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Page 128

116 Endometriosis a nd adenomyosis

rates. However, this widely held viewpoint may well

be brought into question following publication of the

findings from a Canadian multicentre study in which

surgical (laparoscopic) ablation of deposits was com-

pared with no intervention. Surgical destruction did

improve cumulative pregnancy rates in this study, but

further confirmatory trials are awaited. \Afith regard

to hormonal therapy, the evidence is very clear that

this treatment does not improve subsequent fertility.


Patients with endometriosis are often difficult to treat,

not only from a physical point of view, but also often

because of associated psychological issues. For some

patients the label of endometriosis in itself may create

its own problems, since it is known to be a recurrent

disorder throughout the whole of reproductive life.

\Afh ilst there is no standard formula for treatment, nor

indeed a cure, it is important to tailor treatment for

the individual according to her age, symptoms, extent

of the disease and her desire for future childbearing.

Problems also arise when minimal endometriosis is

detected in a patient presenting with pain and there is

real uncertainty as to whether the condition is coinci-

dental or causal. In this situation a full explanation of

the associated diagnostic uncertainty is required.

Drug therapy

Non-steroidal anti-inflammatory drugs (NSAIDs) are

potent analgesics and are very helpful in reducing the

severity of dysmenorrhoea and pelvic pain. However,

they have no specific impact on the disease and its

progression and hence their use is for symptom con-

trol. There may be additional benefit in combining

these agents with paracetamol or codeine, so as to avoid

the main adverse effect of NSAIDs, which is gastroin-

testinal upset.

Combined oral contraceptive agents
Oral contraceptive agents are known to reduce the

severity of dysmenorrhoea and menstrual blood loss

in many patients. They may be of some benefit, but

are often of little help when given in the standard

manner with regular monthly withdrawal bleeds. Two

or three packs of p ills taken without a break may be

beneficial in avoiding the exacerbation of symptoms

associated with menstruation. Explanation that miss-

ing a withdrawal bleed is n t harmful is often ne ded.

Danazol and gestrinone are hormonal, ovarian sup-

pressive, medical treatments comparable in their effect

of reducing the severity of symptoms fo r endom etrio-

sis . Danazol is given in a dose of between 400 and

800 mg daily and gestrinone in a dose of 2.5 mg twice

weekly. In most instances the d rugs are well tolerated,
but many women do experience and rogenic side

effects, e.g. weight gain, greasy skin and acne. The

drugs are normally given in courses of between 3 and
6 months. In longer-term adm inistra tion of the drugs

there may be alterations in lip id profiles o r liver func-

tion, which need to be monitored . Prescribing of

danazol has recently been restricted owing to a possi-

ble association with ovarian cancer.

Synthetic progestogens such as medroxyprogesterone

acetate and dydrogesterone have been given on a

continuous basis to produce pseudo-decidualization

of the endometrium and comparable changes in

endometriotic lesions. The dose of agents required to

be effective is quite high, and side effects, including

breakthrough bleeding, ","eight gain, fluid retention

and weight changes, are not uncommon.

Gonadotrophin-releasing hormone agonists
Gonadotrophin-releasing hormone agonists (GnRH-

A) are as effective as danazol in relieving the severity

and symptoms of endometriosis and differ only in their

side effects. These drugs induce a state of hypo-

gonadotrophic hypogonadism or pseudo-menopause

with low circulating levels of oestrogeh. Side effects

include symptoms seen at the menopause, in particular

hot flushes and night sweats. Despite th~se side effects,
the drugs are well tolerated and they have become

established agents in the treatment of endometriosis.

They are available as multiple, daily-administered

intranasal sprays or as slow-release depot formulations,

each lasting for 1 month or more. Apart from the

symptomatic side effects described above, the low

circulating oestrogen levels can affect bone meta-

bolism in ways comparable to those seen at the natural

menopause. Therefore, with continuing long-term use

there can be reduction in bone mineral density, seen

Page 129

most acutely in the trabecular bone of the lumbar

spine. Bone loss of some 5 per cent can occur over a 6-

month course of treatment, but for the majority of

patients this is readily replaced as ovarian function

returns on ceasing the drug therapy. The administra-

tion of low-dose hormone replacement therapy (HRT)

along with the GnRH -A analogues, the so-called 'add

back' therapy, may offer a way of preventing the adverse

effects of oestrogen deficiency, although information

about the long-term results of this approach to treat-

ment is so far lacking.

Surgical treatment

Conservative surgery
Laparoscopic surgery with techniques such as intra-
abdominal lasers has become the standard for the surgi-

cal management of endometriosis. It is now much

simpler and safer to eradicate visible endometriotic

lesions with diathermy, CO2 or KTP lasers. Likewise,

endometriotic cysts can be drained and opened and the

inner cyst wall or lining destroyed and vaporized with

the laser. In many instances, because of the severe adhe-

sive disease found with endometriomas, open surgery

may still be necessary. Conservative approaches have

reduced the need for open surgery with its long recovery

times, and this allows patients to delay treatment until

such time as definitive surgery may become necessary.

Definitive surgery
Where there are severe symptoms or progressive dis-

ease or in women whose families are complete, defin-

itive surgery for the relief of dysmenorrhoea and pain

is often necessary. This takes the form of hysterec-

tomy and bilateral salpingo-oophorectomy. The

removal of the ovaries and subsequent ovarian hor-

mone production is beneficial in achieving long-term

symptom relief. Paradoxically, such patients can

receive HRT subsequent to surgery. To minimize the

risk of recurrence, the commencement of HRT is

often deferred for a period of time following surgery,

particularly when active disease was found to be pre-

sent at the time of laparotomy, and this delay is typi-

cally a period of 6 months or more.

Definitive surgery is also required for large adherent

endometriotic cysts and for the small proportion of

patients who have deep-seated endometriosis involving

the bowel or bladder. Endometriosis thus remains a dis-

order of which we still have little understanding and, at

Adenomyosis 117

present, little hope of a permanent cure other than

definitive surgery in the form of pelvic clearance. New

treatment options, both medical and laparoscopic

surgery, have expanded the pot ntial for delay in

surgery, but for most sufferers the disease remains one

of repeat recurrences throughout their reproductive life.


Adenomyosis is often incorrectly termed internal

endometriosis because of the histological fe atures of

the disorder in which endometrial glands are found

deep within the myometrium. Adenomyosis i increas-
ingly being viewed as a separate pathological entity

affecting a different population of patients with an as

yet unknown and different aetiology.

Patients with adenomyosis are usually mult iparous

and diagnosed in their late thirties or early forties.

They present with increasingly severe secondary

spasmodic dysmenorrhoea and increased menstrual

blood loss (menorrhagia). Examination of patients

may be useful with the findings most often of a bulky

and sometimes tender uterus, particularly if examined
perimenstruaUy. Ultrasound examination of the uterus

may be helpful on occasions when adenomyosis is par-

ticularly marked or localized to one area. Then ultra-

sound may show alterations of echogenicity within

the myometrium from the localized, haemorrhage-

filled, distended endometrial glands. In some instances

where there is a very localized area of adenomyosis, this

may give an irregular nodular development within

the uterus, very similar to that of uterine fibroids. MRI

provides excellent images of the myometrium, endo-

metrium and areas of adenomyosis and is now the

investigation of choice.

Given the practical difficulty in making the diagnosis

of adenomyosis preoperatively, conservative surgery

and medical treatments are so far poorly developed.

In general, any treatment that induces ameno,r.rhoea \,vill

be helpful as it will relieve pain and excessive bleeding.

Effective agents such as danazol, gestrinone and

GnRH-A used in the treatment of endometriosis may

also be beneficial for this condition. On ceasing treat-

ment, however, the symptoms rapidly return in the

majority of patients, and hysterectomy remains the only

definitive treatment. Where well-localized islands of

adenomyosis can be identified within the myometrium,

there is the potential for laparoscopic laser surgery, and

some reports of benefit have appeared in the literature.

Page 256

244 Index

psychological conditions (Contd)
chronic pelvic pain 221
contraception 221
fertility 220-1
menopause 2 10,218-19,220
menstruation 219
premenstrual synd rome 56-7,219-20
puberty 2 18
referral 219
sexual problems 2 18,22 1-31
transition to parenthood 218

puberty 26-7,30-1,218
pubic hair 27
pubic lice 171
pubococcygeus muscles 16, 16
pudendal artery 18
pudendal nerve 19
pulmonary complications 100,101
pyometra 105

radiology 125

cervical cancer 137-8
endometrial carcinoma 140
ovarian cancer 149
vaginal cancer 165
vulval cancer 163

raised intra-abdominal pressure 201
rectal ampulla 10
rectal artery 18
rec tocele 202, 203, 204-5,204

anatomy IS, 16
examination 5
lymph vessels 19

recurrent herpes 177-8, 177
recurrent miscarriage 54,92,93, 94,95,97
Set-reductase deficiency 24,25
referral for psychological conditions 219
reproductive outflow tract abnormalities SO
resistant ovary syndrome 5 I, 208
retention with overflow 190
ring pessaries 203,204
risk-taking behaviour 218
Rokitansky syndrome 25
round ligament 17

sacrocolpopexy 205, 205
salpingectomy 96, 99
salpingitis 171, 173, 175
salpingo-oopherectomy 117
salpingotomy 96,99
SARA see sexually acquired reactive arthritis
sarcoma of uterus 141
scabies 171
SCJ see squamocolumnar junction
scra tching

see also irritation
pinworms 170
pruritus vulvae 157-8

screening for ovarian cancer 148
secondary amenorrhoea 50,207,208
secondary dysmenorrhoea 49-50
secondary subfertility 76,77
secondary syphilis 178-9
secretory phase of menstrual cycle 39-40, 39
selective oestrogen receptor modulators

(SERMS) 16-17
self-discovery 229
semen 79,80,82, 83-4, 86
sensa te focus 230
SERMS see selective oestrogen receptor

serous cystadenoma 121
serous ovarian carcinoma 145

Sertoli cells 22, 22
Sertoli-Leydigcell tumours 122,15 1
serum markers 125
sex chromosomes 21,22-3,23,27-9,27,28
sex cords 7
sex cord stromal tumours 12 1-2, 123, 151
sexual development 21-3 1,22-5

outflow tract problems 29- 30,30
puberty 26-7
Turner's syndrome 27-8,27,28

sexual differentiation 21 - 2,22
sexually acquired reactive arthritis (SARA) 175
sexually-transmitted diseases (STOs) 66,79,

see also individual diseases

sexual orientation 218
sexual problems

case history 230-1
classification 223
communication 223
counselling 225, 229-30
female sexual behaviour 222, 225-8
history taking 2, 166,224
management 225-9
menopause 226
myths and taboos 223
pain disorders 228-9
physiological changes 224
prevalence 224
psychological conditions 218,221-31
psychosocial factors 222
response cycle 222-4
response staircase 229
sexual abuse 170

shelf pessaries 203,204
side effects, COCP 62, 62
Sim's speculum 3,4
skeletal system 21 0-11
sleep rhythms 209, 210
smears, cervical 133-4
social factors 2, 222
solid vulval tumours 159

intracytoplasmic sperm injection 83-4,

subferti lity 79,80
spiral arteries 38
spontaneous abort ion see miscarriage
squamocolumnar junction (SCn 132, 133
squamous cell carc inoma 131

see also cervica l intraepithelial neoplasia
squamous cell hyperplasia 159

cervical cancer 136, 137
endometrial carcinoma 140
Fallopian tube carcinoma 153, 153
ovarian cancer 146,14 7
vaginal cancer 165
vulval cancer 162, 162

STOs see sexually-transmitted diseases
sterili zation

consent 68
female 68-9, 68, 69
male 69-70,69

steroidogenesis, ovarian 33, 34, 37
Stiefel biopsy punch 157,157
Streptococcus faecalis 192
stress incontinence 189-98, 189, 196-8
subdermal contraceptive implants 64-5,65
subfertility 76-88

abortion 73-4
assisted conception 84-8
counselling 81
definition 76
endometriosis 11 5-16

epidemiology 76- 7
examinations 81
female factors 76-9, 77,8 1,83-8
history 81
investigations 81-3
male factors 77, 79- 80, 82-4
ovarian cancer 143--4
polycystic ovary syndrome 54, 55
psychological effects 220- 1
treatment 83-8
uterine fibroids 106, 107

subtracted cystometry 194, 195
suburethral support mechanism 189,189
superficial dyspareunia 225, 228- 9
superior hypogastric plexus 20
superior rectal artery 18

abortion 72, 73, 73
cervical cancer 137
cervical stenosis 105
ectopic pregnancy 99
endometrial carcinoma 140
endometriosis 11 7
epithelial ovarian cancer 148-9
fibroids 107
incontinence 197-8
menorrhagia 47-9
miscarriage 96,96
prolapse treatment 203-5,205
ureteric trauma 15
vaginal cancer 165
vulval cancer 163

surgical menopause 208
sympathetic nerves 20
sympathy 157,158
syphilis 178-80, 180

TA see transactional analysis
tamoxifen 104
Tanner's stages of puberty 26-7
Taxol see paclitaxel
TOF see testicular determining factor
tension-free vaginal tape (TVT ) 198
teratomas 120, 152
testicular determining factor (TOF ) 21, 22, 23
testosterone 22,22,25,34
TGF see transforming growth factor
theca cells 33, 121, 151
threatened miscarriage 94-5, 94
thrombosis 61,62
thrush see vaginal candidiasis
tibolone 214-15
tolterodine 198
toxic shock syndrome 170
trabecular bone 21G-I]
tranexamic acid 46-7 J
transactional analysis (TA) 219-20
transdermal oestrogen patches 213
transformation zone 132
transforming growth factors (TGF) 9
transvaginal ultrasound examinations 91,91,

transverse vaginal septae 25,29-30
traumatic post-abortion injuries 74
treponematoses 178

see also syphilis
triangular ligament 14, 16
trichomoniasis 167, 167, 168, 170
trigone of bladder 14, IS
Troissier's sign 1
trophoblastic tumours 101
tropical genital ulcer disease 180-1,180
true hermaphrodite 24,24
tubal dysfunction 79,8 1,81,82,82,83
tuberculosis 175-6

Page 257

see also cancer; individual tumours
benign epithelial 120-1
benign germ cell 120
benign ovarian 119-29
benign sex cord stromal 121-2
markers 125, 148
mixed mesodermal 141

Turner's syndrome 23,25,27-8,27,28,51,79
TVT see tension-free vaginal tape
'two cell two gonadotrophin' hypothesis 33

UK Abortion Act (1967) 70, 71

genital 176-81,180,185
vulval 159

ultrasound examinations 124-5, 196
early pregnancy 91-2,91,101
ectopic pregnancy 98-9
endometriosis 114-15
gestational trophoblastic disorders 100, 100
miscarriage 95,96
su bfertility 79, 81-2, 82

ultrasound-guided diagnostic ovarian cyst
aspiration 125, 127-8

United Kingdom contraception use 60
unruptured luteinized follicle see luteinized

ulHuptured follicle
upper genital tract infections 171-6
ureters 15,15

anatomy 10,14-15,14,16
intravenous urethrography 195-6
lymph vessels 19
pressure profilometry 196
suburethral support mechanism 189,189

urgency 191
urinary tract infection 192

diary 192-3, 193
frequency 106,109
incontinence 188
symptoms of menopause 210

urodynamic stress incontinence (US!) 189,

uro[1owmetry 193-4,194
urogenital diaphragm 14,16
urogynaecology 188-':99, 189, 191, 193, 194,

bladder exstrophy 191
ectopic ureter 191

fistula 191
investigations 192-6
vesicovaginal fistula 191, 191
voiding difficulties 191-2

USI see urodynamic stress incontinence
uterine fibroids 105-8

clinical features 106-7,106
degeneration 105, 106
differen tial diagnosis 107
pathophysiology 105-6, 105
treatment 107-8

uterosacral ligaments 17
uterovaginal prolapse 200-6,201,203,204,


anatomy 11, 11
artery 15, 108, 108, 109
benign disease 103-9
cervi.;, see cervix
curettage 96,98, 104-5
development 7,7
maldevelopment 25
malignant disease 138-41, 139, 140,

prolapse 203
rupture 107

vagina 9, 10
anatomy 16
artery 18
atresia 27,29
bacterial vaginosis 167, 168, 169
cancer 164-5,165
candidiasis 167-9,167,168
cervical ectropion 103
children 170
collagen metabolism 205
conditions affecting 163-5
development 7,7
discharge 103,167,167,170
examination, prolapse 202
menopausal dryness 210
septae 25, 29-30
vaginismus 228
vault prolapse 200,201

vaginal bleeding
cervical ectropion 104
complete hydatidiform mole 99
ectopic pregnancy 98
endometrial polyps 104
miscarriage 94-5

Index 245

vaginal hysterectomy 234
vaginal infections see lower geni tal tract

vaginal intraepithelial neoplasia (VAIN)

VAIN see vaginal intraepithelia l neoplasia
vascular endothelial growth factor I VEGF) 38
vas deferens 22, 22
vasectomy 69-70,69
vasoconstrictionof endometri um 39
vault prolapse 205,205
VDRL see Venereal Disease Reference

Laboratory test
veins, pelvic 18
Venereal Disease Reference Laboratory

(VDRL) test 179
venous thromboembolism 62
vertical transmission of syphilis 179
vertical vaginal septal defects 30
vesical arteries 18
vesicovaginal fistula 191, 191
vestibule 8,9
vestigial structures 14
videocystourethrography (VeU) 195, 195
VlI see vulval intraepithelial neoplasia
Virchow's node 1
virilization 26
voiding difficulty 191-2, 198-9

anatomy 8-9,8
cancer 161-3,162
conditions affecting 156-63
nerves 19

vulval intraepithelial neoplasia (VIN) 158,

vulvo-vaginal candidiasis see vaginal
ca nd id iasis

warts, genital 181-2,181
weight 54,55
Wertheim hysterectomy 137, 138
withdrawal method 67
Wolffian ducts 6, 21,22, 24

X chromosomes 21,22-5,23
46XX gonadal dysgenesis 27,28
XY females 24,24,25,27, 28-9
46XY gonadal dysgenesis 27, 29

Y chromosomes 21, 22-5
yolk sac 89,90,91-2,91, 152

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