Pathology 122
Hyperprolactinaemia 97 Microscopic Appearances 122
Hypothalamic Disorders 101 Endometriosis 123
Diagnosis 101 Pathology 123
Causes 101 Secondary Pathology 124
Investigation of Amenorrhoea 102 Histology 125
Investigation 102 Clinical Findings 126
Hirsutism 105 Symptomatology 126
Aetiology 105 Physical Examination 126
Physiology of Testosterone 105 Laparoscopy 126
Virilisation 106 Imaging Techniques 127
Clinical Features 106 Differential Diagnosis 127
Investigation 106 Histogenesis 127
Management of Hirsutism 107 Treatment 127
Local Treatment 107 Premenstrual Syndrome 129
Drug Treatment 108 Clinical Features 129
Menstrual Disorder 109 Investigations 129
Dysfunctional Uterine Treatment 130
Bleeding 110 Management Options for Severe PMS 130
Clinical Features 110
NORMAL AND PHYSIOLOGICAL CHANGES IN THE MENSTRUAL CYCLE
Normal menstrual cycles have a length of 21–35 days (mean 28 days). A normal period lasts for
3–7 days. Menstrual blood loss of 30–50 ml/month is normal. Menstrual blood loss is
considered as excessive when it is greater than 80 ml/month. It is, however, rarely measured in
clinical trials, and heavy menstrual loss should be defined clinically.
AMENORRHOEA
Amenorrhoea is the absence of menstruation for 6 months in a woman who had previously
menstruated normally (sometimes called 2 amenorrhoea)
or
amenorrhoea is the term given when a girl has failed to menstruate by the age of 16
(sometimes called 1 amenorrhoea).
In practice, the distinction between 1 and 2 amenorrhoea is not generally helpful in making
a diagnosis. A similar process of investigation should be carried out whether or not the patient
had previously menstruated. Amenorrhoea occurs in a number of physiological conditions,
and these should be borne in mind when initiating investigation.
MENARCHE
Menarche is the onset of menstruation at puberty. The median age at which menarche occurs
(13 y) is relatively late in the events occurring around puberty. For most young women, the
growth spurt and secondary sexual characteristics, such as breast development (thelarche) and
the growth of pubic and axillary hair, usually precede the onset of menstruation by about
2 years.
Absent or late puberty may present with amenorrhoea. If a girl over the age of 14 presents
with amenorrhoea, investigations should depend on whether or not other signs of puberty are
present.
88
PHYSIOLOGICAL AMENORRHOEA
PREGNANCY
During pregnancy, the levels of oestrogen and progesterone remain high, thus ensuring the
integrity of the endometrium, and causing amenorrhoea. Initially, the corpus luteum is the
source of oestrogen and progesterone. Later in pregnancy, the production of oestrogen and
progesterone is taken over by the placenta. Pregnancy should be considered in the differential
diagnosis of all women who present with amenorrhoea.
LACTATION
Soon after delivery, prolactin is secreted in large quantities by the anterior pituitary. There is
partial suppression of luteinising hormone (LH) production so that ovarian follicles may grow,
but ovulation does not occur, and amenorrhoea is the result. If the mother does not breast
feed, menstruation will return in 2–3 months, but if she does breast feed, the period of
amenorrhoea will be prolonged.
MENOPAUSE
The menopause is the cessation of menstruation (mean age 51 y) due to exhaustion of the
supply of ovarian follicles. Oestrogen production therefore falls. This fall in oestrogen
production is accompanied by a rise in follicle stimulating hormone (FSH) levels, which
continues for a considerable time. In a proportion of women, menstruation ceases abruptly,
but in many, the menstrual cycles alter. Frequently, they become shorter initially, but later
they lengthen and tend to be irregular, before ceasing entirely. This phase is known as the
menopause transition, and the final period is recognised only in retrospect, after 1 year of
amenorrhoea. See Chapter 18.
CAUSES OF AMENORRHOEA
Amenorrhoea may be classified in a number of ways. One of the most helpful classifications is
shown below:
1. Uterine or lower genital tract causes
2. Ovarian causes Psychological
3. Pituitary causes
4. Hypothalamic causes. Hypothalamic
Pituitary
Thyroid Adrenal
Ovarian
Uterine
89
UTERINE AND LOWER GENITAL TRACT DISORDERS
IMPERFORATE HYMEN OR TRANSVERSE VAGINAL SEPTUM

This condition usually presents with primary amenorrhoea. There is no visible bleeding
although the usual cyclical symptoms are present. In that there is no flow of blood, the term
amenorrhoea can be used, but the cause is an obstruction by a vaginal septum or an
imperforate hymen rather than a functional abnormality.
Three degrees are recognised.
Haematocolpos. Only
the vagina is distended Haematometra.
Haematosalpinx. In
by altered blood. The uterus is
long-standing cases the
also distended.
tubes are also involved.
Clinical Features
The patient is usually a girl of 17 or so,
complaining of primary amenorrhoea
and pelvic pain of increasing severity.
In long-standing cases, the pressure of
the distended vagina may cause urinary
retention. Pregnancy must be excluded.
Examination
A pelvic mass is palpated and may even
be visible. The vaginal membrane or
hymen is bulging.
Treatment
Incision and drainage. Very
large amounts of inspissated
blood may be released, and
if the septum is particularly
thick, a vaginal reconstruction
procedure may subsequently
be required.
90
UTERINE AND LOWER GENITAL TRACT DISORDERS
ASHERMAN’S SYNDROME
In Asherman’s syndrome, the uterine cavity is obliterated by adhesions. The condition is
usually caused by uterine surgery: most commonly curettage, for example during termination
of pregnancy. In developing countries, infections such as tuberculosis and schistosomiasis are
commoner causes of Asherman’s syndrome.
The adhesions should be broken down hysteroscopically. High dose oestrogens are used to
stimulate endometrial proliferation following the procedure. Some authorities advocate the
use of a Foley catheter placed in the uterus for a short time after adhesiolysis to prevent
recurrence. Pregnancy rates following treatment are in the order of 80%. Such pregnancies
may be complicated by abnormal placentation, for example by placenta accreta.
MÜLLERIAN AGENESIS
See Chapter 1
The Müllerian ducts fuse by the 10th week of gestation to form the fallopian tubes, uterus and
upper portion of the vagina. Agenesis or lack of development of the Müllerian ducts (the
Mayer–Rokitansky–Kuster–Hauser syndrome) leads to absence of these structures. Absence
or hypoplasia of the vagina is a constant feature, but the uterine abnormalities vary. Provided
there is a cavity lined by endometrium, menstruation can be normal.
The diagnosis of Müllerian agenesis is made in women with primary amenorrhoea and an
absent vagina, but normal female chromosomes. Ovarian function is normal.
Uterine
nodules
Ovary
CONGENITAL ANDROGEN INSENSITIVITY

Previously known as testicular feminisation syndrome, congenital androgen insensitivity is the
third commonest cause of primary amenorrhoea. The individual is phenotypically female
although the uterus is absent. The karyotype is 46XY (see p. 62).
91
OVARIAN DISORDERS
Ovarian disorders
1. Gonadal dysgenesis
2. Premature ovarian failure
3. Resistant ovary syndrome
4. Disorders of ovulation such as polycystic ovarian syndrome
5. Hormone-producing tumours, such as granulosa cell tumours (oestrogen-producing)
or Leydig cell tumours (androgen-producing).
GONADAL DYSGENESIS
Women with gonadal dysgenesis have abnormal ovarian development, leading to absent or
streak ovaries. The number of germ cells that migrate to the ovary during intrauterine life
is reduced. These woman present with primary or secondary amenorrhoea, and have
persistently elevated gonadotrophins on testing.
Tube
In women under 30 years of age at the time of
presentation, a karyotype should be performed.
Turner’s syndrome (p. 60) is the classic form
of gonadal dysgenesis, but other karyotypes,
including 46XX are also found. If a
Y chromosome is present, consideration should
Streak
be given to gonadectomy because of the risk
ovary
of neoplasia.
92
OVARIAN DISORDERS
PREMATURE OVARIAN FAILURE

In this condition, ovarian follicles are depleted from the ovary before the normal age of the
menopause, and a premature menopause ensues. In addition to amenorrhoea, the patient may
complain of menopausal symptoms such as hot flushes, loss of libido, etc. This condition is
not uncommon: 1% of women will have ovarian failure by the age of 40. Premature ovarian
failure is found in around 10% of women with amenorrhoea.
Cause
The majority of women with premature ovarian failure have no obvious cause for their
condition. It is associated with chromosomal abnormalities such as Turner’s syndrome (XO).
It may occur in association with autoimmune disease, following infections such as mumps, or
following chemotherapy or pelvic radiotherapy.
Diagnosis
The diagnosis is made by finding elevated serum FSH levels (>20 IU/L). As FSH levels are
elevated physiologically mid-cycle, at least two FSH levels should be obtained at six weekly
intervals. If a high FSH level is followed 2 weeks later by menstruation, the cause of the
elevated FSH may be more likely to represent ovulation rather than menopause.
Treatment
Women with premature ovarian failure should be advised that they are likely to be infertile,
although spontaneous pregnancies have been reported. Pregnancy can be achieved by IVF
(in vitro fertilisation) with donor oocytes.
Oestrogen replacement should be considered to reduce the risk of osteoporosis and
cardiovascular disease. A progestogen is also required to protect the endometrium from the
stimulatory effects of oestrogen. This can be in the form of hormone replacement therapy,
but, alternatively, the combined oral contraceptive pill would be a suitable option and may be
more acceptable to young women.
RESISTANT OVARY SYNDROME

In this condition, the ovarian follicles fail to develop, despite high circulating levels of
gonadotrophins. The clinical and biochemical features are that of premature ovarian failure.
An ovarian biopsy will reveal ovarian follicles, and thus distinguish the condition from
premature ovarian failure. In practice, this is not helpful; it may stimulate adhesion formation
and the absence of follicles can be reliably determined only after the entire ovary has been
examined. The treatment is the same as for premature ovarian failure.
93
OVARIAN DISORDERS
POLYCYSTIC OVARIAN
SYNDROME
Polycystic ovarian syndrome
(PCOS) is a functional
derangement of the
hypothalamo–pituitary
ovarian axis associated with
anovulation. The
pathophysiology of PCOS Polycystic
remains poorly understood. ovaries
Insulin resistance is a feature,
and a genetic element to the
disorder has been proposed.
Women with PCOS are more at
risk of developing Type II
diabetes.
In women with PCOS, LH levels are relatively high and FSH levels are relatively low, leading
to an elevated LH:FSH ratio. Oestradiol levels tend to be within the normal range. Production
of androgens is stimulated by the elevated levels of LH; increased levels of testosterone,
androstendione and DHA are secreted by the ovary. Some of these androgens are converted to
oestrogen in peripheral tissues. In response to high androgen levels, sex hormone binding
globulin (SHBG) is reduced by about 50%, leading to an increase in the proportion of
unbound, active, androgens. Hence, androgenic side effects are common, despite only a
modest rise or even normal levels of total serum testosterone levels.
Clinical Features
The clinical features of PCOS are variable. In the classic ‘Stein Leventhal’ syndrome,
described in 1935, the presenting features are oligomenorrhoea, hirsutism and obesity. Other
manifestations are common, however, and include menstrual disorders ranging from
amenorrhoea to menorrhagia and signs of androgen excess, such as hirsutism, acne and
infertility.
94
OVARIAN DISORDERS
POLYCYSTIC OVARIAN SYNDROME—(cont’d)

Diagnosis
No specific features of polycystic ovarian syndrome are diagnostic of the condition. According
to the Rotterdam criteria, the diagnosis can be made if two out of three of the following
criteria are present:
1. Oligoamennorhoea
2. Ultrasound
Ultrasound will show
multiple follicular cysts
up to 6–8 mm diameter
within the ovary. This is
described as a necklace
of pearls appearance.
The volume of the
ovarian subcortical
stroma is increased. Such
findings on ultrasound
support rather than
confirm a diagnosis of
PCOS, as 25% of normal
women will demonstrate
these features on
ultrasound.
Thick capsule
6mm
Hyperplasia of ovarian cortex with

multiple follicles
3. Elevated free testosterone levels

A modest increase in total testosterone is accompanied by a decrease in SHBG resulting
in an increase in free testosterone levels.
An elevated LH:FSH ratio may occur but is no longer a diagnostic criteria.
A physiological raised LH level occurs during the LH surge.
95
OVARIAN DISORDERS
POLYCYSTIC OVARIAN SYNDROME—(cont’d)

Long-term Effects of PCOS
1. Women with PCOS who are anovulatory are
at increased risk of endometrial hyperplasia and
subsequent endometrial cancer (3) because of
the high oestrogen and low progesterone levels. Hypertension/
2. The hyperinsulinaemia associated with insulin cardiovascular
resistance leads to an increased risk of diabetes disease
mellitus.
3. Women with PCOS who are obese and insulin
resistant have an increased risk of hypertension Diabetes
and cardiovascular disease.
Endometrial
carcinoma
Treatment of PCOS
The treatment for PCOS is aimed at relieving
symptoms and preventing adverse long-term effects.
For women who are overweight, weight loss should
be strongly supported as it reduces the clinical
features of the condition and provides long-term
health benefits.
1. Infertility
Anovulatory women with infertility should be treated with clomiphene in the first
instance. Women who fail to respond may require gonadotrophins gonadotrophin
releasing hormone (GnRH) analogues.
2. Amenorrhoea
Women with amenorrhoea may be treated with the combined oral contraceptive pill if
contraception is required, or cyclical gestogens (e.g. medroxyprogesterone acetate 10 mg
daily from day 15 to 25) if contraception is not required. The prevention of amenorrhea is
important in PCOS to reduce the risk of endometrial carcinoma. The Mirena IUS is also
useful to reduce the long-term risk of endometrial hyperplasia.
3. Hirsutism
See p. 106.
96
PITUITARY DISORDERS
1. Hyperprolactinaemia
2. Pituitary adenoma
3. Craniopharyngioma
4. Other tumours such as meningioma
5. Pituitary necrosis (Sheehan’s syndrome/
Simmond’s disease).
Pituitary tumours are normally benign. However,
as they grow in a confined space, they may cause
symptoms by compressing surrounding tissue and
structures. Functioning pituitary tumours may
exert effects because of the hormones they release.
The commonest of these are prolactin secreting
pituitary tumours, accounting for 50% of all
pituitary adenomas.
‘Double floor’ appearance of the

pituitary fossa due to tumour
HYPERPROLACTINAEMIA
Prolactin is secreted from the anterior pituitary,
and the normal blood level is between 150 and 600 mU/L depending on the laboratory.
During pregnancy, there is a 10-fold increase in serum prolactin levels. Non-physiological
hyperprolactinaemia, which occurs when the woman is non-pregnant, can cause amenorrhoea
or galactorrhoea (inappropriate lactation) or both. Hyperprolactinaemia is the principal cause
of amenorrhoea in around 20% of women with this condition.
Hypothalamus
TRH Dopamine
(VIP) g -aminobutyric acid
+ -
Pituitary
+
E2
PrL
Suckling
Breast
Control of prolactin release
97
PITUITARY DISORDERS
Aetiology
1. Pituitary tumour Hypothalamus
microadenoma <10 mm diameter
macroadenoma >10 mm diameter T4 - TRH
+
2. Hypothyroidism
Thyroid function tests should be
Pituitary
performed on all women with
hyperprolactinaemia. In primary PrL +
hypothyroidism, TRH is increased.
As TRH stimulates pituitary TSH
prolactin production, +
hyperprolactinaemia results.
Treatment with L-thyroxine should
restore prolactin levels to normal. Thyroid
3. Drugs
Drugs with dopamine agonistic activity
cause hyperprolactinaemia by attenuating
the inhibitory action of dopamine on
pituitary prolactin production.
Commonly used dopamine agonists
Phenothiazines
e.g. chlorpromazine
thioridazine
prochlorperazine
Butyrophenones
e.g. haloperidol
Benzamides
e.g. metoclopramide
Cimetidine
Methyldopa
Other drugs which may cause hyperprolactinaemia
Tricyclic antidepressants
Monoamine oxidase inhibitors
Opiates*
Cocaine*
*especially during chronic abuse
4. Idiopathic
98
PITUITARY DISORDERS
Diagnosis of Hyperprolactinaemia
The diagnosis of hyperprolactinaemia can be made on a single serum measurement. In the
presence of oligo- or amenorrhoea, a serum prolactin of 800 mU/L or greater is likely to be of
pathological significance. In the absence of an obvious alternative cause, radiological
examination such as computerised tomography (CT) scanning or magnetic resonance imaging
(MRI) should be performed to exclude a pituitary tumour.
Mechanism of Amenorrhoea
Raised prolactin
Disturbance of normal hypothalamic GnRH release
LH pulsatility suppressed
Anovulation/amenorrhoea
99
PITUITARY DISORDERS
Treatment
Medication
Dopamine is the prolactin release inhibiting factor produced by the hypothalamus, and
medical treatment for hyperprolactinaemia is based around dopaminergic stimulation.
1. Bromocriptine
This is a semi-synthetic ergot 50
alkaloid. Side effects include
Serum prolactin (µg/L)

nausea and giddiness with fainting
(syncope). Side effects may be 40
minimised by commencing with a 2.5mg
small dose and increasing Bromocriptine
gradually. 30
2. Quinagolide Normal
Quinagolide, a dopamine agonist, 10
is given daily and may be tolerated
better than bromocriptine.
0
4 8 12 16 20
3. Cabergoline Hours
Cabergoline is a dopamine agonist
Effect of bromocriptine on serum
with a long half-life. It is
prolactin. Duration 12–16 h.
administered weekly.
Surgery
Transnasal
Trans-sphenoidal surgery can be used to resect both micro- and macroadenomas. Symptoms
of hypopituitarism, particularly diabetes insipidus, may be a long-term consequence of
surgery. The results of treatment vary greatly between centres. Knowledge of local data can be
used to determine whether surgery or medical treatment is most appropriate for each patient.
100
HYPOTHALAMIC DISORDERS
Intermittent release of GnRH (gonadatrophin releasing hormone) stimulates production of

FSH and LH by the anterior pituitary. Increased concentration of endogenous dopamine and
opioids can affect the release of GnRH. This can be provoked by a number of conditions,
detailed below.
Disorders of the hypothalamus result in hypogonoadotrophic hypogonadism, and hence
amenorrhoea.
DIAGNOSIS
The diagnosis is made by exclusion. These patients have low gonadotrophins, normal
prolactin levels, a normal pituitary gland on radiological evaluation, and they fail to bleed in
response to progesterones.
CAUSES
1. Anorexia nervosa
This is an eating disorder characterised by low body weight. It is much more common in
women than in men and usually starts in the mid-teen years. The patient’s weight is more
than 15% below normal for her age and height.
In moderate to severe disease, it is important to treat the psychological cause of the
condition and this is best done by referral to a psychiatrist. Treatment with hormone
replacement therapy will relieve symptoms of oestrogen deprivation and initiate the
resumption of menstrual periods.
2. Exercise
Female athletes are commonly amenorrhoeic, and the mechanism is one of suppression of
GnRH production. This condition is related to the much reduced body fat (although not
necessarily body weight), stress and to exercise itself. Again, oestrogen replacement (with
added cyclical gestogens) should be considered.
3. Kallmann’s syndrome
This is a rare condition of congenital hypogonadotrophic hypogonadism in association
with anosmia. Secondary sexual characteristics are absent. Ovulation can be induced with
gonadotrophins.
101
INVESTIGATION OF AMENORRHOEA
In most cases, the failure to menstruate is due to some abnormality in the control mechanism
involving the hypothalamic–pituitary pathway. A careful history and physical examination is
essential and may provide pointers to likely abnormalities.
The history should include the following:
change in weight
presence of galactorrhoea
presence of hirsutes (excess body or facial hair)
presence of stress
questions about excessive exercise.
A full physical examination should be performed. This should include the following:
assessment of patient’s body mass index (BMI) (weight in kg2/height in m)
presence of galactorrhoea
presence of hirsutes
blood pressure
urinalysis
assessment of secondary sexual characteristics
assessment of external genitalia
pelvic examination to assess internal genitalia.
In women who are virgo intacta, a pelvic examination should not be performed. If necessary,
information about the presence of a uterus can be gained from ultrasound or MRI. However,
inspection of external genitalia can still be performed and may reveal a condition such as cliteromegaly.
INVESTIGATION
The simplified scheme of investigation shown will identify which compartment is responsible
for the amenorrhoea. In practice, estimation of serum prolactin and thyroid stimulating
hormone (TSH) is performed concurrently with a progesterone challenge test.
Estimation of blood prolactin and TSH
High prolactin High TSH Normal prolactin

Normal TSH Normal TSH
CT scan Hypothyroidism Investigate

as below
Prolactin Idiopathic
secreting hyperprolactinaemia
102 adenoma
The progesterone challenge test involves giving a progesterone, for example,

medroxyprogesterone acetate 10 mg daily for 5 days. It is essential to exclude pregnancy first.
If the woman bleeds after progesterone is withdrawn, this indicates firstly that a uterus is
present, and secondly that there is some circulating oestrogen. If the progesterone challenge
test is negative, it is appropriate to give oestrogen and progesterone, (e.g. 1.25 mg of
conjugated oestrogens for 21 days, with the addition of a progesterone for the last 5 days).
Failure to bleed in response to this treatment confirms a uterine problem.
Normal prolactin
Normal TSH
Progesterone challenge test
+ve withdrawal -ve withdrawal

bleed bleed
Anovulation Oestrogen and

probably PCOS progesterone challenge
+ve -ve
FSH/LH Uterine
abnormality
Low Normal High
CT scan of Ovarian
pituitary failure
Abnormal: Normal:
Pituitary disease Hypothalamic disease
103
If the results of these tests are inconclusive, it suggests that the cause lies between the pituitary
and ovaries, and further laboratory exploration must be undertaken.
Estimation of FSH LH
High Low High
Estimate blood oestrogen Estimate androstenedione and testosterone
High Low
Ovarian tumour or
polycystic ovaries
Refractory Ovarian
Ovaries failure
104
HIRSUTISM
Hirsutism in the female means an excessive production

of hair with a tendency to male distribution.
‘Excessive’ is defined as beyond social acceptability or
causing embarrassment to the patient.
Normal pattern hair is of two types:
(i) fine downy, vellus hair which is non-pigmented.
(ii) coarser pigmented terminal hair as in the
axilla and pubis.
About one-third of women have some visible
pigmented hair on the upper lip, and 5% have it on
the chin and sides of the face.
AETIOLOGY
1. Rise in secretion of free androgens.
2. Reduction in SHBG.
3. Increased end organ sensitivity to androgens.
SHBG level falls when testosterone production increases, and probably also in the case of drug-
induced hirsutism. Oestrogen increases the levels of SHBG and lowers the amount of free androgen.
PHYSIOLOGY OF TESTOSTERONE
The three principal androgens are dihydrotestosterone, testosterone and androstenedione; the
last mentioned is the least potent but is converted to dihydrotestosterone in the follicle cells.
Hair follicle cells 50% 3% Testosterone remains free Androgen

receptors in
follicles
Adrenal 25% 97% Testosterone bound
to SHBG or albumin
Ovary 25%
Causes: testosterone is greater than 5 nmol/L

or if the history is of sudden onset.
1. Idiopathic hirsutism
By far the commonest, it has no apparent 4. Congenital adrenal hyperplasia
androgen increase, and is probably due to This is an adrenal disease, caused by an
increased local testosterone production enzyme defect (commonly 21-
at the target organ. hydroxylase deficiency) resulting in
elevated androgens.
2. Polycystic ovary disease
17-hydroxyprogesterone is elevated.
There is usually a higher level of free active
testosterone because of reduced SHBG. 5. Drugs such as:
See page 95. phenytoin
diazoxide
3. Androgen-producing tumours minoxidil
These may arise in the ovary or adrenal
androgen-containing compounds 105
glands. They should be considered if serum
VIRILISATION
Masculinisation and virilisation are terms for extreme androgen effects.
CLINICAL FEATURES
The symptoms and signs include the following:
male pattern balding
cliteromegaly
deepening of the voice
increased muscle mass
male body habitus.
Alopecia
Growth of moustache and beard

Changes in larynx cause
deepening of voice
Flattened breasts
Hirsutes of chest
Hair on abdomen
Enlargement of clitoris
These symptoms are more likely to represent an androgen secreting tumour, but mild
symptoms such as male pattern balding can occur with PCOS.
INVESTIGATION
serum testosterone
serum dehydroepiandrosterone sulphate (DHAS)
(elevated in adrenal disease)
17-hydroxyprogesterone (17-OHP)
(elevated in congenital adrenal hyperplasia)
24 h urinary free cortisol if Cushing’s syndrome is suspected.
If the testosterone levels are significantly elevated, an androgen secreting tumour of the ovary
or adrenal gland is likely. Ultrasound, CT scanning and perhaps even laparoscopy may be
required to make the diagnosis.
106
MANAGEMENT OF HIRSUTISM
If the woman is untroubled by her symptoms, no treatment is needed. Women who are
overweight should be advised to lose weight.
LOCAL TREATMENT Depilatory Creams

These are alkaline solutions, which
Ferriman Galwey Charts
dissolve the hairs and allow them to be
These charts provide a semi-objective
wiped away. They will injure the skin if left
scoring system for hirsutism. If they are
on too long.
completed at each patient visit, the change
in symptoms may be assessed. Depilatory Waxes
The wax is melted and spread on to the
Shaving
skin. When it sets, it is pulled off, plucking
This method has to be repeated
the hairs with it. This is painful and leaves
frequently.
the skin tender and reddened.
Electrolysis
Decomposition of the hair follicle by the
passage of an electric current. Low
galvanic current is used through a fine
electrode. The hair is electrolysed after
about 10 s and plucked out painlessly.
Diathermy Probe
The follicle is coagulated instantly and the electrode
hair pulled out.
Electrical destruction of individual hairs is
permanent, but prolonged treatment is
tedious and expensive and may cause
scarring.
107
MANAGEMENT OF HIRSUTISM
DRUG TREATMENT
1. Combined oral contraceptive pill (COCP)
These drugs act firstly by suppressing LH production and thereby attenuating ovarian
androgen synthesis. Secondly, the oestrogens stimulate SHBG production by the liver.
The effect of the progestogen component can vary as some such as norethisterone and
levonorgestrel have an androgenic derivation. Some of the available preparations contain
antiandrogenic progestogens, these include Cyproterone Acetate and Drospirenone.
2. Antiandrogens
As mentioned above, cyproterone is a progesterone, which inhibits LH production. It also
binds to the androgen receptor and therefore acts as an antiandrogen. It can either be
administered as with ethinyloestradiol (the contraceptive pill ‘Dianette’) or daily from
days 5–14, with ethinyloestradiol on days 5–25 (the ‘reverse sequential’ regimen).
Other antiandrogens include flutamide, a non-steroidal, and finasteride, a 5a reductase
inhibitor. Finasteride inhibits the conversion of testosterone to dihydrotestosterone.
3. Insulin sensitising agents

Metformin will improve insulin sensitivity and reduces free androgens in women with
PCOS.
4. Dexamethasone
Dexamethasone inhibits adrenal androgen production, and is useful in hirsutism caused
by adrenal disease.
5. GnRH analogues with addback hormone replacement therapy (HRT)

This treatment is expensive, but has been shown to be effective in clinical trials.
6. Eflornithine cream locally slows hair growth by inhibiting the enzyme orthinine
decarboxylase.
NB. With all of the above, it may be 3 months or more before an improvement in symptoms
can be expected, and the patient should be counselled regarding this.
108
MENSTRUAL DISORDER
Heavy menstrual bleeding is one of the commonest reasons why women in the Western world
consult a gynaecologist. The vast majority of these women have benign or no pathology;
however, the illustration demonstrates that for a minority of women there will be a malignant
pathology.
Clearly, the age of the patient has a major influence on the likely cause of bleeding, for
example, endometrial carcinoma is uncommon in premenopausal women and, similarly,
endometriosis is uncommon in postmenopausal women.
Endometrial
cancer
Adenomyosis Endometriosis
Fibroid
Pelvic inflammation
Endometrial polyp
Cervical polyp
Cervical tumour
Careful history taking is crucial in the assessment of menstrual disorder. Women with heavy
regular bleeding and no additional symptoms of concern such as intermenstrual or postcoital
bleeding are most likely to have dysfunctional uterine bleeding. Benign pathologies such as
fibroids are a common cause of heavy menstrual bleeding. See Chapter 11.
109
DYSFUNCTIONAL UTERINE BLEEDING
Dysfunctional uterine bleeding is one of the commonest causes of excessive menstrual

bleeding in women of reproductive age.
Dysfunctional uterine bleeding is the term applied to cases of excessive bleeding where no
organic lesion can be found. Presumably the cause lies in an abnormal function of the ovarian
and endometrial control mechanisms associated with the menstrual cycle.
Where appropriate investigation may be required. This will depend on the age of the patient
and any additional symptoms.
Pelvic ultrasound (ideally transvaginal) should be performed. Hysteroscopy and endometrial
biopsy may be required, depending on scan findings, age of the woman, and presenting
symptoms.
CLINICAL FEATURES
The patient will complain of heavy and/or irregular bleeding. Normal menstrual cycles have a
length of 21–35 days (mean 28 days). A normal period lasts for 3–7 days. Menstrual blood
loss of 30–50 ml/month is normal. Menstrual blood loss is considered as excessive when it is
greater than 80 ml/month. It is however rarely measured during clinical trials, and heavy
menstrual loss should be defined clinically.
ESTIMATION OF BLOOD LOSS

1. Subjective methods
The subjective estimation of menstrual blood loss is often difficult. What is normal to one
woman may be regarded as abnormal by another. The simplest method of determining
excessive menstrual loss is to ask the patient about the number of sanitary pads and/or
tampons used daily. The use of pictures to indicate the amount of staining on each
pad/tampon may improve accuracy. The passage of significant clots usually indicates
excessive menstrual loss. The social effect of heavy menstrual loss can be considerable and
symptoms such as flooding through sanitary protection are important.
2. Objective methods
Haemoglobin measurements will indicate if the patient is anaemic. An estimation of
serum ferritin may show a depletion in iron stores. Whilst the detection of anaemia has
important clinical implications, many women with a good diet are able to maintain
normal haemoglobin levels, despite excessive menstrual loss.
The optimum method of assessing menstrual blood loss accurately is to ask the patient to
collect her used pads and tampons over the course of one menstrual period. These can
then be soaked in sodium hydroxide, and the optical density compared to a known
standard. This technique is generally only used as a research tool, but reveals that many
women who complain of menorrhagia have a menstrual loss within the normal range.
A blood loss of 80 ml is thought to represent the upper limit of a ‘normal’ period. Studies
have also shown that some women with a blood loss of greater than 80 ml do not perceive
that they have heavy periods.
110
INVESTIGATION OF THE ENDOMETRIUM
Transabdominal scanning can be useful and should be used for women who have never been
sexually active (virgo intacta). The bladder requires to be full so that overlying bowel is moved
away to optimise the view of the pelvis. Even with a full bladder, views of the endometrium
may be limited and particularly difficult to obtain in obese patients.
Transvaginal ultrasound scan This technique offers a close view of the uterus and adnexae.
Features noted during transvaginal scanning of the pelvis
Thickness and regularity of the
endometrium; in
postmenopausal women, the
endometrial thickness (ET) is
less than 3 mm in an AP
diameter. A thickened
endometrium may represent a
polyp or endometrial
hyperplasia; however, the
normal endometrial thickness
varies in premenopausal women
during the menstrual cycle, and
it may be physiological.
Presence of uterine fibroids The
size and site of fibroids are
important. Small fibroids of less
than 3 cm are very common
and usually do not change the
treatment options.
Adnexal pathology can also be
visualised in detail. Hysteroscopy Bladder
OUTPATIENT
PROCEDURES
Hysteroscopy
Hysteroscopy is a technique used
to visualise the endometrium
under magnification. Abnormal
areas of the endometrium can be
seen, and a targeted biopsy
Hysteroscope
taken. The procedure may be inserted into
performed as an outpatient cervix
procedure if a sufficiently narrow
hysteroscope and distension
media are available. The
distension media can be fluid: Uterus
saline or dextrose or CO2 gas.
111
INVESTIGATION OF THE ENDOMETRIUM
The main purpose of endometrial biopsy is to assess for endometrial hyperplasia or identify
endometrial carcinoma. The risk of endometrial cancer in premenopausal women is very low, but
biopsy should be performed for women over 45 with menstrual disorder. In women under 45, the need
for biopsy (possibly with hysteroscopy) should be guided by other factors including intermenstrual or
irregular bleeding, and scan findings. See page 201 hyperplastic conditions of the uterus.
METHODS OF ENDOMETRIAL BIOPSY
Pipelle de Cornier
The Pipelle is inserted into the uterine cavity
and the plunger withdrawn to produce a vacuum.
A small sample of endometrium is thereby sucked
into the tube and subsequently expelled into fixative.
Vabra Curettage
This method of obtaining material for
histological examination can be done in the
outpatient clinic. Adequate specimens can be
obtained, but the procedure is painful. Vabra curette
DILATATION AND CURETTAGE

As a sole procedure, dilatation and curettage is
now considered to be an outdated procedure;
however, occasionally it may be required to
provide a better sample of the endometrium. It is
usually accompanied by hysteroscopic assessment
of the cavity prior to sampling. It is often necessary
to dilate the cervical canal in order to pass the
curette. This procedure is normally performed
under general anaesthesia as an inpatient.
Technique
The dilator must be held firmly in one hand and
pressed into the canal against traction in the opposite
direction exerted by the other hand. Resistance must be
overcome slowly, and the dilator must not be passed farther
than the length of the uterine cavity measured by the sound.
Curettage
Dilatation of the cervix is followed by curettage of the
endometrium. The endometrium can then be examined histologically. Hysteroscopy and endometrial
biopsy are largely diagnostic tools, but in the uncommon situation in which pathology such as an
112 endometrial polyp is present, they may be therapeutic.
INVESTIGATIONS OF ENDOMETRIUM - COMPLICATIONS
1. Trauma to cervix
The volsellum
forceps may tear the
anterior lip of cervix
if pulled on too
forcibly.
The cervix
splits at about
8mm dilatation
The next dilatation

enlarges the false
passage
2. Perforation of the uterus or cervix

This is not an uncommon occurrence
and usually no ill-effects result. The
usual site is the midline of the fundus,
and it becomes evident when the curette
passes farther than the length of the
cavity as shown by the uterine sound.
Immediate laparoscopy and/or
laparotomy is required if there is any
suspicion of damage to extrauterine
viscera. This risk is higher during
pregnancy as the uterus is softer.
3. Uterine synechiae
Over-vigorous curettage may remove all the endometrium from areas of anterior and
posterior walls, permitting the myometrium to heal together forming adhesions –
Asherman’s syndrome. This is diagnosed and treated hysteroscopically.
113
MANAGEMENT OF HEAVY MENSTRUAL BLEEDING
MEDICAL MANAGEMENT
Tranexamic Acid
Administration: tranexamic acid 1 g qds during menstruation.
Mode of action: inhibits clot breakdown within endometrial vasculature.
Side effects are usually mild but can include nausea, vomiting and diarrhoea.
Up to 40% reduction in menstrual loss can be achieved.
Prostaglandin Synthetase Inhibitors
Administration: for example mefenamic acid, 500 mg tid during menstruation.
Mode of action: alters imbalance of vasodilator prostaglandin PGE2 and the vasoconstrictor
prostaglandin PGF2a.
Side effects can include, diarrhoea, rashes, thrombocytopenia and haemolytic anaemia.
A 25% reduction in menstrual loss can be achieved.
Combined Contraceptive Pill
Administration: usual contraceptive regimen.
Mode of action: suppression of ovulation limits hormonal stimulation of the endometrium.
A reduction in menstrual loss can be seen in women both with and without menorrhagia.
Levonorgestrel Intrauterine System (LNG-IUS) Mirena
Administration: intrauterine system releasing 20 mg of levonorgestrel daily.
Mode of action: inhibits endometrial proliferation.
This device was originally designed as a contraceptive agent but is one of the most effective
medical methods for reducing menstrual blood loss. One year after insertion, menstrual blood
loss is reduced to 5% of the original amount. The main side effect of treatment is irregular
bleeding in the first 3–6 months after insertion.
Progesterone
This is most useful for anovulatory bleeding.
Cyclical gestogens.
Administration: for example norethisterone 5 mg bd from days 5–26 of the menstrual cycle.
Mode of action: thought to provide progestogenic support to the endometrium when
endogenous progesterone is lacking.
114
SURGICAL MANAGEMENT
Endometrial Ablation
Hysterectomy
Abdominal – total
subtotal (conservation of cervix)
Vaginal – laparoscopically assisted vaginal hysterectomy
total laparoscopic hysterectomy
ENDOMETRIAL ABLATION TECHNIQUES

These techniques use a variety of energy sources and can either be performed under
hysteroscopic guidance or as a blind procedure. Endometrial ablation does not guarantee
amenorrhoea, but symptoms are improved in most women. The major advantage of
endometrial ablation over abdominal hysterectomy is the shorter inpatient stay and recovery
associated with this operation. Complications of the procedure include excessive fluid
absorption and uterine perforation with damage to intra-abdominal organs.
Endometrial ablation is only appropriate for women who have completed their family and
effective contraception should be continued following the procedure.
Hysteroscopic Procedures
Trans-cervical resection of endometrium (TCRE)
Using an operating hysteroscope, the uterine cavity is distended with a glycine solution and
either a wire loop diathermy instrument is used to cut strips of endometrium and underlying
myometrium or a ‘roller ball’ electrode is used to coagulate the endometrium. These
techniques are performed under direct vision.
‘Roller ball’
Wire loop
115
Second Generation Techniques

These techniques use a variety of thermal energies
and are not performed under direct vision. They are
relatively simple to perform; however, if the
instrument is displaced, there is a risk of thermal
injury to extrauterine structure, for example, bowel
injury. The common techniques are microwave
(MEA), a fluid filled balloon that is heated,
Thermachoice and electrical energy, Novasure.
There are a variety of safety mechanisms that these
techniques employ; however, none of them is
infallible, and recent advice has recommended that
hysteroscopy should be performed prior to the
procedure and that ultrasound should be used to
confirm that the device is within the endometrial
cavity during treatment.
An endometrial biopsy to exclude endometrial
carcinoma is essential as part of any endometrial
ablation procedure.
Total Hysterectomy (Removal of Uterus

and Cervix)
Line of
division
1. Division of adnexa. The ovarian 2. Vesicouterine peritoneum is opened up

ligament, fallopian tube and round and bladder is being dissected off cervix.
ligament are clamped and divided. (The ‘lateral vesicouterine ligament’ –
marked by the arrow – conceals the
ureter.)
116
Total Hysterectomy (Removal of Uterus and Cervix)—(cont’d)
3. Parametrium containing the uterine 4. The uterosacral ligaments are clamped

arteries is clamped and divided. and divided.
5. The top of the vagina is now clear of bladder and ureters and can be opened to allow
excision of uterus and cervix.
117
Subtotal Hysterectomy
Subtotal hysterectomy involves removal of
the body of the uterus only. The cervix is
conserved. The operation is easier and safer
than total hysterectomy, particularly if there
are adhesions around the cervix (e.g. from
previous caesarean section). The risk of
ureteric damage is much less than with total
hysterectomy. The major disadvantage of
subtotal hysterectomy is that cervical
smears continue to be required as there
remains a risk of cervical cancer. There is a
small risk of persistent light bleeding from
the remnant of endocervix.
Bilateral Oophorectomy
Hysterectomy is often accompanied by
bilateral oophorectomy. The pros and cons
of this procedure are summarised below.
Advantages
reduces risk of ovarian cancer
effective treatment for premenstrual syndrome
may improve efficacy of treatment if pelvic pain is included in symptoms.
Disadvantages
leads to premature menopause and effects of oestrogen withdrawal, unless patient takes
HRT.
118
Vaginal Hysterectomy
In vaginal Vaginal hysterectomy
hysterectomy, the
uterus and cervix are
removed via a vaginal
approach. The
operation is technically
difficult in women
without some degree of
uterine prolapse. This
approach avoids the
need for an abdominal
scar, and recovery is
usually more rapid;
however, the risk of
major complications is
slightly higher than
with an abdominal
procedure. There are a
number of factors that
may make an
abdominal procedure
the better option,
for example, large
fibroids, severe
endometriosis.
Laparoscopically Assisted Vaginal Hysterectomy (LAVH)
A laparoscopically assisted hysterectomy procedure allows the ovaries to be removed; this is
difficult with a standard vaginal hysterectomy. The broad ligaments, including the ovarian
vessels, the round ligaments, and the uterine arteries may be ‘clamped and cut’ by an
endoscopic device which inserts multiple rows of stainless steel staples and divides the tissues.
Alternatively, diathermy may be used to coagulate the tissues prior to division. The uterus is
then removed vaginally and the vaginal vault closed per vaginam.
Total Laparoscopic Hysterectomy
The entire procedure is completed laparoscopically, and the uterus is removed per vaginam.
119
DYSMENORRHOEA
Dysmenorrhoea implies pain during menstruation, and most women experience some degree of
pain at least on the first day of the period, when the loss is heaviest.
Cramp may occur premenstrually; if this is severe, it may be more likely to suggest underlying
pathology, such as endometriosis.
The pain may be secondary to organic disease such as endometriosis or infection, but primary
dysmenorrhoea, which is being discussed here, occurs in the presence of a normal genital
tract.
NATURE OF THE PAIN

It is usually described as having two components: a continuous lower abdominal pain
attributed to vascular congestion, which radiates through to the back and sometimes down the
thighs, and an intermittent cramping pain.
Premenstrual Increased PAIN

epithelium uterine
contraction
Myometrial PAIN
ischaemia
Prostaglandin Products of tissue breakdown

PAIN
and bradykinin
AETIOLOGY
There is increased myometrial activity during the periods in women with dysmenorrhoea and
uterine blood flow is reduced, especially during intense contractions. It is thought that this
hyperactivity is the result of excessive quantities of prostaglandins synthesised during the
breakdown of the premenstrual endometrium.
120
DYSMENORRHOEA
CLINICAL FEATURES OF PRIMARY DYSMENORRHOEA

This condition is typically present from the time when ovulation is established, usually the late
teens.
Prostaglandin (PG)
synthetase inhibitors Pain
have been shown
experimentally to
Uterine blood flow
abolish uterine
contraction and
ischaemia and the
pain that
accompanies them.
200 Intrauterine pressure
mmHg
0
0 10 20 30 40 50 min
PG synthetase
inhibitor
MANAGEMENT
In mild or moderate disease, treatment can be commenced after a full history and
examination. In severe or unresponsive disease, investigation should be performed.
A transvaginal scan and possibly laparoscopy should be considered.
DRUG TREATMENT
1. The contraceptive pill. Dysmenorrhoea is very unlikely in the absence of ovulation, probably
because of the pseudo-atrophy of the endometrium. The disadvantages of this efficacious
treatment are the well-known side effects and perhaps the prevention of pregnancy.
2. Prostaglandin synthetase inhibitors such as mefenamic acid inhibit prostaglandin
production, reduce uterine contractions, and thereby alleviate dysmenorrhoea.
In controlled studies, up to 90% of women report an improvement of symptoms with
mefenamic acid.
3. Levonorgestrel intrauterine system MIRENA
Progesterone is a smooth muscle relaxant and intrauterine administration will significantly
reduce dysmenorrhoea.
121
ADENOMYOSIS
This is an infiltration of the myometrium by ectopic deposits of endometrium. It is usually

only diagnosed once the uterus is examined histologically following hysterectomy. It can be
visualised with ultrasound but MRI is better at differentiating adenomyosis from fibroids.
PATHOLOGY
The gross appearances are quite
striking. The uterus is usually
enlarged and this may be quite
marked.
MICROSCOPIC
APPEARANCES
The appearance of the endometrial deposits
within the myometrium varies. In many cases,
they consist of typical glands and stroma although
the stroma may be more prominent than the
glands. Cyclical changes may be observed, but this
is not common. More often, the endometrium is
of immature type, and if it does react, it usually
shows only proliferative changes. Clinical features
are pain and menstrual upset.
Endometrial deposits in the myometrium. Note
the non-secretory gland epithelium. The
surrounding myometrium undergoes moderate
hyperplasia.
122
ENDOMETRIOSIS
Endometriosis is a condition where deposits of endometrium develop outside the uterine cavity.
Its manifestations are very variable and often bear no relation to the extent of the disease.
PATHOLOGY
The gross appearance shows ectopic deposits,
which can vary in number from a few in one
locality to large numbers distributed over the
pelvic organs and peritoneum.
The commonest sites of these deposits are
the following:
• Ovary
• Peritoneum of the rectovaginal
cul-de-sac of the Pouch of Douglas
• Sigmoid colon
• Broad ligament
• Uterosacral ligaments.
Less common are the following sites:
• Cervix
• Round ligament
• Bladder
• Umbilicus
• Appendix
• Laparotomy scars.
Endometriosis
of a laparotomy
scar
Endometriosis of the
reco-vaginal septum
Endometriosis
Orifice
in the bladder
of ureter
123
ENDOMETRIOSIS
The commonest appearance of a typical

lesion is that of a round protruding vesicle
that shows a succession of colours from blue
to black to brown. The variation in colour is
due to haemorrhage with subsequent
breakdown of the haemoglobin. Ultimately
the area of haemorrhage heals by the
formation of scar tissue. The result is a
puckered area on the peritoneum.
Commonly, however, the haemorrhage
results in adhesion to surrounding
structures. These adhesions are more apt to
form between fixed structures such as the
broad ligament, ovary, sigmoid colon, or
the posterior surfaces of the vagina and
cervix.
The ectopic deposits of endometrial tissue vary in size from pin-point to 5 mm or more. It is
these larger deposits which tend to rupture leading to adhesions. These adhesions over the
ovary can lead to the formation of quite large haemorrhagic cysts due to continued bleeding
from deposits, the blood being unable to escape.
Investigation has shown that many lesions do not have a ‘typical’ appearance. The following is
a list of other appearances which have been described.
• White, slightly raised opacities due to retroperitoneal deposits.

• Red flame-like or vascular swellings, more common in the broad ligament
or uterosacral ligament.
• Small excrescences like the surface of normal endometrium.
• Adhesions under the ovary or between the ovary and the ovarian fossa peritoneum.
• Café-au-lait patches often in the Pouch of Douglas, broad ligament or peritoneal
surface of the bladder.
• Peritoneal defects on uterosacral ligament or broad ligament.
• Areas of petechiae or hypervascularisation usually on the bladder and the broad ligament.
SECONDARY PATHOLOGY
This is due to the adhesions between the endometriotic deposits and adjacent organs.
In long-standing cases, the pelvic cavity is obliterated by these adhesions. Retroversion of
the uterus can occur as the adhesions form.
124
ENDOMETRIOSIS
HISTOLOGY
While the deposits consist of endometrial elements, rarely do they mirror the appearance of normal
endometrium, especially in their architecture. In place of the compact orderly arrangement of
glands and stroma, there are scattered patches of gland formations with some surrounding stroma.
Sometimes gland formations predominate; occasionally only stromal cells can be seen.
Sometimes the deposits show evidence of cyclical activity, but the activity does not always
coincide with what is happening in the uterine endometrium.
THE AMERICAN FERTILITY SOCIETY

REVISED CLASSIFICATION OF ENDOMETRIOSIS
FO
U N D D 1 94
Patient’s name _______________________________________________ Date ___________________________________

Stage I (Minimal) – 1–5 Laparoscopy _________ Laparotomy ________ Photography __________
Stage II (Mild) – 6–15 Recommended Treatment ________________________________________
Stage III (Moderate) – 16–40 ____________________________________________________________
Stage IV (Severe) – >40 ____________________________________________________________
Total __________________________ Prognosis ____________________________________________________
PERITONEUM
ENDOMETRIOSIS <1 cm 1–3 cm >3 cm

Superficial 1 2 ?
Deep 2 4 6
R Superficial 1 2 4
OVARY
Deep 4 16 20
L Superficial 1 2 4
Deep 4 16 20
POSTERIOR Partial Complete
CUL DE SAC
OBLITERATION 4 40
ADHESIONS <1/3 Enclosure 1/3 – 2/3 Enclosure >2/3 Enclosure

R Filmy 1 2 4
OVARY
Dense 4 8 16
L Filmy 1 2 4
Dense 4 8 16
R Filmy 1 2 4
Dense 4a 8a 16
TUBE
L Filmy 1 2 4
Dense 4a 8 a
16
aIf the fimbriated end of the fallopian tube is completely enclosed, change the point assessment to 16
125
ENDOMETRIOSIS
CLINICAL FINDINGS
The incidence of endometriosis has been estimated at 3–7% of women, but the true incidence
is unknown. Quite often, deposits are found incidentally in women who have no symptoms of
endometriosis and are undergoing laparoscopy or laparotomy for some other condition. In
addition, as indicated in the section on pathology, many peritoneal changes now known to be
due to endometriosis were undiagnosed in the past.
The prevalence of endometriosis peaks between the ages of 30 and 45 years. As ectopic
endometrium is stimulated by the same ovarian steroid hormones as the endometrium lining
the uterine cavity, endometriosis is almost never found outside the reproductive years.
SYMPTOMATOLOGY
A. Pain affects more than 80% of women with endometriotic deposits. The pain tends to
begin premenstrually, reaching a peak during menstruation and subsiding slowly.
The character of pain may vary as does its apparent origin. It may be generalised
throughout the abdomen and pelvis like the pain of severe dysmenorrhoea. Alternatively,
pain may be localised to a particular site within the pelvis. Deep dyspareunia affects
around 40% of women with endometriosis.
B. Menstrual disturbance Menstrual disturbance affects around 20% of women with

endometriosis. It may take the form of premenstrual ‘spotting’, menorrhagia or
infrequent periods. Lesions in the wall of the bladder may result in ‘menstrual
haematuria’.
C. Infertility Endometriosis is found more commonly in women undergoing investigation

for infertility than in the ‘normal’ population. It is not clear which condition arises first.
Approximately 30% of patients with endometriosis complain of infertility. When
endometriosis is extensive, and both fallopian tubes are occluded, the mechanism by
which endometriosis prevents conception is obvious. However, milder forms of
endometriosis are also associated with subfertility, and here the pathophysiology is less
clear. The most likely mechanism appears to be that immunological factors within the
peritoneal cavity inhibit normal gamete function, thus reducing fertilisation rates.
PHYSICAL EXAMINATION
Endometriosis cannot be diagnosed by physical examination alone. However, enlargement of
the ovaries, fixed retroversion of the uterus, and tender nodules within the pelvis may each
raise the suspicion of the disease. Endometriosis should always be considered when patients
have symptoms referable to the pelvic cavity.
LAPAROSCOPY
Laparoscopic examination is the gold standard investigation for endometriosis. The lesions
can be seen and their number and location estimated. Endometriosis of long standing may be
very difficult to diagnose because of obliteration of the pelvic cavity by adhesions.
126
ENDOMETRIOSIS
IMAGING TECHNIQUES
Ultrasound, CT and MRI may
suggest the presence of
endometriosis (e.g. by the
demonstration of a particular
type of ovarian cyst) but are by
themselves insufficiently reliable
to make the diagnosis.
DIFFERENTIAL
DIAGNOSIS
Owing to the mixture of
symptoms and the variation in
appearance of the pelvic
structures, conditions such as
pelvic inflammatory disease and
tumours of the ovary and bowel
must be considered and Endometrioma right ovary
eliminated.
HISTOGENESIS
There are three theories:
1. Retrograde spill of menstrual debris through the tubes. Retrograde menstruation takes
place in most women, but it is unclear why some women should develop endometriosis
while others are unaffected.
2. Metaplasia of embryonic cells. These are derived from the primitive coelom and may
remain in and around the pelvis and differentiate into Müllerian duct tissue.
3. Emboli of endometrial tissue may travel by lymphatics or blood vessels and become
established in various sites.
The first of these theories is the most favoured.
TREATMENT
Medical Treatment
Any treatment must be aimed at treating symptoms. As ovarian hormones are responsible for
growth and activity in endometrium, many medical therapies are designed to reduce ovarian
steroid production or oppose their action.
1. Progestogens
Progestogens in a relatively high dose (e.g. medroxyprogesterone acetate 10 mg tid)
induce decidualisation, and sometimes resorption of ectopic endometrium. Side effects
include weight gain, bloating and irregular vaginal bleeding.
2. Combined contraceptive pill
The combined oral contraceptive pill also induces decidualisation of ectopic
endometrium. It may be given continuously for up to 3 months.
127
ENDOMETRIOSIS
3. Danazol
Danazol is a steroid hormone closely related to testosterone, which inhibits pituitary
gonadotrophins, and is antioestrogenic, antiprogestational, slightly androgenic, and
anabolic. It is an effective treatment but is now outdated as irreversible androgenic effects
such as hirsutism and deepening of the voice are common.
4. Gonadotrophic releasing hormone analogues (GnRH analogue)
GnRH analogues are administered by
GnRH Pituitary receptors depot injection or nasal spray. Their mode
analogue desensitised of action is shown above. These drugs are
generally effective in treating symptoms
caused by endometriosis; however,
FSH and LH output reduced menopausal side effects are common.
Add-back hormone replacement therapy
will usually prevent the vast majority of
Ovarian function depressed vasomotor symptoms without stimulating
endometriosis. These preparations are
licensed for 6 months of use as there is
Hypo-oestrogenism
concern that long-term use will increase
the risk of osteoporosis and other effects of
Regression of endometrioid deposits oestrogen deprivation.
Conclusion
As with medical therapies for other conditions, the optimum treatment is dictated by the side
effect profile which is most acceptable to the patient. None of the drug treatments described
will prevent recurrence of endometriosis once therapy has been stopped, although there may
be a period of some months between stopping treatment and the re-emergence of symptoms.
No medical treatment has been shown to improve subsequent fertility.
Surgical Treatment
Where the woman has completed her family, radical surgery to remove both ovaries is likely to
provide a lasting cure for endometriosis as it removes the oestrogenic stimulus to endometrial
growth.
In many cases, the patient wishes relief from pain but also desires to retain the possibility of
future pregnancy. In these circumstances, only conservative surgery can be employed.
The intentions in conservative surgery are the following:
1. To ablate as many endometrial deposits in the pelvic cavity as possible.
2. To restructure the pelvic anatomy by destroying adhesions that interfere with ovarian
and tubal function.
3. To destroy endometrial deposits in the ovaries.
128
PREMENSTRUAL SYNDROME
The premenstrual syndrome (PMS) includes a large group of symptoms, which appear
regularly and predictably in the week before the onset of menstruation. The symptom pattern
varies with the individual, but 95% of women are likely to acknowledge at least one of the
symptoms listed below. Symptoms resolve completely by the end of menstruation. The
severity can vary significantly and it has been classified as follows:
Mild – does not interfere with personal/social and professional life.
Moderate – interferes with personal/social and professional life, but the woman is still able to
interact, although may be suboptimally.
Severe – unable to interact personally/socially/professionally – withdraws from social and
professional activities.
Water retention Pain Autonomic reactions

Weight gain (up to 7lb) Headache Dizziness/faintness
Painful breasts Backache Cold sweats
Abdominal distension Tiredness Nausea/vomiting
Feeling of bloatedness Muscle stiffness Hot flushes
Mood changes Loss of concentration Miscellaneous

Tension Forgetfulness Feelings of suffocation
Irritability Clumsiness Chest pains
Depression Difficulty in making decisions Heart pounding
Crying spells Poor sleeping Numbness, tingling
CLINICAL FEATURES
Although the aetiology of PMS is unknown, it is clearly related to cyclical ovarian activity.
Women who have no cyclical variation in sex steroids (e.g. postmenopausal women, pregnant
or breastfeeding women, and women who have had bilateral oophorectomy) do not have
PMS.
INVESTIGATIONS
There is no test that ‘confirms’ a diagnosis of PMS. It is helpful to ask the patient to complete
a symptom diary on a daily basis over the course of several cycles in order to demonstrate that
symptoms are related to the premenstrual phase.
In a few women, it may be helpful to institute treatment with a GnRH analogue for 3 months.
This drug reliably suppresses ovarian activity. If symptoms are still present by the third month
of treatment, they are unlikely to be related to PMS.
129
PREMENSTRUAL SYNDROME
TREATMENT
General advice to minimise stress, maintain a sensible diet and have regular exercise have
been shown to have beneficial effects for women with PMS.
MANAGEMENT OPTIONS FOR SEVERE PMS

1. Pyridoxine (vitamin B6)
This is based on disordered tryptophan metabolism in sufferers from endogenous
depression. Pyridoxine corrects the reduced brain 5-hydroxytryptamine. High doses are
associated with peripheral neuropathy and a maximum of 10 mg daily is recommended.
2. Oil of evening primrose
Oil of evening primrose is widely prescribed for the treatment of PMS. It is available ‘over
the counter’ and has few adverse effects. Its main benefit appears to be in the
management of cyclical mastalgia.
3. Progesterone
Progesterones are widely prescribed for the treatment of PMS. In the many placebo-
controlled studies in which they have been evaluated, they have repeatedly been shown to
be ineffective.
4. The combined oral contraceptive pill (COCP)
The COCP abolishes cyclical hormone fluctuations; however, it has been shown to have
been of limited benefit in the management of women with severe PMS. This may be due
to the effect of the progestin component as newer progestogens may be beneficial.
Preparations containing drospirenone, an antiandrogenic, antimineralocorticoid progestin
appears to be effective in the treatment of PMS.
5. Oestrogen
Oestrogen patches and implants are beneficial in the management of severe PMS. Doses
of 100 mg patches were shown to be effective. Progestin is required and the Mirena IUS
may be of benefit to minimise systemic side effects.
6. Selective serotonin uptake inhibitors (SSRIs)
SSRIs such as fluoxetine have been shown to be significantly better than placebo for the
treatment of PMS in controlled trials. As altered serotonergic function has been
demonstrated in women with PMS, there is a clear rationale for their use.
7. GnRH analogues
GnRH analogues are extremely effective in the treatment of PMS, and indeed may be useful
in making the diagnosis (see above). Unfortunately, the menopausal side effects, associated
bone loss, and expense mean these drugs are unsuitable as long-term treatment. Add-back
HRT should be given at the same time as treatment with GnRH analogues for PMS.
8. Bilateral salpingo-oophorectomy
Bilateral oophorectomy is extremely effective in the treatment of PMS. When combined
with hysterectomy, oestrogen replacement can safely be given with no increase in
symptoms. Clearly, hysterectomy and bilateral oophorectomy will rarely be indicated for
the treatment of PMS alone. However, in women undergoing hysterectomy, the presence
of significant PMS may be an indication for bilateral oophorectomy.
130
CHAPTER 7
GYNAECOLOGICAL INFECTIONS
Inflammation in the Lower Granuloma Inguinale 143

Gynaecological Tract 132 Chancroid 143
Defence Mechanisms 132 Gonorrhoea 144
Vulval Inflammation 133 Clinical Features 144
Treatment 133 Examination 144
Vaginal Discharge and Infection 134 Treatment 144
Composition 134 Sexual Partners 144
Source of Vaginal Discharge 134 Syphilis 145
Clinical Features 134 Primary Syphilis 145
Complaints of Vaginal Diagnosis of Syphilis 146
Discharge 135 Signs and Symptoms of
Examination 135 Syphilis 147
Leucorrhoea 135 Toxic Shock Syndrome 147
Vaginal Discharge 136 Physiological Variation of the
Candida Albicans 136 Cervix 148
Bacterial Vaginosis 137 Cervical Ectopy 148
Trichomonas Vaginalis 137 Pelvic Inflammatory Disease 149
Vaginitis 139 Acute PID 149
Atrophic Vaginitis 139 Bacteriology 149
Vulvovaginitis in Children 139 Differential Diagnosis 149
Foreign Bodies 139 Management 149
Other Causes of Vaginitis 139 Chronic PID 150
Genital Herpes 140 Genital Tuberculosis 151
Clinical Findings 140 Clinical Features 151
Diagnosis 140 Diagnosis 151
Treatment 140 Pathology 151
Genital Warts 141 Treatment 152
Clinical Findings 141 Human Immunodeficiency Virus 153
Differential Diagnosis 141 Transmission 153
Histology 141 Acquired Immune Deficiency
Treatment 141 Syndrome (AIDS) 153
Bacterial Infections 142 Intercurrent Infections Frequently
Chlamydia Trachomatis 142 Found in AIDS Patients 154
Tropical Sexually Transmitted Paediatric AIDS 154
Infections 143 Treatment 154
Lymphogranuloma Venereum Antiretroviral Drugs are the
(LGV) 143 Mainstay of Treatment 154
INFLAMMATION IN THE LOWER GYNAECOLOGICAL TRACT
Under normal conditions, the vulva, vagina and ectocervix are the habitat of various types of
infective agents, but they are a threat only if normal defence mechanisms are altered.
Normal vaginal flora

DEFENCE MECHANISMS
1. Vaginal acidity
Glycogen is produced by vaginal epithelium
influenced by oestrogens and is converted to
lactic acid by Doderlein’s bacillus (a type of
B. acidophilus). This maintains the vaginal pH
between 3 and 4 which inhibits most other
organisms.
2. Thick layer of vaginal squamous epithelium

This is a considerable physical barrier to Desquamated Organisms
infection. Continual desquamation of the cells mostly lactobacilli
superficial kerato-hyalin layer and glycogen (Note absence of pus cells)
production, both dependent upon ovarian
oestrogen action, combat bacteria. In children
and postmenopausal patients, the epithelium
lacks oestrogen stimulation and is thin and
easily traumatised or infected.
3. Closure of the introitus

The vaginal canal is only a potential space
kept closed by the surrounding muscles and
provides another physical barrier. This,
however, alters following sexual activity and
pregnancy.
Functional vaginal epithelium:

intermediate cells rich in glycogen
4. Glandular secretions from the cervix and Bartholin’s glands maintain an outward fluid
current helping to clear the canal of debris. In addition, cervical secretion contains
immunoglobulins, especially IgA, and there are varying numbers of polymorphs, lymphocytes
and macrophages.
132
VULVAL INFLAMMATION
Vulval inflammation is not uncommon but is usually an extension of infection from the
vagina. A mild reaction may arise because of physical and anatomical conditions in the area,
such as (a) moistness and (b) proximity of urethra and anus.
The area is not only naturally moist but also warm, particularly in obese patients. The folds of
fat harbour moisture, and chafing occurs between them. The proliferation of bacteria is
encouraged. Urinary incontinence and unsuspected glycosuria may add to this. It is important
to test the urine for sugar in all patients.
Incidental factors may intensify any reaction resulting from these conditions, for example, the
wearing of nylon underwear which is heat-retaining and non-absorptive. Chemical factors
such as washing underclothes with detergents, and using toilet powders, perfumes and
deodorants, which intensify the reaction, may be associated with this. The clinical result is
irritation and itching leading to scratching. Continual itch-scratch-itch leads to maceration of
the skin and may invite infection. Careful attention to personal hygiene is essential. Obese
patients should be encouraged to lose weight and all the incidental factors mentioned above
should be avoided.
Search for lice or scabies should be made where appropriate.
One of the complications of
vulvar inflammation is
obstruction of the duct of
Bartholin’s gland. Cystic
dilatation and abscess
formation are apt to follow. Bulb of
The condition occurs during a vestibule
woman’s sexual life. Any
organism, staphylococcal,
coliform or gonococcal, may be + infection
found.
The gland lies partly behind the Bartholin’s
bulb of the vestibule and is covered Orifice gland
by skin and the bulbospongiosus
muscle. The duct is 2 cm long
and opens into the vaginal
orifice lateral to the hymen.
TREATMENT
Marsupialisation (Gk. marsipos, a bag). The cyst or abscess is
widely opened within the labium minus and drained, and its
walls sutured to the skin leaving a large orifice, which it is hoped
will form a new duct orifice and allow conservation of the gland.
A ribbon-gauze pack is inserted for 48 h by some surgeons.
133
VAGINAL DISCHARGE AND INFECTION
A small amount of vaginal discharge is normal in adult life and may be excessive in the
presence of cervical ectopy. Cervical ectopy is where the glandular epithelium from the
endocervix is visible on the ectocervix.
COMPOSITION
The vaginal discharge is composed of tissue fluid, cell debris, carbohydrate, lactobacilli and
lactic acid. The pH is about 4.5, a degree of acidity that inhibits the growth of organisms other
than the lactobacilli.
SOURCE OF VAGINAL DISCHARGE

Vulva: Greater vestibular glands, glands of vulval skin.
Uterus
Vagina: Mainly desquamated epithelial cells which
liberate glycogen. The lactobacilli metabolise the +
glycogen to lactic acid. Vaginal transudate (secretion
from tissues and capillaries of the mature vagina) Cervix
is often described; vaginal epithelium is certainly +
not water resistant (like transitional epithelium).
There are no mucosal glands. Vagina
Cervix: Alkaline mucous secretion which becomes
+
copious and watery during ovulation.
Uterine glands also discharge into the vagina. Greater
vestibular
glands
CLINICAL FEATURES
Volume: The need to wear a pad or tampon continuously suggests excessive discharge.
Onset: Onset can be associated with the end of a pregnancy, the contraceptive pill, a course of
antibiotic.
Colour: Normal discharge is white but stains yellow or pale brown on clothing or pads.
A greenish-yellow colour suggests pyogenic infection, commonly accompanied by an
unpleasant odour. Red or dark brown suggests blood.
Irritation: Any discharge can in time excoriate the vulva, but often Candida and Trichomonas
cause itching.
134
COMPLAINTS OF VAGINAL DISCHARGE
Women will complain under the following conditions.

(a) There appears to be an excessive amount of staining on the clothing.
(b) They detect an offensive smell.
(c) They suffer local irritation.
There is often little correlation between symptoms and signs. Some women will complain of
what is really normal; and gynaecologists regularly observe heavy and purulent discharge in
women who deny any symptoms at all.
EXAMINATION
1. Vulva, perineum and thighs are inspected for signs of excoriation. The vestibular glands
and urethral meatus are observed and palpated.
2. Vaginal walls and cervix are examined through a speculum. Normal vaginal epithelium
is pink, the rugae are well marked and the epithelial surface of the cervix smooth and
moist. Normal discharge is white and odourless.
3. A bimanual examination should always be made.
4. Specimens of discharge are taken for microscopy and culture. Chlamydia must be
excluded. Cervical rather than vaginal swabs should be taken and a separate swab and
appropriate medium are essential for Chlamydia. A urine sample can also be taken for
Chlamydia DNA analysis.
LEUCORRHOEA
This means an excessive amount of normal discharge – a very subjective assessment. The
patient will complain of constantly having to change her clothes but there will be no irritation
and appearance will be normal. The smell will be the normal vulval odour (from the action of
commensal bacteria on the secretions of the apocrine sex glands); microscopy will reveal
normal appearances and culture will grow only lactobacilli.
The patient should be reassured and given an explanation of normal physiology. No local
treatment is necessary.
135
VAGINAL DISCHARGE
CANDIDA ALBICANS
This is yeast and exists in two forms – slender
branching hyphae or as a small globular spore which
multiplies by budding.
Source of Infection
This organism may exist as a normal commensal in
the rectum and small numbers may be found in the
vagina. Sexual transmission is also possible.
Symptomatic infection is most likely to arise when Mycelia and spores of C. albicans.
there are predisposing conditions, examples of which Note the presence of leucocytes.
are given below:
1. Pregnancy. The vagina provides a tropical
microclimate and the high concentration of sex
steroids in the blood maintains an increased glycogen formation in the vaginal epithelium
and may alter the local pH.
2. Immunosuppressive therapy. This includes cytotoxic drugs and corticosteroids. There is also
thought to be a natural degree of immunosuppression during pregnancy.
3. Glycosuria. This may be due to undiscovered diabetes, but again a mild degree of
glycosuria may exist in a normal pregnancy because of the lowering of the renal threshold
for sugar.
4. Antibiotic therapy. Systemic antibiotics destroy the normal bacteria, thus reducing the
competition for nutrients, leaving the field clear for C. albicans.
Clinical Features
The patient is usually between 20 and 40, when oestrogen support of the epithelial glycogen
content is at its highest. The complaint is of irritant discharge and dyspareunia. Examination
reveals an inflamed and tender vagina and vulva with white
plaques resembling curdled milk adhering to the vaginal wall
and vulva. Removal of the plaque reveals a red inflamed
area. Pre-pubertal or postmenopausal infection is less
common.
Treatment
A single 500 mg clotrimazole pessary, with external
Plaque
application of 1% clotrimazole cream, offers convenient
therapy. Routine treatment of partners is unlikely to reduce
recurrence rates. In persistent or recurrent infection, Small
confirmation of the diagnosis by culture and determination early
of sensitivity to treatment are important. plaque
Oral antifungal medication can also be used.
136
VAGINAL DISCHARGE
BACTERIAL VAGINOSIS
For a long time, a large number of cases of vaginitis were labelled non-specific because of
disagreement regarding the infective agent. These cases were characterised by a non-irritating,
foul-smelling discharge. The discharge contains a mixture of bacteria.
Clinical Features
The patient complains of a foul-smelling discharge, and examination confirms both the
discharge and the odour. In appearance, the discharge is thin, greyish and sometimes shows
bubbles. A vaginal smear reveals the presence of ‘clue’ cells. Gram staining is usually negative
but can be variable.
‘Clue’ Pus cells tend to be few in number. Lactobacilli are

cell Vaginal squame also scanty but frequently many other bacteria are
showing present. The pH of the fluid is raised. Although the
stippling of
main complaint is of malodorous discharge, some
cytoplasm due
patients will have pruritus, frequency, dysuria and
to adherent
cocco-bacilli dyspareunia.
Treatment
Oral metronidazole appears to be effective. Clindamycin vaginal cream may also be employed.
Male partners should also be treated.
TRICHOMONAS VAGINALIS
T. vaginalis is a protozoan organism, which infests the vagina
in women and the urethra, prepuce and prostate in men. It is a
common cause of irritant vaginal discharge.
T. vaginalis is a single-cell organism about 20m 10m, with four
flagellae and an undulating membrane which gives it a
characteristic jerky movement. It is transmitted mainly during
sexual intercourse.
137
VAGINAL DISCHARGE
TRICHOMONAS VAGINALIS—(cont’d)
Clinical Features
In the acute phase, the patient complains of severe vaginal tenderness and pain, and an irritant
discharge. The vagina is seen to be inflamed, sometimes with a patchy strawberry vaginitis,
and there is a copious, offensive, frothy discharge. Frequently there is a burning sensation,
pruritus, dysuria and dyspareunia. In the latent or dormant phases, there are no symptoms
although the presence of the organism can be demonstrated, often in a cervical smear.
Incidence
T. vaginalis affects perhaps 18% of the female population. It is commonly found in patients
with gonorrhoea and is associated with cervical dysplasia. No cause-and-effect relationship has
been proved.
Diagnosis
Diagnosis is by observation of the motile organisms in a fresh smear diluted with saline and by
laboratory culture.
Treatment
Always systemic and, if possible, including the patient’s sexual partner. Metronidazole
(Flagyl) 400 mg thrice daily for a week, or 2 g orally once daily.
Pathology
Passing from host to host during coitus,
T. vaginalis attaches itself to the vaginal
epithelium and multiplies rapidly, taking
glycogen away from lactobacilli, which
disappear. The vaginal pH rises to about 5.5,
allowing the increase of bacterial pathogens that
aggravate the infection and resulting discharge.
138
VAGINITIS
ATROPHIC VAGINITIS
This occurs at times when ovarian activity ceases with the onset of menopause, after surgical
removal of the ovaries or following ablation by radiotherapy or chemotherapy.
Clinical Features
Symptoms consist of irritation and vaginal dryness.
Discharge may occur if superimposed infection has
occurred. Examination of the vaginal mucosa reveals a
rash of petechial haemorrhages and there may be
ulceration. Smears show rounded epithelial cells, with
no glycogen, many polymorphs and bacteria. In
neglected cases intravaginal adhesions may develop.
Topical vaginal oestrogen quickly reverses the changes.
This is available as creams or pessaries. There is also a
silicon vaginal ring containing oestrogen for Vaginal smear of atrophic type, with
management of atrophic changes. numerous polymorphs, a mixed bacterial
content and para-basal epithelial cells.
VULVOVAGINITIS IN CHILDREN
This is a less common condition and arises only in
certain circumstances, for example, those given below.
(a) Sexual interference.
(b) Insertion of foreign bodies by a child herself.
(c) Threadworm infestation.
With reference to the above points.
(a) the changes will be those of physical damage to the tissues. Infection will depend to
some extent on whether the person guilty of the offence is a carrier of a specific agent.
(b) infection may arise from bowel commensals.
(c) the diagnosis may be made by applying Sellotape (Scotch tape) to the vulva then
pressing the tape onto a microscope slide for microscopic examination.
Many of the cases of vulvovaginitis may arise from the irritation caused by threadworms. Scratching
will lead to maceration of the skin, which in turn will encourage bacterial contamination.
FOREIGN BODIES
Vaginitis due to foreign bodies is sometimes seen in adults. Tampons, contraceptive devices
and supportive pessaries used for prolapse may be left, forgotten, in situ. These give rise to an
offensive purulent discharge. Bacteriological investigation will give an indication of the type of
infection and appropriate treatment following removal of the offending body.
OTHER CAUSES OF VAGINITIS

Secondary vaginitis may arise because of contamination of the vagina through fistulous openings
(vesicovaginal or rectovaginal) following injury, surgical operations or tumour growth. Repeated
attacks of infection may occur. Treatment is obviously repair of the fistula where this is possible.
In all cases of vaginal discharge, the possibility of malignant disease in the tract must be
considered. 139
GENITAL HERPES
Herpes simplex virus (HSV) types 1 and 2 may affect the lower genital tract or the mouth.
It is highly infectious – 80% of women in contact with male carriers become infected.
The initial attack may be severe. There may be, in 50% of victims, less severe recurring attacks
every 3 or 4 weeks and they represent a potential for wide dissemination to others in the
immediate environment. The incubation period is short – 3–7 days.
CLINICAL FINDINGS
The disease affects the vulvovaginal and peri-anal regions but may be transmitted to the
mouth. The patient complains of burning, itching and hyperaesthesia of the area and the skin
shows evidence of acute inflammation – oedema and erythema. There is usually a vaginal
discharge. If the peri-urethral area is involved, there may be dysuria and retention of urine.
The specific lesions start as small indurated tender papules which become vesicles and quickly
break down to form shallow ulcers, 5 mm or more in diameter, with a yellowish grey slough in
the base. These can be seen on the vulva and labia, but in some cases they are confined to the
vagina and cervix and there may be no external evidence of the disease. In these circumstances
the ulcers may be large and could be mistaken for carcinoma of the cervix. The inguinal nodes
are enlarged. The infection is accompanied by general symptoms of malaise, headache and
even encephalitis. Sacral ganglion involvement causes neuralgia.
The acute phase lasts for 4–5 days. The lesions heal over 8–10 days and then a latent period
ensues during which the virus remains in the sacral ganglia. Further attacks may follow.
Infection of the neonate can lead to herpes encephalitis with a primary infection.
DIAGNOSIS
Clinical suspicion is confirmed by tissue culture isolation of virus or detection of virus antigen by
immunofluorescence or ELISA techniques. Some degree of immunity may be conferred during
recurrent attacks and a search for antibodies will help to differentiate primary from second attacks.
TREATMENT
Ice packs, local analgesia (2% lidocaine), non-steroidal
analgesic creams, saline bathing and systemic analgesics help
relieve acute local symptoms. Aciclovir 3% ointment, applied
repeatedly, is effective only if commenced at the onset of signs
and symptoms.
Oral antiviral agents such as aciclovir for 5 days may be
commenced within 5 days of onset of a first episode.
Antibiotics may be required if there is secondary infection.
Antiviral agents do not eradicate the virus and recurrent
episodes may occur.
Chromatin at nuclear membrane
Eosinophilic inclusion bodies

140
GENITAL WARTS
Genital warts are a common viral infection. They are caused by human papilloma viruses
(HPVs) which are transmitted sexually, with more that 50% of contacts developing lesions.
Numbers 6 and 11 are particularly associated with warts or condylomata. Infectivity is greatest
just after appearance of a wart. Incubation varies from a few weeks to 9 months or more.
CLINICAL FINDINGS
A single warty growth quickly spreads to form multiple growths showing a tendency to fuse.
They are pinkish with dry surfaces unless macerated and are of softer consistency than the
ordinary skin wart. The growths develop in moist areas and especially during pregnancy. They
affect the labia, peri-anal area, perineum and the lower part of the vagina, and may even
spread to the thighs. Secondary infection may give rise to purulent discharge.
DIFFERENTIAL DIAGNOSIS
1. Syphilitic condylomata. These are more
widespread and not confined to the genital
area. They are also flatter and more rounded.
Treponemes can be found in the tissue fluid.
Serological tests will of course confirm the
diagnosis.
2. Benign papilloma. This is commonly single
and similar to ordinary skin warts.
3. Verrucous carcinoma. This is a locally
malignant lesion, but vulval carcinoma is rare
in premenopausal patients. Biopsy will
differentiate the two conditions.
4. Sometimes, genital warts affect the cervix and
can resemble carcinoma.
HISTOLOGY
The warts have a central core of connective tissue covered by a thick layer of prickle cells.
Chronic inflammatory changes are present in the dermis.
TREATMENT
Podophyllotoxin, a cytotoxic agent, can be used. It is topically painted on the lesions. It is
toxic if used systemically and may not be used in pregnancy.
Imiquimod cream is an alternative. It works by stimulating the immune response but is also
unsuitable during pregnancy.
Cryo-cautery, electro-cautery and laser ablation can be employed. Lesions may recur and may
also regress spontaneously.
141
BACTERIAL INFECTIONS
CHLAMYDIA TRACHOMATIS
This is a widespread gynaecological infection.
Clinical Features
The initial symptoms in women are often mild and may in fact be asymptomatic. Discharge
may be present, varying from watery to frankly purulent according to the severity of the
reaction to the disease. In severe cases, there is obvious cervicitis which looks like an infected
erosion. Sometimes, there is a punctate haemorrhagic inflammation with microabscesses.
Occasionally, there are few changes in the vagina and the first evidence of infection is the
appearance of a salpingitis. It is an important cause of chronic pelvic inflammation.
A gelatinous exudate is formed in the Pouch of Douglas which proceeds to multiple adhesions
and tubal occlusion.
It is an important cause of infertility. Ophthalmia neonatorum
occurs if there is transmission to the neonate during delivery.
Reiter’s syndrome with urethritis, arthritis and conjunctivitis is
more common in the infected male.
It may spread to cause perihepatitis with so-called violin string
adhesions to the parietal peritoneum. This is accompanied by
acute pain in the upper right quadrant and is known as Fitz–
Hugh–Curtis syndrome. It can be mistaken for cholecystitis or Chlamydia
pancreatitis.
Diagnosis
Culture of Chlamydia requires sampling of endocervical cells, urethral cells or endosalpinx
cells (salpingitis detected at surgery). They should be sent in special transport medium to
an appropriate laboratory.
Nucleic acid amplification techniques are now commonly used to diagnose chlamydia from a
vulval swab or a first-void urine sample, with 30% greater sensitivity than viral culture.
The organism can be seen under the microscope. It is intracellular. Staining by an
immunofluorescence technique confirms the diagnosis. It multiplies like bacteria, but like
viruses can only do so within cells. It contains both DNA and RNA.
Treatment
Azithromycin 1 g as a single dose or doxycycline 100 mg orally, twice a day for 7 days.
Azithromycin and doxycycline are equally effective. The primary advantage of azithromycin is
that it is administered in a single dose. Erythromycin should be given in pregnancy.
142
TROPICAL SEXUALLY TRANSMITTED INFECTIONS
LYMPHOGRANULOMA VENEREUM (LGV)

LGV is attributed to a strain of Chlamydia. This is rare in the developed countries.
Clinical Findings
The primary lesion is a small painless ulcer with raised
irregular borders which may involve the labia, clitoris
or urethra. It appears 1–3 weeks after infection. Several
weeks later the inguinal and iliac lymph nodes enlarge,
become soft and fluctuant and this is followed by
rupture creating discharging sinuses. The lesions
eventually heal with the creation of large fibrous scars.
In the process, the urethra may be virtually destroyed
and the rectum stenosed. The pelvic organs may be
involved in the same way giving rise to intestinal
obstruction and various fistulous communications.
Histologically, the reaction is of granulomatous type.
Lymph channels are often obstructed giving rise to
elephantiasis of the vulva. The picture shows an
advanced case of LGV.
Treatment: Tetracyclines, doxycyline or
erythromycin is effective.
GRANULOMA INGUINALE
Granuloma inguinale is another tropical ulcerative condition, caused by Klebsiella
granulomatis; this begins as a painless genital, inguinal or peri-anal nodule, which ulcerates.
Local lymphatic glands enlarge, but do not ulcerate.
Prolonged antibiotic treatment is required.
CHANCROID
This lesion is due to infection by Haemophilus ducreyii.
After a short incubation period, a red macule appears,
which quickly changes to a pustule and then an ulcer. The
ulcers are numerous and vary in size from millimetres to
several centimetres. They are well defined with projecting
margins but shallow with a greenish slough in the base.
These ulcers are soft and painful. This, together with the
short incubation period, helps to differentiate them from
syphilitic lesions. The labia major, clitoris and peri-anal
regions are affected. Two weeks later the local lymph
nodes tend to enlarge and suppurate. There is usually
secondary infection and the discharge is foul smelling.
Chancroid
Treatment
Azithromycin, ceftriaxone or erythromycin may be used.
143
GONORRHOEA
Gonorrhoea in women carries a high risk of salpingitis and sterility, but early diagnosis is
difficult to achieve. Symptoms are often mild or absent.
CLINICAL FEATURES
The classical history is of urethritis, vaginal
discharge and menstrual upset of sudden onset, but
any infection in the genital area, however it
presents, may be gonococcal. After the acute phase,
vaginal discharge will persist, followed in
approximately 15% of cases by signs of pelvic
inflammatory disease (PID).
Systemic signs – conjunctivitis, dermatitis,
arthritis – are rare in women.
EXAMINATION
The labia are held apart, and the urethra, Skene’s
ducts and Bartholin’s ducts examined for signs of
infection. Swabs are taken from the cervix which is
the main reservoir of infection.
Diagnosis is a laboratory procedure. Intracellular diplococci may be seen with Gram staining,
or the more time consuming immunofluorescent method. Alternative tests include nucleic
amplification tests (NAATs) and nucleic acid hybridisation tests. NAATs are more sensitive
than culture and can also be used as diagnostic/screening tests on non-invasively collected
specimens (urine and self-taken vaginal swabs). Caution is required in interpretation of
positive results as the specificity of NAATs is not 100%. Confirmation of a NAAT positive
result by culture is advisable. This is also useful to assess for antibiotic sensitivities.
TREATMENT
Uncomplicated anogenital infection in adults:
ceftriaxone 250 mg IM as a single dose or cefixime
400 mg oral as a single dose. Antimicrobial therapy
should take account of local patterns of
antimicrobial sensitivity to Neisseria gonorrhoeae.
The chosen regimen should eliminate infection in
at least 95% of those presenting in the local
community. Alternative regimens may be required
when an infection is known to be unresponsive to
these antimicrobials.
SEXUAL PARTNERS
Partner notification should be pursued in all
patients identified with gonococcal infection,
preferably by a trained health adviser in genito-
urinary medicine.
144
SYPHILIS
Syphilis is an uncommon disease in gynaecological practice, but any genital sore should come
under suspicion. It is less uncommon in association with human immunodeficiency virus.
Pregnant women continue to be screened for syphilis in the UK despite its very low levels, as
transmission can occur to the fetus.
PRIMARY SYPHILIS
The chancre (a corruption of ‘cancer’)
has an incubation period of about a
month and its appearance is often
accompanied by pyrexia and malaise.
The most common site is the vulva and
then the cervix, but infection can occur
anywhere. The chancre is the point at
which the treponema enters the body.
The typical chancre is about 1 cm in
diameter and begins as a reddish papule
which becomes ulcerated. It is painless
and highly infective. The inguinal glands
are markedly enlarged.
Primary ulcer
Diagnosis requires the identification of

Treponema pallidum in the exudate of
the chancre or in material aspirated
from an enlarged gland. Treponemata
are not easily recognisable in stained
preparations and the dark-ground
illumination of fresh specimens is used.
Light is reflected off the edges of the
organisms, making them easy to
perceive and they are recognised by
their shape and movement. T. pallidum
must be distinguished from other
treponemata.
145
SYPHILIS
DIAGNOSIS OF SYPHILIS
Positive identification of T. pallidum is difficult for various reasons including the failure, so far,
to grow the organism in vitro. The usual method of diagnosis is by serological tests, which
become positive 4–6 weeks after infection.
Enzyme immunoassay (EIA) tests which detect antitreponemal IgM and IgG antibodies are
useful as screening tests. Confirmation is required in the context of a positive EIA.
These include TPHA (Treponema pallidum haemagglutination) and fluorescent treponemal
antibody absorption. False positives can occur.
Fluorescent Treponemal Antibody
Principle of Fluorescent Treponemal Antibody tests (FTA)
AHG F
1. Antihuman globulin
(AHG) is combined
with fluorescein.
} +
2. Dead treponeme is
Trep. Glob. antibody
combined with test
serum. If subject is
infected, the treponeme +
acquires a coating of
globulin antibody.
3. 1 and 2 are combined

and the treponeme
becomes fluorescent. }
146
SYPHILIS
SIGNS AND SYMPTOMS OF SYPHILIS

Signs and symptoms of the spread of T. pallidum throughout the whole body appear usually
about 2 months after the primary stage, and the disease may present in this phase to the
gynaecologist.
There is likely to be a mild pyrexia and malaise,
but the dominating signs are a generalised
lymphadenopathy and mucocutaneous lesions.
‘Snail track’ ulcers appear on mucosal surfaces,
and the skin develops a very wide variety of
macular and papular rashes. In warm moist areas
such as the breast flexures and the vulva, the
papules become hypertrophic and flattened and
present as ‘condylomata lata’, which are highly
infective.
Diagnosis is by the demonstration of T. pallidum in
the lesions and by serological tests.
Treatment of Early Contagious Syphilis
T. pallidum is sensitive to many antibiotics, but Condylomata
reactions are common and care is required in lata
treatment. Prolonged antibiotic treatment,
mainly penicillin based, is required and long-term
follow-up should be performed by an infectious
disease specialist.
If not treated in the early stages, syphilis leads to a complex immune reaction and the patient
can develop cardiovascular and neurological complications many months or years later.
TOXIC SHOCK SYNDROME

This is a very rare syndrome which can arise in women using tampons. It is caused by
exotoxins produced by staphylococci which may be carried by the woman herself in various
sites such as the vagina, cervix, perineum or nasopharynx.
Clinical Signs
There is a rapid onset of fever often with vomiting, diarrhoea, muscular aches and skin
erythema. It can be a life-threatening condition.
Treatment should provide general supportive measures and antibiotic treatment, usually
clindamycin.
147
PHYSIOLOGICAL VARIATION OF THE CERVIX
CERVICAL ECTOPY
Columnar epithelium appears on the cervical surface. This is usually because of physiological
changes, for example, eversion which occurs as the cervix develops during puberty and the
squamocolumnar junction becomes visible. This is physiological and no treatment is required.
It is also common in pregnancy and while on the contraceptive pill.
Abraded area Squamous

Columnar epithelium (seen epithelium
covering part of occasionally) (normal)
vaginal surface
of cervix
External
os
Columnar
Simple ectopy epithelium
in canal
Women who have symptoms relating to an ectopy may opt for local treatment with the aim of
ablating the columnar cells so that squamous cells develop. A number of techniques have been
employed. The patient will experience a prolonged heavy discharge and the ectopy may recur.
148
PELVIC INFLAMMATORY DISEASE
Infection of the fallopian tubes usually involves the ovaries and peritoneum, and the combined
infection is called pelvic inflammatory disease (PID). It results from ascending infection by
micro-organisms from the vagina or cervix. Its incidence is closely related to that of sexually
transmitted diseases and it is predominantly a disease of young, sexually active, women.
ACUTE PID
The following clinical features are suggestive of a diagnosis of PID: bilateral lower abdominal
tenderness (sometimes radiating to the legs); abnormal vaginal or cervical discharge; fever
(greater than 38 C); abnormal vaginal bleeding (intermenstrual, postcoital or ‘breakthrough’);
deep dyspareunia; cervical motion tenderness on bimanual vaginal examination and adnexal
tenderness on bimanual vaginal examination (with or without a palpable mass).
BACTERIOLOGY
N. gonorrhoea and C. trachomatis are said to be the commonest pathogens, but anaerobic
organisms are often found in pelvic abscesses.
Appendicitis
Signs are mainly right sided, and the menstrual cycle is undisturbed.
Diverticulitis
This is a disease mainly of older women and signs are left sided.
Torsion of Pedicle of a Cyst
There may be a history of intermittent pain over several months. A cyst should be palpable.
Tubal Pregnancy
A positive HCG pregnancy test should suggest ectopic pregnancy.
MANAGEMENT
In the Outpatient Setting
An intrauterine device, if in the uterus, should be removed. After swabs have been taken from
the vagina and cervix, a broad spectrum antibiotic such as doxycycline, azithromycin or
ampicillin should be given. This should be on the basis of one of the following regimens
recommended by the Royal College of Obstetricians and Gynaecologists, UK (Greentop
Guideline 32, Management of Acute Pelvic Inflammatory Disease):
• Oral ofloxacin 400 mg twice daily plus oral metronidazole 400 mg twice daily for 14 days
• Intramuscular ceftriaxone 250 mg single dose followed by oral doxycycline 100 mg
twice daily plus metronidazole 400 mg twice daily for 14 days.
If acute signs and symptoms persist, an ultrasound should be carried out to search for abscess
formation. Surgical intervention to drain abscesses may be required.
Referral to a genito-urinary medicine clinic is advisable. Without tracing and treatment of
contacts, reinfection is likely. Acute PID may be relatively asymptomatic, but this does not
preclude tubal damage, infertility and ectopic pregnancy. Ectopic pregnancy follows in almost
10% of subjects compared with a background rate of 1.5%.
149
PELVIC INFLAMMATORY DISEASE
CHRONIC PID
The patient complains of pelvic pain
made worse during the periods, which
are irregular and heavy. Dyspareunia is
common. There is a 10-fold increase in
hysterectomy after PID.
Examination
Some swelling may be felt, but often
there is little to find except tenderness
in the fornices.
Pathology
All degrees of inflammation are met with, from salpingitis alone to a widespread inflammatory
reaction involving all the pelvic tissues. It is rare to recover any organism in chronic PID, other
than in the case of tuberculosis. The ascending infection first attacks the tubes which are
sealed off by oedema and adhesions. The tubes either swell up with watery exudate forming a
hydrosalpinx or pyosalpinx; or they become highly thickened and adherent to the ovary. The
ovary may also be the seat of abscess formation, and the uterus and adnexa, normally mobile,
become fixed by adhesions.
Blocked and distended tubes in PID
Treatment
The course of chronic PID is not predictable, and mild degrees may resolve spontaneously.
Where possible, any infective agents should be identified and treated. Hydrosalpinx and any
abscess formation must be relieved by laparotomy and drainage. In advanced cases however,
the only effective treatment is operation to remove the uterus and tubes and perhaps the
ovaries as well.
150
GENITAL TUBERCULOSIS
Tuberculosis is a rare disease in gynaecology. It attacks the fallopian tubes and the
endometrium. Lesions elsewhere in the genital tract are uncommon.
CLINICAL FEATURES PATHOLOGY

The patient is usually a young This infection is blood borne, usually from a primary
woman seeking treatment for focus in the lung or kidney, and it infects the tubes,
primary infertility or complaining spreading thence to the endometrium.
of irregular menstruation or
perhaps abdominal pain.
DIAGNOSIS
1. Histological evidence
from curettings. This is
the commonest method
and it is assumed that
the tubes are also
infected.
2. Laboratory culture.
3. Biopsy from any suspicious
ulcerated area in the
vagina or vulva.
4. By laparoscopic inspection
and biopsy.
The tubes may appear normal (endosalpingitis) but
usually display the distortion and swelling of
chronic infection, and small pinhead tubercles
appear on the serosa.
Once evidence of genital

infection is obtained, the Giant
respiratory and urinary tracts cells
must also be investigated.
The endometrium also shows tuberculous follicles,

best developed in the premenstrual phase. There
may be debris in endometrial glands.
151
GENITAL TUBERCULOSIS
TREATMENT
Antituberculous Chemotherapy
A combination of rifampicin, isoniazid and ethambutol has been used effectively in recent
years. This should be managed by an infectious disease specialist.
Surgery
Surgery may be required when chemotherapy has failed (about 5% of cases) or in combination
with chemotherapy in older women. All infected tissue must be removed to avoid subsequent
fistulous openings in the bowel or bladder.
Tuberculosis and Infertility
Failure to conceive is probably the most important consequence of genital tuberculosis, and
90% of women presenting with the disease will never have a pregnancy. There is also an
increased chance of ectopic gestation.
152
HUMAN IMMUNODEFICIENCY VIRUS
TRANSMISSION
The following are the main modes of transmission of human immunodeficiency virus (HIV):
• Unprotected penetrative sex with someone who is infected.

• Injection or transfusion of contaminated blood or blood products, donations of semen
(artificial insemination), skin grafts or organ transplants taken from someone who is
infected.
• From a mother who is infected to her baby; this can occur during pregnancy, at birth
and through breastfeeding.
• Sharing unsterilised injection equipment that has previously been used by someone
who is infected.
The course of the disease is erratic, associated with progressive loss of immune resistance.
Death is almost inevitable but may be delayed for years with appropriate antiviral treatment.
ACQUIRED IMMUNE DEFICIENCY SYNDROME (AIDS)

The progress of the disease can be roughly divided into six phases, but these phases are
ill-defined, and variable in time of onset and duration:
1. Infection
2. Window period
3. Seroconversion
4. Asymptomatic period
5. HIV/AIDS-related illness
6. AIDS.
The duration of the different phases of HIV/AIDS is variable. It is not possible to predict the
course of the disease in an individual. Factors affecting the course of HIV/AIDS include
nutrition, emotional stress and access to health care. People infected with HIV can infect
others at any phase of the disease.
Three conditions are particularly characteristic of the immunodeficiency state:
1. Kaposi sarcoma, usually an indolent growth in the skin, becomes aggressive.
2. Hairy leukoplakia of the tongue.
3. Lymphomas are common in AIDS patients and lymphoma of the brain is almost
diagnostic.
153
HUMAN IMMUNODEFICIENCY VIRUS
INTERCURRENT INFECTIONS FREQUENTLY FOUND IN AIDS PATIENTS

Minor infections and infestations, which remain localised in normally immune persons and
produce mild symptoms if any, spread rapidly and cause life-threatening clinical conditions in
the AIDS patient whose immunity is seriously compromised.
Infective agents Clinical results

Parasites
Pneumocystis carinii Pneumonia
Cryptosporidium Severe diarrhoea
Strongyloides stercoralis Severe diarrhoea
Toxoplasma gondii Chorio-retinitis
Viruses
Herpes Pneumonia
J.C. virus Leuco-encephalopathy
Bacteria
Species usually causing minor lesions, e.g. skin spots Septicaemia
Fungi
Cryptococcus neoformans Pneumonia, meningitis
PAEDIATRIC AIDS
Infection of the fetus
or newborn from the Infected Baby at
mother can occur in mother delivery
utero, intrapartum or,
through breastfeeding,
post-partum.
Zidovudine has been
shown to reduce
vertical transmission Fetus
of HIV-1. Placenta
Direct Infection due to mixing
transplacental Uterus of maternal and fetal
TREATMENT spread
Specialised knowledge bloods at delivery
and experience are
essential.
ANTIRETROVIRAL DRUGS ARE THE MAINSTAY OF TREATMENT

Combination therapy is used and for many patients can significantly control the disease
within developing countries access to antiretroviral therapy may be limited. There is ongoing
research to develop a vaccine.
154
CHAPTER 8
DISEASES OF THE VULVA
Vulval Dermatoses 156

Classification 156
Lichen Sclerosus 157
Benign Tumours of the Vulva 158
Vulval Intraepithelial Neoplasia 159
Vulval Intraepithelial Neoplasia (VIN) 159
Paget’s Disease of the Vulva (Adenocarcinoma
In Situ) 159
Carcinoma of the Vulva 160
Aetiology 160
Histology 160
Lymphatic Spread 161
Surgical Treatment 162
Complications 164
Radiotherapy and Chemotherapy 164
Prognosis of Vulval Carcinoma 164
Diseases of the Urethra 165
Prolapse of the Urethral Mucosa 165
Caruncle 165
Urethrocele 165
VULVAL DERMATOSES
Vulval dermatoses is the term applied to non-infective

non-neoplastic diseases of the vulval skin. Their
management has evolved into a multidisciplinary
approach involving specialist nursing staff,
dermatologists and gynaecologists. Specialist clinics
may have direct referrals, but the symptoms of itching,
soreness and dyspareunia will usually take the patient
in the first place to the gynaecologist.
Normal vulva
CLASSIFICATION
The following classification is recommended by the International Society for the Study of
Vulvar Disease (ISSVD – 2004).
Non-neoplastic disorders of the vulva
lichen sclerosus
lichen planus
other dermatoses
Vulval intraepithelial neoplasia (VIN)
VIN, usual type
(i) warty
(ii) basaloid
(iii) mixed
VIN, differentiated type
Paget’s disease
156
VULVAL DERMATOSES
LICHEN SCLEROSUS
Lichen sclerosus is a common condition
found in postmenopausal women complaining
of vulval itch. Premenopausal women may
also be affected, as well as men and children.
The aetiology is unknown, but it appears to be
associated with autoimmune disorders.
It is most commonly seen in the vulvo-
perineal skin of women, but can affect skin in
any region of the body. Lichenification
Appearance
The disease starts as a flat pinkish-white macula.
As it progresses, there is atrophy of the labia as
well as clitoral recession with loss of normal
architecture. With further Some Thin atrophic
deterioration, labial fusion and hyperkeratosis epithelium
perineal fissuring occur. Scratching
may induce lichenification
(thickening).
Histology
There is atrophic thinning of the
epidermis with some hyalinisation
of the dermis. The keratinised
layer is thickened, giving a
whitened appearance
(‘leukoplakia’). Hyalinisation of dermis
Differential Diagnosis of Vulval Itch

Lichen planus, lichen simplex, candidiasis, VIN, psoriasis.
Management
Ultrapotent steroid such as clobetasol propionate (suggested regimen)
Apply once daily 4 weeks.
Apply alternate days for 4 weeks.
Apply twice weekly for 4 weeks.
NB maintenance/interval treatment with clobetasol at previous minimal effective frequency.
Soap substitute
There is an extremely limited role for vulval surgery in the management of this condition,
unless there is suspected malignancy.
If asymptomatic, no treatment is required.
Malignant Associations
A recent estimate suggests that 5% of women with lichen sclerosus will develop invasive
cancer.
157
BENIGN TUMOURS OF THE VULVA
The complaint is usually of a ‘lump’ or ‘swelling’ at the vaginal introitus. (In many cases, the
patient may mistake prolapse of various types for tumour growth.)
Cyst of Bartholin’s gland This is the commonest simple
tumour of the vulva. Caused by obstruction of the
duct, the cyst often becomes infected and requires
surgical treatment (see p. 133).
Sebaceous cyst of the vulva occurs in the hair-bearing
vulval tissue. The cyst may become infected and cause
pain. The cyst contains whitish, cheesy sebaceous
material. If painful, it can be removed.
Vulval haematoma is a result of direct violence or
wounding (it is most commonly found with
childbirth). Treatment is by incision, evacuation and
drainage if the patient is symptomatic.
Lipoma, fibroma and myoma are found rarely

and can become sarcomatous. Treatment is
by excision, following appropriate imaging
assessment. Magnetic resonance imaging
(MRI) is usually the imaging modality of
choice.
Lipoma
158
VULVAL INTRAEPITHELIAL NEOPLASIA
VULVAL INTRAEPITHELIAL NEOPLASIA (VIN)

There are two main types of VIN – usual and differentiated. Usual type is associated with
oncogenic human papilloma virus (HPV), whereas differentiated type is not always associated
with HPV infection; however, both can be precursors of vulval carcinoma.
HPV infection can infect all cloacal origin epithelium causing intraepithelial neoplasia.
The site of epithelium affected dictates the term used to describe it: vaginal intraepithelial
neoplasia (VAIN); anal intraepithelial neoplasia (AIN); and peri-anal intraepithelial
neoplasia (PAIN). As such, intraepithelial neoplasia can often be a multifocal disease with
histological features similar to that of cervical intraepithelial neoplasia (CIN). The malignant
potential of VIN is thought to be less than that of CIN. However, the mechanism whereby
it causes dyspaltic change is the same and can be reviewed on page 175.
VIN may present with vulval itch, burning or pain. However, it may be detected when
abnormal skin is identified by the patient or when the patient is undergoing gynaecological
examination for other reasons.
There is no distinct appearance, with the changes often being subtle. Lesions may be macular,
papular with the abnormal area appearing mainly white but also red or pigmented in some
cases. Diagnosis can be confirmed by biopsy.
Treatment of VIN
1. Careful observation only as spontaneous resolution can occur.
2. Wide local excision to achieve a clear margin, with or without plastic surgery.
3. CO2 laser vaporisation.
Following treatment, patients should be seen regularly in the clinic as recurrent or new
intraepithelial neoplasia can occur necessitating further treatment.
PAGET’S DISEASE OF THE VULVA

(ADENOCARCINOMA IN SITU)
This malignant disease starts as an
erythematous, irritant plaque which becomes
eczematous (oedema and exudate) and spreads.
The disease is multi-focal and the true margins
are indistinct. To determine the margins,
mapping biopsies from the periphery are
required. Histology shows the characteristic
Paget’s cells – large round, clear-staining cells
with large nuclei, often mitotic.
Thirty percent patients may have an underlying
adenocarcinoma of the vulva, cervix, bladder,
ovary, rectum or breast. Wide local excision of
the lesion is the treatment of choice and plastic
surgical reconstruction may be required.
159
CARCINOMA OF THE VULVA
Vulval cancer is very rare in young women.

Incidence
1 per 100,000 women aged 25–44
3 per 100,000 in those aged 45–64
13.2 per 100,000 in women aged 65 and over (UK).
AETIOLOGY
The aetiology of squamous vulval cancer is related to the underlying
vulval skin disorder.
The differentiated type is associated with underlying conditions such
as lichen sclerosis and is not HPV related. The remaining squamous
cancers are associated with oncogenic HPV infection. The mechanism
for oncogenic HPV cancer induction can be reviewed on page 175.
HISTOLOGY CLINICAL FEATURES

Squamous carcinoma: 85% The majority of patients with vulval cancer are over 60.
Melanoma: 5% The presenting features include vulval irritation and
pruritus (70%), a vulval mass (60%) and bleeding (30%).
The diagnosis is often delayed, partly due to the patient’s reluctance to seek medical help, and
partly because of delay in performing a clinical examination once the patient presents.
Any lump on the vulva must be examined and if suspicious biopsied.
The inguinal lymph nodes may be enlarged, but absence of enlargement does not guarantee
absence of lymphatic spread.
The FIGO staging of vulvar cancer 2009
Stage Definition
Stage I Confined to vulva.
IA Tumour 2 cm or less maximum diameter. Stromal invasion no greater than 1 mm. No
nodal metastases.
IB As for IA, but stromal invasion greater than 1 mm.
Stage II Tumour of any size with extension to adjacent perineal structures (lower 1/3 urethra,
lower 1/3 vagina, anus). Negative nodes.
Stage III Tumour of any size with or without extension to adjacent perineal structures (1/3 lower
urethra, 1/3 lower vagina, anus) with positive inguino-femoral lymph nodes.
III A (i) With 1 lymph node metastasis (5 mm), or
(ii) 1–2 lymph node metastasis(es) (<5 mm).
III B (i) With 2 or more lymph node metastases (5 mm), or
(ii) 3 or more lymph node metastases (b5 mm).
III C With positive nodes with extracapsular spread.
Stage IV A Tumour invades any of the following:
(i) upper urethral and/or vaginal mucosa, bladder mucosa, rectal mucosa, or fixed to pelvic bone, or
(ii) fixed or ulcerated inguino-femoral lymph nodes.
160 Stage IV B Any distant metastasis, including pelvic lymph node.
LYMPHATIC SPREAD Superficial fascia

1. To the superficial inguinal glands (superficial layer)
which lie along the inguinal ligament (deep layer)
and the saphenous vein (vertical Lymph
group). These nodes lie between glands
the layers of the superficial fascia Inguinal
ligament
in relation to numerous
superficial vessels.
Long Fat
saphenous vein
2. Then to the deep femoral nodes

accompanying the femoral vessels,
and from there to the external iliac,
common iliac, and para-aortic glands.
3. This path is not invariably followed. The

superficial nodes are occasionally
bypassed. To detect aberrant pathways,
techniques such as sentinel lymph node
biopsy are being increasingly used. Using
patent blue dye and radioactive tracer
injection techniques, the primary
drainage lymphatic pathway can be
identified. This technique may also
reduce the risk of lymphoedema.
161
SURGICAL TREATMENT
Surgery is the optimum treatment for
vulval cancer.
The conventional operation was radical
vulvectomy with dissection of the
superficial and deep inguinal glands and
the external iliac glands. Such surgery
increased the five-year survival for the
disease.
The whole vulva,

skin and
subcutaneous
tissue are excised
down to the
periosteum.
The wound would be closed

completely if possible, undercutting
and mobilising skin if necessary. In
this picture, closure is incomplete, but
the small raw area would heal in a few
weeks. Drains are shown, which
remain in place for the first few days.
Surgery for vulval cancer has evolved
with the above illustrations providing
a context for the need to improve and
reduce morbidity.
162
Radical vulvectomy with en bloc dissection and removal of the inguinal and iliac lymph glands
is associated with significant morbidity. The following variations in technique have been
introduced to reduce morbidity.
1. Separate groin incisions

In vulval cancer, lymphatic
metastases develop initially by
embolisation. In early disease, there
is no need to remove the lymphatic
channels between the tumour and
the groin nodes. Therefore, separate
incisions can be used to remove the
tumour and the nodes on the side(s)
where lymphadenectomy is
required. Such an approach is
associated with lower morbidity
than conventional surgery.
2. Modified radical vulvectomy

If the primary tumour is small, and
confined to one area, a more limited
operation may be as effective as
radical vulvectomy. In modified
radical vulvectomy, the lesion and
surrounding area are removed,
leaving the remainder of the
perineum intact. A 1–2 cm margin
of healthy tissue should be removed
along with the tumour.
3. Ipsilateral lymphadenectomy
If the tumour is confined to one side of the vulva only, at least 1 cm from
a midline structure such as clitoris or anus, and the groin nodes appear
clinically tumour free, ipsilateral lymphadenectomy may be sufficient to detect
lymph node disease.
163
COMPLICATIONS
1. Wound breakdown and
infection.
2. Thromboembolic disease.
3. Bleeding.
4. Lymphoedema.
5. Paraesthesia over the upper
legs.
6. Impaired sexual function.
7. Psychological sequelae.
The incidence of wound
breakdown and infection is
reduced by the use of the three
incision technique. The
incidence of thromboembolic
disease may be minimised by
the use of low molecular weight
heparin and thromboembolic
disease stockings. The use of
plastic surgery to restore normal
anatomy, form and function of
the tissues is very important in
reducing morbidity and
minimising sexual and
psychological problems.
Lymphoedema can also be
treated using techniques such as
massage and limb wrapping
available with referral to
specialist clinics.
RADIOTHERAPY AND CHEMOTHERAPY

Radiotherapy is useful for treatment of positive groin node disease after inguino-femoral
lymphadenectomy. Preoperative chemoradiotherapy has been used for advanced tumours
with impressive local response. It may reduce morbidity in advanced tumours, often
facilitating surgical removal.
PROGNOSIS OF VULVAL CARCINOMA

Stage 1 93%
Stage 2 87%
Stage 3 62%
Stage 4 20–30%
Where a patient has involved groin nodes, survival is poorer.
164
DISEASES OF THE URETHRA
PROLAPSE OF THE
URETHRAL MUCOSA
This forms a swelling round
the meatus. Symptomatic
urethral mucosal prolapse
may be treated by cautery.
CARUNCLE
A small polypoid area arising from the lower end of the urethra.
It is composed of a very vascular stroma and covered with
squamous or transitional epithelium.
Clinical Features
Caruncles are red in colour because of their vascularity, and extremely sensitive. The patient is
usually an elderly woman complaining of dysuria and bleeding.
Treatment
Caruncles can be excised and sent for histological examination if suspicious or symptomatic,
although malignant change is rare. The base of the tumour on the urethral mucosa should be
cauterised.
URETHROCELE
This is a descent of the urethra from its position
under the pubic arch. It is sometimes a cause of
stress incontinence and may exist by itself or
more commonly with a cystocele.
Treatment is described in the section on prolapse.
165
CHAPTER 9
DISEASES OF THE VAGINA
Benign Vaginal Disease 168

Benign 168
Traumatic Epithelial Cysts 168
Vaginal Infections 168
Malignant and Premalignant Disease 169
Vaginal Intraepithelial Neoplasia (VAIN) 169
Carcinoma of the Vagina 170
Site and Spread 171
Treatment 171
Plastic Surgery of the Vagina 172
Additional Procedures 172
BENIGN VAGINAL DISEASE
Vaginal diseases can manifest as benign, premalignant or malignant conditions
BENIGN
Vaginal cysts are not uncommon but are rarely large. They are found in the anterior or lateral
walls of the lower third of the vagina and in the posterior wall of the upper third, are seldom
larger than a walnut, are sometimes multiple, and may be mistaken for a cystocele. These
cysts are occasionally a cause of dyspareunia but they usually cause no symptoms at all.
Treatment is by excision or marsupialisation.
TRAUMATIC EPITHELIAL CYSTS

Traumatic epithelial cysts (inclusion cysts) are found usually in the lower vagina and are
caused by an infolding of epithelium at repair operations. If they cause any symptoms, they
should be excised or marsupialised.
VAGINAL INFECTIONS
See pages relating to infection.
168
MALIGNANT AND PREMALIGNANT DISEASE
VAGINAL INTRAEPITHELIAL NEOPLASIA (VAIN)

This can be a very difficult condition to treat. It is rare, can affect any point on the vaginal wall
and may progress to an invasive malignant disease. Its aetiology is likely to be due to human
papilloma virus infection. The mature epithelium and a lack of metaplastic change may
explain its reduced incidence when compared to cervical intraepithelial neoplasia.
It is often asymptomatic but symptoms may include irregular vaginal bleeding or discharge.
Diagnosis is usually by colposcopy with directed biopsy, but it may also be detected
incidentally in histology after a hysterectomy.
Treatment will depend on the age of the patient, previous treatment (some may have had a
hysterectomy or treatment for cervical cancer), general health and desire to retain normal
sexual function. Surgical excision (partial or total vaginectomy) and laser ablation have been
employed and some authors report the use of topical 5-fluorouracil (5-FU) chemotherapy.
Due to the rarity of this condition, treatment should be undertaken by a clinician with
specialist skills in this area.
169
CARCINOMA OF THE VAGINA
Primary growths of the vagina are rare. The most common vaginal cancers are squamous
cell carcinomas, however, adenocarcinomas, melanomas and sarcomas may also be seen. 30%
of patients will have a history of CIN or of a carcinoma of the cervix.
Its aetiology is mixed, with oncogenic human papilloma virus being implicated in squamous
carcinoma development. Although rare, VAIN is being diagnosed more frequently and it
may proceed to cancer. Historically, intrauterine exposure to diethylstilboestrol (DES) has
carried a risk of causing vaginal adenocarcinomas, but more commonly, vaginal adenosis.
Metastatic deposits are also seen, especially as extensions from cervical cancer and
endometrial carcinoma.
CLINICAL FEATURES
The patient is usually postmenopausal and
asymptomatic. The most common symptoms are
bleeding (60%), discharge (15%) and pelvic pain
(10% or less). If the bladder is involved, patients
may experience pain and dysuria.
The tumour is not at first painful, and unless it
appears in a woman who is still sexually active, it
is not likely to present until it has penetrated the
vaginal wall and caused bleeding. An early
tumour can easily be missed if it is obscured by
the blade of a speculum. The whole vagina
should always be inspected, and a biopsy be taken
from any unusual lesion.
A thorough examination, including

colposcopy, cystoscopy and
proctosigmoidoscopy, may be
indicated to detect its spread. In
addition, magnetic resonance imaging
(MRI) scans can provide information
on local and regional disease.
170
CARCINOMA OF THE VAGINA
SITE AND SPREAD

The most common site of disease Upper third: approximately same
is the upper vagina. The disease drainage as the cervix.
can have a variety of appearances Middle third: any pelvic
depending on its histology, such lymphatic channel may be
as a mass lesion, plaques of involved.
abnormal tissue or ulceration.
Lower third: approximately same
drainage as the vulva.
Clinical staging Five-year survival rates (%)

Stage I Invasive. Confined to the vaginal mucosa. 75–90
Stage II Invading paravaginal tissue, but not to the 45
pelvic side wall.
Stage III Extension to the pelvic side wall. 30–40
Stage IVa Extension to mucosa of bladder or rectum. ≯20
Stage IVb Extension beyond the pelvis. ≮20
Prognosis depends on the clinical stage of the disease.
TREATMENT
Treatment will be tailored to the patient; size and stage of the disease and psychosexual
impact of the treatment will also be taken into consideration. If the disease is localised to the
vagina in a fit patient, it may be treated by radical surgery (radical hysterectomy, vaginectomy,
lymphadenectomy). More advanced disease and disease in the mid to lower third of the vagina
may be treated with radiotherapy. Some authors are also exploring the use of chemotherapy
(cisplatin and 5-FU) alongside radiotherapy.
The vaginal melanoma carries a poor prognosis, with radical excision and radiotherapy
currently being employed in its treatment.
Sarcoma botryoides is a rare tumour of young children, presenting as grape-like masses with
bleeding. Chemotherapy with vincristine, actinomycin D and cyclophosphamide gives good
results.
171
PLASTIC SURGERY OF THE VAGINA
This is required when the patient is found to have a congenital absence of the vagina, is having
the vagina removed as a part of radical cancer surgery, or distortion and contractures due to
injury or genital mutilation. Such a situation is rare, but various operations have been devised.
The small bowel has been used successfully in male to female sex change procedures.
The placement of a skin graft
1. A plastic mould is covered with skin

from the thigh. (This is done by
a plastic surgeon.)
3. The mould and the graft are inserted and

kept in place by suturing the split ends of
the labia minora. The moulds can now be
fashioned from inflatable plastic and in
varying sizes. The vaginal orifice may
need enlarging later on by the plastic
surgeon.
The mould must be kept for a prolonged
time, and once it is removed, the patient
should use vaginal trainers or have regular
sexual intercourse to prevent closure of the
neovagina.
ADDITIONAL PROCEDURES
The techniques available to the plastic
surgeon have allowed the evolution of a
2. The space between the urethra/bladder variety of procedures to create a neovagina.
and the rectum is opened up. A finger Some may raise myocutaneous flaps from
in the anus helps the surgeon to avoid the rectus abdominus muscle or the gracilis
damaging the rectum. muscle.
172
CHAPTER 10
DISEASES OF THE CERVIX
Normal Cervical Epithelium 174 Carcinoma of the Cervix 183

Anatomy of the Cervix 174 Clinical Findings 183
Benign Squamous Metaplasia 174 Symptoms 183
The Role of Human Papilloma Carcinoma of the Cervix 184
Virus in Cervical Disease 175 Squamous Cell Carcinoma 184
Risk Factors 175 Spread 185
Screening for Cervical Cancer 176 Diagnosis of Cervical Carcinoma 186
Screening Process 176 Staging of Cervical Carcinoma 187
Cervical Smears 177 Radiotherapy and Chemotherapy
Interpretation of Cervical Smears 177 in Cervical Carcinoma 189
Premalignant and Malignant Brachytherapy 189
Cervical Disease 178 External Beam Therapy 189
Dysplasia 178 Complications 189
Microinvasive Cervical Carcinoma 178 Surgery for Cervical Carcinoma 190
Risk of Progression of Microinvasive Cervical Carcinoma 190
Cervical Intraepithelial Radical Hysterectomy and Node
Neoplasia 178 Dissection 190
Colposcopy 179 Radical Surgery for Cervical
Identification of Atypical Cancer 192
Epithelium 179 Treatment of Cervical Carcinoma:
Treatment of Cervical Surgery or Radiotherapy? 193
Intraepithelial Neoplasia 180 Prognosis 193
Ablative Techniques 180
Excisional Techniques 181
NORMAL CERVICAL EPITHELIUM
ANATOMY OF Fallopian tube

THE CERVIX
The cervix
constitutes the lower
third of the uterus. Ovary
Uterus Endometrium
} Endocervix
}
Vagina
Ectocervix
Vulva
It is in two parts, the
endocervix and the
ectocervix. Before puberty, the Tall mucus secreting
dividing line between the endo- epithelium
and ectocervix is sharp, and is
determined by the character of Stratified
the lining epithelium: the squamous
ectocervix is covered epithelium
with squamous epithelium non-keratinised
and the endocervix is covered Branching
with columnar epithelium. glands
Ectocervix Endocervix
Transitional zone
BENIGN SQUAMOUS Under the influence of oestrogen (e.g. at puberty, during

METAPLASIA pregnancy or when the combined pill is taken), the cervix
Stratification well defined with: enlarges, so that the columnar epithelium of the
Squames endocervix can be seen on the ectocervix. This region,
at surface formerly the endocervix, which is now anatomically the
ectocervix, is known as the ‘transformation zone’. The
Oval polygonal
transformation zone is a dynamic area that responds to
cells for several changes in endogenous or exogenous oestrogen. As it
layers undergoes changes, it becomes a squamous metaplasia,
which is a benign condition. The transformation zone is
Basal cells usually important as it is susceptible to infection with the human
a single layer at papilloma virus (HPV), which is known to lead to
right angles to possible dysplastic change, and this in turn may lead to
the surface cervical cancer.
174
THE ROLE OF HUMAN PAPILLOMA VIRUS IN CERVICAL DISEASE
RISK FACTORS
Human Papilloma Virus (HPV) Infection
HPV infection is now known to be the viral agent required for the development of, initially,
cervical intraepithelial neoplasia (CIN), and, ultimately, a cervical carcinoma. Approximately
80% of women will be infected with at least one of the more than 100 genotypes of HPV. 70–
90% of women infected with HPV will clear the infection spontaneously within 1–3 years.
HPV is a DNA virus that can integrate into the human genome, and each genotype has a
number. The most prevalent HPV genotypes in cervical carcinoma are 16 and 18. They are
responsible for at least 70% of all cervical cancers.
The HPV genome encodes early (E) proteins that are responsible for viral regulation, cell
transformation and late (L) proteins that make the viral capsule. HPV infects the basal cells
and the expression of genes E6, E7 in high risk genotypes allows them to act as oncogenes via
a variety of mechanisms to cause unregulated cell growth that may lead to dysplasia and
cancer. Two tumour suppressor proteins that are affected by the E6/E7 gene products are p53
and retinoblastoma.
Suggested co-factors that may increase the likelihood of developing cervical cancer include:
smoking, low socioeconomic status, immunosuppression (e.g. HIV infection, organ transplant),
multiple sexual partners and combined oral contraceptive pill use for more than 10 years.
Prophylactic vaccines HPV Surgery

Chemotherapy
Radiation
Neutralising antibody
Squamous
tion
epithelium
Infec
Superficial
zone
Midzone
Basal layer
Basement
membrane
Columnar epithelium
Normal Low grade High grade Invasive
CIN 1 CIN 2/3
175
SCREENING FOR CERVICAL CANCER
Screening for cervical intraepithelial neoplasia (CIN) can be done by performing cervical
smears and offering subsequent colposcopic assessment if significant dyskaryotic change is
found. Treatment of CIN significantly reduces the incidence of and mortality associated with
cervical cancer. For these reasons, many countries, including the UK, have set up a national
screening programme.
SCREENING PROCESS
The Cervical Smear
A cervical smear is taken by a trained healthcare professional, often in their local practice. The
cervix is visualised using a speculum. A wooden spatula or small plastic broom is placed in the
cervical canal and rotated through 360 . The superficial layer of cells overlying the
squamocolumnar junction is removed. If a wooden spatula is used, it is then smeared on a
slide and fixed. If the broom is used, it is placed into a vial of liquid fixative (liquid-based
cytology – LBC). Both methods then stain the specimen using Papanicolou’s method and the
cells are examined under a microscope. The LBC technique is automated once the sample is
sent for processing and this method produces cleaner specimens for analysis, thus reducing
the number of unsatisfactory slides. If abnormal cells, dyskaryosis, are identified, the patients
are referred for colposcopy.
In Scotland, the current cervical screening programme includes the following:
– All women between 20 and 60 years are invited for a smear test every 3 years.
– Immunocompromised/immunosuppressed women are offered annual screening.
– A national electronic database records and monitors the cervical smear process from
the point of invitation to the completion of a colposcopic assessment. This is the
Scottish Cervical Call-Recall System (SCCRS).
An abnormal smear is usually an indication for colposcopy
(see p. 179).
Cervix brush and pot
176
CERVICAL SMEARS
INTERPRETATION OF CERVICAL SMEARS

Smears are reported in the
following categories:
Endocervical cell
Normal
Inflammatory changes Mature squame
Borderline nuclear change
Mild dyskaryosis
Moderate dyskaryosis
Severe dyskaryosis
Invasion suspected
Glandular abnormality Normal
The smear shows a mixture of

normal cells and dyskaryotic
(abnormal nuclei) cells.
Binucleate cells
Some variation
in size of nuclei
Polymorphs
Mild dyskaryosis Moderate dyskaryosis
The cells are almost all

abnormal and show larger
nuclei with coarse chromatin.
Severe dyskaryosis
In general, the more severe the dyskaryosis, the more likely the patient is to have high grade
CIN. However, even in women with a mildly dyskaryotic smear, the incidence of high
grade CIN can be 50%.
A referral for colposcopy is made for all women with, moderate or severe dyskaryosis. A
repeat smear is justified in women with inflammatory or borderline nuclear changes.
However, if these abnormalities persist, colposcopy is indicated. Colposcopy is also indicated
if there are three or more abnormal smear tests of any grade in a 10-year interval. 177
PREMALIGNANT AND MALIGNANT CERVICAL DISEASE
DYSPLASIA
Dysplasia occurs when the epithelium CIN 1 low grade dysplasia
shows changes such as nuclear
enlargement, increased
nucleocytoplasmic ratio and abnormal Upper two thirds stratified
mitoses. It is regarded as the first step squames i.e. normal
in a series of changes that may lead to
cervical intraepithelial neoplasia (CIN)
and subsequently to invasive Cells of basal third have
carcinoma. The pathological features high nucleocytoplasmic
of mild, moderate and severe dysplasia ratio; pleomorphic nuclei in
are shown. In practice there can be layers at this level.
inter- and intra-observer variation
between these categories.
CIN 2 high grade dysplasia CIN 3 high grade dysplasia
Upper half of epithelium (1) There may be one

shows stratification or two layers of stratified
and maturation epithelium on surface.
(2) Remainder is immature

with large nuclei.
Abnormal basal cells
occupy lower half (3) Abnormal mitoses are
common.
MICROINVASIVE CERVICAL
CARCINOMA
The histological appearance of an early cervical
invasion with spread through the basement
membrane is shown here.
RISK OF PROGRESSION OF CERVICAL INTRAEPITHELIAL NEOPLASIA

CIN has the potential to develop into a malignant cervical disease but it may also regress or
persist as CIN without undergoing any malignant change. The risk of developing cervical
cancer following dysplasia is 10–20%. The risk is also influenced by the grade of CIN,
oncogenic potential of the HPV type, and environmental factors such as smoking and the
178 immune status of a patient.
COLPOSCOPY
Colposcopy means binocular inspection of the cervix with magnification.
The transformation zone

lies between the cervical canal
and the squamocolumnar junction.
The colposcopist recognises two kinds of epithelium, the

‘native’ epithelium which may be squamous or columnar;
and the metaplastic squamous epithelium which arises in the
physiological transformation zone.
IDENTIFICATION OF ATYPICAL
EPITHELIUM
Following the insertion of a speculum, the cervix is
swabbed with 3% or 5% acetic acid. This
dehydrates cells and the abnormal areas with larger
and denser nuclei reflect light, appearing white. Mosaicism
The vascular pattern within the white area can also
be examined. Any changes are described with
terms such as mosaicism and punctation. Trained
Punctation
colposcopists establish areas of abnormality and
perform a small biopsy. Those patients with a high
grade smear and an abnormal colposcopic
appearance may be offered treatment at their first
visit. Other patients requiring treatment will
usually return as an outpatient.
Patients can find the whole process stressful and
this is taken into account when seeing patients in
the clinic and arranging management for the
patient.
179
TREATMENT OF CERVICAL INTRAEPITHELIAL NEOPLASIA
There is a high rate of spontaneous regression within the first 2 years after a diagnosis of low
grade CIN (CIN1). For this reason, the majority of CIN1 cases are usually kept under review
to establish if the changes regress cytologically and colposcopically.
High grade CIN (CIN2/3) has a lower rate of regression and is associated with a malignant
transformation rate of up to 22%. Treatment is therefore offered to women with high grade
CIN. This is usually done as an outpatient, under local anaesthetic, but some women may
require admission for a general anaesthetic. The method of treatment chosen will depend on
training, availability of technique and the need to minimise morbidity.
ABLATIVE TECHNIQUES
All these techniques destroy abnormal cervical tissue. In contrast to the excisional methods,
there is no tissue for analysis after treatment and any occult invasive disease may not be
recognised. Hence it is essential to have:
Excluded invasive disease by colposcopically directed biopsy, prior to treatment.
No discrepancy between cytology/colposcopy/histology.
No evidence of microinvasion/invasion.
No evidence of a glandular lesion.
Satisfactory colposcopy.
Morbidity with these techniques is often lower compared to the excisional techniques and
there is less bleeding and no increased risk of adverse pregnancy outcomes such as preterm
delivery and preterm rupture of the membranes.
Cold Coagulation
This involves the application of a probe,
heated to 120 C, to the cervix, for between
20 and 30 s over one to five applications,
depending on the size of the area to be
treated. This simple technique can be
performed under local anaesthetic, it is Cold coagulator probes
inexpensive and it has been shown to
adequately treat CIN.
CO2 Laser
This is a precise method that vaporises tissue to a
depth of 7 mm. However, it is an expensive technique
that requires significant training and attention to
safety issues.
180
Cryosurgery
This allows destruction of affected tissue to a depth of
3–5 mm. It is a rapid treatment but it may not treat the Cervix
cervix to an adequate depth to destroy all CIN. For this
reason this technique is not employed.
EXCISIONAL TECHNIQUES
Excisional techniques have a major advantage over
ablative methods in that tissue is obtained and can be
examined histologically. The diagnosis can be
confirmed and the completeness of excision can be
assessed.
Many operators prefer to perform excisional techniques
on all patients. However, increasingly, in response to the
data concerning pregnancy-related morbidity, some
individuals are more selective and offer excision rather
than ablation when they
1. Suspect invasive disease
2. Are treating a glandular abnormality
3. Cannot visualise the squamocolumnar junction
4. Are managing a patient with previous cervical surgery
The following techniques are currently in use:
Large Loop Excision of the Transformation Zone (LLETZ)
This has become one of the most popular methods for treating premalignant cervical disease.
A thin wire loop is used to excise the transformation zone using a blended diathermy current.
It is also known as a LEEP (Loop Electrosurgical Excision Procedure). Ball diathermy is
applied for haemostasis at the treated the excision base.
Ball Diathermy
being used
for haemostasis.
Wire
Cervix
loop
Tissue removed
by wire loop
181
Knife Cone Biopsy

This technique was extremely popular prior to the introduction of LLETZ. However, it
requires a general anaesthetic and is now less commonly used. Complications include
bleeding, infection, and cervical stenosis or incompetence during a subsequent pregnancy.
Laser Cone Biopsy

In a laser cone biopsy, a cone of tissue is removed as above. However, the procedure may be
done under local anaesthesia. The costs of the equipment and the training required have
reduced its potential popularity. Laser does have the advantage that co-existing VAIN may be
treated at the same time.
Follow-Up
The above techniques are effective in treating CIN but recurrence can occur in 5% of the
patients. All women who have had CIN should be followed up with increased smear cytology
surveillance for a minimum of 5–10 years; there is regional variation within the UK.
182
CARCINOMA OF THE CERVIX
Worldwide, carcinoma of the cervix is the commonest malignancy of the female genital tract.
Its incidence varies from country to country and is significantly reduced where there is an
organised screening programme. In developed countries, such as the UK, cervical cancer is
the twelfth most common malignancy in females.
CLINICAL FINDINGS
The cervix becomes
very indurated; Later, a large fungating
necrosis and mass is produced.
ulceration Sloughing may leave
commonly follow an excavated crater.
quickly.
The tumour may Sometimes the

form a proliferating spread is in the
growth which substance of
protrudes into the the cervix – called
vagina – a ‘excavating’,
‘cauliflower’, ‘endophytic’,
‘exophytic’, ‘inverting’ growth.
‘everting’ growth. The cervix
This tumour type becomes stony,
bleeds easily and hard and enlarged
soon becomes – the ‘barrel-shaped’
ulcerated. cervix.
SYMPTOMS
Cervical cancer may present with no symptoms or may be detected at the microscopic stage
through a screening programme. If symptoms are present, then, they may include:
1. Irregular vaginal bleeding. It is not often due to carcinoma but the possibility must be
kept in mind. The bleeding may be due to intermenstrual bleeding, postcoital bleeding or
postmenopausal bleeding.
2. Vaginal discharge. The growth may become infected and produce offensive discharge.
3. Symptoms of advanced disease. Pain, bladder/bowel pressure symptoms, haematuria and
cachexia.
183
The two commonest cancers are squamous cell carcinomas and adenocarcinomas. 70% are
squamous cell carcinomas and 15% are adenocarcinomas with the remainder being the less
common types.
SQUAMOUS CELL CARCINOMA

The appearances are typical, but cell nests are absent and keratinisation is rarely seen.
Adenocarcinoma
This less common form of cervical malignancy usually arises from the columnar epithelium of
the endocervix.
The appearances in this form are typical of adenocarcinomas in other organs.
Low power. Tubular processes spread

out from the lumina of the glands. The
characteristic pattern is an aggressive
adenomatous formation with very little
fibrous stroma.
Many indeterminate patterns are seen on microscopic examination. Sometimes, both

glandular and squamous malignant cells appear together – an adenocanthoma – and
squamous metaplasia is common.
High power appearance of squamous

epithelium, which appears to originate
by metaplasia of the columnar
184 epithelium.
SPREAD
Direct spread into adjacent tissues such as
the vagina or parametrium can occur. In
postmenopausal women, it can also lead to
a uterine outlet obstruction and pyometra.
Its spread to the parametrium may induce
pain and tenderness.
Spread downwards into the

vaginal wall, if not diagnosed or
treated, may involve the bladder
or rectum and lead to the
formation of fistulae. A
backwards spread along the
uterosacral ligaments can lead to
an involvement of the sacral
plexus causing intractable sciatic
pain that can be felt in the hip or
the leg.
Lymphatic spread also occurs and may
precede direct spread. This is why Aortic
Common iliac
lymphadenectomy is still important in the
assessment of cervical cancers. From the
cervical lymphatics, the spread is usually
along the paracervical lymph tract to the iliac Internal iliac
and obturator nodes. Blood borne spread is
Sacral
less likely to occur in early stage disease but
may be significant in advanced disease. External
Ovarian involvement is rare. iliac
Obturator
Paracervical
185
DIAGNOSIS OF CERVICAL CARCINOMA
Biopsy is necessary for histological confirmation of the carcinoma. If the growth is early, some
normal tissue should be removed as well, and a diagram provided to show the pathologist
from where the biopsy was taken. It should be no bigger than necessary and a punch biopsy,
millimetres in size, may be sufficient. LLETZ biopsy can be performed for diagnosis but is
generally not performed in the presence of evidence of malignant growth that is visible to the
naked eye. Very occasionally, what appears to be a definite malignant lesion turns out to be
benign.
Some differential diagnoses include:
Cervicitis with ectopy, the commonest Mucous cervical polyps, when infected, can
cervical lesion and, if florid, can be most present with a very suspicious appearance.
misleading. (But all polyps require examination.)
Tuberculosis is rare in the cervix. There is A primary chancre (syphilis) can appear in
nearly always a history of genital the cervix and is ulcerated, hard and
tuberculosis. indurated. In the United Kingdom, this is
rare.
186
STAGING OF CERVICAL CARCINOMA
Each growth is allocated to a stage according 5m

m 4mm
to the extent of spread (FIGO). 3mm 3m m
m
2mm
1m
Stage IA Microscopic Cervical Cancer.
Stage 1A1
Stromal invasion 3.0 mm in depth and Stage la1 Stage la2
7.0 mm in horizontal spread.
Stage 1A2
Stromal invasion 5.0 mm in depth and Squamo-
7.0 mm horizontal spread.

columnar
junctions
Stage IB The growth is confined to the cervix.

Stage 1B1
Clinically visible lesion 4.0 cm dimension.
Stage 1B2
Clinically visible lesion >4 cm in greatest
dimension.
3 cm
5 cm
Stage II Tumour invades beyond the uterus but

not to pelvic wall or to lower third of the vagina.
IIA Without parametrial invasion.
IIA1 Clinically visible lesion 4 cm greatest
dimension.
IIA2 Clinically visible lesion >4 cm greatest
dimension. IIB Extension into the parametrium but not
as far as the pelvic wall.
187
STAGING OF CERVICAL CARCINOMA
Stage III Extension to lower third of vagina or to pelvic wall.
IIIa Carcinoma involving the lower third of IIIb Carcinoma extending to the pelvic side
the vagina. wall and/or hydronephrosis due to tumour.
Stage IV Extension through vagina into

bladder or outside the pelvis.
IVa Carcinoma involving adjacent organs. IVb Carcinoma extending to distant organs.
Omentum Periaortic
nodes
Inguinal nodes
Staging is clinicopathological and, currently, imaging that demonstrates hydronephrosis due

to tumour involvement can be used for staging purposes. Whilst magnetic resonance imaging
(MRI) is commonly available in developed countries, it is less so in developing countries.
Therefore, although MRI is useful in assessing the local spread of disease and may be used in
188 clinical decision, it is not included in the FIGO staging.
RADIOTHERAPY AND CHEMOTHERAPY IN CERVICAL CARCINOMA
Chemotherapy combined with radiotherapy is equivalent in terms of treatment efficacy,

compared to radical surgery, for early stage cervical cancers. The choice of treatment will
depend upon patient fitness, size of tumour and likelihood of requiring adjuvant treatment
based on preoperative factors; the aim being to deliver the most effective combination of
treatments to minimise morbidity.
Chemotherapy given along with radiotherapy has been shown to improve treatment
outcomes, with chemotherapy given at the same time as radiotherapy further sensitising
tumours to radiotherapy. A haemoglobin >11 g/dl will also increase efficacy.
The radiotherapy is delivered by two modes – external beam therapy and brachytherapy
(delivered close to tumour site).
BRACHYTHERAPY Intracavity therapy

Hollow carriers are placed in
the uterus and vaginal
fornices under general
anaesthesia. Radioactive
sources can then be loaded
into these tubes for treatment
at a later date. Intracavity
therapy allows high doses of
radioactivity to be targeted to
the cervix. The activity falls
with increasing distance from Radioactive
the source, therefore the sources
tissues around the cervix
(bladder, bowel, etc.) receive
a lower dose.
EXTERNAL BEAM
THERAPY
External beam therapy is applied to the pelvis to control spread outside the cervix. The total
radiotherapy dose is divided into smaller doses or fractions that are delivered over short daily
treatments, usually as 20–25 fractions. Treatment, therefore, lasts for 4–5 weeks.
COMPLICATIONS
Short term Long term

Diarrhoea Persistent bowel and bladder symptoms
Urinary frequency Radiation menopause
Nausea Vaginal stenosis/scarring/dryness
Vulval inflammation Late secondary tumours
189
SURGERY FOR CERVICAL CARCINOMA
MICROINVASIVE CERVICAL CARCINOMA

This may be treated with a LLETZ biopsy or if the patient has completed her family, by a
simple hysterectomy.
RADICAL HYSTERECTOMY
AND NODE DISSECTION Ureter
This consists of removal of the uterus,
upper 2 cm of the vagina, the tissues/
ligaments adjacent to the cervix
(parametrium) and the lymph glands
overlying the iliac vessels and the
obturator nerve at the sides of the pelvis.
It can be performed abdominally,
vaginally or laparoscopically, with
robots being increasingly used for
laparoscopic dissection.
The broad ligament is opened up and
the ureter dissected off the uterus and
cervix. This is a vascular area. This
diagram shows the ureter being
identified by palpation but it is also
directly visualised and dissected.
Ureter
The ureter is identified at the common iliac

division and followed downwards. The
ureter has to be mobilised to protect it, but
this does lead to the possibility of a fistula
due to avascular necrosis.
The ureter has been dissected clearly down to the bladder and the uterine vessels, divided at
their origin, form the internal iliac artery.
190
RADICAL HYSTERECTOMY AND NODE

DISSECTION—(cont’d)
After division of the ligamentous attachments (uterosacral
and cardinal) of the uterus, the vagina is transected. The
vaginal opening may then be over sewn around its margin
to provide haemostasis and allow fluid to drain. This will
seal within a short time following surgery.
In this description the hysterectomy is shown first,
followed by the lymphadenectomy; but many surgeons
carry out the lymphadenectomy first followed by the
block dissection of the radical hysterectomy.
The vagina is severed below the

Wertheim clamp in this example but
similar clamps may also be used.
Dissecting out the fatty tissue and glands Dissecting out the external iliac glands.
from the obturator fossa. (Other accessible groups of nodes are
also removed.)
191
RADICAL SURGERY FOR CERVICAL CANCER

Special Circumstances
Fertility sparing surgery
Removal of the uterus leads to loss of fertility and many women in the age range for the
development of cervical cancer may not have any children or have completed their family.
Daniel Dargent, Lyon, France, has developed a technique for a radical vaginal excision of the
cervix and retaining the uterine body. This technique has the potential to preserve fertility.
Lymph node spread is assessed by laparoscopic lymphadenectomy. This is now an accepted
technique and is being performed in specialist centres. Pregnancies have been recorded but
there are potential pregnancy-related complications such as pre-term labour, pre-term rupture
of the membranes and late miscarriages.
Exenteration for relapsed disease
Localised, central, pelvic relapsed carcinoma can be salvaged by radical excision of the pelvic
tumour. Due to the proximity of the bladder and the rectum to the vagina, such surgery may
involve – in addition to removal of the vagina – removal of the bladder (anterior exenteration),
bowel (posterior exenteration) or both (total exenteration). This is a long and complex procedure
that may require urinary diversion, colostomy formation and the creation of a new vagina.
Surgical complications of surgical treatment for cervical cancer
Early Late
Haemorrhage Atonic bladder
Infection Lymphoedema
Damage to ureters or Ureteric/bladder
bladder fistulae (1–2%)
Venous thromboembolic
disease
192
TREATMENT OF CERVICAL CARCINOMA: SURGERY OR RADIOTHERAPY?

Early stage cervical cancer is normally treated by surgery up to and including Stage 1B1. Later
stage cervical cancer (Stage 1B2 onwards) is usually treated by chemo-radiotherapy.
The advantages of the two treatment types are shown below.
Advantages of Surgery
Ovarian function is retained.
Normal vaginal function is retained.
Avoidance of the effect of radiotherapy on the bladder and bowel.
Advantages of Chemo-Radiotherapy
As effective as surgery for treatment.
Suitable in women who are unfit for surgery or do not wish surgery.
May allow avoidance of surgery where, at diagnosis, there is strong indication that it will be
required.
PROGNOSIS
5-Year Survival Figures According to Stage
Palliative care
In women with advanced cancer, it may be unrealistic to seek to cure the disease with surgery,
radiotherapy or chemotherapy. In some women, these procedures may be performed
palliatively, to reduce symptoms.
The care of patients with advanced or terminal disease is now a specialty in itself, and help
should be sought from palliative care specialists at an early stage. Such specialists are
invaluable in minimising symptoms, including pain, whilst maximising the quality of life.
193
CHAPTER 11
DISEASES OF THE UTERUS
Uterine Polyps 196 Local Spread 206

Endometrial Polyp 196 Lymphatic Spread 206
Placental Site Trophoblastic Aetiological Factors in Endometrial
Tumour 196 Carcinoma 207
Fibroids 197 Prognosis of Endometrial
Fibroids (Leiomyoma) 197 Carcinoma 208
Pressure Symptoms 198 Treatment of Endometrial
Diagnosis 199 Carcinoma 209
Complications 199 Stage I 209
Treatment 200 Stage II 209
Endometrial Hyperplasia 201 Stage III/IV 209
Clinical Findings 201 Recurrence of Endometrial
Simple Hyperplasia 201 Carcinoma 210
Complex Hyperplasia 201 Sites 210
Atypical Hyperplasia 201 Treatment for Recurrence 210
Aetiology 202 Sarcoma of the Uterus 211
Investigation 202 Clinical Features 211
Treatment 202 Histological Appearances 211
Carcinoma of the Endometrium 203 Endometrial Stromal Sarcomas 212
Presentation 203 Carcinosarcoma (Malignant Mixed
Diagnosis 203 Mesodermal Tumour) 212
Histology 204 Leiomyosarcoma 212
Staging of Endometrial Carcinoma 205
Spread of Endometrial Carcinoma 206
UTERINE POLYPS
ENDOMETRIAL POLYP
Symptoms
Enlarged Symptoms are heavier but regular periods,
tip of
postmenopausal bleeding, and irregular
polyp
bleeding on hormone replacement therapy
(HRT).
Cramping pain occurs as the uterus tries to
expel the polyp.
Intermenstrual bleeding – usually occurs
due to congestion or necrosis, but a
malignant change must always be
considered.
The polyp may be visible in the external os
and there may be more than one polyp.
Endometrial polyps may be identified by
transvaginal scan but hysteroscopy will allow
direct visualisation.
PLACENTAL SITE TROPHOBLASTIC

TUMOUR
This is due to the survival of chorionic tissue from a
recent pregnancy. The tissue remains adherent to the
uterine wall and enlarges with the accretion of fibrin and
fibrous tissue. This can produce either high or low
grade disease.
Symptoms
Menorrhagia and intermenstrual bleeding may present
some time after the pregnancy has terminated or
miscarried. Examination can reveal an enlarged uterus.
Treatment
All polyps must be removed and submitted to
pathology. The final treatment will depend upon the
histology, malignant potential and patient’s symptoms.
Surgery, including hysterectomy, may be required in
some cases, especially where malignant transformation
is known or is suspected.
196
FIBROIDS
FIBROIDS (LEIOMYOMA)
Fibroid is the gynaecological term for
a leiomyoma of the uterus or, occasionally,
of the cervix.
It is a circumscribed tumour of non-striped
muscle with supporting fibrous tissue.
Fibroids develop in the myometrium and are not
encapsulated, but they develop a false capsule of
compressed myometrial tissue.
The cut surface is

whorled, white
and bulges.
Intramural
fibroid Fibroid
becoming
subserous
Fibroid
becoming
submucous
Cervical
fibroid
The location of the fibroid describes the type.

They are sometimes conglomerate and multiple, and vary in size from tiny (millet seed) to
large, which may be many centimetres in diameter.
Some fibroids develop a long pedicle and present as polyps.
197
FIBROIDS
Fibroids are common tumours found in 15–20% of women. They may make the uterus bulky
and irregular and may enlarge the cavity so that there is a greater area of endometrium to be
shed at menstruation. Menstruation tends to be heavy but the cycle is usually regular. Fibroids
are associated with infertility and nulliparity.
A fibroid polyp starts as a submucous fibroid and develops a

pedicle. It causes dysmenorrhoea as the uterus tries to expel it.
It may be extruded through the cervix and become necrotic,
giving a foul discharge with irregular staining, and may even be
mistaken for cervical cancer.
Bladder
Bladder
compression
Bladder displacement
PRESSURE SYMPTOMS
A palpable abdominal tumour

The bulk of
fibroids in the Urinary frequency
uterus gives
A growth filling the pelvis leading to bladder
displacement, retention and overflow and difficulty with
defecation.
198
FIBROIDS
DIAGNOSIS
Pedunculated
Symptoms and Signs
Menstrual disorders, pressure
Intramural
related symptoms and abdominal
distension are all potential
symptoms. A palpable mass per
abdomen and/or on bimanual
examination may be elicited
during examination. The mass is
usually firm, smooth and can be Submucous
irregular.
Pedunculated
Investigations submucous
Patients may be anaemic if
suffering from menorrhagia and
Subserous
investigations for this should be Adenomyoma
undertaken with full blood count
and possibly assessment of Cervical
ferritin, folate and B12 levels, Intraligamentary
where appropriate.
The suspicion of a fibroid on
clinical assessment should be
confirmed with imaging.
Imaging will assess the size, site
and nature of the fibroid. While
rare, some fibroids can show Necrotic Malignant Cystic Red
signs of malignant change degeneration degeneration
(leiomyosarcoma). Ultrasound
will suffice for the assessment of
most but further information
may be gained by the use of
magnetic resonance imaging
(MRI), especially when the nature of the mass is being considered.
COMPLICATIONS
Sarcomatous change. This is rare but can occur, and large or complex asymptomatic fibroids
must be kept under observation if not being removed surgically.
Degeneration. Fibroids tend to outgrow their blood supply and are subject to various forms of
degeneration. Necrobiosis (‘red degeneration’) occurs in pregnancy and is a cause of pain.
Usually, this remits and no treatment is needed.
Hyaline, mucoid, cystic degeneration. These changes may produce soft or hard fibroids,
confusing the diagnosis. Torsion of the pedicle. This can arise in the case of a polypoid subserous
fibroid, and will give rise to acute abdominal symptoms. If the torsion is subacute and the
blood supply is gradually reduced, the fibroid may develop a new vascularity through
199
adhesions (parasitic tumour).
FIBROIDS
TREATMENT
Conservative management.
Small, asymptomatic fibroids need not be treated.
Medical treatment
Gonadotropin releasing hormone (GnRH) analogues may give 50% reduction in 6 months,
but rapid return to former size may follow cessation of therapy. Treatment for longer than 6
months can lead to osteoporosis.
Surgical treatment
Uterine artery embolisation – radiologically guided arterial embolisation
Myomectomy – conserving the uterus but removing the fibroid may preserve fertility.
Hysterectomy – removal of uterus with the fibroids.
Myomectomy
The approach to the tumour is made
through the uterine wall following an
injection of a vasopressor to minimise
blood loss. The fibroid is shelled out by
sharp and blunt dissection. The false
capsule may make the plane of dissection
difficult to identify. It can be performed
by open or laparoscopic techniques.
Myoma screw
can be used to
steady fibroid
The resultant cavity is obliterated by buried

sutures and the uterine wall flapped over to bring
the suture line as low on the uterine wall as
possible to reduce the risk of adhesions to the
bowel.
The disadvantages of myomectomy are possible blood loss and the recurrence of fibroids.
200 Hysterectomy is the treatment of choice unless the patient wishes to retain fertility potential.
ENDOMETRIAL HYPERPLASIA
Being less accessible than lesions of the vulvar, vaginal or cervical epithelium, endometrial
premalignant conditions are less easily diagnosed and followed up. Any hyperplastic condition
raises the question of development of cancer and assessment of risk is important. Hyperplasia
and carcinoma may coexist.
Endometrial hyperplasia may be classified as simple, complex or atypical.
CLINICAL FINDINGS
Most patients are in the 3rd and 4th decades of life, but hyperplasia is not confined to these
age groups. It may be found in association with anovulation in teenage girls and in
postmenopausal women. Heavy and/or irregular vaginal bleeding are the presenting symptoms
but its severity or frequency is not related to the degree of pathological change.
SIMPLE HYPERPLASIA
This is the most common type. The endometrium has a characteristic appearance, often
termed ‘Swiss cheese’ or cystic glandular hyperplasia.
At low power magnification the pattern is a
mixture of glands of varying sizes, a significant
proportion of them being cystic. There is no
crowding of the glands which are lined by cubical
or columnar epithelium. Mitotic figures are present
in small numbers. A similar gross picture may be
seen in atrophic endometria but the mitotic activity
is absent. Other associated pathology is rare.
COMPLEX HYPERPLASIA
In this grade of hyperplasia the most
striking feature is the quite obvious hyperplasia –
crowding of glands so that they are back-to-back,
the epithelium is stratified and mitoses are
relatively frequent. There is, however, no
epithelial atypia.
ATYPICAL HYPERPLASIA
At this stage nuclear atypia is present. Intra-
glandular polypoid formations and abnormal
mitotic figures are seen. Severe cases may be
indistinguishable from a carcinoma and adjacent
areas of endometrial carcinoma may occur.
201
ENDOMETRIAL HYPERPLASIA
AETIOLOGY
Exogenous or endogenous unopposed oestrogens are primarily implicated in the pathogenesis
of hyperplasia. Anovulatory cycles in perimenopause, obesity, polycystic ovarian disease,
oestrogen secreting ovarian tumours (granulosa cell tumours), tamoxifen therapy (selective
oestrogen receptor modulator) and unopposed oestrogen hormone replacement therapy can
cause hyperplasia of endometrium.
INVESTIGATION
Imaging of the uterus with ultrasound to assess the endometrium is indicated. To obtain a
diagnosis, an endometrial biopsy, with or without hysteroscopic assessment, will be required.
Investigation will usually be in an outpatient setting but inpatient general anaesthetic
assessment may also be needed.
TREATMENT
This depends principally on the types of hyperplasia. The age of the patient and a desire
to retain fertility are factors to be considered.
Simple hyperplasia, with 1% risk of progression to carcinoma requires no routine follow-up.
Symptomatic patients can be treated with progestogenic agents such as oral preparations or,
increasingly, with the levonorgestrel releasing intrauterine device (IUD) (MirenaW). Recurrent
abnormal bleeding would, of course, merit investigation.
Complex hyperplasia is not thought to merit hysterectomy. Progestin therapy, such as
levonorgestrel releasing IUD, is again indicated for symptomatic management. Subsequent
care after diagnosis can reasonably be dictated by the presenting symptoms.
Atypical hyperplasia, with estimated risks of co-existence of, or progression to, endometrial
carcinoma of between 20% and 50% merits hysterectomy and a bilateral salpingo-
oophorectomy in most cases. Women who wish to remain potentially fertile may be treated
with oral progestogens or by levonorgestrel releasing IUD but long-term data is lacking.
Recurrence on cessation of therapy has been reported and long-term surveillance with
repeated endometrial sampling is mandatory.
Hysteroscopy Endometrial biopsy
202
CARCINOMA OF THE ENDOMETRIUM
One of the commonest gynaecological cancers, it occurs most often in postmenopausal women
(up to 80% of cases) with less than 5% diagnosed under 40 years of age. Its association with
obesity, diabetes and polycystic ovarian syndrome is common. Postmenopausal American
women may run a 1 in 1000 risk of endometrial carcinoma each year. There is no effective
screening programme, but postmenopausal bleeding may be a cardinal symptom prompting
urgent investigation.
PRESENTATION
The usual presenting symptom of endometrial carcinoma is postmenopausal bleeding which carries
a 10% risk of associated malignancy. However, patients may also present in the perimenopause
with frequent, irregular bleeding or before the menopause with irregular vaginal bleeding. An
awareness of the risk factors will prompt appropriate investigation. Pyometra also carries a high
risk of underlying carcinoma
Increased risk is associated with obesity, nulliparity, late menopause, tamoxifen, polycystic
ovarian disease, oestrogen secreting tumours.
DIAGNOSIS
Patients presenting with
postmenopausal bleeding should be
reviewed urgently and investigated with
an abdomino-pelvic ultrasound
including a transvaginal ultrasound.
This will allow an assessment of the
ovaries and the endometrium. Where
the endometrial thickness is measured to
be less than 3 mm in women not on
HRT and less than 5 mm in women
taking HRT, there is an extremely low
incidence of endometrial cancer and the
patient can be reassured. Recurrent
bleeding should prompt further
investigation.
Transvaginal scan showing thickened
endometrium
Typical early
polypoidal fundal
growth
Patients with abnormal scans and all
women with irregular bleeding on
tamoxifen should undergo
hysteroscopy and endometrial biopsy.
In addition, careful inspection of the
cervix, vulva and vagina should be
undertaken to exclude these as a source
of bleeding due to malignant change. 203
CARCINOMA OF THE ENDOMETRIUM
HISTOLOGY
Distribution of Subtypes
Endometrioid 85%
Adenosquamous 4%
Serous carcinoma 4%
Clear cell 3%
The majority of tumours are adenocarcinoma and they are divided into three groups
according to the degree of glandular differentiation.
Single
cell
columns
Grade 1 – Well differentiated. Grade 2 – Moderately differentiated. Gland forms

are much less prominent and many of the deposits
consist of infiltrating single cell columns or solid
masses.
Grade 3 – Poorly
differentiated. This type
consists of solid masses of
malignant cells of varying sizes
Clear cell carcinoma
and shapes with little or no
This tumour has a poor prognosis
stroma. Mitoses are
and is included with the Grade 3
numerous.
adenocarcinomata. It occurs mainly
in the elderly.
204
STAGING OF ENDOMETRIAL CARCINOMA
The classification given below is that of the International Federation of Gynecology and
Obstetrics (FIGO 2009).
Stage I Growth
confined to Endometrium
A Inner half of the uterus Stage Ia Stage Ib
Myometrium
B Growth into the outer
Stage II
half of the uterus
Stage II Stage II
The growth has extended

to the cervix.
Endocervical
Stage III canal
The growth has extended

to
A Serosa and/or adnexa
B Vagina
C Pelvic or paraaortic
lymph nodes
Pelvic Paraaortic
nodes nodes
adnexal
spread
Stage IV Omentum
The growth has invaded
(a) the rectum or bladder or
(b) structures beyond the
pelvis.
Histological grading, G1,
G2 or G3 is applied to
Stages I, II and III only.
205
Inguinal nodes
SPREAD OF ENDOMETRIAL CARCINOMA
Magnetic resonance imaging is preferable to an ultrasound for the assessment of myometrial

invasion and pelvic spread. To assess distal metastases, a computerised tomography (CT)
scan of the chest, abdomen and pelvis may also be of value.
LOCAL SPREAD
Invasion of the myometrium and cervix is the commonest spread. It may produce
considerable uterine enlargement.
LYMPHATIC SPREAD
Lymphatic spread is more likely to occur when the tumour is poorly differentiated and the
uterine wall is deeply invaded. The incidence of pelvic nodal metastases is in the region of 10%.
Most metastases occur in the adjacent structures and in the peritoneum. In advanced cases,
distant metastases do occur, most commonly in lung, but occasionally in liver, vertebrae or
other bones and in the supraclavicular lymph nodes.
Pelvic organs Lymph nodes
Aortics
Common iliacs
Loose cancer cells Hypogastrics
in peritoneal cavity
External
iliacs
Small bowel
implants
Involved
ovary
Extension to
broad ligament
Obturator
Vaginal Inguinals
Paracervical
206
AETIOLOGICAL FACTORS IN ENDOMETRIAL CARCINOMA
There are two suggested types of endometrial carcinoma, based on aetiology.

Type 1 – arising in patients with a background history of oestrogen excess.
Type 2 – arising without evidence of oestrogenic stimulation.
Type 1 tumours would appear to have a better prognosis with a better differentiation pattern
and a less invasive component. They would appear to be derived from a hyperoestrogenic
stimulus. Type 2 tumours, including serous and clear cell cancers, arise from a atrophic type
endometrium and have a more aggressive phenotype with greater invasion, poorer
differentiation, more metastatic disease and, as such, they carry a poorer prognosis. Type 2
tumours have been associated with abnormalities in tumour suppressor genes.
Obesity, in particular, appears to be a developing issue in terms of the risk of endometrial
carcinoma. Obese patients convert peripheral androgens to oestrogens via the action of the
aromatase enzyme in adipose cells. Countries where the incidence of obesity is rising have
started to also see an increase in the incidence of endometrial carcinoma. In some countries,
it is now the commonest cancer of the female genital tract, overtaking ovarian carcinoma.
Hereditary non-polyposis colorectal cancer (Lynch II) syndrome is an inherited mutation in
DNA mismatch repair genes. In those affected, the endometrial carcinoma occurs more
frequently, together with breast and colon cancer.
207
PROGNOSIS OF ENDOMETRIAL CARCINOMA
The overall 5-year survival rate is approximately 80%. Fortunately, over 80% of cases are
diagnosed at Stage I. The survival is affected by multiple prognostic factors including:
Stage at diagnosis
Histological grade
Depth of myometrial invasion
Lympho-vascular space involvement (LVSI)
Non-endometrioid type
5-year survival rates according to clinical staging are as follows:
Stage 5-year survival (%)

I 85
II 75
III 45
IV 25
Assessing 5-year survival rates according to International Federation of Gynecology and

Obstetrics (FIGO) histological grading is reported as follows:
Grading 5-year survival (%)

G1 92
G2 90
G3 81
Using both methods on similar cases, we find that the 5-year survival rates for Stage I are the
only ones altered significantly:
Stage and histology 5-year survival (%)

I, G1 and 2 80
I, G3 60
208
TREATMENT OF ENDOMETRIAL CARCINOMA
This is essentially surgical, with postoperative adjuvant radiotherapy added when unfavourable
prognostic features are found at surgery. Adjuvant therapy for endometrial cancer is a
contentious, evolving field. To date, it provides improved local control but without improved
survival. Many believe that the addition of adjuvant chemotherapy may add a survival
advantage and research is underway.
Progestogen therapy is probably only of value in recurrent disease, but has been studied in early
stage, well-differentiated, disease where fertility preservation is an issue and in patients not fit
for radical therapy. If a woman is unfit for surgery then radiotherapy may be used alone, but it
is less effective.
STAGE I
Surgery for total abdominal hysterectomy and bilateral salpingo-oophorectomy without partial
removal of vagina is the treatment of choice. Peritoneal saline washings are taken for cytology
on opening the abdomen during surgery and the abdominal contents are carefully examined.
The procedure can also be performed laparoscopically with equivalent 5-year survival and a
lower operative morbidity. Evidence from randomised trials does not support
lymphadenectomy as a therapeutic intervention.
STAGE II
Stage II carries a prognosis that is similar to Stage I, and is usually treated as for Stage I and
diagnosed by pathology. Where preoperative assessment suggests obvious cervical
involvement then a radical hysterectomy with pelvic lymphadenectomy may be undertaken.
STAGE III/IV
Treatment of this stage is designed to control tumour growth and alleviate symptoms.
Treatment will depend upon tumour burden at the preoperative assessment and imaging.
Many cases may only be identified as Stage III, following surgical management. Surgery,
radiation therapy, chemotherapy and adjuvant progestogen therapy all have a place.
209
RECURRENCE OF ENDOMETRIAL CARCINOMA
The majority of recurrences appear within 3 years of treatment. Early recurrence has a poor
prognosis.
SITES
Recurrence can be local but endometrial carcinoma can also recur outside the pelvis. Vault
recurrence is less common after adjuvant vaginal vault irradiation but distal recurrence is
found more frequently if vault irradiation has been performed.
TREATMENT FOR RECURRENCE

Where recurrence is localised to the central pelvis, its salvage with radiotherapy and/or surgery
can be successful. Progestogens have been used as part of a combined primary treatment, as
well as for recurrent or metastatic growths. Between 15% and 50% of recurrences will respond
to therapy. Tumour response is especially noted in those patients with progesterone receptors
in the tumour. Medroxyprogesterone acetate is most commonly employed and the addition of
tamoxifen may improve the response. Chemotherapy also has a place in recurrent disease.
Combination treatment with adriamycin and cisplatin gives response rates between 20% and
40%.
210
SARCOMA OF THE UTERUS
These are rare tumours and include:

Endometrial stromal sarcomas
Leiomyosarcomas
Carcinosarcomas
This group of cancers has undergone changes in nomenclature and even now some consider
that uterine sarcomas are best described as high or low grade uterine sarcomas. They share a
common presentation with other uterine cancers, with irregular and/or postmenopausal
bleeding.
CLINICAL FEATURES
The patient is usually over 50 years old and presents with a complaint of fairly heavy bleeding
of recent origin, accompanied by pain. Pelvic examination reveals a large intrauterine mass
with friable tissue palpable through the os. The tumour may originate from the vagina in
younger women and from the cervix in the child; but these are, indeed, very rare conditions.
Sarcomatous change may occur in 0.1% of fibroids.
HISTOLOGICAL APPEARANCES
Tumour tissue may infiltrate the whole myometrium and fill the uterine cavity or arise from a
pedicle. This type often presents as a cervical or vaginal polyp. The tissues of origin are the
connective tissue and muscle of the myometrium or leiomyoma, or the endometrial stroma.
These are composed of undifferentiated round- or spindle-cell masses. In children, striated
muscle is often a feature and a characteristic polypoidal growth occurs – sarcoma botryoides.
High power appearance of Low power view of spindle-cell

round-cell sarcoma sarcoma
High power view of smooth muscle

sarcoma 211
SARCOMA OF THE UTERUS
ENDOMETRIAL STROMAL SARCOMAS

These are tumours of the endometrial stromal cells and form two groups:
Low Grade Stromal Sarcomas
The clinical course is often uncomplicated and cure may follow surgery. They can recur, often
years later, and recurrence up to 25 years later has been reported.
High Grade Stromal Sarcoma
This type of stromal tumour shows numerous mitoses and is infiltrative from the start. There
is early recurrence and widespread metastases occur even if there has been little local invasion
of the myometrium. The prognosis is poor.
CARCINOSARCOMA (MALIGNANT MIXED MESODERMAL TUMOUR)

In this variant, both epithelial and stromal elements are malignant. It forms a soft polypoid
mass that is usually haemorrhagic. Microscopically, most of the growth is sarcomatous but
there are foci of carcinoma – adeno, squamoid, undifferentiated or various mixtures of these.
The prognosis is poor. Treatment is surgical with hysterectomy, bilateral salpingo-
oophorectomy and pelvic lymphadenectomy.
LEIOMYOSARCOMA
Usually these cases do not present with postmenopausal bleeding and are found in patients
thought to have a uterine fibroid. Fibroids of a very large size or those which increase rapidly
in size should be suspected as having a higher chance of malignant change.
Treatment is usually hysterectomy and bilateral salpingo-oophorectomy. It is often not
suspected at diagnosis. If detected postoperatively, then CT scan of chest, abdomen and pelvis
should be undertaken to look for metastases. 10% of cases at diagnosis may have pulmonary
metastases. Haematogenous spread is most common.
Pelvic examination, in this case, A diffuse infiltrating sarcoma.

212 would suggest a cervical origin.
CHAPTER 12
PROLAPSE AND UROGYNAECOLOGY
Retroversion of the Uterus 214 Genuine Stress Incontinence 238

Symptoms and Treatment of Symptoms 238
Displacement 215 Genuine Stress Incontinence 238
Uterovaginal Prolapse 216 Other Incontinence Mechanisms 239
Vaginal Prolapse 218 Overflow Incontinence 239
Anterior Prolapse 218 Neurological Disease 239
Prolapse of the Posterior Wall 219 Other Symptoms and Signs
Clinical Features of Prolapse 220 Associated with Incontinence 239
Differential Diagnosis of Prolapse 221 The Urethral Syndrome 240
Pessary Treatment 222 Investigation of Incontinence 241
Alternative-Shaped Pessaries 222 Examination 241
Indications for Pessary Treatment 222 Demonstrations of Stress
Anterior Colporrhaphy (and Repair Incontinence 241
of Cystocele) 223 Urodynamic Investigation of
Anterior Repair 223 Bladder Function 242
Manchester Repair 225 Cystometry 242
Posterior Colpoperineorrhaphy Abnormal Cystometry 242
(Including Repair of Indications for Urodynamic
Rectocele) 227 Assessment 243
Repair of Enterocele 228 Other Investigations 243
Vaginal Hysterectomy 229 Treatment of Stress Incontinence 244
Indications 229 Conservative Treatment of Stress
Operative and Postoperative Incontinence 244
Complications 230 New Surgical Developments in the
Late Complications 230 Treatment of Stress Incontinence 244
Urogynaecology 231 Surgical Treatment of Stress
The Anatomy of the Urinary Tract 231 Incontinence 245
Blood Supply of the Ureter 233 Marshall–Marchetti–Krantz
Histology of the Ureter 233 Urethropexy 246
Physiology of Micturition 234 Burch’s Colposuspension Operation 247
Intravesical Pressure 234 Stamey Needle Suspension
Intraurethral Pressure 234 Procedure 247
Innervation of Bladder and Urethra 235 Sling Procedures 248
Mechanism of Voiding 236 Treatment of Detrusor Instability 249
Detrusor Instability 237 Bladder Retraining 249
Symptoms 237 Drug Treatment 249
RETROVERSION OF THE UTERUS
An alteration from the usual anteverted position of the uterus often with a change in the curve
of the uterine axis. Most of the so-called displacements are merely variations of the normal
and are of little clinical significance.
Anteverted Uterus
The uterus is approximately
at right angles to the vagina
and has a slight forward
curve.
Retroversion Retroflexion
The long axis of the uterus is This is a variation of retroversion but the
directed backwards. The uterus is uterus is curved backwards. The cervix may
displaced backwards and this is simply a remain in the normal position but is usually
physiological variation for the vast positioned as in retroversion.
majority of women. It occurs in
approximately 20–30% of women.
214
RETROVERSION OF THE UTERUS
Causes of Displacement
Displacement may be due to the Fibroid
presence of some other condition such
as a cyst or fibroid or endometriosis.
Diagnosis is by bimanual palpation. The

vaginal hand palpates a mass in the Pouch
of Douglas, the abdominal hand detects
the absence of a uterine corpus in the
expected place. The possibility of pelvic
pathology should be considered and
ultrasound may be used to confirm the
clinical findings.
SYMPTOMS AND TREATMENT OF

DISPLACEMENT
Consequences of Uncomplicated
Displacement
Usually none. However, if there is pelvic
pathology present, the woman may
complain of deep dyspareunia. If such
pain occurs, it can easily be reproduced by
pressing with the examining fingers. It is
quite possible for the patient to present
with a complaint of dyspareunia and to
have a retroverted uterus which has
nothing to do with her complaint.
215
UTEROVAGINAL PROLAPSE
Herniation of the genital tract through the pelvic diaphragm.
Sacrum
Stretched Stretched
Sacrum
uterosacral cardinal
Uterosacral Cardinal ligament ligament
ligament ligament
Side
wall
of
pelvis
Stretching and
gaping pelvic floor
Pelvic floor
The uterus and vagina are held in the pelvis When these ligaments and muscles become
by the cardinal and uterosacral ligaments ineffective, the uterus and vagina descend
and by the pelvic floor musculature, (prolapse) through the gap between the
mainly the levatores ani. muscles.
The causes of prolapse are the following:
• The stretching of muscle and fibrous tissue which occurs with childbirth and damage
to the innervation of the pelvic floor.
• Age and menopausal changes lead to changes in connective tissue support.
• Increased intra-abdominal pressure, for example, chronic cough, heavy manual work;
congenital predisposition to stretch the ligaments.
• Distortion of pelvic anatomy by previous surgery, for example, vault prolapse after
hysterectomy or entercoele after colposuspension.
The incidence of this condition in the United Kingdom has been greatly reduced because
of smaller families and higher caesarean section rates.
216
UTEROVAGINAL PROLAPSE
The uterus gradually descends in the axis

of the vagina taking the vaginal wall with
it. It may present clinically at any level,
but is usually classified as one of three
degrees.
First degree: cervix

still inside vagina.
Second degree
Third degree
Second degree: the

cervix appears at the
level of the introitus.
Bladder
Third degree: complete prolapse. In

the picture, the uterus is retroflexed
and the outline of bladder can be seen.
There may be a rectal prolapse as well.
This is sometimes called complete Course
procidentia. The vaginal mucosa of
is non-keratinised and the tissues ureter
can become very dry and ulcerated
with a 3rd degree uterine prolapse. Uterus
Bleeding and infection can also
occur.
217
VAGINAL PROLAPSE
The prolapse involves the vaginal walls and the related viscera. Prolapse of several sites may
co-exist and a uterine prolapse may also be present.
Cystocele
Cystocele
ANTERIOR PROLAPSE
When the upper part of the anterior wall prolapses, there is an underlying failure of the
investing fascia, and the bladder base also descends. This is called a cystocele.
Stretched
Urethrocele urogenital Urethrocele
diaphragm
Sometimes the lower part of the vaginal wall prolapses and the urethra also descends.
This is called a urethrocele.
218
VAGINAL PROLAPSE
PROLAPSE OF THE POSTERIOR WALL
Rectocele
If the prolapse is at the level of the middle third of the vagina, the rectovaginal septum is often
involved and rectum prolapses with vaginal wall. This is called a rectocele. If the lowest part of
the vagina prolapses, the perineal body is involved rather than the rectum.
Enterocele
If the upper part of the posterior vaginal wall prolapses, the Pouch of Douglas is elongated and
small bowel or omentum may descend. This is called an enterocele. Enterocele is often
associated with uterine prolapse, as in the picture.
Where the uterus has been removed, prolapse of this region is known as a vault prolapse. This
is a difficult condition to treat. The technique depends on suspending the vaginal vault from
fixed ligaments within the pelvic and often requires insertion of a non-absorbable mesh. 219
CLINICAL FEATURES OF PROLAPSE
• Asymptomatic. It is not uncommon for women to palpate a prolapse, for example,

during washing or attempting to insert a tampon. For some women, simple reassurance
that there is no sinister cause is all that is required. It can also be identified during
routine smear, etc., and if asymptomatic no treatment is required.
• ‘Something coming down’ within the vagina is the commonest symptom. It tends to be
worse when the woman has been on her feet and it disappears when she lies down.
• Backache. Some women will experience a dragging feeling or bearing down sensation.
This is sometimes resolved with treatment of the prolapse, but mechanical back pain is
very common and it may be unrelated to prolapse.
• Coital problems. This is relatively unusual but the woman may admit to difficulties with
intercourse, only on direct questioning.
• Increased frequency of micturition. This can be due to anatomical changes that make it
difficult to empty the bladder fully. Detrusor instability is also common in older women
and may co-exist. A careful urinary history should be taken including fluid and
caffeine intake.
• Stress incontinence. This is by no means always present. Sometimes, it is found that
reduction of the prolapse causes stress incontinence.
• Difficulty in voiding urine and defecating. The patient may find that it is impossible to
initiate micturition except by pushing up the cystocele with her finger. In the same way,
the rectocele must be pushed back to allow emptying of the rectum.
The onset may be gradual or quite sudden and is commoner after the menopause when the
genital tract tissues begin to atrophy.
220
DIFFERENTIAL DIAGNOSIS OF PROLAPSE
Prolapse should be confirmed by vaginal examination. The following conditions resemble

prolapse on superficial examination; however, careful examination will detect the difference.
Large
cervical
polyp Cyst of
Bartholin’s
gland
Vaginal cyst
Cyst of Skene’s duct
Chronic inversion of uterus 221

PESSARY TREATMENT
There are a number of different shapes of vaginal pessaries, the simplest to insert is a ring
pessary. This is usually made of semi-rigid plastic and is inserted into the vagina so that the
vaginal walls are stretched and they cannot prolapse through the introitus.
The pessary is compressed into a long ovoid shape, lubricated and gently pushed into the
vagina, where it resumes its circular shape and takes up a position in the coronal plane. It must
not be too tight; and correct fitting is learnt by experience. To an extent, pessary fitting is trial
and error and the woman should be warned that the pessary may dislodge. A point of contact
should be given so that she can be seen again without delay if this is the case.
ALTERNATIVE-SHAPED PESSARIES
The ‘shelf’ pessary can be particularly useful for
uterine prolapse but it is slightly less malleable and
insertion can be more difficult.
INDICATIONS FOR PESSARY TREATMENT

• The patient prefers a pessary. Pelvic surgery with
its unavoidable risks should only be applied to a
willing patient.
• The prolapse is amenable to pessary support. If the perineal muscles are very deficient
they will not hold a pessary and the pessary will fall out. If too big a ring is required, the
vaginal wall or cervix will prolapse through it. Posterior vaginal wall prolapses are
poorly supported by pessaries.
• The patient is not fit for surgery.
• The patient wishes to delay operation temporarily (e.g., another pregnancy is anticipated).
Plastic rings should be changed once or twice a year, and if it has been properly fitted, the
patient will be unaware of its presence in her vagina even during coitus. An ill-fitting pessary is
ineffective and may cause dyspareunia and discomfort. If it is too tight or left too long,
ulceration of the vaginal wall will occur, and malignant change has been reported. Vaginal
222 oestriol cream or vaginal oestradiol tablets (0.025 mg) help prevent atrophic vaginitis.
ANTERIOR COLPORRHAPHY (AND REPAIR OF CYSTOCELE)
Surgical restoration of the normal anatomy is

the purpose of treatment. Reconstitution of
the fibrous ‘scaffolding’ of the pelvic organs
aims to allow the musculature to function
efficiently
Cystocele and rectocele are dealt with by
anterior and posterior colporrhaphy. Uterine
prolapse may require vaginal hysterectomy.
Cervical amputation or Manchester repair
may be adequate if the cervix is
hypertrophied and the uterus is well
supported. Each ‘repair’ must be adapted to
the extent of the prolapse and this may often
be fully appreciated only at examination
under anaesthesia. Women should be
counselled regarding the possible surgical
consequences prior to surgery and consent
should reflect this. ANTERIOR REPAIR
1. Opening up the anterior vaginal wall.
Gauze
swab on
finger
2. Mobilising cystocele from vaginal walls. 3. Mobilising cystocele from cervix.
223
ANTERIOR COLPORRHAPHY (AND REPAIR OF CYSTOCELE)
ANTERIOR REPAIR—(cont’d)
The next step is obliteration of the
cystocele protrusion by tightening the
fascial layer between it and the vaginal
wall, a layer which is often very difficult
to identify.
4. Placing the tightening sutures as far

laterally as possible.
5. Obliteration of the cystocele completed. 6. Removing redundant vaginal wall.

This is followed by closure with
224 interrupted absorbable sutures.
MANCHESTER REPAIR
This involves at the least some shortening

of the transverse cervical ligaments and
usually amputation of the elongated
supravaginal cervix. It is often done in
conjunction with anterior and posterior
repairs.
1. The cystocele has been repaired.

The cervix is being stripped of vaginal
wall.
2. Posterior vaginal wall being stripped 3. Elongated transverse cervical and

back. uterosacral ligaments are sutured and
divided.
225
MANCHESTER REPAIR
4. Amputation of cervix. 5. Covering the posterior stump with

vaginal wall.
6. Tying the transverse cervical ligaments 7. Covering cervical stump and closing
in front of the cervix and so shortening the vaginal wall. On release of the
them and raising the uterus. (This is cervical stump, the uterus returns to
the so-called Fothergill suture: the pelvis.
226 sometimes two are put in.)
POSTERIOR COLPOPERINEORRHAPHY
(INCLUDING REPAIR OF RECTOCELE)
1. Mobilisation of the posterior vaginal 2. Separating rectocele from posterior

wall. vaginal wall.
Perineal
muscle
3. Obliterating the rectocele by tightening 4. Excess vaginal skin is removed. The

the fascial layer (cf. obliterating the perineal muscles are sutured over the
cystocele). obliterated rectocele. The skin and vagina
are closed.
227
REPAIR OF ENTEROCELE
An enterocele is a prolapse of the Pouch of Douglas peritoneum in between the upper vagina
and rectum, and must be distinguished from a rectocele. Repair of enterocele is often
combined with repair of uterine prolapse which is not shown here.
Bowel
1. Dotted lines show the

area of vaginal wall
which will be removed. 2. The enterocele sac is
identified and opened.
3. Once the sac is mobilised the neck is 4. The vaginal wall is closed in the usual
sutured up as far as possible to way.
obliterate the enterocele.
228
VAGINAL HYSTERECTOMY
INDICATIONS
Cystocele
• When the uterine prolapse is significant.
repair
• When hysterectomy is required for a
non-malignant uterine condition –
menorrhagia.
It may be difficult to remove the ovaries by the
vaginal route and laparoscopically assisted
vaginal hysterectomy may facilitate this.
Appropriate access is required to the remove
the uterus. The blood supply has to be divided
from the uterus and the pedicles secured.
The bladder has to be mobilised so that it is
not injured during the procedure. Access
may be limited by a number of factors, for
example, an enlarged fibroid uterus or if there
is pelvic adhesion related to endometriosis.
This procedure is always easier in women
who have had vaginal deliveries. 1. The bladder has been mobilised.
The uterine ligaments are put
on the stretch and divided.
Tube and
round ligament
Body of
uterus
2. Uterovesical pouch has been entered. 3. The lateral pedicles are sutured
Broad ligament structures are put on together to support the Pouch of
the stretch and divided. The uterus is Douglas. The vaginal vault is closed.
then removed.
229
VAGINAL HYSTERECTOMY
OPERATIVE AND POSTOPERATIVE COMPLICATIONS

Selection of Patients
• Neither youth nor age is a contraindication, but the patient must be reasonably fit, with
adequate cardiorespiratory and renal function. Oestradiol vaginal cream may be
used to treat atrophic vaginitis prior to surgery.
• The prolapse should be symptomatic.
Perioperatively
• Bleeding pedicles are more difficult to control than during abdominal surgery.
The parametric structures should be clamped, divided and ligated in small rather than
large bites.
• With the uterus gone, there is a risk of distorting the ureters if the bladder fascia is
tightened too much during repair of the cystocele.
Postoperatively
If uncomplicated, the recovery following vaginal surgery is usually associated with less pain
and more rapid mobilisation than with abdominal surgery. There is a higher risk of vault
haematoma with vaginal hysterectomy when compared to abdominal hysterectomy. This may
become infected; however, this usually responds to antibiotics and usually discharges per
vaginam. Insertion of a vaginal pack at the end of the procedure is often performed to provide
local pressure and reduce the risk of haematoma. A urinary catheter is required when a pack is
used.
LATE COMPLICATIONS
Recurrence of prolapse
This is a relatively common problem. The prolapse that returns within the first months of a
repair may be due to a break down or herniation within the primary repair. There may
have been a history of postoperative infection. In the long term, women who have undergone
pelvic floor repair are at an increased risk of prolapse. It is likely that the fundamental
weakness of the fibrous supports of the pelvic floor continues but it may also be that a repair in
one area of the pelvic floor transits pressure to another area of the pelvis.
Urinary incontinence
Urinary symptom can appear for the first
time after a pelvic floor repair. This is often
due to an underlying problem when the
anatomy returns to normal.
Dyspareunia
The surgeon must enquire before the
operation about the patient’s sexual activity
and must be careful to leave a functional
vagina where this is required (although this
may make support of the prolapse more
difficult). Occasionally, dyspareunia may be Vaginal wall adhesions
caused by vaginal adhesions.
230
UROGYNAECOLOGY
THE ANATOMY OF THE

URINARY TRACT
The Ureters
The ureter enters the pelvis
retroperitoneally by crossing
over or near the bifurcation of Ureter
the common iliac artery. Sacral
promontory
The ureter is itself crossed by Ovarian
the ovarian vessels and is near vessels
the fold of peritoneum which
forms the infundibulo-pelvic External
ligament. iliac artery
Internal
iliac artery
Infundibulopelvic ligament
Uterus
It passes down and medially behind the ovarian fossa and is in close relation to the internal
iliac artery. In the healthy subject, its shape can be made out beneath the peritoneum and
peristatic movements can be observed (vermiculation).
Internal iliac artery
Ureter Ureter
Ovary
Internal iliac artery
Ovary
Sacrum
Uterine artery
Uterus
Bladder
Bladder
231
UROGYNAECOLOGY
The ureter then passes

beneath the base of the broad
ligament, through the
Ureter
transverse uterine ligament
and into the bladder. In this
parametrial part of its course,
it lies alongside the vaginal Transverse
ligament
fornix and passes under the
Uterus
uterine artery.
(cut)
Uterine
artery
Uterus
Ureter Vagina
This picture shows the
parametrial part of
Trigone of the ureter with the Relationship of bladder
bladder (cut) connective tissue base to vagina
removed. Note that
the asymmetry of the
uterus and vagina
makes the left ureter
have a much closer
relationship with the
vaginal fornix than the
232
right.
BLOOD SUPPLY OF THE URETER
The ureter is supplied by branches from

the main arteries with which it is in
relation, principally the renal and ovarian
arteries. The pelvic vessels are variable
and because the blood enters mostly at the
upper and lower ends, the peri-ureteric
anastomoses are important. From renal artery
From ovarian artery
Ureter
From internal iliac artery
Common iliac artery From uterine artery

Uterus
From vaginal artery
From vesical artery
Bladder
HISTOLOGY OF THE URETER

The adventitia is a fibrous sheath
containing the peri-ureteral arterial
network, the autonomic nerves and
the lymphatics.
The muscularis consists of two or

three layers of smooth muscle
irregularly arranged.
The lumen is lined by plicated

transitional epithelium on a loose
areolar stroma. This arrangement
allows for distension of the ureter as
required (cf. the fallopian tube).
233
PHYSIOLOGY OF MICTURITION
Incontinence of urine is very common in women. The assessment and treatment call for an
understanding of bladder and urethral physiology.
INTRAVESICAL PRESSURE INTRAURETHRAL PRESSURE

The bladder displays the phenomenon of Urethral pressure is maintained by the
adaptation to increased urinary volume. ‘internal sphincter’ made up of longitudinal
Pressure remains below 10 cm H2O until and circular plain muscle and elastic tissue;
over 500 ml of urine are contained. and an ‘external sphincter’ which contributes
striated muscle.
Intravesical
pressure (cmH2O)
50 Cough Striated
muscle
40 Plain
muscle
30 Elastic
tissue
20
Awareness Mucosa
of filling
10 Cross section of urethra
0 200 400 600

Volume of urine (ml)
100 cmH2O
Maximal
A ‘urethral pressure profile’ shows the urethral
changes in pressure along the length of the closure
urethra. This is normally much greater 50 pressure
than the intravesical pressure, thus
ensuring continence.
Bladder
Length of
pressure
urethra
0
centimetres
234
PHYSIOLOGY OF MICTURITION
INNERVATION OF BLADDER
Cortex
AND URETHRA
There is an intercommunicating
Inhibition
sympathetic, parasympathetic and Sensation
Relaxation
somatic supply. The parasympathetic
stimulates detrusor contraction, and
the sympathetic fibres (chiefly through T10–L2
the alpha receptors) stimulate Sympathetic via
hypogastric
contraction of the bladder neck and
plexus
urethra. (Contraction of
bladder neck)
S2–S4
Parasympathetic
(nervi erigentes)
(Contraction of
detrusor;
contraction of
external sphincter)
The striated muscle has been shown to

have a dual autonomic/somatic supply Smooth muscle
via the pelvic plexus. In normal urethral of detrusor/urethra
closure, all the components of the
sphincter mechanism must function
Levator ani
together and the striated muscle has
muscle
more to do than merely contract
voluntarily when the desire to micturate
must be resisted. Striated
muscle
Diagram of urethral closure mechanism
235
MECHANISM OF VOIDING
Cystometry recording Intra-abdominal

demonstrates the timing of events. pressure
1. Intra-abdominal pressure 1.
increase. (Measured with a
vaginal or rectal probe.) Intravesical
2. Detrusor contracts. pressure
(Intravesical pressure 2.
increase.) Sphincter activity
3.
3. Sphincter relaxes.
(Electromyogram of anal
sphincter.) Urine flow
4.
4. Urine flow begins.
Time
The urethra and bladder neck are maintained in the closed state by the trigonal condensation
of muscle (the base plate) and the urethral sphincter (plain and striated muscle).
Sphincter Sphincter
closed open
Funnelling
Base
plate
Flattening
Urethrovesical angle
of UV
Sphincter
angle
When cortical inhibition is withdrawn, the detrusor contracts and the bladder neck
relaxes (funnelling). The sphincter also relaxes and urine is voided. As the flow
continues, the bladder neck moves downwards and backwards and the urethrovesical
(UV) angle is obliterated.
236
DETRUSOR INSTABILITY
For most women with this condition, it may be associated with neurological conditions,
for example, multiple sclerosis and stroke.
The normal bladder does not contract unless voiding is desired. For reasons that are poorly
understood, patients with detrusor instability experience detrusor contractions at other times.
This can occur spontaneously but may also be provoked, for example, with coughing. The
mechanism is altogether different from that of genuine stress incontinence, but some women
will have both pathologies.
SYMPTOMS
The patient experiences an irresistible and sudden desire to micturate (urgency). Detrusor
instability is the commonest cause, but it may also be due to inflammatory disease of the
bladder without detrusor contraction. All forms of bladder pathology must be considered
including calculus and carcinoma. There is usually an associated complaint of frequency.
237
GENUINE STRESS INCONTINENCE
SYMPTOMS
When a sudden increase in intravesical
pressure is caused by a contraction of the
detrusor muscle or by an increase in intra-
abdominal pressure as by coughing or
straining, the stimulus is usually applied to
the intra-abdominal urethra as well, and
there is no leakage of urine. If urine does
escape, the symptom is called stress
incontinence.
GENUINE STRESS INCONTINENCE

(alternatively named urethral sphincter incompetence)
Involuntary leakage occurring in the absence of a detrusor contraction. This leakage is
attributed to weakness and displacement of the bladder neck so that it cannot respond
normally to a sudden increase in intra-abdominal pressure. The cause is likely to be a pelvic
floor weakness as a result of parturition and/or oestrogen deficiency.
238
OTHER INCONTINENCE MECHANISMS
Fistula incontinence is described in Chapter 14 Complications of Gynaecological Surgery.
OVERFLOW INCONTINENCE
Retention of urine is relatively unusual in women; however, it can occur after surgery
and is particularly common after regional anaesthesia. Spasmodic detrusor contractions
force a little urine into the urethra and the stretched muscle takes several days to
regain its tone.
When obstruction to outflow occurs gradually, as from pressure by a pelvic tumour or an
incarcerated retroverted gravid uterus, the detrusor has time to hypertrophy and, for a time,
forces urine out; but eventually the bladder becomes atonic and painless, and urine dribbles
out only when the intra-abdominal pressure is raised.
NEUROLOGICAL DISEASE
Failure of detrusor inhibition is the commonest symptom and is the cause of senile
incontinence. It is also a symptom, although not usually the presenting one, of multiple
sclerosis. Full sensation is present, but the incontinence is of the urgency type and cannot be
resisted.
Failure of bladder sensation is a result of diseases which interrupt the posterior columns of the
cord, for example, tabes, syringomyelia and occasionally multiple sclerosis. Chronic
overdistension leads to an atonic bladder and overflow incontinence, and infection is a
common complication.
OTHER SYMPTOMS AND SIGNS ASSOCIATED WITH INCONTINENCE

Frequency
Increased frequency of micturition may arise from any source of irritation including infection,
detrusor instability, tumour or incomplete emptying. It is usually diurnal – during waking
hours only – but in severe cases will awaken the patient from her sleep. It is one of the earliest
symptoms of pregnancy.
Urgency
This is defined as a desire to void urine before the bladder contains 50 ml of urine. True
urgency occurs in the absence of a detrusor contraction, and is often associated with infection.
Severe urgency leads to ‘urge incontinence’.
Dysuria
This means pain associated with micturition and indicates an infection either of the bladder
and urethra, or of the vulval and perineal epithelium which is irritated by the dribbling of
urine.
Nocturia
Requiring to pass urine during the night.
239
THE URETHRAL SYNDROME
The urethral syndrome includes complaints of frequency, dysuria, urgency and a sensation of
incomplete emptying in a patient in whose urine no evidence of infection can be
demonstrated. The cause is not known and there are several views.
Urinary infection is strictly defined as being present only when 104 or more typical urinary
pathogens are grown per ml of freshly voided mid-stream urine and it may be that the urethral
syndrome is simply a condition caused by fewer than the usual number of organisms, or by
organisms which cannot be cultured in the media used for conventional organisms. Clinically,
these patients must be regarded as suffering from a possible urinary tract infection and
investigation should be persevered with. Even if no evidence of infection is obtained, empirical
antibiotic treatment may be of benefit. In menopausal women, topical oestrogens will treat
atrophic changes in the urethral epithelium which can predispose to infection.
240
INVESTIGATION OF INCONTINENCE
It is useful to distinguish between genuine stress incontinence and detrusor instability as their
treatment is different although it is important to remember that some women will have dual
pathologies.
History and clinical examination are useful but investigation of bladder function may be
required particularly where surgical intervention is being considered.
Incontinence may be due to the following:
1. Genuine stress incontinence

Usually occurs after one or more pregnancies.
Urine appears only after effort (stress) such as coughing, laughing or running for a bus.
Usually only small quantities of urine are passed, whether the bladder is full or not.
2. Detrusor instability
Complaints of urge incontinence and frequency, especially at night (nocturia).
May pass large volumes of urine when bladder muscle contracts.
Stress incontinence combined with urgency incontinence due to bladder infection or cystocele
is quite common. Continuous incontinence suggests fistula (p. 292).
The social effects of urinary incontinence should be considered when planning treatment.
EXAMINATION
Signs of infection (urethritis) and scarring from previous surgery are looked for, and the usual
bimanual and speculum examinations are performed (Chp. 5).
DEMONSTRATIONS OF STRESS
INCONTINENCE
The patient is asked to strain and cough
and, if stress incontinence is present,
small amounts of urine will be observed
escaping from the urethral meatus.
Unfortunately, this test is really valid
only in the erect position when
observation of the meatus becomes
almost impossible.
241
URODYNAMIC INVESTIGATION OF BLADDER FUNCTION
This means an investigation of bladder movements and tensions during different levels of
filling, and involves measurement of bladder activity (cystometry) and urethral flow
(uroflowmetry).
CYSTOMETRY Intravesical
The bladder pressures are continuously pressure
recorded as the bladder is filled. In twin 100 cmH2O
channel cystometry, the intra-abdominal
Filling Standing
pressure is simultaneously recorded by a
transducer in the rectum or vagina. The Cough
detrusor pressure is calculated by
subtracting abdominal pressure from
intravesical pressure. 50
0
200 400 600ml
Bladder volume
ABNORMAL CYSTOMETRY
If detrusor contractions are seen in the filling phase (up to 400 ml infused into bladder), a
diagnosis of detrusor instability can be made.
In stress incontinence, leakage on acts such as coughing occurs in the absence of a rise in
detrusor pressure.
Recorder
Bladder
Rectum
Bladder line
Rectal line
242
INDICATIONS FOR URODYNAMIC ASSESSMENT
These investigations are invasive, but their application would be justified in the presence of
the following indications:
1. Continuing difficulty in distinguishing genuine stress incontinence from detrusor
instability.
2. After failure of surgery to relieve a complaint of incontinence.
3. Where there are other complicating factors such as neurological disease.
4. Where difficulty in voiding urine is complained of or is suspected. Such a condition
may be met with after pelvic surgery and leads to incomplete emptying and perhaps
retention overflow.
5. Some clinicians would advocate urodynamic assessment prior to surgical treatment for
stress incontinence. The purpose of this is to assess for underlying detrusor instability
which may be exacerbated by surgery.
OTHER INVESTIGATIONS
Bacteriological Culture of Urine
This must be carried out in every case.
Fluid Balance Chart
The patient is asked to record the volume of oral fluid intake and urine output over the course
of a week. Recordings of urine production should include the volume and the time of each
micturition. Any episodes of incontinence should also be recorded. This procedure is useful
for identifying the patient with an excessive oral intake. An estimate of the patient’s normal
bladder capacity can also be made.
Neurological Disease
This possibility must always be borne in mind and the gynaecologist should test for reflexes in
the usual manner. Where there is doubt, the patient must be referred to a neurologist.
Endocrine Diseases
Diseases such as diabetes mellitus and insipidus may present with frequency of micturition.
243
TREATMENT OF STRESS INCONTINENCE
General measures:
The following should be treated if present:
1. Chronic urinary tract infection
2. Obesity
3. Chronic cough.
CONSERVATIVE TREATMENT OF STRESS INCONTINENCE

1. Physiotherapy – pelvic floor exercises
Pelvic floor exercises may be of value, especially in the puerperium. The best results
are achieved when the patient has input from a physiotherapist with an expertise in pelvic
floor exercises. Repeated contraction of the pelvic floor will strengthen the muscle tone.
A number of techniques are used to achieve this including vaginal cones and biofeedback.
This is where the woman’s pelvic floor strength is measured to enable her to be aware
of her own pelvic floor tone.
2. Mechanical devices to occlude urethra or support the bladder neck

These devices are usually placed within the vagina and efficacy is variable. Urinary tract
infection, expulsion of the device and patient discomfort are reasonably common.
NEW SURGICAL DEVELOPMENTS IN THE TREATMENT

OF STRESS INCONTINENCE
1. Peri-urethral injections
Substances such as collagen or subcutaneous fat are injected around the urethra using a
vaginal approach. This procedure is suitable for frail patients. Cure rates of up to 80%
have been reported in the short term but this is reduced in longer follow-up.
2. Artificial urinary sphincters

Implantation of an artificial urinary sphincter may be considered as a last resort in the
treatment of stress incontinence.
244
SURGICAL TREATMENT OF STRESS INCONTINENCE
All operations attempt to elevate the bladder neck above the pelvic floor and behind the
symphysis so that increases in intra-abdominal pressure will compress the urethra and not
force it downwards. There are three conventional methods, each with several variations.
1. Anterior colporrhaphy
This procedure may be useful in women with coexisting anterior vaginal wall prolapse,
but the rate of objective cure for stress incontinence is less than 40%.
2. Urethropexy
The bladder neck is approached through a
suprapubic incision and elevated by suturing the
paraurethral tissues to adjacent structures such
as the rectus sheath or the ilio-pectineal ligament.
These operations are more difficult than vaginal

urethroplasty, especially in obese women. Some
operators employ a laparoscopic technique.
3. Urethral sling operations

A sling of synthetic material,
sutures or tendon is passed under
the urethra and attached to the
rectus muscles or adjacent
ligaments. This requires a
combined vaginal-suprapubic
approach and is the most
difficult of the three methods.
The urethropexy operations are probably most likely to be successful when the inconti-
nence is due to urethral inadequacy and not detrusor instability.
245
MARSHALL–MARCHETTI–KRANTZ URETHROPEXY
The urethrovesical junction is made to adhere firmly to the anterior vaginal wall by suturing
the vaginal tissue to the back of the symphysis pubis.
Back of
symphysis pubis
1. The urethrovesical junction is exposed 2. A Foley’s catheter in the bladder helps to

in the space of Retzius. Adhesions are identify the urethrovesical junction.
divided and all bleeding points picked Sutures pick up vaginal tissue on either
up. The urethra must be dissected to side and suture it to the pubic
within 1 cm of the external meatus. periosteum.
Bleeding from paravesical blood vessels is

common and a drain can be useful to reduce
the risk of a pelvic collection.
Periosteitis is sometimes a late complication and the operation is difficult in the presence of
excessive obesity. If too acute an angle is produced, the patient may have difficulty in
emptying her bladder.
246
BURCH’S COLPOSUSPENSION OPERATION
This operation elevates the anterior vaginal wall, bringing the urethra up with it.
1. Through a suprapubic incision,

the bladder neck area is
mobilised from the paravaginal
fascia. This procedure may be
accompanied by a good deal of
bleeding which can be controlled
by tightening the sutures.
2. The paravaginal fascia (and
some vaginal tissue as well) is
sutured on each side to the Bladder
inguino-pectineal ligaments,
using four or five sutures.
Inguino-
pectineal
ligament
The wound is closed with drainage as for the Marshall operation, and the possible
complications are similar. Suprapubic operations can be difficult when the patient is very
obese. This procedure may now be performed laparoscopically by appropriately trained
surgeons.
STAMEY NEEDLE SUSPENSION

PROCEDURE
The Stamey procedure is one of a number of
needle suspension procedures. They are less
invasive than conventional colposuspension.
A long Stamey needle is passed through a
small incision above the pubis on each side,
behind the pubic bones, into the vaginal lumen.
A nylon suture is attached to the vaginal wall
and tied to the rectus sheath, to elevate the
vagina and bladder base.
A cystoscope is passed to ensure that the
needle has not entered the bladder after each
pass of the Stamey needle.
247
SLING PROCEDURES
Slings can be made from either the patient’s own tissues (abdominal fascia) or synthetic
material. These materials are placed under the urethra to achieve compression when
the intra-abdominal pressure increases.
The synthetic materials are meshes, which are non-absorbable and permanent. They are
inserted vaginally either side of the urethra. They can be a source of infection and can
occasionally erode through tissues.
Tape
Bladder
Pubic bone (pelvis)

Urethra
TVT: retropubic approach
TVT: transobturator approach
248
TREATMENT OF DETRUSOR INSTABILITY
BLADDER RETRAINING
Women with symptoms suggestive of detrusor instability should be advised to cut out bladder
stimulants such as caffeine and alcohol.
This may be done as an inpatient or an outpatient, although inpatient treatment is more
effective. The patient is instructed to void only at defined intervals (to start with, this is
normally 1.5 h). When the patient can achieve continence between scheduled voiding, the
interval is increased gradually. A normal fluid intake should be allowed. Support and
enthusiasm from medical and nursing staff is required for this procedure to be effective.
DRUG TREATMENT
Antimuscarinic agents (oxybutynin, tolterodine). These agents act by blocking
parasympathetic stimulation of the detrusor muscle. Improvement is seen in 70% of patients
who can tolerate the drug.
Non-compliance is common, because of the anticholinergic side effects of dry mouth, blurred
vision, tachycardia, drowsiness and constipation.
Tricyclic Antidepressants (Imipramine)
These drugs are useful if nocturia is a significant compliant. Anticholinergic side effects may
be a problem.
Oestrogen
Although few trials have formally evaluated the efficacy of oestrogens, they appear to have a
role in postmenopausal women.
249
CHAPTER 13
DISEASES OF THE OVARY

AND FALLOPIAN TUBE
Clinical Features of Ovarian Tumours 252 Fibroma 272

Symptoms Due to Size 252 Androgen-Producing Tumours 273
Pressure Symptoms 252 Other Hormone-Producing Tumours 275
Differential Diagnosis 255 Carcinoid (Serotonin-Producing
Ascites 255 Tumour) 275
Uterine Fibroids 256 Struma Ovarii (Thyroid Type Tumour) 275
Pelvic Inflammation 257 Choriocarcinoma of the Ovary 275
Rectus Sheath Haematoma 257 Hormone Production by Non-Functioning
The Obese Abdominal Wall 257 Tumours 275
Broad Ligament Cysts 258 Surgical Treatment of Ovarian Tumours 276
Ectopic or Transplanted Kidney 258 Treatment of Ovarian Cancer 277
Retroperitoneal Tumours 258 Spread of Ovarian Cancer 277
Ovarian Cyst Accidents 259 Incision 278
Complications of Ovarian Tumours 259 Inspection 278
Clinical Features 259 Organs Removed 278
Differential Diagnosis 259 Cytology 278
Management 259 Staging of Ovarian Cancer 279
Rupture of Ovarian Cyst 260 Principles of Chemotherapy 281
Benign and Malignant Ovarian Tumours 262 Malignant Tumour Growth 281
Clinical Features 262 Mode of Chemotherapeutic Action 281
Investigation 262 Chemotherapeutic Agents in Ovarian
Histological Classification 263 Cancer 282
Risk Factors for Ovarian Cancer 264 Chemotherapy Toxicity 282
Carcinoma of the Ovary 264 Present Prognosis for Invasive
Ovarian Cancer Risk Factors 264 Epithelial Ovarian Cancer 282
Epithelial Ovarian Tumours 265 Broad Ligament Cysts 283
Serous Cystadenoma 265 Broad Ligament Cysts (Parovarian
Serous Cystadenocarcinoma 265 Cysts) 283
Mucinous Cystadenoma 266 Diagnosis 284
Mucinous Cystadenocarcinoma 266 Operation 284
Germ Cell Ovarian Tumours 267 Cysts of Kobelt’s Tubules,
Clinical Features 267 Hydatids of Morgagni,
Treatment 267 Fimbrial Cysts 284
Germ Cell Ovarian Tumours – Carcinoma of Fallopian Tubes 285
Undifferentiated 268 Pathology 285
Teratomata 269 Clinical Features 285
Other Ovarian Tumours 270 Clinical Staging 285
Hormone-Producing Tumours 271 Treatment 285
Oestrogen-Producing Tumours 272
DISEASES OF THE OVARY AND FALLOPIAN TUBE
CLINICAL FEATURES OF OVARIAN TUMOURS
SYMPTOMS DUE TO SIZE

Ovarian tumours are often large by the time the doctor is consulted because of the lack of any
specific symptoms. Menstrual function is usually normal, and any irregularity is attributed to
perimenopausal change. The patient may have noticed that her clothes are getting tight and
have attributed this to weight gain or, if the abdominal swelling has coincided with
amenorrhoea, she may believe herself to be pregnant.
PRESSURE SYMPTOMS
There are commonly increased frequency of micturition, gastrointestinal symptoms and a dull
pain in the lower abdomen. Very large tumours may cause shortness of breath, peripheral
oedema or varicosities in the legs.
252
Small tumours remain in the pelvis

and will only be detected on bimanual
examination or by ultrasound.
Larger tumours fill the pelvis and usually lie

between the uterus and the sacrum. If the
patient is not too obese, the uterus can be
distinguished on palpation as separate
from the tumour.
A tumour occupying the abdomen causes a midline swelling and is usually tense.
Little can be done at this stage to classify the tumour or exclude a malignancy. Further
information can be gained by undertaking imaging and tumour marker assessment including
CA125 and CEA (AFP, and B-HCG are included in younger patients).
253
If the patient is very thin,

irregularities may be palpated and
sometimes two tumours may be
suspected.
Some tumours of moderate size

may have a long pedicle composed of
the attenuated broad ligament and
the fallopian tube, which allows the
tumour to be displaced from side to side
or to occupy a high abdominal position.
Such cysts are at increased risk of
torsion.
The upper pole can usually be

distinguished and the lower pole
can be palpated per vaginam.
Adhesions, inflammation and
displacement of pelvic organs may
all exist along with a tumour,
making examination difficult.
254
An experienced examiner will recognise an ovarian tumour mainly because ovarian tumour is,
in the circumstances, the most likely diagnosis. All abdominal swellings should be subjected to
further imaging with a combination that may include ultrasound, computerised tomography
(CT) and magnetic resonance imaging (MRI) scan examination.
Two very obvious mistakes must be avoided.
1. The midline swelling due to a full 2. The 16-week pregnancy. The gravid
bladder. uterus at this stage has a very soft
isthmic region, which can resemble the
pedicle of a cyst.
ASCITES
A fluid thrill may be elicited from an ovarian cyst, and ascites and tumour may coexist; but as
a rule, the distinction should be easily made. The presence of ascites raises the suspicion of
cancer.
(See ‘Shifting dullness’, page 77.)
With ascites With ovarian cyst
The bowel floats on the fluid. The Percussion note is dull over the top of the
percussion note is resonant over the top of swelling and resonant in the flanks.
the swellings and dull over the flanks.
255
UTERINE FIBROIDS
A large midline intramural fibroid may be indistinguishable from a solid ovarian tumour until
the abdomen is opened and an entirely different surgical problem
encountered.
An ovarian tumour will displace the An intramural fibroid will obscure the
uterus forwards or downwards where it uterus. The cavity is often elongated.
may, sometimes, be identified on vaginal
examination.
Ultrasound examination should be able to distinguish between a fibroid and an ovarian cyst;
but many ovarian tumours are solid, and some fibroids undergo cystic degeneration. Vaginal
ultrasound gives a more detailed picture of the pelvic contents and a more precise diagnosis.
256
PELVIC INFLAMMATION
The swelling palpated per vaginam may
be due to an adherent mass of the uterus,
the tubes, ‘chocolate’ ovarian cysts,
and the bowel.
A pyosalpinx may give the same
sensation.
RECTUS SHEATH
HAEMATOMA
This rare condition presents as a fixed
abdominal mass, accompanied by
pain, and usually follows sudden
exertion such as severe coughing.
THE OBESE ABDOMINAL WALL

The obese patient may be convinced she has a tumour although she is only putting on
weight (phantom tumour). Palpation is difficult; but the percussion note in the lower half of
the abdomen will be resonant.
g
Mesenteric cyst These are all rarities in the UK but must be considered if
Hydatid cyst the physical signs are equivocal and especially if the swelling
Pancreatic cyst is not in the midline. Modern imaging techniques should
Large hydronephrotic kidney differentiate.
257
BROAD LIGAMENT CYSTS

The distinction is not likely to
be made before laparotomy,
even with imaging, if the
intact ovary is observed on
the back of the swelling.
ECTOPIC OR TRANSPLANTED
KIDNEY
These abnormalities are rare, but as they
are usually detected for the first time on
bimanual examination, they must be
borne in mind. The ectopic kidney can lie
anywhere in the pelvis and derives its
blood supply from the iliac vessels. The
ureter often runs a tortuous course.
RETROPERITONEAL TUMOURS
Retroperitoneal, in the surgical sense,
means behind the peritoneum of the
posterior abdominal wall. Such
tumours are rare but may arise from any
connective tissue, a lipoma being the
commonest. Examination reveals
a fixed tumour. The tumour may
displace the ureter and is in close
relation to the large vessels.
258
OVARIAN CYST ACCIDENTS
COMPLICATIONS OF OVARIAN
TUMOURS
Torsion of the Pedicle
(Axial rotation)
This is the commonest complication
and may occur with any tumour except
those with adhesions. The thin-walled
veins of the pedicle are obstructed first
while the arterial supply continues. As a
result there is haemorrhage into the
tumour and into the peritoneum, and
if not treated, significant infection
may occur.
CLINICAL FEATURES
Subacute
The patient complains of recurrent abdominal pain which passes off as the pedicle untwists.
There is a rise in pulse and temperature during the bleeding, and over a period, anaemia
develops.
Acute
The signs and symptoms are those of an acute abdominal condition. The problem becomes
one of a differential diagnosis to exclude those conditions in which a laparotomy is not needed
and those in which a laparoscopy may be useful.
Pain tends to be intense and continuous.
‘Surgical conditions’ (i.e. those conditions commonly seen and dealt with by a general
surgeon).
Acute appendicitis
Inflammatory bowel disease
Obstruction of bowel
Diverticulitis/diverticular abscess
MANAGEMENT
Patients presenting with an acute abdomen should first be stabilised. Once
stabilised, investigations to establish wellbeing and potential causes may then be
undertaken with blood tests and imaging. In cases where there is no resolution with
conservative treatment, then, a diagnostic laparoscopy and/or a laparotomy may be
needed. If the ovulation bleeding is greater than usual the woman may show quite,
marked signs of peritonism. The corpus luteum may thereafter become exaggeratedly
cystic and mislead the examiner.
259
RUPTURE OF OVARIAN CYST

Rupture may be either traumatic or spontaneous and may occur in the following conditions:
1. Following torsion of a pedicle. 2. During bimanual examination.
3. During labour when the cyst is 4. Spontaneous rupture. This is not

impacted within the pelvis. uncommon, especially with malignant
cysts, where the epithelial tissue outgrows
the connective tissue.
260
Differential Diagnosis for an Ovarian Cyst Accident
Acute pelvic inflammation with

tubo-ovarian abscess. Torsion of a fibroid
Normal organs very rarely, if ever, develop
Signs of infection are more marked.
axial rotation, but a uterus, enlarged by a
A cyst which has undergone rotation is
fibroid, may do so.
usually larger than the diffuse swelling of
pelvic inflammation.
Ectopic pregnancy Ovulation bleeding

The swelling is usually small although
extremely tender and the history usually
suggestive; but in a young woman this
condition must always be considered.
261
BENIGN AND MALIGNANT OVARIAN TUMOURS
Ovarian cysts can grow to a significant size before causing any symptoms. Ovarian cancer has
been described as the ‘silent killer’ as approximately 60% of women present with advanced
disease. While many patients, in retrospect, do have symptoms, they are non-specific and do
not at first seem to be due to ovarian disease.
CLINICAL FEATURES
The patient usually has non-specific symptoms and appears well. Symptoms may
include abdominal pain, bloating, changes in bowel habits, urinary symptoms and pelvic
symptoms. Not unsurprisingly, many women are initially misdiagnosed with irritable
bowel syndrome and/or are initially referred for general surgical review. However, referral
from primary care was not found to be significantly delayed and did not have an impact
on survival.
INVESTIGATION
Once a pelvic mass is suspected it should be investigated with tumour markers, as previously
discussed. Imaging with ultrasound will delineate complex features (ascites, bilateral masses,
thick septa, metastatic deposits, solid areas) and allow the calculation of a risk of malignancy
index (RMI). This is calculated as below:
Score Menopausal status Ultrasound

1 Premenopausal 1 abnormality
3 Postmenopausal 2 or > abnormality
RMI ¼ CA125 VALUE MENOPAUSAL SCORE ULTRASOUND SCORE
Using a cut-off value of 200, the RMI has an 80% positive predictive value for ovarian
malignancy. CT scanning will provide further information on the extent of disease. Using both
the RMI and CT findings, patients can then be referred directly to specialist gynaecological
oncology surgeons.
262
BENIGN AND MALIGNANT OVARIAN TUMOURS
HISTOLOGICAL CLASSIFICATION
Ovarian tumours can arise from the ovarian epithelium, stroma or the germ cells. The
embryonic coelom, from which the epithelium develops, also gives rise to the Müllerian duct
from which develop the structures of the genital tract; and it is this common origin which
accounts for the great variety of epithelial patterns encountered.
Epithelial Tumours
Serous cystadenoma or cystadenocarcinoma.
Mucinous cystadenoma or cystadenocarcinoma.
Endometrioma or endometrioid carcinoma.
Clear cell carcinoma.
Brenner tumour.
Sex Cord Stromal Tumours
Fibroma or sarcoma.
Oestrogen-producing:
Granulosa cell tumour.
Thecoma.
Androgen-producing:
Sertoli-Leydig cell tumour (arrhenoblastoma).
Hilar cell tumour.
Lipoid cell tumour.
Germ Cell Tumours
Dysgerminoma.
Teratoma.
Gonadoblastoma.
Yolk sac tumour.
Carcinoid hormone-producing
Thyroid tumour choriocarcinoma
There is one well-known secondary tumour of the ovary, the Krükenberg tumour, which is
secondary to a Gastric carcinoma. This term is now being widely used to describe metastases
to the ovary from other cancers such as breast and colon cancers.
263
RISK FACTORS FOR OVARIAN CANCER
CARCINOMA OF THE OVARY

In developed countries, women have a lifetime risk of about 1.4% for developing ovarian
cancer, which is slightly greater than the risk of cervical or endometrial cancers, but well below
the 13% lifetime risk of breast cancer.
5–10% of ovarian cancers are related to genetic factors such as BRCA gene mutations or the
Lynch syndrome of familial breast, colorectal and ovarian cancers. The induction of ovulation
with Clomiphene for more than a year carries a 10-fold increased risk of ovarian cancer. Long-
term oral contraceptive use reduces the incidence of ovarian cancers.
BRCA 1
The mutation is located on chromosome 17. Those affected carry a 30–60% risk of developing
ovarian cancer. Survivors of breast cancer have a 13% risk of developing ovarian cancer within
10 years.
BRCA 2
The mutation is located on chromosome 13. Those affected carry a 20% risk of developing
ovarian cancer. Survivors of breast cancer have a 7% risk of developing ovarian cancer within
10 years.
If family members are identified as having a mutation, then, they may be offered risk reducing
surgery such as prophylactic bilateral salpingo-oophorectomy.
OVARIAN CANCER RISK FACTORS
Increased Decreased
Low parity High parity
Infertility Combined contraceptive pill
Endometriosis Breastfeeding
Ovarian metastases from extra-genital tumours are not uncommon. The commonest
sites of primary growth are the breast, stomach and the large intestine. They usually
occur in functioning ovaries and their importance lies in the fact that these metastases
grow to a large size while the primary growth is small and give rise to no clinical
manifestations. The metastases usually reproduce the histological characteristics of
the primary cancer.
264
EPITHELIAL OVARIAN TUMOURS
SEROUS CYSTADENOMA
It can be a unilocular or a multilocular cyst. They are the most common benign epithelial
tumours and form 40% of all epithelial tumours. They are bilateral in 10% of cases. They
show one of three structures:
(1) A simple cystic form with a smooth

surface and a smooth lining.
(2) A cystic structure with intracystic
papillary formations. The latter may
be sessile buttons or pedunculated,
frond-like projections.
(3) An adenomatous form where many
of the loculi are small and the
papillary structures are solid and
complex.
Microscopically, the tumour has a fibrous capsule.

Septa support the cysts which are lined by cuboidal
epithelium and contain thin serous fluid.
SEROUS CYSTADENOCARCINOMA
This is by far the commonest primary carcinoma, and in over half the cases, it is bilateral.
The cysts are always of the papillary type and the epithelium burrowing through the capsule
produces papillary processes on the serous surface. Extension of the growth to the pelvis and
adjacent organs fixes the tumour. It commonly spreads across the peritoneal surface tissues
becoming densely adherent, but at times, it can invade tissues directly. Ascites are frequently
present.
265
EPITHELIAL OVARIAN TUMOURS
MUCINOUS CYSTADENOMA
It is a unilocular or multilocular cyst of an ovary lined by a tall columnar epithelium,
resembling that of the cervix or the large intestine. They can be large and may reach immense
proportions, occupying the whole peritoneal cavity and compressing other organs.
It may occur at any age.
The surface of the

cyst is often
completely
smooth and
round, but may be
slightly nodular,
due to the
projecting loculi.
The cut surface of the cyst is

multilocular and has a mosaic pattern.
Microscopically, the tumour has an
outer fibrous capsule from which
the septa extend to support the walls
of the cysts. The latter are lined by
tall columnar epithelium with basal
nuclei and contain a gelatinous
glycoprotein or mucin.
The signs and symptoms are similar to those generally associated with any non-functioning
ovarian tumour. Rupture may occur and seeding of the epithelium on the peritoneal surface
may cause a pseudomyxoma peritonei.
Pseudomyxoma Peritonei
This rare condition, occasionally, but not inevitably, follows the rupture of a mucinous
cystadenoma (page 260). The epithelial cells get implanted on the peritoneum and continue
to secrete mucin. The abdominal cavity is eventually filled with the jelly, while the secreting
cells spread over the parietal and the visceral peritoneum. The disease develops slowly over
several years and may require multiple operations to strip the mucin plaques. Current research
is focusing on hot intraperitoneal chemotherapy. This disease is, commonly, chronically
progressive.
MUCINOUS CYSTADENOCARCINOMA
This is only a third as common as the serous variety. Malignancy in a mucinous cyst is
characterised by the formation of areas of solid carcinoma in the wall. The cells are columnar,
266 show mitoses and tend to form glandular structures.
GERM CELL OVARIAN TUMOURS
Germ cell tumours may be:

Undifferentiated Dysgerminoma
Gonadoblastoma
Differentiated Embryonal
Teratomas
Extra-embryonal
Yolk sac tumour
Choriocarcinoma
CLINICAL FEATURES
97% of these tumours are benign but they comprise 20% of all ovarian tumours. Patients are
usually young, in the 20–30 year-old age group. They may present with an acute abdomen as
the pelvic masses undergo torsion or rupture. In some, the pain can be of a more chronic
nature. However, many women are often diagnosed incidentally, while undergoing
investigations for other reasons.
TREATMENT
This will depend upon the age of the patient, the extent of the disease and fertility
wishes. Where fertility is not an issue, then usually, bilateral salpingo-oöphorectomy
and hysterectomy are indicated. Where fertility preservation is an important issue,
evidence supports the strategy of unilateral salpingo-oöphorectomy with
thorough assessment. All disease should be cyto-reduced at a laparotomy to the
smallest possible level.
Disease is staged as for an ovarian carcinoma. If the disease is greater than Stage 1A, then
postoperative chemotherapy is indicated to reduce the risk of recurrence and provide patients
with a good long-term outcome or even a cure.
267
GERM CELL OVARIAN TUMOURS - UNDIFFERENTIATED

Dysgerminoma
This is the only solid ovarian tumour of characteristic appearance. Usually ovoid with a
smooth capsule, it is of rubbery consistency and greyish colour. It is most common in the
younger age groups and is bilateral in 20%. About 70% of the cases are Stage 1A at diagnosis.
Lactate dehydrogenase (LDH) levels may be elevated. Survival rates are greater than 90% for
stage 1 tumours.
Microscopically, it consists of masses of large,
clear, epithelial cells with large nuclei, resembling
primitive germ cells, in cords or alveoli. Fine
connective tissue that has been infiltrated by
lymphocytes separates the bundles of epithelial
cells. The malignancy varies, but many appear to
be relatively benign and do not recur. Those in
children tend to be more malignant.
Gonadoblastoma
This is a tumour associated with dysgenetic
gonads, usually streak gonads. The patient is an apparent female and may have a diminutive
uterus, tubes and vagina, but usually there is a sex chromosome mosaicism such as 45X/
46XY.
The tumour is composed of two types of cells: (a) a large primitive germ cell and (b) small
cells of the granulosa type. Call-Exner bodies (small rosettes) may be seen in the latter. These
two types of cells form epithelial islands in a stroma which may contain Leydig-like cells.
Sometimes, the germ cells may undergo rapid proliferation and give rise to a dysgerminoma.
Some of the dysgerminomata in children
probably arise in this way. Choriocarcinoma
may also originate in a gonadoblastoma.
About 60% of women show some signs of
virilisation and 17-ketosteroid excretion
may be raised.
268
TERATOMATA
These are broadly divided into mature and immature forms.
Mature Cystic Teratoma or Dermoid
This is one of the commonest ovarian tumours and is usually diagnosed during the child-
bearing period, but may be found at any age and may be bilateral in 10% of cases.
It is often ovoid. The wall consists of dense fibrous tissue lined by stratified squamous
epithelium. The cyst may contain sebaceous glands, teeth, hair, nervous tissues, cartilage,
bone, respiratory and intestinal epithelium and thyroid gland tissue.
Thick yellow sebaceous
material fills the cyst and
if it ruptures o a severe
granulomatous reaction
can occur.
They are particularly liable to
have a long pedicle and easily
undergo torsion in up to 15% in
some series. Malignant
transformation is rare and an
ovarian cystectomy is adequate
for most cases.
Immature Teratoma
These occur at an earlier age than dermoids, often in childhood. They are solid
and may contain any tissue from the three germinal layers, mixed in a completely
disorderly fashion. They are particularly liable to undergo malignant change, with
the malignancy arising in any one of the tissues present.
269
Yolk Sac Tumour

This is a rare tumour found in children and young adults. It has a variable histological
structure and is highly malignant. The main interest lies in the fact that it produces alpha-
fetoprotein and therefore its blood levels can be used as a diagnostic test and as a means of
monitoring response to treatment.
Choriocarcinoma is mentioned in the succeeding part that deals with hormone-producing
tumours.
OTHER OVARIAN TUMOURS

Krukenberg Tumour
This is a secondary carcinoma of the ovary. It is remarkable for its characteristic histological
appearance and the fact that the primary growth, which is usually seen in the stomach and less
commonly in the large intestine, is often clinically silent. The ovarian tumours are frequently
bilateral, of equal size, smooth and lobulated. They remain freely mobile with no adhesions.
Being firm and fibrous in appearance they are frequently mistaken for fibromata, but these are
usually unilateral.
Histologically, they have a well-defined

appearance. There is a very cellular stroma,
resembling a sarcoma, in which there are
large epithelial cells lying singly or in alveoli.
These epithelial cells have a clear
cytoplasm with a crescentic nucleus that
has been pushed to one side, giving a
signet-ring appearance that is typical.
The cytoplasm is full of mucin.
The majority of patients with this tumour
have a poor prognosis.
270
HORMONE-PRODUCING TUMOURS
Brenner Tumour
A benign tumour, mainly solid and most common in the 6th decade, it is composed of fibrous
and epithelial elements in varying proportions. It forms 2% of all solid ovarian neoplasms.
It is usually solid and resembles a fibroma. Occasionally, there may be microcysts or even an
associated large mucinous cyst. Microscopically, it is mainly composed of fibrous tissue with
small islands of clear epithelial cells of squamous appearance. Sometimes the islands become
cystic and the epithelial cells become mucinous.
271
The most common tumours of this kind are steroid-producing, particularly sex steroids. Both
androgenic and oestrogenic effects have been described with every histological variety as some
tumours have a mixed steroid cell composition, but certain tumours of well-defined
histological structures are commonly associated with the production of only one type of
steroid.
OESTROGEN-PRODUCING TUMOURS
These belong to the granulosa-theca cell group and are found in all ages. They account for 3%
of all solid tumours of the ovary.
Oestrogen excess can cause hyperplasia of:
1. Myometrium ! enlarged uterus.
2. Endometrium ! Irregular and/or postmenopausal bleeding.
3. Breast tissue ! enlargement, tenderness of breasts.
In childhood there is accelerated skeletal growth and appearance of sex hair.
5% of these occur in children ! precocious puberty.
60% occur in child-bearing years ! irregular menstruation.
30% occur in postmenopausal women ! postmenopausal bleeding.
Diagnosis
Granulosa cell tumour in childhood may be found as the cause of female precocity with a
pelvic mass being demonstrated on imaging. Following puberty, and even into
postmenopausal years, diagnosis on clinical grounds is difficult owing to the multiplicity of
factors that can cause irregular vaginal bleeding. Often, the diagnosis is made following the
removal of an abnormal cyst or ovary.
Pathology
These tumours vary very much in function. Large tumours may be virtually functionless. In
childhood and early adult life, the tumours are composed mainly of granulosa cells. In later
life they are usually thecomata. The granulosa-cell type of growth should be considered as a
carcinoma. Recurrence may occur many years after removal of the primary growth. It is not
possible to accurately correlate malignancy with histological appearances. In 14% of the cases
endometrial hyperplasia becomes atypical and an
endometrial carcinoma develops.
FIBROMA
This is composed of fibrous tissue and resembles
the fibromata found elsewhere. It is most common
in the elderly and accounts for 4–5% of all ovarian
neoplasms.
The fibroma is believed by many to be a thecoma
which has undergone fibrous transformation. It is
sometimes associated with Meig’s syndrome
where a pleural effusion is also noted.
272
ANDROGEN-PRODUCING TUMOURS
Three distinct types of masculinising ovarian tumour are recognised: (a) Sertoli-Leydig cell tumour
(arrhenoblastoma), (b) Hilar cell tumour, (c) Lipoid cell tumour. All the three can cause amenorrhoea.
Sertoli-leydig Cell Tumour
This is a rare tumour and accounts for much less than 1% of all ovarian tumours. It occurs in
young adult females. Clinically two stages are recognised:
Pathology
It usually appears as a small white or yellowish tumour within the ovarian substance. Cystic
degeneration may occur. These tumours are usually only of a low-grade malignancy.
Histologically it consists of primitive
tubules surrounded by Leydig cells
which contain crystalloids of Reinke.
These are rod-shaped structures in
the cytoplasm of Leydig cells and are
said to be diagnostic of these cells.
273
ANDROGEN-PRODUCING TUMOURS—(cont’d)
Biochemistry
The symptoms are due to the secretion of testosterone. The quantities of 17-ketosteroids are
within the normal range, unlike in adrenal virilising tumours where their levels may be
elevated. Direct estimations of blood testosterone can be made. Some of these tumours
secrete oestrogens. Removal of the tumour results in regression of symptoms in the same
order as their appearance. Menstruation returns within a month or two. Voice changes tend to
be permanent.
Hilar Cell Tumour
This is a very rare tumour found in postmenopausal
women. Defeminisation occurs but signs of virilism are
usually mild, consisting of hirsutes, alopecia and an
enlargement of the clitoris.
Pathology
Hilar cell tumours are small, brown, simple tumours of
the ovarian hilum consisting of polyhedral Leydig cells.
Crystalloids of Reinke are occasionally present.
17-ketosteroids are usually within the normal
postmenopausal range. Small quantities of androgen
are produced.
Lipoid Cell Tumour (Ovoblastoma,
Masculinovoblastoma, Adrenal-like
Tumour)
This is also a rare tumour that causes masculinisation and
produces symptoms and signs of Cushing’s syndrome such
as skin striae, obesity, polycythaemia, impaired glucose
tolerance and hypertension.
Pathology
The tumour consists of cells with high lipid content
and are commonly large and yellowish.
Unlike other virilising tumours, the 17-ketosteroid
output is greatly increased and the excretion of
17-hydroxycorticosteroids is also raised. ACTH or
chorionic gonadotrophin will cause a further increase,
but dexamethasone does not diminish the output, thus
helping to differentiate the condition from virilising
adrenal tumours.
274
OTHER HORMONE-PRODUCING TUMOURS
CARCINOID (Serotonin-Producing Tumour)

This tumour arises in association with a cystic teratoma of the ovary from cells related to the
respiratory or intestinal epithelium that are sometimes found in these cysts.
It may give rise to a typical carcinoid syndrome with patchy cyanosis, flushing, diarrhoea,
intestinal colic, oedema and cardiac failure due to a tricuspid valve lesion. Usually the
syndrome does not appear until the tumour has metastasised to the liver.
STRUMA OVARII (Thyroid Type Tumour)

Small foci of thyroid tissue are common in ovarian
teratomata, but large amounts are rare and functioning
thyroid tissue is even rarer. When the thyroid tissue
actually proliferates and forms a tumour, 5–10% of
these become malignant.
CHORIOCARCINOMA OF THE OVARY

This is an extremely rare tumour of the ovary. It is also known as a non-gestational
choriocarcinoma, in that it does not arise as a consequence of conception. Most commonly,
it is associated with a dysgerminoma and both, in turn, may be derived from germinal
cells in a dysgenetic gonad. A syncytiotrophoblast is always present, but sometimes a
cytotrophoblast is also formed. The principal hormone produced is b-human chorionic
gonadotrophin (bHCG). This can prove to be useful in the diagnosis and follow-up of
these tumours. Metastases may occur, as in any choriocarcinoma.
HORMONE PRODUCTION BY NON-FUNCTIONING TUMOURS

Occasionally, the presence of tumour growth in the ovary induces a thecal transformation of
the ovarian stroma which in turn produces steroids, sometimes androgenic, but more
commonly oestrogenic. This has been reported in association with benign and malignant
cysts, Brenner tumours, fibroma and secondary carcinoma of ovary. The secretion of steroids
can result in menstrual disorders, and in the case of androgens, virilisation.
275
SURGICAL TREATMENT OF OVARIAN TUMOURS
Benign ovarian tumours that are greater than 10 cm in diameter must be removed, but
clinically and ultrasonically diagnosed cysts below 10 cm in women under 35 years of age may
be reviewed in a few months if there is no suspicion of a malignancy. A follicular or luteal cyst
may resolve spontaneously.
Cystectomy: It involves enucleation of

the tumour from its capsule of ovarian
tissue, which is then rolled into a little
bundle and held together with sutures,
thus preserving ovarian function.
Indications:
A tumour that is apparently benign.
This operation would not be feasible in
the case of a very large tumour, or
where there had been previous
inflammation.
Ovariotomy: Removal of an ovary
containing a tumour. (Removal of an
ovary not containing a tumour is called
oöphorectomy.)
Indications:
(a) Malignancy. (The uterus and other
ovary are also removed.)
(b) The patient declines a hysterectomy
and the other ovary is normal.
Laparoscopy: This may be diagnostic and/

or therapeutic – small benign cysts may be
removed. Where a malignancy is not
suspected on the basis of preoperative
investigations, some larger simple cystic
lesions can be placed in a laparoscopic bag
for removal and then aspirated to reduce
their size before removal.
276
TREATMENT OF OVARIAN CANCER
Epithelial ovarian cancer is now the most frequent cause of death from gynaecological
malignancy. The principles of treatment are:
1. Surgical staging.
Ovarian carcinoma is staged surgically, so laparotomy is an essential part of its management in
most patients.
2. Surgical debulking of tumour volume.
Surgical removal of as much malignant tissue as possible, even if this should call for resection
of structures outside the normal field of the gynaecologist.
3. Adjuvant chemotherapy.
This is followed-up with intensive chemotherapy. Currently, the most commonly used
regimen is taxanes (paclitaxel) combined with the platinum compound, carboplatin.
Surgery remains an important aspect of management and referral to a specialised
gynaecological oncology surgeon at the initial laparotomy has been shown to provide the best
outcomes. Co-operation with a colorectal surgeon may be necessary. Increasingly, some
centres offer chemotherapy prior to surgery, with an operation after three of the six planned
chemotherapy treatments so as to reduce the incidence of surgical morbidity.
The diagnosis of ovarian cancer is often delayed due to the non-specific nature of the
symptoms. Accordingly, as many as 66% of patients will be at an advanced stage, at the time
of presentation.
SPREAD OF OVARIAN CANCER

It is important to know the direction of spread
of ovarian cancers, so that the true extent of Pleura
Diaphragm
the disease and the symptoms that it may
induce can be recognised and managed. Liver Stomach
1. Direct Omentum
Serosal
Spread directly into neighbouring
bowel
structures – uterus, bladder or bowel. implants
2. Transcoelomic Colon Nodes
Cancer cells are carried across the
peritoneum and achieve widespread seeding. Ovaries
This results in tumour deposits in the Pelvic
peritoneum, bowel mesentery, visceral peritoneal
surfaces and the omentum. The tumour implant
marker CA125 is usually raised in advanced
ovarian cancer and is used to assess the
response to chemotherapy.
3. Lymphatics
Ovarian drainage is to the para-aortic glands, but sometimes also to the pelvic and even the
inguinal groups. Cells seeded on to the peritoneum are drained via the lymphatic channels on
the underside of the diaphragm into the subpleural glands and thence to the pleura.
4. Blood stream 277
Blood spread is usually late and is to the liver and the lungs.
TREATMENT OF OVARIAN CANCER
All patients with an elevated risk of malignancy should be discussed at a preoperative

multi-disciplinary meeting. The management of all patients remains as a combined surgical
and chemotherapeutic regimen – primary surgery followed by adjuvant chemotherapy.
Surgery may be delayed until three cycles of chemotherapy have been administered in selected
cases – ‘delayed primary surgery’.
The objectives are:
1. To classify the growth according to its extent of spread (staging) as accurately as possible.
2. To remove as much cancerous tissue as possible (‘surgical debulking’; ‘cyto-reductive treatment’).
Chemotherapy is recommended for all stages of ovarian tumour greater than Stage 1B grade 2.
INCISION
A vertical incision, which can be extended, is essential to allow a full inspection. Reduction of
a cyst by tapping and extraction through a suprapubic incision is not an acceptable practice.
Surgical rupture of a cyst will increase its staging to a 1C tumour from what may have been a
Stage 1A tumour. This has important implications for patient management.
INSPECTION
The entire peritoneal cavity must be palpated, including the liver, subdiaphragm, bowel and
mesenteries, omentum and nodal areas. Suspicious areas are to be biopsied or removed.
ORGANS REMOVED
These must always include the uterus, tubes, ovaries, appendix and the omentum. Partial
resection of bladder and bowel may also be required, but an epithelial cancer tends to spread
over invaded tissue rather than penetrate it, and a plane of cleavage can often be found. The
best patient outcomes are
associated with either a
complete or an optimal
cytoreduction. The
definition of optimal can
vary but at least to a size
of <2 cm largest tumour
deposit or, preferably
<1 cm largest tumour
deposit.
CYTOLOGY
Before handling the
tumour, specimens of
ascitic fluid or peritoneal
saline washings for
cytological examination
must be taken.
278
STAGING OF OVARIAN CANCER

Positive
STAGE I Growth limited to ovaries. ascites or
peritoneal
washing
IA. Limited to one ovary. IB. Limited to both ovaries. IC. Ascites or positive
No ascites. No ascites. peritoneal washings also
present or tumour on
surface of one or both
ovaries or capsule ruptured.
STAGE II Pelvic extension.

Positive
ascites or
peritoneal
washing
IIA. Spread to uterus/tubes. IIB. Spread to other pelvic IIC. IIB with ascites or positive
tissues. peritoneal washings or tumour on
surface of one or both ovaries or
capsule ruptured.
279
STAGING OF OVARIAN CANCER
Stage III Extrapelvic, Stage IIIA: microscopic

intraperitoneal spread and/or peritoneal metastasis
retroperitoneal or inguinal positive beyond pelvis, including
peritoneal surface of liver
nodes, or superficial liver
metastases.
Stage IIIB: macroscopic

peritoneal metastasis
beyond pelvis 2 cm
in greatest dimension,
including peritoneal
surface of liver
Tumour on
liver capsule
Omental
cake
Lymph node
metastases IIIC Abdominal implants >2 cm
diameter or positive retroperitoneal or
inguinal nodes.
Pleural fluid Lung parenchymal

(positive metastases
cytology)
STAGE IV Distant
metastases or pleural
effusion with positive
cytology or parenchymal
liver metastases.
280
Liver parenchymal
metastases
PRINCIPLES OF CHEMOTHERAPY
MALIGNANT TUMOUR GROWTH

Tumour growth is a result of the failure of normal cell cycle control and a failure of apoptosis
(the natural mechanism for removal of abnormal cells). Tumour cells multiply at the same
rate or more slowly than normal cells, but have more actively dividing cells that are not
subjected to the same physiological control, so that a cancer gradually develops.
MODE OF CHEMOTHERAPEUTIC ACTION
Antimetabolite
5-fluorouracil
X DNA
Alkylating agent
Cisplatin RNA
Carboplatin
Antimitotic Nuclear
Liposomal doxorubicin receptor
Hormonal Cell division

Progestogens apparatus
Oestrogen receptor modulator
Aromatase inhibitor
Plant derivatives
Taxane derivatives (Pacific yew tree)
Paclitaxel
281
CHEMOTHERAPEUTIC AGENTS IN OVARIAN CANCER
The current first line agents used in ovarian cancer treatment are carboplatin and paclitaxel.
Carboplatin is an alkylating type agent that forms DNA cross links that prevent cell
replication, ultimately leading to cell death. Paclitaxel similarly prevents cell replication by
acting on another aspect of the cell, namely interfering with cell microtubule formation.
The antimetabolites inhibit DNA synthesis by disrupting essential metabolic events in nucleic
acid synthesis. Another currently used treatment is liposomal doxorubicin which is an anti-
mitotic agent with a complex mechanism of action that includes prevention of RNA synthesis,
where the agent is delivered in liposomes to enhance its mechanism of action.
Hormonal therapies are employed to either directly bind to nuclear steroid receptors or
influence the production of steroids that can bind to the nuclear steroid receptors. By binding
to such receptors they can influence steroid gene regulation to bring about an antitumour
effect. Response rates have been noted in ovarian cancer treatment and they are well-tolerated
therapies.
Targeted anticancer therapies are currently being investigated as new therapies to increase the
efficacy and decrease the toxicity of traditional chemotherapy. They target different pathways
that are important for cancer growth and metastasis such as angiogenesis, cell cycle and the
apoptotic pathways.
Chemotherapy trials are leading to evolutions of standard therapies. It has been noted that
patients involved in chemotherapy trials have better outcomes than those not involved in these
trials.
CHEMOTHERAPY TOXICITY
Common adverse effects of chemotherapy include nausea, vomiting and fatigue. Such side
effects can be controlled well with antiemetics. Other side effects are related to the individual
drugs. Carboplatin is well tolerated in general but is often myelosuppressive, necessitating
blood transfusions or delayed treatments. Paclitaxel will lead to alopecia and it can also cause
neuropathy, arthropathy and myalgia. Liposomal doxorubicin has a particular side effect called
palmar/plantar erythema and it can also be cardiotoxic.
PRESENT PROGNOSIS FOR INVASIVE EPITHELIAL OVARIAN CANCER
Stage 5-year survival (%)

I 76
II 37
III 27
IV 15
Borderline epithelial tumours have excellent 5-year survival rates of 90–95% and a 15-year
survival rate of 70–85%.
282
BROAD LIGAMENT CYSTS (Parovarian Cysts)
The epoophoron lies in the mesosalpinx and is

parallel to the uterus. At about the level of the
internal os it penetrates the muscle of the uterus and
descends into the cervix and vaginal wall, to the
hymen.
Parovarian cysts derived from the epoophoron
are unilocular and contain watery fluid without
mucin. The wall is thin and lined with a layer of
cuboidal cells that can sometimes be ciliated.
If one imagines any of these locations (marked X)

expanding like a balloon, the resulting
displacement of tissues is easily understood.
283
DIAGNOSIS
On palpation, the cyst, which is not mobile, may displace the uterus and may be closely
related to it. An ovarian cyst with adhesions may feel very similar and it is seldom possible to
distinguish between the two before a laparotomy.
OPERATION
Great care must be taken while identifying tissues, as the location of the original site of the cyst
determines its displacement and its characteristics.
In the outer third of the broad ligament, the cyst tends to develop a pedicle.
In the middle of the broad ligament, the tumour is sessile but relatively fixed.
The ovarian vessels are displaced and may be stretched leading to interference with the
ovarian blood supply.
It is possible for the ureter and uterine artery to be displaced outwards, but usually they are
below and medial to the cyst.
The tumour may increase in size and strip the peritoneum off the pelvic walls and spread
laterally and posteriorly, obliterating the Pouch of Douglas.
The broad ligament is incised anteriorly
where the blood vessels are few, and the
cyst is enucleated digitally. The oozing
area is now exposed and should be
obliterated. Care is necessary to avoid
damage to the blood vessels, ureter and
bladder. Redundant broad ligament may
have to be excised.
CYSTS OF KOBELT’S TUBULES, HYDATIDS OF MORGAGNI,

FIMBRIAL CYSTS
These are names given to small cysts found in the mesosalpinx and around the terminal
portion of the fallopian tubes. They are of indeterminate embryonic origin and are of no
clinical significance.
284
CARCINOMA OF FALLOPIAN TUBES
The fallopian tubes are often involved in an ovarian carcinoma but an isolated fallopian tube
carcinoma is very rare. There is, however, some evidence to suggest that ovarian carcinomas
in BRCA gene mutation patients may actually arise from the distal fallopian tube.
PATHOLOGY
The growth is usually an
adenocarcinoma of the tubal
epithelium which grows inwards
and secretes a copious amount of
serosanguinous fluid which
discharges per vaginam, if the
proximal tube remains patent. This
classical sign of a tubal carcinoma
is rare.
CLINICAL FEATURES
The patient is usually in her fifties and often nulliparous or of low parity. She may complain
of postmenopausal bleeding, pain, and sometimes, a watery vaginal discharge. In the absence
of definite symptoms the diagnosis is often made rather late. Pelvic signs suggestive of
infection in a postmenopausal woman should always be investigated. The differential
diagnosis includes carcinoma of the uterus or the ovary.
Aetiology is unknown, but increasing evidence suggests that some are BRCA linked.
CLINICAL STAGING
Stage I confined to one or both tubes
Stage II pelvic extension
Stage III spread to other structures (omentum, bowel, etc.), positive retroperitoneal or
inguinal nodes or superficial liver metastases
Stage IV distant metastases (including bladder), pleural effusion with positive cytology
or parenchymal liver metastases
TREATMENT
Total hysterectomy and bilateral salpingo-oöphorectomy should be done as a minimum,
followed by chemotherapy, as for an ovarian carcinoma.
285
CHAPTER 14
COMPLICATIONS OF
GYNAECOLOGICAL SURGERY
Urinary Tract Injuries 288

Injury to the Ureter 289
Management of Ureteric Injury 290
Bowel Injury 291
Fistula Formation 292
Urinary Fistula 292
Adhesions 293
Lymphoedema and Lymphocyst 294
Infectious Morbidity 294
Hernia 294
Venous Thrombosis 295
Pathology 296
Sites of Thrombus Formation 297
Clinical Features of Deep Venous Thrombosis 298
Investigations for Deep Venous Thrombosis 299
Fibrin D-Dimer Assay 299
Ultrasound 299
Methods of Thromboprophylaxis 300
General Measures 300
Mechanical Methods 300
Unfractionated and Low Molecular Weight
Heparins 301
Treatment of DVT 301
Pulmonary Embolism 302
Peripheral Pulmonary Embolism 302
Central Pulmonary Embolism 302
Pulmonary Embolism Management 303
Investigations 303
Treatment of Pulmonary Embolus 305
Mortality 306
COMPLICATIONS OF GYNAECOLOGICAL SURGERY
URINARY TRACT INJURIES
Gynaecological surgery, in common with other surgical specialties, can be associated with
complications. Most complications are minor, self limiting and have no long-term
consequence for the patient, but they must still be avoided where possible, and actively
managed where necessary, to make sure they do not become major complications.
Gynaecological surgery involves close dissection to viscera including the bladder, rectum,
ureters as well as the great vessels of the pelvis. Complications can occur during difficult
surgical dissections, especially when the anatomy is distorted (e.g. malignancy, endometriosis
or infection).
Other complications, such as pulmonary embolus, myocardial infarction, pneumonia, or fluid
or electrolyte imbalance are common to all surgery. For the purposes of this chapter, the most
common complications related only to gynaecological surgery will be discussed.
URINARY TRACT INJURIES

Bladder Injuries
If a bladder injury is suspected intraoperatively, it can be localised by intravenous injection of
indigo carmine, retrograde instillation of methylene blue through the urethral catheter or by
opening the dome of the bladder and inspecting the mucosa. Subtle injuries can also be
diagnosed using cystoscopy. Early involvement of an urologist is advised.
Primary closure of a cystotomy can be performed using a simple one or two-layered running
closure with absorbable suture.
In general, it takes approximately 3–4 days for the bladder to re-epithelialise and about 3
weeks to regain its normal strength. A catheter can be left in situ for about 7 days with a
cystogram performed just prior to its removal, to confirm healing.
In circumstances where a primary closure is difficult (e.g. vaginal surgery, unstable patient,
history of pelvic irradiation) and there is a small injury (3 cm or less) in the bladder dome, a
suprapubic catheter can be placed. A Foley catheter is placed through the cystotomy, with the
bulb remaining in the bladder and the catheter exiting through a stab wound in the lower
abdomen.
Women who have received prior lower pelvic radiation or have severe bladder injury require a
stronger repair. A carefully dissected omentum, from the hepatic flexure to the splenic flexure,
can be used over the two-layer closure to provide neovascularity.
After any repair to the bladder, it must be ensured that the ureteral orifices near the trigone are
not compromised. This can be done by passing a stent, retrograde from the bladder toward
the kidney or by dissection and visual identification of the distal ureter.
288
INJURY TO THE URETER
The ureter will occasionally be damaged no matter how much skill and care are exercised. It is
essential to directly visualise the ureters at surgery to check for peristalsis, gross dilation
(obstruction) or urine leakage, in order to prevent ureteral damage.
The operating surgeon must have a thorough knowledge of the location of the ureter and
where it is most susceptible to trauma. The three most common sites of ureteral injury, in the
order of frequency of occurence are:
1. While dividing the infundibulopelvic ligament
2. During division of the uterine artery
3. When mobilising the bladder.
The ureter’s course is to some extent variable, and when under pressure, it will gradually
change its position in the pelvis. A large tumour filling the pelvis will displace it laterally.
A tumour in the broad ligament may displace the ureter outwards and upwards. Duplex
(double) ureters are occasionally met with.
A ureter displaced by
a fibroid which has
occupied the broad
ligament.
Radical surgery may destroy so much of the pelvic blood

supply that the pelvic ureter becomes ischaemic, leading
to fibrotic narrowing or fistula. Damage to the blood
vessels may also be produced by pelvic irradiation.
289
MANAGEMENT OF URETERIC INJURY
Ureteric injury should be managed in consultation with a

urologist, or a gynaecologist with subspecialty training in
urogynaecology.
1. Types of ureteric injury identified at operation.

a. Crush injury from clamp or ligature.
The clamp or ligature should be removed,
and a ureteric stent inserted.
b. Ligation of the ureter.
The ligation of the ureter should be treated by an
end-to-end anastomosis, reimplantation of the ureter
into the bladder or by uretero-ureteric anastomosis
into the opposite ureter.
2. Ureteric injury identified postoperatively.
Clinical Features
The signs and symptoms relate to the leakage of urine into the ureteric fistulae, and to ureteric
obstruction, when the ureter has been ligated. If a ureteric fistula is present, urine leakage may
be observed in an abdominal drain, or from the surgical incisions. The patient may develop
lower abdominal pain and pyrexia. If the ureter has been ligated, the patient may develop loin
pain and pyrexia.
Investigations
1. Ultrasound.
If ureteric obstruction is suspected, an ultrasound may be a useful initial test to
identify hydronephrosis.
2. Computerised tomography (CT).
This is becoming another useful test with an increase in the widespread availability
of CT scanning. It has the advantage of showing clear anatomical relationships as well
as the site of any injury.
3. Intravenous urography.
Intravenous urography (IVU) is useful in the investigation both of ureteric
fistulae and of ureteric obstruction. The urinary tract is outlined by radio-opaque dye
and the site of leakage or obstruction of urine can be identified. Small fistulae may
not be identified by this approach.
290
MANAGEMENT OF URETERIC INJURY
4. Percutaneous nephrostomy followed by

antegrade pyelography.
This manoeuvre is both therapeutic and
diagnostic. Percutaneous nephrostomy is
carried out under an ultrasound or X-ray
control. Using local anaesthesia, a catheter is
passed through the skin and into the renal pelvis
or ureter (percutaneous nephrostomy). This
allows drainage of the kidney, and prevents
further renal damage. Contrast medium can
then be injected through the catheter (antegrade
pyelography), and this gives further information
on the extent of ureteric damage.
Treatment of Ureteric Injury
When ureteric injury is diagnosed, the principle of
treatment, in the first instance, is to relieve the
ureteric obstruction, thus preventing back
pressure on the kidney and subsequent renal
necrosis. Clearly, if both ureters have been
damaged, and renal compromise/failure is already
apparent, consideration should be given to renal
dialysis. The following manoeuvres may be useful
in the short term:
1. Percutaneous nephrostomy with or without antegrade stenting (see above).
2. Cystoscopy and retrograde insertion of ureteric stents.
In the longer term, formal repair of the ureter is necessary, and this may be achieved using one
of the techniques outlined above. It should be emphasised again that these techniques are
outside the areas of expertise of most gynaecologists.
BOWEL INJURY
Serosal abrasions should be assessed and repaired where appropriate, particularly when it is a
diathermy injury. Injuries involving the muscularis or both the muscularis and the mucosa
should also be repaired.
For colonic injury, the lack of a preoperative bowel prep is not an indication for colostomy.
After the bowel is repaired, the abdomen is copiously irrigated. Occasionally, a segment of the
bowel must be resected, and if reanastomosis is performed, routine care can resume. If bowel
reanastomosis cannot be performed due to extensive injury or pathology (i.e. dense adhesions
or inflammatory changes), a diverting colostomy may be required.
291
FISTULA FORMATION
URINARY FISTULA
(L. fistula: a pipe) It is a pathological connection between the urinary tract and an adjacent
structure through which urine escapes. A fistula between the bladder base and the vagina is
the condition that is most often seen.
Aetiology
1. The exposed bladder wall is torn
or penetrated during a vaginal
operation, or during total
A tear
abdominal hysterectomy. This is
develops
the commonest cause in this
during
country.
mobilisation
of the
bladder.
Prolonged pressure of vertex on

the vagina during obstructed
labour. In a few days, a slough
forms. (This should not occur
with modern obstetrics in
developed countries.) 2. The vaginal wall and
bladder are torn during
an obstetric operation,
or pressure necrosis
develops during a
prolonged and difficult
labour.
3. The ureter is damaged or made

ischaemic during a pelvic operation,
especially during radical hysterectomy.
This produces a ureterovaginal fistula.
Exposing ureter in
292 radical hysterectomy
FISTULA FORMATION
4. Radiation burns following treatment for carcinoma of the cervix. This fistula may appear
several years after treatment.
5. Untreated or recurrent cancer of bladder or the genital tract. (This may also be
complicated by radiation effects.)
6. Chronic tuberculosis or syphilis. Fistulae may complicate the surgical treatment of
pelvic tuberculosis.
7. Congenital fistula. An accessory ectopic ureter may open into the vagina. This
condition should be recognised in childhood.
Symptoms
Incontinence may immediately follow the injury, but, usually, the patient has several days of
dysuria and haematuria with symptoms of urinary infection. A discharge appears followed by
sloughing, and the patient finds that her vulva and perineum are constantly wet. This is soon
followed by excoriation of the skin, accompanied by a strong ammoniacal smell and an
incrustation of the vulva and vagina with urinary salts. The area becomes extremely tender.
Diagnosis
The fistula is localised by cystoscopy, an intravenous pyelogram and retrograde studies of the
ureter. Further imaging with CT or magnetic resonance imaging (MRI), where available, can
help to localise the fistulae.
Treatment
Simple vesicovaginal fistulae can be managed by prolonged bladder drainage to allow an
opportunity for spontaneous healing. When healing fails to occur, surgical correction is
necessary and this may be performed through a vaginal or transabdominal approach.
Simple ureterovaginal fistulae usually heal after being stented, preferably by percutaneous
antegrade stents as they have higher success rates. If this fails, surgical repair will be necessary.
Complex ureterovesicovaginal fistulae require stenting and drainage until inflammation and
infection have resolved and surgical procedures may also be required for their resolution.
ADHESIONS
One function of the peritoneal surface of the pelvic and abdominal structures is to prevent
adherence of these structures when they touch. If the peritoneum is injured as a result of
surgery, the damaged areas may stick to each other and a permanent adhesion may form. This
typically occurs within the first 5 days after surgery.
Postoperative adhesions occur in 60–90% of women undergoing major gynaecologic surgery.
The incidence of adhesion-related intestinal obstruction after gynaecologic surgery is greater
upon surgery for malignant conditions and pelvic radiation, compared to benign conditions.
Symptoms may occur from weeks to several years after the procedure.
293
LYMPHOEDEMA AND LYMPHOCYST
Unilateral or bilateral lymphoedema of the lower extremities can

occur after radical surgery, and the risk is greater when
postoperative radiation is given.
This is a chronic problem for the resolution of which a referral to a
specialist clinic can help. Support hosiery and leg wraps will
minimise the oedema, elevation of the extremities while sitting and
elevation of the foot of the bed also help to control the problem.
Women with lymphoedema should be warned to take care of their
skin and pay special attention to the development of erythema or
tenderness, as these may indicate infection and a need for systemic
antibiotics. Diuretics do not improve lymphoedema, and may lead
to electrolyte abnormalities.
Lymphocysts are uncommon after pelvic lymphadenectomy, occurring in about 1–3% of
women, 11–12 days after surgery. They are seldom symptomatic and are detected when
radiologic studies are performed for the purpose of surveying the woman for recurrent
neoplastic disease. Symptoms consist of vague, colicky, lower abdominal pain. Symptomatic
lymphocysts and those causing hydronephrosis can be drained percutaneously. Recurrent
lymphocysts should be re-drained by tetracycline instillation to sclerose the cavity.
INFECTIOUS MORBIDITY
Fever within the first 48 h of surgery is almost always cytokine related. Fever-associated
cytokines are released due to tissue trauma and do not necessarily signal infection. Fever due
to the trauma of surgery usually resolves within 2–3 days.
Chest radiography, urinalysis, and blood and urine cultures are NOT indicated for all
postoperative patients with fever. The need for laboratory testing should be determined from
the findings of a careful history and physical examination. The febrile postoperative patient
should be evaluated systematically, taking into account the timing of the onset of fever and its
many possible causes.
Significant febrile morbidity after gynaecological surgery is usually attributable to infection of
the urinary tract, wounds (including the vaginal cuff and necrotising fasciitis), or pelvic
cellulitis and abscess. After the first two postoperative days, a thorough inspection of the
wound and a good rectovaginal examination are the most important components of the fever
work-up. Empiric broad spectrum antibiotics may then be started.
It may be appropriate to arrange further investigations to determine any septic source.
HERNIA
Incisional hernia can occur in areas of weakness in incompletely healed surgical wounds. An
approach to their prevention is the closure of the incision by incorporating a permanent suture
of a length that is at least four times the length of the incision. Symptomatic or cosmetically
unacceptable hernias are repaired surgically.
294
VENOUS THROMBOSIS
Deep vein thrombosis (DVT) of the lower limbs is a common disease and is often
asymptomatic. Complications include pulmonary thromboembolism (PE) and post
thrombotic leg syndrome (PLS).
Patients undergoing major general or gynaecological surgery, who are aged 40 years or more,
or who have other risk factors (see below) have a significant risk of venous thrombosis. In
many of these patients DVT remains asymptomatic, but, in others, it can cause serious
morbidity and, potentially, mortality.
There is evidence that routine prophylaxis reduces morbidity, mortality and costs in
hospitalised patients at risk of DVT and PE, as highlighted in national and international
guidelines. In contrast, screening for asymptomatic DVT and its treatment, are expensive,
insensitive and not cost-effective compared to routine prophylaxis in at-risk patients.
Risk factors for venous thrombosis
(SIGN Guidelines October 2002)
Age Exponential increase in risk with age. In the general population:

<40 years annual risk 1/10,000
60–69 years annual risk 1/1000
>80 years annual risk 1/100
May reflect immobility and coagulation activation
Obesity 3 risk if obese (BMI 30 kg/m2)
May reflect immobility and coagulation activation
Varicose veins 1.5 risk after major general/orthopaedic surgery
But low risk after varicose vein surgery
Previous VTE Recurrence rate 5%/year, increased by surgery
Thrombophilias Low coagulation inhibitors (antithrombin, protein C or S)
Activated protein C resistance (e.g. Factor V Leidin)
High coagulation factors (I, II, VIII, IX, XI)
Antiphospholipid syndrome
High homocysteine
Other thrombotic states Malignancy 7 risk
Heart failure
Recent myocardial infarction/stroke
Severe infection
Inflammatory bowel disease, nephrotic syndrome
Polycythaemia, paraproteinaemia
Bechet’s disease, paroxysmal nocturnal haemoglobinuria
Hormone therapy Oral combined contraceptives, HRT, raloxifene, tamoxifen 3 risk
High dose progestogens 6 risk
Pregnancy, puerperium 10 risk
Immobility Bedrest >3 days 10 risk (increases with duration)
Hospitalisation Acute trauma, acute illness, surgery, 10 risk
Anaesthesia 2 general vs. spinal/epidural
295
VENOUS THROMBOSIS
PATHOLOGY
Virchow’s triad encompasses the three broad categories of factors that are thought to
contribute to the formation of venous thrombosis:
1. Changes in the vessel wall
Injury or trauma to the vascular endothelium encourages the platelets to adhere
to the exposed collagen tissue and these then release substances which further facilitate
platelet aggregation. Fibrin and leucocytes then adhere to the platelets. Recent work
suggests that a balance is maintained between different groups of prostaglandins.
2. Changes in the pattern of blood flow 3. Changes in the constituents of blood

(flow volume) (hypercoagulability)
Venous flow in the legs is much Increased procoagulant activity, including
reduced in the postoperative period elevated platelet count, platelet ‘stickiness’
and is a result of inactivity and and fibrinogen levels, contribute to
poor muscle tone. hypercoagulability. Fortunately, there is
also a compensating increase in fibrinolytic
activity so that nearly all thrombi
are naturally broken down.
296
VENOUS THROMBOSIS
SITES OF THROMBUS FORMATION

Common sites of thrombus formation include: External iliac
(1) The calf veins extending to the popliteal
(2) The long and short saphenous veins,
Proximal
especially those lateral to the knee Deep femoral
(3) The ilio-femoral segment extending to
the vena cava Great saphenous
(4) Superficial thrombosis in the distal
leg veins.
Popliteal
Distal
Anterior tibial
Posterior tibial
297
CLINICAL FEATURES OF DEEP VENOUS THROMBOSIS
In many cases deep venous thrombosis (DVT) is asymptomatic. It is, therefore, imperative
to carefully look for clinical features, particularly in the presence of any risk factors (see Risk
Factors for Venous Thrombosis). The classical symptoms of DVT include swelling, pain and
discoloration in the affected extremity. Physical examination may reveal the palpable cord of
a thrombosed vein, unilateral oedema, warmth and superficial venous dilation. Other signs
include the Homan’s test of dorsiflexion of the foot for eliciting pain in posterior calf (it
should be noted that it is of little diagnostic value and is theoretically dangerous because of
the possibility of dislodgement of a loose clot) and Pratt’s sign – the ability to elicit pain by
squeezing the posterior calf.
Palpation of the calf

demonstrates tenderness and oedema.
The femoral vein must also
be palpated in the groin.
The affected leg may

feel warmer to the back
of the hand.
Careful measurement
may reveal some
swelling compared
with the other leg.
298
INVESTIGATIONS FOR DEEP VENOUS THROMBOSIS
Diagnostic imaging (venography, ultrasound) should be performed expeditiously (within 24 h

if possible) in patients with suspected DVT. In all patients with clinically suspected DVT, the
diagnosis should be confirmed or excluded by diagnostic imaging, either by non-invasive
testing by ultrasound (compression or Duplex scanning) followed by contrast venography, if
negative (to detect calf and non-occlusive proximal DVT) or contrast venography (to detect
both calf and proximal DVT). It may be necessary to carry out serial (repeat after 7 days)
ultrasound examinations to detect a proximal extension of a calf DVT. A single negative
ultrasound may be sufficient to exclude DVT in patients with low clinical pre-test probability
and/or a normal fibrin D-dimer assay.
FIBRIN D-DIMER ASSAY

Plasma D-dimers are specific cross-linked derivatives of fibrin that are produced when fibrin is
degraded by plasmin, so its concentration is raised in patients with venous thromboembolism.
Although sensitive for venous thromboembolism, high concentrations of D-dimers are
insufficiently specific for making a positive diagnosis because they occur in other disorders
such as a malignancy, pregnancy and after operations. Nevertheless, D-dimer tests generally
have a high negative predictive value and are useful rule-out tests that reduce the need for
imaging when used in conjunction with clinical probability, plethysmography and the
ultrasound.
ULTRASOUND
This is the best non-invasive technique for diagnosing venous thrombosis. It has a better
sensitivity and specificity (97%) in diagnosing of proximal DVT compared to the distal calf
vein thrombosis (approximately 75% sensitivity).
Colour flow duplex ultrasonography evaluates blood flow characteristics within the vessel
using a pulsed Doppler signal.
299
METHODS OF THROMBOPROPHYLAXIS
GENERAL MEASURES
(1) Early ambulation – immobility increases the risk of DVT by about 10 fold and,
hence, early mobilisation and leg exercises should be encouraged in postoperative
patients.
(2) Postoperative physiotherapy – the physiotherapist encourages the patient to perform
deep breathing and exercises to restore muscle tone.
(3) Hydration – haemoconcentration increases blood viscosity and reduces blood flow,
especially in the deep veins of the leg in immobile patients; hence adequate hydration
should be ensured in immobilised patients.
MECHANICAL METHODS
Mechanical thromboprophylactic methods have been shown to increase mean blood flow
velocity in the leg veins and to reduce venous stasis. Unlike pharmacological methods, they do
not increase the risk of bleeding. Mechanical methods are contraindicated in patients at risk of
ischemic skin necrosis, for example those with critical limb ischemia or severe peripheral
neuropathy. Mechanical methods include:
(1) Graduated elastic compression stockings (GECS) – these reduce the pooling of blood in the
leg veins. Graduated static compression stockings exert a greater pressure at the ankle
than at the thigh.
(2) Pneumatic stockings – inflatable lower leg stocking device that applies intermittent pneumatic
pressure to the legs during an operation.
300
METHODS OF THROMBOPROPHYLAXIS
UNFRACTIONATED AND LOW MOLECULAR WEIGHT HEPARINS

Unfractionated heparin (UFH) and low molecular weight heparins (LMWHs – dalteparin,
enoxparin, reviparin and tinzaparin) are effective in the prophylaxis of VTE in both surgical
and medical patients.
The risk of wound haematomas can be minimised by avoiding injection sites close to wounds.
TREATMENT OF DVT
The goals of treatment for DVT are to stop clot propagation and to prevent clot recurrence,
pulmonary embolism (PE), and pulmonary hypertension (a potential complication of multiple
recurrent PEs). These goals are usually achieved with anticoagulation therapy using heparin
followed by warfarin, according to local protocols.
301
PULMONARY EMBOLISM
An embolism arises from a thrombus which was non-occlusive in the vessel in which it was
formed and it is therefore symptomless. This then travels to the lung, causing occlusion of the
pulmonary vessels.
PERIPHERAL PULMONARY EMBOLISM

Small emboli are lysed rapidly and are symptomless unless an infarction occurs. They often
precede a major embolism, unless treatment is given.
Symptoms Signs
Fever Pyrexia
Tachypnoea Pleural rub
Pleural pain Crepitations
Haemoptysis (40%) Perhaps opacity on lung X-ray
CENTRAL PULMONARY EMBOLISM

A large embolus impacting the main
pulmonary artery will be immediately fatal,
but if it is a little more peripheral, circulatory
obstruction will be incomplete and there is a
chance of survival.
Symptoms Signs
1. Collapse 1. Shock
– vasoconstriction
– hypotension
2. Faintness 2. RV failure
– distended neck
veins
– Gallop rhythm
3. Respiratory 3. Cyanosis
distress
4. Pain
The cardiac output drops at once and there is intense reflex vasoconstriction leading to
tachycardia, hypotension and syncope if the patient is sat up. The respiratory distress is very
severe and pulmonary cyanosis may be aggravated by a right-to-left shunt through a patent
foramen ovale which exists in 25% of the individuals.
302
PULMONARY EMBOLISM
PULMONARY EMBOLISM MANAGEMENT

1. Remember the risk factors for thromboembolism.
2. Suspect PE in all women presenting with a sudden onset of shortness of breath, chest
pain, unexplained tachycardia or cardiovascular collapse.
3. Involve senior medical staff.
4. Assess and ensure adequate airway, breathing and circulation. Commence
cardiopulmonary resuscitation if the patient is in cardiac arrest.
5. Transfer the patient to the high-dependency area when appropriate and commence
monitoring: non-invasive blood pressure, pulse oximetry, ECG, urine output.
6. Send samples for a full blood count, clotting studies, urea and electrolytes, liver
function tests and thrombophilia screen.
7. Request ECG, arterial blood gas and chest X-ray.
INVESTIGATIONS
ECG
ECG is non-specific for the diagnosis of a PE. Right axis deviation and right ventricular strain
pattern may be present with a large PE. S waves in lead 1, Q wave in lead 3 and inverted T
waves in lead 3 (s1Q3T3) patterns are very rare.
Chest X-Ray
This will help to exclude a pneumothorax and pneumonia. The non-specific radiological
changes in PE include segmental collapse, a raised hemi diaphragm, consolidation and
unilateral pleural effusion. A wedge-shaped infarction is a rare finding.
Arterial Blood Gases

With massive PE, PaO2 may be reduced with and a normal or low PaCO2. 303
PULMONARY EMBOLISM
Ventilation/Perfusion (V/Q) Scans

V/Q scanning is the most useful initial
test in patients with suspected PE.
They are interpreted using
standardised criteria and, based on the
extent of ventilation-perfusion
mismatches, the scan is interpreted as
normal, low probability, intermediate
probability or high probability for a
PE. A normal scan reliably excludes
PE and a high-probability V/Q scan is
considered as sufficient evidence for
the diagnosis of a PE in a patient with a
high clinical suspicion. Perfusion scan
alone can be performed with a
ventilation scan being performed only
if the perfusion scan is abnormal.
Duplex Doppler Leg
Ultrasound
Bilateral Doppler ultrasound leg
studies should be performed in all
cases of suspected PE.
CT Pulmonary Angiography
CT, after contrast injection,
permits excellent visualisation of
the pulmonary arteries and a
direct visualisation of pulmonary
arterial clots in larger vessels – all
during a single breath hold.
304
TREATMENT OF PULMONARY EMBOLUS
In most cases, anticoagulant therapy is the mainstay of the

treatment. Heparin or LMWHs (such as enoxaparin and
dalteparin) are administered initially, while warfarin therapy
is commenced.
Massive PE causing haemodynamic instability is an indication for
thrombolysis, the enzymatic destruction of the clot with
medication. The aim of this therapy is to dissolve the clot, but
there is an attendant risk of bleeding or stroke.
Surgical management of acute PE (pulmonary thrombectomy) is
uncommon and has largely been abandoned because of poor
long-term outcomes.
Chronic PE leading to pulmonary hypertension (known as chronic
thromboembolic hypertension) is treated by a surgical procedure
known as a pulmonary thromboendarterectomy.
If anticoagulant therapy is contraindicated and/or ineffective, or to
prevent new emboli from entering the pulmonary artery and
combining with an existing blockage, an inferior vena cava filter
may be implanted.
305
MORTALITY
A retrospective study of 1.45 million gynaecology inpatients in England reported a

mortality rate of 0.2% within 30 days of admission and 0.5% within 90 days.
The 30-day death rate in patients with cancer was higher than for patients without cancer
(5.1% vs. 0.1%).
306
CHAPTER 15
EARLY PREGNANCY
Miscarriage 308 Complications of Termination of

Threatened Miscarriage 308 Pregnancy 319
Inevitable Miscarriage 308 Ectopic Pregnancy 320
Complete Miscarriage 308 Aetiology 320
Incomplete Miscarriage 309 Diagnosis of Tubal Pregnancy 321
Missed Miscarriage 309 Symptoms 321
Other Terms 309 Signs 321
Management 310 Diagnosis of Tubal Pregnancy 321
Early Pregnancy Loss (12 Weeks’ Sites of Implantation 323
Gestation) 310 Rupture of the Tube 323
Late Pregnancy Loss (>12 Weeks’ Rupture into Lumen of Tube 323
Gestation) 313 Treatment of Tubal Pregnancy 324
Recurrent Miscarriage 314 Methotrexate 324
Introduction and Definitions 314 Salpingectomy 324
Causes of Recurrent Miscarriage 314 Salpingostomy 324
Investigation and Treatment of Conservative 324
Recurrent Miscarriage 316 Gestational Trophoblastic Disease 325
Termination of Pregnancy 317 Pathology 326
First Trimester Termination of Presentation and Genetics 327
Pregnancy 317 Treatment 328
Second Trimester Termination of Gestational Trophoblastic Neoplasia 328
Pregnancy 319 Chemotherapy for Choriocarcinoma 330
EARLY PREGNANCY
MISCARRIAGE
Miscarriage occurs in 10–20% of clinical pregnancies, and in the UK it is defined as a

pregnancy loss before the 24th week of gestation. In Australia, miscarriage is a pregnancy that
spontaneously ends before 20 weeks. After the 20th week of pregnancy, the loss of a fetus is
called a stillbirth.
THREATENED MISCARRIAGE
Technically this refers only to bleeding from the placental site, which is not yet severe enough
to terminate the pregnancy. Usually the bleeding is slight and the cervix remains closed. The
pregnancy is likely to remain viable.
INEVITABLE MISCARRIAGE
Clinically, the amount of bleeding is variable but the cervix is open. On ultrasound
examination, the bleeding is retroplacental and often, fetal heart activity is absent.
COMPLETE MISCARRIAGE
A miscarriage in which the fetus, membranes and chorionic tissue are completely expelled
from the uterus is termed a complete miscarriage.
308
EARLY PREGNANCY
MISCARRIAGE
INCOMPLETE MISCARRIAGE
A miscarriage in which the fetus or membranes or chorionic tissue are incompletely expelled
from the uterus. An ultrasound will show debris (retained products of conception) within the
uterine cavity.
MISSED MISCARRIAGE
It is defined as the retention of a non-viable fetus for several weeks without any clinical
symptoms.
OTHER TERMS
The term early fetal demise is now used to describe what used to be known as an anembryonic
pregnancy or a blighted ovum and denotes pregnancies in which a gestational sac is present
without the development of a fetal pole.
309
EARLY PREGNANCY
MANAGEMENT
The method of management of miscarriage depends upon the gestation of miscarriage and
clinical facilities available. Apart from expectant management, these methods are identical to
those performed during an elective termination of pregnancy.
EARLY PREGNANCY LOSS (12 Weeks’ Gestation)

Surgical
Clinical indications for surgical evacuation include: persistent excessive bleeding,
haemodynamic instability, evidence of infected retained tissue, suspected gestational
trophoblastic disease and patient choice. Surgical uterine evacuation for a miscarriage should
be performed using a suction curettage. Where infection is suspected, delaying surgical
intervention for 12 h is recommended to allow intravenous antibiotic administration.
Preoperative cervical preparation essentially softens the cervix making it easier to dilate and, in
doing so, minimises force of dilatation required, haemorrhage and uterine/cervical trauma.
The cervix can be prepared using:
– gemeprost (prostaglandin E1) given as a vaginal pessary 3 h before surgery
– misoprostol (a prostaglandin analogue) given vaginally 3 h before surgery
– mifepristone (an antiprogesterone) given orally at least 12 h before surgery
– laminaria tents inserted into the external cervical os.
Surgical Evacuation of the Products of Conception
Curettage
The patient is anaesthetised and the cervix is dilated. Once dilatation is sufficient, vacuum
aspiration of the uterine contents is carried out.
A plastic suction curette is commonly used and is less likely to damage the uterus than metal
instruments. Plastic curettes are available in diameters from 4 to 12 mm. The cervix is
conventionally dilated to a diameter that is 2 mm less than the gestation age in weeks.
310
EARLY PREGNANCY
MANAGEMENT
Surgical Evacuation of Products of Conception—(cont’d)
Complications
1. Incomplete uterine evacuation.
2. Uterine perforation and/or damage to
abdominal viscera.
3. Sepsis. Broad spectrum antibiotics have been
shown to minimise the risk of post-abortal
infection.
4. Haemorrhage. Blood loss can be minimised
by the use of prostaglandins for preoperative
cervical ripening. Bleeding during or after the
procedure can be reduced by oxytocic agents
such as ergometrine or Syntocinon.
5. Rhesus isoimmunisation. Anti-D should be
administered to all rhesus negative women.
Further tissue can be removed with a sponge forcep or a curette. The concave side of the
curette loop is pressed against the uterine wall and pulled down. A ‘clean’ uterine wall gives a
characteristic sensation to the operating hand.
Reported serious complications of surgery include perforation of the uterus, cervical tears,
intra-abdominal trauma, intrauterine adhesions and haemorrhage.
311
EARLY PREGNANCY
MANAGEMENT
EARLY PREGNANCY LOSS (12 Weeks’ Gestation)—(cont’d)

Medical
Medical methods are an effective alternative in the management of a confirmed first-trimester
miscarriage. Various medical methods have been described which use prostaglandin analogues
(gemeprost or misoprostol) with or without antiprogesterone priming (mifepristone).
Protocols should be developed locally with appropriate selection criteria, therapeutic regimens
and arrangements for follow-up. To avoid unnecessary anxiety, women should be informed
that bleeding may continue for up to 3 weeks after medical uterine evacuation.
Expectant
Expectant management is a method that can be offered in cases of confirmed first trimester
miscarriage. Patient counselling is particularly important for those women with an intact sac
who wish to adopt an expectant approach. They should be aware that complete resolution
may take several weeks. Expectant management for incomplete miscarriage is highly effective.
Occasionally, the passage of tissue may be associated with heavy bleeding.
Medical and expectant management should only be offered in units where women have access
to 24-h telephone advice and emergency admission, if required.
Anti-D Immunoglobulin
Non-sensitised rhesus (Rh) negative women should receive anti-D immunoglobulin in the
following situations: ectopic pregnancy, all miscarriages over 12 weeks of gestation (including
threatened) and all miscarriages where the uterus has been evacuated (whether medially or
surgically).
Anti-D immunoglobulin is not required threatened miscarriages under 12 weeks of gestation
unless the bleeding is heavy or is associated with significant pain. It is not required in cases of
complete miscarriage under 12 weeks’ gestation and when there has been no formal
intervention to evacuate the uterus.
312
EARLY PREGNANCY
MANAGEMENT
LATE PREGNANCY LOSS (>12 Weeks’ Gestation)

Surgical
Surgical uterine evacuation remains an option for some women. Dilatation and suction
curettage is commonly performed up to 14 weeks’ gestation. Beyond this point, dilatation and
evacuation (D & E) can be carried out which involves cervical dilatation to a maximum
diameter and the removal of intrauterine contents, usually following a destructive procedure.
This procedure is not commonly performed in the UK.
Medical
Again, medical methods are effective in the management of a second trimester miscarriage.
As in the case of first trimester loss, there are various medical regimens that have been
described using prostaglandin analogues (gemeprost or misoprostol) with or without
antiprogesterone priming (mifepristone). Again, local protocols should be developed
appropriately with selection criteria, therapeutic regimens and arrangements for follow-up.
In cases where antiprogesterones and vaginal prostaglandins are not available, PGE2 can be
very slowly instilled into the cervix through a Foley catheter to facilitate cervical ripening.
313
EARLY PREGNANCY
RECURRENT MISCARRIAGE
INTRODUCTION AND DEFINITIONS

Recurrent miscarriage, defined as the loss of three or more pregnancies, is a distressing
problem that affects up to 1% of women. Recurrent miscarriage is a heterogeneous condition
that has many possible causes; more than one contributory factor may underlie the recurrent
pregnancy losses.
CAUSES OF RECURRENT MISCARRIAGE

Maternal Age
This is an independent risk factor. Advanced maternal age adversely affects ovarian function,
giving rise to a decline in the number of good quality oocytes and resulting in chromosomally
abnormal conceptions that rarely develop further.
Previous Number of Miscarriages
This is an independent risk factor in so far as the more miscarriages an individual has had, the
more likely she is to have another one.
Genetic Factors
In approximately 3–5% of couples with recurrent miscarriage, one of the partners carries a
balanced structural chromosomal anomaly. These are most commonly balanced reciprocal or
Robertsonian translocations.
Abnormalities in the Embryo
Recurrent pregnancy loss may be owing to an abnormal embryo which is incompatible with
life. As the number of miscarriages increases, the presence of a chromosomal abnormality
decreases and the chance of a recurring maternal cause increases.
Uterine Abnormalities
It is difficult to assess the exact contribution that congenital uterine anomalies make to
recurrent miscarriage. The estimates of the number of women with recurrent miscarriage, who
also have uterine abnormalities, range from 2% to 37%. Women who have serious anatomical
abnormalities and have not had treatment for them seem to be more likely to miscarry or give
birth early. Minor variations in the structure of the womb generally do not cause miscarriage
Cervical Weakness
The diagnosis of cervical weakness (previously known as incompetence) is usually based on a
history of late miscarriage, preceded by spontaneous rupture of membranes or a painless
cervical dilatation. This is often over diagnosed as there is currently no satisfactory, objective
314 test that can identify women with cervical weakness in the non-pregnant state.
EARLY PREGNANCY
CAUSES OF RECURRENT MISCARRIAGE—(cont’d)

Endocrine Factors
Maternal diabetes and thyroid disease
Systemic endocrine disorders have been associated with miscarriage. However, they do not
cause recurrent miscarriages as long as they are treated and well controlled.
Hyperprolactinaemia
There is insufficient evidence to assess the effect of hyperprolactinaemia as a risk factor for
recurrent miscarriage.
Polycystic ovarian syndrome (PCOS)
The characteristic features of this condition are polycystic ovaries associated with an
imbalance of hormones. Approximately 50% of women with recurrent early miscarriages have
polycystic ovaries (almost double the number of women in the general population). The link
between PCOS and recurrent miscarriage is not clear. Many women with PCOS and
recurrent miscarriage have elevated levels of luteinising hormone (LH) in their blood.
However, reducing the level of LH prior to pregnancy has not been shown to improve the
chances of a successful birth.
Thrombophilias
Inherited thrombophilic defects including activated protein C resistance (most commonly
owing to factor V Leidin gene mutation), deficiencies of protein C and S and antithrombin III,
hyperhomocysteinaemia and prothrombin gene mutations are established causes of systemic
thrombosis. Studies have established an association between inherited thrombophilias and
fetal loss and late pregnancy complications, with the presumed mechanism being thrombosis
of the uteroplacental circulation. Women with recurrent miscarriage who carry the factor V
Leidin (FVL) mutation are at a significantly increased risk of miscarriage compared to those
with a normal factor V genotype. However, carriage of the FVL mutation did not preclude an
uncomplicated pregnancy that could be delivered at term. There is currently no test that can
reliably discriminate those women with recurrent miscarriage and the FVL mutation who are
destined to miscarry from those who are destined to have a successful pregnancy.
Autoimmune Factors
Approximately 15% of women who have recurrent miscarriages have the antiphospholipid
syndrome. This syndrome is characterised by some or all of the following: recurrent
miscarriage, thrombosis, thrombocytopenia, poor obstetric history. Anticardiolipin antibodies
and lupus anticoagulant levels are also often abnormal.
Infections
Any serious systemic infection can potentially lead to a miscarriage. The presence of bacterial
vaginosis in the first trimester of pregnancy has been reported as a risk factor for second
trimester miscarriage and preterm delivery but the evidence for its association with first
trimester miscarriage is inconsistent.
Environmental Factors
Smoking and alcohol may play a role.
315
EARLY PREGNANCY
INVESTIGATION AND TREATMENT OF RECURRENT MISCARRIAGE

Even after careful investigation, the majority of women have no obvious cause for recurrent
miscarriage. Notwithstanding, the prognosis is generally good, with a mean probability of a
live birth in the next pregnancy being around 70%.
1. Genetic factors
Essentially no treatment is available.
2. Uterine abnormalities
All women with recurrent miscarriage should have a pelvic ultrasound to assess
uterine anatomy and morphology. Uterine surgery may correct the abnormality, but
may not necessarily improve the prognosis. Ironically, these procedures may cause
intrauterine adhesions and, thus, reduce fertility.
3. Cervical weakness
The diagnosis is based on a history of mid-trimester miscarriage preceded by a
spontaneous rupture of the membranes or a painless cervical dilatation. A transvaginal
ultrasound assessment of the cervix during pregnancy may be useful in predicting preterm
birth in some cases of suspected cervical weakness. Cervical cerclage is associated
with potential hazards that are related to the surgery and the risk of stimulating uterine
contractions and, hence, should only be considered in women who are likely to benefit.
Incompetent Non-absorbable suture

internal os inserted at a level of
the internal os.
4. Endocrine problems
The aim is to obtain optimal control of the condition.
5. Immunological factors
In women with the anticardiolipin antibody syndrome, treatment with low dose aspirin
and heparin has been shown to improve the outcome of future pregnancies.
6. Thrombophilias
If protein C and protein S deficiency are found, thromboprophylaxis should be
considered. A few well-conducted trials exist for the treatment of these conditions,
although there is a rationale for low dose aspirin therapy.
7. Environmental factors
All women wishing to become pregnant should be advised to stop smoking and to
minimise their alcohol intake.
316
EARLY PREGNANCY
TERMINATION OF PREGNANCY
Some people elect to terminate their pregnancy for various reasons which must fall within the
Indications for Therapeutic Abortion under the Abortion Act (1967, UK) which was
amended 1992. These include:
1. . . .the continuance of the pregnancy would involve risk to the life of the pregnant
woman greater than if the pregnancy were terminated.
2. . . .the termination is necessary to prevent grave permanent injury to the physical or
mental health of the pregnant woman.
3. . . .the pregnancy has NOT exceeded its 24th week and the continuance of the
pregnancy would involve risk, greater than if the pregnancy were terminated, of injury
to the physical or mental health of the pregnant woman.
4. . . .the pregnancy has NOT exceeded its 24th week and the continuance of the pregnancy
would involve risk, greater than if the pregnancy were terminated, of injury to the physical
or mental health of the existing child(ren) of the family of the pregnant woman.
5. . . .there is substantial risk that if the child were born it would suffer from such physical
or mental abnormalities as to be seriously handicapped.
To facilitate this process, a certificate of opinion is given by two medical practitioners prior
to commencement of the termination process to which it refers.
A single practitioner may give an emergency certificate before termination or, where not
reasonably practical, within 24 h of termination, and terminate a pregnancy if it is necessary to
save the life of the pregnant woman or to prevent grave permanent injury to her physical or
mental health.
FIRST TRIMESTER TERMINATION OF PREGNANCY

In the first trimester of pregnancy termination can be carried out by surgical or medical
methods.
1. Surgical termination of pregnancy (Stop)

This is usually performed up to 14 weeks’ gestation. It involves preoperative cervical
ripening with prostaglandin agents preceded by the administration of an antiprogesterone,
and (mifepristone) followed by dilatation of the cervix and suction curettage of the
products of conception. The methods are almost identical to those already described
for the surgical management of a miscarriage.
317
EARLY PREGNANCY
2. Medical termination of pregnancy

Mifepristone is an antiprogestogen which offers a medical alternative to vacuum
aspiration of an early pregnancy and can be used up to 63 days from the first day of
the LMP or as dated by an ultrasound. The use of mifepristone is strictly controlled
to approved NHS hospitals and premises that have been approved under the
Abortion Act. Mifepristone is contraindicated in a suspected ectopic pregnancy, in
smokers over 35 years of age, in chronic adrenal failure, porphyria, corticosteroid
therapy, coagulation disorders and in women on anticoagulant therapy.
200 mg mifepristone is taken orally and the patient is admitted 36–48 h later for a vaginal
administration of prostaglandins (in certain situations prostaglandins can be also given orally).
Over 95% of pregnancies are completely aborted. In a small number of cases, surgical
evacuation of uterus may be required for any retained products of conception. Side effects
include abdominal pain with up to 20% of the patients requiring opiate analgesia following
prostaglandin administration. Blood loss is similar to that following surgical termination of
pregnancy at the same gestation.
318
EARLY PREGNANCY
SECOND TRIMESTER TERMINATION OF PREGNANCY

1. Surgical termination – dilatation and evacuation (D&E)
Dilatation and evacuation (D & E) involves cervical dilatation to a maximum diameter of
20 mm and removal of the intrauterine contents. This is not commonly performed in the UK.
2. Medical termination
Again mifepristone and prostaglandins are used to facilitate the process, in accordance
with the local protocols. The use of mifepristone significantly reduces the interval from
induction (prostaglandin administration) to abortion, and so, the vast majority of patients
abort within 24 h. Curettage for retained products of conception may be required in up to
30% of patients undergoing a second trimester abortion using medical methods.
3. Extra-amniotic termination
This method may be used if the mifepristone
and prostaglandin pessaries are unavailable.
PGE2 is very slowly instilled into the cervix
through a Foley catheter.
COMPLICATIONS OF TERMINATION OF PREGNANCY

Immediate
Major complications occur in approximately 2% of the cases and include haemorrhage,
thromboembolism, operative trauma and infection. Minor complications (10%) include lower
abdominal pain, bleeding and pelvic infection.
Late
Infertility can occur if a termination is complicated by infection as this increases the risk of
tubal occlusion. In general, if women are screened and treated for genital tract pathogens prior
to an evacuation procedure, the risk of postoperative infection is significantly reduced.
However in the absence of infection, results from several well-designed studies have shown no
adverse effects on a future pregnancy from a single uterine evacuation procedure.
Rhesus isoimmunisation can be minimised by administering anti-D to rhesus negative
women.
319
EARLY PREGNANCY
ECTOPIC PREGNANCY
The term ‘ectopic’ comes from the

Greek ‘ektopis’ meaning
‘displacement’ (‘ek’, out of þ ‘topos’,
place ¼ out of place). An ectopic
pregnancy is an extrauterine
pregnancy. This occurs with an
incidence of approximately 11.1 per
1000 pregnancies. It is still a cause of
maternal death with 10 deaths being
reported in the UK between 2002 and
2005.
An ectopic pregnancy is usually caused
by various conditions that block or
slow the movement of a fertilised egg
through the fallopian tube to the uterus.
The trophoblast can successfully implant on any tissue that has an adequate blood supply.
The most common site for an ectopic pregnancy is within the fallopian tube. Other less
common sites include the cervix, ovary, liver, spleen, stomach and the intestine.
AETIOLOGY
Often unknown, but there are a number of
associated factors:
Pelvic Inflammatory Disease
About half the patients will have signs of
salpingitis or a history of infection, including
gonorrhoea or chlamydia or tuberculosis.
This may affect tubal ciliary activity.
Intrauterine Devices (IUDs)
The IUD may introduce infection. As the aim of the IUD is to prevent implantation in the
uterine cavity, a relative increase in ectopic pregnancy is to be expected.
Tubal Damage
Previous tubal damage such as an ectopic pregnancy treated conservatively, previous pelvic
surgery leading to adhesion formation, endometriosis or reversal of sterilisation may also be
causes.
Assisted Conception
This is associated with an increased incidence of ectopic pregnancies.
320
EARLY PREGNANCY
DIAGNOSIS OF TUBAL PREGNANCY
Tubal pregnancy can present in many ways and misdiagnosis can occur. Many patients now
present with mild symptoms as methods of investigation that detect early pregnancy problems
such as ectopics, can do so earlier than previously. However, acute ruptures with significant
patient compromise still occur.
SYMPTOMS SIGNS
Pain Abdominal Tenderness
Pain in the lower abdomen is always present Tenderness may be elicited on the left, right
in the acute presentation. Described as or across the lower abdomen.
either stabbing or cramp-like, it may be
Pelvic Tenderness
referred to the shoulder if blood tracks to the
Care should be taken when examining the
diaphragm and stimulates the phrenic nerve,
patient to make sure that an ectopic
and may be so severe as to cause fainting.
pregnancy is not ruptured during the process.
Vaginal Bleeding
Adnexal Mass
In about 75% of the cases, a tubal
Gentle bimanual palpation may reveal a
pregnancy presents with vaginal bleeding.
pelvic adnexal mass.
Fainting/Collapse
These pregnancies will cause pain and
fainting, leading to anaemia.
If haemorrhage is severe the usual signs of
collapse and shock will appear.

1. Serum hCG tracking On-going
can aid in its diagnosis. intrauterine
An ongoing intrauterine pregnancy
pregnancy should have a
Ectopic
doubling (minimum of 2/3)
pregnancy
of serum beta hCG in Serum beta
48 h. A non-continuing hcg level
pregnancy will usually show Non-continuing
a fall in beta hCG. An pregnancy
ectopic pregnancy will show Time
a suboptimal rise, static
value or a decline.
2. Ultrasound Features of ectopic pregnancy include:
– absence of a gestation sac within the uterine cavity
– presence of a gestation sac outside the uterus (usually in the adnexal regions)
– demonstration of a live embryo with fetal heart activity outside the uterus.
– free fluid or blood in the adjacent parts of the pelvis.
321
EARLY PREGNANCY
Ovary
Ectopic Pregnancy
contatining yolk sac
A transvaginal ultrasound is the diagnostic modality used. In general, ultrasound findings in

association with serum beta hCG tracking can help establish the diagnosis of an ectopic
pregnancy. In general, there is a serum hCG level at which it is assumed that all viable
intrauterine pregnancies will be visualised by a transvaginal ultrasound. This is referred to
as the discriminatory zone. When serum hCG levels are below the discriminatory zone
(<1000 iu) and there is no pregnancy (intra- or extrauterine) visible on transvaginal
ultrasound scan, the pregnancy can be described as being of unknown location.
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EARLY PREGNANCY
SITES OF IMPLANTATION
Sites of Implantation
The tubal ampulla is the commonest location followed by the isthmus, but the developing
ovum can implant anywhere inside or outside the uterus.
Ampullary implantation: note the thinning Cornual implantation is not common but is very
of the tube wall. dangerous because its rupture is accompanied
by bleeding from uterine arteries.
RUPTURE OF THE TUBE RUPTURE INTO LUMEN OF TUBE
The muscle wall of the tube does not Tubal Abortion

have the capacity of uterine muscle for This is usual in an ampullary pregnancy at
hypertrophy and its distension and a about 8 weeks. The conceptus is extruded,
tubal pregnancy nearly always end in its complete or incomplete, towards the
rupture and the death of the ovum. fimbriated end of the tube.
Rupture into the Peritoneal Cavity

This usually occurs spontaneously, and often
from the narrow isthmus before 8 weeks, or
from the interstitial portion at 12 weeks.
Haemorrhage is likely to be severe.
323
EARLY PREGNANCY
TREATMENT OF TUBAL PREGNANCY
Patients presenting with collapse and shock with a positive pregnancy test must be assessed
and managed like any other critically ill patient. Intravenous access with appropriate blood
tests including a full blood count, a coagulation screen and an emergency blood cross match
should be established. Fluid resuscitation and an emergency theatre should be organised to
deal with the bleeding. In such cases, all procedures are performed as traditional open
operations.
If the patient is stable, then management can be medical (using methotrexate intramuscular
injection) or surgical.
METHOTREXATE
Most ectopics follow a chronic course and are confidently diagnosed with ultrasound and
bHCG. To avoid surgical intervention, women can be offered this treatment if the bHCG is
<3000 and there are no symptoms of rupture. If bHCG levels do not fall, then, 14% may
need a further injection and only <10%, in this group, will eventually need surgery if the
treatment fails or if the ectopic shows signs of rupture during treatment. The dose is usually
50 mg/m2 body surface area.
SALPINGECTOMY
This can be performed following the
diagnosis at surgery. Before removing the
tube, the other fallopian tube should be
examined, because if it is abnormal, then
a more conservative surgical approach
may have to be adopted. Laparoscopic
salpingectomy is the preferred method.
SALPINGOSTOMY
This is a conservative approach to the
surgical management of ectopics. An
incision is made over the antimesenteric
border of the tube, the ectopic is
removed and the tube left to heal once haemostasis is achieved. There is a risk of a persistent
trophoblast that may need to be treated, so follow up bHCG values should be checked. There
is also an increased risk of a recurrent ectopic pregnancy.
CONSERVATIVE
If there is a raised bHCG of <1000 with no further increase in the bHCG levels and no intra-
uterine pregnancy on an ultrasound scan, then the pregnancy can be described as being of
unknown location. Such cases can be treated conservatively as up to 70% will resolve by
themselves. Surgery or medical therapy will be required in some cases.
324
EARLY PREGNANCY
GESTATIONAL TROPHOBLASTIC DISEASE
Hydatidiform Mole
The incidence of molar pregnancies in Europe and North America is approximately 0.2–1.5
per 1000 live births but there may be a higher incidence in Africa and Asia.
Complete and partial are two distinct forms of a molar pregnancy. The gross specimen from
a complete molar pregnancy shows diffuse hydropic placental villi. On scanning, this gives a
multicystic appearance to the uterine contents. A partial molar pregnancy can have a similar
appearance but the findings can be variable and subtle.
Table 15.1 Features of Partial and Complete Hydatidiform Moles (From DISAIA Clinical
Gynecologic Oncology 7E Mosby 2007)
Feature Partial mole Complete mole
Karyotype Most commonly Most commonly
69, XXX or –, XXY 46, XX or –, XY
Pathology
Fetus Often present Absent
Amnion, fetal RBC Usually present Absent
Villous edema Variable, focal Diffuse
Trophoblastic proliferation Focal, slight–moderate Diffuse, slight–severe
Clinical presentation
Diagnosis Missed miscarriage Molar gestation
Uterine size Small for dates 50% large for dates
Theca lutein cysts Rare 25–30%
Medical complications Rare 10–25%
Post-molar GTN 2.5–7.5% 6.8–20%
RBC, red blood cells; GTN, gestational trophoblastic neoplasia.
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EARLY PREGNANCY
GESTATIONAL TROPHOBLASTIC DISEASE – PATHOLOGY

Premalignant
Complete Hydatidiform Mole
In a complete hydatidiform mole, the villi are grossly swollen and are likened to ‘bunches of
grapes’. There is no embryo. Microscopically, the villi are enormously distended.
Hyperplasia of both the syncytio-trophoblast and the cytotrophoblast can be observed.
Partial Mole
In this case, there are two
populations of villi. Some
are of normal size and
configuration, and contain
fetal vessels, while others
show the typical grape-like
appearance of hydatidiform
change. Frequently, an
embryo or embryonic tissue
is present. Trophoblast
hyperplasia is very focal and
is usually confined to the
syncytio-trophoblast.
326
EARLY PREGNANCY
GESTATIONAL TROPHOBLASTIC DISEASE – PRESENTATION

AND GENETICS
Presentation
Early pregnancy bleeding
The degree of bleeding is variable but can be significant.
Excessive nausea and vomiting in early pregnancy
This is related to high levels of serum bHCG.
Symptoms of hyperthyroidism
bHCG is a thyrotropic molecule and
when in excess, they bind to the TSH
receptor
Larger than expected uterine size
for gestation
Cytogenetics
Genetics of hydatidiform mole
1. Complete Mole
The karyotype of a complete
mole is 46XX in 95% and
46XY in 5%, but all of the
chromosomes are of paternal
origin. The pronucleus of the
ovum is absent. The empty
egg is fertilised by a haploid
23X sperm which duplicates
its chromosomes without cell
division (less commonly) or
by two different sperm. Why
the ovum should fail to
contribute to the process is
not known. As complete
moles are more likely to
become malignant, the
karyotype of every mole
should be determined.
2. Partial Mole
In a partial mole, fetal tissue of some type is
present and the karyotype is entirely different. It is
usually triploid – 69XXX or 69XXY with both
maternal and paternal DNA. This is due to
fertilisation of the egg by two sperm. Partial moles
are less likely to undergo malignant change. 327
EARLY PREGNANCY
GESTATIONAL TROPHOBLASTIC DISEASE – TREATMENT

The diagnosis is made using an ultrasound (see p. 326) and bHCG levels. Partial moles
may appear as a missed miscarriage and may not detected until the pathology is available. If
a molar pregnancy is suspected, then uterine evacuation should be performed.
Prior to Evacuation
A full blood count, clotting studies and crossmatching for blood type should be performed.
Renal and liver function analysis.
bHCG levels.
Chest X-ray.
Evacuation
No cervical ripening agents to be used, for example misoprostol.
There is increased incidence of post-evacuation neoplasia.
Suction evacuation using a large suction cannula should be performed.
Post Evacuation
Registration with a gestational trophoblastic disease centre should be done.
Serial bHCG estimation should be performed.
Advise use of reliable contraceptive during follow-up.
Advise not to attempt pregnancy for at least 6 months following treatment.
bHCG levels to be checked after any subsequent pregnancy.
Post-Molar Gestational Trophoblastic Neoplasia
7.5–20% incidence following complete molar pregnancy
2.5–7.5% incidence following partial molar pregnancy.
Chemotherapy is indicated where there is persistent post-molar disease.
GESTATIONAL TROPHOBLASTIC NEOPLASIA

Malignant
Invasive mole
This is a condition in which the molar tissue invades through the decidua and into the
myometrium and its associated blood vessels. It almost always results from a complete,
rather than a partial, mole. Perforation of the uterus may occur, resulting in invasion of the
parametrium.
Spontaneous resolution can occur, but to prevent morbidity and mortality these lesions are
treated with surgery where fertility is of no concern and with chemotherapy if fertility
sparing is required.
328
EARLY PREGNANCY
Gestational
Choriocarcinoma
This occurs most commonly
after a complete molar
pregnancy but can also occur
after any pregnancy. This is a CXR Evidence of
rare condition and a non- Pulmonary
Metastases
gestational variant can arise
directly in the ovary. Only about
2% of moles give rise to a
choriocarcinoma but the risk is
1000 times greater than the risk
after normal delivery.
These tumours metastasise, with
the lung being the commonest
site.
Placental Site Trophoblast

Tumour
This is a rare lesion in which a few
villi are formed. The bulk of the
tissue consists of the chorionic
epithelium, much of which has not
properly differentiated into the
usual two types. These can occur
at variable lengths of time after CT Evidence of
pregnancy. Pulmonary
Metastases
329
EARLY PREGNANCY
CHEMOTHERAPY FOR CHORIOCARCINOMA

A choriocarcinoma is very chemosensitive and its rates of cure can be high. Prognostic
variables which help determine a suitable chemotherapeutic regimen are calculated following
patient referral to a specialist centre.
Patients in the Low Risk Group Patients in High Risk Group
They are treated using a single agent They are treated with multiagent chemotherapy
chemotherapy regimen. regimen.
Recurrence rates <5%
330
CHAPTER 16
SEXUALITY AND CONTRACEPTION
Physiology of Coitus 332 Vascular Disease 343

Excitement Phase 332 Hypertension 343
Plateau Phase 332 Oral Contraceptives and
Orgasm 333 Neoplasia 344
Postcoital Phase or Resolution Endometrium and Ovary 344
Phase 333 Progestogen-Only Pill (POP) 344
Sexual Problems 333 Other Routes 344
Loss of Libido 333 Vaginal Rings 344
Failure to Achieve Orgasm 333 Injectable Progestogens 344
Dyspareunia 334 Progestogen-Only Implants 345
Dyspareunia (Painful Coitus) 334 Intrauterine Devices (IUDs) 346
Sexual Problems Affecting the Mode of Action 346
Male 335 Principle of Insertion of IUDs 347
Premature Ejaculation 335 Complications of Intrauterine
Erectile Dysfunction 335 Devices 348
Treatment Options for Erectile Diaphragms and Caps 349
Dysfunction 336 Condoms 350
Organic Causes 336 The Sponge 350
Psychosexual Counselling 336 Contraception Based on Time
Sildenafil (Viagra) 336 of Ovulation 351
Sex Hormones 336 The Rhythm Method
Papaverine 336 (‘Safe Period’) 351
Ejaculatory Failure 336 The Ovulation Method
Medico-Legal Problems 337 (The Billings’ Method) 351
Rape 337 Postcoital Contraception 352
Methods of Contraception 338 Postcoital Contraception
Failure Rates in Contraception 339 (‘Morning After’
Patient Suitability for Contraception) 352
Contraception 339 Irreversible Methods 353
Hormonal Contraception 340 Sterilisation 353
Combined Oral Contraception 340 Laparoscopic Sterilisation 355
Minor Side Effects of OCs 342 Vasectomy 356
Failure of the Pill 342
Oral Contraception: Risks 343
PHYSIOLOGY OF COITUS
It is important to understand the physiology of sexual function as sexual dysfunction cannot

only be the primary reason for a referral to gynaecology, but often may be a secondary issue
that is related to other complaints, for example pain and fertility. Sexual history should be
taken sensitively and the patients should be able to express their concerns in a non-judgmental
environment.
The response to sexual stimulation is primarily an autonomic nervous reflex which can be
reinforced or inhibited by psychological, hormonal and social factors. These factors are
infinitely variable and understanding the social and psychological influences that are affecting
an individual cannot be easily covered during a single consultation. Referral to a specialist
psychosexual counselling service should also be considered.
The normal sexual response has been categorised into a series of phases by researchers
Masters and Johnson in the 1960s. These are excitement, plateau, orgasm and refractory. The
initial interest in sex, also known as libido, is probably harder to define, but as a
generalisation, it may be said that the female responds to the consciousness of being desired as
a whole person, while satisfaction in the male depends to a greater extent on visceral
sensation.
EXCITEMENT PHASE
Female Male
Vasodilatation and vasocongestion of all Penile erection occurs and may be transient
erectile tissue. Breasts enlarge, the vaginal and recur if this stage is prolonged. Scrotal
ostium opens and secretion from the skin and dartos muscle contract and draw
vestibular glands and vaginal exudations testes towards the perineum
cause ‘moistening’
PLATEAU PHASE
In both, the male and the female, the pulse rate, blood pressure and respiratory rate increase.
Both partners make involuntary thrusting movements of the pelvis towards each other.
Female Male
Vasocongestion increases, and contraction The intensity of penile erection increases
of the uterine ligaments (which contain and the testes are enlarged by congestion.
muscle) lift the uterus and move it more into Seminal fluid arrives at the urethra as a
alignment with the axis of the pelvis. The result of sympathetic nervous stimulation
cervix dilates. There is engorgement of the of the vas deferens, seminal vesicles and
lower third of the vagina and ballooning of the prostate. There is some pre-ejaculatory
the upper two thirds penile discharge which may contain sperm
332
PHYSIOLOGY OF COITUS
ORGASM
Pulse and respiration rate are at double their resting rate, and blood pressure may reach 180/
110. Pelvic and genital sensations are completely dominating, and there is a noticeable
reduction in the sensory awareness in other parts of the body. The pelvic floor contracts
involuntarily, with rhythmic contraction of the vagina, urethra and the anal sphincter.
Female Male
Climactic sensations appear to be caused by Strong contractions pass along the penis
spasmodic contractions of vaginal muscles causing ejaculation of seminal fluid. The
and uterus. The female is potentially capable greater the volume of ejaculate (after several
of repeated orgasm days’ abstinence) the more intense the
sensations of orgasm
POSTCOITAL PHASE OR RESOLUTION PHASE

Pulse, respiratory rate and blood pressure rapidly return to normal and there is marked
sweating. Vasocongestion recedes over about 5 min and there is complete relaxation of all
muscles and a detumescence of erectile tissue. In the male, but less so in the female, there
occurs a refractory period, which varies with individuals, from a few minutes to several hours
during which there is no response to further stimuli.
SEXUAL PROBLEMS
Normal sexual activity and behaviour change with a number of factors including age, social
circumstances, background and values, but it can also be affected by illness or medication and
adverse psychological experiences.
LOSS OF LIBIDO
As previously discussed, interest in sex is a more complex process for women and it can be
adversely affected by a number of common social factors, for example having a baby, stress at
work, bereavement, etc. There is some evidence that it is influenced by hormonal factors; in
particular, it has been shown that women who have had their ovaries removed have lower
levels of androgens and these women may benefit from testosterone supplementation. For
some postmenopausal women standard hormone replacement therapy may be of benefit.
FAILURE TO ACHIEVE ORGASM

The failure to achieve an orgasm is a common problem in women, although relatively few
women seek medical advice. As with the loss of libido, there may be a number of causative
factors. However, many women do not experience orgasm during penetrative intercourse and
require stimulation of the clitoris or other erogenous zones. Psychosexual counselling should
be offered.
333
DYSPAREUNIA
DYSPAREUNIA (PAINFUL COITUS) 6. Painful perineal scar.

Superficial Dyspareunia This may be due to an inflamed or
It is vaginal pain during sexual intercourse. fibrous scar following childbirth, or to an
imperfectly repaired episiotomy or tear.
Causes include:
1. Vulvovaginitis (especially infection by
trichomonas or candida).
2. Vaginal cysts. Small ones are usually
symptomless.
3. Infection of the Bartholin’s gland.
4. Postmenopausal atrophy.
5. Rarely, there is a congenital narrowing
of the ostium or a thick hymen.
Deep Dyspareunia
Pain is due to pressure on an area of tenderness near the vaginal vault. The cause is often difficult to
identify and there may be no obvious disease but a number of pelvic pathologies should be considered.
Examples include:
Pelvic infection.
Endometriosis.
Pelvic masses including an ectopic pregnancy.
Scarring of the vaginal vault following
hysterectomy.
Vaginismus
It is a partly voluntary contraction of the pelvic
muscles that takes place when the introduction
of the penis is attempted, making coitus
impossible. It can also occur with insertion of
tampons or during a vaginal examination.
Causes are as those for the other forms of
sexual dysfunction.
Treatment
Referral to psychosexual counselling can often be helpful in treating vaginismus and should be
a key element of any treatments offered.
Vaginal dilators of graduated sizes are useful. The purpose is not to dilate a narrow vagina but
to give the patient control over her vaginal muscle and the confidence that sexual intercourse
will not be painful.
Mild vaginismus usually responds well to these simple measures, but in severe cases the results
are poor.
Botox therapy is a new technique which may be beneficial in severe cases. The pelvic floor
muscles are temporarily paralysed and for many women normal sexual function continues
334 after muscle function has resumed.
SEXUAL PROBLEMS AFFECTING THE MALE
The gynaecologist is not normally called upon to deal directly with the male, but it can be
useful to be aware of their sexual problems and know something of their management.
PREMATURE EJACULATION
The male ejaculates with minimal sexual
stimulation or before he wishes it to occur.
There are a number of behavioural techniques
that can prolong the sexual episode, such as
stopping repeatedly or the squeeze technique
where intermittent pressure is applied to
the penis by the partner.
There are also some medications that may be
beneficial, including some antidepressants, but
referral should be made to a specialist with an
interest in male sexual disorders.
ERECTILE DYSFUNCTION
This is also known as impotence, is the inability to
achieve or sustain an erection. Erectile dysfunction
becomes more common with age and may have
either a physical or psychological basis. Social,
domestic and relationship pressures can have
significant effects, but it has been increasingly
recognised that organic causes are common.
These include:
• Diabetes mellitus
• Vascular disease and hypertension
• Neurological conditions such as multiple sclerosis, spinal injury
• Radical surgery: extended prostatectomy or abdomino-perineal resection
• Drugs: antihypertensives, antidepressants
• Endocrine causes: prolactinoma, testosterone deficiency
• Urological conditions such as Peyronie’s disease.
335
TREATMENT OPTIONS FOR ERECTILE DYSFUNCTION
ORGANIC CAUSES
These may be reversible, as in endocrine lesions and drugs, and, where possible, treatment of
the underlying condition may be of benefit.
PSYCHOSEXUAL COUNSELLING
This is most useful when social and psychological factors predominate and is often used in
conjunction with drug treatment.
SILDENAFIL (VIAGRA)
An oral therapy for erectile difficulties, this does not produce an erection without sexual
stimulation. Side effects have been reported in men with cardiovascular problems who are on
cardiovascular medication.
SEX HORMONES
Simple prescription of a male sex hormone is seldom successful and its part in the physiology
of erection and ejaculation is not yet known. It has been shown that testosterone levels do
decline with age, but there does not appear to be a male equivalent of the female menopause,
and the role of testosterone replacement therapy remains unclear.
PAPAVERINE
This is a smooth muscle relaxant. Intracavernosal injection is an effective treatment for
impotence.
EJACULATORY FAILURE
It is the inability to ejaculate although there is no loss of erotic drive, erection and intromission
are normal.
The ejaculatory reflex requires intact pathways in both the autonomic and somatic systems.
Somatic nerves receive the sensory stimuli of coitus and pass these impulses to the
sympathetic nerves which then stimulate the delivery of seminal fluid to the urethra by the
vasa deferentia, seminal vesicles and prostate, and prevent retrograde ejaculation into the
bladder by causing contractions of the internal urinary sphincters.
Sympathectomy from T12 to L3 will abolish ejaculation without affecting erectile ability or
the sensations of an orgasm, producing a phenomenon known as ‘dry sex’.
336
MEDICO-LEGAL PROBLEMS
RAPE
The doctor may on occasion be asked to examine a victim of alleged rape. This crime has
heavy penalties and the examination must be thorough and careful. Ideally, the examination
should be performed by a clinician with requisite specialist training and experience. The
victim is likely to have experienced significant trauma and an appropriate supportive
environment and staff trained in counselling techniques, should be available. Major police
forces have specially trained rape investigation teams whose expertise is invaluable.
The following preliminary notes should be made:
1. Authority for examination.
2. Consent for examination.
3. General appearance of person and clothing.
4. History of the circumstances of crime.
Rape is defined as unlawful sexual intercourse with a woman by force and against her will.
Sexual intercourse is described as the slightest degree of penetration of the vulva by the penis
and entry of the hymen is therefore not necessary. (Use of vaginal tampons by virgins may
confuse the issue.)
The vulva should be inspected for signs of
bruising, scratching or tearing. The hymen
may be torn and bleeding.
When the orifice is small or the hymen is
vestigial, bruising may be present because of
the force needed for penetration against the
resistance of the victim. The presence of
seminal fluid in the vagina and cervix may,
sometimes, be the only sign. This fluid is
removed and examined microscopically.
General examination of the patient may show
injuries and bruising, confirming a story of
resistance that has been overcome by
violence.
Skin should be swabbed for blood, semen or
saliva, if there is evidence of these fluids,
using a swab moistened with sterile water, for
DNA analysis. Finger nail clippings should be
taken if there is blood or debris under them.
Comb the head and pubic hair for hairs from the assailant and cut 10 hairs from each site of
the victim for comparison. Blood and urine samples should be taken. These may require to be
tested for drugs.
Careful record keeping is essential. Collection, storage and transport of specimens must
comply with legal requirements so that their source cannot be challenged.
337
METHODS OF CONTRACEPTION
Natural methods Rhythm or Billings

Breastfeeding (while baby is
totally breast fed)
Barrier methods Diaphragm
Cervical cap
Condoms male and female
Spermicides (usually used in Creams, films, foams, jellies, (These are mainly Nonoxynol
conjunction with barrier pessaries, sponges based)
methods)
Hormonal methods Oral contraceptive Combined oestrogen/
progestogen
Progestogen only
Depot progestogens Injections
Subcutaneous silicone
implants
Vaginal Silicone rings releasing
oestrogen and progestogen
Intrauterine devices Inert
Copper bearing
Progestogen releasing
(Mirena).
Surgical methods Laparoscopic sterilisation
Hysteroscopic tubal occlusion
(Essure)
Intrauterine quinacrine
producing tubal fibrosis, in
developing countries
Vasectomy
The ideal contraceptive would have a 100% success rate, have no side effects, and be
completely reversible and totally convenient. Clearly, none of the above fulfil all of these
conditions. Many people are often ill-informed about contraception, and fears about possible
side effects, together with problems experienced by friends and relatives, may play a greater
role in influencing choice than medical advice and statistics. Some medical professionals have
limited knowledge of the details of contraceptive choices and are therefore unable to give
appropriate advice. An informed choice should provide information and counselling, and
written details should, ideally, be supplied along verbal details. Within the UK, specialist
family planning services offer free contraception and advice.
338
METHODS OF CONTRACEPTION
FAILURE RATES IN CONTRACEPTION

There are four factors that affect the failure rate of any method of contraception:
1. Inherent weakness of the method

For example, the rhythm method, which depends on the accurate determination of the
time of ovulation, can never be as reliable as an oral contraceptive (OC).
2. Age
With all methods, the failure rate declines as age increases and fertility and frequency of
intercourse also decrease.
3. Motivation
Every method depends on the determination of the woman to use it correctly. Thus pills
may be forgotten, diaphragm users ‘take a chance’, even with intrauterine devices (IUDs),
a suspicion that the device is out of place may be ignored.
4. Duration of use
The failure rate, especially with occlusive methods, declines as duration of use and
therefore habit, increase.
PATIENT SUITABILITY FOR CONTRACEPTION
Many factors need to be taken into consideration when choosing an appropriate contraceptive
method. These include age, parity, recent pregnancy, smoking, body mass index, medical
history and concomitant medication. The Faculty of Sexual and Reproductive Healthcare
provides evidence-based guidance on its website www.fsrh.org.uk
Potential contraindications are categorised as below
UKMEC categories Definition

UKMEC 1 A condition for which there is no restriction for the use of the
contraceptive method
UKMEC 2 A condition for which the advantages of using the method generally
outweigh the theoretical or proven risk
UKMEC 3 A condition where the theoretical or proven risks usually outweigh
the advantages of using the method. The provision of a method
required expert clinical judgement and/or referral to a specialist
contraceptive provider since the use of this method is not generally
recommended, unless other more appropriate methods are not
available or are unacceptable
UKMEC 4 A condition which represents an unacceptable health risk if the
contraceptive method is used
339
HORMONAL CONTRACEPTION
COMBINED ORAL
CONTRACEPTION
The pill is a mixture of oestrogen
and progestogen, the combined
oral contraceptive pill (COCP)
Mode of Action
The high oestrogen and progestogen
levels reduce the negative feedback
effect so that follicle stimulating
hormone (FSH) secretion is depressed
and the luteinising hormone (LH)
peak is abolished. The combined pill,
therefore, reliably prevents ovulation.
The absence of a corpus luteum inhibits the preparation

of an endometrium that is suitable for implantation,
and a ‘pseudo-atrophy’ develops.
Changes in cervical mucus make

sperm penetration less likely.
All these effects are the result of a
synergistic action between
oestrogen and progestogen.
340
HORMONAL CONTRACEPTION
Constituents
Oestrogens (O) Progestogens (P)

Ethinyloestradiol Levonorgestrel
Norethisterone
Mestranol (ethinyloestradiol- Ethynodiol diacetate
3-methyl-ether) Desogestrel
Gestodene
Norgestimate
Drospirenone
Choice of Pill
There are over 30 brands available, using different drugs in different proportions.
Low dose preparations contain 20 mg of ethinyloestradiol and are particularly suitable for
women with risk factors for circulatory disease.
Standard strength preparations contain 30–35 mg of ethinyloestradiol; however, the risk of
venous thromboembolism varies with the progestogen used.
There are a range of different progestogens, and may have a variety of effects, depending on
their derivation. Side effects such as acne are more likely to be associated with progestogens
that have an androgenic derivation. Drospirenone, a new progestogen, is derived from
spironolactone and has antiandrogenic and anti-mineralocorticoid activity. It is been found to
be useful in women who have fluid retention and is useful in women with the premenstrual
syndrome.
Women should however be offered levonorgestrel- and norethisterone-containing pills as a
first line and alternatives considered only if side effects are problematic.
Risk of venous thromboembolic disease

Non-pregnant, not on the pill 5–10 women per 100,000 per year
Levonorgestrel-and norethisterone-containing pills 15 women per 100,000 per year
Desogestrel and gestodene 25 women per 100,000 per year
Pregnancy 60 women per 100,000 per year
341
MINOR SIDE-EFFECTS OF OCs
Oestrogen Oestrogen and progestogen Progestogen

Breakthrough bleeding Weight gain Acne
Nausea Post-pill amenorrhoea Depression
Painful breasts Dry vagina
Headache Loss of libido
Higher doses of 50–60 mg (taking two pills) can be used by women who are on enzyme
inducing drugs that affect hepatic metabolism. However, this not an ideal long-term option
and it may be best for the woman to consider an alternative approach of contraception that is
not affected by hepatic metabolism.
In the combined pill, the oestrogen and progestogen component is usually given as a uniform
dose for 21 days. This is followed by a 7-day pill-free interval. This break is usually associated
with a withdrawal bleed. Some women opt to exclude the pill-free interval to avoid a
withdrawal bleed. This works well but may be associated with breakthrough bleeding if used
for long periods and it may be best to ‘tricycle’ the COCP, meaning that they run three
packets together at a time followed by a 7-day break to allow a withdrawal bleed.
FAILURE OF THE PILL

The failure rate of the combined pill is very small, between 0% and 1%, and there is often an
avoidable factor.
1. The patient may forget to take the pill. Packing by the pharmaceutical firms is
ingenious but not foolproof. If one pill is missed, two are taken the next day and
additional precautions should be undertaken.
2. Gastroenteritis may impair absorption.
3. Certain groups of drugs such as anticonvulsants, usually phenytoin and phenobarbitone,
and the antibiotic rifampicin are known to increase the metabolic activity of hepatic
enzymes and increase the rate of excretion of contraceptive steroids.
4. Several antibiotics, including ampicillin, are associated with an increase in breakthrough
bleeding, and pregnancy has been reported. Oral contraceptives are conjugated in the
liver, excreted in the bile, and partly reabsorbed. If gut bacteria are inhibited by
antibiotics, reabsorption may not occur, leading to increased bowel excretion but lower
circulating levels of steroids.
342
ORAL CONTRACEPTION: RISKS
Conditions where COCP is contraindicated or special precaution is required:
History of cardiovascular disease Collagen diseases

Hypertension Otosclerosis
Smoking Diabetes mellitus
Obesity Sickle cell anaemia
Chronic hepatitis Severe varicose veins
Depression Migraine
Acute porphyria Arterial or venous thrombosis
A great deal of clinical and laboratory research and epidemiological analysis are available to
support an association between COCPs and thromboembolism and stroke, and there is a
increase in the risk of ischaemic heart disease in women with underlying risk factors. Women
on the COCP, who are over 35 and smoke, have a significant increase in the risk of stroke.
Women with migraine on the COCP are more at risk of
stroke.
VASCULAR DISEASE
The risk of vascular disease, either venous or arterial,
depends on the dose of oestrogen and also on the type of
progestogen (see above). The risk remains low, but
traditional risk factors increase the risk during pill use.
These include thrombophilic tendencies, hypertension and
obesity.
HYPERTENSION
OCs gradually raise the blood pressure, sometimes to the
hypertensive range. The blood volume is increased by fluid
retention, and the secretion of angiotensin is increased.
343
ORAL CONTRACEPTIVES AND NEOPLASIA

No causal link has yet been established between OCs and any kind of neoplasia, but there is
evidence of a small increase in risk of cervical and breast cancer. There has been much
epidemiological debate about the possible mechanisms. It may be that pill users are less likely
to use barrier contraception and, as such, have a higher risk of human papilloma virus
infection.
ENDOMETRIUM AND OVARY

Prolonged OC use depresses mitotic activity in the endometrium and follicular maturation in
the ovary, and these effects significantly reduce the risk of both cancers.
There is also a lower risk of benign conditions such as fibroids. Dysmenorrhoea, premenstrual
syndrome and menstrual loss are also reduced.
PROGESTOGEN-ONLY PILL (POP)

Some 50% of women, on progestogen-only oral contraceptives, ovulate and menstruate, and
the main contraceptive effect is a change in the cervical mucus. Some women bleed irregularly
and around 15% of women are amenorrhoeic with no follicular development. The POP
should be taken at the same time every day for maximum efficacy. Cerazette, a new POP
containing desogestrel, has a 12-h missed pill window similar to COCP, and its contraceptive
efficacy is over 99%.
OTHER ROUTES
VAGINAL RINGS
Silastic ring pessaries have been developed which release either a progestogen alone or both
oestrogen and a progestogen, which are absorbed vaginally, thereby avoiding the first pass
through the liver that results in a subsequent reduction in dosage.
INJECTABLE PROGESTOGENS
The most widely used injectable progestogen is medroxyprogesterone acetate (Depo-Provera),
an intramuscular injection.
Three-monthly injections offer an effective method for contraception for women. The higher
dose of progesterone inhibits ovulation and many women will be rendered amenorrhoeic.
Irregular bleeding is common in the first months of use and some weight gain may also occur.
Long-term use is associated with some loss of bone mineral density and careful consideration
should be given to the risks and benefits. Particular caution should apply in adolescents as
skeletal development is ongoing.
344
PROGESTOGEN-ONLY IMPLANTS
Implanon is available in the UK. It consists of a single rod for subdermal insertion in the
inner aspect of the upper arm and releases etonogestrel. The mode of action involves
inhibition of ovulation but irregular bleeding is common and it may sometimes be persistent.
Insertion and removal should always be performed by someone trained in the procedure.
345
INTRAUTERINE DEVICES (IUDs)
Intrauterine devices (IUDs) have been made from a number of

different materials. Inert coils simply contain plastic but the
common devices also contain a copper or progestogen implant
(Mirena). Most devices have threads that hang through the cervix
to enable easy removal of the device.
MODE OF ACTION
Intrauterine devices prevent fertilisation and implantation. Copper is toxic to both the ova and
the sperm and an inflammatory reaction is induced in the endometrium. Progestogen
releasing intrauterine systems deliver the progestogen directly to the endometrium, rendering
it unreceptive to implantation, and cervical mucus is thickened.
There is an increased risk of pelvic infection. It is thought
that lower genital tract organisms enter the uterus either
during insertion of the device or via the threads. The risk
of pelvic infection is much lower with Mirena as it thickens
the cervical mucus which in turn helps prevent lower
genital tract organisms from entering the uterus.
These devices can also be colonised by actinomyces.
This does not merit a removal of the coil, but
occasionally, pelvic actinomycosis can occur. This is a
chronic, granulomatous infection which should be treated
aggressively with antibiotics and, possibly, surgery.
The length of time that an IUD can last for
depends on the type of device.
The Mirena
This levonorgestrel releasing (20 mg/24 h) intra-
uterine system is licensed for 5 years. It is said to be
as effective as female sterilisation, but the effects are
immediately reversible upon removal.
IUDs commonly cause heavy painful periods but
the Mirena reduces menstrual loss and
dysmenorrhoea due to the local effect of the
progestin on the endometrium and its muscle
346 relaxant effect on the myometrium.
INTRAUTERINE DEVICES (IUDs)
PRINCIPLE OF INSERTION OF IUDs

Insertion Technique
Insertion of an IUD is always easier when a woman has had a previous vaginal delivery. Coil
insertion can also be achieved in nulliparous women. The woman should be examined vaginally
to assess of the size and direction of the uterus, to reduce the risk of uterine perforation.
1. The IUD is first of all folded and pulled into a 2. The introducer is then
plastic tube called the introducer. inserted into the uterus
until it reaches the fundus.
3. The surrounding 4. The rod and introducer is now removed carefully and the
introducer is drawn threads are trimmed to about 4 cm.
back holding the rod in A local anaesthetic and a tenaculum forceps can be useful.
place so that the device The Mirena has a specific introducer that makes insertion
has now opened out in simpler, although it is very slightly thicker than most
the uterine cavity. copper coils, at 4 mm.
Occasionally some sedation or even a general anaesthetic
may be required to insert a coil.
347
COMPLICATIONS OF INTRAUTERINE DEVICES
1. Increased menstrual loss

The cause may be due to the increased fibrinolytic activity that occurs around the IUD. It
can be minimised by the use of antifibrinolytic agents such as tranexamic acid.
Antiprostaglandin agents, such as mefenamic acid or diclofenac, are also effective.
Progestogen releasing devices decrease loss.
2. Infection
There is an increase in the risk of pelvic inflammatory disease, especially during the first
months after insertion. Inert IUDs can be associated with actinomycosis infection if
retained for long periods. Women with active pelvic infection should not have a coil fitted.
Women with an existing coil in place may be given antibiotic treatment with the coil left in
place, but with severe or persistent infection, consideration should be given to coil
removal.
Progestogen releasing systems reduce the incidence of infection as the cervical mucus is
thickened due to the effect of progestin.
3. Pregnancy
The chances of pregnancy are about 1–1.5 per 100 woman years and it is most likely to
occur in the first 2 years. It is lower with copper-bearing coils and may be as low as 0.1 per
100 with the Mirena.{ The risk of ectopic pregnancy is lower in IUD users as the risk of
pregnancy is very low, but in those women who become pregnant with a coil in situ, the
risk of ectopic pregnancy is higher.
4. Expulsion
There is a 5–10% incidence, usually in the first 6 months. It is recommended that a
speculum examination be performed at 6 weeks after coil insertion to check that the
threads are visible. If the threads are not visible, an ultrasound scan should be performed
to check for the presence of an intrauterine coil.
5. Translocation
The IUD passes through the uterine wall
into the peritoneal cavity or the broad
ligament. It is thought that this begins at
the time of a faulty insertion.
An intrauterine coil is usually identified on
scan but an extrauterine coil can be very
difficult to visualise using the ultrasound. If
an intrauterine location has not been
confirmed, an abdominal/pelvic X-ray
should be performed. If the coil is outside
the uterus, a laparoscopy, and possible
laparotomy, may be needed to locate it.
{
348 Sivin I, et al. Contraception (1991) 44:473.
DIAPHRAGMS AND CAPS
The diaphragm is inserted into the vagina prior to intercourse.

It is used in conjunction with a spermicidal cream and it acts
by preventing sperm cells from reaching the cervical canal.
It has a higher failure rate compared to oral contraceptives
or IUDs but it has few side effects.
1. The diaphragm is smeared with 2. The front end is tucked up behind the
spermicidal cream round the edges symphysis pubis.
and on both sides, and guided into
the posterior fornix.
The diaphragm must not be removed until

6 h after intercourse, and if intercourse is
repeated in that period more cream must first
be injected using an applicator.
Caps act in a similar way but are designed to
fit over the cervix.
349
CONDOMS
A thin rubber sheath fits over the penis. Condoms can interfere with sensation; however, they
reduce the risk of sexually transmitted infections and may be used in addition to other
contraceptive methods. Condoms can split and they are liable to come off as the penis is
withdrawn after the act. The failure rate is higher
than for oral contraceptives. Lubricants, such as
‘baby oil’, can weaken condoms.
THE SPONGE
A disposable plastic sponge, impregnated with
spermicide, is inserted into the vagina and can be
left in situ for at least 24 h. Sponges need no fitting
and are comfortable; however, they have a higher
pregnancy risk than the diaphragm.
350
CONTRACEPTION BASED ON TIME OF OVULATION
THE RHYTHM METHOD (‘Safe Period’)

The woman must take her temperature every morning and watch out for the sustained rise
which indicates ovulation. Women with regular periods can often usually identify the peri-
ovulatory time with a fair degree of accuracy. However, an episode of hormonal irregularity
may occur without warning and this can put the woman at risk of pregnancy.
However, assuming the cycle is regular and
lasts for 28 days, ovulation usually occurs
between the 12th and 14th days of the
cycle. 24 h are allowed for ovum survival
and 3 days should be allowed as survival
time of the sperms in the genital tract,
although sperm have been shown to survive
for up to a week.
This means that intercourse must be
avoided from the 9th to the 15th day and a
24 h safety margin at either end increases
the avoidance period from the 8th to the
17th day, both inclusive.
THE OVULATION METHOD (The Billings’ Method)

The woman is taught to identify the peri-ovulatory phase by noting the changes in cervical
mucus.
This method provides the same opportunities for coitus as the rhythm method. In practice,
many women will use these methods concurrently. The failure rate depends very much on the
motivation of the couple and on an understanding of the method. It may be more useful to
help women understand and know if they are fertile when they wish to conceive.
Say 5 days Menstruation

2–3 days ‘Early safe days’ Sensation of vaginal dryness
4–5 days Moist days – not safe Increasing amounts of sticky mucus
2 days Ovulation peak – not safe Copious, clear ‘slippery’ mucus
3 days Post-ovulation Peak – not safe Gradual decrease in secretion
11 days ‘Late safe days’ Minimal secretion
Breastfeeding
For many women, particularly in the developing world, lactational amenorrhoea is an effective
method of contraception. It is most effective where an infant is exclusively breast fed, and
ovulation is more likely to occur when the frequency of feeding is reduced. This is usually due
to supplementary milk feeds or weaning of the infant (introduction of solid foods).
351
POSTCOITAL CONTRACEPTION
POSTCOITAL CONTRACEPTION (‘Morning After’ Contraception)

Effective postcoital contraception has been sought for many years, usually in the form of
douching with various liquids, but these have been unsuccessful because of the rapidity with
which the sperm leave the vagina and enter the cervical canal and uterus. Modern methods are
extremely effective, if started early enough.
Hormonal Methods
Levonorgestrel is given as a once-only dose, as soon as possible after unprotected intercourse
(up to 72 h). This is available over the counter, in the UK, to maximise accessibility.
Method of Action
The preparation of the endometrium for implantation is prevented.
Insertion of IUD
This method is highly effective and can be used for up to 5 days after coitus or 5 days after the
estimated date of ovulation. The IUD can be used for continued contraception, if desired.
352
IRREVERSIBLE METHODS
STERILISATION
For Women
The reasons for seeking sterilisation as a contraceptive method are numerous, but many
women seek a method by which they no longer need to be concerned with, for example,
remembering to take pills, etc., and can essentially forget about.
Careful counselling is required as this method should be considered as irreversible and the
woman needs to be sure that her family is complete. It is useful to explore how long she has
felt that this is the case, and it is best to avoid making such a decision at a time of particular
stress, such as the early postnatal period. Possible future change in circumstances should be
considered in a sensitive manner. Careful consideration should be given before patients under
30, and those who have no children, are sterilised. Reversal operations have a success rate of
around 50% but are now only funded, under exceptional circumstances, by the NHS.
Many women come with the expectation that female sterilisation is 100% successful. This is
not the case and this procedure has a failure rate of 1 in 200. The failure rates for long-acting
reversible contraceptives (LARCs) are similar. LARCs include Mirena and Implanon in the
UK. Only a vasectomy is more successful, with 1 in 2000 women becoming pregnant after
their partner has been sterilised.
Alternative contraceptive options should also be discussed. Experience of previous
contraceptive methods should be considered. Clearly, if a woman has conceived or has had
side effects with another method, she may well be unwilling to use it again.
The method of sterilisation should be explained to them, including the need for anaesthesia,
recovery period and risks associated with the procedure. In most women, this will be
performed as a day-case under laparoscopic guidance, but, occasionally, laparotomy may be
the only feasible procedure, for example in extensive adhesions. There is a small risk of
visceral injury as with any laparoscopic procedure, and laparotomy can occasionally be
required as an emergency procedure.
Some women request sterilisation during a caesarean delivery. There is a higher failure rate
and, possibly, a higher incidence of regret. This should be carefully discussed in the antenatal
period. The Royal College of Obstetricians and Gynaecologists recommend that consent for
sterilisation, at the time of a caesarean section, should be taken at least 1 week prior to the
procedure.
If a woman does become pregnant after sterilisation, it is more likely to be a tubal pregnancy
and she should be counselled to seek medical advice.
The woman should be made aware that her periods are likely to be unchanged by sterilisation,
unless she has been on hormonal contraception which may make them lighter. This is not
unusual, and, in women who expect this to be the case, it may be best to opt for the Mirena.
353
IRREVERSIBLE METHODS
It is important to remind the woman to continue with her current contraceptive method until
the next menstrual period, after the procedure is performed.
All of this information should be clearly documented and written information should be given
to the patient.
CLINICAL/COUNSELLING NOTES
FOR FEMALE STERILISATION ADDRESSOGRAPH
LABEL
DATE:
AGE: PARITY: LMP: BMI:
REASONS FOR WANTING STERILISATION:
CURRENT CONTRACEPTIVE METHOD: PREVIOUS CONTRACEPTION:
ALTERNATIVE CONTRACEPTION DISCUSSED: DISCUSSED INTERESTED
Vasectomy – failure rate 1/2000, can be done under local anaesthetic, complications less urology
Mirena - >99% effective, lasts for 5 years, periods less heavy, may cause initial menstrual upset FPC
Implanon - >99% effective, lasts for 3 years, local anaesthetic, initial menstrual upset, weight gain FPC
Depo-provera – (‘The Jag’) >99% effective, lasts for 12 weeks, periods may be irregular or stop, weight gain GP/FPC
IUCD - 99% effective, lasts 3 to 10 years depending on type, periods may be heavier & more painful GP/FPC
Oral contraception (COCP/POP) – COCP >99% effective, periods less heavy; POP 99% effective; GP/FPC
compliance issues
FEMALE STERILISATION DISCUSSED
GENERAL ANAESTHETIC, usually undertaken laparoscopically with clips as day surgery
LAPAROTOMY may be required if surgical complications are encountered ACTION
IRREVERSIBLE – difficult to reverse and NHS may not fund reversal
FAILURE RATE 1/200; if subsequent pregnancy, risk of ECTOPIC is approx. 5%
SURGICAL RISKS greater in high risk women (BMI, abdominal scars, medical disorders)
CONTINUE current contraception until after the procedure
PERIODS will be unchanged (unless on hormonal method pre-op, or an IUCD is removed)
MEDICAL/SURGICAL HISTORY: DRUG HISTORY:
ALLERGIES:
EXAMINATION: ABDOMINAL VAGINAL
CERVICAL SMEAR NEEDED: YES / NO
PREVIOUS ABDOMINAL SURGERY
CONSENT FORM SIGNED LEAFLET GIVEN
COMMENTS/PLAN:
SIGNATURE/PRINT NAME & GRADE: Patient signature:
Instillation of chemical substances. In developing countries with limited facilities and budgets,
insertion of a pellet of quinacrine into the uterine cavity through the cervical canal on two
occasions, 4 weeks apart, has proved to be effective.
354 Hysteroscopic insertion of implants within the fallopian tubes has recently been used to
achieve permanent contraception.
LAPAROSCOPIC STERILISATION
The tubes can be occluded by the application of clips or rings under laparoscopic vision. (Two
clips are applied to each tube by some operators.)
The Hulka-Clemens Clip Applicator
The clip has two jaws of inert

plastic material, locked together by a gold-
plated stainless steel spring. Filshie Clip
Filshie clips, made of titanium lined with
silicone rubber, are smaller.
Disposable Filshie applicator
The Yoon Ring Applicator

Yoon and Falope silicone rubber rings render
a slightly greater length of tube avascular.
The forceps grip the tube and

draw it through a silicone
plastic ring which is then
pushed off the end of
the applicator.
These applicators, whether for clips or rings, are passed into the abdominal cavity through
a trocar, after the passage of a laparoscope. The clips should be placed about 1 cm
from the cornu, and the rings as near to that point as possible. Thick and vascular tubes 355
are more difficult to occlude by these methods.
VASECTOMY
The same principles apply when counselling for male

or female sterilisation (see above). The major
difference is that vasectomy can be performed by a
simple operation that can be done under local
anaesthesia and the success rate is significantly better.
Only 1 in 2000 women become pregnant after their
partner has had a vasectomy.
It takes several months for the storage system to
become clear of sperm, and a few non-motile ones
may persist whose significance is uncertain. It may take
a year before the ejaculate is completely sperm free.
About 5% of patients demonstrate minor
complications, including vaso-vagal reactions,
haematoma and mild infection. There are occasional
reports of severe infection. Possible long-term
complications include the development of sperm
autoantibodies. This can lower the success rate of
reversal of the procedure.
356
CHAPTER 17
INFERTILITY
Infertility 358 Contraindications to the Assessment

Causes of Female Factor Infertility 359 of Tubal Patency 369
Causes of Male Factor Infertility 359 Assisted Conception 370
Investigations 360 Assisted Reproduction Techniques 370
Investigations in the Primary Fertility Drugs 371
Setting 360 Tubal Surgery 373
Investigations in the Secondary Efficacy 373
Setting 360 Side Effects 373
Evidence of Ovulation 361 Assisted Conception Techniques 374
Features Suggestive of Ovulation 361 In Vitro Fertilisation 374
Tests that Confirm the Occurrence Risks of IVF Treatment 376
of Ovulation 362 Intrauterine Insemination
Seminal Analysis 364 (IUI) 378
Tests which Confirm Normal Sperm Intracytoplasmic Sperm Injection
Production 364 (ICSI) 378
Sperm Production Tests 365 Donor Conception 378
Abnormalities in Sperm Gamete Intrafallopian Transfer
Production 366 (GIFT) 378
Sperm Function Tests 367 In Vitro Maturation (IVM) 379
Postcoital Test 367 Reproductive Immunology 379
Measurement of Antisperm Pre-Implantation Genetic Diagnosis
Antibodies 367 (PIGD) 379
In Vitro Assessment of Fertilisation Assisted Conception 380
Ability of Sperm 367 HFEA 380
Abnormal Sperm Function 367 Counselling 380
Tests of Tubal Patency 368
Requirements for the Assessment
of Tubal Patency 369
INFERTILITY
INFERTILITY
Approximately one in seven couples has difficulties in conceiving. In general, 80% of the
couples who have regular sexual intercourse and do not use contraception will get pregnant
within a year. The majority of the remaining 20% achieve a pregnancy within 2 years of trying.
Percentage of couples pregnant after varying time periods of unprotected intercourse
(Gutmacher 1965)
Definitions
Primary infertility is a condition where a couple, who have had no previous pregnancies, are
unable to conceive.
Secondary infertility is a condition where a couple, who have had at least one previous
pregnancy that may have ended in a livebirth, stillbirth, miscarriage, ectopic pregnancy or
induced abortion, are unable to conceive.
Aetiology of Infertility
Lifestyle factors such as heavy smoking or being significantly over- or underweight and stress
can adversely affect both male and female fertility.
358
INFERTILITY
INFERTILITY
CAUSES OF FEMALE FACTOR INFERTILITY

With increasing age, women become less fertile.
There are many causes of infertility (see below). Sometimes, failure to conceive can be due to
a combination of factors. However, in approximately 30% of cases, a clear cause is never
established.
Unexplained infertility 28%

Male factor infertility 21%
Ovulatory disorders 18%
Tubal disease 14%
Endometriosis 6%
Coital problems 5%
Cervical factors 3%
Other factors that may play a part include chronic medical conditions such as diabetes,
epilepsy and thyroid and bowel diseases.
CAUSES OF MALE FACTOR INFERTILITY

Infertility is often thought of as a female issue, but in around 30% of cases, it is because of a
problem in the male partner. As in women, male fertility is also thought to decline with age,
although to what extent is unclear. Possible causes of male infertility include:
• problems with the tubes carrying sperm

• erectile dysfunction
• ejaculatory problems
• previous orchitis
• a past bacterial infection that caused scarring and blocked tubes within the
epididymis as it joins the vas
• past medical treatment such as drug treatment, radiotherapy or surgery – for example,
to correct a hernia, undescended testes or twisted testicles
• genetic problems
• chronic diseases such as diabetes
• drugs.
359
INFERTILITY
INVESTIGATIONS
INVESTIGATIONS IN THE PRIMARY SETTING

When a couple presents to their general practitioner with the issue of infertility, these initial
investigations should be carried out.
Female partner Cervical smear test.

Urine test for Chlamydia (this can cause blockages of the fallopian tube).
Serum progesterone level to check ovulation. This is taken 1 week prior to
menstruation, hence day 21 for a 28-day cycle or day 28 for a 35-day cycle
(see below).
Rubella immunity – if rubella is contracted during the first 3 months of
pregnancy it can seriously harm the developing fetus Women who are not
immune to rubella should be vaccinated, and advised to avoid pregnancy
for 3 months.
Measuring serum FSH (follicle stimulating hormone), LH (luteinising
hormone) and oestradiol to identify hormone imbalances or possible early
menopause.
Male partner Semenalysis to check for abnormalities of the sperm such as number,
motility, and morphology (see below).
Urine test for Chlamydia, which, in addition to being a known cause of
infertility in women, can also affect sperm function and male fertility.
INVESTIGATIONS IN THE SECONDARY SETTING

These are done in the context of a tertiary fertility clinic and after the primary investigations
have been carried out. Some or all of the following tests will be done:
Female partner Measuring serum FSH, LH and oestradiol to identify hormone imbalances or
possible early menopause.
Serum progesterone level to check ovulation. This is taken 1 week prior to
menstruation, hence day 21 for a 28-day cycle or day 28 for a 35-day cycle.
A pelvic ultrasound scan to look at uterine and ovarian anatomy.
Serial ultrasound tracking of the ovaries for looking at developing follicles
(see below).
Checking of tubal patency – either by hysterosalpingogram,
hysteron-contrast sonography or laparoscopic hydrotubation.
Diagnostic laparoscopy – to check for problems with tubal and uterine anatomy.
Hysteroscopy – to check for uterine conditions such as fibroids or polyps
Endometrial biopsy (in rare cases) see below.
Male partner Semenalysis to check for abnormalities of the sperm such as number,
motility and morphology (see below).
Sperm antibody test to check for protein molecules that may prevent sperm
360 from fertilising an egg.
INFERTILITY
EVIDENCE OF OVULATION
FEATURES SUGGESTIVE OF OVULATION

1. Clinical symptoms and signs
Regular menstruation is usually associated with ovulation, however, no clinical symptoms
or signs are sufficiently reliable to confirm ovulation. Supportive laboratory tests are
always required.
2. Changes in basal body temperature

The secretion of progesterone by the corpus luteum induces a rise of around 0.5 C in basal
body temperature (BBT). If BBT is recorded throughout the menstrual cycle, a fall in
temperature is often observed at the time of the LH surge. Charts typical of those generated
by A) a woman with a normal ovulatory cycle, and B) a woman with an anovulatory cycle, are
shown below. The differences in BBT between ovulatory and anovulatory women are not
sufficiently consistent for a diagnosis of ovulation to be made without further tests.
A. Normal BBT chart

from an ovulating
woman
B. Abnormal BBT chart

from a woman who is
not ovulating
361
INFERTILITY
TESTS THAT CONFIRM THE OCCURRENCE OF OVULATION

1. Serum progesterone levels
Estimation of serum progesterone is a simple method for confirming ovulation.
Progesterone is produced by the corpus luteum and its levels reach a peak in the mid-
luteal phase (i.e. 7 days prior to menstruation). If the measured serum progesterone levels
are low, this may indicate either that the patient is not ovulating, or that the blood sample
was withdrawn at an inappropriate time in the cycle. Information about the time of the
subsequent menstrual period is required to accurately interpret the relevance of serum
progesterone levels.
2. Endometrial biopsy
The presence of a secretory endometrium confirms that ovulation has taken place.
Under the influence of progesterone, the endometrial glands dilate, and secretory
vacuoles may be observed within the glandular cells. If an endometrial biopsy is taken
in the luteal phase and examined histologically, secretory changes can be observed.
A biopsy of the endometrium is a relatively invasive process, but it gives useful
information, especially if sensitive progesterone assays are unavailable.
362
INFERTILITY
3. Serial ovarian ultrasound

Over the course of the menstrual cycle, an ovarian follicle develops, grows to 20 mm and
the oöcyte is then released at ovulation. This process can be visualised by a transvaginal
ultrasound examination every 2–3 days during the follicular, ovulatory and early luteal
phases. This procedure is too invasive and expensive to be used in an unselected
population of women complaining of infertility. However, it is often used to monitor the
number and size of the developing ovarian follicles in women undergoing ovulation
induction. The serial ultrasound is the only method of detecting the luteinised unruptured
follicle syndrome (LUF).
Early follicular phase (no ovarian follicle

visible on ultrasound).
Mid-follicular phase (12 mm follicle

visible on ultrasound).
Immediate pre-ovulatory phase (ovarian

follicle on 20 mm diameter).
363
INFERTILITY
SEMINAL ANALYSIS
TESTS WHICH CONFIRM NORMAL SPERM PRODUCTION

Semen Analysis
A basic semen analysis assesses the number, morphology and motility of spermatozoa. The
patient is asked to provide a sample (usually by masturbation), which should be analysed
within 2 hours of production. The sample should be kept warm (15–38 C) during the interval
from production to analysis. Abstinence from sexual activity for a period of 2–3 days is
required before submitting a sample for analysis; otherwise an abnormally low count may be
recorded. The patient should also be advised to keep the sample away from spermicidal
agents, such as those in condoms.
The criteria for normal spermatogenesis may vary from laboratory to laboratory. The WHO
criteria are shown below:
1. Volume: 2 ml
2. Concentration: 20 million/ml
3. Motility: 50% with forward motility (within 60 min of ejaculation)
4. Morphology: 30% normal forms
5. White blood cells: <1 million/ml
Normal human sperm (from Abnormal sperm (from scanning electron

transmission electron micrograph). micrograph).
364
INFERTILITY
SPERM PRODUCTION TESTS
Spermatogenesis takes at
least 72 days. Events such
as viral infection may
influence the result. For
completeness and accuracy
two samples should be
analyzed each taken at
least 3 months apart.
Semen analysis is conventionally

performed by a trained technician
using a microscope with a heated
stage. More recently, computerised
forms of semen analysis have become
available which have the advantages
of speed, reproducibility and
cost-effectiveness.
Sperm movement analysed by a computerised image analysis system: a linear progressive tracks of a 365
non-capacitated sperm population; b high amplitude, non-progressive tracks of a hyperactivated,
capacitated sperm population.
INFERTILITY
ABNORMALITIES IN SPERM PRODUCTION
The causes of abnormalities in sperm production include:
1. Acute and chronic infection of the male genital tract. Gonococcal and coliform infections
respond to antibiotics but chronic prostatitis can be difficult to treat. Spermatozoa are
reduced in number and tend to be malformed and non-motile.
Chlamydial infection may be found in both partners. Sperm motility is reduced, causing
infertility. Both partners should be treated and follow-up examinations of the ejaculate
carried out.
Viral infections can be important, especially mumps. Testicular atrophy may follow this
infection.
2. Immunological reactions in the form of auto-antibodies occur in a variable number of men

(3–12%). Formation of these antisperm antibodies may be stimulated by infection or by
injury, but in most cases the cause is obscure. Steroids in short courses may be helpful.
3. Environmental factors
These include social habits such as smoking, alcohol and drugs.
Also included under this heading are occupational hazards such as working with heavy metals,
welding processes, exposure to high temperatures, pesticides and radioactive materials.
The list of occupations involving substances that are toxic to sperm count is remarkably long:
Agriculture and gardening – handling pesticides, weed killers.
Car industry, painters, battery workers, domestic decorators, smelters – all using
lead products.
Textile industry – exposure to carbon disulphide.
Plastic manufacturing – exposure to chlorinated biphenyls.
Grain storage – exposure to benzine hexachloride.
A large number of therapeutic agents also affect spermatogenesis.

1. Chemotherapeutic agents – these depress sperm production and cause germinal epithelial
aplasia. Rising FSH levels are an indication of these changes.
2. Sulfasalazine reduces sperm motility and number. These effects are reversed if treatment
is stopped.
3. Cimetidine, spironolactone and ketoconazole interfere with androgen action and may
affect spermatogenesis.
4. Anabolic steroids profoundly depress spermatogenesis, but the effect is reversible when
the drug is withdrawn.
5. Antihypertensive drugs, antidepressants and some sedatives cause impotence and may
depress sperm count or motility.
6. Nitofurantoin, antimalarial drugs and corticosteroids depress spermatogenesis.
366
INFERTILITY
SPERM FUNCTION TESTS
Other tests which may be used to assess sperm function:
POSTCOITAL TEST
The postcoital test assesses the ability of sperm to penetrate the human cervical mucus.
Healthy sperm are able to swim through the cervical mucus secreted at mid-cycle. To perform
the test, the couple is advised to have intercourse mid-cycle, and a sample of the cervical
mucus is obtained 9–24 h later. The presence of
20 motile sperm per high powered field
(400 magnification) indicates a positive result.
Although the postcoital test is still widely used, the
requirement for careful timing of intercourse and
cervical mucus recovery means that the test can be
difficult to perform. An alternative is to assess the
distance travelled by sperm through a layer of ‘artificial
mucus’, normally, a polymer of hyaluronic acid. This
test is more easily quantified, and when used in Positive postcoital test showing
combination with antisperm antibodies, gives similar presence of 20 motile sperm in one
information. high powered field.
MEASUREMENT OF ANTISPERM ANTIBODIES

Antisperm antibodies may be found in the serum, seminal fluid or the cervical mucus. Each of these
may adversely affect fertility. Many tests have been devised to assess antisperm antibodies. The
immunobead test (IBT) detects both IgA and IgG antibodies. In the presence of antisperm
antibodies, polyacrylamide beads covered with bound antibody react with the spermatozoa. The
test has good sensitivity and specificity, and this test can also be used to identify the antisperm
antibody binding site – antibodies bound to the head of the sperm have the most serious effect on
fertility.
IN VITRO ASSESSMENT OF FERTILISATION ABILITY OF SPERM

In practice, many couples with male factor infertility are treated with in vitro fertilisation
(IVF). Some sperm are so abnormal that they are unable to fertilise the egg in vitro, and this
will be detected during the course of a conventional IVF regimen. More specialised treatment,
such as intracytoplasmic sperm injection (ICSI), may then be required.
ABNORMAL SPERM FUNCTION

Spermatogenesis may be adversely affected by conditions such as a viral illness; hence it is
important to obtain two samples of sperm, more than 3 months, apart for complete analysis.
Persistent abnormalities in spermatogenesis are rarely treated successfully without recourse to
assisted reproductive technologies. Further investigation and treatment of such men is outside
the scope of this book, but these should be considered before assisted reproduction
technologies are embarked upon.
367
INFERTILITY
TESTS OF TUBAL PATENCY
1. Laparoscopic hydrotubation
Tubal patency can be assessed at laparoscopy. A cannula is inserted into the cervix, and
5–20 ml of methylene blue dye is injected into the cavity of the uterus. If the fallopian
tubes are patent, the dye can be seen spilling out of the end of each tube. An important
advantage of laparoscopic hydrotubation is that it enables inspection of the pelvic organs
during the procedure. Conditions such as pelvic adhesions and endometriosis, both of
which may reduce fertility, can be noted. The major disadvantage of laparoscopy is that it
is an operative procedure that requires a general anaesthetic.
2. Hysterosalpingography
Hysterosalpingography is the radiological visualisation of the genital tract after the
injection of a radio-opaque contrast medium through the cervix. Hysterosalpingography
may be a useful supplementary test in women who have tubal blockage that is
demonstrated at laparoscopy. Hysterosalpingography allows the site of tubal blockage to
be determined, which is helpful if surgery is contemplated.
This is a normal salpingogram. Note:

1. The anteverted uterus is foreshortened.
2. The long thin tubal outline.
3. The ill-defined shadow of peritoneal spill.
4. Cervico-vaginal leakage.
368
INFERTILITY
TESTS OF TUBAL PATENCY
3. Hysterosalpingo-contrast sonography.
Tubal patency can also be assessed by an ultrasound examination. A solution containing
galactose microparticles, visible on ultrasound, is injected though the cervix. If the
fallopian tubes are patent, the solution can be observed passing along the tubes and out
through the fimbrial ends.
4. Falloposcopy
Advances in imaging techniques have allowed the manufacture of hysteroscopes that are
small enough to be passed into the fallopian tube. Internal tube morphology can be
directly assessed. This procedure is only available in specialised centres, but it can be
combined with operative treatments to relieve fallopian tube blockage.
REQUIREMENTS FOR THE ASSESSMENT OF TUBAL PATENCY

1. The patient should have a clear understanding of the procedure that is going to be
performed.
2. To avoid inadvertently performing the procedure when the patient is pregnant, the
procedure should be done during the first half of the menstrual cycle, or may be done at
any phase of a cycle if adequate contraceptive precautions have been taken.
CONTRAINDICATIONS TO THE ASSESSMENT OF TUBAL PATENCY

1. Pregnancy or possible pregnancy.
2. Active pelvic or vaginal infection.
369
INFERTILITY
ASSISTED CONCEPTION
Pre-Pregnancy Infection Screening

Prior to the storage of patient sperm, eggs or embryos a number of screening tests are carried
out to assess the risk of contamination. These include HIV 1 and 2 (anti-HIV – 1, 2), hepatitis
B (HBsAg/Anti-HBc) and hepatitis C (anti-HCV-Ab).
Folic Acid Administration
Folic acid is thought to reduce the risk of neural tube defects in the offspring of pregnant
women. All women planning a pregnancy should be advised to commence folic acid.
ASSISTED REPRODUCTION TECHNIQUES

The treatment of subfertility is very much dependent on the cause. Available techniques
include:
• Fertility drugs
• Surgery
• In vitro fertilisation (IVF) with or without pre-implantation genetic diagnosis (PIGD)
• Intrauterine insemination (IUI)
• Donor insemination (DI)
• Intracytoplasmic sperm injection (ICSI)
• Gamete intrafallopian transfer (GIFT)
• In vitro-maturation (IVM)
• Reproductive immunology
• Surrogacy.
370
INFERTILITY
FERTILITY DRUGS
FERTILITY DRUGS
These are used for inducing ovulation. Some women may become pregnant with these drugs
alone, or alternatively, these may be used in combination with other treatments such as IVF or
IUI. Commonly used drugs include:
1. Clomiphene
Clomiphene is a non-steroidal antioestrogen. It has complex actions, including an
oestrogen-agonistic activity at the endometrium. The major effect of clomiphene is at the
hypothalamus, and it induces ovulation by increasing pituitary gonadotrophin production.
Its side effects include hot flushes, mood swings, nausea, breast tenderness, insomnia,
increased urination, heavy periods, spots and weight gain. The risk of ovarian cancer can
also increase slightly if it is taken for over a year.
2. Metformin
This is an oral insulin sensitising medication
that helps stimulate ovulation in women with
the polycystic ovarian syndrome. Potential side
effects of this drug include nausea, vomiting,
diarrhoea, abdominal pain, a metallic taste,
itching, allergic reactions and rarely hepatitis.
3. Gonadatrophin releasing hormone

analogues (GnRHa)
This is administered by a small pump, which
injects pulses of the drug into the bloodstream.
It is used mainly in ovulation failure caused by
a lack of GnRH. Possible side effects include
abdominal pain, nausea, vomiting, heavy
periods and headaches.
371
INFERTILITY
FERTILITY DRUGS
4. Gonadotrophins
Follicle stimulating hormone (FSH), Gonal-f and Puregon
Luteinising hormone (LH), such as Menogon, Menopur and Merional
The use of gonadotrophins to induce ovulation should only be carried out in specialised
centres. The patient should be monitored by ovarian ultrasound (to determine the
number of follicles and their diameter) combined with serum or urinary oestrogen assays.
These drugs are generally used before treatment cycles during assisted conception, or for
polycystic ovary syndrome in which clomiphene has not been effective. They are
administered as once-daily injections and act by stimulating follicle production in the
ovaries. When the follicles are mature (as deemed by ovarian tracking), an injection of
human chorionic gonadotrophin hormone (hCG) is given to trigger the release of an egg(s).
Ovarian hyperstimulation syndrome (OHSS), risk of multiple pregnancies when used for
ovulation induction, allergic reactions and skin reactions are the potential side effects.
5. GnRH analogues/pituitary agonists (nafarelin, buserelin and goserelin)

These are administered via nasal sprays, daily injections, or as monthly depot injections.
They downregulate the ovarian cycle which results in low levels of FSH, LH and
oestradiol. They are often used before an IVF cycle is commenced. Some side effects
include hot flushes, night sweats, headaches, vaginal dryness, mood swings, changes in
breast size, acne and muscle aches.
6. Gonadotrophin releasing hormone antagonists (cetrotide and orgalutran)

These are given daily by subcutaneous injection and simultaneously with FSH injections.
These drugs act by blocking the release of LH and are administered while the ovaries are
stimulated to produce eggs, in readiness for IVF treatment. Possible side effects include
nausea, headache, injection site reactions, dizziness and malaise.
7. Progesterone (Cyclogest, Gestone, Crinone, Progynova)

This is generally given after the hCG injection or on the day the embryos are returned to
the womb. Its purpose is to prepare the endometrium for nurturing an embryo. This may
help maintain the pregnancy after IVF or IUI.
8. Bromocriptine and carbergoline

These tablets reduce high levels of prolactin, which can be a cause of subfertility. Side
effects include nausea, headache, constipation, dry mouth, skin reactions, hair loss and a
lowering of the voice.
372
INFERTILITY
TUBAL SURGERY
When tubal disease has been confirmed, tubal patency may be improved by surgery. The best
results are obtained when surgery is performed by an operator trained in these techniques,
using an operating microscope. Surgery may be performed laparoscopically, or as an open
procedure. The aim of surgery is to restore tubal patency and mobility. However, the
restoration of tubal patency does not guarantee pregnancy, since tubal function (e.g. the
movement of cilia) may have been permanently destroyed or impaired.
Laparoscopic salpingostomy with laser or

diathermy to (a) incise the tube and scar
the serosa to cause (b) eversion of the
mucosa.
EFFICACY
The efficacy of tubal surgery depends on the extent of the pre-existing disease and on the
particular procedure that is carried out. The best results are achieved after surgery for
sterilisation reversal as pregnancy rates as high as 60%, have been reported. However, with
severe disease, the cumulative pregnancy rate at 24 months after surgery is low at 10%, which
is a little greater than could have been expected after no treatment.
SIDE EFFECTS
– complications of surgery
– increased risk of ectopic pregnancy during a future pregnancy.
373
INFERTILITY
ASSISTED CONCEPTION TECHNIQUES
IN VITRO FERTILISATION
This technique involves the fertilisation of human oöcytes ‘in vitro’. The eggs are harvested
from ovarian follicles that are approximately 20 mm in diameter (i.e. immediately before
ovulation). The eggs are then placed in a culture medium, in an incubator, and fertilised
several hours later. Gonadotrophins are commonly employed to increase the number of pre-
ovulatory oocytes available for collection. The use of a GnRH analogue allows better control
of the timing of egg collection.
Indications for in vitro Fertilisation
1. Unexplained infertility when anatomy and function appear to be normal, and all treatable
causes of infertility have been eliminated.
2. Tubal disease.
3. Lack of success with other techniques such as fertility drugs alone or IUI.
4. Minor degrees of male subfertility, for example, when the sperm count is low, but not so
low that fertilisation is impossible (see ICSI).
Example of a Treatment Schedule

Suppression of the Natural Monthly
Hormone Cycle
The patient is usually given a GnRH
analogue, which blocks the pituitary
receptors and stops the normal
production of GnRH.
Boosting the Egg Supply
Once the natural cycle has been
suppressed, a FSH (e.g. human
menopausal gonadotrophin, hMG) is
administered by daily injection.
Follicle Tracking
This is done by a transvaginal
ultrasound scanning which helps
monitor follicular growth. When the
follicles reach 20 mm in diameter, The diagram shows the sequence of hormone treatments,
ovulation is imminent. At this point,
compared with the normal (shaded).
•
and the much improved luteal progesterone profile ( )
an injection of hCG is given to
facilitate the egg maturation process.
374
INFERTILITY
IN VITRO FERTILISATION—(cont’d)
Collection of Eggs
Egg collection is
carried out by a
transvaginal
ultrasound-guided
aspiration of the
ovarian follicles. Light
sedation may be
required for this
process.
Egg Fertilisation
The eggs and sperm are then cultured, in vitro, for 16–20 h to allow fertilisation to occur. The
fertilised eggs (embryos) are then grown to the 4–8 cell stage. The best one, or two, embryos
are then chosen for transfer back to the uterus.
Human egg, 18 h
after fertilisation Normal human embryo
at the 4 cell stage
48 h after fertilisation
and ready for transfer
Two pronuclear back to the uterus
bodies (one
from the sperm
and one from
the egg itself)
After egg collection, progesterone is often given to prepare the lining of the womb for embryo
transfer. This can be in the form of pessaries, an injection or a gel.
375
INFERTILITY
Embryo Transfer
For women under 40 years of age, one or two embryos can be transferred. If the woman is
over 40, however, a maximum of three embryos can be used. A restriction on the number of
embryos used is to prevent multiple births and its associated risks. Any remaining embryos
can be frozen for future IVF attempts, if they are suitable.
RISKS OF IVF TREATMENT

(1) Side effects of hormonal therapy – hot flushes, mood changes, headaches, restlessness.
(2) Multiple births (twins, triplets or more) – this is the single greatest health risk associated with
fertility treatment. The Human Fertilisation and Embryology Authority (HFEA) has
imposed restrictions on the number of embryos that can be transferred during IVF in
order to reduce the number of multiple births. Multiple births carry risks for both the
mother and fetuses. The babies are more likely to be premature and tend to have below-
normal birth weight. The perinatal mortality rate has been shown to be four times greater
in twins compared to singletons, and for triplets, the risk is seven times greater than for
singletons. In addition, the risk of cerebral palsy is five times higher for twins and 18 times
higher for triplets, compared to singletons.
376
INFERTILITY
(3) Ovarian hyperstimulation syndrome
The ovarian hyperstimulation syndrome is a potentially dangerous overreaction to certain
drugs that are used to stimulate ovarian follicle production. It is characterised by a sudden
increase in vascular permeability with a massive extravascular exudate. The condition is
categorised into mild, moderate and severe disease. In severe disease, there is evidence of
intravascular loss, with ascites and pleural effusion. The resulting haemoconcentration
can lead to hepatorenal failure and thrombosis. The condition can be fatal and should be
carefully managed by fluid balance, thromboprophylaxis and, where necessary, dialysis
and paracentesis. The mainstay of management is prevention, which involves careful
monitoring of ovarian stimulation and a withholding of hCG in women at risk.
(4) Ectopic pregnancy – there is a higher chance of this occurring after IVF (especially in the
context of tubal disease) when compared to a spontaneous conception.
EFFICACY
The success of IVF is dependent on the age of the female partner, the indications for
treatment, the number of embryos replaced and the skill of the IVF treatment centre. The
cumulative conception rate, after three treatment cycles, varies from over 40% (in women
aged 20–24) to 20% (in women aged 40–45). The live birth rate is considerably lower at 377
around 30% (in women aged 20–24) to less than 15% (in women aged 40–45).
INFERTILITY
INTRAUTERINE INSEMINATION (IUI)

IUI involves a laboratory procedure that separates fast-moving sperm from more sluggish or
non-moving sperm. The fast-moving sperm are then placed into the woman’s womb, close to
the time of ovulation, when the egg is released from the ovary in the middle of the monthly
cycle. Prior to IUI, it is essential that fallopian tubes are
proven to be patent. IUI can be carried out with or
without the use of fertility drugs.
INTRACYTOPLASMIC SPERM
INJECTION (ICSI)
ICSI involves the injection of a single sperm into an egg.
This technique is used when, in the male partner, the
sperm count is so low, or if the sperm function is so
abnormal, that they would not normally be able to
fertilise an egg, either in vitro or in vivo.
DONOR CONCEPTION
Donor conception involves using sperm, eggs or
embryos from donors. DI uses sperm from a donor to
achieve conception. Sperm donors are screened for
sexually transmitted diseases and some genetic disorders. In DI, sperm from the donor is
placed into the cervix at the time of ovulation.
Donor eggs are fertilised in vitro, frozen, and placed in a recipient who has been treated with
oestrogens and progesterones, as described above. Such treatment may be useful in women
with premature menopause.
GAMETE INTRAFALLOPIAN TRANSFER (GIFT)
GIFT involves the replacement of harvested sperm and eggs into the fallopian tube, before
fertilisation occurs. The advantage of this technique is that the expertise of an embryologist is
not required. Clearly, GIFT is unsuitable for women with tubal disease. Pregnancy rates are
similar to those achieved by conventional IVF. However, the clinical guidelines on fertility,
issued by NICE (the National Institute for Health and Clinical Excellence) state: ‘There is
insufficient evidence to recommend the use of GIFT . . . in preference to IVF in couples with
unexplained fertility problems or male factor fertility problems.’
378
INFERTILITY
IN VITRO MATURATION (IVM)

With IVM, eggs are removed from the ovaries and collected when they are still immature.
They are then matured in the laboratory, before being fertilised. The difference between IVM
and conventional IVF is that the eggs are immature when they are collected. This means that
the woman does not need to take as many drugs before the eggs can be collected as she might
if using conventional IVF, wherein mature eggs are collected. This is a useful technique,
particularly in patients who are susceptible to developing the ovarian hyperstimulation
syndrome.
REPRODUCTIVE IMMUNOLOGY
Reproductive immunology (still in its infancy) is a method which offers treatments aimed at
the patient’s immune system, in an effort to sustain a pregnancy. The theory behind this is that
the natural killer (NK) cells, found within the endometrium, may be attacking the implanting
embryo, thus resulting in miscarriage. Uterine NK cells are present in large numbers in the
wall of the womb at implantation and in the early months of pregnancy. They appear to
facilitate the placental link between the mother and the fetus – the mechanism of this is,
however, not clear.
Treatments to ‘suppress NK cells’, offered by some clinics, include high-dose steroids,
intravenous immunoglobulin and tumour necrosis factor-a (TNF) blocking agents. These
treatments are not licensed for use in reproductive medicine. As with all medical
interventions, they carry risks and potential side effects.
PRE-IMPLANTATION GENETIC DIAGNOSIS (PIGD)

PIGD testing involves carrying out tests on embryos, created through IVF or ICSI, to detect
certain inherited conditions or abnormalities. The embryo is grown in the laboratory for 2–3
days until the cells have divided and the embryo consists of around eight cells. An
embryologist then removes one or two of the cells (blastomeres) from the embryo. The cells
are tested to see if the embryo from which they were removed contains the gene that causes a
genetic condition in the family. Embryos unaffected by the condition are transferred to the
womb for development. Any suitable remaining unaffected embryos can be frozen for later
use. Those embryos that are affected by the condition are allowed to perish. Another method,
known as the trophectoderm biopsy, is also available, wherein the embryo is allowed to
develop for 5–6 days such that there are 100–150 cells. At this stage, cells within an embryo
have separated into two types: cells which will form the fetus (inner cell mass) and cells which
will form the placenta (trophectoderm). More cells can be removed at this stage (from the
trophectoderm) without compromising the viability of the embryo, possibly leading to a more
accurate test.
379
INFERTILITY
ASSISTED CONCEPTION
HFEA (HUMAN FERTILISATION AND EMBRYOLOGY AUTHORITY)

HFEA was created by an act of the UK parliament in 1990. Its function is to license and
monitor clinics that carry out ART (e.g. IVF, DI, etc.). The HFEA inspects each clinic on an
annual basis. It also lays down criteria on what is considered as acceptable treatment (e.g.
women under the age of 40 can have either one or two embryos transferred (if however, the
woman is 40, or over, a maximum of three can be used) it requires clinics to make counselling
facilities available to patients; it forbids the payment of donors, etc.). In other countries (e.g.
the USA), there are no legal restraints on treatment; however, clinics have an ethical
obligation to treat their patients with clinical, rather than commercial, principles in mind.
COUNSELLING
Infertility is not just a medical condition, as it also affects the couple’s perceptions of
themselves as individuals, their relationship and their functioning in society. The use of
assisted reproductive technologies, such as IVF, has allowed many couples to bear children
when they could not conceive naturally. However, these technologies may be a mixed
blessing – they are stressful to undergo and are by no means completely effective.
It is important, while dealing with subfertile couples, to give them an accurate description of
the cause of their infertility and their prognosis, both with and without treatment. The efficacy
and the side effects of the various treatment options should be discussed. In addition to this
detailed medical information, the couple should be encouraged to explore their feelings about
their situation. The use of professionals with counselling skills is invaluable, and, indeed, the
provision of counselling facilities is required by the HFEA, as a prerequisite for their licensing
of ART providers.
380
CHAPTER 18
THE MENOPAUSE
The Menopause 382

Signs and Symptoms 383
Common Menopausal Symptoms 383
The Greene Climacteric Scale 384
Changes in the Genital Tract 385
Osteoporosis 386
Cardiovascular Disease and the Menopause 389
Risks and Benefits of HRT 390
HRT and the Breast 390
Hormone Replacement Therapy 391
Factors Influencing Prescription of HRT 391
Severity of Symptoms and Quality of Life 391
Duration of Therapy 391
Screening 391
Choice of Treatment 392
Pros and Cons of Different Routes 392
HRT: Miscellaneous 393
THE MENOPAUSE
THE MENOPAUSE
The word menopause means the cessation of menstruation, but it is commonly also used to
describe events leading up to, and following, the final menstrual period. For about 10% of
women, menses cease suddenly, but for a majority of women, the final period is preceded by
several years of erratic periods. This phase is known as the perimenopause.
Oestrogen levels fall over the 5 years preceding
ovarian failure, which occurs usually between
45 and 55 years of age, with an average of
around 50 years. The fall in oestradiol has a
positive feedback effect on the pituitary,
increasing the production of follicle stimulating
hormone (FSH) and luteinising hormone (LH).
Once menopause has occurred, the FSH level is
usually above 30 iu/l. FSH levels increase in the
perimenopause but levels can fluctuate. The
anti-Müllerian hormone (AMH) is a better
marker of ovarian reserve. The ovary eventually
produces only androstenedione, also produced
by the adrenals, which is converted in the
peripheral fat to the weak oestrogen, oestrone.
Cause of Menopause
Ovarian failure occurs when only a few thousand primordial follicles remain – an insufficient
number to stimulate cyclical activity. Now that women in developed countries have a life
expectancy of around 80 years, at least one-third of a woman’s life is spent in the post-
reproductive, ‘menopausal’ phase.
Premature menopause may occur due to surgical removal of the ovaries, radiotherapy or
chemotherapy; however, for most women, the cause is less clear. Premature ovarian failure is
associated with auto-immune conditions, but in some women there may be a genetic element.
There is a slightly higher chance that conserved ovaries may fail following a hysterectomy.
Menopause occurs 6–18 months earlier in smokers.
Differential Diagnosis
Before the days of immunological pregnancy tests and effective contraception, pregnancy
and menopause were easily confused. Other causes of amenorrhoea, for example, polycystic
ovarian syndrome or a prolactinoma should also be considered (see Chapter 6).
FSH (U/l) LH (U/l) Oestradiol (rmol/l)

Principal changes Premenopausal 2–20 5–25 100–600
in serum hormone
Postmenopausal 40–70 50–70 60
levels:
382
THE MENOPAUSE
THE MENOPAUSE
SIGNS AND SYMPTOMS

These are related to changes in circulating oestrogen levels, and the symptoms may start to
occur some years before menstruation ceases.
COMMON MENOPAUSAL SYMPTOMS

Vasomotor Symptoms
Hot flushes are the classic menopausal symptom. When they occur at night, they are known
as night sweats. This often affects sleep quality and this in turn can affect the quality of life.
In a vast majority of women, these will settle within the first few years of menopause, but for
some women there will be a long-term problem.
Psychological Symptoms
Emotional liability and mood disturbance.
Poor memory and concentration.
Loss of libido.
Urogenital Atrophy
The epithelium of the genital tract and lower part of the urethra is highly sensitive to
oestrogen deprivation. Symptoms include:
Vaginal dryness and dyspareunia
Urinary urgency and frequency
Severity and Duration
of Symptoms
It can be useful to attempt
to quantify these
symptoms, and the
following questionnaire
demonstrates the variety
that can occur.
383
THE MENOPAUSE
THE GREENE CLIMACTERIC SCALE
Please indicate the extent to which you are troubled at the moment by any of these symptoms
by placing a tick in the appropriate box.
SYMPTOMS Not at all A little Quite a bit Extremely Score

0–3
1. Heart beating quickly or strongly
2. Feeling tense or nervous
3. Difficulty in sleeping
4. Excitable
5. Attacks of panic
6. Difficulty in concentrating
7. Feeling tired or lacking in energy
8. Loss of interest in most things
9. Feeling unhappy or depressed
10. Crying spells
11. Irritability
12. Feeling dizzy or faint
13. Pressure or tightness in head or body
14. Parts of body feel numb or tingling
15. Headaches
16. Muscle and joint pains
17. Loss of feeling in the hands or feet
18. Breathing difficulties
19. Hot flushes
20. Sweating at night
21. Loss of interest in sex
Psychological (1–11) = Somatic (12–18) = Vasomotor (19–20) =
Anxiety (1–6) = Depression (7–11) = Sexual dysfunction (21) =
[Greene, J.G. (1991), Guide to the Greene Climacteric Scale. University of Glasgow.]
This scale may be used to measure climacteric symptoms and their response to treatment or to
compare different treatment regimes.
An Anxiety score of 10 or more indicates severe, and possibly clinical, anxiety. A Depression
score of 10 or more indicates severe, and possibly clinical, depression.
384
THE MENOPAUSE
CHANGES IN THE GENITAL TRACT
These changes are of atrophic type and affect the external genitalia as well as the internal
organs. These changes occur over a number of years.
Not only are the main pelvic structures reduced in size but, more importantly, the fascial
framework and the intrapelvic ligaments supporting the bladder and genitalia are weakened;
this may lead to vaginal prolapse and urinary incontinence.
Vulva: There is flattening of the labia Uterus: The uterus becomes small
majora, the minor labia become more with a relatively large cervix – a
evident. Sexual hair becomes grey and return to infantile proportions.
sparse. The clitoris shrinks.
Tubes and ovaries: These show great

shrinkage, the tubes becoming thin while
the ovaries are reduced to small white
wrinkled bodies, about 2–3 cm in length.
In addition to shrinkage of the vaginal introitus, the vagina diminishes in length and its
secretions are limited, leading to vaginal dryness and dyspareunia. Changes in the vaginal
epithelium are also seen. There is loss of rugosity and the epithelium becomes atrophic, with
petechial haemorrhages in some cases and loss of glycogen.
Normal premenopausal vaginal Smear of premenopausal vaginal epithelium.

epithelium. Note the thick cornified The cells are large with small nuclei and
layer. characteristic folded edges. Polymorphs are
385
few in number.
THE MENOPAUSE
OSTEOPOROSIS
Osteoporosis is the most common metabolic bone disease. Postmenopausal osteoporosis

results from an excess of bone resorption over bone formation, and is associated with the loss
of oestrogen. Women have 20% less bone than men at peak skeletal development, and hence
they have less bone to lose before reaching the fragility threshold. More than 50% of
Caucasian women suffer one or more osteoporotic fractures by the age of 70. Osteoporotic
fractures, particularly of the neck of the femur and vertebrae, have significant impact on the
lives of the affected women, and for society as a whole.
Risk factors for osteoporosis are:
1. Female sex.
2. White or oriental race.
3. Family history of osteoporosis.
4. Early menopause (natural or oophorectomy).
5. Sedentary life-style.
6. Low weight for height.
7. Tobacco and alcohol.
8. Low calcium intake.
Incidence of classical osteoporotic fractures

by decades of life (stipple). Note the loss
of height and the development of dorsal
kyphosis with age.
DEXA (dual X-ray densitometry) is currently the favoured technique for measuring the
lumbar spine and femoral neck densities, even though loss of height or the radiological
demonstration of vertebral crush fractures also give clear evidence of osteoporosis. Bone
mineral density (BMD) above minus 1 SD below the young adult mean is normal, osteopenia
lies between 1 and 2.5 SD and osteoporosis below 2.5 SD of the young adult mean.
Ultrasonic densitometry of the calcaneum is of some value, but is not at present a substitute
for DEXA scanning.
386
THE MENOPAUSE
OSTEOPOROSIS
BONE DENSITOMETRY
L2–L4 BMD (g/cm2) 0.809 0.01

L2–L4% young adult 67 3
L2–L4% age matched 79 3
BMD Young adult Age matched

Region g/cm2 % T % Z
L2–L4 0.809 67 3.26 79 1.80
At –3.26 SD of young adult, there is definite osteoporosis of lumbar spine
Neck BMD (g/cm2) 0.614 0.02

Neck % young adult 63 3
Neck % age matched 75 3
NECK :BMC (g) ¼ 3.06 Area (cm2) ¼ 4.99

WARDS :BMC (g) ¼ 1.50 Area (cm2) ¼ 2.76
TROCH :BMC (g) ¼ 4.47 Area (cm2) ¼ 9.45
BMD Young adult Age matched
Region g/cm2 % T % Z
NECK 0.614 63 3.05 75 1.73
WARDS 0.542 60 2.83 78 1.18
TROCH 0.473 60 2.88 67 2.07
387
Osteoporosis at all three sites in this hip
THE MENOPAUSE
OSTEOPOROSIS
Comparative cortical bone thicknesses:
Normal vertebral body. Note Vertebrae from postmenopausal

the thick trabeculae of bone. woman showing extreme
rarefaction of the trabeculae.
Oestrogens have an antiresorptive effect on the bone, and there is good evidence that hormone
replacement therapy (HRT) use is associated with a decreased risk of fractures. HRT is not
recommended as a first line treatment for osteoporosis; however, HRT should be considered
for women who have experienced a premature menopause, whether natural or surgical.
First line treatment for osteoporosis is the administration of bisphosphonates, a non-hormonal
preparation. Other options include raloxifene, a selective oestrogen receptor modulator that
has an antioestrogen effect on the breast and endometrium.
Bone loss recommences on stopping therapy, so withdrawal of HRT at age 65 results in bone
density at ages 75 or 80 being no better than that of untreated women.
388
THE MENOPAUSE
CARDIOVASCULAR DISEASE AND THE MENOPAUSE
In European countries, 40 to 45% of deaths are due to cardiovascular causes, with a relative increase
in risk in females after the menopause. (The actual risk is greater in males even after 75 years.)
Mortality rate for selected causes per 100,000 population in Scotland, 1988.
(Source: Registrar General for Scotland.)
Fractured Ischaemic Cerebro-
Endometrial Cervical Breast Lung femur heart vascular
cancer cancer cancer cancer (estimated) disease disease
All ages 4 7 48 52 <20 316 196
45–64 6 14 88 114 <10 170 62
65–74 12 22 130 206 <25 854 325
The risk of coronary heart disease is increased sevenfold by bilateral oophorectomy before
35 years of age and by premature menopause at 35 years. The rates of coronary heart disease
are lower for women when compared to men, but there is an increase which occurs in the
years after the menopause. Endogenous female hormones have a number of protective effects
on the cardiovascular system and HRT has been shown to replicate some of these features.
Lipid metabolism ................................ oestrogen increases high density lipoprotein

(HDL) cholesterol and lowers low density
lipoprotein (HDL) cholesterol.
Carbohydrate metabolism ......................... oestrogen reduced insulin resistance.
Blood flow........................................... oestrogen increases arterial blood flow.
They also have multiple effects on coagulation and fibrinolysis, with evidence for activation
of coagulation. This is particularly the case with oral HRT. There is also evidence of an
inflammatory effect as CRP increases with oral HRT.
389
THE MENOPAUSE
CARDIOVASCULAR DISEASE AND THE MENOPAUSE
RISKS AND BENEFITS OF HRT

Early observational studies had suggested a number of health benefits associated with HRT
use, specifically a significantly lower risk of cardiovascular disease and osteoporosis. It had
also been shown that HRT use was associated with a small increase in the risk of breast cancer
and that this was higher with long-term use. It had also been shown that HRT use was
associated with an increased risk of venous thromboembolic disease.
Several large randomised placebo-controlled trials were published in the late 1990s and the
subsequent years. These demonstrated no evidence of HRT having a protective effect against
heart disease. The largest of these studies, The Women’s Health Initiative, was stopped before
completion as there was an overall small increase in the risks, when compared to the benefits
of HRT use. A higher risk of breast cancer, venous thromboembolic disease, heart disease
and stroke, but a lower risk of osteoporosis and colon cancer, was demonstrated. There is,
however, some evidence that HRT, started in the early postmenopausal years, has a
cardioprotective effect, presumably before vascular disease has become established.
The results of these studies have significantly reduced HRT prescription and uptake.
However, the women recruited were older than the typical HRT seeking population, for
symptom control. The current recommendation is that women should be prescribed HRT for
menopausal symptoms and not for health benefits such as prevention of osteoporosis. The
lowest effective dose should be used for the shortest time possible. This will vary from woman
to woman.
HRT AND THE BREAST

Fear of an increased risk of breast cancer is the main cause of concern about HRT, in both
patients and doctors.
Breast cancer is increasing in incidence and may affect one woman out of nine in a lifetime.
Alcohol use in young women may increase the risk, and obesity, high socioeconomic status
and delayed first pregnancy are other risk factors. Early menarche, late menopause and
nulliparity are also risk factors. Only 20% of the subjects have a positive family history.
A woman’s risk of developing breast cancer is significantly increased when her mother, sister
or daughter have developed the disease before the age of 50 years. A number of genetic
mutations have been identified, with the commonest being the BRCA gene, and women with
a strong family history of breast and ovarian cancer should be referred for genetic counselling.
Early menopause decreases breast cancer risk (70% reduction with menopause before
35 years).
Between the ages of 50 and 70 years, when most HRT is prescribed, 45 women per thousand
not taking HRT, will develop breast cancer. Using HRT for 5 years between the ages 50
and 70 increases this by only 2 per thousand, 10 years use adds 6 per thousand and 15 years
use adds 12 per thousand.
390
THE MENOPAUSE
HORMONE REPLACEMENT THERAPY
Oestrogen replacement remains the most effective treatment for menopausal symptoms. The
doses required are much lower than those used for oral contraception. For women with an
intact uterus progesterone is also required as oestrogen alone (unopposed oestrogen) is
associated with endometrial hyperplasia and an increased risk of endometrial cancer.
FACTORS INFLUENCING PRESCRIPTION OF HRT

HRT prescription should be considered carefully for any woman, but a number of factors
need to be taken into account and the risks and benefits discussed on an individual basis.
SEVERITY OF SYMPTOMS AND QUALITY OF LIFE

Women who have minimal symptoms may require no treatment. Clearly, women who
experience symptoms that affect their quality of life will be more likely to opt for HRT.
Contraindications Relative contraindications

Pregnancy Cerebrovascular accident
Uninvestigated abnormal vaginal bleeding Severe migraine
Breast cancer or other oestrogen-dependent Thrombophilia
tumour
Venous thromboembolic disease
Myocardial infarction or unstable angina
Severe liver disease
Route of administration: oral preparations, transdermal patches or gels, implants, local preparations.
Concurrent medication: with anticonvulsant, epileptic, or other liver enzyme inducing therapy,
avoid oral HRT.
DURATION OF THERAPY
The main reason for HRT prescription is menopausal symptoms and it may be best to stop
HRT at intervals and recommence if symptoms are an ongoing problem.
Women who have experienced a premature menopause should use HRT until the age of
natural menopause, that is, around 50 years.
Acceptability of therapy: If side effects are problematic then a review of the regimen should be
considered, as well as other treatment options. Withdrawal bleeds and hormonal effects, such
as fluid retention, are common side effects and may settle with time.
SCREENING
Screening before and on HRT is similar to well-woman screening.
Women should be encouraged to take part in national breast and cervical screening programmes.
Pelvic examination should be performed only where clinically indicated.
Blood pressure should be checked every 6 months.
391
THE MENOPAUSE
Hormone levels can be useful in women who have had a hysterectomy with conservation of
the ovaries; however, hormone levels are not required in the vast majority of women. They can
even be normal in the perimenopause. HRT should only be prescribed on a clinical basis.
CHOICE OF TREATMENT
This involves the following considerations:
Routes of administration
1. Oral – tablets.
2. Transdermal – patches. Oral
3. Percutaneous – gel. Low bioavailability.
4. Subcutaneous – implants. Oestradiol dose in mg/day.
5. Vaginal Subject to first pass metabolism
– cream in the liver.
– pessary Serum oestrone
– tablet level > oestradiol level.
– ring (silastic).
Parenteral
High bioavailability.
Oestradiol dose absorbed in mg/day.
No first pass metabolism in the liver.
Serum oestradiol level > oestrone level (more physiological).
PROS AND CONS OF DIFFERENT ROUTES

Oral
1. Economical.
2. Wide choice of preparations and doses.
3. Absorbed into portal system and passes through liver before reaching systemic circulation
with metabolism to oestrone and liver enzyme induction. More effects on lipids and
coagulation.
4. May cause nausea.
Transdermal and Percutaneous

1. More physiological, with absorption into and distribution by systemic circulation, and not
the hepatic portal system.
2. Lesser effect on coagulation.
3. High patient acceptability (if no skin irritation).
4. More costly.
392
THE MENOPAUSE
Subcutaneous Implants (25 or 50 mg pure crystalline oestradiol)

1. Can be effective where other routes fail.
2. Risk of escalation of oestradiol levels, so strict control of dose and frequency of implants is
necessary. Some women will be symptomatic even with supraphysiological oestradiol
levels, this is known as tachyphylaxis.
Vaginal Preparations
Oestriol preparations and low dose oestradiol tablets (0.025 mg) do not have systemic effects,
and can give local benefit in women with contraindications to systemic therapy.
Potent oestrogens given vaginally have systemic effects.
Vaginal preparations relieve atrophic vaginitis, trigonitis, vaginal dryness and dyspareunia.
Vaginal silastic ring pessaries can be low dose oestradiol for local effect, or higher dose
oestradiol to get a parenteral, systemic effect, with each pessary lasting for 3 months.
Alternatives to Oestrogen
When systemic oestrogen is contraindicated, not tolerated or declined, the following may be
useful:
1. Progestogens (norethisterone, megestrol acetate, medroxyprogesterone acetate). In
significant doses, there is an increased risk of thrombosis.
2. Low dose vaginal oestrogen preparations for urogenital symptoms.
3. Selective serotonin reuptake inhibitors have been shown to be effective for some women.
HRT: MISCELLANEOUS
Contraception in the Climacteric
Ovulation may occur after 6 months of amenorrhoea.
Most HRT preparations are not contraceptive.
Effective contraception is recommended until 1 year after menstruation ceases, in the absence
of a vasectomy or female sterilisation. After the age of 45, it is considered that intrauterine
devices (IUDs) do not require to be renewed regularly and that they can be left in situ till there
is no risk of pregnancy. Levonorgestrel releasing IUDs serve a double purpose, giving
excellent contraceptive protection and also countering the effects of oestrogen on the
endometrium.
Barrier contraception has a low failure rate in climacteric women.
393
SUBJECT INDEX
Notes Actinomycin D, sarcoma botriodes menopause 89

vs. indicates a comparison or 171 pregnancy 89
differential diagnosis Acute pelvic inflammation, ovarian primary 71
The following abbreviations have cyst accidents vs. 261 secondary 71
been used: Acute pelvic inflammatory disease treatment 96
CIN - cervical intra-epithelial 149 AMH see Anti-Müllerian hormone
neoplasia Addisonian crisis, congenital adrenal (AMH)
DVT - deep vein thrombosis hyperplasia 63 Ampicillin, pelvic inflammatory
FSH - follicle-stimulating Adenocanthoma, cervical cancer 184 disease management 149
hormone Adenocarcinoma Ampule implantation, tubal
GnRH - gonadotrophin cervical cancer 184 pregnancy 323
releasing hormone Fallopian tubes carcinoma 285 Anabolic steroids, sperm production
HRT - hormone replacement Adenocarcinoma in situ 159 abnormalities 366
therapy Adenomyosis 122 Anaemia, uterine fibroids 199
IUDs - intra-uterine devices microscopy 122 Anaesthetic, IUD insertion 347
LH - luteinizing hormone Adhesions, surgical complications Anal triangle 12
293 Anatomical perineum 12
Adjuvant chemotherapy, ovarian Androgen-producing tumours
Abdominal aorta 34, 41 epithelial tumours 277 hirsutism 105
Abdominal examination 75–77 Adnexal mass, tubal pregnancy 321 ovaries 273–274
ascites 77 Adrenal-like tumours 274 Anembryonic pregnancy 309
hypersplenism 76 Adriamycin, endometrial cancer Anorexia nervosa 101
kidney palpation 76 recurrence treatment 210 Antegrade pyelography 291
liver enlargement 76 Adult uterus 38 Anterior colporrhaphy
obesity 77 Adventitia, ureter 233 stress incontinence 245
ovarian cysts 75, 77 Age, contraception failure rates 339 vaginal prolapse 223–224
palpation 76 Age-related changes 39–41 Anterior fornix, vagina 23
pregnancy 75 ovary 38 Anterior vaginal prolapse 218
uterus enlargement 75 uterus 38 Anteverted uterus retroversion
Abdominal hysterectomy vagina 38 214
endometrial cancer treatment vulva 38 Anti-androgens, hirsutism treatment
209 AIDS 153 108
total 209 intercurrent infections 154 Antibiotic therapy
urinary fistula formation 292 lymphomas 153 broad-spectrum see Broad
Abdominal pain paediatric 154 spectrum antibiotics
pedicle torsion 259 see also HIV infection Candida albicans infection 136
tubal pregnancy 321 Alkylating agents, mechanism of combined oral contraceptive pill
Abdominal ultrasound, action 281 failure 342
obesity 77 Ambulation, DVT 300 Anti-cardiolipin antibody syndrome
Ablation, CIN treatment 180–181 Amenorrhoea 88 316
Abnormal bleeding causes 89 Anti-coagulant therapy, pulmonary
definition 71 history taking 102 embolism 305
see also specific types of hyperprolactinaemia 99 Anti-depressants, sperm production
haemorrhage investigation 102–104 abnormalities 366
Abortion progesterone challenge test 102 Anti-D immunoglobulin,
tubal 323 prolactin levels 102 miscarriage management 312
see also Miscarriage; Pregnancy TSH 102 Anti-hypertensive drugs, sperm
termination physical examination 102 production abnormalities 366
Accessory horn, uterus 65 physiological 89 Anti-malarial drugs, sperm
Aciclovir, genital herpes 140 lactation 89 production abnormalities 366
SUBJECT INDEX
Anti-metabolites Bacterial vaginosis 137 Blood flow, menopause 389

mechanism of action 281 Bacteriology, pelvic inflammatory Blood loss estimation, dysfunctional
ovarian tumour treatment 282 disease 149 uterine bleeding 110
Anti-mitotics, mechanism of action 281 Ball diathermy, CIN treatment 181 Blood stream, ovarian tumour
Anti-Müllerian hormone (AMH) Barrier contraception methods 338 spread 277
complete androgen insensitivity 62 Bartholin’s glands 15 Blood supply
menopause 382 cysts 158 ovary 34
Anti-progesterone priming, ducts 14 uterus 39–40
miscarriage management 312, 313 embryology 8 vagina 39–40
Anti-retroviral drugs, HIV infection histology 15 Blood vessel walls, venous
154 infection, superficial dyspareunia thrombosis 296
Anti-sperm antibodies 367 334 BMD (bone mineral density),
Appendicitis, pelvic inflammatory obstruction, inflammation 133 osteoporosis 386
disease vs. 149 secretions 132 Bone mineral density (BMD),
Arcuate uterus 66 vulval examination 78 osteoporosis 386
Arrhenoblastoma, ovarian tumours Basal body temperature changes, Borderline nuclear changes, cervical
263 ovulation 361 smears 177
Arterial blood gases, pulmonary Benign papilloma, genital warts vs. Botox, vaginismus treatment 334
embolism 303 141 Bowel injury, surgical complications
Artificial urinary sphincters, stress Benign squamous metaplasia, cervix 291
incontinence treatment 244 174 Brachytherapy, cervical cancer 189
Ascites Benign tumours BRCA 1, ovarian tumours 264
abdominal examination 77 vagina 168 BRCA 2, ovarian tumours 264
ovarian tumours vs. 255 vulva 158 Breast(s)
Asherman’s syndrome 91 Bicornuate (double) uterus 65 examination 83–85
Assisted conception 370, 374–379 Bilateral oophorectomy, heavy hormone effects 52, 53
donor conception 378 uterine bleeding 118 HRT 390
ectopic pregnancy 320 Bilateral salpingo-oophorectomy Breast cancer, HRT 390
folic acid administration 370 endometrial cancer treatment 209 Breastfeeding, as contraception
gamete intrafallopian transfer 378 Fallopian tubes carcinoma 285 351
HFEA 380 premenstrual syndrome treatment Brenner tumour 263, 271
intracytoplasmic sperm injection 130 Broad ligament 29, 34–37
378 uterine leiomyosarcoma 212 blood vessels 33
intrauterine insemination 378–379 uterine sarcoma 212 cysts (parovarian cysts) 283
pre-implantation genetic diagnosis Billings’ method (ovulation method) diagnosis 284
379 351 surgery 284
pre-pregnancy infection screening Bimanual pelvic examination 79 cysts vs. ovarian tumours 258
370 uterine retroversion 215 vestigial structures 33
reproductive immunology 379 vaginal discharge 135 Broad spectrum antibiotics
in vitro fertilization see In vitro Biopsies miscarriage management 311
fertilization atypical epithelium identification pelvic inflammatory disease
in vitro maturation 379 179 management 149
Asymptomatic vaginal prolapse 220 cervical cancer diagnosis 186 Bromocriptine
Atrophic vaginitis 139 trophectoderm 379 hyperprolactinaemia treatment
Atypical epithelium identification, Bisphosphonates, osteoporosis 388 100
cervical cancer 179 Bladder infertility treatment 372
Atypical hyperplasia, endometrial blood supply 39–40 Bulb of vestibule, vulva 15
hyperplasia 201 cancer, urinary fistula formation Bulbospongiosus muscle 16
Autoantibodies, sperm production 293 Burch’s colposuspension operation
abnormalities 366 full, ovarian tumours vs. 255 247
Autoimmune factors, recurrent function examination 242 Buserelin, infertility treatment 372
miscarriage 315 injuries, surgical complications
Autonomic nerve supply, pelvis 44 288 CA125, ovarian tumours 253
Azithromycin innervation 235 Cabergoline
Chlamydia trachomatis infection 142 retraining, detrusor instability hyperprolactinaemia treatment
pelvic inflammatory disease treatment 249 100
management 149 Bladder neck relaxation (funnelling) infertility treatment 372
236 CAH (congenital adrenal
Backache, vaginal prolapse 220 Bleeding, intermenstrual hyperplasia) 63
Bacterial infections 142 see Intermenstrual bleeding Call–Exner bodies, gonadoblastoma
396 see also specific infections Blighted ovum 309 268
SUBJECT INDEX
Candida albicans infection 136 stage IB 187 normal 177

Caps, contraception 349 stage IB1 187 severe dyskaryosis 177
Carbohydrate metabolism, stage IB2 187 Cervicitis with ectopy, cervical
menopause 389 stage II 187 cancer vs. 186
Carbon dioxide laser, CIN treatment stage IIA 187 Cervix 26, 27
180 stage IIA1 187 anatomy 174
Carboplatin stage IIA2 187 benign squamous metaplasia
ovarian tumour treatment stage IIB 187 174
277, 282 stage III 188 bimanual pelvic examination 79
side effects 282 stage IIIa 188 cancer see Cervical cancer
Carcinoid ovarian tumours 275 stage IIIb 188 (carcinoma)
Carcinoma, ovarian tumours 264 stage IV 188 diseases 173–193
Carcinosarcoma, uterine sarcoma stage IVa 188 see also specific diseases/disorders
211, 212 stage IVb 188 ectocervix 174
Cardinal ligaments 30, 216 surgery 190–193 ectopy 148
Cardiovascular disease, menopause advantages 193 endocervix 174
see Menopause chemotherapy vs. 193 glands 31
Cardiovascular system, hormone complications 192 secretions 132
effects 53 exenteration for relapsed histology 31
Caruncle, urethra 165 disease 192 normal epithelium 174
Carunculae myrtiformes 14 fertility-sparing surgery 192 physiological variation 148
CEA, ovarian tumours 253 large loop excision of the relationship with ureter 28
Cefixime, gonorrhoea treatment 144 transformation zone 190 trauma, dilatation and curettage
Ceftriaxone microinvasive 190 113
gonorrhoea treatment 144 radical hysterectomy and node vaginal discharge 134
pelvic inflammatory disease dissection 190–191 weakness, recurrent miscarriage
management 149 radical surgery 192 314, 316
Central pulmonary embolism 302 symptoms 183 Cetrotide, infertility treatment 372
Cervical cancer (carcinoma) 178, see also Cervical intra-epithelial Chancre
183 neoplasia (CIN) cervical cancer vs. 186
adenocanthoma 184 Cervical intra-epithelial neoplasia syphilis 145
adenocarcinoma 184 (CIN) 178 Chancroid 143
atypical epithelium identification grade 1 178 Chaperones, gynaecological
179 treatment 180 examination 74
chemotherapy 189 grade 2 178 Chemotherapy
surgery vs. 193 treatment 180 adjuvant, ovarian epithelial
clinical findings 183 grade 3 178 tumours 277
diagnosis 186 treatment 180 cervical cancer 189
differential diagnosis 186 progression risk 178 endometrial cancer recurrence
direct spread 185 treatment 180–182 treatment 210
dysplasia 178 ablation 180–181 mechanisms 281
FIGO staging 188 ball diathermy 181 ovarian tumours 281
microinvasive 178 carbon dioxide laser 180 side effects 282
palliative care 193 cold coagulation 180 sperm production abnormalities
premalignant 178 cryosurgery 181 366
prognosis 193 excisional techniques 181–182 toxicity 282
radiotherapy 189 follow-up 182 vulval carcinoma 164
advantages 193 knife cone biopsy 182 see also specific drugs
brachytherapy 189 large loop excision of the Chest x-ray, pulmonary embolism
complications 189 transformation zone 181 303
external beam therapy 189 laser cone biopsy 182 Chlamydia trachomatis infection 142
screening (cervical smear) Loop Electrosurgical Excision sperm production abnormalities
see Cervical smears procedure 181 366
spread 185 Cervical smears 176 Choriocarcinoma
squamous cell carcinoma 184 borderline nuclear changes 177 gestational see Gestational
staging 187–188 colposcopy referral 177 choriocarcinoma
magnetic resonance imaging glandular abnormalities 177 ovarian tumours 275
188 inflammation 177 Chromosome analysis, genetic
stage IA 187 interpretation 177 abnormalities 59
stage IA1 187 mild dyskaryosis 177 Chronic pelvic inflammatory disease
stage IA2 187 moderate dyskaryosis 177 150 397
SUBJECT INDEX
Chronic thromboembolic heavy uterine bleeding natural methods 338

hypertension 305 management 114 patient suitability 339
Ciliated cells, Fallopian tubes 32 hirsutism treatment 108 postcoital (morning after) 352
Cimetidine, sperm production low dose 341 spermicides 338
abnormalities 366 mode of action 340 sponge 350
CIN see Cervical intra-epithelial premenstrual syndrome treatment success rates 338
neoplasia (CIN) 130 surgery 338
Cisplatin, endometrial cancer side effects 342 time of ovulation 351
recurrence treatment 210 endometrium effects 344 see also specific methods
Clear cell carcinoma hypertension 343 Contrast venography, DVT 299
endometrial cancer 204 neoplasia 344 Copper, IUDs 346
ovarian tumours 263 ovary 344 Cornual implantation, tubal
Clindamycin, bacterial vaginosis 137 stroke 343 pregnancy 323
Clinical syndromes thromboembolism 343 Corona radiata 47
genetic abnormalities 59 vascular disease 343 Corpus albicans, ovary 37
see also specific diseases/disorders standard strength 341 Corpus luteum 36
Clitoris 12, 13–14 venous thromboembolism risk absence, combined oral
embryology 8 341 contraceptive pill 340
Clobetasol propionate, lichen Common iliac artery 39 FSH 36
sclerosus treatment 157 Comparative cortical bone hormones 36, 89
Clomiphene, infertility treatment thicknesses, osteoporosis 388 LH 36
96, 371 Complete androgen insensitivity Corpus, uterus see Uterus
Clotrimazole, Candida albicans 62–63 Cortex, ovary 35, 46
infection 136 Complete hydatiform mole Cortical bone thicknesses,
Coccygeus muscle 19 see Hydatiform mole osteoporosis 388
nerve supply 19 Complete miscarriage 308 Corticosteroids
COCP see Combined oral Complete procidentia 217 congenital adrenal hyperplasia 63
contraceptive pill (COCP) Compliance, combined oral sperm production abnormalities
Coelomic epithelium contraceptive pill failure 342 366
genital ridges 3 Computed tomography (CT) Counselling
sex cords 3 endometrial cancer 206 infertility 380
Coitus hyperprolactinaemia 99 sterilization 353
definition 337 ovarian tumour diagnosis 255 Cramp, dysmenorrhoea 120
excitatory phase 332 pulmonary angiography, Crinone, infertility treatment 372
orgasm 333 pulmonary embolism 304 Cruciate anastomosis 41
plateau phase 332 renogram, ureteric surgical injury Crush injury, ureteric surgical injury
postcoital (resolution) phase 290 290
333 Conception, assisted see Assisted Cryocautery, genital warts therapy
problems, vaginal prolapse 220 conception 141
Cold coagulation, CIN treatment Concurrent medication, HRT 391 Cryosurgery, CIN treatment 181
180 Condoms, contraception 350 CT see Computed tomography (CT)
Colon, surgical injury 291 Congenital adrenal hyperplasia Cumulus oophorus 47
Colpoperineorrhaphy, posterior 227 (CAH) 63 Curettage
Colporrhaphy, anterior see Anterior Congenital adrenal hyperplasia, and dilatation see Dilatation and
colporrhaphy hirsutism 105 curettage
Colposcopy 179 Congenital androgen insensitivity 91 miscarriage management 312
definition 179 Congenital urinary fistula 293 placental site trophoblastic
referral, cervical smears 177 Conservative management, tubal tumour 196
Combined oral contraceptive pill pregnancy treatment 324 Cusco’s speculum 71
(COCP) 340–341 Contraception 331–356 Cyclogest, infertility treatment 372
amenorrhoea treatment 96 barrier methods 338 Cyclophosphamide, sarcoma
choice 341 caps 349 botriodes 171
constituents 341 condoms 350 Cyproterone, hirsutism treatment
drospirenone 341 contraindications 339 108
ethinyloestradiol 341 diaphragms 349 Cyst(s)
progestogens 341 failure rates 339 Bartholin’s glands 158
contraindications 343 history taking 70 uterine retroversion 215
corpus luteum absence 340 hormonal methods 338, 340–341 vagina 168
dysmenorrhoea treatment 121 see also Combined oral Cystadenocarcinoma
endometriosis treatment 127 contraceptive pill (COCP) mucinous 263, 266
398 failure of 342 implantable chemicals 354 serous 263, 265
SUBJECT INDEX
Cystadenoma Diabetes insipidus, incontinence 243 secondary 72

mucinous 263 Diabetes mellitus, incontinence uterine fibroids 198
serous 263, 265 243 Dyspareunia 73, 334
Cystectomy, ovarian tumours 276 Diabetes mellitus type II, polycystic deep 73, 334
Cystic degeneration, uterine fibroids ovarian syndrome 94 menopause 385
199 Diaphragms, contraception 349 superficial 73, 334
Cystoceles 218 Diathermy, hirsutism 107 uterine retroversion 215
anterior colporrhaphy 223–224 Dilatation and curettage 112 vaginal hysterectomy
Cystometry 236, 242 complications 113 complications 230
abnormal 242 pregnancy termination 319 Dysplasia, cervical cancer 178
stress incontinence 242 Dilatation and evacuation, Dysuria, incontinence 239
Cystotomy miscarriage management 313
closure 288 Diverticulitis, pelvic inflammatory Early fetal demise 309
Foley catheter 288 disease vs. 149 Early pregnancy 307–330
Cyst pedicle torsion, pelvic Doderlein’s bacillus 132 bleeding, gestational trophoblastic
inflammatory disease vs. 149 vaginal secretions 15 disease 327
Cytogenetics, gestational Donor conception, assisted Early proliferative phase,
trophoblastic disease 327 conception 378 endometrial cycle 51
Cytology, ovarian tumours 278 Dopamine agonists, Ectocervix 174
hyperprolactinaemia 98 Ectopia vesicae, vulva 68
Danazol, endometriosis 128 Double (bicornuate) uterus 65 Ectopic deposits, endometriosis 123
Deep dyspareunia 73, 334 Doxorubicin, side effects 282 Ectopic kidney, ovarian tumours vs.
Deep perineal pouch 17 Doxycycline 258
Deep vein thrombosis (DVT) Chlamydia trachomatis infection Ectopic pregnancy 320
ambulation 300 142 aetiology 320
clinical features 298 pelvic inflammatory disease assisted conception 320
definition 295 management 149 IUDs 320
hydration 300 Drospirenone, combined oral pelvic inflammatory disease
investigations 299 contraceptive pill 341 320
post operative physiotherapy Drug(s) tubal damage 320
300 detrusor instability treatment 249 Fallopian tubes see Tubal
thromboprophylaxis 300 hirsutism 108 pregnancy
graduated elastic compression hyperprolactinaemia 98 ovarian cyst accidents vs. 261
stocking 300 sperm production abnormalities Ectopy, cervix 148
low molecular weight heparins 366 Eflornithine cream, hirsutism
301 Drug-caused hirsutism 105 treatment 108
mechanical methods 300 Drug interactions, combined oral EIAs (enzyme immunoassays),
pneumatic stocking 300 contraceptive pill failure 342 syphilis diagnosis 146
unfractionated heparin 301 Dual X-ray densitometry (DEXA ), Ejaculatory failure 336
treatment 301 osteoporosis 386 Electrocardiogram (ECG),
Defeminisation Duplex Doppler leg ultrasound, pulmonary embolism 303–304
Sertoli–Leydig cell tumour pulmonary embolism 304 Electro-cautery, genital warts
273 DVT see Deep vein thrombosis therapy 141
see also Masculinization (DVT) Electrolysis, hirsutism 107
Dehydroepiandrosterone sulphate Dysfunctional uterine bleeding 110 ELISA (enzyme-linked
(DHAS), virilisation 106 blood loss estimation 110 immunosorbent assay), genital
Depilatory cream, hirsutism 107 definition 110 herpes diagnosis 140
Depilatory waxes, hirsutism 107 transvaginal ultrasound 110 Embryo abnormalities, recurrent
Dermatoses, vulva 156–157 Dysgenesis, ovary 64 miscarriage 314
Detrusor contraction, micturition Dysgerminoma, ovarian tumours Embryology 1–9
236 263, 268 Bartholin’s glands 8
Detrusor instability 237 Dyskaryosis, severe 177 clitoris 8
stress incontinence vs. 241 Dysmenorrhoea 120–121 Fallopian tubes see Fallopian
symptoms 237 aetiology 120 tubes
treatment 249 clinical features 121 female external genitalia 7–8
Dexamethasone, hirsutism treatment cramp 120 genital (labial) swelling 8
108 definition 72 genital tubercle 8
DEXA (dual x-ray densitometry), drug treatment 121 urethral folds 8
osteoporosis 386 management 121 genital ridges 2, 3
DHAS (dehydroepiandrosterone pain 120 germ cells 2
sulphate), virilisation 106 primary 72 labia minor 8 399
SUBJECT INDEX
Embryology (Continued) atypical hyperplasia 201 Epithelium

male external genitalia 9 classification 201 ovary 46
primary urethral groove 9 clinical findings 201 tumours see Ovarian tumours
scrotum 9 complex 201 vagina 24
testes 9 investigations 202 Epoöphoron 283
mesonephric ducts 6 polycystic ovarian syndrome 96 broad ligament 33
Müllerian (paramesonephric) simple 201 Erectile dysfunction 335
duct 5, 6 treatment 202 treatment 336
Müllerian tubercle 5 Endometrioid carcinoma, ovarian Ethambutol, genital tuberculosis
ovary see Ovaries tumours 263 treatment 152
para-urethral glands of Skene 8 Endometrioma, ovarian tumours Ethinyloestradiol
rete 3 263 combined oral contraceptive pill
urethra 7 Endometriosis 123–125 341
urethral glands 8 clinical findings 126 hirsutism treatment 108
urogenital buds 8 cyclical activity 125 Evening primrose oil, premenstrual
urogenital sinus 7 differential diagnosis 127 syndrome treatment 130
uterus see Uterus ectopic deposits 124 Excisional techniques, CIN
Wolffian (mesonephric) ridge 5 haemorrhage 124 treatment 181–182
Embryo transfer, in vitro fertilization histogenesis 127 Excitatory phase, coitus 332
376 histology 125 Exercise, hypothalamic disorders
Endocervix 174 imaging 127 101
Endocrine disease laparoscopy 126 Explanations to patients,
incontinence 243 medical treatment 127–128 gynaecological examination 74
recurrent miscarriage 315, 316 menstrual abnormalities 126 Expulsion, IUD complications
Endometrial cancer 203–204 pathology 123 348
aetiology 207 physical examination 126 External anal sphincter 16
clear cell carcinoma 204 prevalence 126 External beam therapy, cervical
computed tomography 206 secondary pathology 124 cancer 189
diagnosis 203 surgical treatment 128 External iliac artery 39, 41
grade 1 204 symptoms 126 External urethral orifice 14
grade 2 204 treatment 127–128 vulva 14
grade 3 204 uterine retroversion 215 Extra-amniotic termination,
histology 204 Endometrium 31 pregnancy termination 319
magnetic resonance imaging 206 ablation, heavy uterine bleeding Extremity elevation, lymphoedema
obesity 207 115 294
polycystic ovarian syndrome 96 biopsies 112
postmenopause 203 methods 112 Fainting/collapse, tubal pregnancy
presentation 203 ovulation evidence 362 321
prognosis 208 cancer see Endometrial cancer Fallopian tubes 33
FIGO staging 208 combined oral contraceptive pill abnormalities 64
recurrence 210 effects 344 carcinoma 285
sites 210 hyperplasia see Endometrial clinical staging 285
treatment 210 hyperplasia ciliated cells 32
spread of 206 investigation 111 damage, ectopic pregnancy
local 206 polyps 196 320
lymphatic spread 206 stromal sarcomas 211, 212 development 5–6
staging 205 thickness, transvaginal ultrasound diseases/disorders 251–285
FIGO staging 205 111 see also specific diseases/disorders
stage I 205 Endoscope, laparoscopy 83, 84 menopause 385
stage II 205 Enterocele 219 patency, infertility see Infertility
stage III 205 repair of 228 ‘peg’ cells 32
stage IV 205 Environmental factors pregnancy see Tubal pregnancy
treatment 209 recurrent miscarriage 315, rupture, tubal pregnancy 323
recurrence 210 316 Falloscopy, tubal patency 369
Endometrial cycle 51 sperm production abnormalities Female external genitalia,
early proliferative phase 51 366 embryology see Embryology;
late proliferative phase 51 Enzyme immunoassays (EIAs), specific anatomical features
menstruation 51 syphilis diagnosis 146 Femoral artery 41
secretory phase 51 Enzyme-linked immunosorbent Ferriman Galway charts, hirsutism
Endometrial hyperplasia 201–202 assay (ELISA), genital herpes 107
400 aetiology 202 diagnosis 140 Fertility drugs 371–372
SUBJECT INDEX
Fertility requirements, history FSH see Follicle-stimulating Gestone, infertility treatment

taking 70 hormone (FSH) 372
Fertility-sparing surgery, cervical Full bladder, ovarian tumours vs. GIFT (gamete intrafallopian
cancer 192 255 transfer) 378
Fever, surgical complications Funnelling (bladder neck relaxation) Glandular abnormalities, cervical
294 236 smears 177
Fibrin D-dimer assay, DVT 299 Glycosuria, Candida albicans
Fibroma Gamete intrafallopian transfer infection 136
Meig’s syndrome 272 (GIFT) 378 GnRH see Gonadotrophin releasing
ovarian tumours 263, 272 Gartner’s duct, broad ligament 33 hormone (GnRH)
vulva 158 Gastroenteritis, combined oral GnRHa see Gonadotrophin releasing
FIGO staging contraceptive pill failure 342 hormone analogues (GnRHa)
cervical cancer 188 GECS (graduated elastic Gonadal dysgenesis 92
endometrial cancer 205 compression stocking), DVT 300 Gonadal removal, complete
prognosis 208 Gemeprost, miscarriage androgen insensitivity 62
vulval carcinoma 160 management 312, 313 Gonadoblastoma, ovarian tumours
Fimbrian cysts 33, 284 Genetics 263, 268
Finasteride, hirsutism treatment gestational trophoblastic disease Gonadotrophin(s)
108 327 infertility treatment 372
Fistula formation, surgical recurrent miscarriage 314, 316 in vitro fertilization 374
complications 292–293 Genital herpes 140 Gonadotrophin releasing hormone
Fitz–Hugh–Curtis syndrome, Genital ridges (GnRH)
Chlamydia trachomatis infection coelomic epithelium 3 ovulation 49, 50
142 embryology 2, 3 puberty 54
Flow volume, venous thrombosis mesoderm 3 Gonadotrophin releasing hormone
296 Genital (labial) swelling, analogues (GnRHa)
Fluid balance chart, incontinence embryology 8 endometriosis treatment 128
243 Genital tract hirsutism treatment 108
Fluorescent Treponemal antibody hormone effects 52, 53 infertility treatment 371, 372
tests 146 menopausal changes premenstrual syndrome 129
5-Fluorouracil chemotherapy, see Menopause premenstrual syndrome treatment
vaginal intra-epithelial neoplasia Genital tubercle, embryology 8 130
169 Genital tuberculosis 151–152 uterine fibroid treatment 200
Flutamide, hirsutism treatment 108 cervical cancer vs. 186 Gonadotrophin releasing hormone
Foley’s catheter clinical features 151 antagonists, infertility treatment
cystotomy 288 diagnosis 151 372
Marshall–Marchetti–Krantz pathology 151 Gonorrhoea 144
urethropexy 246 treatment 152 diagnosis 144
Folic acid administration, assisted urinary fistula formation 293 examination 144
conception 370 Genital warts 141 Goserelin, infertility treatment 372
Follicle-stimulating hormone (FSH) differential diagnosis 141 Graafian follicles 36, 47
corpus luteum 36 Germ cells insulin-like growth factor-1 47
follicular phase 50 embryology 2 LH 47
infertility treatment 372 maturation 58 Graduated elastic compression
luteal phase 50 see also Meiosis stocking (GECS), DVT 300
menopause 89, 382 tumours see Ovarian tumours Granuloma inguinale 143
menstruation 50 Gestational choriocarcinoma 329 Granulosa cells 47
ovulation 48, 50 chemotherapy 330 tumour 263
polycystic ovarian syndrome 94 Gestational trophoblastic disease Greene climacteric scale, menopause
premature ovarian failure 93 325 384
Follicle tracking, in vitro fertilization cytogenetics 327 Gubernaculum, ovary development 4
374 genetics 327 Gynaecological examination 74
Follicular atresia, ovary 37 pathology 326 abdominal examination
Follicular phase, hormones 50 presentation 327 see Abdominal examination
Follow-up, CIN treatment 182 treatment 328 bimanual pelvic examination 79
Foreign bodies, vaginitis 139 see also Hydatiform mole breast examination 83–85
Fornices, vagina 23 Gestational trophoblastic neoplasia chaperone 74
Fossa navicularis 14 328–329 explanations to patients 74
Fothergill suture 226 malignant 328 laparoscopy see Laparoscopy
Fourchette 13 placental site trophoblastic principles 74
Frenulum 13 tumour 329 speculum examination 80–81 401
SUBJECT INDEX
Gynaecological examination drug-caused 105 HRT see Hormone replacement

(Continued) Ferriman Galway charts 107 therapy (HRT)
vulval examination 78 idiopathic 105 Hulka–Clemens clip applicator 355
see also Physical examination management 96, 107–108 b-Human chorionic gonadotrophin
Gynaecological perineum 12 drug treatment 108 (bHCG), ovarian
Gynaecomastia, Klinefelter’s local 107 choriocarcinoma 275
syndrome 61 polycystic ovary disease 105 Human chorionic gonadotrophin
Gynatresia, vagina 67 Histology, endometriosis 125 (hCG), tubal pregnancy diagnosis
History taking 69–85, 70–71 321
Haematoma, vulva 158 contraceptive requirements 70 Human papilloma virus(es) (HPVs)
Haematometra 90 difficult situations 70 141
Haematosalpinx 90 fertility requirements 70 benign squamous cervical
Haemoatocolpos 90 menstrual abnormalities 109 metaplasia 174
Haemophilus ducreyi infection menstrual history 71 genome 175
see Chancroid obstetric history 70 infection 175
Haemorrhage parity 70 cervical disease 175
endometriosis 124 smear history 71 see also Genital warts
laparoscopy complications 85 HIV infection 153–154 vulval intra-epithelial neoplasia
miscarriage management 311 anti-retroviral drugs 154 159
uterus see Heavy uterine bleeding transmission 153 Human papilloma virus 16 (HPV-
Hairy leukoplakia 153 see also AIDS 16) 175
Heart disease, HRT 390 Homan’s test, DVT 298 Human papilloma virus 18 (HPV-
Heavy uterine bleeding Hormonal chemotherapy 18) 175
management 114–119 mechanism of action 281 Hyaline degeneration, uterine
medical management 114 ovarian tumour treatment 282 fibroids 199
surgical management 115 Hormonal methods, contraception Hydatid cyst, ovarian tumours vs.
bilateral oophorectomy 118 338, 340–341 257
endometrial ablation 115 Hormone-producing tumours, Hydatids of Morgagni 33, 284
laparoscopy assisted vaginal ovarian tumours see Ovarian Hydatiform mole 325
hysterectomy 119 tumours complete 325–326
microwave endometrial Hormone replacement therapy genetics 327
ablation 116 (HRT) partial 325–326
Novasure 116 benefits 390 genetics 327
subtotal hysterectomy 118 breast cancer 390 pre-malignant complete 326
Thermachoice 116 breasts, effects on 390 Hydration, DVT 300
total hysterectomy 116–117 choice of treatment 392, 393 Hydronephrotic kidney, ovarian
total laparoscopic hysterectomy concurrent medication 391 tumours vs. 257
119 duration 391 Hydrosalpinx, chronic pelvic
vaginal hysterectomy 119 endometrial cancer 203 inflammatory disease 150
Heparin heart disease 390 17-Hydroxycorticosteroids, lipoid
DVT treatment 301 influencing factors 391 cell tumours 274
pulmonary embolism 305 oestrogen 391 21-Hydroxylase deficiency,
Hereditary non-polyposis colorectal oral route 392 congenital adrenal hyperplasia 63
cancer (Lynch II) syndrome 207 osteoporosis 388 17-Hydroxyprogesterone (17-OHP),
Hernia, surgical complications 294 parenteral 392 virilisation 106
Herpes simplex virus type 1 (HSV1) percutaneous 392 Hymen 12
140 quality of life 391 development 6, 14
infection see Genital herpes risks 390 imperforate 90
Herpes simplex virus type 2 (HSV2) route of administration 391, 392 rape 337
140 screening 391–392 Hypercoagulability, venous
infection see Genital herpes stroke 390 thrombosis 296
HFEA, assisted conception 380 subcutaneous implants 393 Hyperinsulinaemia, polycystic
High grade stromal sarcomas, symptoms 391 ovarian syndrome 96
uterine sarcoma 212 transdermal 392 Hyperplasia, endometrium 201
Hilar cell tumours 263, 274 Turner’s syndrome treatment 60 Hyperprolactinaemia 97–100
Hilum, ovary 34, 35 vaginal preparations 393 aetiology 98
Hirsutism 106 venous thromboembolism 390 amenorrhoea mechanism 99
androgen producing tumours 105 Women Health Initiative 390 diagnosis 99
congenital adrenal hyperplasia see also Oestrogen replacement recurrent miscarriage 315
105 therapy surgery 100
402 definition 105 Hormones, corpus luteum 36 treatment 100
SUBJECT INDEX
Hypersplenism, abdominal Immunoglobulin A (IgA) 132 ovulation evidence 361–363

examination 76 Immunological problems basal body temperature
Hypertension, combined oral recurrent miscarriage 316 changes 361
contraceptive pill 343 sperm production abnormalities clinical symptoms and signs
Hyperthyroidism, gestational 366 361
trophoblastic disease 327 Immunosuppressive therapy, endometrial biopsies 362
Hypogastric plexus 44 Candida albicans infection 136 serial ultrasound 363
Hypogonadotrophic hypogonadism Implantable chemicals, serum progesterone 362
101 contraception 354 tests 362–363
Hypothalamus Implantation sites, tubal pregnancy prevalence 358
disorders 101 310 primary 358
hormone effects 52, 53 Implants, subcutaneous, HRT 393 secondary 358
ovulation 49 Incision, ovarian tumours 278 sperm function tests 367
Hypothyroidism, Incomplete miscarriage 309 antisperm antibodies 367
hyperprolactinaemia 98 Incontinence 74, 239 post coital test 367
Hysterectomy bladder function examination 242 in vitro assessment 367
abdominal, urinary fistula dysuria 239 sperm production tests 364
formation 292 endocrine disease 243 abnormalities 366
endometrial hyperplasia treatment fluid balance chart 243 microscopy 365
202 frequency 239 samples 365
with pelvic lymphadenectomy, investigation 241 semen analysis 364
endometrial cancer treatment neurological disease 239, 243 treatment 96
209 nocturia 239 counselling 380
placental site trophoblastic physical examination 241 fertility drugs 371–372
tumour 196 urgency 239 surgery 373
subtotal, heavy uterine bleeding urine bacteriology 243 see also Assisted conception
118 urodynamic assessment 243 tubal patency 368–369
total see Total hysterectomy vaginal hysterectomy assessment contraindications
total abdominal, endometrial complications 230 369
cancer treatment 209 see also Detrusor instability; Stress assessment requirements 369
total laparoscopic, heavy uterine incontinence; specific types falloscopy 369
bleeding 119 Inevitable miscarriage 308 hysterosalpingo-contrast
uterine fibroid treatment 200 Infantile uterus 38 sonography 369
uterine leiomyosarcoma 212 Infections 131–154 hysterosalpingography 368
uterine sarcoma 212 defence mechanisms 132 laparoscopic hydrotubation
vaginal see Vaginal hysterectomy IUD complications 348 368
Hysterosalpingo-contrast laparoscopy complications 85 Inflammation 132
sonography, tubal patency recurrent miscarriage 315 Bartholin’s gland obstruction 133
369 secondary, genital warts 141 cervical smears 177
Hysterosalpingography, tubal sperm function tests 367 Infundibulopelvic ligament 29, 231
patency 368 sperm production abnormalities Inguinal glands, superficial 42
Hysteroscopy 366 Inguinal lymph node, genital herpes
endometrial polyps 196 tropical 143 diagnosis 140
endometrium investigation 111 see also specific infections Inhibin, ovulation 50
Infectious morbidity, surgical Inspection, ovarian tumours 278
ICSI (intracytoplasmic sperm complications 294 Insulin-like growth factor-1,
injection) 378 Inferior mesenteric artery 34, 41 Graafian follicles 47
Idiopathic hirsutism 105 Infertility 357–380 Insulin sensitizing agents,
IgA (immunoglobulin A) 132 aetiology 358 hirsutism treatment 108
Iliococcygeus muscle 20 endometriosis 126 Intermenstrual bleeding
Imaging female factor causes 359 definition 71
DVT 299 genital tuberculosis 152 endometrial polyps 196
endometriosis 127 male factor causes 359 placental site trophoblastic
uterine fibroids 199 pregnancy termination tumour 196
see also specific methods complications 319 Interna; iliac artery 39
Imipramine, detrusor instability definitions 358 Intracytoplasmic sperm injection
treatment 249 examination, laparoscopy 85 (ICSI) 378
Imiquimod cream, genital warts investigations 360 Intra-epithelial neoplasia (AIN)
therapy 141 primary setting 360 159
Immunofluorescence, genital herpes secondary setting 360 Intra-urethral pressure, micturition
diagnosis 140 see also specific investigations 234 403
SUBJECT INDEX
Intra-uterine devices (IUDs) Klebsiella infection see Granuloma LEEP (Loop Electrosurgical
338, 346 inguinale Excision procedure), CIN
complications 348 Klinefelter’s syndrome 61 treatment 181
copper 346 Knife cone biopsy, CIN treatment Left renal vein 34
ectopic pregnancy 320 182 Leg wraps, lymphoedema 294
insertion 347 Kobelt’s tubules 33 Leiomyosarcoma, uterine sarcoma
local anaesthetic 347 cysts 284 211, 212
tenaculum forceps 347 Krükenberg tumours 263, 270 Leucorrhoea, vaginal discharge 135
Mirena 346 Levator ani muscle 19, 216
mode of action 346 Labial (genital) swelling, Levator (anal) fascia 18
pelvic infections 346 embryology 8 Levonorgestrel
post-coital contraception 338–339 Labia majora 12, 13 endometrial hyperplasia treatment
progestin 346 menopause 385 202
Intrauterine insemination (IUI) Labia minora 12, 13–14 post-coital contraception 352
378–379 embryology 8 Levonorgestrel Intrauterine System
Intravenous urography, ureteric menopause 385 (LNG-IUS)
surgical injury 290 Laboratory studies, genetic dysmenorrhoea treatment 121
Intravesical pressure, micturition abnormalities 59 heavy uterine bleeding
234 Lactate dehydrogenase (LDH), management 114
In vitro assessment, sperm function dysgerminoma 268 LGV (lymphogranuloma venereum)
tests 367 Laparoscopy 83–85 143
In vitro fertilization 374–376 complications 85 LH see Luteinizing hormone (LH)
efficacy 377 endometriosis 126 Libido, loss of 333
egg collection 375 endoscope 83, 84 Lice, vulval inflammation 133
egg supply 374 hydrotubation, tubal patency Lichen sclerosus 157
embryo transfer 376 368 differential diagnosis 157
fertilization 375 indications 85 malignancies 157
follicle tracking 374 ovarian cyst accidents 259 vulval examination 78–79
gonadotrophins 374 ovarian tumours 276 Ligaments, uterus 29–30
indications 374 salpingostomy, infertility Ligation, ureteric surgical injury 290
natural cycle suppression 374 treatment 373 Lipid metabolism, menopause 389
risks of 376–377 sterilization 355 Lipoid cell tumours 263, 274
treatment schedule 374–376 technique 83–84 Lipoma, vulva 158
In vitro maturation, assisted trochar 83 Liquid-based cytology, cervical
conception 379 Laparoscopy assisted vaginal cancer screening 176
Ipsilateral lymphadenectomy, vulval hysterectomy (LAVH), heavy Liver enlargement, abdominal
carcinoma treatment 163 uterine bleeding 119 examination 76
Irregular bleeding, definition 71 Laparotomy, ovarian cyst accidents LLETZ see Large loop excision of
Irritation, vaginal discharge 134 259 the transformation zone (LLETZ)
Ischial tuberosity 12, 18 Large loop excision of the LMP (last menstrual period) 71
Ischiocavernous muscle 16 transformation zone (LLETZ) LMWHs see Low molecular weight
Ischiococcygeus muscle 20 cervical cancer 186, 190 heparins (LMWHs)
Ischiorectal fossa 18 CIN treatment 181 LNG-IUS see Levonorgestrel
Isoniazid, genital tuberculosis Laser ablation Intrauterine System (LNG-IUS)
treatment 152 genital warts therapy 141 Local anaesthetic, IUD insertion
Isthmus uteri 26 vaginal intra-epithelial neoplasia 347
IUDs see Intra-uterine devices 169 Local excision, vulval intra-epithelial
(IUDs) Laser cone biopsy, CIN treatment neoplasia treatment 159
IUI (intrauterine insemination) 182 Local spread, endometrial cancer
378–379 Laser vaporisation, vulval intra- 206
epithelial neoplasia treatment Loop Electrosurgical Excision
Kallmann’s syndrome 101 159 procedure (LEEP), CIN
Kaposi sarcoma 153 Last menstrual period (LMP) 71 treatment 181
Karyotype analysis, gonadal Late proliferative phase, endometrial Lower genital tract disorders,
dysgenesis 92 cycle 51 menstrual abnormalities 90–91
Ketoconazole, sperm production Lateral fornices, vagina 23 Low grade stromal sarcomas, uterine
abnormalities 366 LAVH (laparoscopy assisted vaginal sarcoma 212
17-Ketosteroids, lipoid cell tumours hysterectomy), heavy uterine Low molecular weight heparins
274 bleeding 119 (LMWHs)
Kidney palpation, abdominal LDH (lactate dehydrogenase), DVT 301
404 examination 76 dysgerminoma 268 pulmonary embolism 305
SUBJECT INDEX
LUF (luteinised unruptured follicle Maternal age, recurrent miscarriage risk factors 389–390
syndrome) 363 314 physiological amenorrhoea 89
Lumen, ureter 233 Maternal diabetes, recurrent premature 2, 382
Luteal phase, hormones 50 miscarriage 315 signs and symptoms 383
Luteinised unruptured follicle Mature cystic teratoma, ovarian psychological symptoms 383
syndrome (LUF) 363 tumours 269 severity and duration 383
Luteinizing hormone (LH) Mayer–Rokitansky–Kuster–Hauser urogenital atrophy 383
corpus luteum 36 syndrome 91 vasomotor symptoms 383
follicular phase 50 Mayer–Rokitansky syndrome 65, 67 Menorrhagia
Graafian follicles 47 MEA (microwave endometrial definition 71
infertility treatment 372 ablation), heavy uterine bleeding placental site trophoblastic
luteal phase 50 116 tumour 196
menopause 382 Mechanical devices, stress Menstrual abnormalities 87–130,
menstruation 50 incontinence treatment 244 109
ovulation 50 Median sacral artery 41 amenorrhoea see Amenorrhoea
polycystic ovarian syndrome 94 Medical termination of pregnancy causes 109
recurrent miscarriage 315 318, 319 dysfunctional uterine bleeding
Lymphadenectomy Medico-legal problems 337 see Dysfunctional uterine
pelvic, uterine sarcoma 212 Medroxyprogesterone acetate, bleeding
vaginal carcinoma treatment 171 endometrial cancer recurrence endometriosis 126
Lymphatics 42–43 treatment 210 history taking 109
cancer metastases 42–43 Meig’s syndrome, fibroma 272 hypothalamic disorders 101
cervical cancer (carcinoma) Meiosis 58 lower genital tract disorders
spread 185 Melanoma, vaginal carcinoma 171 90–91
endometrial cancer spread 206 Menarche 88 ovarian disorders 92–96
ovarian tumour spread 277 definition 71 see also Ovaries
vulval carcinoma spread 161 Menopause 55, 381–393 pituitary disorders 97–100
Lymphocysts, surgical complications anti-Müllerian hormone 382 uterine disorders 90–91
294 cardiovascular disease 389–390 see also specific diseases/disorders
Lymphoedema blood flow 389 Menstruation
surgical complications 294 carbohydrate metabolism 389 abnormalities see Menstrual
vulval carcinoma surgery 164 lipid metabolism 389 abnormalities
Lymphogranuloma venereum mortality rate 389 blood loss, IUD complications
(LGV) 143 risks 389 348
Lymphomas, AIDS 153 causes 382 changes, menopause 55
Lynch syndrome, ovarian tumours conception possibility 393 endometrial cycle 51
264 contraception 393 FSH 50
definition 71, 382 history taking 71
Mackenrodt’s ligaments 30 differential diagnosis 382 LH 50
Magnetic resonance imaging (MRI) FSH 89, 382 normal cycle 88
cervical cancer staging 188 genital tract changes 385 prostaglandin F2-a 51
endometrial cancer 206 dyspareunia 385 Mesenteric cyst, ovarian tumours vs.
hyperprolactinaemia 99 Fallopian tubes 385 257
ovarian tumour diagnosis 255 labia majora 385 Mesentery, ovary development 3
uterine fibroids 199 labia minora 385 Mesoderm, genital ridges 3
vaginal carcinoma 170 ovaries 385 Mesonephric ducts, embryology 6
Male external genitalia, embryology uterus 385 Mesonephric (Wolffian) ridge,
see Embryology vagina 385 embryology 5
Malignancies vaginal dryness 385 Mesovarium, ovary 34
lichen sclerosus 157 vulva 385 Metastases, lymphatic system
vagina 169 Greene climacteric scale 384 42–43
Manchester repair, prolapse 223, LH 382 Metformin, infertility treatment 371
225–226 menstruation changes 55 Methotrexate, tubal pregnancy
Marshall–Marchetti–Krantz oestrogen 89, 382 treatment 324
urethropexy 246 osteoporosis 386–388 Metronidazole
Marsupialization, vulval bisphosphonates 388 bacterial vaginosis 137
inflammation treatment 133 comparative cortical bone Trichomonas vaginalis 138
Masculinization thicknesses 388 Microinvasive cervical carcinoma
Sertoli–Leydig cell tumour 273 HRT 388 178
see also Defeminisation oestrogens 388 Microinvasive surgery, cervical
Masculinovoblastoma 274 raloxifene 388 cancer 190 405
SUBJECT INDEX
Microscopy Mucous cervical polyps, cervical benign squamous cervical

adenomyosis 122 cancer vs. 186 metaplasia 174
Chlamydia trachomatis infection Mullerian agnesis 91 cyclical changes 51
142 Müllerian (paramesonephric) duct, detrusor instability treatment 249
sperm production tests 365 embryology 5, 6 endometrial hyperplasia 202
Microwave endometrial ablation Müllerian tubercle, embryology 5 high-dose, Asherman’s
(MEA), heavy uterine bleeding Multiple births, in vitro fertilization syndrome 91
116 376 HRT 391
Micturition 234–235 Muscles menopause 89, 382
detrusor contraction 236 pelvis 19 osteoporosis 388
frequency see also specific muscles ovulation 48
incontinence 239 Muscularis, ureter 233 pregnancy 89
vaginal prolapse 220 Myoma, vulva 158 premenstrual syndrome treatment
intra-urethral pressure 234 Myomectomy 130
intravesical pressure 234 disadvantages 200 Oestrogen-producing ovarian
voiding mechanism 236 uterine fibroid treatment 200 tumours 272
Mifepristone Myometrium, uterine fibroids 197 Oestrogen receptors 52
miscarriage management 312, 313 Oestrogen replacement therapy
pregnancy termination 318, 319 Nafarelin, infertility treatment 372 complete androgen insensitivity 62
Mild dyskaryosis, cervical smears Natural cycle suppression, in vitro premature ovarian failure 93
177 fertilization 374 Ofloxacin, pelvic inflammatory
Mirena, IUDs 346 Natural methods, contraception disease management 149
Miscarriage 308–309 338 Oil of evening primrose,
complete 308 Nausea and vomiting, gestational premenstrual syndrome treatment
incomplete 309 trophoblastic disease 327 130
inevitable 308 Necrobiosis, uterine fibroids 199 Oligoamenorrhoea
management 310, 310–312 Neoplasia, combined oral definition 71
anti-D immunoglobulin 312 contraceptive pill 344 polycystic ovarian syndrome 95
complications 311 Nephrostomy, percutaneous 291 Oophorectomy, bilateral, heavy
curettage 312 Nerve supply uterine bleeding 118
dilatation and evacuation 313 coccygeus muscle 19 Operative hysteroscopy, placental
expectant management 312 pelvis 43–44 site trophoblastic tumour 196
less than 12 week gestation Neurological disease, incontinence Ophthalmia neonatorum, Chlamydia
310–312 239, 243 trachomatis infection 142
medical management 312, 313 Nitrofurantoin, sperm production Oral route, HRT 392
more than 12 week gestation abnormalities 366 Orgalytran, infertility treatment
313 Nocturia, incontinence 239 372
surgery 310, 313 Novasure, heavy uterine bleeding Organ removal, ovarian tumours
missed 309 116 278
recurrent see Recurrent Nucleic acid amplification tests Organ systems, pelvic pain 72
miscarriage (NAATs) Orgasm
threatened 308 Chlamydia trachomatis infection coitus 333
Misoprostol, miscarriage 142 failure to achieve 333
management 312, 313 gonorrhoea diagnosis 144 Osteoporosis
Missed miscarriage 309 Nucleic acid hybridization tests, bone mineral density 386
Mittelschmerz 72 gonorrhoea diagnosis 144 menopause see Menopause
Moderate dyskaryosis, cervical Nulliparous adults, vagina 23 ultrasonic densitometry 386,
smears 177 387–388
Mons pubis 12, 13 Obesity Ova/ovum
Montgomery’s tubercles 82 abdominal examination 77 blighted 309
Motivation, contraception failure abdominal ultrasound 77 collection 375
rates 339 endometrial cancer 207 supply 374
MRI see Magnetic resonance ovarian tumours vs. 257 Ovarian arteries 34, 41
imaging (MRI) vulval inflammation 133 ureter 233
Mucinous cystadenocarcinoma, Obstetric history taking 70 Ovarian hyperstimulation syndrome,
ovarian tumours 263, 266 Obturator fascia 18 in vitro fertilization 377
Mucinous cystadenoma, ovarian Obturator internus muscles 19, 20 Ovarian tumours 262–263
tumours see Ovarian tumours Oestradiol tablets, pessaries 222 BRCA 1 264
Mucoid degeneration, uterine Oestriol cream, pessaries 222 BRCA 2 264
fibroids 199 Oestrogen(s) carcinoma 264
406 Mucosal prolapse, urethra 165 actions of 52 chemotherapy 281
SUBJECT INDEX
Ovarian tumours (Continued) non-functioning tumours 275 menstrual abnormalities 92–96

clinical features 252–254, 262 oestrogen-producing 272 see also specific diseases/disorders
large 253 Sertoli–Leydig cell tumour dysgenesis 64
palpation 254 273–274 epithelium 46
pedicles 254 struma ovarii (thyroid type follicular atresia 37
pressure symptoms 252–254 tumour) 275 hilum 34, 35
size 252 investigations 262 histology 35–37
small 253 Lynch syndrome 264 menopause 385
upper pole 254 mucinous cystadenocarcinoma mesovarium 34
complications 259 266 premature failure 93
differential diagnosis 259 mucinous cystadenoma 266 primordial follicle 46
pedicle torsion 259 pseudomyxoma peritonei 266 tumours see Ovarian tumours
differential diagnosis 255–258 risk factors 264 tunica albuginea 35
ascites 255 risk of malignancy index 262 Ovariotomy, ovarian tumours 276
broad ligament cysts 258 serous cystadenocarcinoma 265 Overflow incontinence 239
computed tomography 255 serous cystadenoma 265 Ovoblastoma 274
ectopic kidney 258 sex cord stromal tumours 263 Ovulation 46–50
full bladder 255 spread of 277–278 bleeding vs. ovarian cyst accidents
hydatid cyst 257 blood stream 277 261
hydronephrotic kidney 257 direct 277 evidence, infertility see Infertility
mesenteric cyst 257 lymphatics 277 FSH 48, 50
MRI 255 transcoelomic 277 GnRH 49, 50
obesity 257 staging 279–280 hypothalamus 49
pancreatic cyst 257 stage I 279 inhibin 50
pelvic inflammation 257 stage II 279 LH 50
pregnancy 255 stage III 280 oestrogen 48
pyosalpinx 257 stage IIIa 280 Ovulation method (Billings’
rectus sheath haematoma 257 stage IIIb 280 method) 351
retroperitoneal tumours 258 stage IIIc 280
transplanted kidney 258 stage IV 280 Paclitaxel
ultrasound 255, 256 stromatous tumours 263 ovarian tumour treatment 282
uterine fibroids 256 surgery 276, 277–278 side effects 282
epithelial tumours 263, 265–266 cystectomy 276 Paediatric AIDS 154
adjuvant chemotherapy 277 cytology 278 Paediatric vulvo-vaginitis 139
prognosis 425 incision 278 Paget’s disease of the vulva 159
staging 277 inspection 278 Pain
surgical debulking 277 laparoscopy 276 dysmenorrhoea 120
see also specific tumours organ removal 278 endometriosis 126
germ cell tumours 263, 267–271 ovariotomy 276 tubal pregnancy 321
Brenner tumour 271 tumour markers 253 PAIN (perianal intra-epithelial
clinical features 267 Ovaries 34–37 neoplasia) 159
dysgerminoma 268 abnormalities 64 Palliative care, cervical cancer 193
fibroma 272 age-related changes 38 Palpation
gonadoblastoma 268 blood supply 34 abdominal examination 76
Krukenberg tumours 270 combined oral contraceptive pill ovarian tumours 254
mature cystic teratoma 269 344 Pancreatic cyst, ovarian tumours vs.
solid teratoma 269 corpus albicans 37 257
staging 267 corpus luteum see Corpus luteum Papanicolaou staining, cervical
teratomas 269–270 cortex 35, 46 cancer screening 176
see also specific types cyclical hormonal changes 51 Papaverine, erectile dysfunction
treatment 267 see also specific hormone treatment 336
undifferentiated 268 cysts 259–261 Paramesonephric (Müllerian) duct,
yolk sac tumours 270 abdominal examination embryology 5, 6
histology 263 75, 77 Parasympathetic nerves
hormone-producing tumours 272 differential diagnosis 261 bladder/urethra 235
androgen-producing 273–274 rupture of 260–261 pelvis 44
carcinoid (serotonin-producing development 2–4 Para-urethral glands of Skene 8
tumour) 275 descent 4 Parenteral route, HRT 392
choriocarcinoma 275 gubernaculum 4 Parietal layer, pelvic fascia 21
hilar cell tumours 274 mesentery 3 Parity, history taking 70
lipoid cell tumours 274 diseases/disorders 251–285 Paroöphoron, broad ligament 33 407
SUBJECT INDEX
Paroöphoron tubules, hilum 35 Percutaneous antegrade stents, PMS see Premenstrual syndrome
Parovarian cysts see Broad ligament urinary fistula therapy 293 (PMS)
Partial hydatiform mole Percutaneous nephrostomy, ureteric PMT (premenstrual tension) 53
see Hydatiform mole surgical injury 291 Pneumatic stocking, DVT 300
Partial vaginectomy, vaginal intra- Percutaneous route, HRT 392 Podophyllotoxin, genital warts
epithelial neoplasia 169 Perforation, laparoscopy therapy 141
Patient documentation, sterilization complications 85 Polycystic ovarian syndrome
354 Perianal intra-epithelial neoplasia (PCOS) 94–96
Patient selection, vaginal (PAIN) 159 clinical features 94
hysterectomy complications 230 Perihepatitis, Chlamydia trachomatis diabetes mellitus type II 94
Patients, explanations to 74 infection 142 diagnosis 95
PCOS see Polycystic ovarian Perimenopause 71 FSH 94
syndrome (PCOS) Perineal body 16 hirsutism 105
Pedicles Perineal muscles 17 LH 94
ovarian tumours 254 Perineum 12 long-term effects 96
torsion, ovarian tumour anatomical 12 recurrent miscarriage 315
complications 259 gynaecological 12 sex hormone binding globulin 94
‘Peg’ cells, Fallopian tubes 32 muscles of 17 treatment 96
Pelvic diaphragm 20 see also specific muscles amenorrhoea 96
functions of 20 true 12 hirsutism 96
Pelvic fascia 21 Periosteitis, infertility treatment 96
parietal layer 21 Marshall–Marchetti–Krantz Polyps
relations of 21 urethropexy 246 uterine fibroids vs. 197
visceral layer 21 Peripheral pulmonary embolism 302 uterus 196
Pelvic floor exercises, stress Peritoneal cavity rupture, tubal POP (progesterone only pill) 344
incontinence treatment 244 pregnancy 323 Post-coital bleeding, definition 71
Pelvic inflammatory disease (PID) Periurethral injections, stress Postcoital (morning after)
149 incontinence treatment contraception 352
acute 149 244 Postcoital (resolution) phase, coitus
bacteriology 149 pH, vagina 24 333
chronic 150 Physical examination 69–85 Post coital test, sperm function tests
differential diagnosis 149 amenorrhoea 102 367
ectopic pregnancy 320 incontinence 241 Posterior colpoperineorrhaphy,
management 149 see also Gynaecological vaginal prolapse 227
Pelvic lymphadenectomy, uterine examination Posterior fornix, vagina 23
sarcoma 212 Physiological amenorrhoea Posterior wall vaginal prolapse
Pelvis see Amenorrhoea 219
bimanual examination Physiology 45–55 Postmenopause
see Bimanual pelvic Physiotherapy, stress incontinence bleeding 203
examination treatment 244 endometrial cancer 203
blood supply 39–41 PID see Pelvic inflammatory disease superficial dyspareunia 334
collateral blood supply 41 (PID) uterus 38
see also specific blood vessels Pipelle de Cornier, endometrial Post molar gestational trophoblastic
infections, IUDs 346 biopsy 112 neoplasia 328
inflammation Piriformis muscle 19, 20 Post operative physiotherapy, DVT
ovarian cyst accidents vs. 261 Pituitary 300
ovarian tumours vs. 257 disorders, menstrual Post thrombotic leg syndrome (PLS)
models, bimanual pelvic abnormalities 97–100 295
examination 79–80 tumours, hyperprolactinaemia 98 Pouch of Douglas 23
muscles of 19 Pituitary antagonists, infertility Pratt’s sign, DVT 298
see also specific muscles treatment 372 Pregnancy
nerve supply 43–44 Placenta, hormone production 89 abdominal examination 75
autonomic nerves 44 Placental site trophoblastic tumour Candida albicans infection 136
parasympathetic nerves 44 196, 329 early see Early pregnancy
see also specific nerves Plant chemotherapeutics, ectopic see Ectopic pregnancy
pain 72–73 mechanism of action 281 Fallopian tubes see Tubal
organ systems 72 Plastic surgery, vagina 172 pregnancy
severity of 73 Plateau phase, coitus 332 IUD complications 348
tubal pregnancy 321 Plexus of Frankenhauser 44 oestrogen 89
see also Dyspareunia PLS (post thrombotic leg syndrome) ovarian tumours vs. 255
408 Penicillin, syphilis treatment 147 295 physiological amenorrhoea 89
SUBJECT INDEX
Pregnancy termination 317–319 Progestogen(s) management 303

complications 319 combined oral contraceptive pill mortality 306
immediate 319 341 peripheral 302
late 319 endometrial cancer recurrence treatment 305
first trimester 317–318 treatment 210 Pulmonary thromboembolism (PT)
medical termination of endometrial cancer treatment 209 295
pregnancy 318 endometrial hyperplasia treatment Pyelography, antegrade 291
surgical termination of 202 Pyometra, cervical cancer
pregnancy 317 implants 345 (carcinoma) 185
second trimester 319 injectable 344 Pyosalpinx
dilatation and curettage 319 premature ovarian failure 93 chronic pelvic inflammatory
extra-amniotic termination 319 Progynova, infertility treatment 372 disease 150
medical termination 319 Prolactin ovarian tumours vs. 257
Pre-implantation genetic diagnosis amenorrhoea 102 Pyridoxine (vitamin B6),
(PIGD), assisted conception 379 lactation 89 premenstrual syndrome treatment
Pre-malignant complete hydatiform Prostaglandin(s) 130
mole 326 dysmenorrhoea 120
Pre-malignant disease, vagina 169 pregnancy termination 319 Quality of life, HRT 391
Premature ejaculation 335 Prostaglandin analogues, miscarriage Quinagolide, hyperprolactinaemia
Premature menopause 2, 382 management 312, 313 treatment 100
Premature ovarian failure, FSH 93 Prostaglandin E2, pregnancy
Premenstrual syndrome (PMS) 53, termination 319 Radiation burns, urinary fistula
74, 129 Prostaglandin F2-a, menstruation 51 formation 293
clinical features 129 Prostaglandin synthetase inhibitors Radical hysterectomy
investigations 129 dysmenorrhoea treatment 121 and node dissection, cervical
treatment 130 heavy uterine bleeding cancer 190–191
Premenstrual tension (PMT) 53 management 114 urinary fistula formation 292
Pre-pregnancy infection screening, Protein C deficiency, recurrent vaginal carcinoma treatment
assisted conception 370 miscarriage 316 171
Prepuce 13 Protein C resistance, recurrent Radical surgery, cervical cancer
Presacral nerves 44 miscarriage 315 192
Pressure symptoms Protein S deficiency, recurrent Radical vulvectomy, vulval
ovarian tumours 252–254 miscarriage 316 carcinoma treatment 162, 163
uterine fibroids 198 Pseudomyxoma peritonei 266 Radiotherapy
Previous miscarriage, recurrent Psychological symptoms cervical cancer see Cervical cancer
miscarriage 314 hormone effects 53 (carcinoma)
Primary amenorrhoea 71 menopause 383 endometrial cancer treatment
Primary dysmenorrhoea 72 Psychosexual counselling 333 209
Primary infertility 358 erectile dysfunction treatment 336 vulval carcinoma 164
Primary syphilis 145 vaginismus treatment 334 Raloxifene, osteoporosis 388
Primary urethral groove, Pubertal uterus 38 Rape 337
embryology 9 Puberty 54 definition 337
Primordial follicle, ovary 46 absent/late 88 general examination 337
Progesterone definition 54 hymen 337
actions of 52 GnRH 54 record keeping 337
cyclical changes 51 Pubococcygeus muscle 20 skin swabs 337
endometriosis treatment 127 Pudendal artery 40, 43 vulval examination 337
heavy uterine bleeding Pudendal nerve 18, 43 Record keeping, rape 337
management 114 Pudendal vessels 18 Rectocele 219
infertility treatment 372 Pulmonary embolism 302–304 anterior colporrhaphy 223
ovulation evidence 362 central 302 posterior colpoperineorrhaphy
pregnancy 89 investigations 303 227
premenstrual syndrome treatment arterial blood gases 303 Rectovaginal examination, bimanual
130 chest x-ray 303 pelvic examination 79
Progesterone challenge test, computed tomographic Rectus sheath haematoma, ovarian
amenorrhoea 102 pulmonary angiography 304 tumours vs. 257
Progesterone only pill (POP) 344 duplex Doppler leg ultrasound Recurrent miscarriage 314–316
Progestin 304 causes 314–315
endometrial hyperplasia treatment ECG 303–304 autoimmune factors 315
202 ventilation/perfusion (V/Q) cervical weakness 314, 316
IUDs 346 scans 304 embryonic abnormalities 314 409
SUBJECT INDEX
Recurrent miscarriage (Continued) Scabies, vulval inflammation 133 male 335

endocrine factors 315, 316 SCC see Squamous cell carcinoma orgasm, failure to achieve 333
environmental factors 315, 316 (SCC) see also specific problems
genetics 314, 316 Scrotum, embryology 9 Sexual transmission, Candida
hyperprolactinaemia 315 Sebaceous cysts, vulva 158 albicans infection 136
immunological problems 316 Secondary amenorrhoea 71 Shaving, hirsutism 107
infections 315 Secondary dysmenorrhoea 72 SHBG see Sex hormone binding
maternal age 314 Secondary infections, genital warts globulin (SHBG)
maternal diabetes 315 141 Shelf pessaries 222
polycystic ovarian syndrome Secondary infertility 358 Sidenasil (Viagra), erectile
315 Secretory phase, endometrial dysfunction treatment 336
previous miscarriage 314 cycle 51 Sims’ speculum 81
thrombophilias 315, 316 Selective serotonin uptake inhibitors, Skeleton, hormone effects 53
thyroid disease 315 premenstrual syndrome treatment Skene’s ducts 14
uterine abnormalities 314, 316 130 Skin conditions, vulval examination
definitions 314 Semen analysis 364 78–79
investigation 316 Septated uterus 66 Skin swabs, rape 337
treatment 316 Serial ultrasound, ovulation evidence Smear history, history taking 71
Reiter’s syndrome, Chlamydia 363 Soap substitutes, lichen sclerosus
trachomatis infection 142 Serotonin-producing ovarian treatment 157
Renal artery, ureter 233 tumours 275 Solid teratoma, ovarian tumours 269
Renogram, ureteric surgical injury Serous cystadenocarcinoma, ovarian Specimens, vaginal discharge 135
290 tumours 263, 265 Speculum examination 80–81
Reproductive immunology, assisted Serous cystadenoma, ovarian Sperm function tests see Infertility
conception 379 tumours 263, 265 Spermicides, contraception 338
Resistant ovary syndrome 93 Sertoli–Leydig cell tumours 263, Sperm production, infertility
Rete, embryology 3 273–274 see Infertility
Retroflexion, uterus retroversion Serum human chorionic Sphincter ani 18
214 gonadotrophin (hCG), tubal Sphincter urethrae 17
Retroperitoneal tumours, ovarian pregnancy diagnosis 321 Spironolactone, sperm production
tumours vs. 258 Serum progesterone, ovulation abnormalities 366
Rhesus immunization, miscarriage evidence 362 Sponge, contraception 350
management 311 Severe dyskaryosis, cervical smears Squamous cell carcinoma (SCC)
Rhythm method (safe period) 351 177 cervical cancer 184
Rifampicin, genital tuberculosis Sex chromosome acquisition X vaginal carcinoma 170
treatment 152 (super-female) 61 Squamous epithelium, vagina 132
Right ovarian vein 34 Sex cords Staging
Ring pessaries 222 coelomic epithelium 3 cervical cancer see Cervical cancer
Risk of malignancy index (RMI), stromal tumours 263 (carcinoma)
ovarian tumours 262 Sex development disorders endometrial cancer
Route of administration, HRT 391, 57–68 see Endometrial cancer
392 congenital abnormalities 62–63 Fallopian tube carcinoma 285
Rudimentary uterus 65 cloacal origin 68 ovarian epithelial tumours 277
Rupture into lumen, tubal genetic abnormalities 59–61 ovarian germ cell tumours 267
pregnancy 323 chromosome analysis 59 ovarian tumours see Ovarian
clinical syndromes 59 tumours
Sacral nerves 18 investigations 59 Stamey needle suspension procedure
Sacrotuberous ligament 12, 18 laboratory studies 59 247
Salpingectomy, tubal pregnancy see also specific diseases/disorders ‘Stein Leventhal’ syndrome 94
treatment 324 Sex hormone binding globulin Sterilization 353–354
Salpingo-oophorectomy, bilateral (SHBG) counselling 353
see Bilateral salpingo- hirsutism 105 laparoscopic 355
oophorectomy polycystic ovarian syndrome 94 patient documentation 354
Salpingostomy, tubal pregnancy Sex hormones success rates 353
treatment 324 erectile dysfunction treatment Steroids, lichen sclerosus treatment
Samples, sperm production tests 336 157
365 see also specific hormones STOP (surgical termination of
Sarcoma botriodes 171, 211 Sexual history 332 pregnancy) 317
Sarcoma, ovarian tumours 263 Sexuality 331–356 Stress incontinence 74, 238
Sarcomatous change, uterine Sexual problems 333 cystometry 242
410 fibroids 199 libido, loss of 333 demonstration of 241
SUBJECT INDEX
Stress incontinence (Continued) Surgical termination of pregnancy Total abdominal hysterectomy,

detrusor instability vs. 241 (STOP) 317 endometrial cancer treatment 209
surgery 244 Sympathetic nerves, bladder/urethra Total hysterectomy
treatment 244 235 Fallopian tubes carcinoma 285
vaginal prolapse 220 Syphilis 145–147 heavy uterine bleeding 116–117
Stroke chancre 145 laparoscopic, heavy uterine
combined oral contraceptive pill diagnosis 145, 146 bleeding 119
343 primary 145 Total laparoscopic hysterectomy,
HRT 390 signs and symptoms 147 heavy uterine bleeding 119
Stromatous ovarian tumours 263 treatment 147 Total vaginectomy, vaginal intra-
Struma ovarii, ovarian tumours 275 urinary fistula formation epithelial neoplasia 169
Subcutaneous implants, HRT 393 293 Toxicity, chemotherapy 282
Subtotal hysterectomy, heavy uterine Syphilitic condylomata, genital warts Toxic shock syndrome 147
bleeding 118 vs. 141 TPHA (Treponema pallidum
Sulfasalazine, sperm production haemagglutination), syphilis
abnormalities 366 Tamoxifen, endometrial cancer 203 diagnosis 146
Super-female (sex chromosome Taxanes, ovarian tumours 277 Tranexamic acid, dysfunctional
acquisition X) 61 TCRE (trans-cervical resection of uterine bleeding management 114
Superficial dyspareunia 73, 334 endometrium) 115 Transabdominal scanning,
Superficial inguinal glands 42 Tenaculum forceps, IUD insertion endometrium investigation 111
Superficial transverse perineal 347 Trans-cervical resection of
muscle 16 Teratomas, ovarian tumours 263, endometrium (TCRE) 115
Support hosiery, lymphoedema 294 269–270 Transcoelomic spread, ovarian
Surgery Testes, embryology 9 tumours 277
cervical cancer see Cervical cancer Testosterone Transdermal route, HRT 392
(carcinoma) complete androgen Translocation, IUD complications
complications see Surgical insensitivity 62 348
complications measurement, polycystic ovarian Transnasal surgery,
contraception 338 syndrome 95 hyperprolactinaemia 100
endometrial cancer treatment physiology 105 Transplanted kidney, ovarian
209 Sertoli–Leydig cell tumour 274 tumours vs. 258
genital tuberculosis treatment 152 virilisation 106 Transvaginal ultrasound
infertility treatment 373 Theca interna 47 dysfunctional uterine bleeding
miscarriage management 310, 313 Thecoma, ovarian tumours 263 110
ovarian tumours see Ovarian Thermachoice, heavy uterine endometrium investigation 111
tumours bleeding 116 tubal pregnancy 322
pulmonary embolism 305 Threadworm, paediatric vulvo- Transverse cervical (Mackenrodt’s;
stress incontinence 244 vaginitis 139 cardinal) ligaments 30
uterine fibroid treatment 200 Threatened miscarriage 308 Transverse septum, vagina 67
vaginal intra-epithelial neoplasia Thromboembolism Traumatic epithelial cysts, vagina
169 combined oral contraceptive pill 168
Surgical complications 287–306 343 Treponema pallidum
adhesions 293 venous see Venous haemagglutination (TPHA),
bladder injuries 288 thromboembolism syphilis diagnosis 146
bowel injury 291 Thrombophilias, recurrent Treponema pallidum infection
fever 294 miscarriage 315, 316 see Syphilis
fistula formation 292–293 Thromboprophylaxis, DVT see Deep Trichomonas vaginalis infection
see also specific types vein thrombosis (DVT) vaginal discharge 137–138
hernia 294 Thrombosis, venous see Venous vaginal pH 138
infectious morbidity 294 thromboembolism Tricyclic antidepressants, detrusor
lymphocysts 294 Thrush see Candida albicans infection instability treatment 249
lymphoedema 294 Thyroid disease, recurrent Trochar, laparoscopy 83
ureter injuries see Ureteric surgical miscarriage 315 Trophectoderm biopsy 379
injury Thyroid stimulating hormone True perineum 12
urinary fistula 292–293 (TSH), amenorrhoea 102 TSH (thyroid stimulating hormone),
urinary tract injuries 288 Thyroid tumour choriosarcoma, amenorrhoea 102
venous thrombosis see Deep vein ovarian tumours 263 Tubal abortion 323
thrombosis (DVT); Venous Time of ovulation, contraception Tubal pregnancy 321–322
thrombosis 351 diagnosis 321–322
Surgical debulking, ovarian epithelial Torsion of the pedicle, uterine serum hCG 321
tumours 277 fibroids 199 ultrasound 321 411
SUBJECT INDEX
Tubal pregnancy (Continued) Ureteric surgical injury 289 polyps vs. 197
implantation sites 310 clinical features 290 pressure symptoms 198
pelvic inflammatory disease vs. 149 crush injury 290 prevalence 198
peritoneal cavity rupture 323 investigations 290–291 symptoms and signs 199
rupture into lumen 323 ligation 290 torsion, ovarian cyst accidents vs.
signs 321–322 management 290–291 261
symptoms 321 treatment 291 transvaginal ultrasound 111
treatment 324 Urethra treatment 200
conservative management caruncle 165 uterine retroversion 215
324 closure 235 Uterine sarcoma 211–212
methotrexate 324 diseases 165 carcinosarcoma 211, 212
salpingectomy 324 see also specific diseases/disorders clinical features 211
salpingostomy 324 embryology 7 endometrial stromal sarcomas
tubal abortion 323 glands, embryology 8 211, 212
tube rupture 323 innervation 235 high grade stromal sarcomas
Tuberculosis, genital see Genital meatus, vulval examination 78 212
tuberculosis mucosal prolapse 165 histology 211
Tumour markers orifice 12, 14 leiomyosarcoma 211, 212
ovarian tumours 253 sphincter incompetence 238 low grade stromal sarcomas 212
see also specific markers urethrocele 165 Utero-sacral ligaments 30, 216
Tunica albuginea, ovary 35 Urethral folds, embryology 8 Uterovaginal prolapse 216
Turner’s syndrome 60 Urethral slings, stress incontinence causes 216
gonadal dysgenesis 92 245, 248 first degree 217
premature ovarian failure 93 Urethral syndrome 240 incidence 216
Urethroceles 165, 218 second degree 217
UFH (unfractionated heparin), Urethropexy, stress incontinence third degree 217
DVT 301 245 Uterus 25–31
Ultrasonic densitometry, Urgency, incontinence 239 abnormalities 65–66
osteoporosis 386, 387–388 Urinary catheters 230 absence 65
Ultrasound Urinary fistula, surgical with accessory horn 65
abdominal 77 complications 292–293 arcuate 66
duplex Doppler leg ultrasound Urinary incontinence double (bicornuate) 65
304 see Incontinence menstrual abnormalities
DVT 299 Urinary sphincters, artificial 244 90–91
endometrial cancer 203 Urinary tract recurrent miscarriage 314,
IUD translocation 348 anatomy 231–232 316
obesity 77 infections 240 rudimentary 65
ovarian tumour differential injuries, surgical complications septated 66
diagnosis 255, 256 288 unicornis 66
polycystic ovarian syndrome 95 symptoms 74 uterus bicornis 65
pulmonary embolism 304 Urination see Micturition uterus bicornis bicollis 65
transvaginal see Transvaginal Urine bacteriology, incontinence uterus bicornis unicollis 65
ultrasound 243 uterus didelphys 65
tubal pregnancy diagnosis 321 Urodynamic assessment, adult 38
ureteric surgical injury 290 incontinence 243 age-related changes 38
uterine fibroids 199 Urogenital angle 12 bimanual pelvic examination 79
Undifferentiated germ cell tumours Urogenital atrophy, menopause 383 blood supply 39–40
268 Urogenital buds, embryology 8 corpus 26
Unfractionated heparin (UFH), Urogenital diaphragm 17, 18 cavity 27
DVT 301 Urogenital sinus, embryology 7 development 5–6
Unicornis uterus 66 Urography, intravenous 290 diseases 195–212
Unilateral salpino-oöphorectomy, Urogynaecology 213–249 dysfunctional bleeding
germ cell ovarian tumours Uterine artery embolisation, uterine see Dysfunctional uterine
267 fibroid treatment 200 bleeding
Upper pole, ovarian tumours 254 Uterine fibroids 197 endometrial polyps 196
Ureter 231–232 complications 199 fibroids see Uterine fibroids
blood supply 233 diagnosis 199 heavy bleeding see Heavy
course of 289 dysmenorrhoea 198 uterine bleeding
histology 233 investigations 199 placental site trophoblastic
relationship with cervix 28 myometrium 197 tumour 196
412 relationship with uterus 28 ovarian tumours vs. 256 polyps 196
SUBJECT INDEX
Uterus (Continued) melanoma 171 operative complications 230

prolapse 213–249 prognosis 171 post-operative complications 230
retroversion see below sarcoma botriodes 171 prolapse 223
see also specific diseases site 171 Vaginal intra-epithelial neoplasia
endometrium see Endometrium spread 171 (VAIN) 159, 169
enlargement, abdominal squamous cell carcinomas 170 Vaginal preparations, HRT 393
examination 75 treatment 171 Vaginal rings 344
glands 31 cysts 168 Vaginal ultrasound, uterus
histology 31 superficial dyspareunia 334 dimensions 25
infantile 38 development 6, 14 Vaginectomy
isthmus uteri 26 discharge 74, 134 partial 169
ligaments 29–30 bacterial vaginosis 137 total, vaginal intra-epithelial
see also specific ligaments Candida albicans see Candida neoplasia 169
measurements 25 albicans infection vaginal carcinoma treatment 171
menopause 385 cervical cancer (carcinoma) Vaginismus 73, 334
outlet obstruction, cervical cancer 183 treatment 334
(carcinoma) 185 clinical features 134 Vaginitis 139
post-menopause 38 composition 134 atrophic 139
pubertal 38 examination 135 foreign bodies 139
relationship with ureter 28 leucorrhoea 135 paediatric vulvo-vaginitis 139
retroversion 214–215 source of 134 secondary causes 139
anteverted 214 Trichomonas vaginalis 137–138 Vaginosis, bacterial 137
causes 215 diseases 167–172 VAIN (vaginal intra-epithelial
diagnosis 215 benign disease 168 neoplasia) 159, 169
retroflexion 214 bleeding see above Vascular disease, combined oral
symptoms 215 carcinoma see above contraceptive pill 343
treatment 215 cysts see above Vasectomy 356
septated 66 malignant disease 169 Vasomotor symptoms, menopause
synechiae, dilatation and pre-malignant disease 169 383
curettage 113 prolapse see below Vault haematoma, vaginal
trauma, dilatation and curettage dryness, menopause 385 hysterectomy complications 230
113 epithelium 24 Vault prolapse 219
uterine glands 31 fistulae, cervical cancer Venography, contrast 299
Uterus bicornis bicollis 65 (carcinoma) 185 Venous thromboembolism
Uterus bicornis unicollis 65 fornices 23 HRT 390
Uterus bicornis uterus 65 histology 24 risk, combined oral contraceptive
Uterus didelphys 65 menopause 385 pill 341
nulliparous adults 23 Venous thrombosis 295–297
Vabra Curettage, endometrial biopsy orifice 12, 14 pathology 296
112 pH 24 prophylaxis 295
Vagina 22 Trichomonas vaginalis 138 risk factors 295
abnormalities 67 plastic surgery 172 sites 297
absence 67 prolapse 74, 218 see also Deep vein thrombosis
gynatresia 67 anterior 218 (DVT)
transverse septum 67 anterior colporrhaphy 223–224 Ventilation/perfusion (V/Q) scans,
vertical septum 67 clinical features 220 pulmonary embolism 304
acidity 132 differential diagnosis 221 Vermiculation 231
age-related changes 38 pessary treatment 222 Verrucous carcinoma, genital warts
anterior fornix 23 posterior colpoperineorrhaphy vs. 141
bimanual pelvic examination 227 Vertical septum, vagina 67
79 posterior wall 219 Vestibule 12, 14
bleeding stress incontinence 220 Viagra (sidenasil), erectile
cervical cancer (carcinoma) secretions 24 dysfunction treatment 336
183 squamous epithelium 132 VIN (vulval intra-epithelial
tubal pregnancy 321 transverse septum 90 neoplasia) 159
blood supply 39–40 traumatic epithelial cysts 168 Vincristine, sarcoma botriodes 171
carcinoma 170–171 Vaginal dilators, vaginismus Viral infections, sperm production
clinical features 170 treatment 334 abnormalities 366
clinical staging 171 Vaginal hysterectomy 229–230 Virchow’s triad, venous thrombosis
magnetic resonance imaging heavy uterine bleeding 119 296–297
170 late complications 230 Virilisation 106 413
SUBJECT INDEX
Visceral layer, pelvic fascia 21 lymphatic spread 161 Vulval intra-epithelial neoplasia
Visual inspection, vulval prognosis 164 (VIN) 159
examination 78–79 radiotherapy 164 Vulvectomy, radical 162, 163
Vitamin B6 (pyridoxine), surgical treatment 162, 164 Vulvovaginitis, superficial
premenstrual syndrome treatment diseases 155–165 dyspareunia 334
130 benign tumours 158
Voiding mechanism, micturition 236 carcinoma see above Warfarin, DVT treatment 301
Volume, vaginal discharge 134 dermatoses 156–157 Warts, genital see Genital warts
V/Q (ventilation/perfusion) scans, fibroma 158 Wolffian (mesonephric) ridge,
pulmonary embolism 304 haematoma 158 embryology 5
Vulva 12, 13–14 inflammation 132 Women Health Initiative, HRT trials
abnormalities 68 lipoma 158 390
absence 68 myoma 158
ectopia vesicae 68 Paget’s disease 159 X-rays
age-related changes 38 sebaceous cysts 158 chest, pulmonary embolism 303
bulb of vestibule 15 see also specific diseases/disorders IUD translocation 348
carcinoma 160–164 examination 78 mammography 82
aetiology 160 rape 337
chemotherapy 164 external urethral Yolk sac tumours 263, 270
clinical features 160 orifice 14 Yoon ring applicator 355
FIGO staging 160 menopause 385
histology 160 vaginal discharge 134 Zidovudine, AIDS transmission 154
incidence 160 vestibule 14 Zona pellucida 46
414

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GYNAECOLOGY ILLUSTRATED

Commissioning Editor: Pauline Graham

Kevin Burton MD MRCOG

C Jay McGavigan MD MRCOG FRANZCOG

Robin Callander FFPh FMAA AIMBI

1. Embryology of the 4. Disorders of Sex Development 57

2. Anatomy of the 5. History and Examination 69

Adenomyosis 122 Premalignant and Malignant Cervical

Physiology of Micturition 234, 235 14. Complications of

Contraception Based on Time of Assisted Conception 370

Development of the Ovary 2

DEVELOPMENT OF THE OVARY

The germ cells, which will eventually inhabit Allantois

By 30 days, the gut, complete with its

At the same time, the coelomic epithelium Gut

DEVELOPMENT OF THE OVARY

At this stage, the primitive gonad Mesonephric

The coelomic epithelium, growing

Until this time, that is, around the Mesonephric

The germ cells and most of the sex

DEVELOPMENT OF THE OVARY

DEVELOPMENT OF UTERUS AND FALLOPIAN TUBES

DEVELOPMENT OF UTERUS AND FALLOPIAN TUBES

While this is happening, the ovary is also

DEVELOPMENT OF EXTERNAL GENITALIA

Allantois Hind gut

Ureter Uterus Allantois (or urachus)

DEVELOPMENT OF EXTERNAL GENITALIA

Certain small, but clinically important, glands are

DEVELOPMENT OF MALE EXTERNAL GENITALIA

As in the female, a mesodermal mass, the Glans penis

The ectoderm on the under surface of the

The endodermal plate then becomes hollowed

The Perineum 12 Cavity of the Corpus 27

THE PERINEUM (Gk. ‘around

The gynaecological perineum is the

The anterior or urogenital triangle of the

Subcutaneous: the bulb of the vestibule and

MONS PUBIS AND LABIA MAJORA Mons pubis

CLITORIS AND LABIA MINORA

The VESTIBULE is the area between the labia

The EXTERNAL URETHRAL ORIFICE is, in Vagina

Normal Hymen after

The BULB of the VESTIBULE consists Bulbospongiosus

MUSCLES OF THE PERINEUM

The Perineal body is a

THE UROGENITAL DIAPHRAGM

THE UROGENITAL DIAPHRAGM (Triangular Ligament)

Upper fascia of diaphragm

⎧ Trans. perinei profundus

Lower fascia of diaphragm or perineal

Perineal body Sphincter Anal

MUSCLES OF THE PELVIS

Nerve supply: nerve to levator ani and

Nerve supply: S4 and anococcygeal

The Obturator internus arises

These muscles are primarily

FUNCTIONS OF THE PELVIC DIAPHRAGM

THE PELVIC FASCIA