1

THE GYNAECOLOGICAL PATIENT

- HISTORY TAKING AND EXAMINATION The key to a proper approach to patient care lies in making the correct
diagnosis. There are three main steps in making a diagnosis in the
gynaecological patients. The first is to obtain a good relevant history
taking, the second to perform a thorough medical and gynaecological
examination, and the third is to carry out relevant investigations.
When a gynaecological condition has been diagnosed properly, the
doctors can offer rational treatment and assess the severity of the
condition to produce a prognosis.
The history is probably the major mechanism that leads the doctors
towards a correct diagnosis. Examination of the abdomen and pelvis
adds confirmatory data and sometimes correctly chosen investigations
may help. It is important, therefore, to get a careful and relevant
history, not just a mass of information written down in some
prestructured proformat. The doctors must be specifically to the points
that are productive in making a diagnosis.
This chapter is concerned with the diagnosis of the symptomatic
gynaecological disease and the relevance of the history and clinical
examination in the management of gynaecological problems.

GYNAECOLOGIC HISTORY TAKING

a) Establishing good rapport
Gynaecological patients require a particularly sensitive and
sympathetic approach. It is often not easy for a woman to consult a
doctor with gynaecological symptoms about which she may be
embarrassed. Most of the time the patient is reluctant to discuss her
gynaecological problem until she has assessed the attitude of the
doctor.
The doctors must establish good rapport by a friendly and courteous
attitude appropriate to the age and type of patient.
1

If the patient speaks the same language as the doctor, it is much

easier but should she speak a different language then an interpreter
must be used. Even if the language is not common, the friendliness of
the doctor will show through with a smile or, if it is the custom in her
country, shaking the womans hand and making her comfortable will
definitely a success in establishing good rapport with the patient.
b) Be a good listener
The best way to start taking a history is to allow the woman to tell her
own story in her own words; let her talk about her principle complaint
herself and note from her description those areas about which further
questions are needed.
It has been truly stated that you should listen to the patient,
Doctor, and she will tell you the diagnosis. Certainly, many of
us do not really listen to what the patient are saying. If you truly
devote all of your attention not only to the words but also to the
inflections and overall attitude and composure of the patient, you will
receive a number of messages aside from the patients actual words.
During the interview, you should become very sensitive to the subtle
changes in the patients composure and be aware of her emotional and
psychological responses to your questions.
The doctor must be a good listener and counselor and also must be
able to direct the consultation by asking appropriate questions.
Different patients will respond best to different approaches and the
doctor must adjust to the needs of the patient.
c) Gynaecologic history
The aim of good history taking is to establish the relevant facts and at
the same time is to listen for problems which the patient does mention
overtly. It is very important to perform a complete history and to make
an accurate record of the history of the patient.
The basic data about the patients history, an obstetric,
gynaecological, medical, surgical, drugs, past and present history,
social and family history are an integral part of gynaecological history
taking. Detailed gynaecological questioning, I prefer to perform it after
a general history has been taken and the patients confidence has
been gained.
Gynaecologic history taking includes the following:

Patients identification data:

2

There are certain basic data about the patient that you must obtain
during your evaluation on her.

Age
Race
Maritial status
Parity
Occupation

Age: The patients age is one of the most important pieces of

information you will obtain because it will, to some extent,
determine the types of illnesses that you should consider in the
face of certain complaints.
For example, Vaginal bleeding in:

Premenarcheal girl, is usually due to a foreign body in the vagina

or the child might has ingested some hormonal tablets (commonly
the mothers birth control pills).

Teenage girl, who is not pregnant will almost always have

dysfunctional uterine bleeding due to anovulatory cycle.

Woman of reproductive age, should always suggest pregnancy

first, with all its complications, such as a threatened abortion,
ectopic pregnancy or hydatidiform mole. Others causes include
uterine polyps, fibroids or cervical carcinoma.

Perimenopausal woman should suggest endometrial carcinoma,

although dysfunctional uterine bleeding is also common in this age
group.

Postmenopausal patient, should strongly suggest carcinoma of

the endometrium.

Presenting (Chief) complaint:

You will need to explore the reasons for your patients visit. You should
ask specific information about her complaint in order to define the
problem and provide a set of working diagnoses. You should also ask
about the duration of the complaints.

History of Present Illness:

Once you have determine the patients presenting complaint, you will
need to explore in detail more facts about the patient complaint with a
pertinent review-of-symptoms.
For example, A 30 years-old, Gravida 2 Para 2 female comes in
with the chief complaint of progressive painful period of six
months duration. You will need to elaborate and explore regarding
this painful period such as follows,

For how long always had it or developed recently

The site of occurrence
Relationship to menses and duration
Degree of incapacitation caused
Relieved by what?
Any usage of intrauterine contraceptive device
Any vaginal discharge - colour, amount, duration, itching or irritant

Past Obstetric History:

You also need to know about the womans reproductive performance,

including her gravidity, parity, and previous pregnancy outcomes.
If the woman had any pregnancies, it is important to go through the
past obstetric history systemically. Detail of each pregnancy should be
listed under the year of the pregnancy, what happened in the
pregnancy itself, the stage of gestation at delivery, what happened in
labour, the method of delivery, the birthweight and the stage of the
baby after delivery. If the pregnancy ended as a spontaneous or
therapeutic abortion, the stage of the gestation should be noted and
whether curettage was performed.

Past History (Medical and Surgical):

The past medical and surgical history of the woman herself should be
ascertained. It is wise to start with some general questions like Have
you ever been admitted to hospital? or Have you had any
operations?
These two screening questions cover any serious
medical treatments in the past.

Relevant Family history:

The family history may be relevant, particularly if there are female

family members or, if the symptoms indicate, a possible familial
condition when the patients mothers medical history may be relevant.
For example, a case of primary amenorrhoea may have familial
etiological factors.

Social History:

The social history is important, for it should fit the woman into the
context of her work pattern and conditions at home. She should be
question about her permanent partner (if she had one) and what he
does. Her smoking and drinking habits should be noted.

Drugs and Allergic History:

Any history of drugs usage (particularly hormonal pills) should be

ascertained. Allergic history to drugs, pollens, food or other agents
should be noted.

Menstrual History:

Your patients menstrual history is very important. It is therefore

important to obtain a full menstrual history, particularly that of the
most recent months. The following information about the menstrual
history should be asked.
1) The age when the menstruation began (menarche).
2) The pattern of the regularity of the menstrual cycle is it regular or
irregular. The usual interval between her periods, and the average
duration and amount of menstrual flow should be recorded.
3) The date of the last normal menstrual period (LNMP) should be
obtained and the pattern of the last few periods.
4) You should always find out whether the patient has experienced any
abnormal uterine bleeding.
Any change in the amount of bleeding may be important; this can
be estimated in relation to a change in the number of days of
bleeding at each period and the number of pads used on the
heaviest day.
5

In cases involving intermenstrual bleeding (IMB), or postcoital

bleeding (PCB), the character of the bleeding and its time of onset
during the menstrual cycle may be important factors in arriving at a
correct diagnosis. For example, spotting just prior to the menstrual
period, when associated with a prolongation of the period, may
indicate the presence of irregular shedding of the endometrium due
to hormonal imbalance. Spotting or bleeding on and off during the
cycle may indicate the presence of endometrial polyps. Spotting or
bleeding after coitus may frequently be due to a cervical erosion or
an endocervical polyp.
Enquiry should be made about dysmenorrhoea. Its degree, duration
and site should be ascertained; the relation in time to the period
may be characteristic in pointing to a diagnosis.
If the woman is post-menopausal enquire specifically about postmenopausal bleeding (PMB).

Contraceptive History:
The types of contraceptive usage and for how long should be
ascertained. Intrauterine device and hormonal contraceptives may
be relevant because of their possible effect on menstruation.

Sexual History:

Information is required about a womans sexual history. Sexual

history may not be asked early in the interview. The doctor must
choose the right time to ask such question and should ask them in a
matter-of-fact way which does not cause embarrassment.
Information about dyspareunia ( pain at the time of intercourse) should
be asked and the doctor should determine if dyspareunia is superficial
or deeper in the pelvis. It is also helpful to know if deep dyspareunia is
constant or intermittent. A constant dyspareunia which last for few
hours or days may be indicative of congestive disorders of the uterus
or adnexa.

CLINICAL EXAMINATION
Examination of the abdomen and pelvis adds confirmatory data in
making a correct diagnosis. It is very important that certain practical
6

points should
examination:

be

taken

before

performing

the

gynaecological

1) It is important to establish good rapport with the patient before

attempting to examine her.
2) The patients consent should always be obtained before examining
her.
3) The patients modesty should be considered to be of prime
importance and the examination should be carried out discretely
and without interruption.
4) Whether the doctor is male or female it is preferable for the
examination to be carried out in the presence of a third person.
The clinical examination of a gynaecological patient is performed as
follows:
a) General Examination:
A general examination is carried out with particular regard to general
health and to evidence of anaemia and to endocrine function. The
conjunctiva of an eye is examined to check anaemia. Blood pressure
estimation should be performed.
b) Breast Examination:
An examination of the breasts should always be performed. The
inspection and palpation of the breasts are the mainstays of the breast
examination.

Inspection: With the patient sitting up and lying down in turn, the
doctor should inspect the breast for dimpling, skin retraction,
abnormal contour or depressions, or any deviation of the nipples
from their abnormal position.
Palpation: The breast should be palpated in each of the four
quadrants, and then beneath the nipple, using the flats of the
fingers. Any significant lumps will become apparent in most
instances.
In addition, the supraclavicular areas should be
thoroughly palpated to detect the presence of any enlarged lymph
nodes. An attempt should be made to express secretion from each
nipple.

c) Abdominal examination:

The abdominal examination is performed in the supine position. Before

starting the abdominal examination, the doctor should ensure that the
woman is comfortable on the couch.
The abdomen of the woman is examine in the following ways:

Inspection: The abdomen should be observed for the presence of

any scars.
Inspection of the abdomen may reveal an intraabdominal mass, particularly one arising above the symphysis
pubis. The presence of striae should be noted and hernias should
be excluded in the femoral and inguinal regions.
Palpation: The woman should first be asked to point to any areas
of pain in the abdomen with one finger. The doctor starts the
palpation away from such areas, working towards the points of
maximum tenderness.
Start with a gentle palpation first, and
only if there is no superficial tenderness may this be followed by
deeper palpation. In this manner will enable the doctor not to hurt
the patient.
Always watch the patients face carefully which
performing the examination.
If a mass is felt, it should be described in terms of their shape and
consistency, their location and mobility, and their size.

Where in the abdomen is the mass, central or lateral?

Does the mass arise from the pelvis.
Can the examining hands get below it.
Is the surface of the mass smooth or multilobulate.
Is the consistency of the mass- soft, cystic or hard.

Percussion: Percussion is used if a mass is felt or the presence of

ascites is suspected. Ascites is elicited by tapping from the middle
of the abdomen out towards the flanks.
Auscultation: Rarely does
gynaecological diagnosis.

auscultation

help

in

making

d) Pelvic Examination
Pelvic examination should be carried in a systematic manner in order
to avoid missing important information. Prior to the pelvic the patient
is instructed to empty her bladder. She then should be placed in a
comfortable dorsal position with both of her legs bend at the knee or in
a lithotomy position on the examination couch with her legs in the
stirrups. The patient should be instructed to remain relaxed and to
keep her legs widely separated in order to facilitate the examination.
8

External genitalia:
The external genitalia should be thoroughly inspected for lesions,
masses, inflammation, or other pathology. The labia should be
palpated for cysts or lumps, and the clitoris should be inspected for
size. The labial fold should then be widely separated and the
urethral and vaginal orifices inspected. The palpation of the vaginal
introitus at five and seven oclock will detect the presence of
Bartholins cyst

Vaginal examination:
A vaginal examination is performed in the dorsal or left lateral
position. Speculum examination is usually undertaken next but this
may be preceded by bimanual examination.

Bimanual examination: The bimanual examination of the

pelvis consist of using both of your hands, with one inside the
vagina and the other on the abdominal wall, to palpate the pelvic
and abdominal structures.

With the labia parted by the left hand, the gloved right hand
(the index and middle fingers) is introduced gently into the
vaginal canal. You should place two fingers in the vagina, one
on each side of the cervix initially, and then on further
examination the fingers should be placed in each fornix.
The cervix is gently palpated and the left hand is now placed
on the lower abdomen just above the symphysis pubis in the
mid-line and by gentle ballottement of the pelvic structures
with the hand on the abdominal wall, the location of the
adnexa can be determined (Fig. 1.1).

Fig. 1.1 Bimanual palpation procedure in

gynaecological examination.

Once the uterus has been located, it should be checked for

regular
or
irregular
enlargement,
mobility,
position
(anteflexed, retroflexed, anteverted or retroverted), along with
its consistency and tenderness.
Any pelvic mass that is detected in the bimanual examination
should be define as its position, mobility, consistency, and
size.
The adnexal structures should also be carefully evaluated.

Speculum examination: The speculum examination is usually

performed using a bivalve speculum, known as the Cuscos
speculum (Fig. 1.2).

10

Bivalve or
Cuscos
speculum

Sims speculum

Fig. 1.2 The vaginal speculums

It is very important to explain to the patient prior to the

procedure. Also, it is a good practice to insert a warm
speculum.
A bivalve or Cusco,s speculum is intended for the dorsal
or supine position. This speculum is introduce in the following
ways:1. First, explain to the patient what is going to happen.
2. Choose the appropriate size of the speculum and
lubricated it. Never introduced a cold speculum.
3. After spreading the labia with the fingers of one hand, the
speculum is gently introduced with the flat axis at rightangles to the cough, parallel with the line between the
labia majora. Once it is about 2 to 3 cm in the vagina,
the handle is then rotated anteriorly or posteriorly.
4. The cervix is then inspected for any pathological
conditions. A Papanicolaou smear or a high vaginal swab
may be taken as indicated.
5. During the slow removal of the speculum, the vaginal
mucosa from the cervix to the introitus should be
inspected for the presence of any lesions.

11

A Sims speculum (Fig. 1.2) is introduced with the patient in

the left lateral position (Fig. 1.3), to inspect the walls of the
vagina and to examine for prolapse.

Fig. 1.3 A Sims speculum is introduced with the woman lying left lateral.
This give an excellent view of the vaginal walls and cervix.

Rectal examination:

It is very important to perform a rectal examination on every patient.

Not only will this examination allow to detect rectal pathology, but also
it will provide adequate information.

CONCLUSIONS
Taking a full relevant history and performing a proper examination is
the essence of good gynaecological practice.

SAMPLE CASE HISTORY OF GYNAECOLOGICAL PATIENT

PATIENTS IDENTIFICATION DATA

12

Name : Mrs. R.K

Marital status : Married
Parity : Gravida 3 Para 2

Age : 35 years old

Race :
Occupation : Housewife

CHIEF COMPLAINT;

Painful period of eight months duration.

HISTORY OF PRESENT ILLNESS

Painful period begins about eight months ago, before that had only slight discomfort.
It is usually felt in the lower abdomen with radiation to the lower back.
It begins several days before the menses and gradually increases in severity as menses
approach.
Unable to perform normal housework.
Need to take medications to relieve pain but only last for few hours.
This painful period is causing Mrs. R.K to feel miserable
There was slight increase in the amount of menstrual flow for the first two days. However there
was no history of intermenstrual or postcoital bleeding.
No significant history of vaginal discharge.

PAST OBSTETRIC HISTORY

Had 2 Full term uncomplicated pregnancies which ended in spontaneous vaginal deliveries
at 39-40 weeks gestation. Labour progress was uneventful, and delivered a live baby boy
and girl with the birthweight ranging from 3.5 3.7 Kgs. The third stage and postpartum
recovery was uneventful.

PAST MEDICAL AND SURGICAL HISTORY:

FAMILY HISTORY:
SOCIAL HISTORY:

Married with two healthy children aged 9 and 7 years old.

Husband is running their own business
Mrs. R.K does not smoke nor drink

DRUGS AND ALLERGIC HISTORY: None

MENSTRUAL HISTORY:

Menarche at the age of 13 years old.

Last Normal Menstrual Period:
Cycle regular with an interval of 29 days; 5 days of flow duration and normal amount. Lately there
was slight increase in amount of flow during the first two days and associated with small pieces of
clot.
There was no history of intermenstrual bleeding

CONTRACEPTIVE HISTORY:

Currently has been using intrauterine device for the last 3 years and had regular followup.
Mrs. R.K has been quite happy with this intrauterine as she has no complaint about it.

13

SEXUAL HISTORY:

She describe that her sexual relationship with her husband has been without much problem.
Lately, she experience mild dyspareunia, which was felt, deep in her pelvis. This dyspareunia last
for a short period.

GYNAECOLOGICAL EXAMINATION

General Examination: as indicated by history

Breasts Examination: as a routine

Abdominal Examination: Inspection, Palpation, Auscultation and Percussion.

Pelvic Examination: To be done in either the dorsal or left lateral position.

Inspection of the external genitalia
Bimanual examination
Speculum examination
Rectal examination

SUMMARY: Conclude by writing summary of history and examination

PROVISIONAL DIAGNOSIS: Secondary dysmenorrhoea
DIFFERENTIAL DIAGNOSIS:

2
ANATOMY OF
THE FEMALE REPRODUCTIVE ORGANS
14

External
Genitalia

Internal
Genitalia

VULVA
VAGINA

CERVIX
UTERUS
FALLOPIAN
TUBES
OVARIES

Fig 1.1 Sagittal section of the female reproductive organs

The reproductive system of the female (Fig. 1.1) may be divided into
the external and internal genitalia.

EXTERNAL GENITALIA ORGANS

The external genitalia organ of the female consist of the
Vulva - the visible portion
Vagina the hidden portion
THE VULVA
The vulva (Fig. 1.2) is the visible portion of the female external
genitalia and consists of all the structures visible externally extending
from the pubis to the perineum, i.e.

Mons pubis or mons veneris

Labial majora
Labial minora
Clitoris
Vestibule
Fourchette

MONS PUBIS
15

Clitoris
Labial Majora
Labial Minora
Vestibule
Fourchette

Fig. 1.2 Anatomy of the female external genitalia VULVA

MONS PUBIS
Mons pubis or mons veneris is a fatty cushion which is situated
anteriorly.
It covers the anterior surface of the symphysis pubis.
The skin contains sebaceous and sweat glands and coarse pubic
hairs.
LABIA MAJORA
The labia majora are comprised of two rounded fold of adipose
tissue covered by the skin originating in the mons pubis.
It extended downward from the mons pubis and merged posteriorly
into the perineum where they are joined together by the fourchette
(Fig. 1.2), forming the lateral boundaries of the vulva
Embryologically the labia majora are homologous with the male
scrotum and are formed from the genital swelling.
The labia majora have a full complement of adnexal structures, with
hair follicles, and sebaceous, eccrine and apocrine glands. The hair
follicles are found on the lateral surface of the labia majora.
The round ligaments terminate at the upper border of the labia
majora.
The microscopic structure of the labia majora and its superficial
layers reveals the following:
16

1. The epithelium is cornified stratified squamous, similar in type

to that seen in other areas of the body.
2. Underlying the skin is a thin poorly developed muscle layer
called the tunica dartos labialis.
3. Beneath the dartos layer are thick layer of adipose tissue.
4. Numerous sweat glands are found in the labia majora, the
greater number being present on the medial aspect.
5. In the deeper layer of the labia majora are found fibres of the
round ligament.
The arterial supply to the labia majora comes from the internal and
external pudendals with extensive anastomoses.
The lymphatics of the labia majora are extensive with two systems
being utilized, i.e. superficial and deep drainage (Fig. 1.3).

upper two-thirds of the labia majora drain into the superficial

inguinal nodes which then drain to the deep femoral group and
then into the external iliac nodes.
the lower part of the labia majora has superficial and deep
drainage.

The innervations of the labia majora are from the ilioinguinal and
genito-femoral nerves.
LABIA MINORA
The labia minora are two thin folds of skin, visible when the labia
majora are separated.
They vary greatly in size and shape. In children and postmenopause
women labia minora are more prominent than the labia majora.
They begin at the base of the clitoris. Anteriorly form the prepuce of
the clitoris and beneath the clitoris they unite to form the frenulum
of the clitoris.
The skin of the labia minora is smooth and pigmented. They
contains sebaceous and sweat gland but no hair follicles.
Embryologically the labia minora are homolgous with the phallic
portion of the male urethra and they are formed from the genital
folds.
Microscopic examination reveals:
1. Poor rete pegs and papillae development in the stratified
squamous epithelium.
2. The labia minora are characterized by the absence of adipose
tissue for most of the length.

17

3. The sebaceous glands are found predominantly on the lateral

surfaces, while sweat glands are evident on both medial and
lateral surfaces.
4. Smooth muscle fibres, continuation of the dartos, are found
within the labia minora.
The main source of arterial supply occurs from anastomoses from
the superficial perineal artery, branching from the dorsal artery of
the clitoris, and from the medial aspect of the rete of the labia
majora.
The lymphatics medially may join those of the lower third of the
vagina superiorly and the labia majora laterally, and go to the
superficial subinguinal nodes and to the deep subinguinal nodes. In
the mid-line, the lymphatic drainage goes with that of the clitoris
communicating with that of the labia majora to drain to the opposite
side.
The labia minora are extremely sensitive and supplied with a variety
of nerve endings.

External iliac
group
Deep femoral
group

Superficial
inguinal group

Fig. 1.3 Lymphatic drainage of the vulva.

CLITORIS
The clitoris is the homologue of the penis and embryologically
formed from the genital tubercle.
Clitoris is a small erectile organ at the upper end of the vulva and
below the mons pubis, where the labia minora meet.
The clitoris consists of very sensitive glans, a body (corpus) and two
crura.
18

 The crura and body are composed of erectile tissue.

The glans of the clitoris does not contain a urethra as the penis
does.
The blood supply is from the dorsal artery of the clitoris, the
terminal branch of the internal pudendal artery.
The innervation of the clitoris is through the terminal branch of the
pudendal nerve from the sacral plexus.
The lymphatic drainage of the clitoris is primarly that of the labia
minora.
VESTIBULE
The vestibule is the space between the labia minora.
It is bordered,
Laterally by the labia minora.
Posteriorly by the fourchette.
Anteriorly by the urethra and clitoris.
Inferiorly by the hymenal ring.
The vestibule is perforated by six opening,
Urethra.
Vagina.
Ducts of the two Bartholin glands.
Ducts of the two Skenes glands.
Its (vestibule) floor contains the greater vestibular glands (Bartholin
glands).
Microscopic section (Fig. 1.4) of the vestibule reveals, the squamous
epithelium is non-cornified and bears no adnexae.

Fig. 1.4 Microscopic section of the vestibule.

LARGER VESTIBULAR GLANDS (BARTHOLINS GLANDS)

A pair of small pea-liked glands lie each side posterolateral to the
vaginal orifice at 5 and 7 o'clocks.
These glands are tubular and alveolar in character. It is lined by
columnar epithelium.
19

 The ducts about 2 cm long, lined by transitional epithelium, open

into introitus below the hymen.
Bartholins gland is homologous to the Cowpers (bulbourethral)
glands in the male.
The function of the gland is secretion of mucus (pH-alkaline), which
acts as a lubrication of the vaginal orifice and canal in response to
sexual arousal.
The Bartholin gland near the age of 30 begins to show progressively
diminishing function.
In normal situation, the Bartholins glands are not palpable or
visible.
THE VAGINAL OPENING
The vaginal opening or orifice is also known as the introitus of the
vagina occupies the lower portion of the vestibule.
This orifice is partially closed by a thin membrane, known as the
hymen.
This hymen is originally a membrane composed of connective tissue
and covered by stratified squamous epithelium on both aspects.
During reproductive life intercourse the hymen is broken down. The
remaining tags of hymen are known as carunculae myrtiformes.

Lymphatic drainage of the vulva

Superficial inguinal Deep inguinal Femoral External iliac nodes

Venous

Blood supply of
vulva

drain
age

Accompany
arterial supply
Also via
vesical and

Internal
pudendal artery
Superfficial
external
pudedndal
artery

Nerve supply of the vulva

From branches of the pudendal nerve

INTERNAL GENITALIA ORGANSOF THE FEMALE

20

The female internal genital organs

are situated within the lesser pelvis.
They comprise of the,
Vagina
Uterus, which consist of
Fundus
Body
Cervix
Fallopian tubes
Ovaries

Fig. 1.5 Anatomy of internal female genital organ

VAGINA
The vagina is an elastic musculomembranous canal, which serve as
the intermediary or connecting organ between the external genitalia
and the uterus.
In the adult, it varies in length from 7 to 10 cm, the posterior wall
being approximately 1.5 to 2 cm longer.
In resting stage the anterior and posterior walls of the vagina are
apposed (in closed contact).
In the erect position the vagina runs upwards and backwards from
the vestibule to the cervix uteri.
The upper end of the vagina expands into cup-shaped vault into
which the cervix uteri is fitted.
The vaginal vault is divided into the anterior, posterior and lateral
fornices.
The fornices are of clinical importance, since the internal pelvic
organs can be palpated through the thin walls of the fornices. The
posterior fornix provides surgical access to the peritoneal cavity.

The vagina is closely related to the neighboring structures (Fig. 1.6):

Anterior closely related to urethra and base of bladder.

Posterior closely related to Pouch of Douglas, rectum and
anal canal.

21

Posterior

Fig. 1.6 Anterior and posterior relationship between the vagina and the pelvic
structures.

Histology of the vagina:

The vagina has three layers,
1. Inner layer epithelium
2. Middle layer muscular
3. Outer layer fibrous
The vagina is lined by stratified squamous epithelium which is
thrown into folds (rugae).
Beneath the vaginal epithelium is the muscular layer which is made
up of:
Inner circular layer.
Outer longitudinal layer.
The outer most layer of the vagina is fibrous, derived from the
pelvic connective tissue.
Embryology of the vagina:
Embryologically the vagina is formed from the solid vaginal plate
(which is made up of urogenital sinus epithelium and the
paramesonephric duct) which undergoes canalization and forming
the vaginal lumen.
Blood supply of the vagina:
The vagina receives its blood supply from the,
Vaginal artery, branches of the uterine artery which supply
the upper third of the vagina.
Internal pudendal artery which supply the middle third of the
vagina.
22

Middle and inferior rectal artery which supply the lower third
of the vagina.
The venous drainage of the vagina is by vaginal plexus to internal
iliac veins.

Lymphatic drainage of the vagina:

The lymphatic drainage of vagina:
The drainage of the lower vagina is the same as the vulva.
The drainage from the upper vagina is the same as the cervix.
Physiology of the vagina:
The vagina is kept moist by the cervical mucus and vaginal
transudation.
The vaginal epithelium responds to ovarian hormones.
Under the influence of oestrogen the cells become rich in glycogen
which provides a medium for the Doderleins bacilli.
These bacilli convert glycogen to lactic acid which maintains the pH
of the vagina between 4 and 4.5.
The vagina pH is higher in condition, which produces lower estrogen
level, such as during childhood and post menopause.

THE UTERUS
The uterus is a muscular organ whose function is to provide a nidus for
the developing embryo and fetus until the time of parturition.
The uterus has three anatomical sections, ie fundus, body and
cervix.
FUNDUS

BODY

ISTHMUS
CERVIX
23

Fig.1.7. Coronal section of uterus.

The uterus is situated in the pelvic cavity between the bladder

anteriorly and the rectum posteriorly.
In nulliparous women, the uterus measures about 8-10 cm in length,
6 cm in width and about 4 cm in thickness.
The uterus in children is smaller and the cervix is longer than body.
In menopause women the uterus becomes atropic.
The normal position of the uterus is anteverted and anteflexed in
about 80% of women. It is maintained in this position by the
support of the pelvic floor muscles and the ligaments, especially the
uterosacral ligaments. In about 20% of women the uterus is
retroverted.
The inferior portion ie, the cervix projects into the vagina.
The cornu is the region where the fallopian tubes enter the upper
part of the uterus at the fundus.
The uterine body is covered externally by peritoneum, except for
the lower part anteriorly, where the peritoneum is reflected on to
the bladder.
Fundus:
The fundus is the part above the entrance of the fallopian tubes
(Fig. 1.7).
It is convex in shaped.
The fundus measures about 5 cm from side to side and is about 3
cm thick.
Body of the uterus:
The uterine body is a hollow thick-wall globular muscular organ, the
cavity being roughly triangular.
The anterior surface of the body of uterus is almost flat, whereas
the posterior surface is convex.
The anterior and posterior muscular wall bulged into the uterine
cavity and the inner surfaces of anterior and posterior walls are in
close contact.
The peritoneum covers the anterior and posterior surfaces except at
the sides between leaves of broad ligaments.
The wall of the body of the uterus are made of three layers:

Outer layer serosa

Middle layer muscularis
24

Inner layer mucosa

1. The serosa layer is formed by the peritoneum that covers the uterus
and to which it is firmly adherent.
2. The thickest muscularis layer (myometrium) consists smooth
muscles which are arranged in several layers:

Innermost longitudinal layers.

Middle layer being the thickest vascular layer with bundles
in all directions.
Outermost circular and longitudinal layers.

3. The mucosa layer (endometrium) is composed of columnar

epithelium.
The endometrium varies in thickness at different
phases of the menstrual cycle. The endometrium is divided into:
A superficial layer with an upper spongy and a compact
area. These are the only zone responsive to the hormonal
stimulation and are shed at the time of menstruation.
A basal layer not shed at time at time of menstruation.
Cervix:
The cervix is cylindrical in shape and measures 2.5 cm to 3 cm from
above downwards.
It is delineated inferiorly by the external os and superiorly by the
internal os, now called the isthmus uteri. The isthmus dilates and is
taken up into the uterus during pregnancy. This expansion of the
upper cervix or isthmus constitutes the formation of the lower
uterine segment.
The constriction above the isthmus is called the anatomical
internal os, and below the isthmus where the endometrium
changes into columnar cervical epithelium is termed the
histological internal os.
The cervix is a strong pivotal point for uterine for uterine stability,
being attached to the pelvic walls by radiating fascial condensations
called ligaments
Pubocervical anteriorly
Uterosacral posteriorly
Transverse cervical ligament (Mackenrodt) laterally.
There is a vaginal and supravaginal component of the cervix. Half of
the length projects into the vagina (vaginal cervix) and half lies
above it (supravaginal cervix).
25

 The vaginal portion of the cervix is clasped by the vault of the

vagina. The deep sulcus, which surrounds the protruding cervix, is
known as the fornix of the vagina; it is deepest posteriorly.
Anteriorly the supravaginal part of the cervix is firmly attached by
fibrous tissue to the base of the bladder, but posteriorly it is covered
by the peritoneum of the Pouch of Douglas.
The cervix is composed of fibromuscular and collagenous tissue.
The muscular coat of the cervix is well developed in the region of
the internal os, but the proportion of muscle tissue decreases
rapidly at a lower level.
The vaginal portion of the cervix is covered by stratified squamous
epithelium, which joins the columnar epithelium of the cervical
canal at or near the external os. The columnar epithelium often
extends to cover the central part of the ectocervix, resulting in a
bright-red colour, known as eversion or erosion.
The cervical canal runs from the internal to external os.
The external os is small and circular in nulliparous women and
transverse slit in parous women.
ANATOMY OF
THE CERVIX

FUNDUS

Anatomical
internal os
ISTHMUS
CERVIX

Supravaginal

Histological
internal os

Vaginal

External os

There are numerous cervical glands which extend from the surface
of the endocervical mucosa directly into the subjacent connective
tissue. These glands penetrate deeply into fibromuscular stroma.
Secretion from the cervical glands increases under oestrogen
stimulation to form mucus for penetration of the sperms around
time of ovulation.
Under the influence of progesterone in the second half of the
menstrual cycle, the cervical secretions decrease and become
viscous.
If the ducts of the cervical glands are blocked, retention cyst or also
known as nabothian cysts may form on the surface of the cervix.

26

Embryological development of the uterus

The
female
reproductive
organ
developed
from
the
paramesonephric (Mullerians) ducts during the intrauterine life.
The fundus, body of uterus and the cervix are formed by fusion and
canalization of paramesonephric ducts.
Failure in fusion or canalization of these paramesonephric ducts
may result in congenital formation of the uterus such as (Fig. 1.8),

Double uterus due to failure of fusion.

Unicornuate uterus.
Bicornuate uterus.
Uterine septum.
Rudimentary horn.

Fig. 1.8 Congenital abnormalities of the uterus.

Blood supply of the uterus

Blood supply to the body of uterus and the cervix (Fig 1.9) is from the,

Uterine artery ( anterior branch of internal iliac) .

Ovarian artery ( arise from the abdominal aorta).

Uterine artery:
1. Passes medially across the pelvic floor in the base of the broad
ligament above the ureter.
2. Reaches the uterus at the supravaginal part of the cervix
where it gives off branch to the cervix and vagina.
3. Turns upwards within the leaves of broad ligament to the
entrance of the tubes where it anastomoses end-to-end with
the ovarian artery.
27

Venous drainage is via uterine and ovarian veins.

Ovarian artery

Uterine artery

Anterior branch of
internal iliac artery

Vaginal artery

Fig. 1.9 Blood supply of the uterus, cervix and ovary.

Lymphatic drainage of the uterus

The lymphatics from various segments of the uterus drain into
several sets of lymph nodes.
The lymphatics from the body of uterus are distributed into two
groups of nodes,
1. superficial inguinal then the femoral, and then the
external iliac nodes.
2. Para-aortic nodes (via lymphatics accompanying ovarian
vessels).
From the lower part of uterus and cervix, drainage is mainly to
paracervical, internal and external iliac nodes and the obturator
nodes.
Nerve supply of the uterus
28

 The nerve supply of the uterus is derived chiefly from the autonomic
nervous system, sympathetic and parasympathetic.
Pain from the cervix passes in the nervi erigentes (S2,3).
The body of uterus nerve supply is by the lumbar splanchnics to the
lower thoracic segments. This transmit the painful stimuli of uterine
contractions to the central nervous system.
Relationship of the uterus within the pelvic structures (Fig 1.10)
Fig. 1.10

ANTERIOR

Anterior:
are ,

Bladder
Uterovesical pouch

LATERAL
POSTERIOR

In front of the uterus

Posterior: Behind the uterus are,

Pouch of Douglas
Rectum
Lateral: On

either side are the,

Ovaries
Fallopian tubes
Broad ligaments

Superior: Above the uterus lie the - Intestines

Inferior: Below the uterus is the - Vagina
Supports of the uterus
The uterus is supported by the pelvic floor and maintained in
position by several ligaments.
The most important ligaments are the round ligament of the body of
the uterus and the lateral and uterosacral ligaments of the cervix.

Round ligament:
1. Extends from the junction of uterus and tube to the deep
inguinal ring.
2. It lies in the anterior leaf of broad ligament, below the
fallopian tube.
3. It is continues with the ligament of the ovary.
4. It hold and maintain the uterus in anteverted position.

29

Uteroscral ligaments:
1. The
uterosacral
ligaments
extends
backward
and
posterolaterally from the cervix to the sacrum.
2. They are composed of smooth muscles and connective tissue.
3. The uterosacral ligaments maintain the uterus in anteversion.
Lateral ligaments:
1. This ligament is also known as transverse cervical ligaments
or the cardinal ligaments or the lateral ligaments of
Mackenrodt.
2. These ligaments fan out from the sides of the cervix to the
side walls of the pelvis.
Pubocervical ligaments:
1. Pubocervical ligaments pass forwards from the cervix, under
the bladder, to the pubic bones.

THE FALLOPIAN TUBES

Ampulla

Interstitial
Isthmus

Infundibulum
Fig. 1.11 Anatomy of the fallopian tube

30

Anatomy of the fallopian tubes

1.
2.
3.

The fallopian tube is a fibromuscular tube about 10 cm long,

extending from the uterine cornua to a site near the ovaries.
Each tube lies in the upper part of the broad ligament behind
the round ligament.
The fallopian tube is in four portions (Fig. 1.11)
Intersitial portion is about 1.25 cm and lies within the wall
of the uterus. It is straight and narrow. Its lumen is 1 mm
wide.
Isthmus portion is another narrow (about 2 3 mm in
diameter) and straight part of the tube adjacent to the
uterus. It is about 2.5 cm in length.
Ampulla portion is the widest portion (about 5 8 mm in
diameter) and is somewhat tortuous in shape. It is 5 cm
long. Fertilization usually occurs in the ampulla.
Infundibulum is a funnel-shaped free extremity portion
which is composed of many small finger-liked processes
called fimbrae. One of this fimbrae is longer than the
others, and is attached by its tip to the ovary called the
ovarian fimbria.

Embryology of the fallopian tubes

The fallopian tubes develop from the upper part of paramesonephric
(Mullerian) ducts.

Relations of the fallopian tubes

Anterior and posterior : The peritoneal cavity.

Superior : The intestines
Lateral : Side wall of the pelvis.
Medial : The uterus lie between the two tubes.
Inferior : The broad ligaments and ovaries lies below the tubes.

Histology of fallopian tubes

Histologically, the fallopian tubes consist of three layers
1. Outer layer serous peritoneum.
2. Middle layer two muscular coats, arranged in an inner circular
and outer longitudinal layer.
3. Inner layer mucous membrane which is composed of a ciliated
columnar epithelium. This epithelium are thrown into longitudinal
31

folds or rugae. In the isthmus the folds flatten and the cilia tend
to disappear.
There are three cells types in the mucous membrane.
1. Ciliated cells they propel the ova and keep the tubal lumen
clean.
2. Non-ciliated cells have a secretory function.
3. Peg cells.

Blood supply of fallopian tubes

The fallopian tubes receive its blood supply from
the branches of the ovarian artery, and from

the ascending branch of the uterine artery which

anastamoses end-on with the tubal branch of the ovarian
artery.

THE OVARIES
These are two white ovoid bodies placed one on each side of the
pelvis just below the tube.
The ovaries are the homologues to the testes.
They measure about 3.5 x 2 x 1.5 cm.
The inner pole of the ovary is suspended from the uterine cornua by
the ovarian ligament and attached to the posterior leaf of the broad
ligament by double fold peritoneum called the mesovarium.
The ovary is not covered with peritoneum.
Relations of the ovaries with pelvic organs
Anterior: The broad ligaments.
Posterior: The intestines
Superior: The fallopian tubes.
Medial:
The uterus and ovarian ligaments.
Lateral:
The infundibulopelvic ligaments and the side wall of
the pelvis.
Histologically, the ovaries are composed of stroma and follicles.
The ovary is divisible into an outer cortex and a medulla. The
cortex is the functioning part of the ovary and is covered by a single
layer of cuboidal epithelium called the germinal epithelium. The
cortex of the ovary contains primordial and developing follicles and
32

specialized connective tissue called theca. The medulla is mainly

composed of connective tissue and blood vessels.
Embryologically, the ovaries are formed from coelomic epithelium
of the genital ridge, the underlying mesoderm and the primitive
germ cells.
Several millions of germ cells are formed in the ovary during the
intrauterine life. No new germ cells are produced after birth. By the
time at puberty only few hundred thousands are left to matured into
ova.
Blood supply of the ovary is from the ovarian arteries and, to a
lesser extent, uterine arteries (end-to-end anastamoses).
Venous drainage is by ovarian veins, uterine veins and broad
ligament plexuses.
Lymphatic drainage of the ovaries is to the para-aortic nodes.
The functions of the ovaries are:
1. The production of the ova.
2. The production and secretion of estrogen and progesteron.

3
BLOOD SUPPLY OF PELVIC ORGANS

33

Ovarian artery

Uterine artery
Anterior division of
internal iliac artery

Azygous
vaginal
artery
Vaginal artery

Fig. 1.1 Arterial blood supply of internal reproductive organ of the female.

It is essential to know the details of the blood supply to the pelvic

structures. These blood vessels are the important landmarks for the
identification of important pelvic structures, such as the ureter.
The blood supply of the pelvic genital organs (such as, the uterus,
fallopian tubes and the vagina) is derived in large part from the
anterior division of the internal iliac artery (hypogastric artery) and its
branches. The ovaries receive its arterial blood supply from abdominal
aorta via the ovarian arteries.

OVARIAN ARTERY
The ovarian artery originates from the front of abdominal aorta, behind
the third part of duodenum, just below the level of renal artery. This
artery runs downwards on the anterior surface of the psoas muscles.
Reaching the pelvic brim the ovarian artery crosses over the lumbar
division of the ureter and then enter into the infundibulopelvic fold of
the broad ligament.
The ovarian artery divides into branches which supply the ovary and
the fallopian tubes. The tubal branch of the ovarian artery then form
34

end-to-end anastomoses with the ascending terminal branches of the

uterine artery.
The ovaries have double blood supply from the ovarian and uterine
arteries.

INTERNAL ILIAC ARTERY

( Hypogastric artery )

COMMON
ARTERY

ILIAC

Internal iliac
artery
SACRO-ILIAC
JOINT

Fig. 1.2 Bifurcation of common iliac artery at the sacro-iliac joint into sxternal and
internal iliac artery.

The common iliac artery bifurcate at the sacro-iliac joint into the
external and internal iliac arteries (Fig. 1.2).
The ureter crosses the common iliac artery just superior to its
bifurcation into external and internal iliac arteries.
The internal iliac artery or the hypogastric artery is the smaller of
the two terminal branches of the common iliac artery.
At the bifurcation of the common iliac artery, the internal iliac artery
turns medially and passes backwards and downwards where it soon
divides into anterior and posterior divisions.
The blood supply of the female genital organs is derived in large
part from the internal iliac artery and its branches.
The internal iliac artery has posterior and anterior divisions.
The posterior division has three branches supplying the parietal
structure.
35

1. iliolumbar artery
2. lateral sacral artery
3. superior gluteal artery
The anterior division has three parietal and four visceral
branches.
A). Parietal branches:
1. inferior gluteal
2. internal pudendal
3. obturator artery
B). Visceral branches:
1. superior vesical artery
2. inferior vesical artery
3. uterine artery
4. vaginal artery (may branch from the uterine artery).

The branches, which supply the pelvic organs, are all from the
anterior division of the internal iliac artery.

Fig. 1.3 The branches of the internal iliac artery.

UTERINE ARTERY

The uterine artery arises from the anterior trunk of the internal iliac
or hypogastric artery, this provides the main aterial blood supply to
the uterus.
The course of uterine artery (Fig. 1.4): The uterine artery runs
downward and forward till it reach the pelvic floor and turn medially
to the uterus.
The uterine artery reaches the uterus at the level of internal os
where it turns upward at right angles and follows a spiral course
along lateral border of uterus to the cornua between the two layers
36

of the broad ligament. It gives branches to vagina, cervix, uterus

and uterine tube and ends by anastomosing with ovarian arteries.
The uterine artery supplies a branch to the ureter as it crosses it.
During the vertical part of its course it freely gives off branches,
which penetrate, and runs transversely pass into the myometrium.
These blood vessels are called arcuate arteries and from them arise
a series of radial arteries almost at right angles. These radial
arteries reach the basal layers of the endometrium and from these
derives the straight arterioles of the endometrium.

The branches of uterine artery are:

1.
2.
3.
4.

Branches of artery to the ureter.

Descending vaginal artery.
Circular cervical artery.
Arcuate artery to the myometrium

(The descending vaginal artery united with the circular cervical

artery to form anterior and posterior azygous artery of the vagina)

Relation of the uterine artery to the ureter :- The uterine

artery crosses above the ureter (Fig. 1.4) in the parametrium where
it gives off uriteric branch. The artery runs transversely while the
ureter runs approximately anterior posteriorly through the ureteric
canal of the parametrium.

37

Fig. 1.4 The course of the uterine artery and the relationship of the uterine artery
with the ureter.

VAGINAL ARTERY
The vaginal artery arises from two origins, i.e.
1. Vaginal artery arises from a direct visceral branch of the anterior
division of the internal iliac artery (Fig. 1.5).
2. Vaginal artery may also receive branches from the uterine artery
before it passes vertically upwards at the level of internal os.

Uterine artery
Anterior branch of the internal iliac artery
Vaginal artery

Fig. 1.5 Origins of the vaginal arteries.

38

The vagina artery passes downward through the parametrium to

reach the vagina in the region of the lateral fornix. This descending
branch of the vaginal artery is of great importance during the total
hysterectomy procedure. If not separated and well clamped and
ligated may give rise to post operative haemorrhage.
From the lateral fornix the vaginal artery passes downward along
lateral vaginal wall and sends branches transversely across, which
anastomose with branches from the opposite site to form azygos
arteries of vagina.

The vaginal has a rich arterial blood supply from the vaginal and
uterine arteries, which are the branches of the anterior division of
the internal iliac artery. Also the vaginal receives blood supply from
the azygos vaginal artery.
Vaginal artery supplies the upper third of vagina and lower part of
urinary bladder.

INTERNAL PUDENDAL ARTERY

Blood supply of the perineum and external genitalia is derived from

internal pudendal artery.
Internal pudendal artery is another branch of the anterior division of
the internal iliac artery.
The artery leaves the pelvic cavity through the sciatic foramen and,
after winding around the ischial spine, the pudenda artery enters
the ischiorectal fossa adjacent to obturator internus muscle.
Within the ischiorectal fossa it gives off the inferior haemorrhoidal
artery.

Internal pudendal artery ends as dorsal artery of the clitoris which

supply the clitoris and vestibular bulbs.
Terminal branches of internal pudendal artery amastomose with the
superficial and deep pudendal arteries which are branches of
femoral artery.

39

FALLOPIAN TUBE

UTERUS

Tubal branch of the

ovarian artery
Ascending branch of
uterine artery
Ovarian artery

OVARY
Ovarian arteries

VAGINA
Vaginal artery
Branches of Uterine
artery
Middle and inferior
rectal
IInternal pudendal

BLOOD SUPPLY

OF THE
PELVIC ORGANS

Uterine artery
Ovarian artery

EXTERNAL
GENITALIA

The major artery

involve
is
the
anterior division of
the internal iliac
artery

Internal pudendal
artery
Superficial
external
pudendal artery
Dorsal
clitoris
artery

Fig. 1.6 Diagrammatic presentation of arterial blood supply of pelvic organs.

THE PELVIC VEINS

40

The veins around the pelvic organs form plexuses which

intercommunicate freely. Venous drainage from the uterus, vagina,
bladder usually via the veins that accompany the arterial blood supply.

VENOUS DRAINAGE OF THE OVARY

Venous drainage of the ovaries is by the ovarian veins, uterine veins
and broad ligament plexuses. The right ovarian vein terminates in
the inferior vena cava , while left ovarian vein ends by joining the
left renal vein.

VENOUS DRAINAGE OF THE UTERUS

Venous drainage from the uterus and cervix is via uterine and
ovarian veins and then terminates into the internal iliac veins.

VENOUS DRAINAGE OF THE VAGINA

The vaginal is rich in arterial blood supply. Venous drainage of the
vagina is by the vaginal plexus which then drained into the internal
iliac veins.
VENOUS DRAINAGE OF THE EXTERNAL GENITALIA
The venous drainage of the vulva accompanies arterial supply, also
via vesical and vaginal plexuses

41

LYMPHATICS DRAINAGE OF THE PELVIS

AND GENITAL TRACT

LYMPH NODES OF THE GENITAL TRACT

Lymphatics are developed from veins and lymphatic vessels tend to

follow the course of the veins draining a particular region. Lymphatic
vessels and nodes lie extra peritoneal connective tissue and embedded
in adipose tissue. They are difficult to locate or demonstrate unless
they are pathologic.
The lymphatic drainage of the pelvis are compose of superficial and
deep groups of nods:

Lymphatic of the groins

External iliac nodes
Internal iliac nodes
Obturator nodes
Common iliac node
Para-aortic nodes

Lymphatic of the groins:

The lymphatics of the groin is a superficial lymphatics known as
superficial inguinal nodes which are arranged in two groups:
1. Those situated along the inner two-third of inguinal ligament,
and
2. Those clustered around the entrance of saphenous vein into
femoral vein, which is known as superficial femoral nodes.
Internal iliac nodes
The internal iliac lymphatics follows the internal iliac vessels and
receives drainage from the lower pelvis, perineum and the buttock
muscles.
External iliac lymph nodes
The external iliac lymph nodes which consists of about 8 to 10
nodes are located anteriorly, medially and laterally, follows the
external ilac vessel up to the bifurcation of the common iliac vessel
and drains the inguinal nodes, the clitoris, the cervix, the upper
vagina and bladder.

They are arranged in three groups:

1. Lowest group: Usually very large and lies on the lateral side
of the external iliac artery under inguinal ligament.
2. Anterior group: Smaller in size and lies between external iliac
artery and vein.
3. Medial
group: It is larger in size and lies inferior and slightly
medial to external iliac vein.

Obturator node
Obturator lymph node is larger in size.

It is bounded superiorly by external iliac vessels, laterally by pelvic

wall and inferiorly by obturator nerve.
Afferent from inguinal group.

Common iliac nodes

The common iliac lymph nodes lie on the lateral side of the common
iliac artery.

Para-aortic nodes
They are numerous in number and larger in size.
They follow the course of artery and vein.
The para-aortic nodes are found on the lateral side of the aorta.

LYMPHATIC DRAINAGE FROM THE GENITAL TRACT

The lymphatic drainage from the individual genital organs drains in the
following manner.
Lymphatics drainage of external genitalia and perineum:

The lymphatic drainage from the external genitalia (vulva, clitoris)

and the perineum is via the superficial lymphatic systems which
passes into the superficial inguinal nodes and deep inguinal nodes
and femoral nodes.
From the deep femoral nodes the lymphatic drains into iliac and
obturator nodes.
Contralateral spread also occurs.

Lymphatics drainage of the vagina:

The lymphatic drainage of the vagina follows three separate routes.

Lower third of vagina: drain to the superficial inguinal nodes
(similar as the drainage of the vulva).
Middle third of vagina: drains into the internal iliac nodes.
Upper third of vagina: drains into the external and internal
iliac nodes (the same as the cervix).

Upper third drain into external

and internal iliac

LYMPHATICS
Middle
third drain into internal
iliacDRAINAGE
nodes
OFthird
THE
Lower
drain into
superficial nodes

Fig.1.1 The three routes of lymphatic drainage of the vagina.

Lymphatic drainage of the uterus and cervix:
Upper part of uterus
Lower part of uterus and
cervix

Para-aortic

External iliac

Obturator

inguinal

Superficial inguinal

Deep

Paracervical
nodes
Fig. 1.2 Lymphatics drainage of body of uterus and cervix.

The lymphatic drainage of body uterus and cervix is by the following

(Fig. 1.2):
The lymphatic drainage of the upper part of the uterus follow the
ovarian lymphatic to the para-aortic nodes. The superficial inguinal
nodes drain the area of the round ligaments.
From lower part of the uterus and cervix, drainage is mainly to
paracervical, parametrial, internal and external iliac nodes and the
obturator node.

Lymphatic drainage of ovaries and fallopian tubes:

Lymphatic drainage of the ovaries and the fallopian tubes is to the

para-aortic nodes.

5
THE URINARY TRACT OF THE FEMALE
- URETER, BLADDER AND URETHRA Common
artery

iliac

URETER

RECTUM

UTERUS

BLADDER

Fig. 1.1

URETER

The female urinary system.

The anatomy of the female urinary tract which is located in the pelvis
is of considerable significance in gynecological surgery, in view of its
close relationship with the pelvic genital organs.

THE URETER
The female ureter is a musculo-membranous, paired and symmetrical
tube about 25 30 cm ( the left being a little longer than the right )
which conveys the urine from the kidney to the bladder. It commences
at the inferior border of the pelvis of the kidney and terminates into
the bladder.
The ureter is composed of circular and longitudinal muscle and is lined
by transitional epithelium.

The Course of the Ureter

In its course the ureter is commonly divided into an abdominal and
pelvic portion. At the point where the ureter crosses the iliac vessels,
the abdominal portion of the ureter becomes the pelvic ureter (Fig.
1.2).

It crosses the posterior abdominal wall by running in an oblique

medial direction behind the peritoneum and over the psoas muscle.
It crosses the pelvic brim by descending in front of the bifurcation of
the common iliac artery and in front of the internal iliac artery and
Internal iliac
behind the ovarian fossa.
artery

Psoas
muscl
e

URETER
Round
ligament

Uterine artery

Levator ani
Obturator
internus
muscle
Vaginal artery

The Anatomical importance of the ureter

The left ureter is longer than the right ureter by 1 cm.

Each ureter are divided into two portion, i.e. abdominal and pelvic
ureter.
The ureter has variation of calibers, average diameter is 5 mm.
The ureter is liable to be constricted in four places (Fig. 1.3):
1.
2.
3.
4.

At its junction with the renal pelvis.

Where it crosses the pelvic brim.
Where it is crossed by the uterine artery.
At its termination in the bladder wall.

1st.
constriction

About 2 cm of the ureter lie within the wall of the bladder in oblique
direction.
The terminal part of the ureter is in vulnerable position during the
procedure of abdominal hysterectomy and can be easily damaged
or ligated.
The left ureter has the more extensive relationship to the vagina
and is occasionally crossing the midline.

1st constriction
URETER

2nd constriction

External iliac artery at

the pelvic brim

3rd. constriction
4th constriction

Fig. 1.3 Showing the regions where the ureter is likely to be constricted.

The ureter is most exposed to surgical injury:1. At the pelvic brim when the ovarian vessels are ligated.
2. During division and ligature of the lower part of the broad ligaments.
3. During removal of broad ligament tumours which displace it from the normal
position.
4. During peritonization of the pelvis.

2nd.
constriction

The female ureter: Is below the broad ligament.

Is below the uterine artery
Crosses the lateral fornix of the vagina.
Is closer to the cervix (left ureter).
4th.
constriction

Histological structure of the Ureter

The wall of the ureter is composed of three concentric coats,

The inner coat is a mucosal layer

The middle coat is made up of a muscular layer.
The outer coat consists of a fibrous layer.
Mucosal layer is a smooth inner most layer which consist of an
epithelial lining. The epithelium is of transitional type 4 to 5
cells in thickness. The mucous membrane of the ureter is thrown
into longitudinal folds which give its lumen a stellate appearance in
cross-section.
Muscular layer consists of muscle fibres which are arranged in
inner longitudinal and outer circular muscles.
The upper two- third of the ureter muscular layer is composed of
two layers, i.e. inner longitudinal and outer circular muscle fibres.
The circular muscle in this region becomes prominent.
In the lower one-third of the ureter an additional outer longitudinal
muscular is added.
The muscular layer is extremely complex at the level of the
intramural ureter where the longitudinal fibres of the ureter
coalesce with the most superficial muscle layer of the trigone of the
bladder.

Fibrous coat is produced by the condensation of connective tissue

around the ureter thus forming a peripheral sheath. This fibrous
coat contains many vessels and nerves.
Blood supply of the ureter

The ureter is more abundantly vascularised and is of multiple in origin,

i.e. renal, abdominal aorta, ovarian, common iliac, internal iliac, vesical
and the uterine arteries. Different levels of the ureter has different
arterial supply.
Upper third of the ureter received its arterial blood supply from
the branches of renal artery.
Middle third of the ureter blood supply is from the aorta, common
iliac, internal iliac, inferior mesentric, deep hypogastric and
ovarian arteris.

 Lower third of the ureter is supplied by the branches from the

vesical and uterine arteries.
Lymphatics of the ureter
The lymphatics of the ureter are less nemerous in the mucosa than in
the muscular coats. The lymph channels accompany the arteries.
The lymphatics of the ureter are drain in three directions :

The upper part is drained into the renal nodes.

The lymphatics of the middle part of the ureter drained into the
pelvic and lumbar nodes.
The lower third of the ureter drained towards the bladder.

Innervation of the ureter

The ureter has an extrinsic sympathetic nerve supply from the aortic,
hypogastric and pelvic plexuses, and a para-sympathetic nerve supply
from the sacral plexus. It also has an intrinsic system of nerve fibres
with ganglion cells throughout its course.
Relations of the ureter (Fig. 1.4 and Table 1)
For discussion regarding the relation of the ureter, the abdominal
ureter is divided into lumbar and iliac division; and the pelvic ureter is
divided into pelvic segment proper and intra-mural proper.
Lumbar
division
Iliac division

Pelvic
division
URETER

Intramural
segment

Fig. 1.4 The divisions of the ureter and its relations

Division of the Ureter

LUMBAR division

Relations of the ureter

Lateral relation :
Ureter is closely related to
pole of the kidney.

medial aspect of the inferior

Medial relations :
Right ureter related to the vena cava.

Left ureter related to the aorta.

Posterior relation :
Ureters rest on the psoas muscle and its aponeurosis.
Anterior relations :- The right ureter is in relation anteriorly
with

The posterior parietal peritoneum

The utero-ovarian artery which cross the ureter

The duodeno-pancreas

The ascending colon with its mesocolon and its

vessels
Anterior relations :- The left ureter is in relation anteriorly
with

The posterior parietal peritoneum

The utero-ovarian artery

The descending colon

Division of the Ureter

ILIAC division

Relations of the ureter

Anterior relations of right ureter :
Root of the mesentry

Terminal ileum, caecum and appendix

Anterior relations of left ureter :
Transverse mesentry

Sigmoid colon

Superior sigmoid artery

Posterior relations ;- The ureter is related posteriorly with

Iliac vessels

Obturator nerve

Ilio-lumbar vessels

Lumbo-sacral trunk
Right ureter crosses the external iliac artery
Left ureter crosses the common iliac artery

PELVIC division

Anteriorly parietal peritoneum

Posteriorly ureter lies on the internal iliac artery
Medial rectum
Lateral- uterine artery

INTRAMURAL portion

The ureters pierce the posterior aspect of the bladder,

obliquely and medially for a distance of 1.5 cm and terminate
at the ureteral orifice

Table 1 . The relations of the ureters with the pelvic structure

THE URINARY BLADDER

The urinary bladder is a hollow muscular organ which is lined with
transitional epithelium and the wall is composed of layers of muscle
fibres, known as the detrusor muscle. The bladder collects urine from
the ureters and stores it until it is excreted by the body through the
urethra.
Anatomy of the Urinary Bladder

The bladder is smaller in the female than in the male and is located
much lower, anterior to the uterus and upper vagina.
The bladder is separated from the pubic bones by the retropubic
space, known as the Cave of Retzius.

When empty the bladder lies in front of the uterus and vagina and
behind the pubis bones. As it fills it rises above the pelvic brim into
the abdominal cavity.
Urinary bladder is somewhat pyramidal in shape, with its apex
directed forwards and slightly upwards, and its base directed
backwards and slightly downwards. The neck of the bladder rest on
the superior surface of the urogenital diaphragm.
The apex is continued upwards to the umbilicus as the urachus
(median umbilical ligament).
The base of the bladder is separated from the anterior vaginal wall
by loose connective tissue.
The neck is continuous with the urethra. Both the neck and the
bladder base remain stationary as the bladder fills.
The fundus of the bladder lies behind the pubic bones. The body or
fundus of the bladder is mobile as the bladder fills and it has
superior and two lateral surfaces.

Superior surface is flat and concave when the bladder is

empty but becomes globular or convex as the bladder fills. It is
covered by the pelvic peritoneum and is in direct contact with
the uterus which lies directly upon it.

Lateral surface is in relation anteriorly with the retropubic

pad of fat, levator ani and obturator internus.

The trigone or the base of the bladder is immobile and it is held in

position by the lateral ligaments of the bladder and being fixed to
the cervix and anterior vaginal fornix.
The trigone is a triangular area lying between the internal urethral
orifice and the orifices of the ureters. It is a smooth-walled.
The ureteric orifices appear as small slit-like openings at the lateral
angles of the trigone. The ureters pass through the bladder wall
obliquely. The ureteric orifices are connected by a transverse ridge
called the interureteric bar or Merciers bar.
The function of
Merciers bar is to close the ureteric orifices during micturition, thus
preventing reflux of urine along the ureters when intravesical
pressure rises.

Histological structure of the Urinary Bladder

Ureter

Orifices Tunica muscularis

Of ureters
Tunica
mucosa

Trigone
Tunica serosa
Internal sphincter

Urogenital
diaphragm
Urethra

External urethra
sphincter

Fig. 1.5 The structure of the - Urinary Bladder.

The urinary bladder is composed of three main layers:

1. Inner mucosal layer:- This layer is lined with transitional
epithelium (the tunica mucosa) that allows the bladder to stretch
and contract. When the bladder is empty, the tunica mucosa is
thrown into folds called rugae or trabeculae.
2. Middle muscular layer:The thick middle layer (tunica
muscularis) consists of three layers of meshed smooth muscle
which is arranged as,
Inner layer of longitudinal fibres
Middle layer of circular fibres
Outer layer of longitudinal fibres
These three layers of muscle forms the detrusor muscle.
3. Outer serosal layer:- The outer layer of the bladder is the
adventitia (tunica serosa). It is derived from the peritoneum and
covers only the upper and lateral surfaces of the bladder. It is a
moist tissue that lubricates the upper surface, eliminating friction
when the distended bladder presses against the other organs.
Relations of the Urinary Bladder

Coils of intestines, ileum and

sigmoid colon.

Anteriorly :The bladder lies behind

the,
Muscles of the lower
abdominal wall
Symphysis pubis
Retropubic space
Posteriorly :The bladder lies in intimate
relationship with the,
Uterus
Cervix
Upper vagina ( anterior
fornix )
Superiorly :Above the bladder
the,
Pelvic peritoneum

are

Fig. 1.6 Relations of the Urinary Bladder.

The Sphincters of the Bladder

The sphincters of the bladder are known as the internal and external
sphincters. The internal sphincter consists of internal and an external
portion and forms a loop around the neck of the bladder which extend
as far as the superior layer of the urogenital diaphragm.
The external sphincter lies between the two layers of the urogenital
diaphragm, and is known as the sphincter of the membranous urethra.
Blood Supply of the Bladder
The superior vesical artery supplies the anterior superior and lateral
surface of the bladder.
The inferior vesical arteries from the internal iliac supply the base and
neck of the bladder and the proximal part of the urethra.
Lymphatic Drainage of the Bladder

Lymphatic drainage is into the external and internal iliac groups of

lymph nodes.
Innervation of the Bladder
The bladder has a symphathetic supply from the hypogastric nerves, a
parasymphathetic supply from the nervi erigentes, while part of the
external sphincter is supplied by the pudendal nerves.

THE FEMALE URETHRA

The female urethra extends from the neck of the bladder to the
external urethra orifice and is S-shaped. It is about 3.5 cm long, and it
has a slight posterior angulation at the junction of its lower and middle
thirds.
The urethra passes through the two layers of the urogenital diaphragm
and the deep transverse perineal muscle where it is surrounded by the
sphincter of the membranous urethra.
The upper half of the urethra is separated from the anterior vaginal
wall by connective tissue and relatively mobile, but the lower half is
firmly embedded in the wall.
Histologically, the upper two-thirds of the urethra are lined with
transitional epithelium, and the lower third is lined by the stratified
squamous epithelium. The smooth muscle of its wall is arranged in
outer longitudinal and inner circular layers.
The lymphatic drainage from the urethra drain for the most part into
the external and internal iliac lymph nodes in the pelvis, those from the
distal end of the urethra near the external meatus drain into the
superficial inguinal nodes in the groin.

6
THE NORMAL MENSTRUAL CYCLE

FSH , LH
OVARIAN CYCLE
HORMONAL EVENTS

Feedback
mechanism

ENDOMETRIUM CYCLE

Estrogen
Progesterone

Fig 1.1
menstrual cycle.

Diagrammatic representation of events that occur throughout the

Menstruation, a periodic discharge of sanguinous fluid and sloughing of

the uterine lining in response to the cyclic interplay between the
hormones of the hypothalamus, the pituitary, and the ovaries.
Menstruation in most women occurs at regular intervals, 28 days on an
average.
The menstrual cycle, that is the interval between the onset of two
successive menstruations, is under the control of complex
neurohormonal influences. Interactions between the central nervous
system, pituitary, ovary and the uterus result in the preparation of the
uterus for implantation of the fertilized ovum around day 21 of the
average 28 day cycle. If implantation does not take place functional
layers of the uterine endometrium along with the menstrual blood are
shed and the new cycle begins. An abnormality at any of these levels
(hypothalamic-pituitary-ovary-uterine axis) can result in disruption of
the normal menstrual cycle.

The normal menstrual cycle occurs usually every 21 35 days during

the reproductive years. The average length of the menstrual cycle is
frequently quoted to be 28 days.
The duration of the menstrual bleeding varies considerably with the
individual. Menstrual bleeding usually lasts for 4-5 days.
It is
considered that menstrual periods lasting 2 7 days are within
physiologic limits.
The amount of the menstrual flow also varies considerably between
women and may depend upon environmental as well as genetic
factors. Blood loss is normally less than 30 ml, the average being 30
40 ml; losses in the excess of 80 ml are classed as menorrhagia .
Irregularities of the menstrual cycle are more likely to occur during the
first years following menarche and at the opposite end of the
reproductive life, just prior to menopause.
Serious emotional
disturbances, chronic debilitating disease, abrupt changes in climate
and environmental factors may also be the cause of menstrual
irregularities.

REGULATION OF THE MENSTRUAL CYCLE

The events of the normal menstrual cycle may be divided into the
ovarian and endometrium cycle.
THE OVARIAN CYCLE
The events of the ovarian cycle during the normal menstrual cycle can
de divided into: (1) the follicular phase, (2) ovulation, and (3) the luteal
phase.
Follicular phase
The follicular phase is the period during which an ovum matures. The
ovaries are in the follicular phase starting on the first day of
menstruation and ending on the day ovulation (usually lasts for 12 to 13
days).
During menstruation, the secretions of ovarian steroid hormones are at
their lowest ebb. The fall in oestrogen and progesterone secretion by the

ovary just before menstruation stimulates secretion of FSH and LH by

the anterior pituitary. As the FSH and LH levels increases, a group of
follicles (6 to 12 graafian follicles), each containing an immature ovum
begins to grow. As the follicles grow, the granulosa cells secrete an
increasing amount of oestradiol (the principal oestrogen), which
accelerates their maturation. Toward the end of the follicular phase one
follicle in one ovary outgrows all the others to reach maturity (the
mechanism by which this follicle is chosen is unknown). All other
follicles recede entirely and cannot be matured again.
Hormonal changes during follicular phase The amount of FSH
secreted during the early follicular phase is believed to be slightly greater
than the amount secreted in the late follicular phase. FSH stimulates
follicular growth but also facilitates steroidegesis by increasing the
activity or number of LH receptors.
As follicles grow, the granulosa cells secrete an increasing amount of
oestradiol, which reaches its highest concentration in the blood at about
day twelve of the cycle, two days before ovulation.

GnRH
FSH and LH
LHLH

LH surge

FSH
LH

Developing
Follicles

Mature
Follicle

Follicular phase

Day

Ovarian hormones

Oestrogen

Ovulation
Ovulation

14

Formation of
Corpus luteum

Regressive
Corpus luteum

Luteal phase

21

28

Progesterone
Fig. 1.2. The ovarian cycle showing changes in hormonal secretion from the
anterior pituitary and interrelated changes in the ovary

The oestrogen rises slowly then rapidly to peak just before ovulation. The
effect of oestradiol on the pituitary (positive feedback) results in an
increase in LH secretion in the late follicular phase that culminates in a
LH surge. The LH surge begins about 24 hours before ovulation and
reaches its peak about 16 hours before ovulation. It is this surge that
acts to trigger ovulation. Since GnRH stimulates the anterior pituitary to
secrete both FSH and LH, there is a simultaneous, though smaller, surge
in FSH secretion (Fig.1.2).
This follicular phase (preovulatory phase) of the ovarian menstrual cycle
varies in length from woman to woman. Almost all variations in cycle
length are the result of variations in the length of the follicular phase.

Ovulation
During the late follicular phase, the maturing follicle secretes large
amount of oestrogen, and the rapidly increasing blood oestradiol levels
stimulate the hypothalamus and the anterior pituitary to initiate both
the LH and FSH midcycle surge.
Before ovulation, there are general dissolution of the entire follicular wall
and localized disintegration of that portion of the wall that is on the
surface of the ovary, both presumably caused by proteolytic enzymes.
With degeneration of the cells on the surface, a stigma form, and the
follicular basement membrane finally bulges through the stigma. When
this ruptures, the oocyte is expelled into the peritoneal cavity, and
ovulation occurs.

FSH stimulates rapid follicle growth granulosa cells produced oetrogen .

Follicle becomes a thin-walled blister on the
surface of the ovary more oestrogen been
produced

A rapid increasing in oestrogen levels trigger

the LH surge and this LH surge triggers off
ovulation within 24 hours.

Degeneration of the collagen in the follicular wall

and ovulation occurs
Ovulated oocyte is picked up the fimbriated end of the
fallopian tube.
Fig. 1.3 The ovarian cycle ovulation phase

In ovulation, a secondary oocyte, arrested at metaphase II of meiosis, is

released into a uterine tube. The ovulated oocyte is still surrounded by a
zona pellucida and corona radiata as it begins its journey to the uterus.
Hormonal changes at and after ovulation During the LH surge the
secretion of GnRH and gonadotropins is episodic. An increased in FSH is
stimulated by positive feedback from oestradiol. A sharp drop in plasma
oestrogen levels and the increase in progesterone accompany the end of
the LH surge.

Luteal phase
After ovulation and under the influence of LH, the granulosa cells or the
ruptured follicle undergoes luteinization. This luteinized granulosa cells,
plus the surrounding theca cells, capillaries, and connective tissue, form
the corpus luteum. The corpus luteum secretes large amounts of
progesterone and some oestrogen to prepare the endometrium for a
fertilized ovum. The normal functional life span of the corpus luteum is
about 14 days.
The combined high levels of oestradiol and progesterone during the luteal
phase exert a negative feedback inhibition of FSH and LH secretion.
FSH and LH levels decrease during this phase. This serves to retard
development of new follicles, so that further ovulation does not normally
occur during that cycle.

If the ovum is not fertilized, the fall in FSH and LH levels causes the
corpus luteum to regress and stop functioning. With the declining
function of the corpus luteum, oestrogen and progesterone fall to very
low levels by day 28 of the cycle. The withdrawal of ovarian steroids
causes menstruation and permits a new cycle of ovarian follicle
development to progress. The old corpus luteum is replaced by fibrous
tissue called the corpus albicans.

Luteal phase

Day 14 ovulation
Day 15-22
Formation
Formation and function of the corpus luteum:

23
28
Regression

After ovulation, the empty follicle is stimulated by LH to become the corpus luteum
Day 15-18: The granulosa cells
- Increases in size
- accumulate lutein (a yellow pigment)
- secrete progesterone
Day 22-23
- the corpus luteum has become vascularised by capillary network
- peak levels of progesterone and oestradiol are reached.
Day 23 onwards period of regression of corpus luteum
- the corpus luteum begins to decline unless pregnancy supervenes
- in the absent of pregnancy the oestrogen and progesterone begins to
fall

by day 28 oestrogen and progesterone are at the lowest level

Fig. 1.2 Hormonal changes during the events of the menstrual cycle.

THE ENDOMETRIAL CYCLE OF THE NORMAL MENSTRUAL CYCLE

Soiral atterioke
Uterine gland

BL
FL = Functional layer

Fig. 1.3

BL = Basal layer

Endometrial cycle of the normal menstrual cycle

The endometrium responds to fluctuating levels of ovarian steroids

(estrogen and progesterone). It is this responsiveness that gives rise to
menstruation and makes implantation and pregnancy possible.
Functionally, the endometrium is divided into two zones: (1) the upper
portion, or the functionalis, that undergoes cyclic changes in morphology
and function during the menstrual cycle and is sloughed off at
menstruation; (2) the lower portion, or the basalis, that remain relatively
unchanged during each menstrual cycle and, after menstruation,
provides stem cells for renewal of the functionalis.
The cyclic changes of the endometrium can be divided into three stages:
(1) the menstrual phase; (2) the proliferative phase, and (3) the secretory
phase. Cyclic changes affect all components of the endometrium:
glands, stroma and vasculature.
Menstrual phase
If fertilization does not occur, the corpus luteum regresses and its
production of oestrogen and progesterone falls. About 2 days before the
onset of the menses, vasospasm of the endometrial blood vessels causes
the endometrium to become ischaemic and necrotic. The necrotic areas
of the functional endometrium separate from the basal layers, resulting
in the menstrual flow. The first day of menstruation is taken as day one
of the menstrual cycle. The first four days of the cycle are defined as the
menstrual phase.
During a menstrual period, women lose about 40 ml of blood.

Proliferative phase
The most rapid growth of the functional layers occurs between days 5 to
7 and the day of ovulation and is known as the proliferative phase. In a
28-day cycle, ovulation occurs on day 14 (range of 13 to 15 days).The
proliferative phase occurs during the follicular and ovulatory phases of
the ovarian cycle, lasting about 11 days. Endometrial growth during
proliferation is dependent on estrogen produced by ovarian follicles
before ovulation.

After completion of a menstrual period, the endometrium is very thin.

The basal layers of the endometrium remain after menstruation and
begin to proliferate to form new endometrial epithelium and endometrial
glands under the influence of the rising oestrogen secretion by the ovary.
Numerous mitosis is present in these tissues. During the proliferative
phase, the glands are tubular or columnar in shape. There is an increase
in the length of the spiral arteries. By the end of the proliferative phase,
cellular proliferation and endometrial growth have reached a maximum,
the spiral arteries are elongated and convoluted.

Secretory phase
The secretory phase occurs during the luteal phase of the ovarian cycle
as the uterus is prepared to receive a fertilized ovum. This phase last
about 14 days. Following ovulation, progesterone secretion by the corpus
luteum stimulate further thickening of the endometrium and also
stimulate the glandular cells to secrete glycogen, mucus and other
substances. The glands become tortuous, and the lumen are dilated and
filled with secretion. The stroma becomes edematous. The spiral arteries
continue to extend into the superficial layer of the endometrium. The
endometrium reaches the thickness of heavy, soft velvet and becomes
luxuriant with blood and glandular secretions, a suitable protective and
nutritive bed for a fertilized ovum. The endometrium is therefore well
prepared to accept and nourish an embryo if fertilization occurs.
In the fully matured secretory endometrium, three strata are noted: the
two functional or compact layer and spongy layer; and basal layer.
COMPONENTS OF MENSTRUAL FLOW
The haemolysed blood from endometrial arterioles and capillaries,
mucus and the shed functional layers of the endometrium are the
majors components of the menstrual flow.
Lacking of clotting is a
characteristic feature of the menstrual blood. Discovery shows that
the menstrual blood does not contain fibrinogen and it possesses
fibrinolytic properties.
In addition to blood cells and endometrial cells several other cellular
elements are found in the menstrual flow. These includes
macrophages, histocycytes, mast cells and vaginal epithelial cells.

Menstrual flow has been known to contain potent smooth muscle

stimulants, i.e. the prostaglandins. Prostaglandins PGF2 and PGE has
been isolated from the menstrual flow. PGF2 stimulates uterine
contractions during menses, and PGE may relax uterine muscle. In
patients with severe dysmenorrhoea there is an increased ratio of
PGF/PGE.
MECHANISM OF MENSTRUATION
The exact mechanism of menstrual bleeding remains unknown.
However, several theories attempt to explain this phenomenon. Among
the theories are:

Estrogen and Progesterone Withdrawal

The withdrawal of the ovarian sex steroid hormones, i.e. estrogen
and progesterone, leads to spasm, ischaemia and finally rupture of
the spiral arterioles and vascular lakes in the endometrium.
Therefore, withdrawal of both estrogen and progesterone is
necessary for the initiation of normal menstrual bleeding.

Depolymerization Theory
Endometrial enzymatic activity, is also responsible for the menstrual
breakdown. During the proliferative and early secretory phases,
under the influence of estrogens and progesterone, hydrolytic
enzymes such as exopeptidases, acid phosphatases and other
proteases are manufactured and stored in the Golgi-lysosomal
complex of the endometrial cells. Estrogens are also responsible for
the production of acid mucopolysaccharides (AMPS) in the stroma
and the polymerization of these substances of these substances in
the stromal ground substances.
When implantation does not take place, there is an increased in
hydrolase activity which result in the destruction of the lysosome
membranes. The destruction of the lysosome membranes causes
the release of the destructive hydrolytic enzymes leading to tissue
destruction. Activation of hydrolytic enzymes will disintergrate AMPS
of the ground substances with subsequent cell separation and
endometrial breakdown. The onset of menstruation is triggered by
acute release of lysosomal enzymes in the surrounding tissue.

Arteriolar Vasoconstriction
A potent vasoconstrictor factors selectively affecting the spiral
arterioles that supply the superficial layers of the endometrium, was
noted to play an important role in the initiation of menstruation.
There is considerable experimental evidence to suggest that
prostaglandins are the potent vasoconstrictor factors. The rise in
prostaglandins results in vasoconstriction of the spiral arterioles. As
a consequence of this vasoconstrictive effect, tissue ischaemia,
necrosis and bleeding would ensue.

Table 1: Summary of the phases of the menstrual cycle

Phase of Cycle
Ovary

Endometrial

Hormonal Changes
Pituitary

Ovary

Tissue Changes
Ovarian

Endometrial

Follicular
(Day 1-4)

Menstrual

Follicular
(Day 5-13)

Proliferative

Ovulation
(Day 14)

Proliferative

Luteal
(Day 15-28)

Secretory

FSH and
are low

LH

Oestradiol and
progesterone
remain low

Primary
follicles grow

Sloughing
of
stratum
functionale with
accompanying
bleeding

FSH are
slightly higher
than LH

Oestradiol
secretion rises

Follicles
continue to
grow and
single graafian
follicle
developed and
matured

Development of
new layer;
Mitotic division;
Increase
thickness
of
endometrium;
Spiral arteries
developed

LH surge
FSH increase

Fall in
oestradiol
secretion

Graafian follicle
ruptured
and
ovum
is
extruded and
pick up by the
tube

No change

LH and FSH
decrease

Progesterone
and oestrogen
increase, then
fall

Development
of corpus
luteum;
Regression of
corpus luteum

Glandular
development

7
NORMAL DEVELOPMENT
AND
CONGENITAL ANOMALIES
OF THE

FEMALE REPRODUCTIVE ORGANS

UTERUS 1

UT
Fig 1.1 Double uterus (uterus didelphys) - congenital malformation of the genital
tract.

Although the chromosomal and genetic sex of an embryo is

determined at fertilization, male and female morphological
characteristics do not begin to develop until the seven weeks of
intrauterine life.
The early genital systems in the two sexes are similar, therefore, the
initial period of early genital development is often referred to as the
indifferent stage of sexual development.
The genital organs arise in the intermediate mesoderm on either side
of the root of the mesentery, beneath the epithelium of the coelom.

NORMAL DEVELOPMENT OF THE FEMALE

REPRODUCTIVE SYSTEMS
The female genital tract will develop from the paramesonephric
(Mullerian) ducts.
The paramesonephric ducts is an ingrowth of the
coelomic epithelium. The development of the female reproductive
organs will be discussed under the following heading.

The internal genitalia

Development of the uterus and fallopian tubes.
Development of the vagina.
Development of the ovaries.

The external genitalia

NORMAL DEVELOPMENT OF THE INTERNAL GENITALIA

Both male and female embryos have two pairs of genital ducts,
mesonephric (wolffian) ducts and paramesonephric (mullerian) ducts.
The paramesonephric have a leading role in the development of the
female reproductive system.
During the fifth-week intrauterine life when both pairs of genital ducts
are present, the genital system is in the indifferent stage.
In the female embryos the mesonephric ducts almost completely
disappear (only few nonfunctional remnants persist) due to the lack of
testosterone, and the paramesonephric ducts develop due to the
absence of mullerian-inhibiting factor (MIF). The paramesonephric
ducts form most of the female genital tract.

DEVELOPMENT OF THE UTERUS AND FALLOPIAN TUBES

1. The paramesonephric ducts appear at five weeks after
conception in the intermediate mesoderm as buds of coelomic
epithelium at the cranial end of the urogenital ridge.
2. The two ducts then extend caudally until they reach the
urogenital sinus, about 9 weeks.
3. Each paramesonephric duct grows down lateral to the
mesonephric duct until they reach the future pelvic region of the
embryo. At this level it crosses anterior to the mesonephric duct
and joins the paramesonephric from the opposite side, and fuse
to form a Y-shaped uterovaginal primordium ( Fig. 1.2).
4. Fusion of the ducts begins at 7 to 8 weeks and is complete by 12
weeks.

5. The fallopian tubes develop from the cranial (upper half),

unfused portions of the paramesonephric ducts. The anterior
open end of the upper part of the paramesonephric ducts will
become the ostium, and around this the fimbriae later develop
(Fig. 1.2).
6. The uterus is formed by the fused caudal portions of these
ducts.
7. Formation of the uterine cavity:-The characteristic shape of
the uterus is now formed, with cellular proliferation at the upper
portion and simultaneous dissolution of cells at the lower pole,
thus establishing the first uterine cavity. This cavity is at the
lower pole, with a thick wedge of tissue above. The upper thick
wedge tissue (septum) is slowly dissolved, creating the ultimate
cavity. This process usually completed by the 20 th week of
intrauterine life.
Any failure to fuse the two paramesonephric ducts or failure to
reabsorb the tissue between them would result in separate
uterine horns or some degree of persistence of the uterine
segment.
8. Fusion of the paramesonephric ducts also brings together two
peritoneal folds that form the right and left broad ligaments.

Gonads
Mesonephros
Mullerian ducts

Wolffian ducts
Fusion of the lower half of the
Mullerian ducts

UNDIFFERENTIATEDUTERUS
STAGE
Ovaries
TUBE

Fig. 1.2 The normal development of the internal female genital organ from Mullerian ducts.

DEVELOPMENT OF THE VAGINAL

The vagina forms from the vaginal plate at the junction of the
caudal end of the paramesonephric duct where it abuts with the
urogenital sinus.

The vaginal plate is formed from a pair of sinovaginal bulbs . The

sinovaginal bulbs fuse to form a solid vaginal plate. The plate
lengthens from the vestibule upwards.

Later, the central cells of this plate break down and begins the
process of canalization. This process formed the lumen of the
vagina (Fig. 1.3).

The hymen is formed by the invagination of the posterior wall of the

urogenital sinus.

Lower end of
Mullerian duct
Vaginal plate
( tissue of
sinovaginal
bulbs )

Urogenital sinus

Vagina canal
Hymen

Before canalization
canalization of the

After fusion and

vaginal

plate
Fig. 1.3

The normal development of the vagina.

DEVELOPMENT OF THE OVARIES

In human embryos, the gonads begins development during the fifth

and sixth weeks of gestation.

The gonads (testes and ovaries) are derived from three sources:
a) From the coelomic epithelium of the genital ridge.
b) From the underlying mesoderm, and
c) From the primordial germ cells.

In the early stages (before the seventh weeks) the gonads of the
two sexes are indentical in appearance and are referred to as
indifferent or undifferentiated.

The complete differentiation of normal gonads depends upon the

arrival at the genital ridges of the dorsal mesentery of sufficient
numbers of viable primordial germ cells. If they fail to arrive,
gonads do not develop (gonadal agenesis) and only a fibrous streak
will exist.

In embryos with an XX sex chromosome complex, the

undifferentiated gonads begins to develop into the ovaries in the
absence of testis-determining factor (TDF).

There is a proliferation of cells in and beneath the coelomic

epithelium of the genital ridge and by five or six weeks these cells
will form the primitive sex cords into the ridge. The primary sex
cords do not become prominent and normally degenerates and
disappear.

Migration of the primordial germ cells. During the sixth week

the primordial germ cells migrate by ameboid movement from the
wall of the yolk sac and enter the underlying mesechyme of the
genital ridges and are incorporated in the primitive.

The cortical epithelium of the female gonad continues to develop

and by the seventh week a second sex cord

UNDIFFERENTIATED GONADS
Primordial germ
cells

5 weeks

Gonadal ridge
Migration of primordial germ cell from the wall of the
yolk sac to the epithelium of gonadal ridge

6-7 weeks

Cortical epithelium development and formation

of primarysex cords.

Fig. 1.4 Development of the ovary .

indifferent gonads into ovaries.

Degenerating
primary sex cords

20 weeks

Primordial follicle forms from the

cortical cords.

Diagrams illustrating differentiation of

Cortical cords, extends from the surface epithelium of the

developing ovary into the underlying mesenchyme. As the cortical

cords increases in size, primordial germs are incorporated into

them.
Germ cells subsequently develop into oogonia by mitotic division.
Active mitosis of oogonia occurs during fetal life, producing
thousands of these primitive germ cells.
No oogonia form
postnatally. These oogonia undergo meiotic division and form the
primary oocycte. The primary oocyte remains in the prophase
stage of the first meiotic division until puberty and achieve its
complete at ovulation.
During the fetal life the ovary gradually descends into the pelvis.

NORMAL DEVELOPMENT OF THE FEMALE EXTERNAL

GENITALIA
In the development of the embryos until the seven weeks of
intrauterine life , the external genitalia are similar in both sexes
(undifferentiated stage).
The external genitalia are not fully
differentiated until the twelfth week.
Stages of development of the female external genitalia (Fig. 1.5):

The primitive cloaca becomes divided by a transverse

septum into an anterior urogenital portion and the posterior
rectal portion.
Early in the fourth week, the proliferation of the mesenchyme
produces a genital tubercle at the cranial end of the cloacal
membrane.
Two pairs of swellings, a lateral pair (genital
swellings) and a medial pair (genital folds) are then formed on
each side of the cloacal membrane by proliferation of mesoderm
round the end of the urogenital sinus. The genital tubercle soon
elongates to form a phallus.

Genital tubercle
Genital swelling

Genital fold

Genital tubercle

A
Genital fold

Genital swelling

B
Mons pubis
Clitoris
Labia minora
Labia majora

Fig. 1.5 Development of female external genitalia. (A) Undifferentiated stage. (B) 5 months intrauterine
life. (C) Newborn female.

Factors controlling development of the external genitalia of the

female are not clear, but estrogens play a role.
The genital tubercle elongates slightly and forms the clitoris.
The genital (urethral) folds do not fuse and develop into the labia
minora. Labia minora are homologous to the penile part of the
male urethra.
The genital swelling enlarges to becomes the labia majora. The
labial majora are homologous to the scrotum (in male these genital
swelling fused to form the scrotum).
The mons pubis and the anterior labial commisure are formed by
the fusion of the genital swelling anteriorly; whereas the posterior

fusion of the genital swelling forms the posterior labial commisure

(fourchette).

Skenes ducts and Bartholin glands develop as

urogenital sinus.

buds from the

Table 1. SUMMARY OF GENITAL TRACT DEVELOPMENT

Organs

Origin

Normal development

Ovary

Yolk sac; genital ridge

Primordial germ migration and cortical

development.

Fallopia
n tube

Upper end of Mullerian

ducts

Remain separate

Uterus

Middle part of Mullerain Form by fusion and canalization.

ducts

Vagina

Lower end of Mullerian Fusion and formation of vaginal plate

ducts and urogenital and recanalization to form vaginal
sinus
lumen.

Labia
minora

Genital folds

Form in the vestibule region.

Labia
majora

Genital swelling

Enlarges and remained separated.

Clitoris

Genital tubercle

Remains small

CONGENITAL ANOMALIES OF THE FEMALE

REPRODUCTIVE TRACTS
Numerous malformations of the female reproductive tract have been
mentioned, some of little clinical significance, others of considerable
importance.
Although the exact aetiology of these malformations is unknown, the
three most commonly accepted theories for their occurrence are,

teratogenesis
genetic inheritance, and
multifactorial expression

Many variations and combinations of anomalies occur. Malformations of

the genital tract occur when one of the following errors occur.

Lack of development (agenesis).

Incomplete development (hypoplasia).
Failure of recanalization process (atresia).
Failure of the two Mullerian duct to fuse (completely separate
development).

Anomalies of the fallopian tubes, uterus, cervix and vagina are

uncommon.
ANOMALIES OF FALLOPIAN TUBES
The fallopian tube may be malformed or absent if the uterus is
malformed. Total absence of Mullerian ducts may result in complete
absence of the fallopian tubes and these abnormal development are
rare. Congenital diverticula or.accessory may occur, but of no clinical
significance.
ANOMALIES OF THE UTERUS

The most common anomalies are the result of failure of the Mullerian
ducts to form or fuse. One or both tube may fail to form. Fusion
anomalies are of various kinds and are not uncommon.

Failure of the Mullerian ducts to form:

Agenesis or arrested development of one Mullerian duct will result in

one of the following.

Unicornuate uterus If the development of one Mullerian duct is

completely arrested, the uterus and fallopian tube may be formed
entirely from the other. This so-called uterus unicornus seldom
causes any clinical abnormality.

Fig. 1.6 . Unicornuate uterus

Rudimentary uterine horn When the development of one

Mullerian duct is normal and the other very imperfect, various
degrees of rudimentary horn are produced.
Most of these
rudimentary horn are non-communicating and are connected to the
opposite unicornuate uterus by a fibrous band. If the endometrium
of the rudimentary horn are non-functional there will be no clinical
problem. However, if the endometrium is functional, retention of
menstrual blood in the rudimentary horn will cause haematometra .

Rudimentary uterine
horn

Fig 1.7
Unicornuate uterus plus some form of rudimentary horn. (This patient
complaint of severe dysmenorrhoea.
At laparoscope a distended rudimentary
uterine horn was noted . Dysmenorrhoea ceases after surgery).

Blind uterine horn occurs when the two Mullerian duct develop
equally but one failed to communicate with the other. Subsequently
the patient develops increasing dysmenorrhoea with the
development of haematometra (Fig. 1.7).
Failure of fusion of the Mullerian ducts:
Failure of, or incomplete, fusion of the Mullerian duct may produce
the following:
1.
2.
3.
4.

Double uterus (didelphys) with septate vagina.

Double uterus with normal vagina.
Arcuate deformity.
Septate or subseptate uterus.

Double uterus (Fig. 1.8) Duplications of the uterus result from

lack of fusion of the Mullerian ducts in a localized area or throughout
the length of the ducts. In more extreme forms of failure of fusion,
the uterus is entirely double, also known as uterus didelphys ( i.e.
each duct forms one cervix and one uterine body with one fallopian
tube attached to each). This duplication may continue down into the
vagina in that part of the vagina formed by the Mullerian ducts.
Double uterus may be associated with septate or subseptate
vagina.
Pregnancy can occur in either or both sides. However, there is an
increased risk of abortion, malpresentation or obstruction of labour.
If double uterus produces, surgical reconstruction of the uterus to
form a single uterine cavity may be advocated (Strassmanns
operation).

Fig. 1.8 Uterus didelphys. Duplication of the uterus result from complete fusion of
the two Mullerian ducts.

Uterus bicornis - However, most reduplicated uteri are not so

complete, and the fusion may be only in the upper portion so that
there will be a double uterus with a single cervix and a single
vagina. This anomaly of the uterus is designated a bicornuate
uterus (Fig. 1.9). Uterus bicornis is one of the more common
anomalies.

Fig. 1.9 Uterus bicornis the most common abnormalities of the uterus which is the
result of partial fusion of the Mullerian ducts.

Septate and subseptate uterus In this form of anomalies

fusion of the Mullerian ducts does occur but the is incomplete
canalization to form the uterine cavity, therefore resulting in the
persistence of the septum within the uterine cavity.
The septum may be complete (extending until the internal or
external os) or partial (Fig. 1.10).
There is an increased risk of abortion, malpresentation or premature
labour in women with septate uterus. Surgical removal of the
septum is advocated if this produce problems and have a good
outcomes after repair.

SEPTATE

COMPLETE
Fig. 1.10

PARTIAL

Various form of septate uteus.

Absence of the uterus

Complete absence of the uterus is very rare. This type of anomaly is usually
found when the vagina is absent. This combination of features ( absence of
uterus and vagina) should suggest a diagnosis of testicular feminization
which is the result of androgen insensitivity. No treatment is of course
possible for this type of uterine abnormality.

ANOMALIES OF THE VAGINA

The more common anomalies of the vagina include

Septate vaginacommon
Double vagina
Absence of vagina rare

Absence of vagina
Congenital absence of the vagina is relatively uncommon, occurring
once in every in every 5000 20,000 female births. This results
from failure of the sinovaginal bulbs to develop and form the vaginal
plate (Fig. 1.11). When the vagina is absent, the uterus is usually
absent because the developing uterus (uterovaginal primordium)
induces the formation of the vaginal plate.
Congenital absence of the vagina may be associated with possible
renal tract anomalies.

Patients with absence of the vagina seek help after puberty because
of the failure of the onset of menstruation or inability to have sexual
intercourse. Since the uterus is usually absent, treatment is aimed
to allow adequate coitus by constructing a functional vagina. A
number of procedures are available.
1. Non-surgical method Repeated pressure with glass obturator
and attempted coitus if already present.
2. Surgical reconstruction of a vaginal (a) Wlilliams operation, by
suturing the posterior edges of the labia majora together in the
midline to form a perineal pouch (vulvo-vaginoplasty).
(b) McIndoe-Read operation is a more extensive surgical
procedures, where an artificial vagina is created by making a
space between the bladder and urethra in front and the rectum
behind. The created cavity is lined with a skin graft on the
vaginal mould. This mould is kept in placed until the whole
surface of the cavity is covered with living skin. The surgery is
done 3 6 months before regular coitus is anticipated.

Mullerian
ducts
Vaginal
plate
Sinovaginal bulbs

Fig. 1.11 Failure in the formation of the sinovaginal bulbs result in

congenital absent of the vagina
Double vagina
Duplication of the vagina (double vagina) occurs when the two
sinovaginal bulbs failed to fuse. It is difficult to distinguish double
vaginal from completely septate vagina. The true double vagina
includes a double introitus and separate vaginal lumen connecting
to the separate cervix.
Septate vagina
The vaginal septum (septate) may be longitudinal or transverse.

1)

Transverse septate vagina result from faulty canalization of the

united paramesonephric ducts and sinovaginal bulbs. A patient with
a tranverse vaginal septum can easily be mistaken for a patient
with congenital absence of vagina and uterus if the septum is
misinterpreted as the vagina apex. This tranverse septum may
have a small opening or imperforated. If there is a small opening
the problem will be difficulty at intercourse. If the septum is
imperforate, there will be retention of menstrual blood.
These septum can be broken down with manual dilatation or
surgical excision.

2) Longitudinal septate vagina

A mid-line longitudinal septum often creates a double vagina.
Longitudinal vaginal septate may be complete or partial. The
septum may deviated from the centre and be fused with the
lateral wall.

A vaginal septum without obstruction may be

asymptomatic.
Sometimes the septum causes
dyspareunia or may obstruct delivery.
Excision of the vaginal is advocated if it causes
problem.
ANOMALIES OF EXTERNAL GENITALIA

Imperforate hymen
The hymen is formed by invagination of the posterior wall of the
urogenital sinus, resulting from expansion of the caudal end of the
vagina. Failure for the hymenal membrane to perforate results in a
condition as imperforate hymen (Fig. 1.12).

Fig. 1.12 Imperforate hymen occluding the vaginal intoitus.

It is unusual for an imperforate hymen to be discovered before the

onset of puberty. If the condition is discovered the onset of
menarche, the hymen should be incised.
The possible complications of unrecognized imperforate hymen (Fig.
1.13) after menarche are
Imperforate hymen

Complications

Haematosalphinx

Haematometra

Haematocolpos

Imperforate hymen

Fig. 1.13 Complications of an imperforate hymen

Haematocolpos: Most girl with haematocolpos prsent between the

age of 14 and 16 years, but may be much older. The common
complaint is primary amenorrhoea. The features of haematocolpos
are,
1)
2)
3)
4)

Amenorrhoea.
Abdominal discomfort or pain which has a cyclical pattern.
Interference with micturition.
Bulging occluding membrane at the vaginal introitus.

The diagnosis is obvious on inspection of the vulva, when a bluish

bulging membrane is seen occluding the vaginal introitus. The
examination will reveal a lower abdominal swelling; per rectum a
large, bulging mass in the vagina may be palpable.
The treatment is to establish drainage for the accumulated
menstrual blood, by excising the membrane. The risk of infection is
significant, so the surgical technique must be meticulously aseptic.
A vaginal examination is best avoided.

In newborn infants a similar condition known as hydrocolpos may

occur. Hydrocolpos is the result of the accumulation of mucoid fluid
secreted by the cervix as the result of passive hormones
stimulation. Most cases of hydrocolpos become manifest during the
first week or so of life. Treatmet for hydrocolpos is to excise the
imperforate hymenal membrane to allow drainage of the
accumulated fluid.
Haematometra: This condition is the result of a long-standing accumulation of the
menstrual blood which extended into the uterine cavity and may cause
haematosalpinx.

Fusion of the labia

The labia majora and minora developed from the genital swelling
and genital folds respectively.
In normal embryological
development of the female these genital swelling and folds are not
fused. If fusion or closure occurs the labia minora and the majora
may be held together in the mid-line giving the appearance of the
median raphe of a male perineum. This congenital anomalies may
cause doubt about the sex of a child.

Genital tract anomalies

FALLOPIAN TUBES

Absence
UTERUS

Absence

Pathogenesis of the anomalies

Complications

Upper or proximal end of Mullerian

ducts failed to form

Infertility

Absence of the middle part of

Mullerian duct

Menstrual disorders

Menstrual disorders ; obstructed

labour

Double uterus

Failure of fusion of Mullerian ducts

Uterus unicornis

Failure of development of one side

of the Mullerian duct.

Uterus bicornis

Incomplete (partial)
canalization.

and

Recurrent abortion; preterm

labour; malpresentation.

Rudimentary horn

Incomplete or partial development

of one side of the Mullerian ducts.

Dysmenorrhoea

Septate uterus

Recurrent abortion; preterm

labour ; malpresentation

Menstrual and sexual problems.

Dyspareunia

Primary amenorrhoea
Hydrocolpos or hametocolpos
Haaematometra
Haematosalpinx

Sexual ambiguity

Sexual ambiguity

VAGINA

Absence

fusion

Failure of canailzation

Failure of fusion of lower Mullerian

duct and urogenital sinus and
formation vaginal plate.

Septate vagina

Failure of canalization.

Imperforate hymen

Failure to form perforation of the

urogenital sinus membrane.

External genitalia

Fusion of labia

Clitoromegaly
(enlarge)

Closure or fusion of the genital

swelling and folds
Enlargement
of
the
genital
tubercule associated with intersex
disorders.

Table 1.1 Summmary of the anomalities of the genital tract, its pathogenesis and
complications.

PUBERTY
THE ONSET AND NORMAL PUBERTAL
DEVELOPMENT
The puberty is defined as the period of sexual maturation which
the child becomes physiologically capable of reproductive
function.
In normal circumstances the first sign of pubertal
development in girl normally occurs between the ages of 9 and 13
years. During this transition period from childhood to womanhood, it is
associated with many complex physical, endocrinologic, psychologic
and behavioural changes. Changes occurring in the hypothalamicpituitary-ovarian axis are mirrored by changes in body habitus and
appearance.
THE ONSET OF PUBERTAL DEVELOPMENT
The onset of puberty is determined by a process of central nervous
system maturation leading to increased pituitary secretion of follicle
stimulating hormones (FSH) and luteinizing hormones (LH), increased
ovarian maturation, increased circulating estrogens, and increased
development of secondary sexual characteristics, culminating in the
development of an individual capable of reproduction.
The specific events that initiate the onset of puberty is not completely
understood. Many factors that influence the onset and pubertal
development has been postulated.
Factors influencing onset and pubertal development

A critical weight and body mass relationship theory:

- It has been suggested that puberty may be triggered by a
specific body weight or fat content achieved by an individual. It
has been noted that obese girl ( 20% - 30% over normal weight)
experience an earlier menarche than do thinner girl. Therefore,
this observation support the theory of critical weight and body

mass relationship as a trigger factor for initiating the onset of

puberty.

Increased ovarian follicular maturation (Gonadostat theory):

- Before puberty, between the ages of 7 and 10, there is usually
slow increase in the secretion of estrogens and androgens. The
concentrations of these sex hormones remain inadequate,
however, to promote the development of secondary sex
characteristics, such as body hair or genital organs. These low
levels of sex steroids inhibit the secretion of FSH and LH. At the
start of puberty, the hypothalamus begins to release luteinizing
hormone-releasing hormone (LHRH), which stimulates the
secretion of FSH and LH from the pituitary. It is these pituitary
gonadotropic hormones that stimulate the ovarian follicular
maturation to secrete estrogens at full capacity. The increasing
estrogen levels initiate breast development and eventually
sufficient endometrial development to cause the first period to
occur.
Adrenal activity:
- There is an increase in the activity of the adrenal gland to
secrete more dehydroepiandrosterone (DHEA) at the time of
puberty, and are probably responsible for the physical changes of
adrenarche (Adrenarche is the time of first occurrence of the
effects of androgens, usually manifest by pubic or axillary hair).
The role of the pineal gland:
- New evidence suggests that the pineal gland is an important
factor in the hormonal changes that initiate puberty. The pineal
gland secretes the hormone melatonin, which inhibits the
production of sex hormones during early childhood. At the onset
of puberty, however, there is an abrupt drop in the secretion of
melatonin, allowing estrogens and androgens to promote sexual
change.
Sleep-related increases in gonadotrophin levels:
- The onset of puberty is associated with pulsatile secretion of LH
that occurs during sleep. This pattern of LH does not occur
either before or after puberty, but only at its onset.

SEQUENCE OF BODY CHANGES AT THE TIME OF PUBERTY

The events of puberty usually occur in a definite sequence. The

changes that accompany puberty in a girl start about two years earlier
than those for boys, and they also happen more rapidly and closer
together.
The first physical sign of puberty is ordinarily breast budding, which
usually precedes pubic hair growth, which occurs earlier than axillary
hair growth.
The usual sequence of events at the time of puberty is as follows:
1.
2.
3.
4.

Breast development (thelarche)

Pubic and axillary hair development (adrenarche)
Maximum growth spurt
Menarche ( the onset of menses )

Breast development: The first physical sign of puberty is the

development of the breast.
The whole sequence of the breast
development, starting with the breast buds increasing in size and the
nipples beginning to protrude, usually takes two and a half to three
years. Breast developments have been adequately described by
Tanners classification system (Fig.1.1).

STAGE 1 (prepubertal)

Elevation of nipple only

Areola not pigmented

STAGE 2 (9 13 years)

Breast bud stage breast tissue

begins to grow beneath the nipple
and cause elevation breast mound

Areola enlarging.
STAGE 3 (10 14 years)

Further enlargement of breast

mound with no separation of
areola contour
STAGE 4 (11 15 years )

Elevation of papilla and areola to

form second mound above breast
contour
STAGE 5 (12 17 years)

Only papilla is elevated

The areola recessed to general

contour of the breast

Fig. 1.1 Tanners classification of breast development.

STAGE 1 (Prepubertal)

No pubic hair growth

STAGE 2 (9 13 years)

Sparse
growth
of
long
pigmented hair along the labia
majora

STAGE 3 (10 - 14 years)

Sparse growth of dark

coarse hair over
mons pubis

STAGE 4 (11 15 years)

Abundant adult hair spread

over a small area mainly the
mons pubis

No spread to the medial thigh

STAGE 5 ( 12 17 years)

Normal adult female hair

pattern and distribution

Spread to the medial thigh

Fig. 1.2
development.

Tanners classification of pubic hair

Pubic and axillary hair development (adrenarche) follow the

development of the breast. The mean age of adrenarche is 11 years.
Usually the development of the pubic hair occurs much earlier than
axillary hair growth.
The growth of the pubic hair have been
adequately describe by Tanners classification (Fig. 1.2).
Axillary hary : Pigmented, crinkly hair appears in the axilla, usually
one to two years after its appearance on the pubes.
The growth spurt begins at about the age of 9 10 years and
extends through the age of 13.5 years, with a peak at about 11.5
years. Hormonal control of the adolescent growth spurt in girl is via
action of estradiol, growth hormones, and perhaps other ovarian and
adrenal androgens. The adolescent growth spurt can be divided into
three stages:

The time of minimum growth velocity at the beginning of puberty

The time of rapid growth (peak height velocity)
The stage of decreased velocity with cessation of growth at
epiphyseal fusion.

Peak height velocity occurs about a year after the onset of breast
development and about a year and a half before menarche. Peak
height velocity is between Tanners stage 2 and 3 of breast
development and growth of pubic hair.
Menarche is one of the later events of puberty and occurs towards the
end of the growth acceleration; the attainment of at least Tanners
stage 4 breast development is a prerequisite. The onset of menarche
in girls occurs at an average age of 12.8 years, with a range of 10 to
16 years. The first few periods are usually anovulatory, relatively
painless and irregular. They then become regular and more painful as
ovulatory cycles are established.

Area of body

Description of changes

General
changes

bodily Pelvis widens. Fat distribution increases in hip,

buttocks, breasts. Skeletal growth ceases by
about age 18.

External

genital Breast enlarge. Vagina enlarges and vaginal

organs

Internal
organs

wall thicken
stimulation.

as

the

result

of

estrogens

genital Uterus enlages and achieve physiological

functions. Ovaries secrete sex hormones and
maturing of va occurs. Menstruation begins.

Hair growth

Hair appears on pubic arms, axillary region.

Scalp hair increases with female type hairline.

Voice

Voice remains relative high pitched.

Table 1. Major body changes at puberty.

HORMONAL CHANGES OF PUBERTY

An initial surge in gonadotrpin levels follows birth as a result of loss
negative feedback as placental estrogens are withdrawn. Throughout
childhood, there is increasing sensitivity of the gonadostat or
hypothalamic-pituitary axis, and level of FSH, LH, and steroid
hormones fall. There is also evidence for the existence of a central
non-steroidal suppressor of endogenous GnRH and gonadotropin
synthesis. Gonadotropin levels reach a nadir and remained suppressed
throughout childhood.
At puberty, there appears to be a gradual release of inhibition of the
hypothalamic-pituitary axis with the appearance of increasing
amplitude and frequency of GnRH pulses, first at night and then
throughout the day and night.
Gonadotrope cells become more
sensitive to GnRH, and FSH and LH secretion occurs. As gonadotropin
level rise, gonad-derived sex steroids level increase, and positive and
negative feedback of steroid levels to the pituitary and hypothalamus
becomes operational.

ABNORMAL PUBERTY
Abnormalities of puberty can occur as a result of problems at any
level of the hypothalamic-pituitary axis. Aberrations can result in,

The early onset of puberty (precocious puberty), or a

Delay in pubertal development.

DELAYED PUBERTY
Delay in puberty is considered to be abnormal when none of the
physical signs are evident by the age of 13 in girls and if menarche has
not occurred by the age of 17. Delayed puberty is a common cause of
primary amenorrhoea.
Delayed puberty may be due to,

Constitutional delay of puberty

Hypogonadotropic hypogonadism

A few patients may have a simple constitutional delay of menarche.

Others may have disorders of gonadal failure, of steroid synthesis, or of
the hypothalamic-pituitary axis, or they may have a chronic non
endocrine disease.
Constitutional delay occurs in 3% - 4% of teenagers. There is often a
family history of delayed puberty, and these adolescent are usually
short for their chronologic age and have been smaller than their peers
for years.

Evaluation of delayed puberty

A careful history includes detail of the general physical health, analysis
of previous records of height and weight, and a history of the timing of
the onset of puberty in other family members. History of chronic or
intermittent illnesses, injuries and accidents, and details pertaining to
growth and development should be elicited. Details of pregnancy,
labour and delivery might suggest a congenital or neonatal problem
producing the delayed onset of puberty. A history of consanguinity is
important in the detection of chromosomal recessive disorders.
The family history may revealed a delayed onset of menarche in family
members.

Physical examination includes body measurements, staging of

secondary sexual (breast and pubic hair) developments. Visual fields,
funduscopy, and assessment of sense of smell should be elicited.
Possibility of an abnormal vaginal, such as atresia or aplasia ,
imperforate hymen should be looked for when puberty begins normally
but menses are delayed.
Investigation
It is important to determine karyotype, circulating gonadotrophin levels
and bone age. Under certain circumstances a skull x-ray or x-ray of
pituitary fossa may be required. Further evaluation might involve the
use of an LH-RH stimulation test to assess the response of the pituitary.
Also it is important to evaluate the level of growth hormone, thyroid
hormone, sex hormone and excess glucocorticoids.
Differential diagnosis of delayed puberty

Kallmans syndrome and other hypothalamic disorders

Hypothyroidism
Physiological amenorrhoea
Psychogenic amenorrhoea
Chronic illness (rheumatic fever, tuberculosis)
Metabolic disease (Diabetes, thyroidism, adrenal disorders.
Vaginal and uterine defects.
Tumours virilizing and feminizing tumours.
Ashermans disease

PRECOCIOUS PUBERTY
Precocious puberty is defined as a premature initiation of either sexual
development and/or menstrual bleeding before the age of 8 years.
Classification of precocious puberty
The precocious puberty is classified into,
1. True complete precocious puberty
2. Incomplete pseudoprecocious puberty

True complete precocious puberty

This is the most common form of sexual precocious puberty which is

initiated by premature maturation of the hypothalamic-pituitaryovarian axis resulting in total ovarian function with ovulation before
the age of 9. Children with complete precocity are able to conceive.

Incomplete pseudoprecocious puberty

In this condition, only the secondary sexual developments occur
without evidence of ovulation.

Causes of precocious puberty

Precocious puberty may occurs in the following conditions:

Idiopathic or constitutional is probably the most common

form of true precocious puberty. This condition may occur in
families where there is a history of early onset of puberty in other
family members (i.e., constitutional).
Abnormalities in central nervous system - About 5% of
cases of sexual precocity are due to abnormalities of the central
nervous system. Precocious puberty may in the presence of
central nervous system tumours, such as a craniopharyngioma,
a hamartoma, suprasellar cyst or teratoma.
McCune-Albright syndrome consists of caf-au-lait skin
spots, multiple disseminated cystic bone lesions (polyostotic
fibrous dysplasia), and precocious puberty.
Primary hypothyroidism - may be associated with precocious
puberty. In such cases, TRH (thyroid releasing hormone) is
elevated, which in turn elevates TSH, FSH, and LH.
Ovarian tumours - An increased level of sex steroid production
can be a cause for precocious puberty and may be associated
with ovarian tumours. The most common ovarian tumours that
produce estrogens are the granulosa-thecal cell tumours,
teratomas, gonadoblastomas, lipoid cell tumours, and
cystadenomas. Excess estrogen production produces breast
growth and vaginal bleeding, along with skeletal maturation.
A luteoma, a small tumour that produces both estrogen and
progesterone, may produce pseudosexual precocity.

Adrenal tumours are not common, however, an adrenal

carcinoma may secrete estrogen and may be the cause of

precocious puberty.
About 28% of sexual precocity
associated with congenital adrenal hyperplasia.

are

Drug ingestion particular estrogens may be the cause of

precocious puberty.

Clinical features of precocious puberty

Precocious puberty is associated with accelerated growth; accelerated
osseous maturation also occurs, resulting in ultimate short stature.
Also sexual precocity is associated with early sexual maturation and
development.
TRUE PRECOCIOUS PUBERTY

Usually occurs at 8 9 years

Progressive breast development
Progressive
pubic
hair
development
Enlargement
of
external
genitalia
Menstruating
Attain early sexual maturuty

PSEUDOPRECOCIUOS PUBERTY

Usually occurs before the age of

4 years
Breast development or sexual
hair
growth
may
occur
independently
No other signs of sexual
maturuty
Appropriate sexual maturation
and development occur at later
stage

Table 1 : Clinical features comparision between true and pseudoprecocious puberty.

Evaluation of precocious puberty

The importance of evaluating a child with sexual precocity is to identify
the possible causes which may be life-threatening , such tumours of
the central nervous system, ovary or adrenal.

Historical findings A detailed history is required.

Enquiry about the presence of similar conditions in other family

members.
The chronologic order of sexual development should be elicited.

The growth record should be checked to determine the onset of

increase in height velocity, and the degree of correlation
between height and weight measurements.
Enquiry should be made about any central nervous system
symptoms, such as headaches or seizures.
History of sex steroid ingestion, particularly estrogens should be
asked.
A history of encephalitis, meningitis, cranial trauma can be an
important factors in such cases.

Physical examination will consist of:

Measurement of height and weight.

Thorough description of secondary sexual development.

The skin must be examined for acne, hair distribution and
growth, and abnormal pigmentation.
Neurologic examination is essential if there is central nernous
system involvement. This nerologic examinations will include the
assessment of the visual fields and optic discs.
An abdominal and pelvic examination must be performed.
The inspection of the external genitalia may show evidence of
estrogenization.
If vaginal bleeding is present, examination of the vagina may
reveal whether there is any abnormality, including a foreign
body.
Investigations:
A thyroid function test is important if there are any symptoms
or signs of hypothyroidism.

Laboratory evaluation includes estimation of serum FSH, LH,

testosterone and estradiol.
The measurement of DHEA-S ,
progesterone may be valuable
hyperplasia is suspected.

and 17-alpha-hydroxyif congenital adrenal

Radiological examination of the left hand-wrist will usually

define the skeletal age.
Radiological examination of the long bones should be done if
there is any suspicion of McCune-Albright syndrome.
A CT scan of the brain, with particular emphasis on the
hypothalamic and sellar regions, is the most sensitive
radiological means of identifying a CNS tumours associated
with sexual precocity.
Ultrasonic
tumours.

examination

will

reveal

ovarian

and

adrenal

Treatment:
Management of precocious puberty depends on the accuracy of
diagnosis. The treatment goal in true precocious puberty is to stop
the growth process so that patients ultimate height will be
protected. Also the aim of the treatment is to suppress
menstruation, ovulation and fertility.
Principal of treatment
Suppression of menstruation Treatment with progesterone ,
preferably those without androgen or estrogen activity , will
suppress the menstrual cycle.
Alternatively, medroxyprogesterone acetate (MPA), Depo-Provera, Cyproterone acetate
are effective in suppressing ovarian function and menstruation.
Cyproterone acetate usage is limited by side-effects, the most
important of which is adrenal suppression.

Suppression of breast development can be achieved with

the usage of medroxy-progesterone acetate (MPA). MPA in doses
of 100 200 mg intramuscular weekly or biweekly is the
treatment of choice.
MPA stops breast development and
menses. Danazol, a 2,3-isoxasol derivative of 17-alpha-etinyltestosterone is a weak androgen, effectively stops menstruation
and breast development.
To prevent short stature - GnRH agonist has been successfully
used in the treatment of precocious puberty patients. This
treatment delays the closure of the epiphyses so that the
patients ultimate height will be protected. GnRH agonist
treatment will also eliminate the menstrual periods and inhibits
the development of the secondary sexual characteristics.

Psychological support and counseling - Children with sexual

precocity have a physical appearance that outstrips their
psychosexual maturation. Thus many have severe psychological
disturbances, are shy and withdrawn. Therefore, it is important to
provide psychological counseling and support for the patient and
for her family.
Specific treatable condition - When a specific treatable
condition is identified, treatment is directed against the
condition.
CNS tumours may be treated surgically.
Hypothyroidism is treated with thyroxine
Congenital adrenal hyperplasia is treated with glucocorticoids
or mineralocorticoids.
Adreanal and ovarian tumours are treated surgically.

9
DISORDERS OF MENSTRUATION

Menstruation is normal as mentioned in Chapter 2 (The Physiology of

Normal Menstrual Cycle) if it occurs at interval of 21-35 days; if the
duration of menstrual flow is less than 7 days and if the amount of
menstrual loss is less than 80 ml.
Disorders of menstruation may relate to the,

Changes in the length of the menstrual cycle, i.e.

1) Oligomenorrhoea if menstruation occurs at intervals longer
than 35 days.
2) Secondary amenorrhoea if menstruation does not occur for
more than 70 days (in the absence of pregnancy).
3) Primary amenorrhoea if menstruation has not commenced
by the age of 16 years.
4) Epimenorrhoea or polymenorrhoea if menstruation occurs at
interval of less than 21 days.

Changes in the amount of menstrual loss, i.e. the quantity of

menstrual loss may vary, without altering the cyclicity of
menstruation.
1) Hypomenorrhoaea scanty menstrual loss.
2) Menorrhagia heavy bleeding.
3) Dysfunctional uterine bleeding heavy menstrual flow in the
absence of any detectable uterine pathology.

Disturbances in cyclicity and amount of menstrual loss.

1) Metrorrhagia In this disturbance the cyclicity of
menstruation is loss, bleeding occurring at irregular intervals,
and the quantity of menstrual loss varying considerably.

AMENORRHOEA
- When Period Disappears Amenorrhoea is the absence of menstruation. For most sexually
active women in their reproductive years, is a clear signal of
pregnancy. And in older non pregnant women, amenorrhoea may
mean that menopause is approaching or has arrived particularly if

she is in her late 40s or 50s. In both groups of women, amenorrhoea is

perfectly normal.
However some cases amenorrhoea is can indicate an underlying
medical problem. There are two main types of amenorrhoea:

Primary amenorrhoea : A condition when a young woman has not

started to menstruate by the age of 16 years.

Secondary amenorrhoea : Refers to women who have missed

three or more period after their regular menstrual cycle has been
established.

PRIMARY AMENORRHOEA
Primary amenorrhoea is present when a young woman has not started
to menstruate by age 16. This is because she has some hormonal
imbalance or developmental problem, which can often be treated with
hormones and/or surgery. Primary amenorrhoea may occur with or
without other signs of puberty.
Signs of puberty are:
Breast growth
Pubic hair
Axillary hair
Growth spurt
Menarche
Causes for primary amenorrhoea vary from chromosomal abnormalities
and malformation of the reproductive tract, to less common disease of
the pituitary gland, thyroid, or adrenal.
The causes of primary
amenorrhoea are best classified according to whether these secondary
sexual characteristics are present, absent or heterosexual (signs of
virilization).

Secondary sexual
characteristics
PRESENT

Conditions causing primary

amenorrhoea

Imperforate hymen
Testicular feminization
Absence or hypoplasia of vagina

ABSENT OR POOR

Delayed puberty
Kallmans syndrome (hypothalmic)
Pituitary tumour
Gonagal dysgenesis (Turners syndrome)
Gonadal agenesis

HETEROSEXUAL

Intersex
Congenital adrenal hyperplasia
Tumour (adrenal or ovary)

Table 1.1 ; Causes of primary amenorrhoea according to secondary sexual

characteristics.

Imperforate hymen
A condition called cryptomenorrhoea, or hidden menstruation, may
be mistaken for true menstruation. The menstruation occurs, but
menstrual discharge cannot exit the body due to disorders
(blockage) of outflow tract either the vagina or the cervix. The most
common is an imperforate hymen which is due to the failure of
recanalization. The menstrual blood accumulates in the vaginal
canal and gradually distends it to forms haematocolpos.
Haematometra is the accumulation of blood in the uterus.

Fig.1.1 Imperforate hymen

Features: Primary amenorrhoea in a teenage girl with normal

sexual development complaining of:
Intermittent abdominal pain (due to menstruation)
Difficulty with micturition
Lower abdominal swelling (haematometra)
Bulging, bluish membrane
at lower end of
vagina
(haematocolpos)

Management: A cruciate incision in the hymen is made and the

accumulated menstrual discharge is drained slowly.

Testicular feminization
Testicular feminization is the development of female characteristic
in a male. Patient are genetically male (genotype XY), but have
normal female appearance. Testicular feminization is inherited by
an X-linked recessive gene resulting in absence of cytosol androgen
receptors. Testes are present, but female internal organs are
absent due to Mullerian Inhibitory Factor. This condition is often not
discovered until the patient has difficulty with infertility and no
menses. Primary amenorrhoea in testicular feminization occurs
because the uterus is absent or rudimentary.
Features: The appearances are of a normal girl, with good breast
development.

Normal growth and development

At puberty there is normal development of breasts and female
characteristic
Pubic and axillary hair are scanty
The vagina usually ends blindly, and the uterus and uterine tubes
are absent or rudimentary
Testes are situated either intrabdominal, in the inguinal canal or
in the labial
No menstruation (primary amenorrhoea)

Management: These patients are female.

Diagnosis is by
chromosomal analysis and serum testosterone. The gonad (testes)
should be removed after puberty because of a high incidence of
testicular malignancy. Hormonal replacement therapy should be
started.

Fig. 1.2 Testicular feminization. The external genitalia are female, but the patient
has a 46 XY karyotype and testes.

Absence or hypoplasia of vagina

This is one of the causes of primary amenorrhoea which account for
15 to 20 per cent of the cases of primary amenorrhoea. In cases
with complete absence of the vagina it is unusual to find a
functioning uterus.
Features: Growth, sexual development and ovarian function are
usually normal. The vagina is absent and the uterus may be normal
or rudimentary.
Management: A functional vagina can be created by surgery,

McIndoe-Read operation creating a functional vaginal by

dissecting of a space in the fascial space between the rectum
and the bladder and urethra. The cavity is lined with skin graft
from the thigh which is wrapped round a mould.

Williams operation a vagina is constructed by vulvovaginoplasty method.

Turners syndrome (45,XO) gonadal dysgenesis

Primary amenorrhoea occurs with ovarian dysgenesis (Turners
syndrome). Turners syndrome is a disorder in women caused by an
inherited chromosomal defect.
This disorder inhibits sexual
development and causes amenorrhoea and infertility.
Turners syndrome is caused by a missing X chromosome. It
affects 1 out of 3000 live birth.
Features:
There are many manifestations of this syndrome, but the main
features are:

Short stature
Webbing of the skin of the neck
Absent or retarded development of sexual characteristic
Absent of menstruation (usually primary amenorrhoea)
Coarctation (narrowing) of the aorta
Abnormalities of the eyes (dropping of eye lids)
Abnormal bone development
Low hairline
Simian creases
Pectus excavatum (a caved-in appearance of the chest)
Increasing carrying angle
Streak ovaries are present

Fig. 1.3

Turners stndrome

Diagnosis:
Turners syndrome is diagnosed by:
a) Signs :

A physical examination reveals:

Underdevelop genitalia
Webbed neck
Short stature
Abnormal development of the arm

b) Karyotyping: Turners syndrome is diagnosed by chromosomal

analysis. The most frequent chromosome constitution in Turners
syndrome is 45,X (also written as 45,XO)

Fig 1.4 Chromosome constitution in Turners syndrome 45,XO . Note the missing X
chromosome

c) Hormonal profile :
Serum FSH high
Serum LH high
The high levels of gonadotrophins are due to streak ovaries.
Treatment
Management is supportive. Growth hormone replacement may or
not be prescribed; it may help the child to achieve a more normal
height.
Estrogen therapy (cyclical ethinyloestradiol 0.02 mg for three weeks
and followed by norethisterone 5 mg daily for one week) is started
at 12 0r 13 years to stimulate development of secondary sexual
characteristics, breast development and cyclical bleeding so that
girl affected with this disorders will have normal appearance as an
adult. Estrogen therapy, however, will not reverse infertility.
Cardiac surgery is sometimes necessary to correct heart defects.

Delayed puberty
Primary amenorrhoea occurs with delayed puberty.
Girl with
delayed puberty will definitely have delay in their sexual
characteristic development. Usually there is a family history of late
puberty in one parent to aid diagnosis.

Pituitary disorders
Rare cases of pituitary disorders such as pituitary infantilism may
occur. The features are of child-like stature and proportions, with
primary amenorrhoea. The level of gonadotrophins are absent or
low.
Pituitary tumours (e.g. craniopharyngioma) may cause an excessive
secretion of prolactin and consequent primary amenorrhoea.
Hyperprolactinaemia may be diagnosed if the prolactin level
exceeds 1000 mIU/L.

 Kallmans syndrome
Rare hypothalamic causes of primary amenorrhoea are Kallmans
syndrome. Kallmans syndrome consists of anosmia, amenorerhoea
and specific failure to secrete FSH and LH.

Amenorrhoea associated with heterosexual conditions

Primary amenorrhoea which occurs as the result of heterosexual
include:

Congenital adrenal hyperplasia (CAH)

Intersex
Tumour (adrenal and ovary)

Congenital adrenal hyperplasia Is an autosomally recessive

inherited disorder, in which there is a deficiency of the 21-hydroxylase
( an enzyme that is requires for the conversion of 17hydroxyprogesterone to cortisol) and therefore insufficient cortisol and
aldosterone are produced. Reduction of cortisol in congenital adrenal
hyperplasia will result in excessive production of androgens. A female
fetus will be exposed to an excess of adrenal androgens and virilization
will result and the female child will be born with the degree of
masculinization of the external genitalia.
Virilizing tumours of the ovary are suspected as a cause of
amenorrhoea if hirsuitism is prepubertal or suddenly develops some
years after puberty.

SECONDARY AMENORRHOEA
Secondary amenorrhoea, more commonly, affects women who had
previously had normal periods. It is defined as absent of three or more
periods after regular menstrual cycle has been established. Secondary
amenorrhoea is caused by a variety of different factors ranging from
general illness to emotional disturbances to the use of various drugs or
medication.

Often a hormone imbalance is responsible for secondary amenorrhoea.

A hormone imbalance and amenorrhoea can result from
Breast feeding
Premature ovarian failure
Thyroids conditions
Tumours
Anorexia
Problems with adrenal glands
Secondary amenorrhoea may be:
Physiological
During pregnancy
During lactation
After the menopause
Pathological
Disorders of
Disorders of
Disorders of
Disorders of

hypothalamus
anterior pituitary
ovary
uterus

Disorder of the hypothalamus

The most common reason for hypogonadotrophic secondary
amenorrhoea and often associated with stress.
Diagnosed by
exclusion of pituitary lesions.
a) Anorexia nervosa
A loss of weight of more than 10 kg is frequently associated with
amenorrhoea. It usually occurs in young women who become
obsessed with their body images and starve themselves. There is
no loss of appetite in anorexia nervosa. Oestrogen levels are
suppressed. Periods return when the lost weight is regained.
b) Athletic amenorrhoea
Strenuous and continued exercise with diet restriction, such as in
preparation for a major athletic events, may often lead to
amenorrhoea.

 Disorders of the pituitary

Hyperprolactinaemia
1. Pituitary tumour
2. Hypothyroidism
3. Drugs

Deficient pituitary
function
1. Sheehans syndrome

HYPERPROLACTINAEMIA
Excessive secretion of prolactin by the anterior lobe of the pituitary
gland inhibits the secretion of the FSH and LH. This will cause
amenorrhoea and galactorrhoea may also occur.
Hyperprolactinaemia may occur in the following condition:
1. Pituitary tumours

Anterior lobe pituitary tumours

causing hyperprolactinaemia
causes amenorrhoea and galactorrhoea. High prolactin levels
inhibit FSH and LH, and this imbalance of hormone is responsible for
secondary amenorrhoea. About one-third of women with secondary
amenorrhoea will hav a pituitary adenoma. Hyperprolactinaemia
may be diagnosed if the prolactin level exceeds 1000 mIU/L. The
tumours may be small or large. If the tumour is large it may press
on the optic nerve and causes disturbances of the vision. Pituitary
fossa x-rays must be taken in all cases of amenorrhoea, particularly
secondary. CT scan or magnetic resonance imaging is requested
when the x-rays of the pituitary fossa suggest abnormalities.

Small prolactinoma may be treated with dopamine agonist,

bromocryptine. Bromocryptine will suppress prolactin secretion and

it may reduce the size of small tumours. Small tumours can also be
removed surgically.

Large tumours need to be removed surgically if eyesight is to be

preserved.

2. Hypothyroidism

Disorders of the thyroid gland, particularly hypothyroidism with high

thyroid stimulating hormone (TSH) may cause secondary
amenorrhoea. High level of TSH will elevate prolactin.

3. Drugs - Dopamine antagonists

Pharmacological causes of amenorrhoea are appearing more
commonly. Patients on treatment with drugs that are dopamine
antagonists (phenothiazines, haloperidol, methyldopa, cometidine,
metoclopramide) may cause secondary amenorrhoea.
The
mechanism for amenorrhoea in these patients is pharmacological
induction of hyperprolactinaemia.
4. Sheehans syndrome

Sheehans syndrome refers to a condition where there is ischaemic

necrosis of the anterior pituitary. It is the result of thrombosis of the
pituitary blood vessels following severe postpartum haemorrhage.
It is a very problem today.

The anterior pituitary gland loses its function and the production of
gonadotrophin, thyrotrophic and adrenotrophic ceases or
inadequate.

The patients with Sheehans syndrome have the following features,

a). amenorrhoea
b). hypothesion
c). lethargic
d). low metabolic rate
e). gain weight

Treatment includes,
a) Thyroxine and cortisol therapy
b) Oestrogens to produce cyclical bleeding

Amenorrhoea Cause By
Disorders of the ovary
The ovarian causes of secondary amenorrhoea are:

Chromosomal abnormality
Polycystic ovarian disease
Ovarian failure

Chromosomal abnormality

A mosaic chromosome pattern of Turners syndrome ( e.g. XX/XO)

will lead to various degrees of gonadal dysgenesis, secondary
amenorrhoea and premature menopause.

Polycystic ovarian disease (PCOD)

Polycystic ovary or also known as Stein-Leventhal syndrome is the

most commonly recognized cause for secondary amenorrhoea.
Stein-Leventhal syndrome refers to a condition where there is an
accumulation of many incompletely developed follicles in the ovary.
This condition is characterised by scanty or absent menses, multiple
cyst on the ovary, and infertility. Many of these patients are obese,
and have an excessive growth of facial and body hair.

Causes: Although the cause of Stein-Leventhal syndrome is not

fully understood, there are several theories suggesting that
problems with oestrogen production and hypothalamic-ovarian
feedback may be responsible.

Pathogenesis: How the process starts is not clear but it can be

initiated by excessive androgen secretion by the adrenal gland. The
sequence of events may be as follows:
a) Androgens from ovary or adrenal are converted
estrogens. Rate of conversion will be greatest in obesity.
b) High oestrogen will be
development is curtailed.

suppressed

and

to

follicular

c)High LH level is stimulated by the persistently high oestrone

but no LH surge occurs and ovulation is prevented. Multiple
lutein cysts formed.
d) The raised LH level stimulate the theca cell to produce androgens which
causes hirsuitism and virilisation and perpetuates the whole process.

e) Amenorrhoea may occurs

Pathology :

Fig 1.5 . Gross pathology of polycystic ovarian disease seen at laparoscopy.

The ovaries are enlarged and show:

a)
b)
c)
d)

Thicken and very tough outer covering (ovarian capsule)

Numerous small cystic follicles
Hyperplasia of theca cell
Atresia of granulosa cell

Hormonal changes :

FSH: The secretion of FSH is within normal range.

LH: The LH level is elevated.

LH to FSH ratio : Increase

Testosterone: The serum testosterone may also be raised.
Urine 17-ketosteroi : Increase

Diagnosis :
The diagnosis of polycystic ovarian disease or Stein-Leventhal
syndrome is made on the case history and confirmed by
transvaginal ultrasound and the finding of a raised LH : FSH ratio.

Treatment :
Treatment depends on the presenting symptoms and on the wishes
of a woman. Medication used to treat the symptom of SteinLeventhal syndrome includes:

Oral contraceptive/clomiphene citrate

Clomiphene induces the pituitary gland to produce more FSH
which in turn stimulates maturity and release of the ova.

If fertility is not required the combined contraceptive pill is

advised.

A wedge resection or ovarian drilling of the ovaries may

be used to remove the multiple cyst.

Weight reduction is also very important

Ovarian Failure
Secondary amenorrhoea from ovarian failure may occur. This include :
a).
a

Resistant ovarian syndrome

b).

A rare condition in which FSH is elevated despite normal

ovarian development.
It may resolve spontaneously
otherwise no treatment is possible except oestrogen therapy
for any hot flushes.

Premature menopause

If ovarian biopsy shows absence of ovarian follicles the term

premature menopause is used. Ovarian failure may be due to:

(i)
(ii)
(iii)

Auto-immune disease
Viral infection (e.g. mumps)
Cytotoxic drugs

Hormone replacement therapy will be required to avoid immediate and longterm menopausal symptoms.

Amenorrhoe Cause By
Disorders of the Uterus

In general uterine causes of secondary amenorrhoea are rare.

Destruction of the endometrium by surgical procedures (e.g. excessive
curettage, endometrial ablation), or radiations, and advance infection
results in amenorrhoea.
Uterine causes of amenorrhoea include,

Ashermans syndrome
Ashermans syndrome is a condition associated with secondary
amenorrhoea as the result of the removal of the basal endometrial
layer by excessive curettage, particularly following an abortion or
postpartum this may result in obliteration of the uterine cavity and
permitting multiple synechiae to form. The diagnosis is made by
hysteroscopy or from hysterogram.
Treatment is by breakdown intrauterine adhesions through
hysteroscope and inserts an intrauterine contraceptive device (IUCD)
to deter reformation.

Infection (e.g tuberculosis)

Advanced pelvic tuberculosis may caused destruction of the
endometrium and this results in amenorrhoea. Tuberculosis infection
still occurs in the developing countries.

Weight loss / eating disorders

Excessive exercise
Psychological disturbances

Hyperprolactinaemia condition
Pituitary tumours, Drugs
Thyroid disturbances

Polycystic ovarian disease

Ovarian failure due to
Premature menopause
Resistant ovarian syndrome

Ashermans syndrome

Fig. 1.6 The common causes of pathological secondary

amenorrhoera

INVESTIGATION OF AMENORRHOEA
There are several possible ways to investigate amenorrhoea. It is best
to discuss according to the type of amenorrhoea, i.e primary or
secondary.

PRIMARY
AMENORRHOE
A
If a girl has not begun to
menstruate by the age of 17

TAKE A DETAILED MEDICAL

HISTORY

This includes a family and personal history. Any other female sibling
has the similar problems. At what age does the other female
siblings has their menarche (this is to exclude the case of delayed
puberty). Pubertal development is also important.

PHYSICAL EXAMINATION

a) Physical examination includes general examination with special

relation to secondary sex characters.
b) Look for signs to suggest gonadal dysgenesis (Turners
syndrome) , such as :
1) short stature
2) webbed neck
3) wide carrying angles at the elbow
c) Patients with adrenogenital syndrome (congenital
hyperplasia) may present with signs of virilization.

adrenal

d) The breast should be examine,

Patients with poor breast development are likely to have
gonadal dysgenesis.

If breast development has taken place, look for abnormality

of the lower genital tract such as imperforate hymen.

e) Consider the possibility of testicular feminization in a female

child with inguinal hernia and primary amenorrhoea.
f) Pelvic examination should be conducted. A normally developed
uterus can be felt easily by rectal examination in cases where
vaginal examination is not possible.

SPECIFIC TESTS

1) Chromosome analysis:
If a chromosomal anomaly is
suspected checked the karyotype to exclude Turners syndrome
or testicular feminization.
2) Ultrasound of the pelvis is useful to determine the internal
reproductive organ

3) Hormonal assay FSH, LH, TSH and prolactin

Patients with hypogonadotrophic hypogonadism will have low
levels of plasma FSH and LH.
High FSH and LH levels suggest gonadal dysgenesis.
High TSH suggests thyroid disturbances.
4) Laparoscopy is useful in cases of vaginal atresia to determine
whether the uterus is present.

SECONDARY AMENORRHOEA
A patient who has previously menstruated

Work up for secondary amenorrhoea

HISTOR :
Complete history is important Any chronic or systemic illness
Eating disorder
Weight loss
Any stress factors
Drug use (not to forget hormonal contraception)
Previous menstrual pattern
Any history of galactorrhoea
Any history of curettage, particulary following abortion or
postpartum.
Contraceptive history
PHYSICAL EXAMINATION:
General examination of characteristics,
- obese
- hirsutism
- signs of thyroid disorders
Breast examination - look for the presence of galactorrhoea.
Complete gynaecological examination.
Ultrasound of the abdomen and pelvis to exclude adrenal or
ovarian mass.
LABORATORY EXAMINATION:

Step 1:
Carried out pregnancy test. If pregnancy test negative proceed to step
2.
Step 2:
a) Performed thyroid function test. TSH assay are needed
b) Prolactin level. If level exceed 1000 mIU/L, performed x-rays of
pituitary fossa. CT scans and MRI will confirm the presence of
pituitary tumour.
c) If androgen excess suspected, performed DHEA-S and
testosterone level.
Step 3:
If above tests are negative
- Carried out progestational challenge test with 10 mg
medroxyprogesterone acetate. If there is withdrawal bleeding in
2 to 7 days then the women must be well oestrogenized and is
simply having anovular cycles.
Step 4:
If no withdrawal bleed may use oestrogen-progesterone to determine
whether the uterus is functional. If this still fails to cause a withdrawal
bleed then hormonal assays are necessary.
Step 5:
Obtain FSH, LH assay:
- High level indicates ovarian failure (premature menopause). If
women is under 35 years of age check her karyotype.
-

High LH, increase LH:FSH ratio are suggestive of polycystic

ovarian disease.

HYSTEROSCOPE / HYSTEROGRAM:
This procedure is to diagnose Ashermans syndrome.
synechiae show up on hysterogram or hysteroscope.

Multiple

TREATMENT OF AMENORRHOEA
There are several available treatments, depending on the cause of
amenorrhoea.

Treatment
amenorrhoea

of

primary

The aim of treatment should be to attain the maximum physiological

function of which the individual patient is capable.
The treatment depends on the cause of primary amenorrhoea. Young
women with primary amenorrhoea, found to be caused by
developmental abnormalities, may require hormonal supplementation,
surgery or both. In ant case, psychological support and counseling for
the patient and family is necessary to address specific concerns and
provide guidance regarding anticipated sexual development. If the
problem causing the amenorrhoea is not correctable, than one should
consider the possibility of creating pseudo-menstruation (menstruation
that is caused by hormonal treatment).

Gonadal dysgenesis (Turners syndrome)

The only treatment for this patients is to achieve sexual maturation
with exogenous steroids. Estrogen therapy is started at 12 or 13 years
to stimulate development of the secondary sexual characteristics so
that girl affected with this disorders will have normal appearance as an
adult. This hormonal treatment causes breast development and
cyclical bleeding and can be continued unchanged into adult life.
Estrogen therapy, however, will

not reverse infertility.

Testicular feminization
The testes should be removed from patients with the testicular
feminizing syndrome because of the risk of development of a
malignant gonadal tumour. Estrogen replacement maintains breast
development and prevents hot flushes.
Gynaetresia

Imperforate hymen (causing cryptomenorrhoea) obviously requires

surgical treatment as soon as the diagnosis is made. Usually a cruciate
incision is made on the membrane of the imperforate hymen.
When there is total absence (complete atresia) of the vagina, the
definitive treatment is to construct an artificial vagina at a suitable
age.
Congenital adrenal hyperplasia
If this conditions presents a the time of puberty, it is treated
specifically with corticosteroids.

Disorders of hypothalamus and pituitary glands

Those who have panhypopituitarism should be treated initially with
human growth hormone, made sexually mature with gonadal steroids,
and then treated with pituitary gonadotrophins to induce ovulation
when pregnancy is desired.

Treatment of secondary
amenorrhoea
Obviously the primary treatment must be directed to the primary
cause. There are several available treatments.
Hyperprolactinaemia
The causes for hyperprolactinaemia should be determined, if due to:
a) Drugs: Discontinuation of drugs that cause hyperprolactinaemia
will result the returning of prolactin level to normal.
b) Prolactinoma: Large pituitary tumour may require surgery.
Uncomplicated small pituitary tumour
may be treated with
bromocryptine. Treatment with bromocryptine wills restores
prolactin level to normal and may reduced the size of the tumour.

The common observed side-effects are nausea, vomiting, postural

hypotension and headache.
Radiation therapy for pituitary is usually reserved for situations
where other medical or surgical treatments are not successful.
Ashermans syndrome
The treatment for this syndrome includes:a) The breaking down of intra-uterine adhesions which is done under
general anaesthesia blindly or under hysterscope view.
b) Insertion of the intrauterine device (IUCD) after the procedure to
keep the uterine wall apart
c) The used of oestrogens in order to increases chances of
endometrial proliferation from the damaged basal layer of the
endometrium.
This approach is successful in reestablishing menstrual bleeding.
Ovarian failure
In premature ovarian failure (premature menopause) fertility cannot be
restored and only HRT (hormone replacement therapy) can be offered.
Resistant ovarian syndrome
In cases of resistant ovarian syndrome, ovulation may sometimes be
induced with clomiphene, or with LH-RH ( gonadotrophin releasing
hormone).
Polycystic ovarian disease
Treatment will depend on the desire of the patient.
a) No desire for pregnancy - Oral contraceptive or estrogen plus
progesterone is advised, in order to reduce risk of endometrial
carcinoma.

b) Desire pregnancy Clomiphene induces the pituitary gland to

produce more FSH which in turn induces ovulation.
c) If hirsutism is present, the woman may need anti-androgen
medication (cyproterone acetate).
d) Weight reduction should be advised in obese woman with
polycystic ovarian disease, as obesity is thought to initiate or
aggravate the condition.

PROGNOSIS
Overall the prognosis is good, depending on the cause of the
amenorrhoea. If amenorrhoea is caused by the following conditions,
there is good possibilty of correcting the amenorrhoea, through
medication, life style change, or surgery.
-

Drastic weight reduction

Extreme obesity
Hypogonadotropic hypogonadism
Chronic illness
Hypothyroidism
Imperforate hymen
Adrenogenital syndrome

If the amenorrhoea is caused by one of the following conditions it is

unlikely that the amenorrhoea can be corrected by any intervention.
-

Congenital abnormality of the genital system

Gonadal dysgenesis (Turners syndrome)
Testicular feminization
True hermaphroditism

If the amenorrhoea cannot be corrected, as long there is a uterus, it

may be possible to create a pseudo menstruation with medication to
help the young women feel more like her friends and/or family.

DYSMENORRHOEA

- A Painful Time -

There are probably few women who can truthfully claim theyve never
had dysmenorrhoea, the medical term for painful periods or menstrual
cramps. The majority of women are thought to experience some
degree of dysmenorrhoea.
TYPES OF DYSMENORRHOEA

There are two types of dysmenorrhoea:

Primary or spasmodic dysmenorrhoea.
Secondary or congestive dysmenorrhoea.
Primary dysmenorrhoea are those without evident of pelvic disease,
whereas secondary dysmenorrhoea are associated with pelvic disease.

PRIMARY DYSMENORRHOEA
This is the commoner type of dysmenorrhoea and frequently affects
women in their teens and early 20s, who have never had a baby. With
primary dysmenorrhoea, no disease or medical cause can be found.
Definition
Primary dysmenorrhoea is defined as painful periods or menstruation
for which no organic or psychological causes can be found.
Features
1. It usually occurs in teenage girls. It is commonest in single women
or in infertile married women.
It is a limiting disease which
improves as years gone by with peak incidence between 15 to 25
years old.
2. Primary dysmenorrhoea usually begins with the onset of ovulatory
cycles, typically 6 to 12 months after the onset of menarche.
3. The pain is spasmodic or colicky in nature and usually begins shortly
after or at the onset of menses. The good thing about primary
dysmenorrhoea is that usually the symptoms dont last very long. It
tends to last for only 24 to 48 hours.
4. Lower, mid-abdominal colicky pain, often radiating to the lower back
and upper thighs, is the most frequent complaint.
Pathophysiology

The pain of dysmenorrhoea is probably caused by ishaemia due to the

powerful contractions of uterine muscle. There are several factors
associated with the etiology of dysmenorrhoea:
a) Neuronal Factors :
The preception of pain requires neuronal transmission from the
uterus to the higher brain centers.
Disruption of these
pathways by denervation procedures, such as presacral
neurectomy can alleviate dysmenorrhoea symptoms. Thus,
neuronal factors must somehow participate in the aetiology of
menstrual pain. It is reasonable to assume that the adrenergic
and cholinergic nerves of the uterus may play a role in the
etiology of primary dysmenorrhoea.

b) Hormonal and Prostaglandin Theories :

The clinical efficacy of the combination oral contraceptives and
progesterone in many dysmenorrheic women and the
observation that anovulatory women do not suffer from
primary dysmenorrhoea suggest that these hormones may
participate in its etiology. However, their causal relationship to
dysmenorrhoea is unclear.
It is possible that that the
production of uterine prostaglandin is progesterone and
estrogen dependent.

The symptoms are caused by prostaglandin, a natural

hormone produced by cells in the uterine lining (endometrium).
The level of prostaglandin increases in the second half of the
menstrual cycle. When a womens period begins, the cells in
the uterine lining release prostaglandin (PGF2 and PGE2) as
they are shed. Women with severe primary dysmenorrhoea
have significantly higher prostaglandin level in their menstrual
fluid than do other women. Prostaglandins increase myometrial
contractions and cause constriction of small endometrial
vessels,
resulting
in
tissue
ischaemia,
endometrial
disintegration, bleeding, and pain. Thus, prostaglandins may
be the underlying cause of the dysmenorrhoea.

It has been suggested that vasopressin and/or oxytocin may

increase uterine tone, which in turn may lead to
dysmenorrhoea.
Vasopressin
increases
prostaglandin
synthesis.

c) Myometrial Activity :
It has been shown conclusively that in most women primary
dysmenorrhoea is associated with increased myometrial
activity.
d) Obstructive Theories :
It has been postulated that dysmenorrhoea was due to
mechanical obstruction ( e.g. cervical stenosis, cervical
narrowing due to severe uterine fundus anteflexion) of the free
flow of menstrual blood. It is interesting that this theory
remained popular in spite the occurrence of dysmenorrhoea in
the absence of mechanical obstruction, the absence of
dysmenorrhoea with cervical stenosis, and the not uncommon
finding of severe dysmenorrhoea with excessive menstrual
flow.

Investigation
A comprehensive history and examination is vital.
a) History: A complete history should be taken with special reference
to the location, severity, duration, character, and radiation of pain,
as well as its relationship to the onset of menarche, menses,
mittelschmerz, bowel movements, coitus, voiding and other
possible associated symptoms. Documentation of previous pelvic
infections, endometriosis, pelvic masses is important.
Family
history of painful menses must be sought.
b) Examination: A physical examination should be made to exclude
any gross lesion. The physical examination should include a careful
pelvic
examination,
with
special
attention
to
detecting
endometriosis, pelvic inflammatory disease, pelvic masses, or
uterine enlargement.
Usually in most case of primary
dysmenorrhoea no abnormality is found.
Diagnosis
The history and physical examination should enable the physician to
evaluate the pain and determine the etiology. The diagnosis of primary

dysmenorrhoea can be made only on eliciting the characteristic history

and after excluding pelvic pathology.
Treatment
Primary dysmenorrhoea is a limiting disease which improves as years
gone by and it is nearly always cured by childbirth. Reassurance and
explanation are important.
There are several approaches used in the treatment of primary
dysmenorrhoea. The three main approaches to treatment are:
a) PHARMACOLOGIC AGENTS
Analgesics and antispasmodic preparation has been used for
treating dysmenorrhoea.

Prostaglandin synthesis inhibitors such as the NSAIDS (e.g.

mefenamic acid, ibubrufen, diclofenac sodium or naproxen) have
been effectively used for symptomatic relief. NSAIDS may be
preferred by women who do not wish to use hormone and prefer
to take medication for as short time as possible. The chosen
medication is taken at the first sight of pain and continued for 5
days.

b) TO SUPPRESS OVULATION
Oral contraceptives (combined estrogen/progestogen pill) are
another option, as it suppresses ovulation and decreases
prostaglandin levels. It is now generally accepted that combined
oral
contraceptives
are
highly
effective
in
relieving
dysmenorrhoea, perhaps by decreasing endometrial production.
The women can remain on the pill as long as necessary provided
there is no contra-indication of taking the oral contraceptive pill.
However, the following are guideline:

Stop after 2 years or so to see whether it is still painful or not.

If still painful may carry on.
Stop it if she wants to get pregnant.
It tends to disappear after pregnancy. Hence may not require
after child birth.

c) SURGERY

Cervical dilation to treat dysmenorrhea was used with some

success for many years. It has been suggested that cervical
dilation may result in more efficient blood flow during
menstruation, leading to less accumulation of blood and
prostaglandins in the uterus, thereby decreasing contractility and
pain. However, cervical dilation should not be used as a primary
treatment mode for primary dysmenorrhea.

Presacral neurectomy is of value in treating dysmenorrhea,

but it should be used only after all others of therapy have been
exhausted.

SECONDARY DYSMENORRHOEA
Secondary or congestive dysmenorrhoea is defined as a painful periods
owing to pelvic disease. Secondary dysmenorrhoea is caused by a
physical condition. Women who suffer from it tend to be older than
those with primary dysmenorrhoea.
Features
It usually occurs middle-aged women.
The pain of secondary dysmenorrhoea usually begins few days
before the menses and gradually increases in severity as menses
approach.
The pain is felt in the pelvis and back and made worse by exertion.
The pain is constant rather colicky and is often associated with back
pain, deep dyspareunia and sometimes menorrhagia.
Causes of secondary dysmenorrhoea
Some conditions that may be responsible for dysmenorrhoea are:
Adenomyosis

Endometrial polyp

Endometriosis

Fibroids

Pelvic infection (PID)

Intrauterine device

Fig 1.1 Causes of secondary dysmenorrhoea.

1.
2.
3.
4.
5.
6.
7.

Adenomyosis.
Endometriosis.
Endometrial polyps
Fibroids
Pelvi inflammatory disease (PID)
Use of intrauterine device (IUCD)
Narrowing of the cervix (outflow obstruction)

Management of secondary dysmenorrhoea

The approach in managing a woman with secondary dysmenorrhoea
can be summed up as follows:
1. TO DETERMINE THE CAUSE :
History is important:
A complete history should be taken with special reference
to the menstrual cycle.
Documentation of previous history of pelvic infection,
fibroids, endometriosis is important.
The use of intrauterine device. Are there any
complications with IUCD usage?

Examination:
A careful pelvic examination with special attention to
detecting endometriosis, pelvic inflammatory disease,
pelvic masses or uterine enlargement should be made.

Investigations:

Ultrasound to detect the presence of myomas,

endometrial polyps, and uterine abnormalities.
Hysteroscope can inspect the uterine cavity for
endometrial polyps or submucous myomata.
Laparascope may be necessary to diagnose pelvic
infection, adenomyosis or endometriosis.

2. TO RELIEVE SYMPTOMS :
Analgesics
Symptomatic relief can be achieved with analgesic drugs
such as aspirin, codeine.

Prostaglandin synthesis inhibitors

Drugs which inhibit the production of prostaglandin in the
endometrium (such as mefenamic acid, ibubrufen,
diclofenac sodium or naproxen) may diminish myometrial
contractions and therefore relieve dysmenorrhoea.

3. TO TREAT THE UNDERLYING CAUSE :

Adenomyosis
Adenomyosis may be treated medically or surgically
depending on the need of the patient.

Endometriosis
Hormonal therapy and conservative surgery are the best
form of treatment for younger women and who plans for
future pregnancy. Hysterectomy is preferred for older
women and women who have completed their family.

Endometrial polyps
Polyps are generally removed by means of hysteroscope.

Fibroids
Fibroids may require myomectomy or hysterectomy.

Pelvic infection (PID)

Pelvic inflammatory disease can be effectively treated
with combination of appropriate antibiotic.

Intrauterine device (IUCD)

If an intrauterine device is the cause for the painful period
therefore it should be removed and offer an alternative for
contraception.

Cervical narrowing
Cervical dilation to treat dysmenorrhoea was used with
some success

MENORRHAGIA
- When Period Are Too Much -

UTERINE POLYPS

FIBROIDS

ENDOMETRIAL
HYPERPLASIA
Fig. 1.1

MALFORMATION OF
UTERUS

Causes of menorrhagia.

Heavy periods, longer periods, shorter cycles and premenstrual spotting

are common menstrual disorders amongst women in theirs 40s and
early 50s.
MENORRHAGIA is defined as abnormal uterine bleeding that is
characterized by excessively heavy or prolonged bleeding with regular
menstruation; it may be constitutional or acquired.
The average amount of blood loss during normal menstrual period is 40
to 50 ml. With menorrhagia, a woman may loss 80 ml or more.
Excessive loss can be due to menses which are too long, too frequent,
too heavy, and/or too irregular.
Women with the following risk factors are more likely to have
menorrhagia.
Obesity.
Estrogen administration (without progestin).
Young women who have not established a regular ovulation cycle.
Women who are approaching menopause.
FACTORS THAT INFLUENCE NORMAL MENSTRUATION
At the time of menstruation, various factors play a part to control
excessive bleeding. This include,

Spontaneous haemostatic plug formation.

Vasoconstriction and occlusion of the spiral arterioles by endothelial
proliferation.
Heparin like activity with plasminogen activation and fibrinolysis.

Activities of the various protanoids.

All the above factors are involved in the control of normal

menstruation.
Influences and changes in these activities cause
excessive bleeding.

CAUSES OF MENORRHAGIA
Menorrhagia is excessive uterine bleeding, which may be caused by a
variety of causes. This can be classified under three groups namely: SYSTEMIC CAUSES
GENITAL (LOCAL) CAUSES
HORMONAL CAUSES

Systemic causes include

Blood dyscrasias
Endocrine disorders
Psychiatric disorders

Blood dyscrasias or diseases are rare causes of menorrhagia.

However
menorrhagia
may
occur
in
acute
leukaemia,
thrombocytopenic purpura and hereditary capillary fragility (von
Willebrands disease).
Endocrine disorders such
myxoedema) cause menorrhagia.

as

hypothyroidism

(particularly

Psychiatric disorders: Women treated for psychosomatic

disorders may temporary develop heavy or frequent menses which
resolve when these disorders improve. Menstrual disturbances in this
case are due to disturbances of pituitary functions.

Local or Genital causes:

The causes of menorrhagia under this group includes:

Anatomical causes
Traumatic causes
Infective causes
Hyperplasia of endometrium
Malignant causes

 Anatomical causes include conditions of the uterus such as;

1. Congenital malformation of the uterus, e.g. Double uterus
may causes heavy menses because of increases surface area of
endometrium.
2. Fibroids are very common cause of menorrhagia. Submucous
fibroids are those most likely to causes abnormal bleeding or
menorrhagia as the overlying endometrium is shed in patches.
Intramural fibroids, if small, may not cause symptoms; if larger,
they may distort the endometrial cavity and increase the surface
area from which the bleeding occurs. Subserous fibroids do not in
general affect the menstrual pattern.
3. Endometrial polyps are also involved in the causation of
excessive menstrual bleeding.
4. Diffuse adenomyosis causes gradual increase in menstrual
flow.
Traumatic causes - The most common cause in this category is the
intrauterine contraceptive device (IUCD). This IUCD may cause trauma
to the endometrium and interfere with the normal uterine contraction
which eventually result in excessive menstrual flow (menorrhagia).
Infective condition - of the pelvis (generalised chronic
inflammatory disease, low grade endometritis) is an all too common
cause of irregular, heavy menses.

Fig.1.2 Organic causes of menorrhagia.

GROUP
ANATOMICAL

CONDITIONS

PATHOGENESIS

UTERUS
Congenital malformation Double uterus

Increases the surface

area of endometrium
Fibroids mainly submucous type

Increases the surface

area from which the
bleeding occurs
Uterine polyps

Increases the surface

area of bleeding
Diffuse adenomyosis

Enlarge
increase
bleeding
TRAUMATIC

uterus
area

INTRAUTERINE CONTRACEPTIVE DEVICE (IUCD)

Traumatize
endometrium
interfere with
contraction
HYPERPLASIA
OF
ENDOMETRIUM

with
of

the
and
uterine

ENDOMETRIAL HYPERPLASIA

Thickened endometrial
tissue increases more
menstrual bleeding

NEOPLASTIC
GROWTH

UTERUS Malignancy growth of the uterus

Endometrial carcinoma

OVARY - Functioning ovarian tumours (eg. Theca cell

and granulosa cell tumours)

Estrogen effect on the

endometrium.

 Hyperplasia of endometrium various forms of hyperplasia of the

endometrium (cystic, adenomatous, atypical) is another frequent
cause of menorrhagia. Endometrial hperplasia may be related to
fluctuating unopposed estrogen level from the premenopausal ovary.
Neoplastic growths - Malignancy of the endometrium are involved
in the causation of abnormal uterine bleeding and excessive menstrual
bleeding. Occasionally, functioning ovarian tumours (theca cell and
granulosa cell tumours) or cyst may present with abnormal or
excessive uterine bleeding.

HORMONAL
In a normal menstrual cycle, there is a balance between estrogen and
progesterone, two hormones in the women body. These hormone
regulate and buildup of the endometrium, which is shed each month
during menstruation. Menorrhagia can occur because of the imbalance
between estrogen and progesterone. As a result of the imbalance, the
endometrium keeps building up. When it is eventually shed, there is
heavy bleeding. Because hormone imbalances are often present in
adolescents and in women approaching menopause, this type of
menorrhagia known as dysfunctional uterine bleeding (DUB) is fairly
common in these groups. About 65 per cent of the cases with
menorrhagia are due to dysfunctional uterine bleeding.
Dysfunctional uterine bleeding is defined as abnormal bleeding from
the uterus not due to organic disease (anatomical, infective, traumatic
or neoplastic causes).
Dysfunctional bleeding may be ovulatory
(usually due to insufficient production of progesterone in the luteal
phase of the cycle) or more usually anovulatory. In a woman with
anovulatory cycles, low levels of estrogen result irregular and
prolonged bleeding, whereas high levels of estrogen lead to
amenorrhoea and then heavy bleeding as the endometrium is shed
patchily.
CLINICAL PRESENTATIONS OF MENORRHAGIA
The usual presentations of a woman with menorrhagia are those
related to the menstrual pattern and the sequel of the excessive blood
loss. This includes,

Excessive menstrual flow (varies greatly from woman to woman).

Menstrual period lasts for more than 7 days.
Large clots of may pass.
Paleness and fatigue (anaemia).

INVESTIGATING A WOMAN WITH MENORRHAGIA

Any woman presenting with menorrhagia for several months should be
investigated as follows,
HISTORY TAKING:
An accurate history should be obtained whenever possible.
a)

Description of the menstrual cycle:- A complete description

of the pattern of bleeding (e.g:- cycle length, duration of flow,
regularity of the cycle, amount of blood loss, any association with
clots) is usually more helpful and vital.
Postcoital bleeding
requires thorough investigation and should always be asked about.

b)

Dysmenorrhoea (painful period) and dyspareunia (pain with

intercourse) should be enquired about. Pain with bleeding is more
likely to indicate an organic than functional cause. The possible
organic causes (Table 1.1) include fibroids, endometrial polyps,
enddmetriosis, adenomyosis, and pelvic inflammatory disease.

c)

Possible pregnancy should always be considered in

premenopausal years occasionally an unsuspected pregnancy
presents with bleeding as a complication.

d)

Usage of contraceptive device: The possible presence of an

intrauterine contraceptive device (IUCD) should not be overlooked.

EXAMINATION:
A comprehensive examination should be made. Examination should be
general and specific. The presence of anaemia should be sought.
Thyroid enlargement need to be checked.
Evidence of
coagulopathies, liver disease or systemic malignancies should
not be overlooked, because occasionally this condition may present
with prolonged and heavier periods.

Abdominal examination should always precede vaginal examination.

On vaginal examination it is important to inspect the cervix and
vaginal walls. Blood may be seen issuing through the cervical os.
Cervical polyps, ectropion (erosion), or infective vaginitis may be
noted. Inspection should be followed by bimanual palpation, although
in obese patients the size and shape of the uterus and adnexae may
be difficult to determine.
INVESTIGATION:
Specific laboratory tests need to be checked. These include a full
blood picture, including a coagulation screening if indicated. Thyroid
function may need to be checked and screening for diabetes may be
indicated. Pap smear is mandatory for any woman who has not
recently had one.
If a woman is over the age of 35 it is usual to investigate further. The
additional tests are:
a) Ultrasound: This is a non-invasive method of imaging the uterine
cavity. The vaginal probe (transvaginal ultrasound) is particulary
useful.
An experience operator should be able to accurately
measure endometrial thickness, dtect endometrial irregularities,
outline the uterine contour, and detect congenital malformation of
the uterus, fibroids and adnexal masses.

Using ultrasound to demonstrate

Using ultrasound to demonstrate

Uterine Myoma (M).

Endometrial polyp (P)

Fig. 1.3 Ultrasound procedures

b) Hysteroscopy: Direct inspection of the interior of the cervical

canal and uterus by hysterscopy is a part of gynaecological
examination which can be performed either with or without local
anaesthesia. Hysterscopy is usually accompanied by some form of
direct endometrial sampling.
Mobile pedunculated polyps,
submucous fibroids, endometrial hyperplasia ,and even endometrial
cancer can be detected by hysteroscopic examination.

Fig. 1.4 Hysteroscope view showing the diagnosis of submucous and intracavitary
fibroids

c) Histology (Diagnostic curettage): In the absence of any

pathology visible at laparoscopy, histology of the endomentrial
biopsies provides useful information about the hormonal status.
This procedure is invasive and is performed under general
anaesthesia.
It is performed between bleeding episodes.
Diagnostic curettage should be carried out in women of 35 years of
age or over.
d) Laparoscopy: On occasion, laparoscopy may be indicated when
condition, such as uterine fibroids, endometriosis or pEelvic
infection are suspected.

TREATMENT

Treatment is directed at both the cause of bleeding and the needs of

the particular woman after consideration of her age, lifestyle, parity
and wishes regarding pregnancy in the future. In about a third of the
patients, mere reassurance (when there is no underlying pathology) is
sufficient while the rest may require either medical or surgical
treatment.
Correction of iron deficiency anaemia and attention to diet, exercise
are an important form of treatment. Any endocrine abnormalities such
as hypothyroidism need to be corrected. Removal of the intrauterine
contraceptive device may be required if this is the contributing cause
of menorrhagia.
Emergency Treatment
In situation of severe uterine bleeding whilst investigations are being
arranged, large doses of progestogen (e.g. 30 mg norethisterone daily)
continued over several days are usually effective (if the underlying
cause is benign). Alternatively, injectable conjugated estrogens can
be given for several days.

Medical Treatment
The drugs that can be used are:
1. Nonsteroidal anti-inflammatory drugs (NSAIDs), e.g mefenamic
acid, and naproxen.
2. Hormones Progestogens
Estrogens
3. Danazol
4. Gonadotrophin-releasing Hormones Agonist (GnRH agonist)
5. Antifibrinolytic Agents

NSAIDS: Nonsteroidal anti-inflammatory preparations such

mefenamic acid and naproxen may reduce the amount of bleeding
and also any associated dysmenorrhoea, especially if taken
immediately before the onset of a period.In

Progestogens: The most commonly used progestogens are oral

medroxylprogesterone acetate and norethisterone.
These

treatments are extremely useful in patient with

uterine bleeding or benign endometrial hyperplasia.
are taken from day 14 or 16 of the cycle for 10
withdrawal bleeding occurs two to three days after
course.

dysfunctional
Progestogens
to 12 days
stopping each

Initially, quite high daily doses of progestogen (20 to 30 mg

medroxyprogesterone, or 10 to 15 mg norethisterone ) may be
required, or treatment may need to be given from day 5 to day 26.
After several cycles the dose can be reduced. The preparations are
usually well tolerated. Side effects include mild weight gain,
bloating and mood changes.
In some women, injectable
medroxyprogesterone acetate, giving complete amenorrhoea, is
useful.

Estrogens: Estrogens may be combined with a progestogens in a

cyclical form. This may be in the form of the oral contraceptive pill
in younger women, or synthetic estriol, estradiol or other forms of
hormone replacement with progestogens, in older women. The
combination will bring about regular withdrawal bleeds of
acceptable duration. The use of estrogens may be associated with
breast tenderness, nausea and headaches.
Estrogen should be used with caution in the presence of fibroids of
any size, whose growth may be stimulated.

Danazol: Danazol may be used for short periods of time to shrink

fibroids prior to myomectomy. This drug can be useful in patients
with severe menorrhagia who are responsive to progestogens. This
hormone in a dose of 200mg a day may be chosen. If this dose does
not control the bleeding it is increase to 400mg a day. Danazol
usually cauases complete amenorrhoae and have quite marked side
effects, including weight gain, acne, mood changes and deeping of
voice.

GnRH Agonists: Like danazol, GnRH agonists may be used for

short periods of time to shrink fibroids prior to myomectomy. GnRH
agonists may cause hot flushes, vaginal dryness and loss of bone
mineral.

Antifibrinolytic Agents: Tranexamic acid is an inhibitor or

endometrial fibrinolysis that has been used for the treatment of

menorrhagia. It is reported to reduce blood loss in dysfunctional

uterine bleeding and that associated with fibroids by 50 %.

Surgical Treatment
If an underlying organic condition is causing menorrhagia, it should be
treated. Surgical treatment may be either conservative surgery or
radical surgery (hysterectomy).
a) Conservative surgery :
RESECTION
Submucous fibroids, as well as endometrial polyps, can usually be
resected under direct vision through the hysteroscope; this technique
frequently provides enormous relief of menorrhagic symptoms.
MYOMECTOMY
Intramural fibroids causing symptoms may be amenable to removal at
myomectomy, either by laparotomy or (on occasion) laparoscopically.
Myomectomy is most suitable for woman who wishes to try to
conceive, or at least conserve her reproductive potential. Patients
should always be aware that myomectomy may prove technically
impossible and that hysterectomy may be necessary.
TRANSCERVICAL RESECTION OF ENDOMETRIUM (TCRE)
TRCE or endometrial ablation, under direction hysteroscopic vision has
proven its usefulness in the treatment of menorrhagia. The concept of
this procedure is that by ablating the basal layer of endometrium,
endometrial regeneration is prevented or reduced and menorrhagia is
cured. Preparation of the endometrium with danazol or progestogen is
commonly practiced; this is to reduce endometrium thickness.
Endometrium is either resected, or destroyed using the rollerball
diathermy or laser.

b) Radical surgery Hysterectomy:

For many women with fibroids who have completed their families,
hysterectomy (abdominal or vaginally) may be the initial treatment of
choice and continues to be widely practised.

SUMMARY
In all cases, the management of menorrhagia depends upon the age of
the patient, parity and its severity. The gynaecologist should come to
a proper diagnosis before embarking on the necessary treatment.

DYSFUNCTIONAL UTERINE BLEEDING

Dysfunctional (or abnormal) uterine bleeding (DUB) is a problem that
often affects women as they start to get periods and as they get closer
to menopause. Dysfunctional uterine bleeding is best defined as an
abnormal bleeding from the uterus which is not due to any organic
disease of the genitalia tract. DUB isnt caused by a specific condition

such as polyps or uterine fibroids, cancer, inflammatory disease, or

complication of pregnancy.
DUB occurs because of a hormonal imbalance in the body. It may be
somewhat reassuring for a woman to know her DUB isnt caused by
disease, but it is still troublesome and must be investigated and
treated.
CAUSES
A womans normal hormonal cycle depends upon a delicate balance
between a number of hormones (gonadotrophins, ovarian hormones,
and probably endometrial prostaglandins).
There are many possible causes of hormonal imbalance that may
result in dysfunctional uterine bleeding. For example, if a woman fails
to ovulate her ovary wont receive a cue to produce a hormone called
progesterone. Progesterone is needed to regulate the endometrium,
which is discarded during menstruation. Without progesterone, the
endometrium keeps growing until it starts to break down and is shed
during a very heavy period.
The endometrium may also shed
incompletely and irregularly, and bleeding becomes irregular or
prolonged. Lack of ovulation is a major cause of DUB in women
approaching menopause. Because hormone imbalances are often
present in adolescents and in women approaching menopause,
dysfunctional uterine bleeding is fairly common in these groups.
TYPES OF DYSFUNCTIONAL UTERINE BLEEDING
There are two types of dysfunctional uterine bleeding:
1. Ovulatory DUB

The causes is unknown, but may be mediated through

prostaglandins. There is no consistent endocrine abnormality.
The endometrium is normal.

In ovulatory DUB the heavy bleeding is due to a poor luteal

phase. The luteal phase may be short or long

Features of ovulatory DUB :

-

Heavy regular menses in the 35 to 45 year old woman.

The affected woman often complains of lower abdominal

discomfort and dysmenorrhoea.

2. Anovulatory DUB

In women with anovulatory DUB there are persistently high

estrogen levels causing 6-8 weeks amenorrhoea followed by
prolonged bleeding. The pattern is irregular.

The unopposed estrogen levels are high, resulting in an

increased thickness of endometrium. Endometrial shedding
takes place once the oestrogen level falls. The endometrial
shedding is irregular and incomplete and is associated with
excessive blood loss.

The causes of anovulation are obesity, hypothyroid,

hyperprolactinaemia, or polycystic ovarian disease. Obesity
leads to pheripheral conversion of androgen to oestrogen.

Features of anovulatory DUB :

-

Usually a prolonged cycle ends in heavy and irregular

bleeding.
It is commonest at the extremes of menstrual life.
It can occur as part of the polycystic ovarian disease.
Affected women are usually obese.

PRESENTATION
Dysfunctional uterine bleeding
reproductive age woman.

affects

about

9%

to

12%

of

The main symptoms are prolonged and/or irregulary bleeding. The

bleeding may be irregular spotting during the cycle, but sometimes the
bleeding is so heavy that a woman cant participate in her normal dayto-day activities.
The amount and frequency of abnormal or excessive bleeding can vary
and change over time. Some women may have other symptoms such
as:
cramping or discomfort
inability to do usual activities
tiredness
anaemia

feeling of sadness or nervousness

MAKING A DIAGNOSIS OF DUB

Diagnosis of dysfunctional uterine bleeding is made after the exclusion
of organic diseases of the genitalia tract. The steps taken to diagnose
dysfunction uterine bleeding are: history, examination, and special
investigations.
HISTORY
A detailed menstrual history is very important, which includes:-

the pattern of the cycle.

an assessment of the blood loss.
the presence or absence of associated menstrual symptoms.
symptoms of endocrine or other organic disease.
the patients background, home , marital circumstances.
any history of emotional stress or psychiatric abnormality.

Examination
The general condition of the women must be assessed and any
endocrine or systemic disease excluded. An internal examination of
the reproductive organs (pelvic examination) must be performed in
every women complaining of menstrual abnormalities.
Special tests
Special tests are needed to ensure no medical or organic conditions
are causing dysfunctional uterine bleeding. These tests are commonly
used to explore dysfunctional uterine bleeding. These include:
haematological
endocrine
ultrasonography
endometrial biopsy
hysteroscopy
laparoscopy
dilation and curettage (D&C)
a) Haemological investigation
- All cases of dysfunctional uterine bleeding must have a
haemoglobin estimation. Persistent or unexplained dysfunctional
uterine bleeding should have a blood smear, platelet count,
bleeding test to exclude haematological causes for the bleeding.

b) Endocrine investigation
- When there are clinical suspicion of associated endocrine disease
endocrine test may be required, such as :
- Thyroid fuction test
- Serum prolactin
- Serum FSH , LH
c) Ultrasound
- Ultrasonography are non-invasive method of imaging the uterine
cavity. The presence of uterine myoma, ovarian cyst can be
detected. Thickness of the endometrium can be measured.
d) Hysteroscopy
- Using a hysteroscope the uterine cavity can be inspected for
polpys, submucous fibroids and endometrial hyperplasia can be
inspected.
e) Laparoscopy
- Laparoscopy is useful in the diagnosis of endometriosis, pelvic
inflammatory and unsuspected ovarian tumours.;
f) Endometrial biopsy
- Endometrial biopsy involves removing a small of uterine tissue for
histological examination. This procedure can be performed as day
surgery.
g) Dilation and curettage
- Dilation and curettage is an invasive procedure which is
performed under general anaesthesia. It is usually performed in
the second half of the cycle and preferably 5-6 days before
menstruation. The objects of the curettage are for,
diagnostic
therapeutic effect
If no organic cause for the abnormal uterine bleeding is found, a
diagnosis of dysfunctional uterine bleeding is made.
TREATMENTS
If investigations show a hormone imbalance and no underlying medical
cause, there are several possible approaches to the treatment of
dysfunctional uterine bleeding:
1.

Watchful waiting (monitoring the

treating it).

DUB for a few months before

2.
3.
4.
5.

Hormonal therapy
Dilation and curettage
Endometrial ablation
Hysterectomy

The treatment will depend on a womans age, other medical

conditions, and the seriousness of the bleeding.
HORMONAL THERAPY
When a hormone imbalance causes dysfunctional uterine bleeding,
horme therapy is often the first treatment of choice. It is certainly
more effective than watchful waiting and probably more effective
than dilation and curettage. When hormone therapy works, it offers
very good relief from dysfunctional uterine bleeding. Hormone
treatment may be the first option considered for younger women.
Hormone therapy consists of:
1.

ORAL CONTRACEPTIVE PILLS

Oral contraceptive pills containing synthetic forms of the
hormone estrogen and progesterone may be prescribed to
make menstrual periods lighter and more regular.

2.

PROGESTOGENS
Often a woman receives therapy only with a progestogen.
Progestogen helps to balance the effect of oestrogen, the
hormone that causes the endometrial tissue to grow during the
menstrual cycle. As a result, the endometrium does not grow
as much and so bleeding decreases.
Either norethisterone (5-15 mg daily) or medroxyprogesterone
acetate (10 mg twice or three times daily) is given from day 5
to day 25 of the menstrual cycle for 4-6 menstrual cycles.

3.

4.

DANAZOL
Sometimes a drug called danazol is prescribed for short-term
treatment of dysfunctional uterine bleeding. Danazol affects
sex hormones and their production, which causes menstrual
bleeding to stop completely within a month or so. Danazol is
most often used for women who are near menopause.

Staring dose of 200 mg a day may be chosen. If this does does

not control the bleeding it is increased to 400 mg a day.

Some possible undesirable side effects are dcreased breast

size, acne, weight gains, muscle pains as well as deepening of
the voice.

GnRH Agonists
Agents called gonadotropin-releasing hormone (GnRH) agonist
may be prescribed for short-term treatment of dysfunctional
uterine bleeding. GnRH agonists cause the body to suppress
oestrogen production and ovulation.
Menstrual bleeding
therefore stops or is very much decreased. A problem with
GnRH agonists is that long term use increases the risk of
osteoporosis.

DILATION AND CURETTAGE (D&C)

Dilation and curettage used to be widely employed to treat
dysfunctional uterine bleeding, although today it is usually a testing
tool, like ultrasonagraphy, hysteroscopy, and endometrial biopsy.
By removing the excessive endometrium, D&C may prevent
dysfunctional uterine bleeding but perhaps only temporarily. Many
women experience relief for a few menstrual cycles before
dysfunctional uterine bleeding returns.
ENDOMETRIAL ABLATION
Endometrial ablation a method of removing the uterine lining to
prevent dysfunctional uterine bleeding is an option open to more and
more women with dysfunctional uterine bleeding. In many cases
endometrial ablation can be considered instead of hysterectomy. In
some cases, among very carefully selected women, some preliminary

studies have shown that endometrial ablation may be very effective in

providing long-term relief from dysfunctional uterine bleeding.
Like hysterectomy, endometrial ablation is usually an option for women
whose dysfunctional uterine bleeding hasnt been successfully treated
with hormone therapy. Ablation may also be particularly appropriate
for women who do not want more children, as pregnancy isnt possible
afterwards.
The concept of endometrial ablation is that by ablating the basal layer
of the endometrium, endometrial regeneration is prevented or reduced
and excessive bleeding is cured.
Endometrial ablation involves the use of a tube-like medical instrument
that incorporates an electric current, laser, heated balloon, or other
devices. The instrument is inserted through the vagina into the uterus,
and the fluid is placed directly into the uterus to expand it.
The
endometrium layer is removed by using roller ball electrocoagulation,
loop resection or by laser.
This ablation procedure should only be
performed by a gynaecologist experienced in the technique, or the
results will be poor and the women may be at risk of severe
complications.
Possible risks with ablation include perforation of the uterine wall and
fluid overload from the fluid used to inflate the uterus.
HYSTERECTOMY
The place of hysterectomy in the treatment of dysfunctional uterine
bleeding depends upon the age of the patient, other medical
conditions, and the seriousness of the bleeding. Hysterectomy should
be the last resort. The women must have the opportunity to the
choices of treatment if hysterectomy is recommended to her.

PREMENSTRUAL SYNDROME

Premenstrual syndrome: Taking Control of Symptoms

PREMENSTRUAL SYNDROME, or PMS, is a phenomenon that wasnt

even discussed a generation ago. Now, practically every woman
knows the symptoms of PMS and probably discussed them with other
women. Much about the condition is still unknown and there is little
consensus on its etiology, epidemiology, diagnostic criteria and
effective therapy.
DEFINITION
As such, there is no satisfactory definition of premenstrual syndrome.
PMS consists of various physical and/or emotional symptoms that occur
in the second half of the menstrual cycle, after ovulation.
The
symptoms begin about midcycle and are generally the most intense
during the last seven days before menstruation. Fortunately, a woman
obtains relief when her menstrual period begins. Another feature of
PMS is a symptom-free time for several days every month, in the first
half of the menstrual cycle.
PATIENT PROFILE
Premenstrual syndrome tends to occur in the second half of menstrual
life that is after the age of 30. In about 25 per cent symptoms begin
with menarche. Symptomatology becomes more severe with age.

Women with PMS are likely to develop a major affective illness in the
future. It occurs in all races and classes and differs only in the type of
symptoms.
ETIOLOGY-PATHOPHYSIOLOGY
Theres still some disagreement about what causes PMS. There may be
a genetic component, but the current theory is that PMS is
multifactorial. But it definitely seems to be linked to hormones. PMS
symptoms occur in the second half of the menstrual cycle: at this time,
production of female hormone progesterone increases. Then, about
seven days before the menstrual period, production of both
progesterone and estrogen decreases dramatically. Many women find
that PMS worsens as they get older; this also suggests a hormonal role.
Several mechanisms have been proposed
pathophysiology of premenstrual syndrome.

for

the

etiology-

1. Steroids :
a) Low progesterone: It was hypothesised that women with PMS
have lower progesterone levels, higher estradiol levels and
therefore an altered estradiol-progesterone ratio.
b) Low estradiol: Recently this has been postulated as a possible
cause of PMS.
2. Fluid imbalance :
Alteration in angiotensine and aldosterone has been postulated.
They are responsible for weight gain, abdominal bloating and
edema.
3. Nutrition :
Hypoglycemic episodes have been implicated in emotional
outbursts.

4. Prolactin :
Elevation of this hormone in the luteal phase might be
responsible for some of the symptoms.

5. Prostaglandins :
Level of PGF 2 and PGE are known to be elevated in the luteal
phase. Prostaglandins have been associated with symptoms of
cramping, discomfort, headache and depression.
6. Opioids :
Opioid activity is influenced by the fluctuating levels of gonadal
steroids througout the menstrual cycle. All opioids are elevated
in the luteal phase of the menstrual cycle. It is hypothesized that
the period of highest opioid secretion is associated with features
of depression as noted in PMS.
7. Neurotransmitter alteration :
Many of the central nervous system neurotransmitters that are
altered in depression such as serotonin, dopamine and
norepinephrine have been thought to be altered in the luteal
phase of the menstrual cycle.
CLINICAL PRESENTATION
Generally, PMS is recognizable because it comes and goes at the same
time each month. Patients can present in one of 3 ways:1. A situational depression.
2. An
underlying
psychiatric
disorder
with
premenstrual
exacerbation of their illness and moods swing consistent with
PMS.
3. About 50 % of patients with true PMS symptoms related to the
menstrual cycle. They have a symptom free follicular phase.
Symptoms occur mainly in the luteal phase.

Several different symptoms can accompany PMS.

Some of the physical symptoms are:

Acne.
Backache
Bloating.
Fatigue
Headache
Sore breasts.
Weight gain.

Emotional symptoms might include

Changes in sexual desire.
Depression.
Difficulty concentrating.
Difficulty handling stress.
Irritability.
Tearfulness.
ASSESSMENT
Careful evaluation is of prime importance so that a proper diagnosis is
made and effective instituted. Generally, PMS is recognizable because
it comes and goes at the same time each month. Patients should keep
a PMS diary of their symptoms. This will help to determine whether
PMS follow a monthly pattern. Also symptoms charting helps to
determine which symptoms are the most disturbing and on which day
treatment is needed.
THE MANAGEMENT OF PMS
Theres no cure for PMS, self-help measures can ease symptoms. As
the presentation of PMS is diverse, no single treatment modality works
for all patients. The therapeutic approach must be tailored to the type
and severity of patient symptomatology. Initial treatment should
consist
first
in
explanation,
reassurance
and
supportive.
Approximately 30 % of patients repond to this form of therapy.
Diet:
Diet and exercise are important. Many women find that a
balanced diet and healthy snacks are helpful, as are avoiding
caffeine and reducing salt intake.
Vitamin, mineral supplements:

Some women believe that vitamin B6 (pyridoxine), magnesium,

evening primrose oil, and some other herbal preparations are
useful, although there are no scientific studies to prove.

Medical treatments are available for women with especially severe

PMS. The objectives of medical treatment are to reduce the most
distressing symptoms.
a) Severe fluid retention:
In cases with severe fluid retention, diuretics such as
chlorothiazide, 0.5 g. twice daily for 3 days at a time may help.
Diuretics can reduce bloating.
b) Breast tenderness:
Bromocriptine 2.5 mg twice daily may relieve breast symptoms
but has no other benefits.
c) Nervous tension :
Nervous tension may be relieved by transquillizers.
d) Hormonal treatment :
Hormonal treatment helps some cases of severe intractable PMS.
Estrogens, progestogens, and androgen have all been used.
Progestogens give the best results and are given in the form of
oral progestogens.

Norethisterone acetate may be given in a dose of 5 mg three

times a day for 10 days beginning on the 15th day of the cycle.

Dydrogesterone 10 mg once or twice daily can also be used.

Oral contraceptive pill has been prescribed with varying rates of

success in relieving PMS.

10
THE MENOPAUSE
Menopause is a universal and irreversible part of the overall aging
process involving a womans reproductive system, after which she no
longer menstruates as a result of decreasing ovarian function.
Climacteric is the general term for the time from the period of this
transition to the early postmenopausal phase of a womans
reproductive life cycle.
Perimenopause refers to the time before menopause when vasomotor
symptoms and irregular menses often commence. Menopause, by
definition, begins 12 months after the final menses and is
characterized by a continuation of vasomotor symptoms and by
urogenital symptoms such as vaginal dryness and dyspareunia.
Menopause may be
natural,
artificial, or
premature.
Natural menopause occurs at an average age of 50 to 51 yr. As
ovaries age, response to pituitary-produced gonadotropins (folliclestimulating and luteinizing hormones) decreases, initially with
shorter follicular phases (hence, shorter cycles),
fewer ovulations,
decreased progesterone production, and
more cycle irregularity.
Eventually, the follicle fails to respond and, without feedback of
estrogen, the circulating gonadotropins rise substantially. Circulating
levels of estrogens and progesterone are markedly reduced; androgen
(androstenedione) is reduced by half, but testosterone decreases only
slightly.
This transitional phase beginning before menopause and continuing
after it, during which a woman passes from her reproductive stage, is
properly referred to as the climacteric, although most people refer to
it also as menopause.

Premature menopause refers to ovarian failure of unknown cause

that occurs before age 40. Premature menopause is associated
Smoking is associated with early menopause.
Radiation exposure,
Chemotherapeutic drugs, and
Surgery that impairs ovarian blood supply can also hasten
menopause.
Artificial menopause follows oophorectomy or radiation of the pelvis,
including the ovaries.

Physiology:
Menopause results from loss of ovarian sensitivity to gonadotropin
stimulation, which is directly related to follicular decline and
dysfunction. The oocytes in the ovaries undergo atresia throughout a
womans life cycle, and both the quantity and quality of follicles
undergo a critical decline approximately 20-25 years after menarche.
Thus, the variable menstrual cycle length during perimenopause can
be due to anovulation or to irregular maturation of follicles. Hormonal
fluctuation may not be responsible for all irregular bleeding during this
period; therefore, pelvic pathology (e.g. uterine fibroids, uterine polyps,
endometrial hyperplasia, endometrial cancer), which becomes more
prevalent during this time, must be excluded.
A shorter menstrual cycle length is the most common change in
menstrual cyclicity that occurs during the perimenopausal period in
women who have no pelvic pathology and who continue to be
ovulatory. The follicular phase of the menstrual cycle shortens because
of the decreased number of functional follicles. Because these follicles,
which are stimulated by follicle-stimulating hormone (FSH) during the
first part of the menstrual cycle, have declined in number, less
recruitment of oocytes occurs and the follicular phase shortens
accordingly. However, once ovulation occurs, the luteal phase remains
fairly constant, at 14 days.
Over time, as aging follicles become more resistant to gonadotropin
stimulation, circulating FSH and luteinizing hormone (LH) levels
increase. Elevated FSH and LH levels lead to stromal stimulation of the
ovary, with a resultant increase in estrone levels and a decrease in
estradiol levels. Inhibin levels also drop during this time because of the
negative feedback of elevated FSH levels. With the commencement of
menopause and a loss of functioning follicles, the most significant

change in the hormonal profile is the dramatic decrease in circulating

estrogen levels. Without a follicular source, the larger proportion of
postmenopausal estrogen is derived from ovarian stromal and adrenal
secretion of androstenedione, which is aromatized to estrone in the
peripheral circulation. Testosterone levels also decrease with
menopause, but this decrease is not as marked as the decline in 17estradiol
With cessation of ovulation, estrogen production by the aromatization
of androgens in the ovarian stroma and production in extragonadal
sites continue, unopposed by progesterone production by a corpus
luteum. Perimenopausal and menopausal women are thus often
exposed to unopposed estrogen for long periods, which can lead to
endometrial hyperplasia, a precursor of endometrial cancer. Estradiol
levels decrease significantly because of loss of follicular production
with menopause and postmenopause, but estrone, which is aromatized
from androstenedione from nonfollicular sources, is still produced and
is the major source of circulating estrogen in the postmenopausal
female.
Androgen-to-estrogen aromatization can occur in adipose tissue,
muscle, liver, bone, bone marrow, fibroblasts, and hair roots. Because
most conversion of androgens to estrogens occurs in adipose tissue, it
is frequently assumed that obese women, who have more circulating
estrogen, should have fewer complaints of vasomotor symptoms.
However, this is not always the case, and vasomotor symptoms of
menopause can be as frequent and severe in heavier women as they
are in thinner women.
The clinical indication that menopause has occurred is the measure of
an elevated FSH level. Because the FSH level rises more than the LH
level, owing to the reduced renal clearance of FSH compared with LH,
obtaining an FSH level alone is not helpful. On the other hand, the FSH
level may not be a reliable indicator because of the wide variation of
FSH and LH levels in response to increased release of gonadotropinreleasing hormone (GnRH) by the hypothalamus and increased
pituitary sensitivity to GnRH

Symptoms and Signs:

Menopausal women may be asymptomatic, or they may have severe
symptoms.

Hot flushes and sweating secondary to vasomotor instability affect

75% of women. Most have hot flushes for > 1 yr. and 25 to 50% for > 5
yr.
Psychologic and emotional symptoms of
o fatigue,
o irritability,
o insomnia, and
o nervousness may be related to both estrogen deprivation and the
stress of aging and changing roles.
Lack of sleep due to disturbance by recurrent hot flushes contributes
to fatigue and irritability.
Cardiac symptoms of palpitations and tachycardia may occur; the
incidence of heart disease increases.
Genital tract atrophy predisposes to:
o Atrophic vaginitis is common, causing soreness, dysuria, and
dyspareunia.
o Prolapse
o Urinary incontinence, especially stress and urge incontinence.
CLINICAL EFFECTS OF MENOPAUSE
Throughout the time when the physiologic changes in responsiveness
to gonadotropins and their secretions occur, with resultant wide
variation in hormonal levels, women often experience several
symptoms that are collectively termed the climacteric syndrome.
Typical climacteric symptoms include hot flashes or flushes, insomnia,
weight gain and bloating, mood changes, irregular menses,
mastodynia, and headache. As already noted, the length of time over
which the climacteric occurs is widely variable; symptoms may begin
during perimenopause and continue for 5-10 years after menopause.
Irregular ovarian function and considerable estrogen level fluctuation
not a deficiency of estrogencause climacteric symptoms during
menopause;
thus,
stopping
hormone
fluctuation
with
oral
contraceptive pills (OCPs) and hormone replacement therapy (HRT)
alleviates climacteric symptoms. Ovarian function and menstruation
therefore usually does not resume if the woman has experienced one
year of amenorrhea. Cessation of menstruation in women of the
appropriate age continues to be the best confirmation of loss of
follicular function. As the postmenopause years progress, with an
accompanying loss of ovarian response to gonadotropins, associated
symptoms of the climacteric also decline.

The effects of gonadal hormone depletion can be obvious on pelvic

examination, with changes noted as early as perimenopause in some
women. The reproductive organs of a woman of reproductive age
greatly differ in appearance from those of a woman who is
menopausal. With loss of estrogen, the vaginal epithelium becomes
redder because of thinning of the epithelial layer and increased
visibility of the small capillaries below the surface. Later, as the vaginal
epithelium further atrophies, the surface becomes pale because of a
reduced number of capillaries. A decrease in urine pH leading to a
change in bacterial flora may result in pruritus and a malodorous
discharge. Rugation also diminishes, and the vaginal wall becomes
smooth. Such changes often result in insertional dyspareunia and, for
many women, eventually lead to sexual abstinence if left untreated.
Inside the pelvis, the uterus becomes smaller. Fibroids, if present,
become less symptomatic, sometimes shrinking to the point that they
can no longer be palpated on pelvic examination. Endometriosis and
adenomyosis are also alleviated with the onset of menopause, and
many patients with pelvic pain finally achieve permanent pain relief.
The menopausal ovary diminishes in size and is no longer palpable
during gynecologic examination. A palpable ovary on pelvic
examination warrants a full evaluation in all women who are
menopausal or postmenopausal.
For older women, a general loss of pelvic tone also occurs, and this
may manifest as prolapse of reproductive or urinary tract organs.
Vaginal pressure, lower back pressure, or bulging at the vaginal
introitus is common in women with prolapse. On examination,
cystocele, rectocele, and uterine prolapse are obvious as causes of
these symptoms.
Atrophic cystitis, when present, can mimic a urinary tract infection.
Women report symptoms of urinary frequency, urgency, and
incontinence. However, women are more prone to urinary tract
infection during this time because of atrophic cystitis, and a urine
culture should be obtained in all symptomatic women.
In addition to alterations in the pelvic organs, marked changes occur
throughout the body. Skin loses elasticity, bone mineral density (BMD)
declines, and dense breast tissue is replaced by adipose tissue, making
mammographic evaluation easier.
The most common reason a woman presents at menopause is because
of symptomatic hot flashes. Flashes, or flushes, which are
unpredictable in onset and sometimes occur over many years, are

reported in about 75% of women who are perimenopausal or

postmenopausal. Hot flashes often cause embarrassment and
discomfort, as well as sleep disturbances and emotional labiality,
especially if they are intense and occur frequently. Vasomotor episodes
usually last a few minutes. Episodes vary in frequency from every hour
to every few days.
A woman who flushes to the extent that she has major sleep
disturbances may also complain of cognitive or affective disorders
resulting from sleep deprivation. The vasomotor flush is described as a
feeling of warmth or heat that begins from the umbilical area and
moves upward toward the head, followed by sweating of the head and
upper body. Other cardiovascular or neurological symptoms (e.g.
palpitations, dizziness, light-headedness, vertigo) can also occur, with
or without flushing, making the episode more difficult to classify as
simply a climacteric symptom. Because of the wide range of
symptoms, symptomatic women who have risk factors for a condition
other than menopause should undergo thorough evaluation.
OSTEOPOROSIS
Although osteoporosis is one of the most pervasive conditions in older
women, the condition is often not taken seriously enough by
menopausal women. Osteoporosis is the major health hazard. With
proper intervention, osteopenia is a largely preventable sequela of
menopause. A recently published article by Grady and Cummings
(2001), a meta-analysis of 22 trials with data on a total of 8800
women, found a 27% reduction in risk of nonvertebral fractures in older
women who received HRT. For hip and wrist fractures, the risk
reduction was 40%, increasing to 55% in women younger than 60
years.
With the onset of menopause, BMD is rapidly lost because bone
resorption, uncoupled from bone formation, is accelerated, whereas
formation continues at the premenopausal rate. Trabecular bone is
affected more than cortical bone, and bone loss is therefore more
commonly observed at vertebral, coxal, and radial sites. Normal bone
loss associated with senescence is different from the accelerated bone
loss observed after menopause. Bone loss in just the few years after
onset of menopause may be as high as 20% of lifetime bone loss
(Grady, 2001).
The overall effect of menopausal bone loss is reduction of bone
strength, leading to an increased risk of fracture. The younger the

woman at cessation of ovarian function, the more severe bone loss is

likely to be. Similarly, the lower the womans bone mass when entering
menopause, the more severe the osteoporosis will be. Severity of
osteoporosis is also related to race, being worse in whites than in
Asians, and least severe in women with dark complexions. Other risk
factors are smoking and slender build. Osteoclasts have been shown to
have estrogen receptors, and these are hypothesized to be the
mechanism by which estrogen replacement protects against
osteoporosis.
Bone densitometry is the most accurate clinical predictor of
osteoporosis. If bone mass is less than 1 standard deviation below the
average for the specific bone measured, then the individual is at a
much higher risk of fracture. Other risk factors, such as low serum
estrogen level, female sex, and low serum androgen level, have been
shown to increase fracture risk but have not been found to have as
strong an association as bone densitometry. Bone densitometry testing
is recommended for all postmenopausal women. Neither the age of
initial BMD screening nor the optimal frequency of screening has been
determined.
As noted, estrogen therapy is considered the optimal therapy for
osteoporosis. Oral and transdermal routes have been approved for
osteoporosis prevention in postmenopausal women who are considered
at risk. Postmenopausal women and elderly women should be treated
early and on a long-term basis unless estrogen replacement therapy
(ERT) is contraindicated.
Because loss of ovarian function is a universal occurrence and not all
women can or will use HRT, other therapies have been developed.
These include raloxifene, calcitonin, and bisphosphonates. Raloxifene
acts directly on estrogen receptors and modulates them to decrease
bone resorption, resulting in reduced vertebral fracture risk and
increased BMD. No effect on hip fracture risk has been documented.
Calcitonin is a peptide hormone that acts by inhibiting osteoclasts,
which are involved in bone resorption activity. A decreased vertebral
fracture rate has been demonstrated with this therapy, as has a small
increase in BMD in older women. Serum calcium levels must be
monitored in patients taking this drug.
Bisphosphonates are the most useful pharmacological intervention and
work as antiresorptives. They have been shown to have a beneficial
effect on vertebral and hip fracture rates and to cause a more
significant increase in BMD than raloxifene and calcitonin. Two widely
used and effective bisphosphonates are alendronate and risedronate.

The Vertebral Efficacy With Risedronate Therapy (VERT) study was

conducted at 110 centers and included 2458 postmenopausal women
who had vertebral fractures. Risedronate was administered at a dose of
5 mg for 36 months and showed a statistically significant reduction in
relative risk (RR) of new vertebral fractures (RR = 0.59, 95%
confidence interval [CI], 18-58%). Cumulative incidence of
nonvertebral fractures was also reduced.
Alendronate was first introduced with 10 mg daily dosing for treatment
of osteoporosis. Patients can now be prescribed a weekly 70-mg dose.
Supplementation to 1000-1500 mg of calcium per day remains a
mainstay of prevention therapy, as does vitamin D supplementation
and regular weight-bearing exercise. Excessive salt, animal protein,
alcohol, and caffeine offset these benefits. Unlike estrogens, which are
commonly administered for many years, often decades, the long-term
use of bisphosphonates has not been fully studied and is currently
under investigation.

Fig.1.1 Osteoporosis

CARDIOVASCULAR
Coronary artery disease (CAD) is known to be increasingly prevalent
with older age in both men and women. Menopause increases the risk
for women still further, independent of age. Prior to menopause, the
risk of CAD for women lags behind the risk for men by approximately
10 years. After menopause, women come to have similar risks of CAD
as men of the same age. As a result, the rate of death in women from
CAD is increasing. The Framingham study was pivotal in showing the
relationship between menopause and increased cardiovascular
mortality rate.
The benefit of estrogen on cardiovascular mortality rates is due to
many factors. One mechanism appears to be estrogens effects on lipid

metabolism, which includes reducing low-density lipoprotein (LDL) and

increasing high-density lipoprotein (HDL). Studies have suggested that
the best predictors of CAD in men and women are different (Assman,
1998) and that triglycerides, HDL, and lipoprotein(a) may be more
significant in women (Erikkson, 1999). Women with elevated
lipoprotein(a) levels should be treated more aggressively, and the
treatment considered should include ERT as well as a statin. A positive
relationship between ERT and reduction of primary cardiovascular risk
has been demonstrated in several studies, and the reduction in risk in
women who are taking ERT may be similar to the risk reduction of
those receiving specific lipid-lowering therapy (Darling, 1997).
The Heart and Estrogen/Progestin Replacement (HERS) Study (Hulley,
1998; Wells, 1999; Grady, 1998), a study of 2763 postmenopausal
women with known CAD, compared the effect of continuous combined
HRT versus that of placebo over an average of 4.2 years. No beneficial
reduction of CAD event rates was initially observed in the HRT groups.
In fact, the initial adverse event rate was higher in the treatment arm
than in the placebo arm, which offset a later reduction in risk in the
HRT group. An 11% reduction in LDL level and a 10% increase in HDL
level were apparent in the treatment group. These observations
together suggest that the protective effects of estrogen on
cardiovascular morbidity result from many mechanisms and not solely
from lowering of lipids, and that estrogen alone is not adequate
therapy for secondary prevention of CAD.
The Postmenopausal Estrogen/Progestin Interventions (PEPI) Trial,
which included 875 healthy postmenopausal women, compared
various CAD risk factors as predictors of outcomes in women who
received various HRT regimens by randomizing the participants to
receive placebo or 1 of 5 regimes of estrogen/progestin therapy
(Writing Group for the PEPI Trial, 1995). All treatment groups showed
an overall improvement in HDL and LDL levels compared to the
placebo group. The improvement in HDL level was better in the group
that received unopposed estrogen than in the other treatment groups;
however, individuals using unopposed estrogen also had the highest
rate of endometrial hyperplasia.
The Nurses Health Study demonstrated an approximately 11% risk
reduction for primary cardiovascular disease in postmenopausal
women using HRT compared with women who had never used HRT,
irrespective of duration of use (Grodstein, 2000). The risk reduction did
not appear to be dose dependent. ERT has a role in primary prevention
of CAD.

The greatest beneficial effect of estrogen appears to be on endothelial

function. Women undergoing angioplasty appear to be protected
against restenosis by ERT (Abu-Halawa, 1998). Progression of early
atherosclerosis in postmenopausal women who smoked, as measured
by carotid intimal thickness, was greater over time than in women who
smoked and were on ERT (Teeds, 1999).
BREAST CANCER ISSUES
ERT is known to benefit postmenopausal women in a multitude of
ways, although some data indicate that ERT increases the risk of breast
cancer. Estrogen's possible link to cancer is also suggested by the fact
that the risk of breast cancer is increased in women with an earlier age
at menarche and later age at menopause. With early age at
pregnancy, however, and the interruption of menstrual hormonal
changes, a reduction in risk is observed.
Data suggest a slightly increased RR with estrogen use at
approximately 1.1-1.3 (Schairer, 2000; Collaborative Group on
Hormonal Factors in Breast Cancer, 1997), but not all the evidence
supports this finding (Gapstur, 1999). The risk appears to be related to
duration of use, with longer-term users being more affected (Lando,
1999).
Data suggest that the addition of sequential progestin to the regime
increases the RR of subsequently developing breast cancer beyond the
risk of estrogen alone, although the suggestion has been made that
continuous combined HRT using much smaller doses of progestin
attenuates this risk (Ross, 2000). Most earlier studies evaluating breast
cancer risk and ERT were conducted at a time when the progestin in
HRT was administered on a cyclical basis.
Notably, women with a history of using HRT have more localized
tumors as well as better survival rates. That is, women receiving HRT
who are diagnosed with breast cancer are found to have more
favorable staging at the time of diagnosis (Collaborative Group on
Hormonal Factors in Breast Cancer, 1997), including smaller tumor
size, negative lymph node involvement, and more well-differentiated
tumor histology (Colditz, 1990; Holli, 1990; Strickland, 1992; Squiteri,
1994; Bonnier, 1995; Salmon, 1995; Harding, 1996; Magnusson, 1996;
Fowble, 1999).

A beneficial effect on breast cancer mortality rates has been shown in

postmenopausal women who have received HRT compared with
controls who have no prior history of HRT use (Schairer, 2000). Study
findings do not agree on whether this is due to earlier detection or to
effects of the therapy itself on breast tissue. The general belief is that
any increase in risk is small and that each patient should be evaluated
as a candidate for ERT on an individual basis, with consideration of the
overall balance of risks and benefits. An essential precept in the
management of menopause is that each individual is unique and that
therapy should be tailored accordingly.
CENTRAL NERVOUS SYSTEM EFFECTS
The association of estrogen and memory function is an intriguing area
of research. Normal aging itself induces a decline in certain cognitive
capabilities, and a lack of estrogen may contribute to this process. If
this is the case, postmenopausal ERT may be able to preserve this
function and slow or even prevent decline in certain cognitive
functions. An inherent difficulty in this area of study is the limitations of
objective cognitive testing for functions such as memory. In general,
ERT is associated with better performance on memory testing in
postmenopausal women than in postmenopausal controls who are not
receiving ERT (Sherwin, 1997; Resnick, 1997). The estrogen effect is
one of slowing the decline of preserved memory function. Further
clinical research must be conducted in this area to differentiate the
benefits of estrogen in cognitive function in women who develop
clinical dementia and those who do not.
Currently, data suggest that women have a higher incidence of
Alzheimer disease than men, even after allowing for the longer life
span of women, because Alzheimer disease is primarily an age-related
condition (Anderson, 1999). ERT appears to reduce the RR of
developing this condition and/or to delay its onset (Tang, 1996; Kawas,
1997). Estrogen has not been demonstrated to show an improvement
in cognitive function in patients with Alzheimer disease, that is, it
cannot reverse previous cognitive decline and therefore has no role as
a sole treatment modality in Alzheimer disease. However, estrogen
may be beneficial as adjuvant therapy in conjunction with
cholinesterase inhibitors.
Perimenopause is frequently a time of depressive symptoms
associated with direct hormonal effects through variation in levels and
changes in life circumstances and secondary to effects such as
estrogen-related sleep disturbance and vasomotor symptoms.

However, major depression is associated with the female sex at all

ages, and objective demonstration of a cluster of cases around
menopause has been difficult, although this appears to be anecdotally
true.
Regardless of whether the criteria for a definitive diagnosis of major
depression are met, depressive symptoms should always be
considered in the context of level of functioning; any impairment
warrants consideration of intervention.
In all but a very few cases, distinguishing the etiology of the symptoms
as menopausal versus primary depression is usually not possible.
Treatment of depressive symptoms with estrogen in perimenopause,
the postpartum period (Gregoire, 1996), and premenstrual syndrome is
common, with observed resultant improvement in functioning and
mood, both subjective and objective, in many clinical instances.
Clinical depression, however, warrants treatment with antidepressants,
with estrogen showing benefit as adjuvant therapy in this scenario.
The microcellular effects of estrogen in the CNS have yet to be clearly
outlined but may reveal intricate processes by which estrogen has a
direct effect in CNS functioning. One of these processes may turn out
to be a reduction in free radical damage by ERT.
MENOPAUSE MARKERS
Gonadotropin secretion increases dramatically after menopause. FSH
levels are higher than LH levels, and both rise to even higher levels
than in the surge during the menstrual cycle. The FSH rise precedes
that of LH. The large cyclical variation of estradiol and estrone
observed during the menstrual years ceases, and fluctuation in levels
is small and inconsequential, with the mean being very much lower.
The levels of circulating estradiol have very different ranges before and
after menopause, and these levels are obviously much lower in
menopause. Smears of the vaginal epithelium provide a composite
picture of endogenous and exogenous estrogen stimulation over time;
the more estrogen, the greater the number of superficial cells. No
specific changes related to menopause have been found in thyroid
function.
Endometrial biopsy can show a range of endometrial appearances,
from mildly proliferate to atrophic. No secretory changes are observed

after menopause because no ovulation occurs, and therefore no corpus

luteum forms to produce progesterone. Endometrial hyperplasia is a
sign of hyperstimulation by estrogen from either endogenous sources
or replacement therapy and may be a precursor of endometrial cancer.
Endometrial hyperplasia can also be suggested by ultrasonography (an
endometrial thickness of >5 mm), which is useful in trying to exclude
hyperplasia and cancer of the endometrium in postmenopausal
women.
REPLACEMENT THERAPY
Among the many reasons to treat symptoms of estrogen level
fluctuation prior to actual menopause are to provide relief of
vasomotor symptoms, reduce the risk of unwanted pregnancy, avoid
the irregularity of menstrual cycles, and mitigate the long-term effects
of menopause (e.g. osteoporosis, cardiovascular disease, decline in
cognitive function).
The time to begin therapy depends on the patients current illness(es),
if any, and medical history. Whether a woman is perimenopausal or
postmenopausal helps in choosing the most suitable type of therapy.
Each patient should make a choice after receiving counseling on all the
facts and an explanation of the options. For example, the
perimenopausal woman may be started on HRT if either she or her
spouse has undergone a sterilization procedure, whereas the same
woman may need an OCP if she still needs birth control. Many factors,
including personal history, family history, smoking, peer and
commercial influences, culture, ethnicity, and economics, also play
roles in the final decision, and all must be carefully weighed by the
doctor and patient together.
Adverse effects of replacement therapy may include bloating,
mastodynia, vaginal bleeding, and headaches. Unexplained adverse
effects are often the reason for discontinuation of therapy, and
reassuring counseling as well as options and dose combinations should
be tried before therapy is stopped.
HRT can be administered systemically through the oral, transdermal, or
topical routes or locally via the vaginal route using cream, ring, or
tablet. Topical preparations (e.g., conjugated, natural or synthetic
estrogen cream) are used solely to treat vaginal symptoms (such as
atrophic vaginitis and dyspareunia). The estrogen is readily absorbed
systemically from the vaginal mucosa.

HRT=Hormonal Replacement Therapy

Estrogen administration usually is cyclic.
If the patient has a uterus, a progestin is added to the cycle.
o Estrogen (conjugated estrogen 0.3 to 1.25 mg/day or ethinyl
estradiol 0.02 to 0.05 mg/day) is taken orally once a day from the
first through the 25th day each month.
o Progestins (e.g., medroxy-progesterone acetate 5 or 10 mg) are
given from the 15th through the 25th day of the cycle.

Contraindications to estrogen therapy

Contraindications to estrogen therapy are undiagnosed vaginal
bleeding, severe liver disease, pregnancy, and venous thrombosis.
Well-differentiated and early endometrial cancer, once treatment for
the malignancy is completed, is no longer an absolute contraindication.
Estrogen receptorpositive breast carcinoma has traditionally been a
contraindication, but this has also been challenged recently. Progestins
alone may relieve symptoms if the patient is unable to tolerate
estrogens, but the other concomitant protective effects of estrogen are
lost.
Mammography should be routine in postmenopausal women and
is particularly pertinent as a screen and to provide a baseline in those
receiving estrogen treatment. Most evidence indicates that estrogen
therapy does not increase risk for breast cancer.

11
INFECTION OF THE VULVA
The vulva is the visible portion of the female external genitalia and
consists of all the structures visible externally extending from the pubis
to the perineum, i.e. the mons pubis, labial majora and minora, clitoris
and vestibule. They are covered by squamaous epithelium. The
Bartholins glands, one on each site, are within the vulva and apocrine
glands. They lie in the posterior part of the vestibule and connect to
the surface by short ducts.

Bartholins gland

Fig. 1.1 The external anatomy of the vulva.

The skin covering the vulva are liable to be infected by common skin
pathogens and sexual transmitted disease organisms resulting in
inflammation, irritation, abscess formation and even ulceration of the
vulva. Vulva ulceration is most commonly infective.

BARTHOLINS ABSCESS
Etiology:
The gland may be affected by mixed organisms (E.coli or
staphylococci), but is commonly associated with Neisseria gonorrhoea
and Chlamydia trachomatis.
Clinical Features:
Unilateral or bilateral bartholinitis may occur. The abscess forms a
painful red swelling and expands to the posterior part of labium minus.
It causes considerable discomfort. A tender cystic swelling may be
palpable posterolaterally, and occasionally pus can be expressed from
the duct opening of the affected gland.

The Bartholins gland may ruptured spontaneously or subside to form a

non-painful cyst which may become reinfected.
Diagnosis:
In acute the woman complains of acute tenderness in the region of the
gland. A redness swelling is noted on the affected area where the
gland is situated, i.e. beneath posterior part of the labium majora. A
tender cystic swelling is palpable.

Fig. 1.1 Right bartholins abscess.

Treatment:
1) On first presentation, pus obtained should be sent for culture.
2) To prescribe broad spectrum while waiting for the culture result and
may required modification in the light of microbiological results.
3) If an abscess is formed, marsupialization of the abscess should be
performed.
The vaginal and abscess walls are sutured with
interrupted plain catgut around it edges to maintained patency and
to prevent reformation.

BEFORE

AFTER

1. Elliptical incision is made over

the center of the abscess (A),
i.e. medial to the long axis of
labial majora (M) and lateral
to hymenal ring (L).

1. The vulva and abscess walls

are sutured with plain
catgut at its edges
interrupted sutures

2. The incised elliptical vulval

and
abscess
wall
are
removed.

2. A small wick gauze may be

left for 24-48 hours or a
small drained may be
inserted if required.

3. The contents are drained.

Fig. 1.2 Marsupialization of Bartholins abscess or cyst

LABIAL ABSCESS
This can be mistaken for Bartholins abscess,
but it does not involve the Bartholins gland.
Etiology: It has a similar etiology to skin
abscess and sexually transmitted diseases are
rarely implicated in their etiology.
Clinical Feature:
It causes a tender red
swelling on the labial majora and considerable
discomfort. The Bartholins glands are not
involved.

Treatment:
Surgical intervention with incision and packing may be
required. Broad-spectrum antibiotic should be prescribed.
Fig. 1.3 Labial abscess

GENITAL WARTS (CONDYLOMATA ACUMINATA)

Genital warts are caused by human papilloma virus (HPV), principally
types 6 and 11, which are generally transmitted by sexual contact.
The warts tend to occur in moist areas. The vulva, vagina, cervix and
perianal areas can all be affected, the introitus and labial minora being
the commonest sites. Malignant change can rarely occur.
Clinical features: These genital warts present as cauliflower growth,
occasionally pedunculated, and are variable in size and number. In
most cases the warts are symptomless but some women complain of
vulva irritation and itching. If the warts involve the introitus or the
vaginal, the women may complain of dyspareunia.
Diagnosis: The diagnosis is made on clinical grounds.
Treatment:
Small genital warts may be treated with topical
application of podophyllin (washed off after 4 hours) or cryotherapy.
Large warts are treated by diathermy or surgical excision.

GENITAL ULCERS
Genital herpes infection is the most common form of genital ulceration,
followed by syphilis and rarely, chancroid.

HERPES GENITALIS
Etiology: Herpes simplex virus (HSV) is the commonest cause of
genital ulcerative disease. The herpes simplex virus exists in two
forms, HSV1 and HSV2. HVS2 causes genital herpes in 85 percent of
the cases.
Clinical features:
In primary genital herpes infections, lesions
developed 2-7 days after sexual exposure with an infected person.
Local symptoms tend to be severe and systemic symptoms are
common, including fever, malaise and mucocutaneous lesion. Itching
or burning sensation accompanied by tiny crops of painful vesicles

begins to appear on the inner surfaces of the labial majora. The

vesicles ulcerate rapidly to form multiple shallow painful ulcers (Fig.
1.4) and secondary infection may occur, aggravating the pain.

Fig. 1.4 Herpes ulceration over the labial minora

Progress of the lesions: Complete healing occurs with 7-12 days

after the appearance of the vesicles. After the healing the virus is shed
from the affected area. The virus may also enters myelin sheath of the
sensory nerves and remain in the dorsal root ganglion. It may lie
dormant for the rest of the womens life or may be reactivated to
cause new attack of herpes. Subsequent attacks are less severe.
Diagnosis:
The history and physical examination may often be
sufficiently distinct to permit the diagnosis of herpes genitalis. The
diagnosis of genital herpes infection can be confirmed by isolation of
the virus by culture.
Treatment: The only effective medication is with the antiviral agent
acyclovir.
Acyclovir may be administered intravenously (in the
management of disseminated disease and in patient with central
nervous system manifestations), orally or topically. Oral acyclovir
(200mg five times per day for 5 days) is generally prescribed for
patients with genital ulceration due primary infection. General
measures - During an active attack the women should be advised not
to scratch the infected area and she should wash her hands after
touching the infected area or applying the medication. Analgesia or
local applications of ice or local anaesthetic gel may provide some
relief.

 SYPHILITIC VULVAL ULCER

Syphilis is sexually transmitted caused by the invasion of the tissues
by Treponema pallidum. In women the usual site of infection is one of
the labial majora. The initial lesion is a small papule, which appears at
the site of inoculation and then become a painless ulcer known as hard
chancre. These ulcers or chancres may be painful if secondarily
infected. The infected women are highly infectious during the primary
lesion. The primary lesion disappears in 21 days or so.
Diagnosis:
The diagnosis is confirmed by examining a wet
preparation from the base of the ulcer under dark ground illumination.
This reveals the characteristic morphology and mobility of the
organism.

Fig. 1.5 Treponema pallidum

Six weeks after the primary infection serological tests for syphilis
(VDRL) become positive.
Treatment: A course of intramuscular penicillin remains the therapy
of choice (e.g. procaine penicillin 1.0 mega units for 10 days). For
patients allergic to penicillin, extended courses of erythromycin 500
mg orally 4 times a day for 10 days may be given. Meticulous followup is essential.

12
VAGINAL

DISCHARGE

Fig.1.1 Mucopurulent vaginal discharge of gonococcal cervicitis

Vaginal discharge is a common problem in women, and accounts for a

good proportion of the consultations seen by general practitioners,
gynaecologist in their outpatient clinics. It may be physiological or due
to local vaginal or cervical condition or occasionally to a problem
higher in the genital tract. Sometimes, the problem can be quite
simple, but at times, can be quite complicated, requiring many
sessions before relief can be obtained. Women are also frequently
over anxious about their discharge, because of fear of cancer, or of
sexually transmitted disease and might exaggerated their symptoms.
COMPOSITION OF NORMAL VAGINAL SECRETION
In the adult the normal vaginal secretion consists of vaginal transudate
cointaining desquamated vaginal epithelial cells.
Besides the
transudate across the vaginal epithelial lining, vaginal secretion is also
contributed to by vulval secretions from sebaceous, Bartholins and
Skenes glands, the cervical mucus, and fluids from the endometrial
cavity and oviductal regions.
There is a cyclical variation in the amount of secretion: it is heavier
premenstrually and there is an increased secretion of clear mucus at
the time of ovulation. The vaginal fluid is acidic (the result of glycogen
in the vaginal epithelium been converted to lactic acid by Doderlines
bacilli), pH 4-5, and this prevents the multiplications of most
pathogenic organism.

NATURAL DEFENCE MECHANISMS OF THE LOWER GENITAL

TRACT
Changes in the activity of the vaginal epithelium and in the vaginal
secretion, which occur at different times during a womans life, have a
profound influence on the defense against vaginal infection. There are
various defense mechanisms against the colonisation of microbial in
the vagina.
At vulva level, there is the cohesiveness of the labial folds, its natural
resistance, and the secretion of undecylenic acid by its apocrine gland.
At vaginal level, the cohesiveness of its wall, the stratified epithelial
lining, its acidity, and the presence of vaginal microbial flora, all
contribute in the defense mechanisms.
The cervical mucus possesses bactericidal properties, in addition to its
mucus plug function.
What can alter these defense systems?
During menstruation, there is reduction in mucus as a result of the
outflow discharge.
In the puerperium, a noticeable decrease in vaginal acidity is present,
related to reduced oestrogens levels after child-birth.
Low level of oestrogen, resulting in fall in vaginal acidity and reduced
natural resistance of epithelial lining, also occur in the childhood
period, after menopause.
CAUSES OF VAGINAL DISCHARGE
Vaginal discharge may be either physiological or pathological (infective
and non-infective) in origin.

Physiological causes
Basically, an increase in activity of glands, especially endocervical,
resulting in an increase of normal vaginal discharge may occur in
the following situations
1. Premenstrually

2.
3.
4.
5.
6.

At the time of ovulation

During sexual excitement
During pregnancy
When using the contraceptive pill or an intrauterine device
In anxious women

The discharge is slight to copious, and is clear to mucousy in nature,

occasionally mild white, but with no foul smell or associated priritus
of the vulva.

Pathological causes
There are a various of such factors that could lead to vaginal
discharge.
1. Infections
Various forms of infections, be it, fungal, parasitic, viral or
bacterial, can affect the lower genital tract, leading to vulvitis,
vaginitis or cervicitis. The commonest organism giving rise to an
infective pathological vaginal discharge is Candida albicans.
Other infections causing this symptoms may be due to agents
such as Chlamydia trachomatis, Neisseria gonorrhoeae,
Trichomonas vaginalis, and Gardnerella vaginalis. Cervical
lesions due to herpes, warts, and a syphilitic chancre may also
cause a discharge. Occasionally, infections in the Occasionally,
infections in the allopian tube can also result in vaginal
discharge.
Infective discharge can be copious, usually purulent, foulsmelling and frequently associated with vulval itch and urethral
symptoms.
2. Hormonal
Due to estrogen deficiency, women in premature menopause or
natural menopause can develop atrophic vaginitis, which could
manifest as blood-stained vaginal discharge.
It is believed that development of cervical erosion may be
related to oestrogen predominance, either inherent, as a result of
pregnancy or taking oral contraceptive pills. Such a lesion,
together with the eversion that occurs, lead to increased
secretion from the endocervical glands. It also predisposes to
secondary bacterial infections.

3. Foreign body / Local irritation

Vaginal discharge can arise from over-douching especially with
irritative antiseptics, neglected tampons left in for long periods
of time, missed gauze or cotton swabs left in after vaginal
examinations or childbirth, use of vaginal pessary in the
treatment of vaginal prolapse, and of course, the use of
contraceptive devices like the cervical cap, vaginal diaphragm
or sponge.
4. Cervical ectropion
Local cervical lesions such as ectropion may present with a
vaginal discharge.
5. Neoplasms
Polyps of the cervix or vagina can cause vaginal discharge, so
also pedunculated submucous fibroids of the uterus, especially
with surface ulceration.
More sinister causes could be malignancies of the vagina, cervix,
endometrium, and rarely fallopian tube.
6. Displacements
Utero-vaginal prolapse, especially so when there is decubitus
ulceration of the cervix may present with a vaginal discharge.
7. Fistulae
Fistulae of the genito-urinary type, e.g. vesico-vaginal, may also
cause a vaginal discharge.

COMMON CAUSES OF VAGINAL DISCHARGE

VAGINAL CANDIDIASIS
This is the commonest fungal infection with Candida albicans. This
fungal grows well at pH 5 6.5, i.e. when the vagina is less acid than
normal. Vaginal candidiasis or also known as monilial vaginitis or

thrush is more likely to occurs in pregnancy, in women who are taking

antibiotics or immunosuppressive therapy and in diabetics. Apart from
these, vaginal candidiasis may also occur in patients who are using
oral contraceptives.
This infection may be transmitted sexually.
Moderate to severe vulval itching and burning, with redness and
possibly excoriation suggests candida infection.

Clinical features

May be asymptomatic.
With severe infection the discharge is thick, curdy and white.
Can cause severe itching, soreness and dyspareunia.
Can affect vulva, intergluteal folds and inner aspects of thighs.
On examination there may be white curds in the vagina with
underlying redness and inflammation.

Fig. 1.2 Sever vaginal candidiasis

Diagnosis
This made largely on clinical grounds. Taking smears from the
vagina walls and examining them microscopically for Candida
albicans for spores and hyphae by Gram stain can make an
immediate diagnosis.

Treatment
Principles of treatment:

Application of topical antifungal agents for sufficient time to be

effective
To avoid re-infection from sexual partner - sexual intercourse
should be avoided until cure is complete
Prevention of auto-infection from the bowel
The vulva must be kept cool and dry. This is achieved by careful
hygiene, use of cotton rather than synthetic underwear and
careful drying after washing vaginal area.

Treatment is generally using intravaginal pessaries or cream inserted

high into the vagina at night. Some possible antifungal pessaries
include:

clotrimazole 200 mg pessary, 1 at night, for 3 nights

clotrimazole 500 mg pessary, single dose
miconazole 100 mg pessary, two, for 7 nights

VAGINAL TRICHOMONASIS:
Trichomonas vaginalis is a flagellate protozoan that is acquired venerally. Infection with
T. vaginalis is usually associated with a vaginal pH of 6 or more. Trichomonas infection
is marked by a profuse frothy green vaginal discharge (Fig. 1.3). Infection often
produces a vaginitis and sometimes punctate mucosal haemorrhage of the cervix; the
strawberry cervix (Fig.1.3). Itching is severe. The symptoms are often worse
immediately after menstruation. Occasionally the infection may be asymptomatic.
Clinical features of trichonomiasis:
Vaginal Trichomoniasis (Trichomonas vaginalis) in most cases the
vagina is involved. The patient may complain of:
o
o
o

a vaginal discharge - greenish, offensive, may be frothy

vulvovaginal irritation or pain
dyspareunia and dysuria

On examination there may be reddening of the vulval, vaginal and

cervical mucosae.

Typical frothy vaginal associated with

trichomoniasis

Punctate haemorrhage producing strawberry

cervix appearance in T.vaginalis infection

Fig. 1.3 T. vaginalis infection

Diagnosis
Trichomoniasis can be diagnosed by identifying a flagellate
protozoan from a direct wet preparation of the vaginal discharge.
On microscopic examination, T. vaginalis can be seen as motile,
unicellular flagellated organisms (Fig. 1.4).

Fig. 1.4 Microscopic examination showing Trichomonas vaginalis.

Treatment of trichonomiasis

Metronidazole (Flagyl) is the usual treatment. Alternatives include

tinidazole. Both are administered orally (minimum dose 400 mg b.d.
for 5 days).
In pregnancy a dose metronidazole 200mg t.d.s. for 7 days is a
possible treatment regimen. The male partner should also be
treated; especially if there is a recurrence. During treatment, a
condom should be used during intercourse. It is advisable to treat
an asymptomatic woman in whom trichomonas has been found,
before it becomes an established infection.
Note that when one sexually transmitted disease is found, others
frequently co-exist and should be looked for (Gonorrhoea often coexists with trichomoniasis).

NEISSERIA GONORRHOEA
Gonorrhoea is a sexually transmitted disease caused by Neisseria
gonorrhoea, a gram-negative intracellular diplococcus. The most
common form of transmission is from sexual contact. Non-sexual
transmission can occur - for example an infected mother passing the
infection to a newborn child, usually resulting in gonococcal
conjunctivitis.
Clinical features of the disease vary between gender. About 40% of females are
asymptomatic whereas asymptomatic infection rarely occurs in males.

Clinical features of gonorrhoea

Lower genital tract infection is often asymptomatic, although

mucopurulent cervicitis may be seen on examination.
Symptomatic females present with purulent vaginal discharge,
frequency of micturition and anorectal discomfort. There may be
bartholinitis.
Ascending endocervical infection causes
endometritis and pelvic inflammatory disease (salpingitis).

Disseminated gonococcal infection causes fever,

myalgia and a diffuse pustular and erythematous rash

Gonococcus contracted via anal sex may cause proctitis

malaise,

Diagnosis
Local infection: History and examination are suggestive but
definitive diagnosis can only be made by identifying the organisms
in smears or by culturing them in special media - Thayer Martin.
Smears may be obtained from genital discharge, endocervix,
urethra and rectum. The organisms are gram-negative intracellular
diplococci (Fig. 1.5)

Fig. 1.5 N.gonorrhoea Gram stained showing gram-negative intracellular

diplococci (arrow)

Treatment of gonorrhoea
Compliance and defaulters may be a problem so best to give a
single oral dose, under supervision.
Single-dose treatment (ciprofloxacin or ofloxacin or cefotaxime ) in
uncomplicated infection - choice of antibiotic depends on locality
where the infection was acquired. Co-infection with chlamydia may
occur with gonorrhoea.
For this reason it is justified for
simultaneous treatment for both infections in patient with
gonorrhoea.

 BACTERIAL VAGINOSIS:
Bacterial vaginosis (anaerobic vaginosis, non-specific vaginitis or
Gardnerella vaginitis) is a common condition. It is caused by a
disturbance by a disturbance in the vaginal ecology with an
overgrowth of a variety of anaerobic organisms, including Gardnerella
vaginalis.
Clinical features
The patient complains of an off-white, gray, or yellowish turbid
discharge with a foul or fishy odor that becomes stronger when the
discharge becomes alkaline (e.g., after coitus or washing with soap).
Vulval pruritus or irritation may be present, but redness or edema is
not usually marked.
Diagnosis
This made by finding at least three of the following four criteria:
1.
2.
3.
4.

Offensive off-white discharge

Elevated pH (> or = 5)
Positive amine test
Presence of clue cells when secretions are examined by dark
ground microscope.

Fig. 1.6 Gram stain of clue cell.

Treatment: The most effective treatment is metranidazole 400 mg

b.d for 5 days.

THE INVESTIGATION OF VAGINAL DISCHARGE

The investigation of vaginal discharge consists in taking a history, in
physical examination and in special investigations.
History and examination:
The initial visit should include a complete physical examination and
history, with attention to details of the discharge (color, consistency,
presence of odor, duration, and symptoms). The type of discharge may
suggest the cause, or it may be misleading.
The patient should be asked to describe when the discharge occurs in
the menstrual cycle; whether it is recurrent; how it responded to
previous therapy; whether vulvar itching, burning, pain, or lesion is
present; and what aspect of the problem is most troublesome.
Questions should also include

concern sexual activity;

contraceptive use;

whether the sexual partner has had urethral discharge,

pruritus,

postcoital irritation, or

therapy for infection;

use of chemicals on the vulva or vagina;

recent change in laundry products;

any present or past venereal disease or parasitic infection;

and whether anyone in the household has pubic itching.

Examination:
After the general physical examination, the vulva is examined for
redness, edema, and abnormal lesions. It may be advisable to pass a
speculum before making a bimanual examination. A speculum is
passed to inspect the vaginal walls and cervix. The cervix is inspected
for erosion, ectropion, polyp or carcinoma.
Various aspects of the history and examination may be SUGGESTIVE of
particular infectious causes of an increased vaginal discharge.

Pregnancy, diabetes mellitus, recent antibiotic treatment,

immunosuppression, dyspareunia or itchy vulval irritation suggestive of candidiasis
A recent change in sexual partner, a discharge that is offensive
and copious - suggestive of trichomoniasis
Offensive discharge plus IUCD plus dyspareunia - sugggestive of
bacterial vaginosis
Erythema and oedema of the vulvovaginal area, excoriation of
the vulva and presence of curd-like discharge with white plaques
- suggestive of candidiasis
Yellow/green, offensive, frothy discharge - suggestive of
trichonomiasis
Bacterial vaginosis is suggested by a thin, offensive, grey-white,
adherent discharge

Investigations:

High vaginal swab

Swabs for specific infections e.g. chlamydia

A sample of the discharge is taken with a swab or wire loop; some of

this is suspended in saline and examined immediately for trichomonas
and monilia; cultures may also be made. In cases where gonorrhoea is
suspected a swab is taken from the cervical canal.

13

INFECTION OF THE FALLOPIAN TUBES

- SALPINGITIS -

Fig 1.1

Acute salpingitis

Infection of the fallopian tube is known as salpingitis. The term

salpingitis is used synonymously with pelvic inflammatory disease.
Salpingitis is an acute febrile illness in a woman with pelvic pain and
signs of signs of genital infection.
These infection results from
ascending spread of the lower genital tract infection.
The incidence of salpingitis is closely associated with sexually
transmitted disease. Salpingitis occurs predominantly in women who
are sexually active and results from microorganisms transmitted most
commonly by intercourse, less often by childbirth (puerperal fever) or
abortion.
Patients with intrauterine devices (IUDs) are especially vulnerable,
probably because the transcervical appendage assists pathogen
transport.
Salpingitis may be described as acute, subacute and chronic

ETIOLOGY OF SALPINGITIS
Organisms can reach and affect the fallopian tube by one of the three
routes.
1. Ascending infection from the lower genital tract and uterus (Fig.
1.2).
2. Direct spread infection from nearby pelvic organs.
3. Infection through the bloodstream (blood-borne).

3. Infection through blood stream

2. Direct spread from

nearby pelvic organs
1. Ascending infection from
lower genital tract

Fig. 1.2

Aetiology of salpingitis.

A variety of organisms may be responsible, and secondary infection

readily occurs (Fig.1.3).
Ascending infection from lower genital tract and uterus

In acute salpingitis the route of infection is most commonly

ascending from the vagina and cervix to the uterus and parametrial
tissues.
The most common organism in this route of infection are
streptococci and staphylococci.
An infection which ascends from lower genital tract are due to:
Sexually transmitted disease:

The most common aetiologic agents is salpingitis are caused by

organisms such as:
Neisseria gonorrhoea
Chlamydia trachomotis
Mycoplasma
Ascend of endogenous vaginal and perianal flora (usually
anaerobic organisms).
Iatrogenic
,
e.g.:
Dilation
and
curettage
(D&C),
Hysterosalpingogram (HSG), tubal insufflation, termination of
pregnancy, and insertion of intrauterine contraceptive device
(IUCD). Salpingitis may rarely followed therapeutic abortion,
salpingography or the insertion of an intrauterine contraceptive
device. In rare instances actinomycosis has been found in
association with the use of IUCD.
After delivery or miscarriage Infection of the fallopian tube
may occur following an abortion or after childbirth. In these
cases the infective agents E. coli, staphylococci, sreptococci
and anaerobic. These organisms enter the tissues through
cervical laceration, or more frequently through the placental bed.

These organisms initially cause lower genital tract infection and

then spread into the upper genital tract (fallopian tubes) via the
endometrium.
Many cases are polymicrobial in etiology with two or more of these
organisms involved.

Direct spread infection from the nearby pelvic organs

Most often infection of the right fallopian tube can occur in cases of
acute appendicitis.
Infection from the pelvic peritoneum or
parametrial tissue (e.g. peritonitis or pelvic abscess) may result in
infection of both tubes (bilateral salpingitis).
The most common organisms involved are:
E. coli
Sterptococcus faecalis

Infection through bloodstream

Salpingitis may also occur as a result of spread from blood-borne

infection. The most common organism in this route is tuberculosis.
Tuberculosis usually produced a silent chronic salpingitis.

Pathways of
salpingitis

infection

of

Fig.1.3 Etiology for salpingitis

Why is Salpinigitis (Pelvic inflammatory diseases) important?

Systemic upset
Pain
Recurrence
Infertility
Ectopic pregnancy

Acute salpingitis can be a systemic illness, with fever, rigors &

septicaemia. Long-term pain, dysmenorrhoea and/or dyspareunia occur
in about 15-20% of patients. Chronic pain following an acute attack is
common, lasting up to 6 months.
Following a severe episode of salpingitis (PID), as many as 21% of
women may have tubal compromise. Ectopic pregnancy is more
common following salpingitis (PID).

That sexually transmitted organisms predominantly cause PID is well

established. It occurs rarely in virgins and is much more likely in those
who have multiple sexual partners. Its incidence peaks in women aged
15-25 years, most likely reflecting the sexual activities of this age
group. Remember to take a sexual history - there may be more than
one partner implicated.

The cause may be a single organism or several organisms.

common infective organisms include:

The

Chlamydia trachomatis Chlamydia - has replaced Neisseria

gonorrhea as the most common cause of PID. C. trachomatis
may affect the lower or upper genital tract; often upper genital
tract infections have a deceptively benign onset and seem quite
mild. Chlamydial organisms may remain in tubal mucosa for
many months before manifestations of acute disease appear.

Neisseria gonorrhoeae - usually produces more acute, typical

pelvic inflammation, with rapid onset and development of pelvic
pain shortly after the start of a menstrual period

Gram negative bacilli - e.g. E. coli

Gram positive cocci - e.g. Groups B&D Streptococci
Anaerobes - e.g. Bacteroides species
Mycoplasma hominis
Actinomyces israelii

Clinical features of salpingitis:

Salpinigitis may be described as acute and chronic.
Acute salpingitis: Onset is usually shortly after menses.
Lower abdominal pain becomes progressively more severe, with
guarding, rebound tenderness, and discomfort that increases with
cervical motion. Unless related to an IUD, involvement is usually
bilateral
Vomiting may occur; bowel sounds are normal early, although
paralytic ileus may ensue.

 High fever, leukocytosis, and copious purulent cervical

discharge have commonly been associated with PID, but low-grade
fever, mild to moderate abdominal pain, irregular bleeding,
and vaginal discharge may also signal the disease.

Chronic salpingitis may follow an acute attack with subsequent tubal and pelvic scarring
and adhesions, chronic pain, menstrual irregularities, and possibly, infertility. An
obstructed tube may distend with fluid (hydrosalpinx). In chronic interstitial salpingitis,
the tube is enlarged as a result of a thickened wall.

Acute Salpinigitis
Abdominal pain
Offensive vaginal discharge
Malaise, vomiting, fever
Irregular vaginal bleeding
Pyrexia, tachycardia
Lower abdominal tenderness
Bilateral
adnexal
tenderness,
cervical
excitation

Chronic Salpingitis
General malaise & fatigue
Chronic lower abdominal
pain
Intermittent
offensive
vaginal discharge
Deep dyspareunia
Apyrexial
Generalised
lower
abdominal tenderness
Pelvic tenderness

Bulky, tender uterus

Tubo-ovarian mass
Table 1. Symptoms and signs of salpingitis

Complications following salpingitis(PID)

Although symptoms and signs may predominate on one side, both
tubes are probably affected.
The tubal infection produces a profuse exudate, leading to
agglutination of mucosal folds, adhesions, and tubal occlusion. As a
result of the mucosal destruction and tubal occlusion, infertility is a
common sequela of salpingitis.
Peritonitis, from spread of the exudate to the pelvic peritoneum, is
common; the ovaries tend to resist infection but may also be invaded.

Abscesses may develop in the tubes, ovaries, or pelvis during the

acute or subacute stage. A small perforation may seal off the abscess
and still allow response to antibiotics; those that do not respond
require surgical removal. Massive perforation of an adnexal abscess is
a surgical emergency, rapidly progressing in a characteristic pattern of
severe low abdominal pain, generalized peritonitis, nausea, vomiting,
and shock secondary to peritonitis and endotoxemia.

Pyosalpinx, in which one or both fallopian tubes are filled with

pus, may be sterile but almost always is associated with symptoms of

inflammation. The ovary, if involved, becomes incorporated into the

tubal inflammatory mass, producing a tubo-ovarian abscess.
Hydrosalpinx occurs with late or incomplete therapy, resulting from
closure of the fimbriated end of the fallopian tube. It may be present
without symptoms for years.

ASSESSMENT:
Gynaecological examination

Inspection: Vulva, Lymph nodes

Speculum: Inspect the cervix and vagina
Bimanual Examination
Uterine size, av/rv, axial/deviated
tenderness, cervical excitation
Adnexa: tenderness, masses

laterally,

mobility,

When carrying out a gynaecological examination, it is important to

think methodically about what you are doing.
Inspection: lymph nodes (genital herpes), pubic lice, vulval warts or
ulcers (herpes/syphilis)
Speculum: visualisation of vagina for lesions & presence of discharge.
Swabs
should
be
taken
including
endocervical
for
chlamydia/gonorrhoea and vaginal for trichomonas.
Bimanual: The aim is to be able to document your findings clearly
covering the points above so that a collegue reviewing your notes can
build up a 3D picture of your findings. On pelvic examination, the
most striking finding is that moving the cervix or palpating the adnexa
produces severe pain.

Investigations

Full blood count

Genital swabs specimens for cultures and smear for Gram stain
should be obtained from the cervical, urethral, and rectal areas.
The examinations may help in differential diagnosis as well as in
identifying organisms.
Ultrasound scan
Laparoscopy - should be performed if the clinical diagnosis is
questioned for any reason; it also aids in differential diagnosis

Differential diagnosis
Acute salpingitis must be distinguished from the following condition:
o Acute appendicitis
In acute appendicitis the history of central abdominal pain, settling in the right side, is
typical; fever is generally lower. There is no history of sexual transmitted diseases or
pregnancy.
o Ectopic pregnancy
In ectopic pregnancy there may be severe pain but there is not a high fever and the
leucocytosis is less marked.
o Complication of ovarian tumour torsion or rupture
In this condition pain and vomiting occur but there is no history of infection, fever is
lower and leococytosis is less marked. The swelling is usually unilateral.
o Intestinal obstruction
This is distinguished by the absence of high fever and leucocytosis and by
generalized abdominal distension. Usually there is no pelvic mass.

Treatment
The treatment should always be conservative in acute phase.
Acute salpingitis requires immediate and vigorous treatment to stop
the infection and prevent infertility
Antibiotics should be started (begun with a broad spectrum, such as
ampicillin) as soon as specimens have been obtained for culture and
sensitivity tests, without waiting for the results of these studies. If a
patient can be treated as an outpatient (i.e., findings are minimal),
appropriate therapy includes single doses of cefoxitin 2 gm IM plus
probenecid 1 gm orally followed by doxycycline 100 mg orally bid for

10 days. Patients should be followed up within 48 h; if no improvement

is noted, they should be hospitalized.
Patients who are systemically unwell, vomiting or who have more
severe pelvic signs will require admission and intravenous antibiotics,
otherwise outpatient management may be appropriate.

Ampicillin 500mg qid IV

Metronidazole 1g bd PR
Doxycycline 100mg bd PO

Doxycycline 100mg bd PO x14 days

Metronidazole 400mg bd PO x10 days

There are many antibiotic regimes suitable for the treatment of pelvic
inflammatory disease and local guidelines should be formed in
collaboration with microbiologists. One suitable example is shown
above. In penicillin sensitive patients, a 3rd generation cephalosporin
may be chosen. Ciprofloxacin 250 mg stat is added when there is a
high suspicion of gonococcus (increasing penicillin-resistance).

Surgical treatment:
In acute phase:
Laparotomy may be necessary if there is no response to conservative
treatment or if the diagnosis is in doubt, i.e. other surgical condition
such as appendicitis is suspected. If a laparotomy acute sapingitis is
diagnosed, treatment should be restricted to taking cultures and
draining any collection of pus.
In chronic phase:
Surgery has a limited place in chronic PID with tubo-ovarian mass - the
aim is conservative with drainage of any collection and placement of a
drain, but radical surgery is not unusual and varies from simple
salpingectomy to hysterectomy.

14
ENDOMETRIOSIS

Endometrioti
c nodules
Fig. 1

External endometriosis severe stage

The term endometriosis is defined as the presence of functioning

endometrial tissue in an abnormal sites other than the uterine cavity.
This misplaced endometrial tissue may be found on the ovaries,
uterus, bowel, bladder, uterosacral ligaments, and in the pouch of
Douglas. These ectopic endometriums respond to the cyclical estrogen
and progesterone in the similar ways as the normal endometrium and
continue to act normal, and bleed each month, forming abnormal
growths, scarring lesions and adhesions. It bleeds at the time of
menstruation but the blood, endometrial tissue and tissue fluid are
trapped and forms a miniature blood cyst known as endometriotic
nodules Fig. 1).
It is estimated that as many as 15 per cent of all women of
reproductive age have endometriosis. In women who have chronic
pelvic pain or who are infertile, up to 50 per cent are thought to have
the condition. It can affect any woman, regardless of age, race or

childbearing status. It is one of the leading causes of pelvic pain in

women today.
Endometriosis appears during the reproductive age group and is found
more commonly in infertile woman. Endometriosis is almost certainly a
progressive disease, but the rate of progression and nature of lesions
varies from patient to patient. It can be symptomless even when
extensive. Endometriosis regresses after menopause.
TYPES OF ENDOMETRIOSIS
Depending on the sites at which endometriosis may occur it is further
divided into internal and external endometriosis.

Internal endometriosis In internal endometriosis the functioning

endometrial tissue is confined to the myometrium of the uterus.
Internal endometriosis is better referred to as adenomyosis.

External endometriosis If the presence of endometrial tissue is

found outside the uterus, it is called external endometriosis, or true
endometriosis. This ectopic endometrium may be in the pelvis, or
abdomen, or in more remote sites.

Although the two conditions are histologically similar, they are

probably of different aetiological factors and occur in different types of
patient.
ETIOLOGY
Endometriosis denotes the presence of functioning endometrial tissue
in sites other than the uterine cavity. How does this endometrial tissue
reaches this abnormal location is not entirely understood. There are
numerous proposed theories that attempt to explain how
endometriosis develops, ranging from Dr. John Sampsons theory of
retrograde menstruation to an immune system deficiency theory.
However, no single theory provides an adequate explanation for the
variation and range of location of endometriosis.
There are three main theories describing mechanism which may cause
endometriosis. These include:

Retrograde menstruation (Sampsons theory)

Metaplasia of coelomic epithelium
Vascular spread

Additionally, an alteration in the immune system may play a role in the

development of endometriosis.
Retrograde menstruation theory
Dr. John Sampson discussed the notion that blood is forced backward
into the uterus and tubes, thereby enabling the viable endometrial
tissue to implant itself into the surrounding areas. This endometrial
tissues still respond each month to hormonal instructions, swelling and
bleeding abnormally into the pelvic region. Sampson suggests that
retrograde flow is the primary path for the tissue to grow in the pelvis.
Path
of
the
menstrual flow and
its contents

There is the backflow

of the menstrual flow
and
its
contents
towards the ostium

The
viable
endometrial tissue are
deposited
and
implanted
on
the
structures within the
pelvic
cavity,
e.g.

Fig. 1.1 Possible cause of external endometriosis Retrograde

mesnstruation theory of Sampson.

One interesting question regarding Sampsons theory is if virtually all

women have retrograde flow of endometrial cells in their pelvis during
each menses then why dont virtually all women have endometriosis?
The answer to this is not known, however, there are several proposed
theories. The most widely accepted theory concerns the immune
system.
Basically, the immune system can be thought of as a
housekeeping mechanism that rejects or destroys any tissue that is
foreign. It can also regulate when a tissue will be allowed to grow
within the body.

When the immune system is activated an inflammatory response

occurs and these inflammatory cells help to reject the abnormally
placed tissues. If there is a problem with the immune response the
tissue might be allowed to grow in abnormal locations that is, to form
implants such as endometriosis.
Sampsons theory fails, however, to account for the development of
endometriosis in sites such as the arm or leg, or the brain, where they
have been discovered.
Metaplasia of the coelomic epithelium theory of Iwanoff
In the very early development stages of the fetus, there are only a few
cells present which have the potential to change into a number of
different types of cells. Both epithelial and stromal cells of the
endometrium have a common precursor in the coelomic epithelium
and adjacent mesenchyme. Metaplasia (change from one normal type
of tissue to another type of tissue) of the coelomic epithelium allows
endomterium tissue to replace other types types of tissues outside the
uterus. This could account for all abdominal and pelvic endometriosis,
and the rare cases in the rectovaginal septum and umbilicus.
Vascular spread theory of Halbans
The presence of endometriosis in site distant from the adnexae
(ovaries/tubes) has led to alternate theories. Another theory believes
that endometrial tissue will metastasize from the pelvic organs
throughout the body via the lymph and circulatory system. Vascular
spread of endometrial tissue (via blood vessels or lymphatic supplying
the uterus) from the uterus to distant sites may allow this tissue to be
transported to areas like the lung, brain or the knee. Certainly, the
uterine walls are highly vascularized and endometrial tissue might find
entrance through damaged vessels, such as those that are broken
during the course of menstrual flow.

Immune system deficiency

Another popular theory which is now under study is immunological in
nature.
Immunological defects have been found in women with
endometriosis. Both cell mediated and humoral immunological defects
have been noted. It is thought that in woman with immune system

deficiency, their body is unable to combat the migrating endometrial

tissue and destroy it.
Iatrogenic transplantation
Another theory which provides a basic for the migration of the
endometrial tissue is the iatrogenic transplantation. This means that
during surgery, accidental transference of the tissue is spread from the
uterus and/or other affected areas to another sites. This theory,
however, fails to explain why the endometriosis is there in the first
places.

RISK FACTORS
Numerous factors seem to affect whether a woman will have
endometriosis, the severity of the disease in any particular woman, her
symptoms, and her response to treatment. These include:

Genetics affected female family members double the risk.

Hormonal status higher estrogen level and prolonged heavy
menses increases risk of endometriosis.
Life style low body weight reduced risk of endometriosis by
decreasing estrogen level.
Contraceptive use Oral contraceptive possibly reduces
progression of endometriosis.
Obstetric history pregnancy and lactation reduce risk of
endometriosis.
Anatomic factors cervical stenosis increases risk.
Race caucasions are at higher risk.

PATHOLOGY
Wherever the location, the ectopic endometrial tissues continue to act
normal, and bleed each month, forming abnormal growth, scarring
lesions and adhesions. Deposits of endometriosis may vary in size
from a pin head to a large cyst filled with trapped blood (known as
chocolate cysts).

Cyst The tissue bleeds like endometrium but there is no escape

for the blood so cyst formation occurs. The size of the cyst depends
on its location. If the endometriosis occurs in the ovary the cyst
then to be larger.

Scarring and adhesions Bleeding from the ectopic endometrium

causes severe irritation and a sterile inflammatory reaction to the
adjacent tissues. Pelvic adhesions and fixation develop as a result
of the inflammatory process caused by the longstanding
endometriosis. Leakage of material from the chocolate cyst leads
to dense adhesion to surrounding tissues and leads to the formation
of frozen pelvis.

The essential histological features are the presence of endometrial

glands, stroma and histocytes laden with haemosiderin granules.

SITES OF ENDOMETRIOSIS
Most often, endometriosis is located in the pelvis near or on the
reproductive structures. However, endometriosis can occur in virtually
any tissue of the body, including distant sites like the lung, the knee
and the skin.
Common site

Ovaries
Pouch
Douglas
Uterine
ligaments
Bowel

Uncommon site

of

Urinary tract

Perineum
,
vagina
and
cervix
Abdominal wall

Other sites
(rare):
Limbs
Lungs
Inguinal region

Fig. 1.2 Possible sites of endometriosis.

Ovaries - The ovaries are the commonest sites for endometriosis,

and the lesion may be either superficial or deep. The superficial
lesions have been tought to arise from the implants of the
retrograde menstruation while the metaplastic changes account for
the deeper lesion. Ovarian endometriosis may take the form of
numerous endometrial cysts containing blood or a chocolate cyst
of various sizes.

Pouch of Douglas The next commonest sites are the pouch of

Douglas and the pelvic peritoneum. Peritoneal deposits often
present as a wide spread black nodules (endometriotic nodules)
with scarring and puckering of the peritoneal surface. The pouch of
Douglas may be obliterated by dense adhesions, causing the
formation of frozen pelvis.

Uterine ligaments The utero-sacral ligament are often involved.

Endometriosis deposits may be seen on the ligaments with scarring
and puckering of the utero-sacral ligament.

Bowel The small and large intestine, the appendix and the rectum
may become infiltrated with endometriosis. Edometriosis involving
the rectum may cause rectal bleeding or painful defaecation at the
time of the menses. Longstanding complication is fibrosis in the
wall of the bowel which leads to stricture formation and thus to
obstruction.

Perineum and vagina Deposits of endometriosis may be seen in

the posterior vaginal fornix or vaginal wall or the cervix. The lesions
are bluish-black in colour and cystic.

Urinary tract Endometriosis may also occur in the bladder which

may be seen at cystoscopy as a bluish areas if the mucosa is
involved. Painful micturition, haematuria in the absence of infection
are characteristic of urinary tract endometriosis. Endometriosis
invasion of the ureters may lead to ureteric obstruction.

Abdominal wall Endometriosis may also occur in the umbilicus.

It can also occur in the scar following operation on the uterus or an
abdomen in which there is widespread endometriosis.

PROGRESSION OF ENDOMETRIOSIS
Endometriosis is almost certainly a progressive disease, but the rate of
progression and nature of lesion varies from patient to patient. During
this progression ovarian cyst and dense adhesions may develop.
Endometriosis may progress from mild to severe stage.
Progression of endometriosis is basically described as, mild, moderate
and severe following surgical confirmation.

Mild Endometriosis

Only
endometriotic
nodules
The pelvic is
from adhesions

Moderate Endometriosis

few

free

Endometriotic nodules
abundant
Cyst more larger
Dense pelvic adhesions
develop

Severe Endometriosis

Cyst more larger and

may ruptured
Pouch of Douglas
obliterated with
extensive adhesions
Frozen pelvis develop
Surrounding structures
affected

CLINICAL PRESENTATIONS
Endometriosis is an enigmatic disease affecting reproductive-aged
women between 30 and 45 years. The clinical presentations of
endometriosis are often nonspecific. Although they may suffer
significant symptoms ranging from pelvic pain to infertility, most of
these women do not know that they have endometriosis. The
symptoms of endometriosis are astonishingly variable, depending on
the sites and the activity of the disease.

A) Symptoms
The most typical symptoms occur with endometriosis of the ovaries
and pelvis. Endometriosis primarily presents with pelvic pain (in about
80 per cent of patient). About 20 per cent of patient presenting with
endometriosis are also infertile. The predominant symptoms are:
Pelvic pain between menses
Secondary dysmenorrhoea
Dyspareunia
Heavy, often irregular menses
Infertility
(1)Pain
The extent of a patients pain often does not correlate with severity of
her endometriosis. Pain may occur as the result any or all of the
following:

Endometrial implants secreting irritating factors (e.g. histamine).

Scar tissue adhesions.
Leaking endometriomas.
Compression of other abdominal structures (e.g. bowel, ureters).
Compression of endometriotic nodules deep in the pelvis.
Invasion of the urinary tract.
Invasion of the gastrointestinal tract.

Basically, three main types of pain are found,

1. Dysmenorrhoea is typically of the congestive type, beginning a
few days or up to a week before the onset of menstruation and
relieved when the flow is established. It is felt in the pelvis and
lower back.
2. Ovulation pain is sometimes severe; the menstrual cycle tends
to be shortened so that ovulation pain may continue without
relief into premenstrual and menstrual phases.
3. Dyspareunia is the common complain if the endometriosis
involved the cul-de-sac (pouch of Douglas), particularly if the
uterus is retroverted and fixed by adhesions. Dyspareunia is
generally felt deep in the pelvis and is due to pressure on the
ovaries and recto-vaginal septum.

(2)Disturbances of menstruation
In majority of affected women menstrual disturbances occur.
Menorrhagia is a frequent symptom, which is due to the ovarian
disturbance. Premenstrual staining or spotting, short cycles and
prolonged bleeding may also occur.
(3)Infertility
Endometriosis is associated with infertility. About 20 per cent of patient
presenting with endometriosis are also infertile. Endometriosis is
thought to cause infertility by:
Distorting anatomy of the pelvis.
Creating hormonal abnormalities.
Altering the pelvic biological environment.
Influencing the immune system.
Interfering with sperm function.
Possibly altering the process of embryo implantation.
B) PHYSICAL SIGNS
The most common areas affected by endometriosis are easily reached
during examination of the pelvis or abdomen. The most typical
physical signs of endometriosis are
Fixed retroversion of the uterus with nodularity behind the uterus.
Tender ovarian mass which is not mobile.
Nodularity and scaring of the utero-sacral ligament.
The presence of endometriosis deposits which can be seen as a
bluish areas on the cervix, in the vaginal, or even in the
umbilicus.
DIAGNOSIS
Suspicion of endometriosis is based on the patients history and
description of symptoms, as well as the presence of pelvic pain and/or
palpable nodules during physical examination.
Endometriosis should be suspected in women with any of the following
symptoms.

Dysmenorrhoea (particularly those that worsen with time and are

unresponsive to medical therapy).
Deep dyspareunia.
Dyschezia (pain with bowel movement, particularly noticeable
near menses).
Severe ovulation pain.
Focal or generalised recurrent pelvic pain.
Dysuria and haematuria which is unrelated to infection.

During pelvic examination, endometriosis is suspected when any of the

following are discovered.

Tenderness or nodularity in posterior cul-de-sac, especially on the

utero-sacral ligaments.
Adenexal masses.
Reduced mobility, or fixation of the uterus and ovaries.
Unusual pain associated with examination.

Ultrasound (particularly transvaginal sonagraphy) is commonly used to

evaluate the adnexa for endometriomas. Ultrasound may lead to a
suspicion of endometriosis, but will not confirm it.

Fig.1.4 Ovarian endometriosis (Endometrioma). Sonogram demonstrates a

chocolate cyst (M) posterior to the uterus (U). B = bladder.

The only positive way to diagnose endometriosis is by direct

observation of the misplaced endometrium via surgery. Laparoscopies
are now done routinely to diagnose endometriosi. At laparoscopy, the
extent of the disease should be determined.

Fig. 1.5. Laparaoscopic view showing endometriosis of the ovary

MANAGEMENT OF ENDOMETRIOSIS
Treatment of pelvic endometriosis is essentially conservative and is
directed to relief of symptoms as to removal of their cause.
In order to develop a long-term treatment plan for patient with
endometriosis, the gynaecologist must carefully and thoroughly
evaluate factors, includes

The patient age

Severity of symptoms
Type and extend of disease
Plans for future pregnancy
Physical findings
Life style of the patients

There are several treatment options for endometriosis which includes

expectant management (observation, or a wait and see approach),
medication, surgery, or a combination of both medication and surgery.
The choice of treatment is usually based on the nature of symptoms,
the severity of the disease and the goals of the patient.
Observation may be the appropriate treatment for younger women
with minimal disease and symptoms. It is important to have the

woman maintain a regular schedule of follow-up (every 6 to 12

months) to note any changes or progression of the disease.
Medical Treatment
Treatment with medications may focus on several strategies:
To relief the discomfort of the disease only.
To stop the progression of the disease.
Medical treatments are:
Non-hormonal
Hormonal
Non-Hormonal
Analgesic therapy, treating the discomfort of the disease only, may be
indicated for women with mild to moderate premenstrual pain, with no
pelvic examination abnormalities, and with no immediate desire to
become pregnant.
Temporary pain relief may be possible with non-hormonal medications
such as ibuprofen or others NSAIDs (non steroidal anti-inflammatory
drugs). In more severe cases, narcotic drugs can be prescribed.
Hormonal
This is successful in majority of the cases. The basis of hormonal
therapy of treating endometriosis is to suppress estrogen synthesis
and release. In consequence menstruation ceases and this inhibit
further growth of the lesions. Currently three regimens of hormonal
treatment are widely used,

Progestogens
Danazol
Analogues of gonadotrophin-releasing hormone (GnRH)

Progestogens - The female hormones known as progestins can also

be used in the management of endometriosis. Primolut-N
(norethisterone) may be given starting with 10 mg daily and increasing
up to 40 md daily or more for 9 to 12 months. The injectable form of a
drug known as medroxyprogesterone acetate is one of the more
commonly used progestins, but it may have side effects of unwanted
weight gain, fluid retention, elevated blood pressure, and headache.

Danazol - Danazol, a synthetic derivative of testosterone, a weak

androgenic hormonal drug may be used to reduce natural levels of
estrogen and progesterone to low levels.
Danazol is given in a dose of 200mg 2 4 times a day for 3 12
months, depending on the extent of the lesions and on the response. It
appears that the use of Danazol may be superior to the progestogens
regimens in controlling symptoms and progression of disease in women
with moderate-to-severe endometriosis (Fig1.5). The potential side
effects of Danazol include,

Weight gain
Acne and oily skin
Hirsutism
Headaches
Deepening voice

GnRH analogues (agonist) - GnRH analogues produces a pseudo

menopausal state in women. GnRH analogues make the pituitary
gonadotrophs insensitive to stimulation by endogenous GnRH, and this
stops the ovary from producing estrogen and creating a menopauselike state.
GnRH analogues is u8sually given as a long acting injection for 3 6
months.
Treatment with GnRH analogues may result in side effects that are
similar to the symptoms of menopause including
Hot flushes.
Sleep disturbances.
Mood changes.
Vaginal dryness.
Early loss of calcium from bones (with extended usage over six
months).

Surgical Treatment
Surgery is usually reserved for women with severe endometriosis,
including adhesions and infertility. Surgical procedures can be
accomplished with laparotomy or laparoscopy.

Conservative surgery attempts to remove or destroy all of the

outside endometriosis tissue, remove adhesions, and restore the pelvic
anatomy to as close to normal as possible. A conservative operation is
performed as far as is possible and the aim should always be to leave
some normal ovarian tissue.
Definite (or radical) surgery is appropriate for the woman with
severe symptoms or disease, and no desire for future childbearing.
This type of surgery involves abdominal removal of the uterus, both
ovaries, both fallopian tubes, and any remaining adhesions or
endometrial implants. Hormonal replacement therapy may be
indicated after total hysterectomy and should be tailored to the
individual womans needs.
General surgical principles when treating endometriosis include:
1) Attempt to remove as much of the endometriosis as possible.
2) Retain fertility potential (the ability to become pregnant) whenever
possible.
3) Recreate normal relationships of the pelvic and abdominal organs
and surrounding structures.
4) Only in most severe cases that caused debilitating symptoms and
that have failed multiple other types of therapy, should radical
surgery be performed.

ENDOMETRIOSIS SUSPECTED
CONFIRMATION OF DIAGNOSIS AND EXTENSION OF ENDOMETRIOSIS
( by laparoscopy or laparotomy )

ENDOMETRIOSIS CONFIRMED
MILD

MODERATE

SEVERE

HORMONE THERAPY

CONSERVATIVE SURGERY

GOOD RESPONSE
( symptoms improve )

POOR RESPONSE
( symptoms persist or recur )

CONTINUE HORMONE

NO FURTHER SYMPTOMS

SURGERY

PLAN FOR FUTURE

PREGNANCY

EXTENSIVE DISEASE
OR NO DESIRE FOR
CHILDBEARING

CONSERVATIVE SURGERY

RADICAL SURGERY

RESIDUAL LESION

NO RESIDUAL

NO FURTHER TREATMENT

NO SYMPTOMS
SYMPTOMS PERSIST

HORMONE THERAPY
Fig.1.6. Flow chart in the management of endometriosis

15
DISPLACEMENT OF THE UTERUS
ANATOMY OF POSITION OF THE UTERUS IN PELVIS
The transverse cervical (cardinal) and uterosacral ligaments inserted in
the upper parts of the cervix and of the vaginal support the uterus and
vault of the vagina in their normal position in the pelvis. The round
ligaments help to maintain the uterus in anteversion.
In the adult women the uterus is
situated in the center of the true
pelvis and in the majority is in a
position of anterversion (the
fundus is directed forwards
towards the bladder) and of
anteflexion (the body of the
uterus is bent forwards at almost
a right-angle on the cervix).
The uterus is a partially mobile
organ, fixed in the lower pelvis at
the
cervix.
This
anatomic
relationship permits the fundus
of the uterus to move relatively freely in the sagittal, vertical, oblique,
and anteroposterior planes. Hypermobility occurs during the
nonpregnant state, but it is more common during gestation and
occasionally can result in retroversion and incarceration.
Rarely,
prolapse occurs during pregnancy.

UTERINE DISPALCEMENT
The uterus may be displaced forwards or backwards, or downwards.

FORWARD AND UPWARD DISPLACEMENT of the uterus is due to

previous surgery such as shortening of the round ligaments
(ventrosuspension) or due the presence of tumour in the pouch
of Douglas.
BACKWARD DISPLACEMENT of the uterus, know as retroversion,
may be idiopathic or due to adhesions (such as in chronic pelvic
inflammatory disease, endometriosis or malignancy).
DONWARD DISPALCEMENT of the uterus, i.e. prolapse of the
uterovaginal organ, is due to weakening of the support of the uterus
(see Chapter 16).
LATERAL DISPLACEMENT of the uterus is due to adhesion pulling the
uterus sideway, or due to tumour pushing the uterus to one side.

RETROVERSION OF THE UTERUS

If the fundus is directed backwards with
the cervix pointing into the posterior
fornix, the uterus is said to be retroverted
(Fig. 1.1).
and this is usually
accompanied by backward flexions.
Uterine retroversion is a common and
generally asymptomatic state. One out of
5 women has a retroverted uterus, either
congenitally or due to an acquired
condition.

Fig. 1.1 Retroversion of the

uterus

Types of retroversion:

MOBILE RETROVERSION of the uterus occurs in about 15

percent of the woman and is usually asymptomatic. Occasionally
may cause deep dyspareunia.
No treatment is required for
asymptomatic cases.

If deep dyspareunia is the chief complain,

the uterus can be anteverted with vaginal
pessary Hodge pessary.
Ventrosuspension
procedures
considered in recurrence cases.

can

be

Fig. 1.2 Hodge pessary

FIXED RETROVERSION OF THE UTERUS

Causes:
In instances in which pathology is present, acquired fixed retroversion
of the uterus results from the following conditions:
1) Fixation by adhesions may fasten the body of the uterus in the
retroverted positions. Adhesions commonly result from

Chronic salpingitis
Endometriosis
Malignancy disease, especially ovarian carcinoma

2) Displacement by a tumour The presence of tumour may

displace the uterus backwards.

Tumors distorting uterine shape or position (uterine fibroids)

Ovarian tumour

Symptoms:
Uncomplicated retroversion of the uterus causes no symptoms.
Symptoms traditionally attributed to uterine retroversion include the
following:

Pelvic discomfort, pressure, or pain

Menstruation disturbances
Dyspareunia due to pressure on prolapsed ovaries. This is
commonly seen in some cases of acquired retroversion (e.g.
endometriosis or pelvic inflammatory disease)
Infertility this may be because the cervix points forwards and is
not inseminated during intercourse.
Constipation

Urinary difficulty, urine retention: Because the bladder base,

which is attached to the supravaginal cervix the urethra,
becomes stretched and elongated when the uterus is
retroverted.
Pelvic congestion syndrome

Diagnosis:
The diagnosis of retroversion of the uterus is made on bimanual pelvic
examination and depends on the following physical signs:
1) The cervix points forward.
2) The body of the uterus is felt through the posterior fornix.

Treatment:
If symptoms occur from retroversion alone in nonpregnant individuals,
they are minimal. Pelvic pain and the other symptoms associated with
retroversion are principally due to coincidental pathology. Evidence
that retroversion alone is responsible for abortion or infertility is
lacking. When these conditions are encountered, another etiology must
be sought. For these reasons, uterine suspension procedures have
nearly disappeared from gynecologic surgery. Uterine suspension is
indicated when retroversion is associated with endometriosis or
following microsurgical tubal reconstruction procedures for infertility.
However, the presence of uterine retroversion alone in an
asymptomatic patient is not an indication for a prophylactic uterine
suspension.

IMPACTED RETROVERTED GRAVID UTERUS

A pregnant retroverted uterus wills nearly always anteverted

spontaneously but if this does not occur it will becomes impacted in
the pelvis at about 14 16 weeks gestation. The women will usually
present with urinary symptoms such retention of urine or retention
with overflow.

Predisposing factors for symptomatic incarceration include multiparity

combined with a unique combination of pelvic architecture, uterine
positioning, and laxity of supporting tissues. A prior history of
retroversion/incarceration may be elicited. Women in the latter
category should be evaluated frequently in the late-first and earlysecond trimester to ensure that if the uterus remains retroverted, it
does not fully incarcerate.
Pathophysiology
Most pregnancies complicated by retroversion/incarceration involve a
normal uterus that simply becomes impacted under the sacral
promontory when it enlarges (Fig.1.3). In the remaining cases, other
pathology either alters the normal uterine contour or fixes the uterus,
preventing normal motion. When pathology is present, the findings
may include (1) distortion of the uterine contour by adnexal tumor or
fundal or posterior leiomyomata, or (2) adhesions from endometriosis
or prior pelvic inflammatory disease.

Cervix is usually deviated

anteriorly

As the uterus enlarge it becomes impacted

under the sacral promontory
Fig. 1.3-Impacted retroverted gravid uterus

The uterus rotates posteriorly, and the cervix is forced anteriorly as the
uterus is wedged progressively more firmly into the hollow of the
sacrum. Thus, once the uterus becomes entrapped, the incarceration
worsens with time. Normal voiding becomes difficult or impossible,
with obliteration of the posterior uterovesical angle restricting
funneling of the bladder outlet.

Clinical presentation
The principal symptoms of incarceration include (1) abdominal pain,
pelvic pressure, or uterine contractions; (2) tenesmus, rectal pressure,
or constipation; (3) paradoxical urinary incontinence or frequency or,
more commonly, voiding difficulty or urinary retention (frequently
mandating intermittent or continuous catheterization); or (4) vaginal
bleeding.

Diagnosis
Performing a pelvic examination and reviewing a characteristic history
establish correct diagnosis of incarceration. A common clinical clue is
progressive difficulty with voiding associated with pelvic pain and
pressure or uterine cramping. The clinical examination usually is
striking for the following findings:

Acute anterior angulations of the vagina, with the cervix abutting

or positioned well behind the pubic symphysis
A soft, smooth, nontender mass filling the cul-de-sac
Posteriorly positioned uterine fundus, behind the sacral
promontory

Management
The best treatment for symptomatic midtrimester incarceration of a
normal uterus consists of bladder decompression combined with a
program of patient positioning to facilitate spontaneous replacement.
Prior to attempting any uterine manipulations, the best plan is to leave
an indwelling catheter for 24-48 hours. During this interval, the patient
is instructed to perform repositioning exercises (intermittent kneechest positioning or sleeping prone).
If these maneuvers prove unsuccessful, manual uterine replacement
with the patient positioned in modified knee-chest position can be
attempted. To perform this procedure (Fig.1.4), the anterior lip of the
cervix is grasped with a long Allis or other atraumatic clamp. The
patient is placed in the knee-chest position, and pressure is applied to
the incarcerated fundus by the surgeons finger inserted in the vagina
or rectum. Gentle but constant traction is applied to the cervix, and the

uterus is slowly rotated into the normal position, preferably passing the
fundus to one side or the other of the sacral promontory.
These maneuvers usually prove successful and should be neither
painful nor difficult. Only mild-to-moderate force is required for the
replacement. Excessive force jeopardizes patient compliance, risks a
cervical injury from the cervical grasping instrument, or may possibly
damage the pregnancy by distorting the uterus or obstructing uterine
blood flow.
In unusual instances, when both bladder drainage with repositioning
and a trial of gentle manipulation fail to replace the uterus, uterine and
maternal relaxation by the use of anesthesia combined with a tocolytic
can be considered.
When replacement is successful, instructing the patient to sleep in the
prone position, practice occasional knee-chest positioning, or use a
pessary is often recommended to keep the uterus correctly positioned.

Manual uterine replacement for

impacted retroversion of gravid
uterus

Fig. 1.4 Treatment for impacted retoversion of gravid uterus

SUMMARY
Uterine retroversion with incarceration is an infrequent but by no
means rare obstetrical condition. Clinicians should consider this
disorder when presented with a characteristic set of clinical findings

and symptoms. In uncomplicated second-trimester incarceration,

treatment by patient repositioning or manual uterine replacement is
usually easy. The rare instances involving retroversion persisting
beyond the second trimester, or cases complicated by pelvic adhesions
or permanent distortions in uterine shape, are difficult to manage and
require individualization. In most of these instances, cesarean delivery
is required.

16

PROLAPSE OF THE FEMALE GENITAL TRACT

Pelvic organs such as the uterus and vagina are maintained in position
by supporting ligaments, fascia and muscles of the pelvic floor.
Damage or weakness to these supports may enable one or more pelvic
organs to prolapse within, or less frequently, completely protrude
outside of the vagina.
Genital prolapse is a frequently encountered condition which occurs
mainly in women who have borne children. Prolapse may appear
shortly after chilbirth or may not become apparent until the
menopause or after when there is general shrinking and weakness of
the supports of the pelvic organs.

Types
There are several types of genital prolapse. They may occur separately
but more frequently, are combined.
(A) Vaginal wall prolapse
Vaginal wall prolapse may occur independently of the uterus. Several
types are described:

Cystocoele - descent or bulging of the bladder into the upper two

thirds of the anterior vaginal wall. It denotes weakness in the
investing fascia of the vagina.

Urethrocoele - bulging of the urethra into the lower one third of

the anterior vaginal wall. It is more properly called urethral
displacement, as the urethra is not dilated.

Enterocoele - herniation of the pouch of Douglas into the upper

posterior vaginal wall. The peritoneal sac may contain loops of
bowel

Rectocoele - prolapse of the rectum into the lower posterior

vaginal wall. It is not to be confused with rectal prolapse.

Vaginal vault prolapse indicates a failure of the supports around

the upper vagina. It may be seen after vaginal or abdominal
hysterectomy.

(B) Uterine prolapse

The uterus cannot prolapse without carrying the upper vagina with it.
Three degrees of uterine prolapse are described:

First degree - cervix remains within the vagina (i.e. cervix is

situated between the level of the ischial spines and the vaginal
introitus.

First-degree prolapse

Second degree - cervix protrudes through the introitus, but the

body of the uterus remains within the vagina.

Second-degree prolapse

Third degree or procidentia - uterus lies entirely outside the

introitus.

Third-deree prolapse

Procidentia denotes complete failure of all the genital supports. It must

be distinguished from hypertrophy, elongation, congestation and
oedema of the cervix all of which may cause a large protrusion of
tissue beyond the introitus.

Etiology
Genital prolapse results from weakness and elongation of the
ligaments which hold the uterus in its normal position; these are the
cardinal (transverse cervical or Mackenrodts ligaments) and the uterosacral ligaments.
More frequently, genital prolapse is the result of:

Childbirth - attenuation of the pelvic fascia, ligaments and

muscles from excessive stretching during vaginal delivery. More
likely to follow a difficult delivery.
The cardinal ligaments (Mackenrodts) provide the major support
for the uterus and vagina. These ligaments may be unduly
stretched if the fetus is large or if forceps delivery is attempted
before full cervical dilation. If the cardinal ligaments do not
return to normal after delivery, the uterus will sag backward and
downward into the vagina.

Post-menopausal estrogen deficiency - The more severe

prolapse are seen in postmenopausal women when tissue
atrophy eliminates whatever residual support existed.

Raised intra-abdominal pressure The cardinal and the

utero-sacral ligaments may be unduly stretched in the following
conditions which caused an increased in the intra-abdominal
pressure.
o Chronic cough
o Ascites
o Repeated lifting of heavy weights
o Habitual straining due to constipation
o Large pelvic tumour

Clinical features
Symptoms of genital prolapse are variable and may not bear much
relation to the physical signs found on examination.
Classically, genital prolapse occurs in a parous postmenopausal woman
who complains of "something coming down" or of stress incontinence.
Typically, symptoms are worst after prolonged standing and relieved by
lying down. Symptoms of uterine prolapse reflect sensations produced

by the weight of the descending structures and their protrusion

through the vaginal introitus. Third-degree prolapse may eventuate in
cervical ulceration and bleeding.
The precise clinical picture depends on the organs involved; common
features include:

The commonest complaint is of a lump or mass within the

vagina. The patient may say that there is "fullness down below"
which may become a "lump between the thighs" in the case of
procidentia. This lump may be the uterus, a cystocoele, and
enterocoele, or any combination of these.
Pain is not a prominent feature - but some may complain of low
backache and/or low abdominal dragging pain - usually
worsening during the day and relieved by rest. Backache as
such is seldom caused by prolapse and when it is, it is due to
pulling of the utero-sacral ligaments.
Urinary symptoms present a varied pattern. Urinary frequency,
urgency, incontinence and rarely, retention, may occur in
patients with anterior vaginal wall prolapse
Rectal symptoms many women with prolapse complain of
constipation. Difficulty in defaecation may indicate a rectocoele
Vaginal discharge is a frequent complaint of women with
prolapse. It may due to decubitus ulceration or to an infected
tear or cervical erosion. A blood-stained discharge may occur
when there is ulceration.

Diagnosis
The diagnosis of prolapse is confirmed by good history and
examination.
History a good history may lead to the possibility of the genital
prolapse.
Inspection - a procidentia should be obvious.
Examining a patient with prolapse - The woman should first be
examined lying on her back with her knees drawn up and apart. She
should be asked to strain and cough. In case of doubt she may be
asked to stand up or walked about for a short time before testing for
prolapse again. The degree of descent of the cervix is best tested with
a finger in the vagina. When there is a complaint of stress incontinent,
examination is best made with some urine in the bladder; the urethra

and bladder neck may be supported with two fingers to demonstrate

that this controls the incontinence.
Vaginal examination - using a Sim's speculum to hold back the
posterior vaginal wall. Ask the patient to strain. This should
demonstrate descent of the anterior vaginal wall indicative of a
cystocoele or urethral displacement. Similarly, holding back the
anterior vaginal wall while the patient strains, will demonstrate a
rectocoele.
Rectal examination - to confirm posterior wall prolapse and
distinguish rectocoele from enterocoele.
In cases of difficulty, ask the patient to stand or walk for some time before examination.

Management
The management of prolapse may be operative or palliative (nonsurgical). The management of prolapse will depend upon:

The patient's age, marital status, desire for children

Sexual activity and need for a functional vagina
Degree of prolapse and associated complications
Exacerbating factors which should be controlled - such as
obesity, smoking, constipation

Non-surgical treatments include:

Pelvic floor exercises - although effects are limited because

they do not enhance support from the fascia and ligaments
Pessary treatment Many types of pessary have been devised
for prolapse. Their use is only palliative or temporary. The
indications for pessaries are:
1)
2)
3)
4)
5)
6)

During pregnancy.
When a future pregnancy is desire within a short time.
If patient is medically unfit for surgery.
If there is a long waiting list for definitive repair.
To promote healing of a decubitus ulcer before surgery.
In patients who refuse operation.

Types of pessaries:
Ring pessary

Hodges pessary

Shelf pessary

Complications of pessary: - Ulceration of the vagina and

cervix may result with the used of these pessaries. A neglected
pessary may become embedded in the vaginal wall and may only
be removed with great difficulty.

Surgical treatment:
Surgical repair is the most satisfactory treatment and with appropriate
control of contributory factors, may enjoy a high success rate. It also
may be the most desirable option for patients whom are not
sufficiently motivated to keep to the rigors of pelvic exercises or to
observe the safeguards needed with pessaries.
Options include:

Anterior colporrhaphy - for cystocoele or urethrocoele

Posterior colporrhaphy - for rectocoele
Manchester-Fothergill operation - amputation of the cervix,
shortening of the cardinal ligaments, and repair of the vagina
(anterior and posterior colpoperineorrhaphy).
Vaginal hysterectomy - especially for procidentia
Vaginal vault suspension - for prolapse following hysterectomy

Prevention
Measures that may reduce the likelihood of prolapse include:

Proper episiotomies and perineal repair.

Avoidance of overstretching of the perineum during delivery.
This can be achieved by:
1) The woman in labour must be discouraged from bearing down
before full dilatation, because attempts at delivery before full
dilatation may damage the uterine supports.
2) The second stage of labour should not be prolonged unduly

Regular pre- and post-natal pelvic floor exercises.

Estrogen replacement after the menopause.
Avoidance of exacerbating factors.

17
UTERINE FIBROIDS
Uterine fibroids, sometimes referred to as uterine myomas, are the
commonest of all pelvic tumours. At least 1 out of every 4 women has
fibroids.
Uterine fibroids are benign, growths
presenting about 30% of women over
the age of 30. Uterine fibroids are
extremely common smooth muscle
tumors of the uterus. The tumours are
usually multiple and vary in size from

tiny seedling to huge masses which fill the abdomen. They are usually
detected on pelvic examination, which may reveal the uterus to be
enlarged and/or irregular in configuration. The vast majority of cases is
absolutely silent and causes no symptoms.
Uterine fibroids are uncommon before the age of 30 and tend to occur
in nulliparous or relatively sterile women. The aetiology remained
unclear, but it is believed that it may be associated with female sex
hormones.
There is considerable circumstantial evidence that
estrogenic stimulation plays a role in their pathogenesis.
Consequently, they develop only during reproductive years, enlarge
both during pregnancy and in women using contraceptive steroids and
tend to shrink after menopause.

Types of Fibroids
Fibroids are classified by their location (see figure 1and 2), which affect
the symptoms they may cause and how they can be treated. Fibroids
that are inside the cavity of the uterus (intracavitary myomas) will
usually cause bleeding between periods (metrorrhagia) and often
cause severe cramping. Fortunately, these fibroids can usually be
easily removed by a method called "hysteroscopic resection," which
can be done through the cervix without the need for an incision.
Submucous myomas are partially in the cavity and partially in the wall
of the uterus. They too can cause heavy menstrual periods
(menorrhagia), well as bleeding between periods. Some of these can
also be removed by hysteroscopic resection
Intramural myomas are in the wall of the uterus, and can range in
size from microscopic to larger size. Many of these do not cause
problems unless they become quite large. There are a number of
alternatives for treating these, but often they do not need any
treatment at all. Subserous myomas are on the outside wall of the
uterus. A fibroid may even be connected to the uterus by a stalk
(pedunculated myoma.) These do not need usually treatment unless
they grow large, but they can twist and cause pain. This type of fibroid
is the easiest to remove by laparoscopy.

Fig. 1
Diagrammatic drawing showing - Types of fibroids

Inracavitary myoma

Intramural myoma

Subserous
myoma

Submucous myoma

Fig.2- Uterus with multiple uterine fibroids demonstrating subserosal,

intramural, subnucosal and intracavitary types.

Pathology
Uterine fibroid arises from the uterine muscle and grows slowly. The
tumour composed mainly of smooth muscles with some intermingling
fibrous tissue. A pseudocapsule is formed by compression of the
surrounding uterine muscle.
Gross characteristics
Uterine fibroids may be small, medium sized or large.
They may be single or multiple and large numbers have been
removed from a single uterus.
They are usually firm, but can be soft and cystic, if degeneration has
taken placed.
On cut surface, fibroids appear as rounded, rubbery, pale or white
nodules, which have a whorled appearance.
There is a thin layer of false capsule (pseudocapsule) of compressed
uterine muscle which allows easy enucleation.
Through this
pseudocapsule the blood vessels enter the tumour.

Microscopically basic pattern of uterine fibroids consists of

interlacing bundles of smooth muscles fibres arranged as twist
and whorls (Figure 3).

Fig. 3 Microscopic appearance of uterine fibroids

Clinical presentation of uterine fibroids

The clinical presentations of uterine fibroid will depend on its size, on
their situation in the uterus and their relation to the uterine cavity.
Small fibroids and some large ones may cause no symptoms and are
discovered at routine examination. A woman with uterine fibroids may
present with the following symptoms and signs.
SYMPTOMS:
Asymptomatic - In many (probably most) cases, fibroids do not cause
symptoms. A small fibroid buried deep in the uterine wall should not
produce symptoms.
Abdominal swelling The swelling is a common presentation and
may become evident to the women herself or may be found by her
doctor. The swelling is due to the enlarging fibroid in the abdomen.
The tumour is hard, non tender (unless the fibroid has becomes
complicated) and may causes local discomfort.
Menstrual disturbances Disorders of menstruation is another
common complaint for patients to seek medical advice. Menstrual
disturbances result from submucous fibroids that distort the
endometrial cavity.
The uterine cavity may also be enlarged in
surface area and thus have more blood loss with menstruation. The
most characteristic disturbances of menstruation is menorrhagia, that
is gradual increase in the duration of periods and the amount of blood
lost; they may be accompanied by the passage of clots and the
interval between periods may be reduced. Increased menstrual loss is

usually caused by submucous fibroids. If heavy bleeding persists the

woman may become anaemic.
Another common complaint is
intermenstrual bleeding. Intermenstrual bleeding may be due to a
fibroid poly with an ulcerated tip. Anaemia may result leading to
lassitude and weakness. In addition to menorrhagia, larger fibroids
may also cause, painful periods, and irregular bleeding between
periods.
Pressure symptoms - A large fibroid filling the abdomen may cause
pressure effects to the surrounding structures.
1. Bladder: Pressure symptoms of fibroid most often affect the
bladder either by direct pressure or by incarceration of a mass of
fibroids, in the pelvic cavity. Frequency and retention of urine may
occur.
2. Bowel: Constipation may result from pressure on the rectum
though this is infrequent.
3. Pelvic veins: Oedema of the legs, haemorrhoid and varicose vein
in the legs may occasional occur when fibroid cause pressure effect
on the pelvic veins or on the inferior vena cava. This oedema or
varicose vein of the legs can be unilateral or bilateral.
4. Respiratory system: A large fibroid filling the abdomen may affect
on the respiration and cause dyspnoea.
5. Backache: A large posterior fibroid in the pelvis may cause
persistent backache.
Infertility and miscarriage - Although infertility is probably not very
common in women with fibroids, in some cases a fibroid may alter the
structure of the uterus, making it difficult to conceive or may
contribute for recurrent miscarriages.
Pain- Fibroids are usually silent, as previously mentioned. Pain is not a
common symptom.
Pain if presence may be due to congestive
dysmenorrhoea. Colicky pain may accompany extrusion of a fibroid
polyp through the cervix by uterine contraction.
Frank pain and tenderness, if caused by fibroids, is usually indicative of
a process called "red degeneration". Red degeneration occurs when
the fibroid is rapidly growing or the large fibroid outgrows its blood
supply, the tissues cannot get enough oxygen, and may die and
resulting in acute abdominal pain ("a fibroid equivalent of a heartattack!"). If left untreated, the body will slowly absorb this non-viable

tissue, but the patient could be very uncomfortable for possibly weeks.
Torsion of the pedunculated fibroid may also causes abdominal pain
with signs of acute emergency.
Pelvic pain A large cervical fibroid may cause pelvic pain and make
sexual intercourse impossible
PHYSICAL SIGNS:
The physical signs vary with the size, position and the number of the
fibroids.

Uterine enlargement The uterus feel hard and enlarged. More

often the enlargement is asymmetrical; abdominal and vaginal
examination may show an irregular or knobbly uterus because
there are multiple fibroids. A symmetrical enlargement of the
uterus is found with a submucous fibroid.

Mass non-tender The fibroids are not tender on palpation, unless

the fibroid has become complicated.

Mobility of the mass On moving the cervix the whole firm fibroid
mass moves.

Diagnosis
Fibroids are fairly easy to diagnose. The
diagnosis is best obtained by a good
physical examination and perhaps an
ultrasound. Some women present to their
doctor for the first time with a uterus that
has grown past the umbilicus, as if she
were in the last few months of
pregnancy! The diagnosis of uterine
fibroids depends on finding a hard,
rounded or lobulated mass continuous
with the uterus.
Fig. 4 Abdominal swelling secondary
to uterine fibroids.

They are usually detected on abdominal or bimanual examination. In

general fibroids are not tender to touch and are mobile and the uterus
are usually enlarged and/or irregular in configuration.

Fibroids may be felt during a pelvic exam, but many times fibroids that
are causing symptoms may be missed if the examiner relies just on the
examination. Also, other conditions such as adenomyosis or ovarian
cysts may be mistaken for fibroids. For this reason, an ultrasound
examination should be performed at the time of the first visit when a
woman has symptoms of abnormal bleeding or cramping. This test
involves either a probe placed on the abdomen, or a vaginal probe
placed in the vagina. This ultrasound can be used to diagnose fibroids
that have grown into the endometrial cavity.

Fig. 5

Intracavitary and submucous fibroids

can be diagnosed by a diagnostic
hysteroscope.
Hysteroscopy uses a
hysteroscope,
which
is
a
thin
telescope that is inserted through the
cervix into the uterus.
Modern
hysteroscopes are so thin that they
can fit through the cervix with minimal
or no dilation. Because the inside of
the uterus is a potential cavity, like a
collapsed air dome, it is necessary to fill (distend) it with either a liquid
or a gas (carbon dioxide) in order to see. Diagnostic hysteroscopy can
be done as an outpatient procedure. During diagnostic hysteroscopy
the hysteroscope is used just to observe the endometrial cavity (inside
of the uterus.)
The picture below is a view through a hysteroscope examination. It
shows the inside of a uterus with two intracavitary myomas on the

back wall. The upper portion of the photograph shows the top of the
uterus, which is normal. Fibroids like this can cause dysmenorrhea,
menorrhagia and bleeding between periods.

The Differential Diagnosis

The differential diagnosis is from other causes of uterine enlargement
and from other pelvic tumour.
One of the most common conditions
confused with fibroids is adenomyosis.
This can be a serious error, as the
treatment may be quite different. In
adenomyosis the lining of the uterus
infiltrates the wall of the uterus,
causing the wall to thicken and the
uterus to enlarge. This can cause
severe pain, and heavy bleeding.
Uterine
adenomyosis

The
difference
between
myoma
and
adenomyosis may not be appreciated
until attempted removal reveals the
lack of capsule, but in general
adenomyosis are firmer tumours and
there is severe dysmenorrhoea. On
ultrasound examination adenomyosis will often appear as diffuse
thickening of the wall, while fibroids are seen as round areas with a
discrete border. Adenomyosis is usually a diffuse process, and rarely
can be removed without taking out the uterus

Ovarian tumours The main difference between ovarian tumours

and myoma , as a rule, the uterus can be detected as separate from
the swelling and menstrual disorders are not so common. But difficulty
may arise when the ovarian tumour is adherent to the uterus.
Pregnancy In pregnancy there is amenorrhoea and the uterus is soft,regular and
contracts from time to time. Fibroid never cause amenorrhoea and the uterine
enlargement is harder and generally more irregular. If amenorrhoea and fibroid co-exist,
a pregnancy test and ultrasonic scan are necessary to diagnose pregnancy.

Management
The most important question to ask is whether or not the fibroids need
to be treated at all. Obviously, fibroids that are causing significant
symptoms need treatment. The location of the fibroids plays a strong
influence on how to approach them.
Fibroids may require treatment in the following circumstances:

Fibroids are growing large enough to cause pressure on other

organs, such as the bladder.
Fibroids are growing rapidly

Fibroids are causing abnormal bleeding

Fibroids are causing problems with fertility.

TREATMENT OPTIONS:
There are a number of treatment options available for fibroids:
FOR ASYMTOMATIC UTERINE FIBROID
a) Observation- If a fibroid uterus is "silent", and none of the above
situations present, conservative observation is appropriate. Because
fibroids may continue to grow, regular check-ups are necessary for
ongoing evaluation. Small and asymptomatic fibroids can usually be
managed by an annual examination to check for growth. In cases
where there are symptoms, women can be offered medications or
surgery.
Conservative management is appropriate,

When the fibroids are small, the diagnosis are certain and
symptomless.
During pregnancy.
Near the menopause when there are no symptoms and fibroid is not enlarging.

FOR SYMPTOMATIC UTERINE FIBROID

Two forms of management are available for women with symptomatic
fibroids, and the choice depends in part on their desire to have more
children.
If future childbearing is important to the patient, then conservative
management program should be attempted. This could be medical
treatment or conservative surgery.
Medical Treatment:
a) Hormone therapy- Excessive bleeding may be controlled or
modified by the monthly use of a progesterone-like drug called
medroxyprogesterone acetate ("Provera"). Fibroids that protrude into
the uterine cavity( "submucous myoma") may especially not respond
to this therapy, but it is simple and inexpensive and is worth a try. A
long acting form ("Depo-Provera) is an injection that lasts for more
than 3 months, and may prevent any periods whatsoever. If successful,
medical therapy must be continued indefinitely.
A very special type of drug therapy (called a GnRH agonist) may be
used for temporary control of bleeding or to shrink the size of a fibroid.
GnRH agonists, induce a temporary chemical menopause. In the
absence of estrogen fibroids usually decrease in size. Unfortunately,
while this class of medication is usually successful in shrinking the
fibroids, in some cases even dramatically, it can produce severe side
effects (such as, headaches, joint pain, severe hot flashes, difficulty
concentrating, and other symptoms of menopause. This medication is
usually not used for more than 3-6 months as it can cause loss of bone
tissue. Once stopped, the fibroid uterus will return to its pre-treatment
status within 6 months (in 85% of cases). Therefore, most doctors
prescribe GnRH agonists prior to surgery so that the surgery is easier,
or to women who want to shrink their fibroids prior to becoming
pregnant, or to those nearing menopause, since fibroids often decrease
in size after menopause. Thus any advantage gained using this very
expensive monthly drug therapy is only a temporary window for
surgical intervention of some kind.

b) Anti-inflammatory medication - Heavy bleeding can often be

managed by specific anti-inflammatory medications of the ibuprofen
class, which block an important chemical made by the tissue within the
uterine cavity.

Conservative Surgical Treatment:

Surgical treatment is indicated if:

The fibroids are causing symptoms, such as heavy or prolonged

bleeding.
They are larger than 16 weeks pregnancy.
The diagnosis is in doubt.
The fibroids distort the uterine cavity and are likely to complicate a
future pregnancy
The fibroid grows rapidly which might suggest malignancy change.
The fibroid is situated in the cervix which would complicated
childbirth (Fig 1.5).
Fibroid has undergone torsion.

Conservative surgical treatment consists of myomectomy.

Myomectomy is indicated for women who,
1. are infertile.
2. want more children.
3. wishes to preserve their menstrual functions (refuse to undergo
hysterectomy).
Myomectomy is a uterine sparing procedure in which fibroid tumors are
surgically removed from the uterus. It may be accomplished using
minimally invasive technique ("laparoscopic myomectomy") or through
a standard conventional incision ("laparotomy").
An abdominal myomectomy is done through an abdominal incision. At
the operation, the fibroids are shelled out of their capsules. It is
generally advisable to open the uterine cavity to exclude submucous
fibroid or polyp. The uterus is reconstructed with meticulous care for
haemostatsis. After myomectomy there is about 5 per cent risk of
recurrence of the fibroids.

Here are photographs of an actual abdominal myomectomy.

Here is the abdomen before surgery. The

uterus is the size of a 5-month
pregnancy. It can be seen to protrude up
to the umbilicus

The uterus, which, is greatly enlarged by

the fibroid, is lifted through the incision.
A laser is being used to make an incision
into the uterus so the fibroid can be
removed.

.
The fibroid is being separated from the
wall of the uterus (myometrium). It is
very important to do this in the exact
location between the fibroid and the
myometrium in order to prevent excess
bleeding.

This shows the fibroid almost completely

free from the uterus. It is attached only
at the base. The blood vessels at the
base
are
being
sealed
with
an
electrosurgical device.

The uterus is being reconstructed by

suturing the walls together with
dissolving suture. This is being done in
multiple layers to ensure a precise repair.

The last layer of sutures is placed, and

the uterus is completely restored. A
barrier to prevent adhesions will be
placed before the uterus is replaced into
the abdomen and the abdomen closed.

Fig. 1.6 Fibroids removed following myomectomy in a 34-year-old patient whom

present with infertility.

The advantage of abdominal myomectomy is that large myomas can

be quickly removed. The surgeon is able to feel the uterus, which is
helpful in locating myomas that may be deep in the uterine wall. The
ability to touch the uterus facilitates repairing the uterus. The
disadvantage of an abdominal myomectomy is that it requires an incision, so
recovery is somewhat longer.
Laparoscopic myomectomy
Fibroids that are attached to the outside of the uterus by a stalk
(pedunculated myomas) are the easiest to remove laparoscopically.
Many subserous myomas (close to the outer surface) can also be
removed through the laparoscope.
Fibroids that are deep in the wall of the uterus, or submucous are most
difficult to remove laparoscopically. Although there have been
successful pregnancies after laparoscopic removal of deep or multiple

myomas, the real question is whether or not the uterus can be repaired
as well through the laparoscope as can be done through an abdominal
myomectomy.
The advantage of a laparoscopic myomectomy over an abdominal
myomectomy is that several small incisions are used rather than one
larger incision.
Hysteroscopic submucous resection
This procedure entails the introduction of a small telescope through the
cervix, thus allowing the inside of the uterus to be seen visually.
Protruding fibroids may then be shaved sufficiently to allow the
configuration of the uterine cavity to be returned to normal. This is
appropriate for those patients who wish to maintain their fertility, and
are having heavy or prolonged periods, as the possibility for conception
and uterine implantation will still exist.

Definitive Surgery
Hysterectomy is the definitive treatment because the fibroids
cannot recur, no return of symptoms is possible, and it is easier to
perform and causes less systemic upset than myomectomy. This is the
most satisfactory treatment and is the treatment of choice in woman
over 40 years and in those who do not wish to have children. Total
hysterectomy with removal of cervix is the operation of choice, and the
ovaries, if healthy, should be left unless the patient has reached the
menopause.
Hysterectomy may be done by the abdominal route or by the vagina. Abdominal
hysterectomy is the method of choice in woman with large fibroids and where there may
be other pelvic disease such as an endometriosis. Vaginal hysterectomy gives excellent
results and the operation of choice where small fibroid occurs in association with
prolapsed. This procedure has advantages of less postoperative pain and an abdominal
scar is avoided.

OTHER POSSIBLE MODE OF TREARMENT FOR FIBROIDS

Uterine artery embolization
This is the newest treatment for fibroids. This procedure involves
placing a small catheter into an artery in the groin and directing it to
the uterine arteries, which supply blood to the fibroids. Little plugs are

injected through the catheter to block these arteries. This causes the
fibroids to shrink, although there may be pain for a short time
afterwards requiring the use of narcotics. Uterine artery
embolization is usually successful in treating heavy bleeding caused
by fibroids.
Uterine artery embolization may eliminate the need for surgical
treatment of myomas.

Photo of huge fibroids. Normal uterus is at bottom right of

picture. Normal-sized, white ovary can be seen at very bottom
of photo.

DEGENERATION CHANGES IN UTERINE FIBROID

Uterine fobroids are poorly supplied with blood vessels and tend to
outgrow their blood supply. This causes some but not all of the

degeneration changes. The degeneration changes, which may occur,

are as follows,
1. Hyaline change is seen in all but the smallest myomas. Aseptic
necrosis follows inadequate blood supply. The myoma may be
painful, enlarged and soft. On histological examination the muscle
cells are seen to have lost their structure and replaced by hyaline
material. There is a tendency to liquefaction of larger areas of
hyaline change and this leads on to cystic degeneration.
2. Cystic change this cystic degeneration is preceded by hyaline
degeneration. Tissue breaking down and liquefaction within the
areas of hyaline change result in the formation of fluid and cystic
spaces in the myoma.
3. Red degeneration or necrobiosis this type of degeneration occurs
typically during mid-pregnancy or the puerperium and is due to
infarction of the center of the fibroid. The cause is probably an
interference with the arterial supply by thrombosis of the peripheral
vessels. Characteristically the myoma suddenly enlarges and is
painful and tender. It can be mistaken for placental abruption or
any acute abdominal emergency. The myoma is macroscopically
diffusely red like raw meat while on histological examination there is
extensive necrosis of the tumour cells and thrombosed blood
vessels can be seen, especially in the capsule.
4. Fatty degeneration and calcification is seen most frequently in
pedunculated myomas and postmenopausal women.
Partial
necrosis may result in the appearance of fat globules in the
muscular substance of a myoma, which then undergo
saponification. Calcium may be deposited in this and the result is a
calcified myomas or known as womb stone. These calcified
myomas are visible on an X-ray.
5. Infection infection is commonly seen in a polypoidal fibroid, which
undergo necrosis as the result of interference with its blood supply.
The surface of this polypoidal fibroid sloughs off and become
infected. Usually there is an offensive vaginal discharge with
pyrexia.
6. Atrophy uterine fibroids depend on the trophic action of estrogen
for maintain of size. After menopause, fibroid tend to atrophy.
Large fibroid will not vanish but there is reduction in size.
7. Malignant change malignant change in uterine fibroid is very rare
and occurs in 0.1 to 0.2 per cent of cases. The fibroid may grow

suddenly and be painful and tender. Macroscopically, the center of

the fibroid is soft and homogenous.
The histology shows a
leimyosarcoma.
8. Torsion pedunculated fibroids may undergo torsion, developing
venous infarction. The venous congestion causes the fibroid to
become dark red. Usually the patient will complaints of acute
symptoms like those due to torsion of an ovarian cyst.

FIBROIDS AND PREGNANCY

During pregnancy uterine fibroid tend to become soft as a result of
interstitial oedema and as there is little hypertrophy of the muscle
tissue of the fibroids; there is a tendency for intramural fibroid to be
flatten out. Certain degenerations are more common in fibroids during
pregnancy, and of these are red degeneration is the most common, as
this is the time when it occurs.
Red degeneration in pregnancy is treated conservatively: Bed rest
Reassurance
Analgesics to relieve pain
Usually symptoms and signs of red degeneration will subside within
about ten days.
Torsion of pedunculated fibroids may occur during pregnancy, but it is
most likely to occur in early puerperium when there is,
Rapid uterine involution.
More mobility of intra-abdominal contents associated with laxity of
abdominal wall.
Symptoms and signs of an acute or subacute abdomen follow. Surgery
is indicated when there is evidence of torsion to the pedunculated
fibroid.
The fibroids may influence the course of pregnancy and labour. The
potential effects of fibroids on pregnancy includes,

Recurrence abortion
Pre-term labour
Malpresentations

Obstructed labour (rare)

Third stage problems, postpartum haemorrhage
Delayed involution postpartum

In early pregnancy abortion may result, this is thought to be more

likely if implantation occurs over a submucous fibroid. Abortion may
be recurrence.
Cervical fibroids, or those situated in lower half, may cause nonengagement of the presenting part (head or breech), instability of the
fetal lie, or persistent abnormal lie presentation.
During labour, fibroids if multiple and intramural may interfere with the
uterine contraction. They may cause incoordinate uterine contraction
and may result in prolonged labour.
The presence of fibroids may cause third stage problems. Postpartum
haemorrhage is a more common complication. The presence of the
fibroids interferes with proper contraction of uterus.

18
UTERINE POLYPS

Endometrial
polyp

Cervical
polyp

Fig. 1.1 Types of uterine polyps.

The word polyp is a term applied to a tumour with a pedicle. Uterine

polyps are the common tumour of the uterus, and may occur either in
the body of the uterus (corpus) or the cervix. The uterine polyps are
usually seen in the peri-menopausal age range and may occur after
the menopause. They are usually multiple but can be single. Polyps are
usually benign and rarely malignant.
TYPES OF UTERINE POLYPS

A variety of polyp is found in the uterus. The uterine polyps are

commonly classified into the following types (Fig. 1.1):
Corpus:
Endometrial polyps (adenoma)
Fibroids polyps
Adenofibromatous polyps
Adenomyomatous polyps
Cervix:
Mucous polyps
Fibro-epithelial polyps
PATHOLOGY
Polyps are small, red or pinkish-white tumours projecting from
endometrial surface. Only occasionally do they have a long stalk
allowing them to present through the cervix, or even at the vulva.
Macroscopically they vary in size but usually 1-3 cm in diameter and
are usually sited in the uterine fundus. They appear as firm smooth
nodules within the endometrial cavity.
Microscopically the endometrial polyp (adenoma) is composed of
endometrial stroma and glands covered by a single layer of columnar
epithelium. The fibroid polyps are composed of muscle cells and some
fibrous tissues. Adenofibromatous polyps are differentiated from the
other types by the presence of a fibrous stroma. Fibromyomatous and
adenomyomatous polyps show the characteristic microscopic features.
Mucous polyps consist of mucous secreting gland of cervical type lined
by squamous or columnar epithelium.

CLINICAL FEATURES
The commonest clinical presentations of the women with uterine
polyps are
Menstrual disturbances, such as increased menstrual loss,
intermenstrual bleeding, postmenopausal bleeding in older woman.
Postcoital bleeding may also occur, especially if the polyps are
extruded from the cervix.
Vaginal discharge.

 If the polyp with a long pedicle has been extruded from the cervix,
the woman herself may discover the polyp in the vagina.

DIAGNOSIS
Diagnosis depends on seeing the polyp through a
examination. The polyps can be detected by the following:

speculum

Speculum examination cervical polyps can be noted when

performing a speculum examination.

Ultrasound pathological condition of the endometrium can be

demonstrated by ultrasonic scanning. The vaginal probe is very
useful and gives an excellent result. An experience operator should
be able to detect the presence of endometrial polyp or fibroid
polyps (Fig. 1.2).

Fig 1.2 Using ultrasound to demonstrate endometrial

polyp (P).

Hysteroscopy Direct inspection of the interior of the cervical

canal and the endometrial cavity by hysteroscopy is now a part of a
gynaecological investigation. Endometrial polyps, fibroid polyps
and submucous fibroids can be detected by hysteroscop (Fig.1.3).

Fig 1.3. Photograph of a fibroid polyp taken at hysteroscopy.

TREATMENT
They are easily removed with a small sponge forceps by twisting off
the polyps. Uterine curettage is a form of treatment and this procedure
should be done with great care as the polyp may be missed.
Transcervical polypectomy under direct hysteroscopy vision may give
an excellent result.
Careful histological examination of all polyps is necessary to exclude
malignant change.
CERVICAL POLYPS
This is a common tumour and often associated with chronic cervicitis.
They are called mucous polyps, because of their histological
appearance. They may be single or multiple. They arise in the cervical
canal or at the external os and may protrude into the vagina; a very
large cervical polyp may present at the vulva.
A cervical polyp is bright red in colour (cherry-red swelling) and highly
vascular. It consists of mucous secreting glands of cervical type with
supporting stroma containing numerous blood vessels.
Squamous
metaplasia is common. Inflammation and ulceration of the apex is
common.
Histological examination shows that the cervical polyps are made up of
glandular tissue similar to that of the cervix.
Their main symptoms are mucous vaginal discharge and irregular
bleeding. Intermenstrual bleeding and post-coital bleeding are due to
inflammation and ulceration at the tip of the polyp.
Diagnosis depends on seeing the tumour through a speculum.
Treatment consists in twisting off the polyps (polypectomy) with a
sponge forceps. Large cervical polyp is wiser to be removed under
general anaesthesia because they have vascular stalk.
Uterine
curettage is advisable because cervical polyp may be associated with
other uterine lesions including endometrial polyp and carcinoma.

ENDOMETRIAL POLYP
Protrusions of the endometrium to form polyp are relatively common.
They are thought to be caused by over-proliferation of glands in
response to estrogenic stimuli. Endometrial or adenomatous polyps
are the commonest polyps among the types of uterine polyp. They are
usually multiple before the menopause and may be a component of
endometrial hyperplasia. After the menopause they are usually single.
They tend to recur are removal.
Macroscopically, endometrial polyps are soft red tumour. They are
often flattened and the pedicle is usually short. They are usually found
in the upper part of the uterine cavity (uterine fundus) near the cornual
region (Fig. 1.4).
Histologically they are made up of cystically dilated endometrial glands
in a vascular stroma.
Most of the endometrial polyps are symptomless but they may be
associated with:

Menorrhagia
Intermenstrual bleeding
Postcoital bleeding
Postmenopausal bleeding

Fig. 1.4 Benign endometrial polyp

Diagnosis depends on exploring the uterine cavity with sponge forceps

and curette. Endometrial polyp is best confirmed by hysteroscopy and
biopsy.
Treatments consist of polypectomy with uterine curettage. The entire
polyp should be carefully removed and submitted to histological
examination.
FIBROID POLYP
This is a fibroid which has been extruded by the uterine muscle and
may present in the cervical canal or the vagina. The main symptoms
are heavy bleeding leading to anaemia and colicky uterine pain (due to
the process of extrusion of the tumour).
A fibroid polyp in the uterine cavity is dealt with myomectomy or
hysterectomy. Fibroid polyp, which projects into the vagina, can often
be removed by cutting through its pedicle scissors.

ADENOMYOMATOUS POLYP
This is less common than the other types of uterine polyp.
Adenomyomatous polyps are confined within the uterine cavity. They
give similar features to a fibroid polyp.
Histological examination reveals uterine muscle with endometrial
glands. Adenomyomatous polyps are usually treated by hysterectomy
though they may be removed by curettage.

19
ADENOMYOSIS

Fig. 1.1 Adenomyosis (uterine endometriosis). (a) Macroscopic

appearance noted
the dark coloured spots (nodules) within the myometrium of the uterus.
(b) Microscopic appearance showing both the endometrial glands and stroma lying
deep in
the myometrium.

Adenomyosis (also known as uterine endometriosis or internal

endometriosis) is a benign condition of the uterus where the
functioning endometrial tissues (glands and stroma) are found within
the muscles fibres of the myometrium apart from the normal location
in the uterine cavity and is often associated with local myometrial
hypertrophy. This disease may coexist with external endometriosis and

is an important cause of dysmenorrhoea, menorrhagia and possibly

subfertility.
Adenomyosis usually occurs in women over 30 years old who have
borne children, and rarely occurs in women who have not carried a
pregnancy to term.

AETIOLOGY
The cause of adenomyosis is unknown. Adenomyosis is probably
caused by direct penetration, or lymphatic spread to the myometrium
by viable endometrial tissue.
The most popular theory of the
histogenesis of adenomyosis is that the basal endometrium cells
invade the myometrium to give rise to foci of adenomyosis.
PATHOLOGY
The abnormally located endometrial tissue, like the normal
endometrium, tends to bleed with menses. The blood and debris may
accumulate in the glands creating small fluid collections inside the
uterine wall. This penetrating and functioning endometrial tissue may
lead to swelling: the uterus may become larger and globular.
Adenomyosis is often classified into a diffuse and focal form. Focal
adenomyosis, also termed adenomyoma, refers to isolated implants
surrounded by extensive but focal smooth muscle changes. It is less
common than diffuse adenomyosis and not accompanied by a
characteristic distortion of the inner myometrium.
Macroscopic appearance:

The uterus is uniformly

enlarged, globular and
appears fibrous.
Foci of adenomyosis
can be noted within
the
myometrium as
dark areas.

Fig. 1.2 The gross appearance of adenomyosis is shown in the specimen .

Microscopic appearance:
Islets of endometrial tissue, glands and stroma are found deep in the
uterine wall (myometrium). This may be diffuse or localized.
A
localized adenomyoma is distinguished from a fibroid by the fact that it
possesses no capsule.

Fig. 1.3 The microscopic appearance of adenomyosis showing the presence of

endometrial glands and stroma in the myometrium.

CLINICAL PRESENTATIONS
Adenomyosis usually occurs in older women (over 30 years old) and in
multiparous women than external endometriosis.
Symptoms of adenomyosis:
Adenomyosis may be present and cause no symptoms.
condition presents with symptoms the typical triad is

When this

Menstrual disorders: Prolonged or heavy menstrual bleeding

(severe menorrhagia) is the outstanding symptom. Premenstrual
staining or spotting may also occurs.

Pelvic pain: Progressively increasing pelvic pain, which is most

common during menses (dysmenorrhoea). Pain worsen
throughout menstruation.

Uterine enlargement: The enlarged uterus may give a feeling

of heaviness in the pelvis.
Physical signs:
Pelvic examination may reveal

Uniformly enlarged globular mobile uterus, unless there are

associated fibroids
Slightly softened uterus, and
Uterine tenderness

HOW CAN ADENOMYOSIS BE DIAGNOSED?

Adenomyosis is frequently an incidental, clinically unsuspected, finding
in uteri removed for other reasons.
It is often stated that a
progressive, uniform enlargement of the uterus accompanied by
menorrhagia and dysmenorrhoea is diagnostic of uterine adenomyosis.
Adenomyosis should no longer be a retrospective diagnosis after
hysterectomy. Nowadays, it is possible to perform a presurgical
diagnosis of adenomyosis.
Occasionally adenomyosis is diagnosed by

Ultrasonography: Several studies have addressed the potential

role of ultrasound in the diagnosis of adenomyosis. There is also

evidence that high resolution transvaginal ultrasound, in experts

hands, may provide accurate diagnosis.
ULTRASOUND CHARACTERISTICS
OF ADENOMYOSIS

ill defined hypoechoic areas

hetrogeneous myometrial echoctexture
small anechoic lakes
asymetrical uterine enlargement
indistinct endometrial-myometrial border
subendometrial halo thickening

MRI magnetic resonance imaging- has more recently proved

to be an effective modality, capable of detecting the presence and
extent of adenomyosis and distinguishing it from fibroids. MRI
diagnosis of adenomyosis is based on recognising the distortion of
the normal inner myometrial architecture caused by smooth muscle
hyperplasia, and not the presence of heterotropic implants. The use
of MR imaging in routine practice has been limited by its restricted
avilability and cost.

Myometrial biopsy:
An intrauterine wall sample may be
necessary for pathological evaluation.
Myometrial needle
biopsies can be taken transabdominally at the time of
laparoscopy, or transvaginally under ultrasound guidance. A
positive biopsy should provide evidence of ectopic endometrial
islets (glands and stromas) sandwiched between strips of
myometrium.

TREATMENT OF ADENOMYOSIS
Frequently the moderately enlarged uterus is asymptomatic and no
treatment is necessary.
Medical treatment for symptomatic adenomyosis
Temporary relief of very painful heavy periods can be achieved with
GnRH agonists. These medications cause a menopause-like state
with complete cessation of ovarian function and menses, causing
abnormal tissue to shrink. This temporary reversible state permits an

anemic patient to restore a normal blood count, especially when iron

supplements are prescribed. However, GnRH agonists are not easy to
tolerate, causing menopausal symptoms such as hot flashes. Other
consequences include weakening of bones, alteration of the cholesterol
profile (decrease in HDL and increase in LDL). For these reasons, this
type of medical treatment is usually limited to six months. Upon
cessation of GnRH agonists treatment, the painful heavy periods tend
to resume.
Most treatment attempts with hormonal supplements have been
unsuccessful.
Surgical treatment for adenomyosis
Hysterectomy with conservation of ovaries (unless there are other
indications for their removal) is currently considered by most the only
effective treatment for symptomatic adenomyosis in women who are
not approaching menopause soon.
Conservative surgery may be undertaken in young women who
desire to retain the uterus. This consists of removing only the part of
the uterus containing the bulk of the disease followed by
reconstruction of a close-to-normal size uterus. This results in
resolution of pain and in normal to light periods. Unfortunately, the
uterus after such surgery is unlikely to sustain a pregnancy.
Nonetheless patient satisfaction has been high because this more
limited operation avoids most of the drawbacks of hysterectomy.

20
POLYCYSTIC OVARIAN SYNDROM
(PCOS)
Stein and Leventhal were first to recognize an association between the
presence of polycystic ovaries and a clinical syndrome of infertility,
infrequent or absent periods, hirsuitism and obesity. Polycystic ovarian
disease or syndrome (PCOS) is a heterogenous disorder characterized
by a disruption of the regular processes leading to ovulation. It is
associated with hyperandrogenemia, normal or elevated estrogen
levels, and elevated luteinizing hormone (LH) secretion, with a raised
LHtofollicle-stimulating hormone (FSH) ratio.
PATHOLOGY
The ovaries are enlarged bilaterally and have a smooth thickened
white capsule that is avascular. On cut section, numerous cystic
subcapsular follicles (seldom exceeding 1.0 cm in diameter) in various

stages of atresia are seen in the peripheral part of the ovary. The most
striking ovarian feature of PCOS is hyperplasia of the theca stromal
cells surrounding arrested follicles. Upon microscopic examination,
luteinized theca cells are seen.

UTERUS

Fig.1.1 Laparoscopic view: Gross appearance of polycystic ovaries (white)

PATHOGENESIS
Women with PCOS have abnormalities in the metabolism of androgens
and estrogen and in the control of androgen production. High serum
concentrations of androgenic hormones, such as testosterone,
androstenedione, and dehydroepiandrosterone sulfate, may be
encountered in these patients. Hyperandrogenemia in PCOS could be
due simply to increased follicle number or theca cell hyperplasia. PCOS
also is associated with peripheral insulin resistance and
hyperinsulinemia, and the degree of both abnormalities is amplified by
the presence of obesity. Insulin has been demonstrated to potentiate
the actions of LH on theca cell androgen production.
A proposed mechanism for anovulation and elevated androgen levels
suggests that under the increased stimulatory effect of luteinizing
hormone (LH) secreted by the anterior pituitary, stimulation of the
ovarian theca cells is increased. In turn, these cells increase the
production of androgens (e.g. testosterone, androstenedione). Because
of a decreased level of follicle-stimulating hormone (FSH), the ovarian
granulosa cells are not able to aromatize the androgens to estrogens,
leading to decreased estrogen levels and consequent anovulation.
The sequence of events may therefore be as follows:

1. Androstenedione from ovary or adrenal is converted to estrogen and

estradiol peripherally. The rate of conversion will be greatest in
obese women.
2. Follicle stimulating hormone (FSH) is suppressed by the estrogens
so that follicular development is curtailed.
3. Luteinizing hormone (LH) secretion is stimulated by estrogen but no
LH surge occurs and ovulation is prevented.
4. The raised LH levels stimulate the teca cells to produce androgens
that cause hirsuitism.
5. Menstrual problems (such as oligoamenorrhoea or amenorrhoea)
may occur.
CLINICAL PRESENTATION
History:
Patients with PCOS may present with the following:

Menstrual dysfunction: The most common presentation is

erratic menstruation due to anovulation. Some women have
oligomenorrhea or amenorrhea (no menstrual periods for 3 or
more months).

Hyperandrogenism: This manifests clinically as excess

terminal body hair in a male distribution pattern. This is
commonly seen on the upper lip, chin, around the breast nipples,
and along the linea alba of the lower abdomen. These patients
also may have acne, male-pattern balding or alopecia, increased
muscle mass, deepening voice, or clitoromegaly.

Infertility: In most cases the reason for visiting a doctor is

infertility. PCOS accounts for 30% of overall infertility.
Obesity: Obesity is present in half the women with PCOS.

Diabetes mellitus: Approximately 10% of women who are

obese and have PCOS also have type 2 diabetes mellitus by age
40 years. Approximately 35% of women who are obese and have
PCOS have impaired glucose tolerance by age 40 years.

Physical:
The traditional description of the patient with PCOS is an obese female
with acne and excess body hair. Physical examination findings are
significant for the following:

Hirsutism: Patients may have excess body hair in a male

distribution pattern and acne. In some patients with PCOS,
virilizing signs such as male-pattern balding or alopecia,
increased muscle mass, deepening voice, or clitoromegaly may
be encountered and should prompt the search for other causes
of hyperandrogenism.

Obesity: Approximately 50% of patients with PCOS are obese.

Patients may have palpably enlarged ovaries.

INVESTIGATION:
Laboratory evaluation:
A large number of patients with PCOS have various biochemical abnormalities. Because
of the heterogeneity of this syndrome, no clear consensus has been reached on
hormonal tests that can be used to fully confirm the diagnosis of this condition. The
following abnormalities may be encountered:

Increased androgen levels in blood. Testosterone and DHEA-S

levels may be mildly elevated.
Serum LH concentrations may be high, but serum FSH
concentrations are normal.

Serum LH-to-FSH ratio - LH:FSH ratio more than 2 or 3 suggests

PCOS .

Increased fasting insulin

Increased oestradiol and oestrone level

Glucose tolerance test - Of women who are obese and have
PCOS, 35% have impaired glucose tolerance and 10% have
diabetes mellitus.

Imaging Studies:
Ultrasonography
is
the
most
sensitive
diagnostic
study.
Ultrasonographic criteria for establishing the diagnosis of PCOS are 10
or more cystic follicles that are 2-10 mm in diameter and are
peripherally arranged in a necklace-like formation around an
echodense stroma.

DIAGNOSIS
The minimal criteria proposed for the diagnosis of PCOS include the
following:

Menstrual irregularity must be present.

Evidence of hyperandrogenism, whether clinical (eg, hirsutism,
acne, male pattern balding) or biochemical (elevated androgen
level), must be present.
A raised LH:FSH - LH:FSH ratio more than 2 or 3 suggests PCOS.
Transvaginal ultrasound finding of numerous subcapsular
follicles, measuring 2-10 mm in diameter, arranged in a
necklace-like formation.

TREATMENT
The treatment depends on the presenting symptom and wishes of the woman.
A): Medical Treatment:
Medical management is aimed at treatment of metabolic
derangements, anovulation, hirsutism, and menstrual irregularity.

Metabolic derangements
o Diet and exercise: Weight loss if achieved may reduce
hirsutism and reverse menstrual irregularities and
infertility. Patients with PCOS who are obese benefit from a
low-calorie diet for weight reduction.
Patients with PCOS who are obese have a marked
improvement in their endocrine-metabolic parameters after

4-12 weeks of dietary restriction. They have a 2-fold rise in

their sex hormonebinding globulin (SHBG) levels and a fall
in free testosterone levels. Weight reduction is associated
with normalization of hormonal disturbances and the
resumption of regular ovulation.

o Metformin: This is an antidiabetic medication that has

been shown to improve insulin resistance and decrease
hyperinsulinemia, and promote weight loss in patients with
PCOS. The usual starting dose is 500 mg orally twice a day.
Commonly encountered adverse effects are nausea,
vomiting, and diarrhea. Patients who develop these
adverse effects can be instructed to decrease the dosage
to once a day for a week and then gradually increase the
dosage. Also importantly, inform these patients that they
have a high likelihood of having ovulatory cycles while on
metformin.

Anovulation (Treatment for infertility)

o

Medical treatment of infertility includes antiestrogens

(clomiphene
citrate),
adrenal
suppression
by
dexamethasone along with clomiphene, gonadotropin
therapy,
gonadotropin-releasing
hormone
(GnRH)
analogue, and metformin therapy.

Metformin has been shown to cause an 8-fold increase in

ovulation. When combined with clomiphene citrate, a 10fold increase in ovulation has been observed.
Patients with PCOS who are infertile but desire pregnancy
should be referred to a reproductive endocrinologist for
further workup and treatment of infertility.

Hirsutism
o

Nonpharmacologic measures include the following:

Hair removal: Hirsutism can be treated through
nonpharmacologic measures including shaving; use
of chemical depilatories, bleaching creams, and wax
depilatories; and electrolysis.

Weight reduction: This has been shown to decrease

androgen production in women who are obese;
therefore, losing weight can slow hair growth.

Pharmacologic measures include the following:

Oral contraceptive pills: Women who do not wish
to become pregnant can be effectively treated for
hirsutism
with
oral
contraceptives.
Oral
contraceptives slow hair growth in 60-100% of
women with hyperandrogenemia. Therapy can be
started with a preparation that has a low dose of
estrogen
and
a
nonandrogenic
progestin.
Preparations that have norgestrel and levonorgestrel
should be avoided because of their androgenic
activity.

Other
drugs:
Antiandrogens,
such
as
spironolactone,
are
effective
for
hirsutism.
Spironolactone in a dose of 50-100 mg twice daily is
an effective primary therapy for hirsutism. Because
of the potential teratogenic effects of spironolactone,
it should be prescribed with an oral contraceptive.
The adverse effects of spironolactone include
hyperkalemia,
gastrointestinal
discomfort,
and
irregular menstrual bleeding, which can be managed
by adding an oral contraceptive.

Menstrual irregularity
o This is treated with an oral contraceptive. The oral
contraceptives not only inhibit ovarian androgen
production, but also raise SHBG production.
o Exclude pregnancy before initiating treatment with an oral contraceptive.

B): Surgical Care:

Surgical management is aimed mainly at restoring ovulation.

Ovarian wedge resection: This procedure has fallen out of

favor because of postoperative adhesion formation and the
introduction of ovulation-inducing medications.

Laparoscopic surgery: Ovarian diathermy has replaced wedge

resection, which can result in extensive ovarian, periovarian, and
tubal adhesions. Only minimal damage to the ovary is required to
stimulate ovulation. The method involves 4-point diathermy set
at 40 W for 4 seconds at each point.

FOLLOW UP
Further Outpatient Care:

These patients need regular follow-up to avoid complications that

may result from untreated PCOS.

Complications:

Women with PCOS are at risk for developing diabetes mellitus

type 2, hypertension, intravascular thrombosis, coronary artery
disease, and endometrial cancer.

PROGNOSIS:

With proper diagnosis and treatment, most PCOS symptoms can

be adequately controlled or eliminated.

Infertility can be corrected and pregnancy achieved in most

patients. In some patients, hormonal disturbances and
anovulation may recur.

Monitor patients for endometrial cancer.

endometrial carcinoma are increased

Because of the high rate of hyperinsulinemia observed in PCOS,

women with the disorder should have their glucose levels
checked regularly to monitor for the development of diabetes.

The

chances

of

POLYCYSTIC OVARIAN SYNDROME (PCOS)

Background
Pathogenesis
Pathology

A clinical syndrome of infertility, menstrual problems,

hirsuitism and obesity found to be associated with
enlarged polycystic ovaries
Abnormalities in the metabolism of androgens and
estrogen and in the control of androgen production
Enlarged ovaries and show:

Thickened white capsule

Numerous cystic follicles
Theca hyperplasia
Granulosa cell atresia

Clinical Features

Laboratory
evaluation

Treatment

Infertility
Hirsuitism
Oligoamenorrhoea
bleeding
Obesity

or

Dysfunctional

uterine

Raised LH and normal FSH

LH: FSH ratio more than 2
Raised serum testosterone and DHEA-S level
Ultrasound numerous follicles (>10) of 2-10 mm
in diameter

Will depend on the primary problems

Complication

Obesity advised weight loss

Anovulation induced with clomiphene
Menstrual
problem

used
combined
contraceptive pills
Hirsuitism:
- Non-pharmacological e.g. bleaching,
shaving
- Pharmacological e.g. antiandrogents
pills
Surgical Ovarian drilling
Diabetes mellitus
Increase risk for endometrial cancer

Table 1. Profile of polycystic ovarian syndrome

21
BENIGN TUMOURS OF THE OVARY

Fig.1.1 Dermoid cyst

Benign ovarian enlargement may be cystic or solid. Some ovarian

cysts (e.g. follicular cyst, theca-lutein cysts) are classified as nonneoplastic functional cysts. However, solid ovarian masses are almost
invariably neoplastic. The classification of benign ovarian cysts and
tumours are made on the cell of origin. The classification of benign
ovarian enlargement is as follow:
Benign Tumour

Cell of Origin

Functional
cysts
(follicular, Normal
follicle
theca-lutein, corpus luteum)

Serous cystadenoma

Mucinous cystadenoma

Teratoma (dermoid cyst)

Endometriomata

Fibroma

Brenners tumour

ovarian

Type
Cyst
Cyst

Surface epithelium
Cyst
Surface epithelium
Cyst
Germ cell (oogonia)
Cyst
Ectopic
endometrium

Solid

Surface epithelium

Solid

Mesenchyme

Non-neoplastic functional cysts:

A. Follicular cysts These consist of unruptured Graffian follicles
which continued to secrete fluid. They are thin-walled (lined by
granulose cells), usually unilateral and they rarely exceed 5 cm. In
diameter. Multiple follicular cysts may occur following ovulation
induction therapy (clomiphene or gonadotrophins).

Uncomplicated follicular cysts do not cause symptoms and tend to

disappear spontaneously by resorption of fluid within few months.
Observation and ultrasound examination is all that is required in the
management of this follicular cyst.
Should the cyst persists or increasing in size surgical intervention
should be performed. Aspiration of the fluid can be achieved by
under ultrasonic or laparoscopic guidance.
B. Theca-lutein cysts are found in hydatidiform moles or
choriocarcinoma.
They are caused by the high level of
gonadotrophins (human chorionic gonadotrophin hCG). Thecalutein cysts may be caused by excessive doses of gonadotrophins or
clomiphene which the patient receive for induction of ovulation in
the management of infertility. Both ovaries are enlarged to a
diameter of 10 cm. or more. In a case of hydatiform moles the
ovaries return to normal when the abnormal chorionic tissues are
removed.
Theca-lutein cyst

C. Endometriotic cysts These ovarian cysts are usually associated

with endometriosis. The ovarian cysts are found to contain blood
which become thick and dark the term chocolate cyst is used.
They rarely become malignant.

Fig. 1.2 Endometriotic cyst of the ovaries

D. Corpus luteun cysts These cysts are due to bleeding into the
follicle which has discharged the ovum. If the bleeding is excessive,
the corpus luteum becomes distended with blood and appears
cystic. Haemorrhage into a corpus luteum may cause pain and
symptoms and signs may resemble those of ectopic pregnancy.

New growths - Benign ovarian tumour: New growths of the ovary

are classified according to their cell origin.
Tumours arising from the surface epithelium
1) Benign serous cystadenoma
This tumour is called serous because the fluid it contains is clear,
straw-coloured and is rich in protein. Most benign serous
cystadenomas are either simple or papillary serous cystadenoma.
Serous cystadenoma cysts are more frequently detected in women
aged 35 55. Serous cystadenomas are lined by a singled-layer
cuboidal epithelium (which is similar to that of the fallopian tube),
usually unilocular and are bilateral in 30-50 per cent of cases. They
can be of any size and may grow to about 30-40 cm. in diameter
(Fig. 1.3).

Fig. 1.3 A large benign serous cysadenoma

2) Mucinous cystadenoma
This is the commonest of the new growths of the ovary and is so
named because the contents consist of a viscous fluid, mucin, a
glycoprotein. This is a benign tumour and occurs more commonly
between the ages of 35 and 55. They can grow to a considerable
size. It is multilocular and is usually unilateral. The cyst is lined by
with a tall mucus-secreting columnar epithelium.
If the cyst ruptures the mucus-secreting cells may implant on the
peritoneum and produce pseudomyxoma peritonei.

Mucinous cystadenoma

Rupture of mucinous cystadenoma

result in the formation of
pseudomyxoma peritonei

3) Brenner tumour
This rare tumour is found mostly in postmenopausal women. They
are usually benign and unilateral. Brenners tumours are solid
tumour. Histologically, it shows nests of epithelial cells resembling

squamous or transitional epithelium and enclosed in dense fibrous

tissue. Sometimes the nests have cystic spaces.

Brenners tumour is sometimes found in mucinous cystadenoma. A

feature of this tumour is their association with ascites and
hydrothorax; this association is called Meigs syndrome.
Tumour arising from germ cells
1) Benign teratoma (Dermoid cyst)
This is a common tumour of the ovary making up 20-25 per cent of
all ovarian tumours. It may occurs at any age group, but commonly
found between the ages of 20 and 30 and is the commonest tumour
in this age group. This may be explained by the fact that it
develops from an unfertilized ovum by parthenogenesis and thus
occurs at the height of the reproductive period. These tumours are
often multiple and bilateral. Dermoid cysts are almost invariably
benign.

Fig. 1.4 Dermoid cyst of the ovary containing teeth

It contains variety of tissues derived from two or more primary germ

layers, endoderm, mesoderm and ectoderm.
A dermoid cyst
consists of a thick wall. It does adhere to surrounding structures so
that torsion is common.

In the wall of the cyst are found sebaceous glands, hair follicle,
teeth (Fig.1.4), cartilage, gastrointestinal epithelium and nervous
tissue. Thyroid tissue may also be found.

Mature teratoma

Plain abdominal x-ray showing

calcification (teeth) with ovarian cyst

2) Strauma ovarii
Strauma ovarii is a benign teratoma consisting mainly of thyroid
tissue which takes up iodine and rarely causes hyperthyroidism.
Tumour arising from the gonadal stromal
1) Fibroma of the ovary
This benign tumour arises from the connective tissue stroma and is
a solid non-encapsulated tumour which may be bilateral and may
grow to a moderate size. The normal ovary is compressed but not
invaded. The histological appearance is that of a benign tumour
composed of fibrous connective tissue resembling the ovarian
stroma.
A feature of this tumour is their association with ascites and
hydrothorax; this association is called Meigs syndrome. When the
tumour is removed the fluid collections disappear. The fluid is
probably exudedfrom the surface of the tumour.
Fibroma of the ovary tends to have long pedicles and may therefore
undergo torsion.

Section of the ovarian fibroma

CLINICAL FEATURES OF BENIGN OVARIAN TUMOUR

An uncomplicated ovarian tumour generally causes no symptoms until
it reaches a size large enough to be noticed by the patient or to be
detected at routine examination. They do not cause pain, but if large
may cause discomfort. Menstrual function is not usually affected.
Abdominal swelling may be present when the tumour is large.
Physical signs:
The physical signs depend on the size of the tumour, on its mobility
and on its relation to the surrounding structure. A small tumour tends
to locate in the fornix and is felt bimanually to one side of the uterus.
A cyst lying in the pouch of Douglas is likely to be dermoide. A large
cyst or tumour tends to be displaced above the pelvic brim and present
as a central abdominal swelling.
Benign ovarian tumours are very mobile either in the pelvis or in the
abdominal cavity.
Large benign ovarian tumours are dull to percussion anteriorly with
resonance in the flanks.

Adbominal swelling is one of the clinical presentation of ovarian cyst

Diagnosis:
Ovarian tumours must be distinguished from a whole variety of pelvic
and abdominal swelling. The diagnosis of ovarian tumour can be
confirmed by abdominal or transvaginal ultrasound, which
differentiates the tumour from pregnancy, distended bladder, uterine
fibroids, ascites or tumours of colon.

Cyst

Bladder

Uterus

Ultrasound imaging showing huge ovaraian cyst

MANAGEMENT OF BENIGN OVARIAN TUMOURS

The treatment of ovarian tumours consists in surgical removal as soon

the tumour is diagnosed. The extent of the surgery will depend on the
age of the patient. An exception may be made in the case of a cystic
ovary, which is not more than 5 cm. in diameter. Ovarian cyst less
than 5 cm I diameter and echo-free, can be observed, repeat scans
being made to see if the tumour increases in size.
In young women who wish to conserve reproductive capacity
enucleation of the cyst (cystectomy) is carried out. Larger cysts may
demand removal of the ovary.
In older women past child-bearing it is customary to remove both
ovaries and the uterus (bilateral salpingo-oophorectomy and total
hysterectomy), because of the possibility of malignant change.
COMPLICATIONS OF OVARIAN TUMOURS
The most important complications of ovarian tumors are:
1) Torsion of the pedicle occurs most often in the small more mobile
tumours with long pedicle and is commonest in dermoid cyst and
fibroma. Larger tumours seldom undergoes torsion because they
have no room in which to move freely. Acute or subacute pain may
be accompanied by fever, rapid pulse, and mild shock. Initially it
causes unilateral lower abdominal pain and later may result in
generalized abdominal pain. The patient may vomit repeatedly. The
lower abdomen is tender with guarding and rigidity.
Pelvic
examination reveals a tender adnexal mass.
Laparotomy is
indicated and removal of the ovary usually necessary.
2) Haemorrhage into an ovarian tumour causes pain but generally
less severe than that of torsion. The tumour enlarges and becomes
tender.
3) Rupture of an ovarian cyst may be spontaneous or be caused by
trauma such as a blow on the abdomen. The signs an symptoms
will vary. The content of the chocolate and dermoid cysts are
extremely irritant and therefore may cause severe symptoms. The
diagnosis can only be certain if the patient was known to have a
cyst, which has become impalpable.
Treatment - If the cyst is small it is reasonable to do nothing but
observe the patient. But if the cyst is large, immediate laparotomy
should be undertaken.

4) Infection may occur from invasion with organisms from the bowel
or in association with salpingitis. This is not a common complication
of ovarian tumours.
5) Malignant change can occur at any at any age but is
commonest after menopause. This occurs mostly in serous and
mucinous cysadenoma. The features indicating malignant change
include,

Rapid growth of the tumour

Pain of an aching character and tenderness
The present of ascites
The tumour feels fixed and nodular

OVARIAN TUMOURS IN PREGNANCY

An ovarian tumour may be revealed for the first time at routine
examination during pregnancy.
The effect of the pregnancy on the tumour
The size of the tumour does not change during pregnancy, but the
enlarging uterus may displace it so that it becomes more obvious.
Torsion of the pedicle may occur either during pregnancy or in the
puerperium.
The effect of the tumour on the pregnancy
The only problem is that the tumour may become impacted in the cul
de sac and obstruct the birth canal.
Treatment
Treatment depends on the size and consistency of the tumour and its
appearance on ultrasound examination.
When a benign ovarian
tumour is discovered in early pregnancy it is reasonable to defer
operation until 16th week, provide no urgent symptom appear, because
of the risk of abortion if surgery is undertaken in the early weeks.

A tumour discovered after 30th week may also be left, because it may
be difficult to remove surgically and risk of premature labour. If it is
not obstructing labour it is best to await delivery and remove the
tumour early in the puerperium. Caesarean section may have to be
done if the tumour is obstructing delivery and ovarian cystectomy
performed.

22

CERVICAL INTRAEPITHELIAL NEOPLASIA

(CIN)
THE NORMAL CERVIX
The ectocervix (vaginal portion of the cervix) is covered by squamous
epithelium and the columnar epithelium lined the endocervix. This two
types of epithelial meet at the squamous-columnar junction (SCJ). The
squamous-olumnar junction is not a fixed point but undergoes changes
throughout life due to hormonal influences (Fig. 1.1). It is situated just
inside the external cervical os in young women, rising up the
endocervical after the menopause.
Before Puberty

Reproductive Period

Menopausal Period

The endocervix lies within the

endocervical canal and the SCJ
lies at the level of the external
os

Under the influences of the

hormone the cervix enlarges
and everts and the SCJ is
situated just inside the external
cervical os.

After menopause, the cervix

shrinks
and
the
SCJ
withdrawn into the canal

Fig. 1.1 The SCJ (squamous-columnar junction) at different periods of life.

As a result of hormonal influences, the cervix enlarges and everts

exposing the columnar epithelium of the endocervical canal. The
columnar epithelium that is exposed to the vaginal environment
undergoes metaplasia to squamous epithelium and the part of the
cervix, which is lined by this metaplastic squamous epithelium, is
known as transformation zone (Fig. 1.2).

Fig. 1.2 Transformation zone of the cervix

The transformation zone is an area of rapid cell division, where almost

95 percent of cervical cancer arises. The increased risk of developing
cervical neoplasia, associated with regular sexual intercourse at early
age, may be due to the transformation zone being exposed at early
age to oncogenic viruses (human papilloma virus).
This transformation zone can be visualized by colposcope procedures.

Fig. 1.3 Colposcopy showing transformation zone

CERVICAL INTRAEPITHELIAL NEOPLASIA (CIN)

If the metaplastic process in the transformation zone is disrupted,

dysplastic changes may develop in the epithelium resulting in cervical
intraepithelial neoplasia (CIN). There are three grades of CIN. The
term CIN 1, CIN 2, and CIN 3, are histological terms used to describe
increasing degrees of dysplasia from mild to severe.
1) CIN 1 corresponding to mild dysplasia;
2) CIN 2 corresponding to moderate dysplasia; and
3) CIN 3 corresponding to both severe dysplasia includes and
carcinoma in situ.
The terms broadly correlate with
dyskariosis seen on cervical histology.

mild,

moderate, and severe

NATURAL HISTORY OF CIN

CIN is asymptomatic. It can regress, persist, or progressive to invasive
malignancy lesions. CIN 1 often regresses without treatment, whereas
CIN 2and CIN 3 is likely to persist or progress and rarely regresses
spontaneously. The average time for progression of CIN 3 to invasive
cancer have been estimated to be 10-15 years but rapid progression
may occur within a shorter period of confirmed-negative cervical
smear.
RISK FACTORS FOR CIN
Patient with the following factors are at risk for CIN.

Early age at first intercourse (16 years and younger)

Multiple sexual partners.
History of genital human papillomavirus (HPV) infection various
serotypes of the HPV, particularly 16 and 18, are associated in the
origins of CIN.
Immunodeficiency or HIV.
Others cocarcinogens include repeated sexually transmitted disease
infections, smoking, poor nutrition, and certain chemicals.

DIAGNOSTIC CRITERIA OF CIN

In all cases of CIN, the normal epithelium of the surface is replaced by

neoplastic cells showing varying degrees of differentiation, nuclear
abnormalities, and mitotic activity.
The histological grading of CIN is based on the proportion of the
epithelial thickness occupied by basaloid neoplastic cells:
not more than the lower third in CIN 1
not more than the lower two thirds in CIN 2
more than two-thirds or full thickness in CIN 3
NORMAL

CIN 1

Normal squamous
epithelium of the cervix

CIN 2

CIN 3

Full
thickness
Two-thirds
Thickness

Normal epithelium
replaced by abnormal One-third
thickness
cells

Fig. 1.4 Schematic drawing showing histological grading of CIN

CIN 1 (MILD DYSPLASIA)

Undifferentiated neoplastic cells occupy not more than the lower third
of the epithelium of the epithelium (Fig. 1.4 and Fig. 1.5). Cells in the
upper two-thirds show differentiation of normal cells. The transition
between the lower third and upper epithelial layers is usually well
demarcated. Nuclear abnormality is present at all levels, but is more
marked in the cells in the deeper layers. Mitotic figures occur mainly in
the lower third of the epithelium.
The cervical smear contains neoplastic cells showing mild dyskaryosis.
These are characterized by the presence of one or more irregular
nuclei, which occupy less than one-half of thetotal area of cytroplasm.

Fig. 1.5 CIN 1 Basaloid neoplastic cells occupy not more than the lower third of
epithelium.

CIN 2 (MODERATE DYSPLASIA)

Undifferentiated neoplasia cells occupy more than one-third but less
than two-thirds of the total thickness of the epithelium (Fig. 1.4 and
Fig. 1.6a). The cells in the upper third are differentiated. The degree
of nuclear abnormality in the cells in the superficial layers is more
marked than in CIN 1. Mitotic figures are more marked and include
abnormal forms.

Fig. 1.6 (a) CIN 2 and (b) - CIN 3

CIN 2 Basaloid neoplastic cells occupy up to two-thirds of the thickness of the
epithelium. Mitotic figures, mainly in the lower-thirds of the epithelium, are more
frequent than in CIN I
CIN 3 Basaloid neoplastic cells occupy the full thickness of the epithelium.

CIN 3 (SEVERE DYSPLASIA AND CARCINOMA IN SITU)

Undifferentiated neoplastic cells with a high nucleocytoplasmic ration
occupy more than two-thirds of the total thickness of the epithelium
(Fig. 1.6 b).
The cells have ill-defined boundaries and scanty
cytoplasm, so that loss of polarity and nuclear crowding are
characteristic of this lesion.
The nuclei are large, irregular and
hyperchromatic. Mitotic figures may be found at all levels.
The cervical smear contains neoplastic cells with a severe dyskaryosis.
The nucleocytoplasmic ratio is high and the nuclei occupy more than
two-thirds of the cell cytoplasmic area (Fig. 1.7).

Fig.1.7 Cervical smear Severe dyskaryosis: Note large nuclei, varied size, irregular
shape, coarse chromatin occupying more than two-third of the cytoplasmic area.

MANAGEMENT OF CIN
Ideally, colposcopy is an important technique in evaluation of women
with an abnormal cervical smear or an abnormal-looking cervix. The
colposcopic examination employs 10 20X magnification combined
with green filter and acetic acid to accentuate the colposcopic findings.
Colposcopy is considered to be satisfactory in patients in whom the
entire limits of the dysplastic lesion and squamocolumnar junction are
visible.

It seems reasonable to recommend immediate colposcope for every

patient with a smear suggesting CIN 2 and CIN 3. Patients with
persistent mild dyskaryosis (CIN 1) should have colposcopy.

Abnormal cervical smears

Borderline
Mild
Changes and HPV
dyskaryosis
CIN 1
Repeat within
6 months

Moderate
dyskaryosis
CIN 2

Severe
dyskaryosis
CIN 3

Repeat within
6 months
Persistent

COLPOSCOPY

COLPOSCOPY
CIN 1
CIN 2

Ablative techniques
Cryocautery
Electrodiathermy
Laser vaporisation

Hysterectomy

CIN 3

Treatment has not cleared

the lesion.
Invasive cancer detected in
the specimen.

Recurrent

Excisional techniques
Knife cone biopsy
LLETZ
LEEP
Laser excision

Follow-up with

smear
*LLETZ large loop excision of the transformation
zone
*LEEP - Loop electrosurgical excision procedure
Fig. 1.8 Protocol for the management of abnormal smears/CIN

Conservative treatment:
Treatment options for CIN include:
Ablation techniques:
Cryocautery destroy tissues by freezing.
Electrodiathermy
the transformation
diathermy needle.
Laser vaporization

zone

destroyed

by

Excisional techniques:
Laser excision
Loop diathermy e.g. LLETZ (large loop excision of transformation
zone) simple, produces a good histological specimen
Knife cone biopsy requires general anaesthesia.
Largely
replaced by loop diathermy.
Ablative techniques have the uniform disadvantages.
Excisional
techniques are preferred because they allow for complete histological
analysis of the specimen.
Whichever method of treatment is chosen the end result is similar
where the transformation zone is destroyed or excised down to the
depth of 6 mm.
Hysterectomy:
If the above treatment has not cleared the lesion, particularly in CIN III,
hysterectomy is recommended, depending on the patients
reproductive status, when there is evidence on the follow-up
examination that CIN is still present.
If invasive cancer is discovered in the conization specimen the poatient
is generally treated with hysterectomy, the extent of which depends on
the amount of invasion present.
FOLLOW-UP

After conservative treatment it is imperative that women attend for

regular cytology. Standard practice is to perform a smear 3 to 6
months after treatment. If this is negative, further cytology 6 months
later and every year for 3-4 years may be undertaken. If all are
negative the patient will follow the usual smear program.
Any
abnormality
during
follow-up
should
result
in
colposcopic
reassessment.

23
VULVAL AND VAGINAL INTRAEPITHELIAL
NEOPLASIA
(VIN and VAIN)
VULVAL INTRAEPITHELIAL NEOPLASIA (VIN)
The term vulval intraepithelial neoplasia (VIN) is used for the condition
when the neoplastic cells are present on the surface epithelium of the
vulva. There are two main categories of VIN:

Non-squamous VIN which include Pagets disease of the

vulva and melanoma in-situ.
Squamous VIN.

Pagets disease Derived from the skin appendages vulvar Pagets

disease is rare and occurs most commonly in postmenopausal women.
It appears as scaly, red areas anywhere on the vulval skin.
Histologically, there are large, round cells with pale cytoplasm, lying
singly or in nests within the epidermis:glandular differentiation is seen
in a few cases. Pagets disease can occasionally progress to an
invasive lesion.
Treatment is commonly by wide local excision.
Prognosis is good if the disease is confined to the epithelium.
Melanoma in situ Is the least common of the VIN group.
GRADING OF VIN
Grading of VIN is similar to that of CIN, with VIN 1, 2 or 3 denoting an
increasing depth of neoplastic cells with worsening differentiation.

VIN 1

The cellular abnormalities and lack of stratification

and cytoplasm differentiation are limited to the lower
third of the epithelium.

VIN 2

Extension of the abnormal cells limited to the middle

third of epithelium.

VIN 3

When the extension of the abnormal cells involved

the upper third of the epithelium.

Table 1. Grading of vulval intraepithelial neoplasia (VIN)

Histologically, VIN may be undifferentiated or differentiated. The

undifferentiated VIN may occur in two basic pattern (1) basaloid VIN,
and (2) warty (also known as bowenoid).
VIN 3 can progress to an invasive squamous cell carcinoma. An
invasive disease associated with VIN is more likely to occur in a
postmenopausal patient as compared to a younger woman.
PRESENTING SYMPTOMS
Approximately one-half of the patients present with pruritus and the
remaining cases are usually found incidentally at the time of routine
gynaecologic examination.

Site

Most commonly the posterior third of labia

minora

Symptoms

Pruritis, burning sensation and soreness

Signs

Raised
or
flat,
leukoplakia,
hyperkeratotic, pigmented.

reddened,

Table 2 Characteristics of VIN

VIN may be unifocal or multifocal in distribution. VIN usually is sharply

demarcated and slightly elevated. The surface may be shiny, smooth,
glandular, rough (warty), or keratinized.

EVALUATION
Evaluation consists of careful inspection of the entire perineum. The
most common locations are the labia minora and the introitus.
Colposcopic examination can aid in defining the extent of the VIN.
Multiple biopsies may be required to define the extent of the disease
and to exclude invasion.
TREATMENT
The two options for treatment of VIN are laser ablation and wide local
excision. The former is generally the preferred method of treatment as
it gives excellent cosmetic results in an area where preservation of
appearance is clearly important.
For invasive disease, the preferred treatment method has been
excision for the older woman and laser ablation for the younger
woman.

VAGINAL INTRAEPITHELIAL NEOPLASIA (VAIN)

Cancer of the vagina is a rare condition. The majority of these are
squamous cell lesion.
The precancerous stage of the invasive
squamous cell disease occurs in the form of intraepithelial neoplastic
condition term vaginal intraepithelial neoplasia (VAIN).
VAIN is uncommon of the lower genital tract intraepithelial disease.
The incidence has increased in recent years and it is now found in
younger women and this rise seem to be associated with increased
prevalence of human pappilomavirus (HPV) infection of the genital
tract.

VAIN is seldom seen as an isolated vaginal lesion. It is more usual for it

to a vaginal extension of CIN.
In most cases it is diagnosed
colposcopically.
Untreated or inadequately treated VAIN may progress to frank invasive
carcinoma.
Human papillomavirus is thought to be a major etiologic factor in VAIN,
as well in CIN and VIN. It has been suggested that postmenopausal
atrophy of the vagina is also conducive to the development of VAIN.
The most common location of VAIN is the upper third of the vagina; the
middle and lower thirds of the vagina are involved in less than 10 % of
the cases. The lesion is often multifocal, usually asymptomatic and is
discovered only on routine examination, when it is seen either as an
area of increased vascularity or as a whitish patch.
The histological appearances of VAIN are similar to those of both VIN
and CIN. VAIN is widely regarded as a precursor of an invasive
carcinoma of the vagina.

Table 3 Grading of VAIN

VAIN 1

When undifferentiated cells are

confined to the lower third of the
epithelium.

VAIN 2

When undifferentiated cells extend

into the middle third of the
epithelium.

VAIN 3

When undifferentiated cells either

extend into the upper third of the
epithelium or occupy its full
thickness.

DECTECTION AND EVALUATION

Vaginal cytology is the most important means of detecting VAIN.
Colposcopy is helpful in evaluating pain in VAIN. Biopsy specimens of
the lesions that appear to be invasive (raised, ulcerated) are taken.

TREATMENT OF VAIN
There is presently available wide range of therapies to treat VAIN.
Before any treatment is undertaken, the lesion will need careful
evaluation and biopsy. The therapies available are as follow:

Local excision
Chemotherapy (intravaginal 5-fluorouracil)
Physical destruction methods:
a) Carbon dioxide (CO2) laser
b) Cryosurgery
c) Electrocautery
Radiation
Major surgery partial and total vaginectomy

Local excision Small areas of VAIN are ideal for local excision. This
can be done under local or general anaesthesia.
Carbon dioxide laser Provided invasive disease has been excluded,
laser vaporization is a satisfactory way of treating VAIN 2 and/or 3.
Radiation therapy - Intracavitary radiation therapy is preferred for
the treatment of VAIN 2 and/or VAIN. Most authorities recommend a
dose of 60 Gy (6000 Rads) to the tumour site.
Complications following intracavitary radiation include vaginal
shortening as well as narrowing preventing satisfactory intercourse.
Therefore, radiation therapy is not suitable to younger and sexually
active female.
Major surgical procedure - Major surgical excision (partial or total
vaginectomy) of VAIN gives far more satisfactory results ands is the
only effective modalities of treatment. Total vaginectomy is preferred for
women with multifocal VAIN.
Careful individualization of treatment is needed. For sexually active
women, preservation of vaginal function is vital. Local therapies either

chemical or locally ablative are the most appropriate.

therapy is indicated for older women.

Radiation

In some patients, especially who are young and whose lesion is minor,
i.e. VAIN 1 and 2, it may be justifiable to delay active interference and
adopt watchful expectancy.
Patient must be counseled of the
important of regular follow-up with smears and biopsies.

24
MALIGNANT TUMOUR OF THE CERVIX

Fig. 1.1 Invasive carcinoma of the cervix

Carcinoma of the cervix is the second most commonest female cancer

worldwide. It is rare before the age of 20 years. The peak incidence is
in the 45 - 55 year age group but occurs slightly earlier among those
from lower socioeconomic groups. Mortality from this condition has
fallen in many developed countries with the introduction of cervical
screening.
The
typical
symptoms
of
cervical
cancer
are
postcoital,
postmenopausal and persistent intermenstrual bleeding. The majority
of cases of cervical cancer are squamous cell lesions, with
adenocarcinomas and adenosquamous lesions occurring less
frequently.

RISK FACTORS
There are many known risk factors for cervical cancer and many of
these are surrogates for sexual activity. Among the major risk factors
are

human papilloma virus - types 16, 18 and 33

cigarette smoking
human immunodeficiency virus
age of first coitus - adolescent cervix more susceptible to
carcinogenic stimuli as squamous metaplasia in the
transformation zone is active during this time
multiple sexual partners - increased likelihood to be exposed to
carcinogens; cervical cancer is virtually unknown in celibate
women
young age at first pregnancy - metaplasia most active during
first pregnancy
low socioeconomic status

The low incidence of cervical cancer among Jewish women may

possibly related to their sexual behaviour - abstinence from intercourse
when "unclean" i.e. when menstruating, when have a vaginal
discharge, and for the first 12-16 weeks postpartum. These are periods
of increased metaplasia in the transformation zone. The benefits of
male circumcision are now largely dismissed.

PATHOLOGY
The majority of cases of cervical cancer are squamous cell lesions, with
adenocarcinomas and adenosquamous lesions occurring less
frequently.

75-80% are squamous cell carcinoma - usually arising from the

squamo-columnar junction
20-25% are adenocarcinoma - arising from endocervical glands in
the endocervical mucosa - or mixed adenosquamous carcinoma
less than 1% are due to sarcomas and lymphomas

The time sequence from pre-invasive cervical carcinoma to invasive

cervical carcinoma is difficult to estimate. An approximate sequence
would be:

20 years from CIN to invasive carcinoma

10 years from microinvasive to invasive carcinoma

However, recent studies suggest that this sequence of events is

becoming more rapid.
Untreated, it is estimated that about 20-30% of patients with CIN3
would eventually develop invasive carcinoma.

PRESENTATION
Women with early disease may not have any symptoms and diagnosis
being established after a routine cervical smear.
In clinically detected lesions, symptoms are usually present and
majority present with

postcoital, postmenopausal or intermenstrual bleeding - occurs in

80-90% of patients; initially, irregular but later becomes
continuous
blood stained vaginal discharge.

Features of advanced disease include:

heavy bleeding
offensive blood-stained vaginal discharge
pain - indicating extension beyond the cervix:
o lower abdominal pain may signify a large pelvic mass
o sciatic pain may signify involvement of lymphatic nodes
which have become adherent to the sacral plexus
o back pain may signify vertebral metastases
urinary and/or faecal incontinence - from fistulae formation
leg swelling
uraemia - from ureteric obstruction or ascending pyelonephritis

DIAGNOSIS
A full history and clinical examination should be undertaken.

 HISTORY:
Specific enquiry should be made regarding previous cervical smear,
gynaecological and obstetrical history, sexual history, contraception,
smoking habits and symptoms of advanced malignancy.

PELVIC EXAMINATION:
Speculum examination may reveal an obvious tumour at the cervix,
which is friable and bleeds easily. Early tumours may be seen as a
small nodule or ulcer on the vaginal surface, or as a diffuse patch
resembling erosion. Advanced lesions may appear as a crater shaped
ulcer with high everted edges or as a warty-looking mass. They may
replace the entire cervix.

Fig.1.2 Speculum examination appearance of invasive carcinoma of the cervix

Rectal examination is essential to ascertain the extent of spread.

STAGING OF CERVICAL CARCINOMA

Cervical cancer is staged clinically and includes an assessment of the
extent of disease and sites of spread. Very early cancers are staged

according to information gained from the histopathological specimen.

Clinical staging for cervical cancer should include the following:

examination under anaesthesia (EUA),

rectovaginal examination
cystoscopy (for bladder involvement)

including

sigmoidoscopy (if required)

intravenous urogram (IVU) and chest X-Ray (CXR)

combined

The International Federation of Obstetricians and Gynaecologists

(FIGO) introduced the following system for the staging of cervical
carcinoma:
Histological staging:

0 - CIN III (carcinoma in situ)

IA - microinvasive carcinoma

Clinical staging:

IB - invasive carcinoma confined to the cervix

IIA - invasion into the upper one third of the vagina
IIB - extension to the parametria but not to the pelvic side wall
IIIA - extension to the lower one third of the vagina
IIIB - extension to the pelvic side wall

IVA - tumour involving the bladder or rectum

IVB - extrapelvic spread, e.g. liver or lung metastases

SPREAD OF CERVICAL CARCINOMA

Local spread:

vagina, bladder, bowel, transverse cervical ligaments, arteries,

uterus

Lymphatics:

outwards in the pelvic fascia to internal iliac nodes, then to

common iliac nodes, and para-aortic nodes

 Haematogenous - relatively uncommon; the patient often dies from

the effects of local invasion before metastases to distant sites are
clinically apparent:

principally, to the lung, bone, and brain

INVESTIGATIONS
Possible investigations include:

FBC's - for anaemia

Urea and electrolytes - ureteral obstruction occurs in 30% of

stage III, 50% of stage IV

Calcium - hypercalcaemia may occur in advanced disease, but

not always due to bone involvement

Liver function tests - abnormal if liver metastases

Cone biopsy - a smear is pointless with a gross lesion

Chest Xray - lung metastases seen in 5% of patients with

advanced disease

Cystoscopy and sigmoidoscopy - rarely reveal mucosal invasion

except in advanced disease

Intravenous pyelogram

CT (computered tomogragraphy) scan or MRI (magnetic

resonance imaging) scan useful for planning treatment

Although CT and MRI scans provide additional information about

tumour size and possible node involvement, it does not alter the
FIGO stage.

TREATMENT

The treatment of cervical cancer is based on keeping the patient

informed and counselled. The main choices are between radiotherapy
and surgical therapy, and are largely dictated by the stage of the
disease, and the age and preference of the patient.
Pre-invasive disease may be treated conservatively - by ablative
techniques such as cryosurgery, or by conisation or hysterectomy in
older patients.
Radiotherapy or surgery may be indicated in early invasive disease
depending upon the exact stage of the disease and the patient's desire
for childbearing.
Late invasive disease is generally treated by radiotherapy.
Recurrent disease usually requires chemotherapy or less commonly,
pelvic exenteration.

SURGICAL TREATMENT:
Stage O is usually treated by ablative techniques such as cryosurgery,
but may be treated by cone biopsy if the transformation zone cannot
be visualised. Hysterectomy may be indicated if future child bearing is
not wished.

Stage IA may be treated by cone biopsy or hysterectomy.

Complications associated with conisation include:

cervical stenosis
cervical incompetence

Stage IB and IIA tumours may be treated by radical hysterectomy

and bilateral pelvic lymph node clearance (Wertheims hysterectomy).
Radical hysterectomy entails removal of the uterus with adjacent
portions of the vagina, cardinal and uterosacral ligaments, and bladder
pillars.
Radical hysterectomy in these patients if favoured:

in premenopausal women - as the ovaries can be preserved and

complications of vaginal irradiation e.g. dyspareunia can be
avoided
where the tumour is small
where future child bearing is not wished

Complications associated with radical hysterectomy include:

ureteric fistula or stricture

bladder dysfunction - through interruption of part of the
autonomic nerve supply traversing the cardinal and the
uterosacral ligaments. Dysfunction usually lasts for some months
and may be permanent
DVT and PE - less common with prophylactic measures such as
early ambulation, low dose subcutaneous heparin

RADIOTHERAPHY:
Radiotherapy is the treatment of choice in patients with stage IIB, III
and IV disease, and most patients with stage IIA disease. Stage IB
tumours may be treated by radiotherapy if the lesion is of sufficient
size that extensive surgical resection is required, with consequent
increased risk of postoperative bladder dysfunction.
Stages I, II, and III is usually treated with a combination intracavity
radioisotope and high-energy external radiation therapy, for example
caesium-137.
Stage IV is treated by external radiotherapy if the disease is confined
to the pelvis. Spread outside the pelvis is an indication for
chemotherapy.
Complications of radiotherapy may include:

fatigue and diarrhoea during treatment; the diarrhoea may

persist after the treatment is completed
proctitis, cystitis and rarely, fistula formation
vaginitis and dyspareunia
vaginal stenosis - rare if dilators used regularly during treatment

loss of ovarian function - may necessitate HRT to overcome

abrupt onset of menopausal symptoms in premenopausal women

CHEMOTHERAPY TREATMENT:
Chemotherapy may be indicated in:

advanced disease - with extrapelvic spread

recurrent disease
where radiotherapy has been ineffective

Most treatments are based on cytotoxics based on cisplatin.

Chemotherapy is not a first choice treatment because:

cervical carcinoma is relatively radiosensitive

large, bulky tumours may have necrotic centres which are never
reached
tissue vascularity is reduced following radiotherapy so drug
uptake is sub-optimal

PROGNOSIS
The prognosis of invasive carcinoma will vary according to the skill of
the surgeon or radiotherapist, and to the exact method chosen.
Illustrative values for 5-year survival would be:

Stage
Stage
Stage
Stage

I - 80% or more
II - 60%
III - 30%
IV - 10%

Stages IA and IIB show little difference between surgically treated

disease and ones treated by radiotherapy.
In patients with recurrent disease:

50% show recurrence within one year

75% show recurrence within two years
90% show recurrence within five years

STAGE

SPREAD

TREATMENT

1a

Cervix (micro-invasive)

1b

Cervix (macro-invasive)

2a

Upper vagina

2b

Parametrium

Local
excision

PROGNOSIS
(5-year
survival) %
100
80

Radical
surgery
Radical
surgery
Radiotherapy

60
50

Lower vagina (a), pelvic

walls (b)
Radiotherapy

30

Bladder,
rectum
metastases

10

or
Palliation

25
ENDOMETRIAL CARCINOMA

Fig.1.1 Carcinoma of endometrium

Invasive carcinoma of the uterine corpus is predominantly a disease of

post-menopausal women with a peak incidence at 61 years of age;
75% of cases occur after the menopause, 5% before the age of 40, and
20% between these two limits.
The disease is highly curable if it presents in the early stages. The
overall prognosis is relatively good as most cases are detected early
following investigation for post-menopausal bleeding. Nulliparous
women and those of low parity seem to be affected most frequently.

ETIOLOGY AND RISK FACTORS

The following are risk factors for endometrial carcinoma:

Age:
Endometrial cancer is principally a disease of
postmenaupasal women. The peak incidence is between the
ages of 60 and 75. About 75% of cases occur after the
menopause, 5% before the age of 40
Late menopause: Women undergoing the menopause after the
age of 52 years have a 2-4 times increased risk of developing
endometrial cancer compared with women who became
menopause before the age of 49 years.
Nulliparity: Of the women with endometrial cancer, 20-35%
are nulliparous.
Obesity: Obesity increases the risk 3-10 fold.
Overweight
women have increased conversion of steroids to estrogen in their
peripheral fat.
Stimulation of the endometrium in
postmenopausal women may result. Hypertension and lateonset diabetes are risk factors, chiefly because of their
association with obesity.
Unopposed estrogen therapy, ovarian theca cell tumour:
Unopposed estrogen replacement therapy in postmenopausal
women increases the risk of endometrial cancer by a factor of 68. The disease is also more common in women with polycystic
ovarian disease and estrogen-producing tumours.
Progesterone opposed therapy:
The risk of developing
endometrial cancer is reduced by combined hormone
replacement therapy with at least 10 days of progestogen in a
28-day cycle.
Others risk factors: Women who have had previous pelvic
irradiation are at increased risk of endometrial cancer. Also

women with previous history of cancers of breast, colorectum

and ovaries are at increased risk of developing endometrial
cancers.
An excess of oestrogen is common to all risk factors:

in obese patients, androstenedione is converted to estrone in

adipose tissue
a late menopause is preceded by many anovulatory cycles
resulting in a lack of progesterone to counter the endometrial
proliferation mediated by estrogens
patients with polycystic ovary disease have anovulatory cycles
ovarian theca cell tumours produce estrogens

It is associated with diabetes and hypertension, but unlike cervical

cancer, is not more common among the lower socio - economic groups.
Atypical endometrial hyperplasia carries an estimated 20% risk of
endometrial cancer.

PATHOLOGY
This growth is essentially adenocarcinomas; varying from anaplastic to
well-differentiated. Occasionally, squamous elements are present. If
these are benign, the tumour may be referred to as an
adenocanthoma; when malignant, as an adenosquamous carcinoma.
The latter carries a poorer prognosis. Rarely, endometrial cancer may
be a leiomyosarcoma or a mixed mesodermal tumour.
Spread is usually by direct extension to adjacent structures. The
tumour commonly invades through the myometrium but may also
spread downwards into the cervix. Less commonly, it may involve the
vagina, rectum or bladder.
Exfoliated cells may pass through the fallopian tubes and deposit on
the ovaries, parietal peritoneum, or omentum. Often, it is these
secondary growths which result in death.
Lymphatic spread occurs later and is less frequent than seen in cervical
cancer. Spread is mainly to the pelvic lymph nodes, and subsequently,
to the para-aortic nodes.

Haematogenous spread is rare. Metastases occur most often in the

lungs and liver.

PRESENTATION
Symptoms:
Classically, endometrial cancer presents with bleeding in the
postmenopausal woman. This is usually slight and intermittent at first,
and separated by long intervals. It later may become continuous and
heavy.
Premenopausal women usually present with intermenstrual or irregular
bleeding.
Watery vaginal discharge may be present in postmenopausal women in
the early stage and later becomes offensive.
There may be a sense of discomfort in the pelvis. Pain is a late
symptom, usually indicating extensive disease.

Physical signs:
On examination, enlargement of the uterus is usually unremarkable
except in late cases. Fixation of the uterus occurs late.

STAGING OF ENDOMETRIAL CANCER

FIGO (International Federation of Gynaecology and Obstetrics) have
introduced a surgico-pathological staging system incorporating the
presence or absence of myometrial invasion, positive peritoneal
cytology and involved lymph nodes. So the staging is based on the
amount of differentiation. Thus:

G1 - Well differentiated
G2 - Moderately differentiated
G3 - Poorly differentiated

The degree of differentiation predicts the likelihood of spread.

FIGO staging of endometrial cancer is as follows:
Stage

Degree of
differentiation

Extension of cancer

1a
1b

G123
G123

Tumour confined to the endometrium

Invasion confined to inner half of
myometrium
Invasion in outer half of the
myometrium

1c

G123

2a
2b

G123
G123

Endocervical glandular involvement

only
Cervical stroma invasion

3a

G123

3b
3c

G123
G123

Tumour invades serosa

Positive peritoneal cytology
Vaginal metastases
Metastases to pelvic or para-aortic
nodes

4a
4c

G123
G123

Tumour invades bladder or bowel

Distant metastases

Table 1 FIGO - Surgico-pathological staging of endometrial carcinoma

INVESTIGATION
Any woman who presents with post-menopausal bleeding must be
investigated with a high degree of suspicion, and should have an
endometrial curettage and biopsy. Curettage must be gentle as there
is a risk that the uterus may be thin and easily perforated.
If the curettage is negative, the patient should be reviewed at threemonth intervals and advised to report immediately, should bleeding
recur.
Other causes of post-menopausal bleeding should be considered whilst
remembering that innocent and malignant lesions may co-exist.

TREATMENT
The standard approach is surgical usually involving total hysterectomy,
bilateral salpingo-oophorectomy, removal of a cuff of vagina.

Patients with low risk stage I disease i.e. well differentiated,

only superficially invasive, may be treated with a total abdominal
hysterectomy and bilateral salpingo-oophorectomy

Patients with high risk stage I disease i.e. poorly differentiated,

deeply invasive, are treated as above with additionally, postoperative radiotherapy. This management approach reduces the
risk of local recurrence from 20 to 5% (1)

Stage II disease is managed as for high risk stage I

Stages III and IV - which fortunately, are rare - are managed on

an individualized basis. Surgery is rarely employed. Progestogen
therapy may be helpful. Chemotherapy may occasionally be used
in metastatic disease

PROGNOSIS
This is determined by stage, grade, myometrial invasion and lymph
node involvement:

Endometrial adenocarcinoma confined to the body of the uterus

(Stage I) has an approximate 80% 5-year survival rate
More advanced tumour, but still confined to the endometrium, has an approximate
40% 5-year survival rate

The degree of differentiation may also be used to predict outcome:

G1 - 95% 5 year survival rate

G3 - 50% 5 year survival rate

26
OVARIAN CANCER

Fig. 1.1 Ovarian carcinoma

Ovarian carcinoma accounts for a quarter of all genital tract cancer but
is responsible for half the deaths, primarily due to its late presentation.
Almost three-quarters of women present with advanced (stage III or IV)
disease, this is because symptoms are generally vague and nonspecific. The overall survival rate for women with ovarian cancer is
only 25-30 percent at 5 years.
Approximately 90% of these cancers are epithelial in origin. Most are
serous, mucoid and endometrioid. Dysgerminoma, granulosa cell and
metastatic tumours account for most of the remainder. The tumours
can be solid or cystic.
Epithelial carcinomas of the ovary are rare before the age of of 30
years and the incidence increases with age. Germ cell tumours are
found in children and young women, usually less than 30 years of age.
Ovarian carcinoma has a mean age of incidence of 58 years and
usually occurs between the 3rd and 8th decades.
Epidemiological studies have shown that pregnancy, breast-feeding and oral
contraceptive use appear to be protective against the development of ovarian cancer.

Risk Factors
The causes of epithelial ovarian cancer are not known.
Factors
associated with an increased risk of epithelial ovarian cancer include:
Parity: Ovarian carcinoma is more common in nulliparous and those of
low parity.

Oral contraceptive use:

There is evidence that taking the
contraceptive pill, which suppresses ovulation, reduces the likelihood
of developing cancer of the ovary. Epidemiological studies have shown
a significant reduction in ovarian cancer risk in women who have used
the combined oral contraceptive.
Familial history of cancer: Inheritance plays a significant role in
about 5 percent of epithelial ovarian cancers, usually serous
adenocarcinomas.
Genetic predisposition: A familial association in some patients with
breast and ovarian cancers has been recognized for many years.
BRCA1 and BRCA2 have been identified as tumour suppressor genes.
It is the mutation of these genes being responsible for these familial
cancers. BRCA1 is found on chromosome 17 and BRCA2 on
chromosome 13. Mutation in the BRCA1, gives a higher risk (40-60%)
of developing ovarian cancer.
BRCA1 mutation screening may be useful in familial and early onset
breast and ovarian cancer.

Types of Ovarian Cancers

Generally the ovarian cancers are primary or secondary. There are a
large number of different types of primary ovarian cancers. They are
classified according to the tissue of origin:

Tumours of surface epithelium - 60%

Germ cell tumours - 15-20%
Gonadal stromal tumours - 5-10%
Metastatic - 5-10%

(A) MALIGNANT EPITHELIAL OVARIAN CANCER

Malignant epithelial ovarian tumours account approximately 85-90% of
ovarian cancers. They arise from the germinal epithelium of the ovary,
which develops from the Mullerian duct, and is closely related to the

cells lining the peritoneal cavity. The commonest epithelial tumour is

the serous adenocarcinoma, followed by the mucinous and
endometrioid adenocarcinoma.
There are also undifferentiated
tumours which cannot be classified and mixed tumours which show
more than one type of epithelial cancer. Clear cell carcinomas are very
rare and associated with a poor prognosis.

Serous adenocarcinoma
These tumours, which are usually both solid and cystic, account for
50% of all epithelial ovarian tumours. They are bilateral in about onethird of the cases. Serous adenocarcinomas are characteristically
unilocur. Papillary patterns may be seen in the better-differentiated
tumours and psammoma bodies (small masses of calcified material of
uncertain origin) are often present.

Mucinous adenocarcinoma
These tumours account for 10-15% of malignant ovarian tumours. It is
unilateral and multilocular, each loculus being lined with a tall
columnar epithelium which may be ciliated and proliferate to form
papillary folds. They contain mucinous fluid which can be huge,
virtually filling the abdominal cavity. Rupture of the capsule can give
rise to pseudomyxoma peritonei in which a gelatinous material fills the
peritoneal cavity.

Endometrioid adenocarcinoma
Endometrioid adenocarcinomas are frequently cystic, often unilocular,
and contain brown fluids. They account 10-15% of epithelial ovarian
cancers. There is a definite association with endometrial carcinoma
perhaps as a result of simultaneous neoplasia in tissue of common
embryonic origin.

Clear cell adenocarcinoma

These rare epithelial tumours are usually unilateral. Microscopically
they have a clear cell pattern. Because there is both an association

between clear cell carcinoma and endometriosis and also because

clear cell tumours frequently coexist with endometrioid carcinomas, it
has been suggested that clear cell carcinomas may be a variant of
endometrial adenocarcinoma.

Borderline epithelial tumours

Ten percent of epithelial tumours are borderline tumours.
An
alternative name for these tumours is epithelial tumours of low
malignant potential. The majority is serous or mucinous. These
tumours show features of malignancy such as varying degree of atypia
and increase in mitotic activity, multilayering of neoplastic cells, and
formation of cellular buds and there is no invasion of stroma.
Most borderline tumours remain confined to the ovaries.

(B) MALIGNANT NON-EPITHELIAL OVARIAN CANCER

Non-epithelial ovarian malignancies account for 10-15 percent of all ovarian tumours, the
most common being the germ cell tumours and the sex cord stromal tumours. These
non-epithelial ovarian malignancies tends to

occur in younger women (rare over the age of 40 years)

have a shorter symptomatic history
have a higher percentage with early stage disease.

GERM CELL TUMOURS

Germ cell tumours in the female originate embryonically in the yolk sac
and are present in the ovaries at birth. These cells are known as
totipotent cells and can themselves give rise to tumours forming the
teratoma from embryonic cells and the highly malignant endodermal
sinus tumour from extra-embryonic cells. They are the second most
common cause of ovarian neoplasia, accounting for 15 - 20% of cases.
Overall, 95% are benign with a peak incidence in the third decade of
life. However, in children less than 10 years of age, 85% may be
malignant.
Germ cell malignancies are described in two main categories:

1) Dysgerminoma (female equivalent to seminoma)

2) Non-dysgerminoma, consisting of

Endodermal sinus tumour

Malignant teratoma

Mixed germ cell tumours

Dysgerminoma
Dysgerminoma are the most common of the germ cell tumours. They
occur in women less than 30 years old. They behave in a similar
fashion to seminoma in men, spreading by lymphatics to para-aortic,
mediastinal and supra-clavicular glands.
Macroscopically, dysgerminomas are soft, rubbery solid tumour with a
nodular outer surface. Histologically similar to seminomas of the
testes.
Presentation is non-specific, with abdominal swelling and mass. They
are bilateral in 10-15 percent of cases and can grow to a large size.
About 70-75% of patient will present with stage I.
Treatment is by surgery. Dysgerminomas are highly radiosensitive and
require only low doses of radiation but chemotherapy is both effective.
Dysgerminimas have a good prognosis as the majority are stage I
tumours and are usually stage Ia.

Endodermal sinus tumour

Endodermal sinus tumours are the second most common germ cell
tumours after dysgerminomas. These tumours are also known as yolk
sac tumours and secrete alpha-fetoprotein (AFP). This tumour marker
can be used in diagnosis and follow-up after treatment. Endodermal
sinus tumour most commonly occurs in women under 20 years of age.
They are usually solid tumours. Abdominal pain and a mass are
usually the presenting features.
The definitive treatment is chemotherapy, surgery being conservative
with aim of establishing the diagnosis, removing the primary, and
staging the disease.

 Malignant Teratoma
Teratomas are neoplastic changes of the germ cells from the
embryonic structures.
Teratomas are of two distinct histological
variants immature and mature. Immature teratomas are highly
malignant. Malignant teratoma is the term applied to carcinomatous
cells with a teratoma. The management of malignant teratoma is
surgery followed by chemotherapy.

SEX CORD STROMA TUMOUR

These are tumours derived from the mesenchymal stroma of the gonad
and account for 5 - 10% of all ovarian neoplasms.
Many are endocrinologically functional, able to synthesise gonadal or
adrenal steroid hormones. The ovarian stroma is sexually bipotential,
so the hormones secreted may be male or female.

Granulosa and theca cell tumours

Granulosa and theca cell tumours are the most common sex cord
stromal tumours account for 5-10% of ovarian malignancies. They are
the largest group of functioning ovarian tumours producing steroid
hormones, mainly estrogens, which can cause bleeding in older women
and precocious puberty in girls. These tumours occur more frequently
in postmenopausal women. The effect of estrogens produced by the
tumour can result in endometrial hyperplasia or endometrial cancer.
Macroscopically, these tumours are solid or cystic and the cut surface
is often yellow because of the high lipid content. Call-Exner bodies are
the specific features of granulose-theca cell tumours.
Unlike epithelial ovarian cancers, granulose-theca cell malignancies
presented at an early disease stage.

Sertoli- Leydig
These are very rare tumours, half of which produced male hormone,
androgen, causing virilization in women. Stertoli-Leydig tumour is also
known as arrhenoblastoma. This tumour is potentially malignant and
may be cystic or solid.

METASTATIC OVARIAN TUMOUR

The ovary, perhaps because of its rich blood supply, is a frequent site
for secondary malignancy. About 5 - 10% of ovarian tumours originate
from primary tumours elsewhere. The most common sources of
metastasis are the breast, stomach, colon, and genital tract.
The Krukenberg tumour from the gastrointestinal tract is the most well
known.
Krukenberg tumour
A Krukenberg tumour is a rare metastatic ovarian tumour arising from
a mucus-secreting carcinoma of the stomach or colon as a result of
lymphatic spread. Most are bilateral and the stomach is the primary
site most commonly implicated.
Histologically, they are characterised by "signet ring" cells with the
nucleus displaced to the edge of the cell as a result of the
accumulation of a mucoid substance in the cytoplasm.

CLINICAL FEATURES
Early in their course, ovarian tumours are often asymptomatic (e.g. on
doing a bimanual examination for a smear test) or present with nonspecific symptoms. It may be difficult to distinguish benign and
malignant tumours.
The most common symptoms of ovarian tumours include:

Pain - most commonly from a rapidly enlarging malignant lesion

or one associated with endometriosis. It is unusual in
uncomplicated benign lesions

Abdominal girth - may increase significantly due to tumour or

ascites. Benign lesions usually enlarge slowly and may not be
perceived until the later stages of growth. A large abdominal
mass in a cachectic patient with general weight loss may be a
striking sign of a malignant lesion. An enlarged abdomen may
cause early satiety

Pressure effects - a large tumour in the rectovaginal pouch

may displace other pelvic structures upwards so distorting the

urethra and producing urinary retention. A tumour pressing down

on the bladder may cause urinary frequency. Rarely, an ovarian
tumour may cause obstructed labour

Rupture - peritonitis may occur secondary to rupture of a large

cyst; a rupture of a malignant cyst may result in spread of
malignant cells throughout the abdomen (Pseudomyxoma
peritonei)

Endocrine effects - these are relatively uncommon.

Endometriomatas and lutein cysts may cause menstrual
irregularity. Gonadal stromal tumours may be estrogenic,
androgenic or virilising

Other possible presentations include infarction/haemorrhage of a cyst, torsion of

a cyst.

SPREAD OF OVARIAN CANCER

Fig.1.2 Transperitoneal spread of ovarian cancer

(1) contralateral ovary and other pelvic organs
(2) small bowel
(3) large bowel serosa
(4) omentum

(5) diaphragm
(6) liver capsule
(7) pleural cavity

Transperitoneal spread - the main route of spread of

carcinoma of the ovary is to the peritoneal cavity. Cancer of the
ovary invades the ovarian capsul and then spreads directly
involve the pelvic peritoneum and other pelvic organs. The
peritoneal fluid carries malignant cells through the peritoneal
cavity and gaining attachment to adjacent structures - such as
the uterus, broad ligament, omentum, large and small intestine,
liver and to the surface of the diagram (Fig. 1.2)
Lymphatic spread is mainly along the lymphatics that run
with the ovarian vessels reaching the para-aortic glands and in
time the left supraclavicular glands. Lymphatic spread may also
involve the cervical and inguinal nodes. Malignant cells present
in the peritoneal fluid may spread from diaphragmatic lymphatics
to the pleura resulting in the formation of pleural effusions.
Haematogenous spread - occurs uncommonly and late. The
main spread is to the liver and the lungs, athough metastases to
bone and brain are sometimes seen.

FIGO STAGING OF OVARIAN CANCER

The FIGO staging of ovarian cancer is shown below. This is a surgicopathological staging. It includes cytological examination of ascites or
peritoneal washings and is dependent on the findings at laparotomy.
Parenchymal involvement of the liver is necessary to make a patient
stage IV

Stage I - growth limited to the ovaries

o a - one ovary, no ascites, capsule intact
o b - both ovaries, no ascites, capsule intact
o c- capsule ruptured, capsular involvement,
peritoneal washings, or malignant ascites

positive

Stage II - ovarian growth with pelvic extension

o a - extension to uterus or tubes
o b - to other pelvic organs, e.g. bladder, rectum
o c - extension plus findings as for IC

Stage III - tumour outside the pelvis or with positive nodes

o
o
o
o

a - microscopic seeding outside true pelvis

b - gross deposits less than or equal to 2 cm
c - gross deposits greater than 2 cm or positive nodes

Stage IV- distant organ involvement including pleural space and

liver parenchyma

MANAGEMENT
The initial approach to ovarian cancer is to confirm the diagnosis by an
exploratory laparotomy.
Once confirmed, standard procedure is to perform a total abdominal
hysterectomy,
bilateral
salpingo-oophorectomy,
and
infracolic
omentectomy.
A thorough surgical staging is made. All serosal surfaces are examined;
biopsies are obtained of grossly involved areas, and any free ascitic
fluid or peritoneal washings taken for cytologic studies. Retroperitoneal
lymph nodes should be examined if the disease appears confined to
the ovary, as this will alter management.
Patients with stage IA tumours which are well or moderately
differentiated, and who wish to remain fertile, may receive a unilateral
salpingo-oophorectomy without compromising survival. However, the
patient must be made to understand that there is a 10% risk of
developing a contralateral lesion.
All gross disease should be debulked. If all macroscopic disease cannot
be removed, aim to reduce individual tumour nodules to less than 1.5
cm diameter as nodules larger than this are considered to have a
deleterious impact on outcome. This "cytoreductive surgery" may
necessitate bowel resection in some cases.
Combination chemotherapy is then indicated for patients with
advanced disease - stage III or IV - and is also recommended for stage
IC or poorly differentiated stage I, and any stage II disease. It is
unnecessary for well or moderately differentiated stage IA or B
tumours.
Subsequent management depends on the response to chemotherapy
where indicated.

Chemotherapy
Chemotherapy plays a central role in treating epithelial ovarian cancer
Initial chemotherapy
All women, except those with well-differentiated Stage 1A disease,
should be considered for platinum-based chemotherapy.
The platinum therapy (carboplatin or cisplatin) are the most widely
used drugs in the management of ovarian cancer either alone or in
combination. They are heavy metal compounds. Cisplatin causes
severe nausea and vomiting and give rise to severe renal damage.
Doxorubicin has anti-ovarian carcinoma activity. Systematic reviews of
randomised trials have shown that cyclophosphamide, doxorubicin and
cisplatin is more effective than cyclophosphamide and cisplatin alone.
Single agent therapy, typically melphalan, is commonly used for frail or
elderly patients.

Subsequent management
The majority of patients demonstrate a complete clinical response to
initial debulking and chemotherapy with physical examination, CT scan
and CA-125 levels all normal. But of these, about half still have disease
as defined by negative biopsy specimens on a second look laparotomy.
The discovery of disease itself has little effect on survival so present
day policy is to recommend second look laparotomy only if further
treatment is to be considered. The guidelines for managing persistent
disease are less established. Treatment options include:

Secondary debulking - not curative but may be valuable in

certain cases. For example, patients with imminent bowel
obstruction due to a single dominant pelvic mass; or whom have
relapsed many years after initial therapy, and possibly, would
enjoy a similar disease free period after another debulking.

Intraperitoneal chemotherapy - drugs such as cisplatin are

administered into the peritoneal cavity through an indwelling

catheter. Only effective if a substantial fraction of tumour cells

remain chemosensitive..
.

Radiotherapy for ovarian cancer

radiotherapy was previously widely used in the treatment of

ovarian cancer before platinum chemotherapy was available however the transperitoneal spread made the delivery of
adequate doses of radiotherapy difficult
radiotherapy is now primarily a palliative treatment option in the
management of ovarian cancer

Radiotherapy is little used in modern management of ovarian cancer

where it has been superseded by the development of more active
chemotherapy.

PROGNOSIS
Stage I disease is associated with an 80-95% 5 year survival rate
depending on histology and grade. That for well or moderately
differentiated IA or IB tumours is usually 91-95%; that for poorly
differentiated stage I, about 80%.
Stage II disease has a 70% 5-year survival rate.
The prognosis for advanced disease remains poor despite intensive
chemotherapy. The 5 year survival rate is about 60% for those in whom
a second look laparotomy is negative, and about 20% in those with
clinical evidence of disease after chemotherapy.

Screening (for ovarian cancer)

There is little information concerning the nature of the precursor to a
malignant ovarian tumour and there is, as yet, no proven role for
screening for ovarian cancer.
The common epithelial cancers may develop from ovarian inclusion
cysts. Unfortunately screening by ultrasonography does not reduce
mortality from ovarian cancer.

Carcino-embryonic antigen is insufficiciently sensitive or specific to be

used as a screening test (see linked term).

27
VULVAL CARCINOMA

Fig.1.1 Vulval carcinoma

Malignancy of the vulva accounts for about 3 to 4% of all

gynecologic neoplasms and usually occurs after menopause. The
majority occurs in the elderly with a median age of 60 years. Though
patients can readily visualize and palpate these malignancies, they
may not seek treatment for up to 3 years because of embarrassment
or fear. Also, the physician may delay treatment by striving to provide
symptomatic relief of the accompanying pruritus rather than obtaining
an immediate biopsy.

Risk factors for vulval cancer include other genital carcinomas, chronic
vulval inflammatory disorders (such as lichen sclerosus or epithelial
hyperplasia), genital warts and vulval intraepithelial neoplasms.

Pathology
Cancer of the vulva involves the labia majora in about two-thirds of the
patients; and the clitoris, labia minora, or perineum in the remainder.
About 90% of cases are squamous cell carcinomas and about 4%
are basal cell carcinomas; the remainder includes intraepithelial
carcinomas, such as Paget's disease, adenocarcinoma of Bartholin's
gland, fibrosarcoma, and melanoma.
Most squamous cell carcinomas of the vulva are well differentiated.

Spread of the disease

Spread of vulval carcinoma is by:
Direct extension to adjacent structures - Vulva cancer usually
spreads slowly and infiltrates local tissues before involving the lymph
nodes in the groins. Often, the intraepithelial lesions have multifocal
origins. Growth is initially superficial, but later the tumors extend into
the vagina, the urethra, or the anus. Prognosis depends on the depth
of involvement into the underlying epidermis.
Lymphatic spread - Spread occurs first to the superficial and deep
inguinal and femoral nodes then to the external iliac and obturator
nodes. The common iliac and para-aortic nodes are involved in late
cases. Spread to the contralateral groin nodes occurs in 25 percent of
cases.
Haematogenous spread occurs late and is rare in the absence of
lymphatic involvement. Haematogenous spread is to distant sites such
as lungs, liver, and bone

Clinical features
Symptoms: Most patients with cancer of the vulva complain of
irritation or pruritis. Less frequent symptoms comprise of swelling,
ulceration, pain and offensive discharge.

Until the lesion reaches 1 to 2 cm or more in diameter, it is often

asymptomatic, although carcinoma in situ tends to be pruritic.
When the tumor becomes necrotic and infected, symptoms resemble
those of an ulcer with bleeding and/or watery discharge.

Signs: Carcinoma of the vulva usually appears as an ulcer with

irregular, raised edges (ulceration is an early feature), or as warty
lesions. It may be pigmented.

Diagnosis
Diagnosis usually is made by simple biopsy.
Differential diagnosis
The differential diagnosis is mainly from other causes of a lump in
vulva or of ulceration, and from other malignant tumours.
Differential diagnosis must include the
granuloma inguinale, chancroid, lymphogranuloma venereum,
syphilis
basal cell carcinoma (rodent ulcer)
intraepithelial (in situ) cancers characterized by small red, white, or
pigmented friable papules
melanomas frequently appear as bluish-black, pigmented, or
papillary lesions

Clinical staging of vulval cancer

The FIGO staging for cancer for the vulva is shown below. This is a
surgical staging as pathological assessment is the only accurate
method of determining lymph node involvement.
Stage

0 - Carcinoma in situ (pre-invasive carcinoma)

I - Confined to vulva or perineum. No lymph node metastases

Ia Lesion less than 2 cm in greatest diameter with stromal
invasion no greater than 1.0 mm

Ib - Lesion less than 2 cm in greatest diameter with stromal

invasion greater than 1.0 mm

II - As I but more than 2 cm in greatest diameter. No lymph

nodes metastases

III Tumour of any size with adjacent spread to urethra and/or

vagina or anus;
and/or unilateral regional lymph node
metastases

IVa - Invasion of upper urethra or bladder mucosa or rectal

mucosa or pelvic bone; and/or bilateral regional lymph node
metastasis

IVb - Any distant metastasis

Treatment
Since squamous cell carcinoma of the vulva spreads by local extension
as well as by lymphatic spread, all existing and potential tumor sites in
this region should be removed.
Radical surgery for early disease consists of vulvectomy with
bilateral block dissection of lymph nodes (inguinal and femoral).
Advanced disease requires the addition of exenterative surgery with
subsequent loss of bowel and/or bladder function.
The relative merits of exenterative surgery must be weighed carefully
as most patients are elderly. Mortality reaches 13%. Morbidity is mainly
due to haemorrhage and sepsis.

Radiotherapy is given post-operatively as an adjunct to surgery to

the pelvic nodes and inguinal areas in the presence of nodal
metastases. The combination of radiotherapy and radical vulvectomy
has been shown to give a better prognosis than exenterative sugery
and radical vulvectomy in the treatment of advanced or recurrent
disease.
Preoperative external radiotherapy can be used to sterilize or
decrease the size of large tumors. Radium needle implants may be
used for inoperable tumors and metastases.

Chemotherapy may be used before treatment to reduce the tumour

bulk.

UNCOMMON MALIGNANT TUMOURS OF THE VULVA

Basal cell carcinoma
Usually occurs on the labia majora beginning as a small nodule which
becomes ulcerated centrally (rodent ulcer). Diagnosis is made by
biopsy. They are only locally invasive and are treated by local excision.

Malignant melanoma
This is a highly malignant tumour of the vulva. The prognosis is
related to the depth of the tumour. The treatment consists of radical
vulvectomy, without lymphadenectomy unless the nodes are involved.

Bartholins gland carcinoma

This is a rare malignant tumour of the vulva. It presents as a hard
mass in the region of the gland with ulceration. These tumours are
usually adenocarcinomas. They are usually diagnosed late because of
the deep site of origin.
Treatment is by radical vulvectomy
accompanied by inguinal and pelvic lymphadenectomy.

Sarcoma
These rare malignant tumours of the vulva include leiomyosarcoma,
which tend to grow slowly, and rhabdomyosarcomas, which are rapidly
growing tumours. Treatment is by extensive local excision and groin
node dissection. Distant recurrence is common. The prognosis is very
poor.

28
VAGINAL CARCINOMA
Vaginal carcinoma is rare, accounting for less than 2% of all genital
tract cancer in women, which mainly presents in postmenopausal
women. The posterior upper third of the vagina is the most common
site for the cancer to occur, followed by the lower third in 25 percent of
cases while the middle third is the least common site.
Cancer found in the vagina is usually as a result of direct spread from
cervical or vulval cancer, or it is metastatic (e.g. from endometrium,
ovary). Making a diagnosis of primary vaginal cancer the following
criteria must be met:
1) The primary site of growth must be in the vagina
2) The cervix and vulva must not be involved, and
3) There must be no evidence that the vaginal tumour is metastatic
from a primary elsewhere.

Etiology
The etiology of vaginal cancer is obscure. Occasionally, it follows
chronic ulceration that accompanies complete uterovaginal prolapse,
or from a long retained pessary.
It has been known to occur in women whose mothers were treated with
large doses of stilboestrol during pregnancy.

Pathology

More that 90 percent of primary invasive tumours of the vagina are

squamous in type and 5 percent are adenocarcinomas.

Spread of vaginal cancer

Local invasion: Cancer of the vagina spreads by local invasion to the
rest of the vagina, vulva, paravaginal tissues and parametria.
Lymphatic spread: Lymphatic spread occurs from upper two-thirds of
vaginal lesions to pelvic and para-aortic nodes similar to that of the
cervix. Lymphatic spread from the lower third lesion is similar to the
vulva, spreading first into the groin (inguinal and femoral) nodes and
thence into the pelvic nodes.
Haematogenous spread:
occurs late.

Haematogenous spread is unusual and

Features
Post-coital bleeding is the most common complaint and is often later
followed by an offensive watery discharge. Urinary symptoms, and
pelvic pain are less common and are suggestive of advanced disease.
Spread may occur locally into the paravaginal connective tissues,
bladder and rectum, and occasionally, fistulae may form from the
vagina to the bladder or rectum.

Investigations
Examination under anaesthesia (EUA) - The most important
investigation is examination under anaesthesia. This should include
careful inspection of the whole vaginal and cervix, a combined vaginal
and rectal examination to detect extra-vaginal spread and cystoscopy.
Biopsies are taken of abnormal lesions and must be full thickness for
a ccurate histological diagnosis.

CT and MRI scan - In more advanced cases CT and MRI scanning of

the abdomen and pelvis to assess nodal involvement and extend of the
disease is necessary.

Staging of vaginal carcinoma

The FIGO staging for cancer of the vagina is based on clinical findings.
Stage

Features

Pre-invasive carcinoma

Carcinoma confined to vaginal mucosa

IIa
Involvement of subvaginal tissues. Not extending to
parametrium
IIb

Parametrial involvement but not extending to pelvic wall

III

Carcinoma extend to pelvic wall

IVa

Involvement of mucosa of bladder or rectum

IVb

Spread beyond the pelvis

Treatment
As most cases of vaginal cancer present late radical treatment is not
always possible.
Most patients with vaginal carcinoma are treated with local
radiotherapy using implanted radium or caesium combined with
external radiation to the pelvic lymph nodes is often used.
Radiotherapy leads to vaginal stenosis, but this complication can be
reduced by the use vaginal dilators following treatment.
Alternatively, the whole of the vagina, uterus and pelvic lymph nodes
may be removed surgically. The rectum is included if this too is
involved, necessitating a colostomy.

The use of chemotherapy in vaginal carcinoma is extremely limited.

OTHER RARE VAGINAL CARCINOMA

Clear cell adenocarcinoma

These rare tumours are occasionally associated with intrauterine
exposure to stilboesterol. The Histology of this tumour is characterized
by vacuolated or clear areas in the cytoplasm and a hobnail
appearance of the nuclei of the cells lining the glands. Most of these
tumours are situated in the upper vagina. The treatment is radical
surgery or radical radiotherapy.

Rhabdomyosarcoma (sarcoma botyroides)

Rhabdomyosarcoma occur in girls under the age of 5 years. The
tumours are confined to the anterior vaginal wallThe feature is a grapelike mass protrudes from the vagina. The presenting symptom is
vaginal bleeding. These tumours are sensitive to chemotherapy.
Treatment
involved
conservative
surgery
plus
combination
chemotherapy using vincristine, actimycin D and cyclophosphamide.
An overall survival rate over 80 percent is achieved.

29
CHORIOCARCINOMA
This is a highly malignant tumour of the trophoblast and it invades the
uterine wall causing necrosis and haemorrhage and has a tendency to
metastasizes rapidly via the blood stream, particularly to the lungs,
vagina, brain, livers, kidneys and gastrointestinal tract.
Choriocarcinoma can occur in any types of pregnancy. The commonest
antecedent pregnancy to choriocarcinoma is hydatidiform mole (about
50 percent of patients with choriocarcinoma). In the remaining
patients, choriocarcinoma is preceded by abortion in 30 percent of
cases and 20 percent follow normal pregnancy at term.
Percentage of each type of antecedent pregnancy in
choriocarcinoma
Hydatidiform mole
50%

Outcome:
Spontaneous
regression
Persistent
trophoblastic

Sponataneous abortion
30%

Outcome:
Choriocarcinoma

Normal pregnancy
20%

Outcome:
Choriocarcinoma

disease
Choriocarcinoma

Choriocarcinoma following full term pregnancy are highly aggressive

variant of this disease, with patients presenting within few months of
delivery with wide spread pulmonary and cerebral metastases.
PATHOLOGY
Choriocarcinoma
is
a
tumour
composed
both
cytoand
syncitiotrophoblastic cells. Typically there is circumscribed nodular
lesion with a dominantly haemorrhagic structure. In the uterus the
primary nodules may be simple or multiple, and may project into the
endometrial cavity or extend deeply into the myometrium. Local
metastasis nodules may be present in the cervix or vagina. A distant
metastasis sites the same haemorrhagic nodular pattern is usually
seen.
PRESENTATION
The majority of patients with choriocarcinoma present within a year of
an apparent normal pregnancy or within six months of persistent high
level of hCG. The presentation may be delayed for several years.
Symptoms:

Vaginal bleeding is a common symptom of uterine

choriocarcinoma or vaginal metastases.
Because of the
gonadotrophin secretion (hCG) amenorrhoea may developed
simulating early pregnancy.
Haemoptysis, cough or dyspnoea may occur as a result of lung
metastases.
In the presence of central nervous system involvement, the patient
may complain of headache, dizzy spell, or other symptom of a
space-occupying lesio0n in the brain.
Rectal bleeding or dark stool could represent disease that has
metastases to the gastrointestinal tract.

Signs:

Uterine enlargement may be present, with bleeding coming through

the os, as seen on the speculum examination.

A tumour metastases to the vagina may present with a firm,

discoloured mass.
Neurologic signs, such as partial weakness or paralysis, unreactive
pupils, aphasia, or convulsion indicate probable central nervous
system involvement.
Metastases in viscera such as liver, spleen, kidney or bowel may
also present with haemorrhage intraperitoneally or into the lumen of
the blood.
Occasionally thyrotoxicosis is present in patient with very high hCG
levels because of cross reaction between alpha subunit of hCG and
thyroid stimulating hormone (TSH).

INVESTIGATION
1) HCG: If hCG titre is positive, the work-up of a patient with choriocarcinoma is the
same as for hydatidiform mole. In trophoblastic tumours hCG comes close to being
the ideal tumour marker. The hCG is grossly elevated in choriocarcinoma. In
gestational trophoblastic disease, hCG values give an indication of the volume of
tumour.
2) Ultrasound scan: An ultrasound examination cannot be applied to diagnose a
trophoblastic tumour, but is used to presume the location of a tumour or to evaluate
the effect of therapy. The choriocarcinoma can be shown as an irregular
cystic pattern in the myometrium. It may be presented as a mass
of irregular linear echoes with high brightness.
3) Plain radiograph of the chest (Chest X-ray): This demonstrates
the diverse patterns of metastases to gestational trophoblastic
disease. The most common appearance (Fig. 1.1) is of multiple
discrete lesions but large solitary lesions (cannon ball appearance).

Fig.1.1 Chest X-ray showing cannon ball appearance metastases of choriocarcinoma

4) Computerized tomograph (CT) scan: CT scan is more sensitive

then plain radiography being able to detect metastases of
choriocarcinoma in the lungs (Fig.1.2).

Fig.1.2 CT scan of the lungs showing metastases (arrow heads)

5) Magnetic resonance imaging (MRI): MR imaging can also be

used to give images of choriocarcinoma in the pelvis and liver.
DIAGNOSIS

Choriaocarcinoma is suspected when bleeding persists after

evacuation of a hydatidiform mole or abortion and when there are
persistently raised hCG levels. Diagnosis may be made histologically
on curettage.
PROGNOSTIC FACTORS IN CHORIOCARCINOMA
In general the patient is either cured of her disease or succumbs within
a few months. Low, medium or high risk can often be assigned if the
following factors are taken into accounts:
1) The longer the binterval between the disease and the antecedent
pregnancy the higher the risk and more resistant to therapy.
2) Masse or tumour > 8 cm in diameter in the uterus, lungs or
elsewhere are more liable to be resistant to therapy.
3) If brain metastases developed after treatment has begun the
outlook is poor.
4) Women of blood group AB have a poor prognosis.
SCORE
Prognostic Factors

Age (years)

Antecedent pregnancy

Interval
time
(months)
between end of antecedent
pregnancy
and
start
treatment

HCG (IU) level

ABO group (female x male)

< 39

> 39

Molar
pregnanc
y

Abortion

Tumour size

Site of metastases

Term
pregnancy

46
4

10

> 12
104 - 105

7 12

103 - 104
OxA
AxO

B
AB

> 5 cm
3 5 cm

GI tract

Spleen

Fig.1.2 Scoring system based on prognostioc pressure.

> 105
105
Brains

Total score for patient isn obtained by addition of score for each prognostic.
<4
5.7
5.8

= Low risk group

= Medium risk group
= High risk.

TREATMENT
Chemotherapy:
For low-risk patients, the course of treatment is:
(i)
Methotrexate 1 mg/kg (to a maximum of 60 mg)
intramuscularly every 48 hours for 4 doses and
(ii)
Folinic acid 6 mg intramuscular every 48 hours for 4 doses
after 30 hours after each injection of methotrexate.
A minimum of 4 courses is given with a 7-day interval between
courses. This interval is lengthened if bone marrow depression or
other complications occur. In most patients hCG levels fall to normal
within four weeks of starting treatment.
For patients with poor prognostic disease, combination chemotherapy
is always used. Regimes that have been successfully employed include
methotrexate, actinomycin D and cylophosphamide (MAC) or the
modified regimen (EMA-CO), which is a six drugs regime. The drug
used includes etoposide (VP- 16), methotrexate, actinomycin-D,
cylophosphamide, vincristine, and folinic acid. The number of courses
depends on the extent of the disease and the patients response.
Intracranial metastases should be treated with intrathecal
methotrexate or cytosine arabinoside if resistance develops to the
former.
Surgical:
Hysterectomy is better avoided as initial treatment (because there is a risk of tumour
dissemination following surgery) except in the following circumstances:
(i)
Uterine perforation or intraperitoneal haemorrhage has occurred.
(ii)
In the older and/or multiparous woman with neither metastases nor uterine
enlargement.
(iii)
If the response to chemotherapy is incomplete or there is residual disease in
the uterus.
Monitoring of chemotherapy:

1) Measure serum hCG levels twice weekly during treatment.

2) Chest X-ray on admission and every 2 weeks during treatment thereafter if indicated.
3) White blood cell and platelet count on admission and three times weekly duringt
treatment. If bone-marrow depression occurs measure them daily.
4) Check liver and renal function on admission and weekly thereafter.

30
ABORTION AND MISCARRIAGE
The most common complication of
pregnancy is spontaneous abortion,
which is estimated to occur in 10-15
per cent of pregnancies. The terms
abortion
and
miscarriage
are
synonymous. The term miscarriage
is best used when discussing with
the women.
Abortion or miscarriage is defined as
the expulsion of the conceptus
before fetal viability is achieved.
The World Health Organization (WHO) define that a fetus is viable
when the gestation has reached 24 or more weeks. Abortion or
miscarriage can occurs naturally (spontaneous) or are induced.
Most miscarriage occurs between the 7 th and 13th weeks of pregnancy.
It is estimated that between 10 and 15 per cent of confirmed
pregnancies end as an abortion. The risk of miscarriage is affected by
age and increased parity. Abortion is more frequent among women
over the age of 30. Abortion increases in frequency with increasing
gravidity:-

CLASSIFICATION OF ABORTION
Abortion or miscarriage can occurs spontaneously or induced.
Spontaneous abortions can be categorized as sporadic or recurrent
(more than 3 consecutive) abortions.
SPONTANEOUS ABORTION
Spontaneous abortion is very common, often occurring before a
woman is aware of her pregnancy. This condition is a loss of pregnancy
before the fetal viability is achieved and is often referred to as a
miscarriage. Often the woman will have vaginal bleeding and cramp
like pains in the lower abdomen, and will have passed products of
conception.
The etiology of spontaneous abortion
There are many causes of spontaneous abortion throughout the
gestation period, the causes differing at different stages. The cause of
most spontaneous abortions is uncertain. In general the causes of
spontaneous abortion may be divided into:

Fetal factors.
Maternal factors.

In early pregnancy (less than 10 weeks) fetal factors account for most
of the abortion while in the later weeks (10 24 weeks) maternal
factors are the main contribution for the occurrence of spontaneous
miscarriage.
FETAL FACTOR
The main fetal causes of spontaneous abortion are:
1. CONGENITAL MALFORMATION OF THE ZYGOTE
The commonest identifiable cause of early miscarriage (first
trimester) is malformation of the zygote. About 70 per cent of these
abortions are associated with chromosomal abnormalities such as
trisomy, XO and triploidy.
In many cases when spontaneous
abortion occurs, it is found that the embryo has failed to develop or
has been absorbed. In these cases abortion takes place usually at
about 8 weeks and the amniotic sac contain no embryo
(anembryonic or missed abortion).
2. FAULTY IMPLANTATION

Many fertilized ova fail to implant successfully. This unfavorable

implantation of the fertilized ova causes spontaneous abortion
during the first trimester.
MATERNAL FACTORS
These may be general, local or psychosomatic. Maternal factors can
cause either first or second trimester miscarriage. The known maternal
factors are:

GENERAL CAUSES
Systemic maternal disease, particularly maternal infections, account
for 2 per cent of spontaneous miscarriages. Any acute febrile illness
may lead to miscarriage, especially if there is septicaemia with
infection of the fetus or placenta.
Maternal systemic lupus erythematosus (SLE) are a recognized
cause of repeated spontaneous miscarriage in the first trimester.
Transplacental infection, e.g Toxoplasma, herpes, rubella and
cytomegalovirus may lead to spontaneous miscarriage early in
pregnancy.
Severe hypertension, renal disease (chronic nephritis, chronic
pyelonephritis) may lead to second trimester miscarriage.
Diabetes, hypothyroidism and other endocrine disorder is
sometimes responsible for miscarriage.
Trauma such as fall, accident, blow to the abdomen may lead to
spontaneous miscarriage.
Certain drugs, particularly cytotoxic drugs may cause abortion.

LOCAL CAUSES
Local causes are the main contribution for second trimester
miscarriage. These include:1. Uterine abnormalities (e.g double or septate uterus), account
for about 8 per cent of spontaneous second trimester
miscarriage.
2. Uterine fibroids, particulary submucous myoma, which distort
the uterine cavity, causes second trimester miscarriage.

3. Incompetence of the cervix, (congenital or acquire) is

responsible for repeated or habitual miscarriage.
4. Hormonal deficiencies, e.g corpus luteum failure. Corpus
luteum failure causes deficiency of progesterone, may be
responsible for bleeding in early pregnancy and miscarriage.

PSYCHOSOMATIC FACTOR
Psychosomatic factors have been suggested but not proven as
causes for early miscarriage.

THE MECHANISM OF ABORTION

The immediate cause of abortion is the partial or complete detachment
of the embryo by haemorrhage in the choriodecidual space. As the
placental function fail, uterine contraction begin and the process of
abortion is initiated.
If the abortion occurs before the 8th week, the defective covered with
villi and some decidua is expelled. Some of the products of conception
may be retained.
Uterine bleeding occurs during the expulsion
process.
In the later pregnancy (between 14th and 24th week), when the
placenta is completely formed, the fetus is usually expelled first
followed the placenta.
Less commonly the placenta is retained.
Usually uterine bleeding is not severe.
An abortion resemble a miniature labour; the uterus contracts
rhythmically, the cervical os dilates gradually and the embryo is
expelled with or without its accompanying membranes. If all products
of conception are expelled, the contractions cease and the bleeding
stop. A blood-stained discharge continues for few days but eventually
ceases and the uterus involuted.
SIGNS AND SYMPTOMS OF SPONTANEOUS
In some cases, pieces ABORTION
of products of conception may retained in the
uterine cavity and result in persistent bleeding.

Patients knowledge of pregnancy

Heavy vaginal bleeding

Cramplike pains in lower abdomen

Passage of tissue (products of conception)

In ability to feel the uterus

VARIETIES OF SPONTANEOUS ABORTION

For descriptive purpose the spontaneous abortion is classified
according to the findings when the woman is first examined. One kind
of abortion may change into another if the aborting process continues.
The following terms are used to describe the clinical varieties of
abortion:

Threatened abortion
Inevitable abortion
Complete abortion
Incomplete abortion
Missed abortion

If infection complicates the abortion the term septic abortion is used.

ABORTION

SPONTANEOUS

SPORADIC

RECURRENT

THREATENED

INEVITABLE

COMPLETE

INDUCED

THERAPEUTIC

MISSED

INCOMPLETE

CRIMINAL

SEPTIC

THREATENED ABORTION
Threatened abortion is diagnosed when a pregnant woman develops
uterine bleeding with or without painful uterine contraction, no
passage of products of conception and the cervix is not dilated.
Mechanism of threatened abortion: In threatened abortion there
is bleeding into the choriodecidual space, but this is not sufficient to
kill the embryo. Majority of cases will recover and continue to term
pregnancy successfully.
Clinical features:
The features of threatened abortion are,
A period of amenorrhoea followed by slight vaginal bleeding.
Pain is usually absent, but a few painful uterine contractions may be
felt by the patient.
There is no history of passage of products of conception.
On examination, the uterus is correct size for dates and the cervix is
closed.
Differential diagnosis:
The diagnosis is made from missed abortion, when the uterus is
smaller then would be expected, from ectopic pregnancy, where pain
generally precedes bleeding and from dysfunctional uterine bleeding
(DUB) where the signs of pregnancy are absent.
Management:
The mainstay of management is to confirm the diagnosis by identifying
the signs of viable pregnancy (fetal heart movement on ultrasound) as
soon as possible and to exclude other non-pregnancy related cause of
bleeding (e.g polyps).
No treatment has been proven to alter the prognosis in threatened
abortion. The following guide may be useful:

BED REST: In a patient who is bleeding considerably per vaginam,

to rest is, of course, merely common sense, and the patient would
apply this unguided. If there is only slight bleeding the woman
should not confined herself to rest, however they will be more
comfortable with a lot of rest.

REASSURANCE: Women who have threatened abortions often worry

lest the pregnancy should continue and result in delivery of an
abnormal child at term. They should be reassured that if the fetus
is seriously abnormal pregnancy will unlikely to continue.

SEDATIVES: Mild sedatives, usually barbiturates, may be prescribed

for anxious women; they serve to make resting more acceptable.

AVOIDANCE OF INTERCOURSE: Should be insisted upon because

coitus stimulates uterine contractility.
After the bleeding has
ceased, she should avoid exertion and travelling and intercourse, at
least until well after the 12th week.

MONITORING THE PROGRESS: Hormone measurements, usually

human chorionic gonadotrophin (hCG) and ultrasound, may give
guidance as to whether the pregnancy is likely to continue. The
cervix should be inspected when the bleeding persist or worsen.

THE ROLE OF PROGESTERONE: The question of whether to give

progesterone is controversial.
Many feel that if progesterone
deficiency causes abortion, by the time the bleeding has occurred it
is probably too late to stop abortion with hormone treatment.
Progesterone may cause retention of a dead or abnormal fetus and
thus cause a missed abortion; it may also cause masculinization of a
female fetus. If it is to be given the dosage must be adequate.

INEVITABLE ABORTION
Threatened abortion, progress to inevitable abortion when the cervix
dilates. Once this has occurred, abortion is inevitable. Inevitable
abortion is characterized by:1. Period of amenorrhoea followed by heavy vaginal bleeding.
2. Colicky strong uterine pains.
3. On examination, the internal os of the cervix is dilating and
products of conception may be felt in the cervical canal.
Soon after the onset of symptoms of inevitable abortions, the abortion
occurs either completely or incompletely.
Management:
Once the cervix dilated, abortion is inevitable; the products of
conception need to be evacuated as soon as possible because of the
risk of haemorrhage and sepsis.

Before 12 weeks: It is best to take the patient to the operation

theatre for evacuation of the retained products of conception
(ERPC).

After 12 weeks:
It is better to allow abortion to take place
spontaneously or set up syntocinon infusion to cause reduction in
uterine size before undertaking evacuation.

If there is severe bleeding, ergometrine or syntometrine 0.5mg

intramuscularly should be given to control bleeding. Unless the patient
is known to be rhesus-positive she should be given 250 international
units of anti-D gamma-globulin.

INCOMPLETE ABORTION
Incomplete abortion occurs when part of the products of conception
are retained in the uterus. The features of incomplete abortion are:

A period of amenorrhoea following by a prolonged variable amount

of bleeding, but can be severe enough to provoke hypovolumic
shock.
Uterine pain continues.
The uterus is small than expected.
The cervical os is opened.

Management:
A woman who is diagnosed to have incomplete abortion should be
admitted for evacuation of the retained products of conception as soon
as possible. The risks associated with retained products of conception
are haemorrhage and sepsis. The treatment for incomplete abortion is
directed toward:1. Controlling bleeding
2. Obtaining an empty involuting uterus
3. Prevention of infection
Principle of management
The patient should be admitted to the hospital.
Any signs of shock should be treated first.
If there has been severe haemorrhage resulting in anaemia a blood
transfusion should be given.

In septic cases, antibiotic treatment should begun, preferably 24

hours before operation.
If bleeding is heavy oxytocic drugs (e.g: ergometrine 0.5mg or
syntometrine 0.5mg) should be administered intramusculary or
intravenously and arranged for evacuation.
Evacuation is usually carried in the operation theatre under
anaesthesia. The uterus is evacuated using a sponge forceps,
followed by a careful gentle curettage. Oxytocic drugs is injected
intramuscularly as soon as the uterus has been emptied.

COMPLETE ABORTION
Complete abortion occurs when all products of conception are passed
per vaginam. The clinical features are:
1. There is little bleeding which has now stopped.
2. The uterine pains have stopped.
3. The uterus is smaller than expected.
4. The cervix is closed.
Management:
If it is certain that the abortion is complete, no further treatment is
generally needed.
If there is any doubt the uterus should be
evacuated. An ultrasound scan can be requested to confirm that the
uterine cavity is empty and may help to prevent unnecessary surgical
procedures. The patient should be warned to report at once if bleeding
recurs or has fever. Anti-D globulin is usually given to patients who are
rhesus-negative.
MISSED ABORTION
Missed abortion occurs when the embryo dies in the uterus or fails to
develop and products of conception are retained.
The features of missed abortion are:

A period of amenorrhoea during which an episode of slight vaginal

bleeding may or may not have occurred.
Regression of earlier signs and symptoms of pregnancy.
Uterus small-for-dates.
The cervix is closed.
Pregnancy tests are repeatedly negative.

Ultrasonic scan shows collapsed gestation sac or fails to detect a

fetal heart.

Management:
If left alone resorption or spontaneous expulsion will occur. There is a
slight risk of a coagulation defect developing if a dead fetus is retained
for more than a month. To overcome this risk, therefore it is best to
proceed to evacuate the uterus once a firm diagnosis of missed
abortion has been made.
The termination or evacuation procedure depends on the size of the
uterus:

Uterus at or less than 12 weeks size:- proceed to careful

suction aspiration of uterus under general anaesthesia.

Uterus greater than 12 weeks size:- pretreat with vaginal

prostaglandin E then used an oxytocin infusion. Evacuation of the
uterus will be necessary if the abortion is incomplete.

SEPTIC ABORTION
Septic abortion occurs when the uterine cavity becomes infected as a
result of abortion.
It may occur after spontaneous abortion or
therapeutic abortion, but most cases result from criminal interference.
In certain types of abortion the risk of sepsis is very great and
constitutes a major hazard to life. The spontaneous, complete abortion
carries minimal risk of sepsis, while the criminally induced abortion
carries an extremely high risk.
Mortality / Morbidity

Septic abortion used to be the leading cause of maternal death

around the world. It remains a primary cause of maternal mortality
in the Third World, mostly as a result of illegal abortions.
In most of the European countries, mortality from septic abortion
rapidly declined after legalization of abortions. It now occurs in less
than 1/100,000 abortions.
The risk of death from septic abortion rises with the advance of
gestation.

Pathophysiology
Infection usually begins as endometritis, involving the endometrium. In
the majority of cases the infection is usually mild and limited to the
uterine cavity but if not treated, the infection may spread further into
the myometrium and parametrium. Parametritis may progress into
peritonitis. At any stage of septic abortion, the patient may develop
bacteremia and sepsis and is liable to develop the most dreaded
complication of abortion bacteraemic endotoxic shock. Pelvic
inflammatory disease (PID) is a very common complication of septic
abortion.
Pathogenesis
There are two major factors that contribute to the development of
septic abortion:

Retained products of conception, as a result of incomplete

spontaneous or therapeutic abortion, may cause septic abortion.
Introduction of infection into the uterus may be a cause of septic
abortion. Pathogens causing septic abortion are usually mixed and
derived from normal vaginal flora and sexually transmitted bacteria.
The organisms most frequently involved in abortion sepsis are:
1.
2.
3.
4.
5.
6.
7.

Escherichia coli
Streptococci haemolytic and non-haemolytic and anaerobic.
Staphylococcus aureus.
Clostridium welchii.
Tetanus bacillus.
Neisseria gonorrhea
Chlamydia tricchomatis

Clinical Presentation
A) History:
Patients with septic abortion usually present with the following
complaints:
Fever
Abdominal pain
Vaginal discharge
Vaginal bleeding

History of recent pregnancy

B) Physical Examination:
Abdominal examination reveals
Tender abdomen
Guarding and rebound tenderness
Pelvic examination reveals,
Foul smelling vaginal discharge
Vaginal bleeding
Cervical motion tenderness
Uterine and adnexal tenderness
Diagnosis Diagnosis of septic abortion is made on,

A history of abortion, often criminal.

Signs of pelvic infection and septicemia :-

1. Foul smelling discharge from the uterus and bleeding.

2. Lower abdominal tenderness.
3. Pelvic pain.
4. There is fever.
5. The presence of leucocytosis.
Differentials Diagnosis
The following differential diagnosis should be considered,
1.
2.
3.
4.
5.
6.

Acute appendicitis
Pelvic Inflammatory disease
Ectopic pregnancy
Urinary tract infections in pregnancy
Vaginitis
Septic shock

Management - All cases should be admitted to hospital.

1) Laboratory Studies:
Complete blood count
ESR
Serum electrolytes and urea
Take cervical and vaginal swabs for bacteriology in all cases

Blood cultures if the pyrexia is greater than 38C

2) Imaging Studies:
An ultrasound should be performed to look for retained
products of conception in the uterus.
Both supine and upright radiographs of the abdomen will
assist in the detection of free air or foreign bodies.
3. Treatment:

Monitor vital signs

Stabilize with IV fluids in cases of shock. IV fluids (normal
saline, Ringers lactate) through a large-bore canula should be
administered.
For unstable patients, oxygen should be administered as well
as an indwelling Foley catheter.
Early antibiotic treatment may be guided by gram stain but
broad spectrum (ampicillin and metronidazole) coverage is
recommended while awaiting the results of bacteriological
cultures.
Evacuation of retained tissues from the uterine cavity is
probably deferred until reasonable tissues levels of antibiotic
have been achieved (i.e about 12 hours).
In cases of uterine perforation, bowel injury a laparotomy may
be needed.

Types of abortion

Vaginal
Bleeding

Uterine pain

Uterine
size
in
relation
to dates

Cervical
os

Fetal
Heart

Slight

Pain
usually
absent

Correct
size
for
dates

Closed

Present

Heavy

Colicky strong
uterine pains

Correct
size
for
dates

Open

Present or
absent

Threatened
Abortion

Inevitable Abortion
Heavy

Pain continues

Small

Open

Absent

Stop

Absent

Small

Closed

Absent

Slight

Absent

Small

Closed

Absent

Incomplete
Abortion

Complete Abortion

Missed Abortion

Tablel 1. Comparison between various types of spontaneous abortion

RECURRENT ABORTION
Approximately 5 per cent of woman attempting pregnancy have
recurrent pregnancy loss, more commonly referred to as miscarriage
or abortion. Recurrent (habitual) or repeated abortion is defined as
three or more miscarriages (abortions) in a row. Repeated miscarriages
can occur by chance or are the result of underlying pathology.
Potential causes
The causes of recurrent or habitual abortion are much the same as
those for a single miscarriage. Causes of recurrent abortion include,

Chromosomal Abnormalities
Chromosomal abnormalities can be caused by abnormalities that
exist in the genetic structure of one or both parents. These
abnormalities are not life threatening to the parents, but when

passed to the embryo, they can cause miscarriage. They account

for only 5 per cent of recurrent abortions.

Uterine Defects
Abnormalities of the uterus or cervix can also cause recurrent
miscarriage. Defects of the uterus can be caused by several factors.
Some women are born with defects in the structure of the uterus
caused by genetics (congenital abnormalities).
Among the
congenital abnormalities of the uterus that cause recurrent
miscarriage are septate uterus and other forms of uterine
malformations.
Acquired defects or the uterus can be caused by endometrial polyps
or fibroids which can cause problems with implantation of the
embryo, eventually leading to miscarriage.

Cervical anomalies
Cervical incompetence may be congenital or acquired and cause
recurrent mid-trimester abortions. Cervical incompetence occurs in
only 1 to 2 per cent of all pregnancies. It is the cause of 20 to 25
per cent of miscarriages in the second trimester.

Hormone Deficiencies
This is an uncommon deficiency associated with very early abortion.
The cause is an inadequate corpus luteum functioning on the ovary
at the place of ovulation, which is the gland that produces
progesterone during early pregnancy. Progesterone is the hormone
that is necessary to maintain the pregnancy. If this hormon is not
present in sufficient quantities, the pregnancy will abort, sometimes
even before it is detected.
Endocrine dysfunctions, for example, polycystic ovarian disease
are associated with abnormal endometrial thickness. Thin
endometrial linings have been associated with recurrent
miscarriage, and estrogen inadequacy may be the cause.

Immunologic Factors
This is one of the newest and sometimes most controversial
problems associated with recurrent abortion.
Autoimmune
problems where the body produces antibodies against other
proteins has been linked to miscarriage. These problems are
diagnosed by tests such as Anti-Nuclear Antibodies (ANA) and AntiPhospholipid Antibodies (APA) which detect the presence of these
antibodies in the womans blood. These antibodies may cause an

abnormal clotting event to occur during pregnancy, which causes

interruption of the blood flow to the placenta. As this interruption
becomes more and more severe, the fetus begins to starve for
oxygen and nutrients and eventually dies. This eventually leads to
miscarriage.
Excessive homozygosity for HLA between husband and wife has
been postulated for recurrent abortion.
Infections
Occasionally such infections as cytomegalovirus, toxoplasmosis,
listeriosis, brucellosis or syphilis can be implicated as a cause.
They are uncommon.
Investigation of recurrent abortion
The most important part of treating women with recurrent abortion is
determining the cause or diagnosis.
1. History: A careful history must be taken of the time in pregnancy
when the previous abortions occurred and how they commenced.
Did the fetus die in utero before the abortion? Were there any
episodes of illness about the same time? Medical history and
obstetrical history may reveal systemic disease or suggestive
cervical incompetence.
2. Vaginal Examination:
A thorough vaginal examination may
reveal a uterine abnormality, uterine fibroid or cervical
incompetence.
3. Ultrasound: Ultrasound examination will confirm the diagnosis of
uterine fibroids, endometrial polyps and also detect uterine
malformations.
4. Blood tests: Blood tests for syphilis and iso-antibodies should be
done, together with tests for viral infection and toxoplasmosis, a
glucose-tolerance test.
5. Hysterosalpingogram (HSG): Hysterography is needed, at least if
the abortions have been in the middle trimester. Uterine defects
such
as
septate
uterus
can
be
diagnosed
using
a
hysterosalpingography, a procedure in which dye is injected into the
uterus and then photographed using an X-ray. A carefully carried
out HSG should allow the detection of cervical incompetence.

6. Chromosomal Analysis: Chromosomal analysis of both partners

can be done to determine if abnormalities exist by actually looking
at the chromosomes of blood cells from both partners.
7. Endocrine profile: If endocrine disorders are suspected ( such as
thyroid disease, diabetes) , a complete endocrine workup should be
performed.
8. Immunological Investigation:
Immunological causes for
recurrent abortion are diagnosed by tests such as Anti-Nuclear
Antibodies and Anti-Phospholipid Antibodies.
Systemic lupus
erythematosis (SLE) should be excluded.
9. Endometrial tissue cultures: If endometrial infection is
considered a causative factor for recurrent abortion, endometrial
tissue cultures may be made to detect toxoplasmosis (T. gondii).
Treatment of recurrent abortion
Any woman with a history of recurrent abortion will need considerable
support and care. After diagnosis has determined a cause, the correct
treatment plan can be discussed and decided upon. Generally the
treatment involved general measures and specific treatment plan.

General measures
1. Reassurance and counselling
2. Dietary advice.
3. They should be advised to stop smoking, to avoid sexual
intercourse and not to travel when they becomes pregnant.
4. Careful antenatal supervision should be advised

Specific treatment
1. Counseling: Genetic counseling can offer guidance to couples
on chances of passing abnormalities to their children.
2. Surgical: In cases where recurrent abortions are due to uterine
defects, uterine polyps or fibroids therefore treatment may
include surgery to go in and reshape the uterus or remove
polyps or fibroids.
3. Cervical
cerclage
incompetence.

is

discussed

under

cervical

4. Antibiotics therapy: If endometrial infection is confirmed a

causative factor, treatment is to prescribe appropriate
antibiotics.
5. Immunotherapy: Immunological treatment for recurrent
abortions with leucocytes infusion is contraversial. Various study
has been carried out to immunize woman between pregnancies
with paternal leucocytes, pool donor cells or trophoblast
membrane preparations to enhance her immune system.
Unfortunately this approach have failed to show any statistical
benefit.
6. Hormonal treatment: There have been a lot of argument
regarding the usage of progesterone in the treatment of
recurrent abortion when an inadequate corpus luteum is
suspected. Treatment with progestogens is no more effective
than a placebo.
Systemic progestogens, e.g. 17hydroxyprogesterone caproate, are still used predominantly
because the women are desperate for something positive to be
done.

CERVICAL INCOMPETENCE
Description of Cervical Incompetence
Cervical incompetence is a condition in which the cervix gradually
begins to dilate and efface before the pregnancy has reached term.
Occurring in the second or third trimester, cervical incompetence is a
cause of late miscarriage and premature birth. When a cervix is
incompetence, the muscle of the cervix is weak and the pressure of the
growing fetus causes the weak cervix to open.
There are no
contractions. If a woman is known to have a weak cervix, measures
can be taken to reduce the risk of miscarriage or premature birth in
subsequent pregnancies.
Incidence of cervical incompetence
Cervical incompetence occurs in only 1 per cent to 2 per cent of all
pregnancies. It is the cause of 20 25 per cent of miscarriages in the
second trimeste.
What causes cervical incompetence?

It is thought to be either congenital weakness of the cervix tissues or a

result of forced dilatation or trauma. The risk factors for cervical
incompetence are:
Previous surgical procedure involving the cervix, e.g.
a) Cone biopsy
b) Manchester repair
c) Excessive dilatation of cervix at D & C

Malformation of the cervix

Maternal exposure to DES (diethylstillboestrol) while in utero
Damage to the cervix during a prior difficult delivery
Damage to the cervix during a prior difficult delivery

Studies have found that if surgical dilatation of the cervix is performed,

the risk of cervical incompetence depends upon the number and
degree of dilatation used. It is unlikely to occur because of a diagnostic
D&C (e.g. for irregular periods) or after a miscarriage, when the cervix
is already starting to open.
Diagnosis of cervical incompetence
A diagnosis of cervical incompetence is usually made on the basis of a
womans past pregnancy history. Classically this is following one or
more late second trimester or early third trimester losses.
The diagnosis is based on:
A history of repeated mid trimester miscarriages.
The easy acceptance of a 9 mm Hegar dilator by the cervix when
the woman is not pregnant.
A gradual painless dilatation of the cervix, with membranes bulging
into the vagina during pregnancy as detected by repeated vaginal
examinations.
Treatment of cervical incompetence
If a woman is known to have a cervical incompetence, measures can
be taken to reduce the risk of miscarriage or premature birth in
subsequent pregnancies.
Cervical cerclage is the treatment that is offered once cervical
incompetence is diagnosed. This involves placing a stitch high up
around the cervix to try and keep it closed. The stitches are usually
placed vaginally. These stitches are called McDonald or Shirodkar
stitches.

Shirodkar or McDonald stitches are best performed at about the 14 th

week of pregnancy (after abnormal pregnancy) are excluded. The
cervix is sutured by encircling stitches of non-absorbable suture
material under general anaesthesia (Fig 1.6). The sutures may stay in
placed until the 37th-38th week of pregnancy, unless the woman aborts
or goes into premature labour, and then they are removed.
Complications of the cervical cerclage include:
Some risks associated with general anaesthesia.
Rupture of the membranes at the time of placement of cervical
sutures.
Increased risk of infection.

31
ECTOPIC PREGNANCY
By definition, an ectopic pregnancy
occurs when a fertilized ovum

implants at a site other than the endometrial lining of the uterus. Such
pregnancies are generally not viable and can in fact be life threatening
to the mother. Most ectopic pregnancies occur in females aged 25 to
34. The risk increased higher for women aged above 40 years.
Fig. 1.1 Tubal pregnancy (arrow) - unruptured

INCIDENCE
The incidence of ectopic pregnancy is rising in the developed countries
and is said to be proportional to that of pelvic inflammatory disease.
Currently the incidence of ectopic pregnancy is running at a rate of 1 in
80 150 pregnancies but can be higher as 1 in 25 30 pregnancies in
some areas (e.g. West Indies).
SITES OF ECTOPIC PREGNANCIES
A variety of abnormal implantation sites include the fallopian tube,
interstitial, ovary, cervix and peritoneal (Fig 1.2).
The commonest site of ectopic pregnancy is the fallopian tube which
account for about 99 per cent of cases.
The ampulla portion of the fallopian tube (in 55 per cent of cases) is
the most frequent site of implantation and the isthmus ( in 25 per cent
of cases ) the next most common. Implantation may occur in the
fimbriated end of the fallopian tube (in 17.4 per cent of cases) and only
about 2 per cent of ectopic pregnancy occurs in the interstitial portion
of the tube.
Ectopic pregnancy may also occur, though rarely in the ovary (0.5 per
cent), in the cervix or, secondary in the abdominal cavity.
.
In ampullary
(55%)

In isthmus (25%)

In interstitial ( 2%)

In fimbriated end
(17.4%)
In ovary
(0.5%)
In abdominal cavity (0.1%)

Fig. 1.2 () Sites of ectopic pregnacy

In cervix

AETIOLOGY OF TUBAL PREGNANCY

The aetiology of tubal pregnancy is not known. Tubal pregnancy could
occur if the passage of the fertilized ovum along the fallopian tube is
delayed because of tubal damage. Ectopic pregnancies are primarily
due to prior tubal infection, fallopian anatomic abnormalities or an
abnormal endometrium.
Predisposing factors:
Risk factors include,
Salpingitis is the commonest predisposing cause. In some
population gonococcal salpingitis is the commonest background
factor, while in others tuberculous salpingitis plays a major role.
Salpingitis cause destruction of the tubal cilia or kinking or stricture
of the tube. Salpingitis impedes the progress of the zygote due to
adhesions, fimbrial agglutination, tubal narrowing or destruction of
the cilia of the endosalpinx.

Congenital malformation of the tube such as diverticula or

abnormal length may be a contributing factor.

Tubal surgery whether in attempt to repair damage inflicted by

inflammation or to reanastomoses tubes after female sterilization
carries a higher risk of tubal pregnacy.
Modes of contraception also affect the incidence of tubal
pregnancy. It has been reported that there is a higher incidence of

tubal pregnancy in woman using an intrauterine contraceptive

devices (IUCD) and progestogen-only contraceptive pills. In both
cases, they reduces tubal motility and, if contraception occurs, it is
more likely to lodge in the tube.

Contralateral implantation The ovum that is fertilized may

come from one ovary but may be carried into the opposite tube. Its
passage to the uterus thus takes longer than usual and trophoblast
may develop so that implantation takes place in the tube.

Infertility There is a close correlation between factors leading to

infertility and those leading ectopic pregnancy.

PATHOGENESIS OF TUBAL PREGNANCY

1. The passage of fertilized ovum is delayed along the tube by
contributing factors as stated in the aetiology.
2. The trophoblast shell develops and the zygote implants on the
endosalpinx.
3. HCG (human chorionic gonadotrophin) from the trophoblast
maintains the corpus luteum which produces oestrogen and
progesterone.
4. The endometrium undergoes a decidual reaction.
5. The fallopian tube cannot physically sustain or contain the
pregnancy and the trophoblast invades deep into the muscular layer
of the tube.
6. The pregnancy begins to fail, hCG and therefore oestrogen and
progesterone fall. The decidual begins to shed causing slight
vaginal bleeding.
7. In most cases the tubal pregnancy terminates between the 6 th and
10th weeks. The tubal pregnancy may terminate in one of the
following ways :

Tubal absorption The conception dies and gradually

reabsorbed. This usually occurs in a very early tubal pregnancy.

Tubal mole The embryo dies in the tube, with a certain

amount of bleeding, and surroundrd by blood clot and is retained

in the tube. A firm swelling is formed within the tube and such a
condition is called a tubal mole.
Tubal abortion The conceptus is aborted from the tube (the
usual termination in fimbrial and ampullary implantation) into the
peritoneal cavity. This is the most common outcome. Rarely the
conceptus may still be viable and a secondary abdominal
pregnancy ensues.
Tubal abortion may be completely or
incompletely.

Tubal rupture This is the most dramatic and familiar

termination of a tubal pregnancy.
The tube ruptures and
bleeding occurs requiring emergency treatment. The pregnancy
is often implanted in the isthmus of the tube.

Secondary abdominal pregnancy This is the rarest

termination of all. The embryo is expelled complete from the
tube and acquires a secondary attachment in the peritoneal
cavity. The fetus may develop fully and survive. When a fetus
dies in the abdominal cavity a lithopaedion is formed.

CLINICAL PRESENTATION
The presentation of ectopic pregnancy may be sub-acute or acute.
Sub-acute presentation
Symptoms: The classic clinical presentation for an ectopic pregnancy
is of the following triad of symptoms:
1. Amenorrhoea - as in early pregnancy. Usually a short amenorrhoea
about 6 weeks to 8 weeks duration.
2. Abdominal pain After a short period of amenorrhoea, the patient
complaints of lower abdominal pain perhaps more to one side than
the other. This pain is typically cramp-like and colicky at first and
often unilateral. It is due to spasm of the tube muscle. Abdominal
pain may be minimal or severe.
3. Vaginal bleeding Slight vaginal bleeding arising after the onset
of the abdominal pain. The bleeding is decidual bleeding due to the
falling level of hCG, oestrogen and progesterone. The bleeding is
usually scanty, less than a normal period, and dark brown in colour.

Beside this triad of symptoms, the patient may also present with:
Feeling of faintness, which may due to an episode of intraperitoneal
bleeding.
Shoulder tip pain, which is due to irritation of the diaphragm by
blood leaking from the tubal pregnancy.
Signs:
The physical signs of an undisturbed ectopic pregnancy
(unrupture tubal pregnancy) are as follows:
1. There may be slight activity of the breasts.
2. On abdominal examination there may be slight tenderness over the
tubal point.
3. On bimanual examination ; There may be dark blood oozing from the external os.
The cervix is soft and the uterus slightly enlarged.
There is marked cervical excitation (tenderness on movement of the
cervix from side to side).
A small tender mass may be palpable to one side of the uterus.
(N.B. If the history is strongly suggestive of an ectopic pregnancy DO
NOT carry out a vaginal examination unless rapid access can be
gained to an operating theater. Vaginal examination may cause the
tube to rupture and the patient may be put at severe risk by it)
Acute presentation
Sudden collapse with little or no warning is more common when the
tubal pregnancy occurs in the isthmus portion of the fallopian tube.
As the tube ruptures, there is intraperitoneal haemorrhage and the
usual presentations are:
Symptoms:
1. Acute lower abdominal pain
2. Fainting episodes
3. Shoulder tip pain
Signs: on examination
A) The patient is pale.
B) The patient is in a state of shocked :-

The patient is often restless and may show air hunger.

The skin may be clammy and cold.
Blood pressure will be low (hypotension).
Pulse is weak and rapid.

C) Abdomen:
The whole abdomen is usually distended to some degree.
There may be no localized area of tenderness.
There may dullness on percussion in the flanks.
D) Vaginal examination:
Little dark blood may be seen oozing from the external os.
Marked cervical excitation.
Fullness in the rectovaginal pouch.
Tenderness in the fornices.

DIFFERENTIAL DIAGNOSIS
Differential diagnosis is from a haemorrhagic corpus luteum, a
haemorrhage into a small ovarian cyst, a pelvic inflammatory disease,
pelvic appendix and spontaneous abortion.

Threatened or incomplete abortion: In the former there is no

pain and in the later pain follows vaginal bleeding.

Bleeding in corpus luteum: Laparoscopy is required to make this

differentiation.

Accident to an ovarian cyst: There is usually no menstrual delay.

Laparoscopy is indicated.

Pelvic inflammatory disease: The systemic reaction is more

profound and the signs are usually bilateral and usually there is no
menstrual delay.

MAKING A DIAGNOSIS
The diagnosis may be difficult; however every attempt should be make
to exclude an ectopic pregnancy once suspected. The diagnosis can
be made from the followings:

 History and clinical examination :

A careful history and clinical examination will usually made the
diagnosis clear, or at least establish the need for further investigation.
The most significant points are:1.
2.
3.
4.
5.
6.

Amenorrhoea
Unilateral pain
Vaginal bleeding
Lower abdominal tenderness
Extreme tenderness in the lateral fornix on one side
Marked cervical excitation

When the diagnosis of tubal pregnancy is in doubt the following

investigations may be performed:

Pregnancy test:
A positive pregnancy test associated with pain and bleeding are
highly suspicious of an ectopic pregnancy. The quantitative level of
-hCG found in ectopic pregnancy is variable. Serum -hCG levels
correlate with the size and gestational age in normal embryonic
growth. The discriminatory zone of -hCG is the level above which a
normal intrauterine pregnancy is reliablly visualized. The lack of an
intrauterine pregnancy when the hCG is above the discriminatory
zone represents either an ectopic pregnancy or a recent abortion. A
radio-immuno-assay for levels of -hCG in the serum is of greater
value, especially when used in conjunction with ultrasound
scanning. A negative result indicates that the woman is not
pregnant, and ectopic pregnancy can be excluded.
-hCG level :
Absence
: eliminates pregnancy
Above 6000 mIU/L intrauterine
Below 6000 mlIU/L- extrauterine , or missed abortion

ULTRASOUND SCANNING
Pelvic ultrasound examination, preferably using a transvaginal
probe, should be made to establish if the pregnancy is intra- or
extrauterine.

The most definitive sonographic sign of ectopic pregnancy is an

extrauterine gestational sac containing a live embryo. However,
this sign is present in less than 5 per cent of cases.
On the other hand, a normal-appearing intrauterine gestation can
almost exclude an ectopic pregnancy.
If ultrasound is doubtful or not available, the presumptive diagnosis
should be confirmed by laparoscopy.

LAPAROSCOPY
A certain diagnosis of tubal pregnancy can be made by examining,
the
peritoneal
cavity,
the
uterus
and
fallopian
tubes
laparoscopically. Laparoscopy is the method of choice if it is
available.

TREATMENT
Once the ectopic gestation has been diagnosed, immediate operative
treatment is essential.
In a case of severe haemorrhage the patient must be taken
immediately to the operating theatre. Little time should be wasted in
attempting resuscitation; this may prove useless and will only increase
bleeding. An intravenous drip should be set up and a blood transfusion
given as soon as possible.
Type of operative procedure:
Several approaches are possible. The gynaecologist may:

Perform a laparotomy In most cases the affected tube should

be removed (salpingectomy); an exception (to preserve the tube)
may be made if the woman desires children and the other tube is
missing or seriously diseased. The disadvantage is that there is a
distinct risk of recurrence of ectopic pregnancy. At operation every
effort should be made to salvage parts of the damage tube, as
reconstructive surgery may be possible at a later date.

Insert a laparoscope to inspect the fallopian tube and if

possible, under laparoscopic vision, the affected tube can be
removed or suck the ectopic gestation out of the tube without

resorting to laparotomy.
This laparoscopic procedures can be
performed as day cases and allowing the patient to return to normal
activities much more rapidly than following a laparotomy.

RARER ECTOPIC PREGNANCIES

Cornual (interstitial) pregnancy

Fig. 1.3 Laparosacopic view Cornual pregnancy

An interstitial ectopic pregnancy is

one that implants at the highly
vascular region of the uterus near
the insertion of the fallopian tube.
These types can grow grow larger
UTERUS
than those within the fallopian tube
Cornual
because the endometrial tissue is
Pregnancy
more expandable. Due to the
increased
size
and
partial
endometrial
implantation,
these
advanced
ectopics
can
be
misdiagnosed as an intrauterine
pregnancy. This uncommon form of ectopic pregnancy can have
serious consequences because it is difficult to diagnose early and when
it ruptures it is associated with profuse intraperitoneal bleeding.
Rupture usually takes place later than in cases of ampullary pregnancy.
The treatment is to excise the cornu by a wedge-shaped incision. If the
uterus is extensively damaged a hysterectomy is perform.

Ovarian pregnancy
This is very rare form of an ectopic pregnancy. Ovarian pregnancy
occurs when the spermatozoon enters the cavity of a ruptured
Graffian follicle and fertilized the ovum before it could be expelled out.
The symptoms and signs are those of tubal pregnancy, and diagnosis is
only made at operation.
To make a diagnosis of primary ovarian pregnancy the following three
features must be present:

1. The fallopian tube must be intact.

2. The gestation sac must occupy the anatomical site of the ovary.
3. Ovarian tissue must be demonstrable histologically in the
specimen.

Cervical pregnancy
This is also rare but may cause
Hysterectomy may be necessary.

profuse

vaginal

bleeding.

Abdominal pregnancy
Both primary and secondary abdominal pregnancies are rare events.
The fetus may develop fully and survive. The usual presentation is as
an acute abdomen in the mid-trimester.
When laparotomy (for delivery) is carried out it may not be possible or
advisable to remove the placenta because it is likely to be fixed to the
abdominal viscera. It may be best to leave the placenta in situ.
Usually the placenta becomes organized slowly into fibrous tissue if
infection does not occur.

32
HYDATIDIFORM MOLE

Fig. 1.1 Gross specimens from a patient with Hydatidiform mole.

The characteristic hydropic villi appearance.

Note

This is a term that includes several conditions that are associated with
the results of a pregnancy. Trophoblastic disease is characterized by
hydropic villi and abnormal proliferation of trophoblastic tissue. This
condition is divided into three categories:

Hydatidiform mole(Molar pregnancy)

Invasive mole (chorioadenoma destruens or malignant non-mestatic
trophoblastic disease)
Choriocarcinoma

HYDATIDIFORM MOLE
Hydatidiform
uncommon
Hydatidiform
trophoblastic

mole or also known as Molar pregnancies are an

and very frightening complication of pregnancy.
mole is the most frequent benign type of gestational
disease. A hydatidiform mole is an abnormality of the

placenta, caused by a problem when the ovum and sperm join together
at fertilization. It is a benign tumour of the chorion. A molar pregnancy
or hydatidiform mole occurs when the cells that normally make up the
chorionic villi do not develop properly. Instead, they undergo cystic or
hydropic degeneration.
TYPES OF HYDATIDIFORM MOLE
There are two types of hydatidiform mole, namely:
1. Complete (classical) mole Complete molar pregnancies have
only placental parts, and form when the sperm fertilizes an empty
egg. Because the egg is empty, no fetus is formed. The placenta
grows and produces the pregnancy hormone, called hCG, so the
patient thinks she is pregnant. The conceptus consists solely of
hyperplastic, hydropic chorionic villi; no fetus is present.
2. Partial mole A partial mole occurs when two sperm fertilize an
ovum. Instead of forming twins, something goes wrong, leading to a
pregnancy with an abnormal fetus and abnormal placenta. The
fetus has to many chromosomes and almost always dies in the
uterus.
Hydatidiform moles vary greatly in their rate of growth, in the amount
of chorionic gonadotrophin produced and in the amount of invasion of
the uterine wall.
In most cases a fetus cannot be found, but
hydatidiform degeneration may occur in the placenta in cases of
abortion.
INCIDENCE
The incidence of hyadatidiform mole varies depending on where ones
live. Hydatidiform mole appears to be commoner in women of Far
Eastern than elsewhere in the world. It is said to be low, about 1 in
2000 to 2500 pregnancies, in Western countries. In some Asian
countries, the incidence is 8 times higher, occurs with a frequency of 1
in 200 to 300 pregnancies. Age over 40 is a risk factor for molar
pregnancy, as is having a prior molar pregnancy. In fact, of having
another molar pregnancy is about a 1 out of 100. The reasons for the
geographic and age differences are currently unknown.

PATHOGENESIS
The exact pathogenesis is uncertain. Gestational trophoblastic disease
is caused by genetic disorder in which a spermatozoon enters an ovum
which has lost its nucleus. In most complete moles the chromosome
complement is 46 XX but surprisingly consists of two set of paternally
derived chromosomes with no maternal contribution whatsoever. In
addition they express only one pair of paternal HLA-A and-B antigens.
These findings suggest that complete moles usually result from
fertilisation of the ovum by a haploid sperm which subsequently
duplicate it own chromosomes by meiosis.
Women who have molar pregnancies have an increased incidence of
balanced translocations and this could explain the loss of the ovum
nucleus.
Chromosomal abnormalities (particulary triploidy-69, XXX or XXY) are
often found in partial moles.
PATHOLOGY
1. If a patient has a hydatidiform mole the chorionic villi (the tiny,
finger-like projections that attach the placenta to the uterine lining)
do not develop properly. Instead, there is cystic degeneration of
the chorionic villi which resembles grape-like vesicles appearance
(Fig. 1.1). Hydatidiform mole does not spread outside of the uterus
to other parts of the body.
2. There is excessive production of hCG and this often causes
moderate enlargement of the ovaries by formation of theca-lutein
cysts.

Fig 1.2 Hydatidiform mole (molar pregnancy) microscopic appearance, showing the
distended villi and irregular trophoblastic appearance.

CLINICAL FEATURES
Patients with hydatidiform mole (molar pregnancy) most often present
;Symptoms:

Amenorrhoea - Women with molar pregnancy usually feel

pregnant and develop exaggerated pregnancy symptoms
(nausea and vomiting).
Vaginal spotting or bleeding - Molar pregnancy or hydatidiform
mole is nearly always signaled by bleeding by the 12 th weeks of
pregnancy. There may be irregular vaginal bleeding and the loss
may contain classical vesicles.
Pregnancy-induced hypertension (previously called preeclampsia) may develop unusually early.
Some women may develop rare complications like thyroid
disease.

Signs:

The uterus may be large for dates.

The uterus is doughy to the touch.
No fetal heart can be heard.
Ovaries may be palpablly enlarged (theca lutein cysts- due to high
hCG level).

DIAGNOSIS
Most cases of molar pregnancy are diagnosed in the first trimester.
Bleeding and an hCG levels that is much higher than in a normal
pregnancy are possible warning signs. The diagnosis of a molar
pregnancy are made on the followings:

Pregnancy Test: Urine pregnancy tests are positive in high dilution

and serum -hCG levels grossly elevated.

Ultrasound: The ultrasound will

often shows a cluster of grapes
appearance or a typical snow
storm appearance inside the

uterus, signifying an abnormal placenta. If a fetus is present its a

possible partial mole, while if the fetus is absent its probably a
complete mole.
Fig. 1.3 Hydatidiform mole.
ultrasound scan.

Snowstorm

appearance (arrow head)

on

Making the diagnosis of a molar

pregnancy

Amenorrhoea
Vaginal bleeding (with or without vesicles)
Uterus large for dates
The uterus feels doughy , not cystic
Early pregnancy-induced hypertension
High hCG level
Snowstorm appearance on scan
Table 1 The features of a molar pregnancy

COMPLICATIONS OF HYDATIDIFORM MOLE

Hydatidiform moles are an uncommon and very frigthening
complication of pregnancy. The risks of hydatidiform mole are in three
categories:
1.
2.
3.

Haemorrhage and toxaemia.

Molar mestatases.
Choriocarcinoma.

TREATMENT
Once a firm diagnosis is made the mole tissues need to be removed
completely from the uterus. The aim of treatment is to ensure
complete elimination of all the abnormal trophoblastic tissue from the
maternal system. Treatment of gestational trophoblastic disease
depends on the stage of the disease, and the patients age and overall
condition.

An intact mole should be dealt with any one of the following

procedures:
1.

Suction curettage An intact mole may be evacuated by

dilating the cervix and perform a suction evacuation and
curettage. This must be done very carefully or excessive bleeding
can occur. An oxytocin drip may be set up hours before the
curettage and left running until evacuation is completed.
Intravenous ergometrine may be given to control bleeding. The
use of suction to evacuate the uterus is safest and carries the
least risk of perforation of the uterine wall.

For the above procedures a gentle curettage is performed about 7

days later to remove any residual trophoblast.
This curettage may need to be repeated if
(i)
(ii)
2.

irregular bleeding persists

hCG levels are still elevated 6 weeks after initial evacuation
Hysterectomy In older women who do not desire further
children, a hysterectomy with the mole in situ may be preferable.

FOLLOW-UP OF HYDATIDIFORM MOLE

After the molar pregnancy is evacuated there must be rigorous
surveillance for any sequelae. Follow-up is important as the
consequences of a mole can be persistent mole (between 5 and 10
percent
of
cases),
invasive
mole,
mestastatic
mole
or
choriocarcinoma.
Follow-up usually consists of:
(i)
Baseline chest x-ray
(ii) Review of the pathology specimen
(iii) Physical examination of the vagina and uterus
(iv) Monitoring of -hCG blood level
(v) To provide contraception
During the follow-up period pregnancy should be avoided for at least
one year period. Many women are frustrated when their doctor
recommends waiting one year to be become pregnant. This is actually
important, because a rise in -hCG levels may indicate a normal
pregnancy when the patient is trying to get pregnant, or a recurrent

molar pregnancy, which requires chemotherapy.

To avoid this
confusion the women are advised not to become pregnancy within one
year of follow-up period.

The Follow-up of Hydatidiform Mole

CLINICAL ASSESSMENTS

A careful history particulary with regard to vaginal bleedingmust be

taken at each visit.
Vaginal examinations at 2-weekly to evaluate uterine involution and
the presence of theca lutein cysts.
Alternatively ultrasound examinations may be at 2-weekly intervals if
available.
Chest X-ray to exclude any pulmonary mestatases

PREGNANCY TESTS

Radio-immuno-assay of serum -hCG at 7-10-day intervals.

When -hCG level has been normal for 3 consecutive weeks, test
monthly for 6 months.
If assay show normal -hCG levels for 6 consecutive months, follow-up
can be discontinued.

CONTRACEPTION

During the follow-up period pregnancy should be avoided. A barrier

method of contraception should be used until the hCG levels are
normal: then oral contraception can be used.

Indications for chemotherapy after hydatidiform mole

If the level of serum -hCG falls serially no drug treatment is needed.

The indications for chemotherapy following hydatidiform mole or molar
pregnancy are
(i)
Rapidly rising serum -hCG levels
(ii)
If serum -hCG level plateaus for more than 3 consecutive weeks
(iii) Obvious mestatases are detected
(iv) Histological evidence of choriocinoma at curettage or
hysterectomy
(v)
Persistent or recurrent uterine bleeding with raised -hCG levels
The commonly used chemotherapy is methotrexate or actinomycin-D.
There is usually a good response to chemotherapy.

Future Pregnancy
Treatment of hydatidiform mole or molar pregnancy is successful in
most cases. Fortunately, the risk of having another molar pregnancy is
about 1 % (1 in 100). Most doctors will perform an ultrasound to make
sure the pregnancy is normal when a patient has had a prior molar
pregnancy.
It is also a good idea to send the placenta to the
pathologist after the delivery just to make sure there are no abnormal
areas.

33
THE INFERTILE COUPLE
Infertility is strictly defines as the inability to conceive after 1 year of
unprotected intercourse. About 10 to 15 % of couples are involuntarily
infertile. Most causes of infertility are identifiable and treatable.
Diagnosis and treatment require a thorough assessment of both
partners, the extent and time course of which should be individualized
(e.g. more rapid if the woman is > 35 yr.).
Infertility is primary if the woman has never been pregnant (or the
man has never impregnated a woman). Infertility is secondary if the
woman has been pregnant at least once but has not been able to
conceive again or sustain a pregnancy.
Infertility, whether primary or secondary, occurs in one couple in
five. For 85% of these couple, the underlying cause can be diagnosed;
50% to 70% can be treated successfully.
The incidence of infertility seems to be increasing, probably because of
(1) the trend to delay pregnancy until later in life when fertility
decreases naturally, and
(2) the increase in pelvic inflammatory disease.

Causes of Infertility
Major etiologic factors include male sperm factors (40%), ovulatory
dysfunction (20%), abnormal tubal function (30%), and cervical factors
(5%) and are unidentified in 10%.
Male causes

Female causes

Impotence
Premature ejaculation
Hypospadias
Deficiency in spern count and
motility
Azoospermia

Congenital malformation of
genital tract
Anovulatory cycle (e.g. PCOS)
Tubal
pathology
(e.g.
blockage)
Cervical factor (poor mucus)
Endometriosis

Factors associated with fertility and infertility

Factor required for fertility

Development
reproductive
normal.

tract

Conditions associated with

infertility

of Congenital
or
developmental
is factors

Gynetresia (e.g., absence of

vagina)

Vaginal anomalies (e.g., double

vagina with single or double cervix and
single or double uterus)

Unusual
uterus
(e.g.,
congenitally small, or infantile, uterus)

Uterine and tubal defects from

exposure to DES as embryo/fetus

Abnormalities of ovary

Ovulation:
Absence of ovulation
Hypothalamus-pituitary
Malfunctioning of axis with
gonadal axis is normal. An menstrual irregularities
ovum is released from a
Abnormal ovaries as seen in
mature ovarian follicle.
Turners syndrome

Hormonal
suppression
of
hypothalamus- pituitary-gonadal axis
with birth control medication

Emotional
problems
(e.g.,
severe psychoneurosis or psychosis or
anorexia nervosa, which may be
responsible
anovulatory
cycles,
frequently associated with amenorrhea
or oligomenorrhea)

Menstrual irregularities from

vigorous exercise (sports), especially in
thin women
Tubal: ovum enters fallopian Fallopian tube is blocked or its
tube promptly after ovulation. function is altered.

Spermatozoa
migrate
into
fallopian tube where fertilization
takes place. Fertilized ovum
finds its way down tube into
endometrial cavity to implant
into
hormone-prepared
endometrium 7 to 10 days after
ovulation.

Factor required for fertility

Blockage of tube by scar tissue

formation following infection (pelvic
inflammatory
disease,
ruptured
appendix followed by peritonitis), or
pelvic surgery

Blockage
of
tube
by
compression or Kinking by abnormal
growth such as endometriosis and
neoplasm

Alteration in tubal motility by

birth control medication or from
emotional stress
Conditions associated with infertility

Uterine: uterine endometrium Uterus is malformed or endometrium is

is adequately prepared to unreceptive
to
fertilized
ovum
receive fertilized ovum.
(malfunction of hypothalamus -pituitarygonadal axis; presence of endometrial
infection; presence of intrauterine
device (IUD)
Vaginal-Cervical:
cervical Absence of mucous characteristics
mucus
is
receptive
and
receptive
and
supportive
to
supportive
to
spermatozoa.
spermatozoa
Cervix is competent.
Altered vaginal pH from feminine
hygiene preparations or douches,
infections, antibiotic chemotherapy,
disease
states
(e.g.,
diabetes
mellitus), poor hygiene, or emotional
stress
Presence of spermicidal foams or
other
preparations
used
for
contraception
Development of antibodies (an
immunologic response) against a
specific males spermatozoa
Spermatozoa
are
normal, Poor quality of spermatozoa:
adequate
in
number, and
- Low count (oligospermia)
ejaculated
into
female
- Poor motility
reproductive tract.
- Absent of spermatozoa
(azospermia)

Study Of The Man

The male factors are responsible in about 40 percent of cases. Thus
evaluation of the male forms an important aspect of investigation of an
infertile couple.
History

A detailed history should be obtained. The main points include:

Fertility in pervious marriages A detailed history of previous

marriage, if any, and the number of pregnancies should be noted.
Medical history: A pass history of mumps or exposure to venereal
disease may be a causative factor.
Surgical history: Detailed history of heniorraphy, injuries to genitals,
or other surgery in genital area should be noted.
Environmental factors to consider include exposure to chemicals, xrays equipment, or extreme thermal changes; physical nature of
occupation

Previous tests and therapy done for study of fertility

Duration of infertility

Sex history in detail, with discussion

frequency, ability to ejaculate, etc.

of

actual

techniques,

Adequacy of erection

Physical Examination should be carried out separately. The

examination should include:

General examination: A careful general examination should be

done to look for possible endocrine stigmata. Any operative scar in
the inguino-scrotal area should be noted.
Genital tract examination: A detail examination of the genitals
will reveal the presence or absence of hypospadias or phimosis.
The size, consistency and position of the testis (whether
undescended) should be examined. The epididymis and vas
deferens should be palpated carefully on each side, to note any
abnormality in size and consistency. A rectal examination will reveal
any abnormalities in the prostate and seminal vesicles.

Careful search for varicoceles: The patient must always be

examined in erect position for varicoele. Irrespective of size all
varicoleces are significant.

Laboratory Data
1) Routine urine, complete blood count, and serologic test for syphilis
2) Complete semen analysis is essential. An ideal specimen is that
obtained by masturbation after 2 to 3 days abstinence.
Examination should be carried out within 1 to 2 hours after
ejaculation. The characteristic of a normal semen are as below:
Liquefaction: usually complete within 10 to 30 minutes
Volume: usually 2.5 to 5 mL
Sperm motility: is an important consideration in sperm
evaluation; percentage of forward-moving sperm estimated in
relationship to abnormally motile and non-motile sperm.
(Normal more than 60%).
Cell count: average normal 40 million or more per mL, or total
of 150 to 200 or more million per ejaculate (average of counts
on two or preferably three separate specimens)
3) Additional laboratory studies as indicated
Basic endocrine studies as indicated
1. T4 or other thyroid tests
2. Gonadotropin determination in patient presenting with
severe oligospermia or azoospermia, FSH estimations
are necessary. These are elevated markedly in patients
with semineferous tubular hyalinization and germ cell
aplasia, which are not treatable, thus obviating the
necessity for testicular biopsy.

Testicular biopsy, where correct interpretation is available

(may give a more accurate diagnosis and prognosis in cases
of azospermia and severe oligospermia), vasography if
indicated and available.

Study Of The Woman

History

A detailed history should be obtained. The main points include:

Duration of infertility: length of contraceptive and non contraceptive

exposure
Fertility in other marriages: A detailed history of previous marrages,
if any, and the number of pregnancies should be noted.
Obstetric history should include,
a. Number of pregnancies and abortions.
b. Length of time required to initiate each pregnancy
c. Complications of any pregnancy
d. Duration of lactation
Gynaecologic history: detailed menstrual history and significant
vaginal discharge
Previous tests and therapy done for fertility
Medical history: general medical history including chronic and
hereditary diseases
Surgical history: especially abdominal or pelvic surgery
Sexual history in detail: libido, orgasm capacity, techniques, and
frequency of intercourse.
Psychosomatic evaluation
a. General
b. As regards infertility problem, particularly her reason for
seeking advice at this time

Physical Examination - should be carried out separately. The

examination should include:

General: careful examination of other organs and parts of body;

special attention given to habits, fat and hair distribution, acne.
Genital tract: state of hymen (full penetration); clitoris; vaginal
infection, including trichomoniasis and candidiasis; cervical tears,
polyps, infection, patency of os, accessibility to insemination;
uterus, including size and position, mobility; adnexa, tumors,
evidence of endometriosis.

Laboratory Data

Routine urine, complete blood count, and serologic test for syphilis;
additional laboratory studies as indicated
Basic endocrine studies in women with irregular menstrual cycles or
in amenorrhea, hirsutism, acne, or excessive weight gain.
Other laboratory tests added as desired for more complete
diagnosis of endocrine problems
Rh factor and antibody titer tests - important in abortion and
premature delivery problems
Sperm antibody agglutination studies (special laboratory procedure
involves obtaining a fresh semen specimen from man and a blood
sample from the woman. Sperm are incubated in the blood serum of
the woman and checked at intervals for agglutination. The test is
negative if no agglutinated sperm are found.)

Specific tests and examinations:

There are several examinations and tests for female infertility. Each
method of assessment is discussed under the following headings:
Table 1. Special investigation for the female

Fertility Factor Test or examination

Ovulation

Tubal

Hystrosalpingography or hysterography
Laparoscopic examination

Cervical

Physical examination

Basal body temperature (BBT)

Cervical mucus changes
Timed endometrial biopsy
Plasma progesterone level

 Assessment of cervical mucus changes

Postcoital test
Sperm
immobilization
antigen-antibody

reaction

Basal Body Temperature

Who

Woman

Why

To obtain presumptive evidence of ovulation and an

adequate luteal (progesterone) phase

How

Obtain and maintain a record of daily rectal temperatures

taken each morning after awakening and before any
physical activity; any physical activity increases the
bodys metabolic rate; the increased metabolic rate is
reflected in a thermal increases, which then may be
mistaken for the thermal rise that accompanies ovulation
and the secretory phase of the cycle.

When

Daily throughout several menstrual cycles

Information
Sought

Factors favorable to fertility:

1. 1. The menstrual cycle is biphasic.
2. 2. The elevated temperature persists for 12 to 14 days
before menses.
3. 3. At the time of the slight temperature drop that is
followed by a persistent elevation, midcycle bleeding,
premenstrual syndrome may occur.

Cervical Mucus Characteristics

Who

Woman (and man)

Why

To obtain presumptive evidence

adequacy and progesterone phases

How

Obtain and evaluate cervical

through several menstrual cycles

When

Daily throughout several menstrual cycles

of

mucus

ovulation

and

characteristics

Plasma Progesterone level

Who

Woman

Why

To assess function of corpus luteum and to for

ovulation

How

A blood sample is drawn

When

Late in menstrual cycle, just before menstruation (e.g.

Day 22 in a 28-day cycle)

Information
sought

Findings favorable to fertility: adequate levels of

progesterone are found.

Hormone Analysis

Who

Woman

Why

To assess endocrine function FSH, LH, TSH,

Prolactin

How

Blood and urine specimens are obtained

When

At varying times during menstrual cycle

Information sought

Findings favorable to fertility:

Levels of progesterone, estrogen, FSH and LH are
all appropriate

Endometrial Biopsy

Who

Woman;

Why

To assess function of corpus luteum and receptivity of

endometrium for implantation; and to check for
tuberculosis

How

Sample of endometrium is removed for histologic

study

When

Late in menstrual cycle; 3 to 4 days before expected

menses

Information
sought

Findings favorable to fertility:

1. Endometrium is negative for tuberculosis, polyps,
or inflammatory conditions.
2. Endometrium reflects secretory changes normally
seen
in
presence
of
adequate
luteal
(progesterone ) phase.

Postcoital Test

Who

Both the woman and the man

Why

To test for adequacy of coital technique, cervical

mucus,
spermatozoa,
and
degree
of
sperm
penetration.

How

Assessment of specimen of cervical mucus following

ejaculation of semen into vagina

When

8 to 24 hours following sexual intercourse that is

synchronized with expected time of ovulation (as
determined from evaluation of BBT, cervical mucus
changes, and usual length of menstrual cycle);
performed only in the absence of vaginal infection

Information
Sought

Findings favorable to fertility:

1. Coital technique is adequate if sperm is found.
2. Mucus is supportive if many sperm are motile.
3. If more than 20 motile sperm are found, male most
likely produces at least 20mil/ml.
4. Mucus is clear and abundant, with good
spinnbarkeit

Hysterosalpingography

Who

Woman;

Why

To assess tubal patency and endometrial cavity to a

lesser degree; to assess uterine mobility
Fluoroscopic visualization (image intensification
fluoroscopy) or spread of radio opaque dye

How

When

2 to 6 days after menstruation to avoid flushing a

fertilized ovum out through a tube into the peritoneal
cavity; if the woman has pelvic inflammatory disease
(PID), she is treated with antibiotics first and the test
is rescheduled in 2 to 3 months

Information
sought

Findings favorable to fertility:

1) Spilling of dye into peritoneum within 10 to 15
mutes>
2) Spread of dye throughout peritoneal cavity.
3) Referred shoulder pain. Shoulder pain is indicative
of subphrenic irritation from the chemical if the
chemical spilled into peritoneal cavity.
Possible therapeutic of test:
1) Passage of dye may clear tubes, of mucus plugs,
straighten kinked tubes, or break up adhesions.
2) Cilia may be stimulated in the lining of the tubes.
3) It may aid healing as a result of the bacteriostatic
effect of dye (iodine).

Fig. 1.1 Hysterosalpingogram bilateral hydrsalpinx

Laparoscopic Examination

Who

Woman

Why

To assess visually the organs in the interior of the

abdomen; tubal patency and to perform minor
surgical procedures

How

A small telescope is inserted through a small

incision in the anterior abdominal wall using cold
fibroptical light sources that allow for superior
visualization of the internal pelvis

When

Laparoscopy is timed depending on the purpose; if

sites of endometriosis are to be treated, any day
of the cycle is appropriate.

Information Sought

Findings favorable to fertility:

1. No developmental abnormalities of pelvic
structures.
2. No lesions, infections, or adhesions.
3. No complications occur as a result of the
examination or procedure.
4. If tubal insufflation is done, the tubes are
found to be patent.
5. If there is a problem (e.g., adhesions kinking
the fallopian tubes), it is reparable through
the laparoscope

Fig.1.2. Laparoscopic view Endometriosis of the ovary

Ultrasound Pelvic Examination

Who

Woman

Why

To visualize pelvic tissues for a variety of reasons

(e.g., pelvic tissues for a variety of reasons (e.g., to
identify
abnormalities,
to
verify
follicular
development and maturity to determine timing for
retrieval of ova for preparation of in vitro fertilization
or for planning of artificial insemination, to confirm
intrauterine (vs. ectopic) pregnancy).

Information
Sought

Findings favorable to fertility:

1. Size, shape, position of reproductive structures are
within normal limits.
2. Ovarian
changes
of
follicle
development,
ovulation, and formation of corpus luteum can be
documented and occur within normal limits.
3. No abnormalities such as ovarian cysts, tubal
pathology, masses, or foreign bodies (broken IUDs)
are seen

TREATMENT OF INFERTILITY
It is estimated that at least 50 % of all infertility problems can be
diagnosed and treated by medical or surgical means. Diagnosis and

treatment require considerable physical, emotional, and financial

invesment over several months or years.

Therapeutic Interventions For Female Infertility

Congenital or developmental factors.
If the woman has abnormal tissue and construction of a functional
vagina may permit normal intercourse. If internal reproductive tract
structures are absent, there is no hope for fertility.
Vaginal and uterine anomalies and their surgical repair vary from
individual to individual. If a functional uterus can be reconstructed,
pregnancy may be possible. After surgical repair of the uterus,
cesarean delivery is necessary to prevent uterine rupture during labor.
Women with ovarian agenesis or dysgenesis are sterile, and no
treatment will improve their fertility.
Treatment of ovulatory failure
In cases where ovulation is not occurring attempts may be made to
induce it. Clomiphene citrate (Clomid) causes release of pituitary
gonadotrophin and thus induce ovulation. It is suitable for use in
women who are not ovulating but have normal or only subnormal
estrogen levels. The dose is 50 mg daily for 5 days starting on the
second day of the menstruation. Three courses of clomiphene in a
dose of 50 mg daily may be given; if this is not successful a further
three courses using 100 mg daily for 5 days should be given.
Treatment with human pituitary gonadotrophins combined with human
menopausal gonadotrophin for failure of ovulation is an alternative to
induce ovulation. Such treatment is best given in centers which have
facilities for hormone assays and ultrasound monitoring for follicular
growth.
Bromocriptine is indicated when ovulatory failure is associated with
hyperprolactinaemia. Before starting treatment , imaging (CT or MRI
scan) of the pituitary fossa must be taken to exclude pituitary tumour.
The dose is 2.5 mg daily taken at night to reduce side effects, such as
nausea and vomiting. Failure to ovulate in otherwise healthy women
can usually be treated by using clomiphene or human gonadotrophins.

Treatment for tubal disease

Surgery may be undertaken to restore patency and function in cases
where tubes have been damaged by infection. The surgery includes
salpingostomy where the abdominal end is opened, tubal implantation
where the isthmus is blocked; salpingolysis when peritubal adhesions
are divided. When blockage occurs in the isthmic portion of the tube it
is sometimes possible to excise the blocked segment and performed
tubal reanastomosis.

Treatment for Male Infertility

Drug treatment
There is no simple drug treatment which will increase sperm
concentrations or correct the shape of individual sperm cells. Some
drugs have been used successfully to some cases of impotence,
particularly where the impotence is related to male sex hormone
testosterone.
In addition, in cases where the male has disorder known as
hypogonadotropic hypogonadism in which the testes are unable to
generate sperms due to inadequate or absent hormonal stimulation of
the testes by the hypothalamus or pituitary human gonadotropic
hormones can be given to provide testicular stimulation. Clomiphene
citrate has been administerd with varying result.
Artificial insemination (AI):
Artifical insemination is the non-coital deposition of semen in the
vagina and has been widely used in the management of infertility due
to impotence or anatomical or abnormality in the male, especially
hypospadias. Use of this technique has focused on sperm selection.
Most studies suggest that AI of whole sperm ejaculates, using a
cervical cup, does not enhance pregnancy rates. AI using a split
ejaculate (the first portion, with the greatest sperm density and

motility) may slightly enhance pregnancy rates when ejaculate

volumes are large.
More recently, intrauterine insemination (IUI) with washed semen
samples has been used to treat infertility associated with low sperm
counts, decreased motility, antisperm antibodies, or abnormal cervical
mucus. The ejaculate is washed several times with tissue culture
medium; the motile sperm swim up from the sperm pellet and are
selected for insemination. This approach appears most successful in
men with low sperm counts and normal motility or in couples with
cervical factors; most pregnancies will be achieved by the 6th
treatment cycle.

Fig. 1.3 Intra-uterine insemination (IUI)

Around the time of ovulation, a sample of sperm from the male partner
is prepared and placed high in the uterine cavity of the female partner
through a fine plastic catheter. Because fertilization takes place in the
natural environment (i.e. in the fallopian tube), the female partners
tubes must be patent.

Assisted conception procedures:

Oligospermia, decreased sperm motility, and antisperm antibodies also
can be treated with either the IVF (In vitro fertilization) or GIFT (Game
Intra-Fallopian Transfer) or ICSI (Intracytoplasmic sperm injection)
procedures.
Assisted conception procedures usually require three steps:

Ovulation induction

Preparation of a suspension of motile sperm

Approximation of male and female gamete

IVF (In vitro fertilization) In simple terms, IVF removes several

oocytes from the ovary (usually transvaginally by piercing the ovaries
with a needle under ultrasound guidance), fertilizes them in the
laboratory with a preparation suspension of motile spermatozoa from
the male partners, and transfers a small selection of the resulting
embryos (four-cell embryo) to the uterine cavity for implantation and
pregnancy.
Although IVF was developed to treat couples whose
principal cause of infertility is tubal damage, the technique has also
been found useful in those with endometriosis, sperm disorders, and
even unexplained infertility.
GIFT (Gametes Intra-Fallopian Transfer) GIFT differs from IVF because
the oocytes collected from the ovary (laparoscopic ovum pickup
procedure) are transferred back into the lumen of the fallopian tube
almost immediately after collection (together with a small sample of
prepared sperm). So, unlike IVF, fertilization does take place in vitro
but in its natural environment in the fallopian tube.

Oocytes are retrieved at

laparascopy

Oocytes and prepared

sperm are transferred into
the lumen of the fallopian
tube

Fig. 1.4 GIFT (Gametes Intra-Fallopian Transfer)

This procedure is only suitable for couples who have patent normal
tubes and sperm where fertilizing capacity is expected to be normal.
Pregnancy rates for GIFT will depend on individual circumstances but
have been reported as high as 30 percent per treatment cycle.

GIFT has proved a useful treatment for couples wild unexplained

infertility and in mild cases of endometriosis, provided that the
fallopian tubes are healthy.
ICSI (Intra-Cytoplasmic Sperm Injection) The techniques of ICSI have
finally offered a viable treatment for event the most difficult cases of
male infertility.
The ICSI technique makes use of the most powerful microscopes and
micromanipulators.
A single sperm is directly injected into the
cytoplasm of the oocyte. The results of ICSI have so far been
remarkable, achieving success in men with very poor counts and
quality or event with immotile sperm.

Oocyte

Cytoplasma
B

Fig. 1.5 ICSI (Intra-cytoplasmic sperm injection).

Suction pipette (A) steady the oocyte on one side and on the other side a
microinjection is performed and a single sperm is injected into the cytoplasma of the
oocyte via a very fine needle (B)

PSYCHOLOGICAL ASPECTS
Failure to conceive often generates frustration, emotional stress,
feelings of inadequacy, anger, guilt. The financial burden and time
commitment for diagnostic and therapeutic infertility procedures can
cause marital strife. Provision of counseling and psychologic support is
an important adjunct to treatment. Support groups for infertile couples
have been organized at local and national levels. Despite all efforts,

some couples will fail to achieve pregnancy. They should be counseled

on when to stop treatments and when to consider adoption.

34
MANAGEMENT OF PELVIC PAIN
Pelvic pain is a common complaint in gynaecological practice. Pain is
not felt in the pelvis but also in the perineum, lower abdomen, back, or
thighs. Frequently, the patient suffers from a multitude of symptoms,
some of which are connected with the reproductive organs.
Pelvic pain may present clinically in an acute form lasting for days or
weeks, or in a chronic form lasting for months or years. Pelvic pain is a
symptom indicative of the presence of an underlying disorder, not
always limited to the pelvic organs. In cases of acute pelvic pain, it is
usually possible to diagnose the underlying clinical condition,
treatment of which leads to relief of pain. However, in cases of chronic
pelvic pain, it is often difficult to make such a diagnosis. Sometimes no
cause is found.
Pelvic pain may be due to a surgical emergency (e.g. ovarian cyst
torsion,
ectopic
pregnancy,
ruptured
tubo-ovarian
abscess,
appendicitis, bowel perforation). Chronic pelvic pain (lasting more than
6 months) may require surgical intervention and can be debilitating.

ACUTE PELVIC PAIN

CAUSES OF PELVIC PAIN
Acute pelvic pain of gynaecological origin often starts in the lower
abdomen, spreads to the entire abdomen, and may even be referred to
the shoulder (diaphragmatic irritation). The causes of acute pelvic pain
are summarized in Table 1.

Table 1. Causes of acute pelvic oain

Mechanism
Haemoperiteu
m

Clinical condition

Ruptured
ectopic
pregnancy
Rupture of endometriotic
cyst
Ruptured corpus luteum
or follicular cyst

Ruptured of endometriotic
cyst
Vascular
complication

Torsion of ovarian cyst

Degeneration of fibroid

Torsion of ovarian cyst

Infection

Visceral
distension

Complication of
pregnancy

Acute pelvic inflammatory

disease
Complication
following
IUD insertion
Haemorrhage into ovarian
cyst
Ovarian hyperstimulation
syndrome
Miscarriages all types

Miscarriage
Nongynaecologi
cal

Surgical acute abdomen

- Acute appendicitis
- Intestinal obstruction

Urinary tract condition

- Ureteric calculi
- Urinary tract infection

MANAGEMENT OF ACUTE PELVIC PAIN

These patients often present in the surgical department as cases of
acute abdomen.
The main problem appears to be one of the
diagnosing the underlying pathology. In real clinical life, of course, it is
common not to be able to make a certain diagnosis at the first
examination. The important thing is to try, establish the differential
diagnosis, and at least to establish the distinction between those
conditions that require immediate surgical intervention (ruptured
ectopic pregnancy and acute appendicitis) and those that do not
(salpingitis).
The diagnosis of the underlying disorder can often be made on the
basis of a careful elucidation of history and physical examination.
History: A thorough history--including the type, location, radiation,
status (stable or increasing or decreasing in severity), and onset
(circumstances and suddenness) of the pain--can help identify the
cause. The patient should be asked if any factors exacerbate or
alleviate the pain and if the pain is related to menses, movement,
micturition, defecation, sexual activity, sleep, or eating.
The history should include past surgical procedures and episodes of
pelvic inflammatory disease. The patient should be asked about past
treatment of the pain and its effectiveness. A detailed menstrual
history (including time of menarche, cycle regularity and length,
duration of menses, and amount of blood loss) should be obtained.
Whether the pain began with menarche or is relatively new should be
determined.

A history of ammenorrhoea preceding the occurrence of pain suggests

a pregnancy complication.
Symptoms and signs relating to the gastrointestinal tract or urinary
tract indicate the possible diagnosis of these systems.
Physical examination: General observation may be diagnostically
helpful; e.g. pallor, hypotension, and tachycardia are associated with
haemorrhage whereas the occurrence of pyrexia denotes the presence
of an infective process.
The abdomen is examined for tenderness or masses. If a painful area is
found, the patient should be asked whether this pain is the same as
the primary complaint.
The existence of blood or inflammatory exudae causes tenderness of
the pelvic peritoneum, and can be detected by abdominal or vaginal
examination.
Pelvic examination: - When performing the pelvic exam, visualize
the vagina and cervix. Note the presence of discharge, blood, or
products of conception in the vaginal vault or cervical os. Next,
perform a bimanual exam checking the bladder, urethra, adnexa,
uterus, and finally the cervix. Pay particular attention to the
appearance of the vaginal and cervical mucosa, the presence of any
exudate, the patency of the internal cervical os, the size and shape of
the uterus, the presence of adnexal masses and of course, the
elicitation of uterine, adnexal, or cervical motion tenderness.
Assessment of cervical motion tenderness, vaginal fornix pain, and
adnexal tenderness can help differentiate pelvic inflammatory disease
or endometriosis from adhesions.
During bimanual examination, uterine size, tenderness, and mobility
are evaluated. A markedly enlarged, bulky uterus suggests fibroids; a
mildly enlarged, boggy, symmetric uterus suggests adenomyosis.
Fixation of the uterus may indicate adhesions or endometriosis.
Uterosacral nodularity (confirmed by a rectal examination) suggests
endometriosis. A rectal examination should always be performed.
INVESTIGATION
Laboratory aids to diagnosis include a full blood count, erythrocyte
sedimentation rate (ESR), and a bacteriology of vaginal discharge and
of a midstream specimen of urine. Measuring ESR or C-reactive protein
may help identify an inflammatory or infectious process.

 Radiological examination of the abdomen can be of value in the

diagnosis of intestinal obstruction or ureteric calculus.
Ultrasonography may help if a physical examination is difficult (e.g.
if the patient has pain) or if an adnexal mass is suspected. Ultrasound
scanning may be of value in the diagnosis of disturbed intrauterine
pregnancy (miscarriages) or of an ectopic bpregnancy. Ultrasound
scan may be of use in the demonstration of ovarian cyst, ovarian
enlargement as in hyperstimulation syndrome, or the presence of fluid
in the pouch of Douglas.
Diagnostic laparoscopy - If the clinical assessment aided by
laboratory studies does not lead to a firm diagnosis, laparoscopic
examination is strongly indicated. Laparoscopy can confirm the
diagnosis. Pathological changes different from those suggested by
clinical examination are often seen during laparoscopy (e.g. ruptured
corpus luteum or ruptured ectopic pregnancy).

DIFFERENTIAL DIAGNOSIS
The differential diagnosis of pelvic pain can be divided into four
categories: pelvic infections, complications of pregnancy, adnexal
accidents, and other causes of pelvic pain.
Pelvic infections include pelvic inflammatory disease (salpingitis),
tubo-ovarian abscess, endometritis, and the Fitz-Hugh-Curtis syndrome
(a complication of PID consisting of right upper quadrant abdominal
pain secondary to perihepatic adhesions usually due to dissemination
of a pelvic infection).
Complications
of
pregnancy
include
ectopic
pregnancy,
spontaneous abortion (threatened, inevitable, incomplete, and
complete), placental abruption, and appendicitis in pregnancy.
Adnexal accidents include torsions of the tube and ovary, ovarian
cyst rupture, and persistent corpus luteum cyst with hemorrhage.
Other causes of pelvic pain include Mittelschmerz (rupture of the
graafian follicle and extrusion of the ovary), dysmenorrhea,
endometriosis, and acute appendicitis.

TREATMENT
Treatment should be directed at the specific cause of the pain, if
possible.
If the diagnosis is obvious on examination, that is
appendicitis or ruptured ectopic pregnancy, then appropriate
treatment (laparotomy) is indicated.
In general, all patients who present with pelvic pain, hemodynamically
unstable vital signs (tachycardia, hypotension, altered mental status),
and positive peritoneal signs should undergo rapid a assessment of the
ABC's (airway, breathing, and circulation), stabilization with two large
bore IV's and immediate referral for emergency gynecologic
consultation.
Treatment should be directed at the specific cause of the pain, if
possible. However, symptomatic treatment with NSAIDs is often the
only option. Patients who have a poor or partial response to one NSAID
may respond well to another one.

(a) Acute Pelvic inflammatory disease (PID)

Outpatient treatment of PID is intramuscular Rocephin 250 mg. plus
Doxycycline 100 mg orally twice a day for 10 to 14 days, or
Azithromycin 1 gram as a single oral dose. Patients with PID who
appear toxic (nausea, vomiting, dehydration) or have peritoneal signs
(rebound tenderness, rigidity, decrease bowel sounds) are not good
candidates for ambulatory treatment and should be hospitalised for
further treatment and work-up to rule out tubo-ovarian abscess.
(b) Post-partum or post-abortal endometritis
These conditions are often associated with retained placental tissue or
products of conception and should be referred to the gynecologist for
definitive therapy.
(c) Ectopic pregnancy
Any patient with pelvic pain, bleeding, and a positive pregnancy test
should be carefully evaluated for possible ectopic pregnancy.

(d) Patients suspected of having a tubal or ovarian torsion require

surgical evaluation and should be treated as in-patient. Patients who
are hemodynamically unstable suspected of having an ovarian or
corpus luteum cyst with intra-abdominal bleeding should be stabilized
before any surgical procedures. If these patients are hemodynamically
stable, they can be referred for routine consultation.
(e) Mittelschmerz and dysmenorrhea can be treated with
reassurance, patient education, oral contraceptives and Ibuprofen 600
to 800mg orally three times a day. However, because these are
diagnoses of exclusion, other conditions must be excluded first.

CHRONIC PELVIC PAIN

The proposed definition of chronic pelvic pain is nonmenstrual pain of 3
months duration or longer that localizes to the anatomic pelvis and is
severe enough to cause functional disability and require medical or
surgical treatment.
Chronic pelvic pain is a common problem and presents a major
challenge to health care providers because of its unclear etiology,
complex natural history, and poor response to therapy.
Chronic pelvic pain is poorly understood and, consequently, poorly
managed. This condition is best managed using a multidisciplinary
approach. Management requires good integration and knowledge of all
pelvic organ systems and other systems including musculoskeletal,
neurologic, and psychiatric systems.
A significant number of these patients may have various associated
problems, including bladder or bowel dysfunction, sexual dysfunction,
and other systemic or constitutional symptoms. Other associated
problems, such as depression, anxiety, and drug addiction, also may
coexist.
As with other chronic pain, chronic pelvic pain may lead to prolong
suffering, marital and family problems, loss of employment or
disability, and various adverse medical reactions from lifelong therapy.
Clinical manifestation of pelvic pain may vary not only with regard to
its localization but also in its relationship to menstruation and other

physiological functions. Categorizing pain as cyclic or non-cyclic may

help determine the cause (Table 2.)
Table 2. Classification of chronic pelvic pain
CYCLIC PAIN

Mittelschmerz
Dysmenorrhoea (primary or
secondary)
Premenstrual
tension
syndrome

NON-CYCLICAL PAIN

Chronic
pelvic
inflammatory disease
Endometriosis
Pelvic adhesions
Displacement
of
the
uterus
Cyst and tumours
Intrauterine devices
Pelvic vein thrombosis

Non-gynaecological
Chronic
pelvic
pain
without
organic
abnormality

Cyclic Pelvic Pain of pelvic origin

Premenstrual tension
The premenstrual syndrome (PMS) may produce pelvic heaviness or
pressure and backache, occurring 7 to 10 days before and
disappearing after menses begins.
Mittelschmerz
Mittelschmerz (severe midcycle pain due to ovulation) frequently
occurs. Rupture of the follicle and subsequent irritation of the
peritoneum (by the fluid and/or blood from the ruptured follicle) may
produce the pain. The pain, although sometimes severe, resolves
spontaneously. Patients should be monitored and given NSAIDs.

Dysmenorrhoea
Dysmenorrhea (pain related to the menstrual cycle) can be primary or
secondary. Most women experience primary dysmenorrhea at some
time during their life. The pain is cramping or sharp and lasts the first
few days of the menstrual period. It may radiate to the back, thighs, or

deep pelvis. Occasionally, nausea or vomiting occurs. Secondary

dysmenorrhea may be due to endometriosis or cervical stenosis or, if
associated with heavy menstrual flow, to fibroids, adenomyosis, or
large endometrial polyps. Using gonadotropin-releasing hormone
agonists to suppress secondary dysmenorrhea associated with PMS
may help in diagnosis, but long-term use requires caution and
coadministration of exogenous estrogen. Adjunctive use of
antidepressants relieves pain through peripheral neuroblockade and
central stimulation.

Non-cyclic Pelvic Pain

Of pelvic origin:
Endometriosis
Endometriosis can cause mild to severe pain, probably from irritation of
pain fibers on the peritoneal surface. In its early stages, endometriosis
causes cyclic pain, which starts several days before menses and
continues through the first few days. However, as the disorder
becomes chronic, pain commonly occurs at variable times unrelated to
menses.
The patient is usually in her 30s and infertile; deep dyspareunia or
rectal pain on defeacation during menstruation is often associated with
it. The uterus may be retroverted and tender on movement. Sensitive
nodules may be palpated in the pouch of Douglas and the ovaries may
be enlarged and tender.
Laparoscopic examination shows bluish
darkish spots on the peritoneum, uterosacral ligaments, or the ovaries.

Fig. 1.1 Endometriosis involving the ovary as seen during laparscopic examination

Chronic pelvic inflammatory disease

Lower abdominal discomfort, secondary dysmenorrhoea, dyspareunia,
and menorrhagia are often the presenting symptoms in this condition.
Tenderness is often detected and a pelvic mass such as hydrosalpinx or
ovarian abscess can be felt on pelvic examination. A fixed retroversion
of the uterus may be palpated. Fever, leukocytosis, and a
mucopurulent cervical discharge usually accompany the pain. Nausea
and vomiting are uncommon. Tubo-ovarian abscess is a late
complication, and rupture may temporarily reduce the pain but is
followed by sudden severe, unrelenting pain and deterioration
requiring surgical intervention.

Pelvic adhesions
Adhesions resulting from previous surgery or pelvic infection may
cause pain. These often cause pain, particularly when involving the
intestines or the adnexae. The diagnosis is frequently made by
laparoscopic examination. Patients should be warned that the removal
of adhesions (adhesiolysis) may make the pain worse and that even if
surgery is beneficial, the adhesions may recur and cause further pain.
Cyst and tumours
Ovarian cysts and fibroids are frequently asymptomatic but may cause
pressure, aching, or heaviness. Sudden sharp pain may indicate
rupture, adnexal torsion, or hemorrhage. Hemorrhage into a cyst or
leakage into the pelvis is very common and produces severe pain. A
ruptured dermoid cyst can cause severe chemical peritonitis. For
ovarian cyst torsion, the pedicle can be untwisted if it appears viable.
Fibroids rarely cause pain except when degeneration or sarcomatous
change is taking place.

Displacement of the uterus

Retroversion of the uterus is an uncommon cause of pelvic pain.
Symptoms include pelvic pressure and low back pain. A successful trial
with a pessary predicts a good response to surgery. Vaginal

hysterectomy or uterine suspension may be performed depending on

the patient's desire to have children.

Malignant diseases of the pelvic organs

Pelvic malignancy can cause intractable pelvic pain, especially where
bones or nerve plexuses are infiltrated or where obstruction to the
outflow occurs in a viscera.

Other gynaecological causes

Intrauterine contraceptive devices may cause pelvic pain if it causes
pelvic inflammatory disease. Larger and stiffer intrauterine device
may result in endometrial compression and myometrial distension
which lead to bleeding and pain.
Another rare cause of pelvic pain is pelvic vein thrombosis after an
operation.

Of extrapelvic origin (non-gynaecological):

Diseases affecting the gastrointestinal, musculoskeletal may present
as pelvic pain. Pain may be referred from extrapelvic organs to the
pelvis.
Correlation of pain with eating or defecation suggests gastrointestinal
tract disease. Alternating constipation and diarrhea, lessening of pain
after a bowel movement, prompt urge to evacuate after eating, or
worsening of pain with stress suggests irritable bowel syndrome or
spastic colon. Dyspareunia may be linked with irritable bowel
syndrome. Hard, infrequent stools with pain during or after bowel
movements, rectal fullness, or a sensation of incomplete evacuation
suggests chronic constipation. Recurrent left lower quadrant pain with
fever, especially in a woman > 40 yr, suggests diverticulitis.
Inflammatory bowel disease, suggested by tenderness of the rectum,
and cancer are uncommon but should be ruled out. Surgical
emergencies, such as appendicitis, usually manifest more acutely but
should be considered.

If the pain does not progress, further search for the cause is indicated
before initiating treatment. Ultrasound examinations during the
episode may reveal gallbladder or ureteral stones. In selected patients,
sigmoidoscopy, colonoscopy, or barium enema is appropriate.
Typical symptoms of urinary tract problems include frequency,
dysuria, burning, fever, chills, hematuria, and colicky ureteral pain.
Occasionally, the only finding is tenderness over the suprapubic or
trigone area. Urinalysis, cystourethroscopy, and urodynamic studies
help in diagnosis. Postcoital voiding difficulties suggest the urethral
syndrome (dysuria and frequency without bacteriuria), with or without
chronic urethritis. This syndrome may require urethral dilation. Once
symptoms are alleviated, the woman should regularly void after coitus
to reduce the risk of recurrence.
Pain that radiates down the legs or is worsened by motion suggests a
musculoskeletal problem. Poor posture, abnormal gait, scoliosis,
unilateral standing, marked lumbar lordosis, discrepancy in leg length,
previous surgery with a diagnosis of a normal pelvis, or a history of low
back trauma suggests a musculoskeletal cause.
Backache, a common complaint, is more often caused by poor posture,
lack of exercise, trauma, or a skeletal disease (e.g. osteoporosis,
ruptured disk of the spine, osteoarthritis, bone tumor) than by a
gynecologic disorder.
Separation of the pubic symphysis is a rare cause of pelvic pain, most
commonly secondary to pregnancy. A history of pubic pain during
ambulation and pain on pressure of the pubic bone during the
abdominal or pelvic examination establish the diagnosis. The patient is
treated with pelvic rest and, if not breastfeeding, NSAIDs. The disorder
may take up to 6 months to resolve.
Laboratory studies are needed to rule out organic causes of pain.
Somatization disorder is a common psychogenic disorder in patients
with chronic pelvic pain . Emotional problems may manifest as physical
complaints. Often the patient has multiple complaints for which no
organic cause can be identified. Psychiatric consultation is
recommended.
Victims of physical or sexual abuse in childhood or in adulthood may
present with chronic pelvic pain. These patients are at high risk of
other psychologic or psychiatric disorders. Inquiries must be
compassionate, but the patient must be asked if she has ever been
touched by anyone against her will as a child or as an adult. Referral
for counseling and to a support group may help.

Pelvic congestion syndrome is pain that occurs 7 to 10 days before

menses. It is more severe when the woman sits or stands and is
relieved by lying down. It is thought to be caused by vascular
congestion or varicosities of the pelvic veins. On examination, the
uterus is usually tender, and the pain during the examination is the
same as that during sexual intercourse. The pain usually responds to
NSAIDs.

MANAGEMENT OF PATIENT WITH CHRONIC PELVIC PAIN

HISTORY:
Patient history is important in cases of chronic pelvic pain. Because of
the complex etiology and, often, the presence of associated disorders,
a general approach with a thorough history that directs further
evaluation and appropriate consultations is needed. Perform a detailed
review
of
systems,
including
reproductive,
gastrointestinal,
musculoskeletal, urologic, and neuro-psychiatric. As needed, ask
specific questions, especially if the patient has an associated disorder.
A thorough past history also is important to avoid repeating invasive
and expensive procedures.

Focus history on characterizing the patients pain, which can lead

to appropriate diagnostic and therapeutic plans.
o

Location of pain: The location of pain is an important

part of the history. Ask the patient to describe the pain
location and type on a pain diagram (anteroposterior and
lateral view of human picture).

Precipitating factors: Ask questions about factors that

provoke or intensify pain. This may provide clues for
possible etiologies or associated disorders. For example, in
pelvic congestion syndrome, pain is related to posture and
is worse at the end of day. In endometriosis, pain
commonly is reported during or after intercourse.

Alleviating factors: Alleviating factors may exist. For

example, rest may decrease pain of musculoskeletal or
adnexal origin.

Quality of pain: Various terms can be used to describe

the quality of pain. Such terms include throbbing,
pounding, shooting, pricking, boring, stabbing, sharp

cutting, lacerating, pressing, cramping, crushing, pulling,

pinching, stinging, burning, splitting, penetrating, piercing,
squeezing, and dull aching.

Pain distribution: Spreading or radiation of pain also is

important in the evaluation of neuropathic pain.

Severity or intensity of pain: Use some type of rating

system to evaluate pain severity or intensity with a degree
of objectivity and reproducibility. Different types of pain
scales may be used. Numerical scales are more useful and
reliable. The visual analog scale is one of the commonly
used numerical scales.

Obtain a history specific to different systems and disorders.

o

Gynecologic and obstetric: For example, excessive

bleeding with menses suggests uterine leiomyomas or
adenomyosis. History of previous surgery may suggest
intra-abdominal or pelvic adhesions. Patients with cervical
stenosis usually have a history of chronic cervical infection
or treatment with cryosurgery/laser surgery/loop excision
or endometrial resection. Having multiple sexual partners
is a risk factor for pelvic inflammatory disease.

Urologic: A detailed history to evaluate the urological

system is important. For example, as compared to patients
with pelvic pain, patients with interstitial cystitis report
urgency and increased frequency of urination as the most
distressing features.

Gastrointestinal: For example, deflecting sigmoid

adhesions are common in women with CPP and frequently
are associated with gastrointestinal symptoms.

Musculoskeletal: History of vaginal delivery with

prolonged second-stage episiotomies or tears may suggest
pelvic floor relaxation disorder.

Neurologic: Constant burning pain is a common complaint

in patients with pudendal neuralgia. Patients may report
dysesthesia and vulvodynia but usually not dyspareunia.

Psychologic: A good psychosocial or psychosexual history

is needed when organic diseases are excluded or
coexisting psychiatric disorders are suggested. Obtain

sufficient history to evaluate depression, anxiety disorder,

somatization, physical or sexual abuse, drug abuse or
dependence, and family problems, marital problems, or
sexual problems. Sexual abuse occurring before age 15
years is associated with later development of CPP (Lampe,
2000). Somatization is a common associated psychologic
disorder in women with CPP. Somatization scales can be
used for evaluation.
PHYSICAL EXAMINATION
Good rapport, tolerance, and an open-minded approach are important
in the evaluation of any patient with chronic pain. A thorough
systematic examination usually suggests an appropriate diagnosis and
therapy.

Physical examination focusing on the abdomen and pelvis. The

examiner should probe for abdominal wall trigger points and
evaluate for musculoskeletal disorders and tenderness of the
bladder, urethra, and other pelvic organs.

Perform detailed examinations for other systems (e.g.

gastrointestinal, urologic, neurologic, musculoskeletal) as
required. For example, gait and posture evaluation, spine
examination, and sensory and motor examination often are
useful.

INVESTIGATIONS
Lab Studies:
The decision to perform laboratory or imaging evaluations is based on
the need for confirmation of the diagnosis and to help rule out other
potentially life-threatening illnesses. Certain investigations sometimes
are needed to provide appropriate and safe medical or surgical
treatment.
Complete blood cell count and sedimentation rate: These
tests provide nonspecific findings, but the results can be
sensitive indicators of inflammation or infection and,
occasionally, malignancy.

Urine test

Urinalysis and urine culture are relatively inexpensive and

noninvasive and should be performed when necessary.

If hematuria is present, carefully evaluate the condition

with a history, physical examination, urine culture, urine
cytology, cystourethroscopy, and intravenous pyelography
or CT scan.

Sexually transmitted disease testing

o

Testing for sexually transmitted diseases in women with

chronic pelvic pain includes endocervical swab, syphilis
serology (rapid plasma reagent, microhemagglutinationTreponema pallidum), hepatitis B screening, chlamydial
polymerase chain reaction, and HIV testing.

Other tests used to help rule out specific infections may

include vaginal cultures, vaginal wet preparations, vaginal
pH, and urine analysis and culture.

Imaging Studies:

Magnetic resonance imaging: MRI is a noninvasive tool that

can provide excellent structural information without any radiation
harm.

CT scan: This is useful in patients with pelvic masses and

sometimes is helpful in differentiating an ovarian mass from a
uterine mass, but it is more expensive than sonography.

Ultrasonography

This is a noninvasive diagnostic tool and could be helpful in

many patients with chronic pelvic pain.

It commonly is used to help identify pelvic masses or cysts

and their origin, and pelvic varicosities.

Plain film radiography

o

Obtaining chest and spine x-ray films may be useful in

fractures, infections, tumors, and other structural
abnormalities.

Flat and upright abdominal radiographs may be obtained

to help rule out intestinal obstruction and pelvic infection
(e.g. tuberculosis).

Barium
enema
sigmoidoscopy.
o

radiography,

colonoscopy,

and

These can be used to evaluate a gastrointestinal etiology

of chronic pain.

Other Tests:

Endoscopic procedures used commonly in the evaluation and

treatment of patients with chronic pelvic pain includes
laparoscopy, hysteroscopy, sigmoidoscopy, and colonoscopy.

Laparoscopy can be used as a diagnostic tool in patients with

chronic pelvic pain, as follows:
o

Most commonly, diagnoses made via laparoscopy include

endometriosis, pelvic adhesions, and chronic pelvic
inflammatory disease. Other diagnoses include ovarian
cysts, hernias, pelvic congestion syndrome, ovarian
remnant
syndrome,
ovarian
retention
syndrome,
postoperative peritoneal cysts, and endosalpingiosis.

PRINCIPLES OF TREATMENT OF CHRONIC PELVIC PAIN

In order to treat chronic pelvic pain it is essential to establish a firm
diagnosis of the underlying disorder.
Reassurance:
Simple explanation that the reproductive organs are normal is often of
therapeutic benefit.

Medical Treatment: Treatment of pelvic pain is complex in patients

with multiple problems. It usually requires specific treatment and
simultaneous psychological and physical therapy. A good relationship
should be established between the physician and the patient.

Treatment of chronic pelvic pain must be tailored for the individual

patient.
The goals of treatment must be realistic. They should be focused
toward restoration of normal function (minimal disability), better
quality of life, and prevention of relapse of chronic symptoms.

Analgesics - Analgesic therapy consists of symptomatic

abortive therapy to stop or reduce the severity of the acute
exacerbations and long-term therapy for chronic pain.
Analgesics, particularly prostaglandin synthetase inhibitors, such
as indomethacine or naproxen, are useful.
Hormonal - Cyclic combined oral contraceptive pills, danazol or
GnRH analogue may be tried in endometriosis

Antidepressants. Low doses of tricyclic antidepressants

(imipramine, amitriptyline) taken at bedtime will decrease pain
intensity, promote sleep and reduce depressive symptoms. May
exacerbate constipation.

Physical therapy - Physical therapy techniques include hot or

cold applications, positioning, stretching exercises, traction,
massage, ultrasound therapy, transcutaneous electrical nerve
stimulation (TENS), and manipulations. Heat, massage, and
stretching can be used to alleviate excess muscle contraction
and pain.

Psychologic therapies: Cognitive-behavioral therapy to control

pain: relaxation techniques, stress management, and pain-coping
strategies. Psychotherapy for mood disorders, eating disorders,
abuse survivors, etc. Marital/family counseling, sex therapy,
substance abuse treatment as indicated.

Antibiotics if evidence of chronic endometritis, (positive

cultures or endometrial biopsy), or for urethritis with pyuria.

Surgical management:
Various surgical procedures may be considered to treat chronic pelvic
pain. Surgical procedures include lysis of adhesions, uterine
suspension, uterosacral nerve ablation, and presacral neurectomy.
Endometriosis spots could be treated by electrocoagulation by
diathermy under laparoscopic control.

Hysterectomy is reserved for patients with chronic pelvic pain

unresponsive to medical or conservative surgical therapy. Patients
without known organic pelvic disease must be informed that their pain
may remain or even worsen after hysterectomy.

SUMMARY
Pelvic pain is a symptom indicative of underlying disorders, not always
limited to the pelvic organ. In cases of acute pelvic pain, diagnosis of
the underlying disorder can usually be made and appropriate
treatment given. In cases of chronic pelvic pain clinical evaluation,
laboratory investigation, and laparoscopic examination should
establish the diagnosis of an organic disease, if present. Psychological
factors are often present, particularly when organic disease cannot be
identified. The aim of treatment should be the treatment not only of
the disease processes but also of the woman and her total
environment.

35
MANAGEMENT OF ABNORMAL UTERINE
BLEEDING
Abnormal vaginal bleeding (i.e. excessive or prolonged bleeding or frequent bleeding) is
a very common symptom. Occasionally, abnormal bleeding will be due to a
laceration of the vagina, a bleeding lesion, or bleeding from the surface
of the cervix due to cervicitis. Much more commonly, abnormal
bleeding arises from inside the uterus.

There are really only three reasons for abnormal uterine bleeding:

Pregnancy-related problems
Organic problems
Hormonal problems

The complaint of abnormal uterine bleeding suggests that the source

of the blood is from the pelvic organs. However, the differential
diagnosis of abnormal uterine bleeding includes systemic and
iatrogenic causes. The diagnosis of dysfunctional uterine bleeding can
be established only by excluding other pathological cause (i.e.
reproductive tract disease, systemic disease, and iatrogenic causes).
DIFFERENTIAL DIAGNOSIS FOR ABNORMAL UTERINE BLEEDING
Reproductive tract disease:
The reproductive causes for abnormal uterine bleeding include
complications of pregnancy, malignancy, infection and begin pelvic
lesions.

Pregnancy complications Complications of pregnancy are an

important cause of abnormal uterine bleeding in women of
reproductive age.
These complications include all types of
miscarriage (i.e. threatened, incomplete or missed) , ectopic

pregnancy, and trophoblastic disease. The history and physical

examination must look for symptoms and findings of pregnancy.

Malignancy - Abnormal bleeding can be a symptom of malignancy,

from the vagina, cervix or uterus. Cancer of the vagina is
extraordinarily rare and will demonstrate a palpable, bleeding
lesion. Cancer of the cervix is more common but a normal Pap
smear and normal exam will effectively rule that out. Endometrial
cancer and less frequently estrogen-secreting ovarian tumours can
be the source of abnormal uterine bleeding.

Infection of the upper genital tract Endometritis may cause

abnormal uterine bleeding.
Uterine and/or adnexal pain on
palpation and movement of the pelvic organs, a sensation of
warmth of the vaginal canal, and purulent vaginal discharge should
suggest strongly the presence of infection.
Benign pelvic lesions Benign vaginal disease, including
lacerations, severe vaginal infections, foreign bodies, cervical

polyps, and cervicitis may produce abnormal genital bleeding.

Benign uterine disease involving submucous leiomyoma uteri,
adenomyosis, and endometrial polyps may be the source of
abnormal uterine bleeding.
Systemic disease
This category includes coogulation disorders and hypothyroidism.

Coagulation disorders - Disorders associated with platelet

deficiency (idiopathic thrombocytopenic purpura), disorders of
defective activity (von Willebrands disease) may cause abnormal
uterine bleeding.
Hypothyroidism Women with lesser degrees of thyroid
hypofunction have disruption of their menstrual cycles expressed as
abnormal uterine bleeding.

Iatrogenic causes
The common iatrogenic causes of abnormal uterine bleeding includes
steroid and intrauterine devices. A careful history is required to make
the correct diagnosis.

Steroid Steroid which may lead to genital bleeding include oral

contraceptive, estrogen replacement therapy, androgens and
corticosteroids.

EVALUATION OF ABNORMAL UTERINE BLEEDING

It is important in every patient with abnormal uterine bleeding to
consider the entire differential diagnosis. All women of child-bearing
age with abnormal uterine should have a careful history and physical
examination, cervical smear, complete blood count and endometrial
tissues sampling.
Thyroid function test, studies of the clotting
mechanism, culture of the vaginal discharge, ultraound scanning,
dilatation and curretage or hysteroscopic-directed biopsies are
performed only when indicated by the history and physical
examination.

Hysteroscopy provides the opportunity for direct visualization of the

endometrial cavity and therefore is more reliable diagnostic procedure
for identifying endometrial lesions than dilatation and curettage.
The evaluation of the abnormal uterine bleeding may be approached
by considering the causes as either menstrual or non-menstrual.

ABNORMAL MENSTRUAL BLEEDING

Abnormal menstrual bleeding may classified as:

Excessive:
o with a normal cycle i.e. menorrhagia
o with a short cycle i.e. epimenorrhagia; anovular cycles
o due to disorder of the ovarian endocrine axis
o with a long cycle - usually from dysfunctional uterine
bleeding resulting in the condition known as cystic
hyperplasia of the endometrium
Reduced:
o infrequent - oligomenorrhoea

MENORRHAGIA
Menorrhagia is defined as excessive menses in an otherwise normal
menstrual cycle. It is largely a subjective definition as what constitutes
heavy bleeding to one woman may be quite normal for another.
Menorrhagia is usually reserved for menses associated with, clots, the use of towels
rather than tampons, and flooding.
Objectively, menorrhagia may be defined as blood loss more than 80
mls in an otherwise normal menstrual cycle.
Causes:
The causes of menorrhagia may be
classified into:

Pelvic pathology:
o pelvic endometriosis
o pelvic inflammatory disease
o endometrial hyperplasia

uterine fibroids

fibroids

Fig. 1.1 Uterine

Systemic disorders:
o hypothyroidism - but usually presents with amenorrhoea in
advanced cases
o blood clotting disorders - very rare; examples include von
Willebrand's disease, thrombocytopenia
Iatrogenic factors:
o intra-uterine contraceptive device
o misoprostol
o poorly-controlled anticoagulant therapy
Psychosomatic disturbance - usually subsides when
precipitating factors subside
Dysfunctional uterine bleeding (DUB) - if all other local and
systemic causes have been excluded

Investigations:
Correct investigation of menorrhagia should entail:

gynaecological and medical history - in particular:

o length and interval of periods
o duration of excessive bleeding
o contraceptive use, especially IUCD
bimanual pelvic examination
speculum examination
cervical smear if indicated
pregnancy test
FBC (full blood count) - to screen for anaemia; clotting studies if
abnormal coagulation suspected
thyroid function tests if clinically indicated
endometrial biopsy - mandatory if the patient is over 40 years of
age; may be deferred in younger patients if bleeding not
excessive. Achieved via a pipelle endometrial sampling,
dilatation and curettage or via hysteroscopy.

Management:
Treatment of menorrhagia may be surgical or medical. Surgery is
usually indicated in cases of proven pathology, for example, uterine
fibroids. Non-hormonal and hormonal agents may be used when the

cause is uncertain or the woman is keen to retain her fertility. In all

cases, the need for iron replacement should be evaluated. In
uncomplicated cases, simple reassurance that the condition is
harmless may be adequate.

What to do first?
Since most (90%) of the non-pregnancy bleeding is caused by
hormonal factors, the best bet is to:
1. Obtain a complete history.
2. Examine the patient.
3. Obtain a blood count.
4. Put the patient to bed if the bleeding is heavy.
5. Start on hormonal treatment or anti-fibrinolytic agent.

Stopping heavy menstrual bleeding

This can be achieved with a regime such as:

norethisterone 30 mg bd for 3 days, 20 mg bd for 3 days, 10 mg

bd for 3 days, 5 mg bd for 10 days.

This regime will be followed by a withdrawal bleed.

With bedrest and hormonal treatment, bleeding should be substantially
improved within 24 hours. It should continue to improve with additional
days of treatment. If hormonal control is not succeeding, then a D&C
will be necessary.
The cause for the heavy menstrual bleeding should be investigated.

Medical management
In women under 40 years old, and in older women without organic
pathology, dysfunctional uterine bleeding may be treated with:

1) Non-hormonal agents need only be taken during menstruation.

Options include:

Prostaglandin synthetase inhibitors, e.g. mefenamic acid reduces blood loss by 20-50%
Anti-fibrinolytics, e.g. tranexamic acid. A recent study has shown
that tranexamic acid 1g three to four times per day reduced
blood loss by 54%. However may be associated with nausea and
vomiting in one third of cases

2) Hormonal agents - options include:

Combined oestrogen-progestogen - useful in young women with

ovulatory or anovulatory bleeding; especially useful in women
who also require contraception

Oral progesterone was previously widely used. This may be

indicated if the initial endometrial biopsy shows unopposed
estrogen activity (i.e. only effective in cases of anovulatory
dysfunctional uterine bleeding).
o

examples of regimes used with cyclical progestogens

include norethisterone 5 mg tds days 12-26 or
norethisterone 5 mg tds days 5-26. There is then a
withdrawal bleed. Side effects of cyclical progestogen
therapy include breast tenderness, weight gain and
bloating

In general, women should be offered a 3-6 month trial of drug therapy.

In addition drugs such as Danazol, LHRH analogues and hormonalcontaining IUCDs may be used:

Danazol - competitively binds sex hormones to their receptors

and inhibits their production by direct enzymatic action. Given
orally. May cause endometrial atrophy in older women.
LHRH analogues - used for the short-term treatment of ovulatory
DUB before endometrial ablation. Also used for the shrinkage of
fibroids before surgery.
Mirena coil (progestogerone-containing IUCDs) - are effective in
dysfunctional uterine bleeding; evidence that treatment with a
progesterone-containing IUCD can lead to a reduction in fibroid
volume following 6-18 months of use (3)
Hormone replacement therapy - may be considered if the woman
experiences climacteric symptoms with ovulatory or anovulatory
bleeding

Surgical Treatment
Surgical options for menorrhagia can be divided into hysterectomy or
endometrial ablation.
Hysterectomy - with conservation of the ovaries; occasionally the
ovaries are also removed e.g. if the patient is over 45 years of age and
elects to have removal of ovaries to protect against ovarian carcinoma.

Advantages (1) Hysterectomy generally cures menorrhagia, (2) No

requirement for contraception post-procedure, and (3) risk of
cervical and endometrial cancer is removed (if total hysterectomy
undertaken).
Disadvantages - operation is longer than with endometrial
destruction techniques, hospital stay and return to work is longer
than with endometrial destruction, risks of complications higher;
also if subtotal hysterectomy is performed then the patient will still
be at risk of cervical cancer and require cervical smears.

Endometrial ablation - Menorrhagia can be treated by removal of

the endometrial layer of the uterus. This can be achieved by
destruction of the basal layer, so preventing menstruation. Endometrial
ablation can be carried out by:

transcervical resection of the endometrium

laser ablation
rollerball coagulation
radiofrequency-induced thermal ablation

In comparison with a hysterectomy - there is conservation of the

uterus, there is a smaller risk of complications, operating time is
shorter, there is a shorter hospital stay and the patient returns to work
sooner

NON-MENSTRUAL BLEEDING
Non-cyclical, patternless vaginal bleeding is often described as
metrorrhagia. A useful classification is as:

postcoital bleeding
intermenstrual bleeding
postmenopausal bleeding

The implication is that of a local lesion and the possibility of

malignancy must be always be considered. However, non-focal causes
are common, for example:

abortion - especially in a young woman

dysfunctional uterine bleeding
break-through bleeding due to the progestogen only pill

Assessment may be approached through history, systematic examination, diagnostic

curettage, and biopsy of any visible lesion.

POSTCOITAL BLEEDING
Post-coital bleeding is more likely to originate from the vagina or cervix
than the endometrium. This symptom is the classical symptom of
cervical carcinoma.
Causes include:

vaginal:
o vaginitis
o carcinoma - very rare
cervix:
o cervicitis
o polyps
o carcinoma - the most likely malignant cause of postcoital
bleeding
o trauma - even quite minor lesions may cause severe
postcoital bleeding if co-existent coagulation disorder
o ectropion

INTERMENSTRUAL BLEEDING
Intermenstrual bleeding is defined as bleeding from the vagina at any
time in the menstrual cycle other than normal menstruation.
Etiology - Causes include:

an ectropion which bleeds spontaneously or after intercourse

in low grade infection
cervical polyps or cancer
endometrial polyps or cancer

underdosing with the contraceptive pill causing breakthrough

bleeding.
o too low a prescription
o concurrent antiepileptic treatment
o diarrhoea
anovulatory uterine bleeding
intrauterine contraceptive device - may act as an irritant
progestogen only pill - disturbs hormone levels in some patients
contraceptive injection e.g. depoprovera

Assessment of intermenstrual bleeding - This section outlines

some considerations in the assessment and investigation of IMB.
History:

Are there any features suggestive of anovulatory bleeding? e.g.

painless, irregular menstruation
Is the patient taking the oral contraceptive pill?
Is the intermenstrual bleeding a recent phenomena?
Does the patient suffer from post-coital bleeding and/or
menorrhagia?

Examination:

Speculum will any lesions of the cervix and vaginal mucosa.

Bimanual examination will reveal any pathology of the uterus.

Investigation:

Blood tests (Full blood count, clotting studies, thyroid function

tests) if indicated from history. FSH/LH if the patient is suspected
to be perimenopausal.
Pregnancy test should be considered
Cervical smear if indicated
Consider a pelvic ultrasound
Hysteroscopy and endometrial biopsy is indicated in cases where
the woman is over 40 years of age. In women less than 40 years
old then a hysteroscopy is not generally used as first line
management.

Treatment
This is dependent on cause.
If a patient is suffering from intermenstrual bleeding whilst on the oral
contraceptive pill, then taking two pills on the days when the

breakthrough bleeding is occurring, or changing to a stronger pill

preparation, may resolve the problem.

POSTMENOPAUSAL BLEEDING
This is defined as bleeding from the vagina six months after the last
period. Any post-menopausal bleeding should be assumed to be to
endometrial carcinoma until proved otherwise.
Etiology - Possible causes of postmenopausal bleeding include:

exogenous oestrogens
atrophic endometritis and vaginitis
endometrial and cervical carcinoma
endometrial or cervical polyps, and endometrial hyperplasia
ring pessary
ovarian oestrogen secreting tumour

Assessment of postmenopausal bleeding: - General points are

listed below:
History:

last menstrual period?

bleeding
o like a period?
o associated with intercourse?
o previous episodes?
vaginal discharge
o any features suggestive of infection?
last cervical smear
drug history
o on HRT that is not designed to have cyclical bleeding?
o previous use of oral contraceptive pill?
obstetric history
o nulliparity associated with endometrial carcinoma
functional enquiry - any recent unexplained weight loss, loss of
appetite

Investigation:
All cases must be thoroughly investigated (except perhaps for
withdrawal bleeding which occurs at the expected time in menopausal
women taking HRT).

Investigations must include

Complete abdominal and pelvic examination.

Cervical smear.
Endometrial biopsy.
In general hysteroscopy is indicated.

Treatment:
This is dependent on cause.

36
INCONTINENCE OF URINE IN WOMEN

Urinary incontinence in women is "a condition in which involuntary loss

of urine is a social or hygienic problem and is objectively
demonstrable." Urinary incontinence can be thought of as a symptom
as reported by the patient, as a sign that is demonstrable on
examination, and as a disorder. The affected individual may experience
a decrease in social interactions, excursions out of the home, and
sexual activity. Embarrassment and depression are common.
Contributing factors with regard to age-related increases in urinary
incontinence include a weakening of connective tissue, and
genitourinary atrophy due to hypoestrogenism, Urinary incontinence in
women, which are age related, can either be stress or urge
incontinence. Stress incontinence tends to be more common in women
younger than 65 years. In women older than 65 years, urge
incontinence and mixed (i.e. urge and stress) incontinence are more
common.

TYPES OF URINARY INCONTINENCE

There are four types of urinary incontinence: (1) true, (2) overflow, (3)
urgency, and (4) stress.

True incontinence In this condition the involuntary loss of urine is

due to a defect in the anatomical integrity of the urinary tract. The
urine flows continuously by day and by night. It is caused by some
form of urinary tract fistula, either acquired or developmental.
Overflow incontinence Is the involuntary loss of urine when the
intravesical pressure exceeds maximum urethral pressure due to
bladder distension and in the absence of detrusor activity.
Its
mechanism is not certain but presumably the overdistension of the
bladder pulls open the internal sphincter.
Urgency incontinence Is the involuntary loss of urine associated
with a strong desire to micturate. The sphincter mechanism is normal
but is overpowered by abnormal activity of the bladder muscle.
Stress incontinence is the involuntary loss of urine when the intraabdominal pressure is raised by a sudden movement, coughing,
laughing, sneezing, walking and even in the change of position in the
absence of detrusor activity. In this condition the urethral sphincter
mechanism is faulty.

ETIOLOGY
Urinary incontinence in women may be classified according to whether
it is urethral or extraurethral leakage (Table 1)

ETIOLOGY OF URINARY INCONTINENCE

Urethral causes
Incompetence urethral sphincter
mechanism (stress incontinence)
Uninhibited detrusor activity (urge
incontinence)

Extraurethral causes
Fistula
-

Ureterovaginal fistula

Vesicovaginal fistula

Retention with overflow

Table.1 Etiology of urinary incontinence

STRESS INCONTINENCE
This has a gradual onset. It is precipitated by sudden unexpected
activity causing rise of intra-abdominal pressure such as jumping,
coughing, sneezing, and carrying heavy weights. Urine leakage usually
coincides exactly with the stress, starting and stopping abruptly with
the rise and fall of intra-abdominal pressure.
Symptom: The patient complaint of frequent and repeated involuntary
loss of a small amount of urine during exercise, coughing, laughing,
sneezing, walking or change of position. The symptoms are usually
worse on standing and reduced when sitting or lying flat.
Sign: Examination may reveal evidence of vulva inflammation and an
ammonical odour. Urine loss is easily demonstrated as dribble,
squirting occurring synchronously with a cough in standing or in the
lying position. Elevation of the bladder neck should reduce this loss
(Bonney test).
Condition: The involuntary loss of urine when the intravesical
pressure exceeds the maximum urethral pressure in the absence of
detrusor activity.
Etiology: The basic lesion is descent and weakness of the bladder
neck and damage to the urethral sphincter mechanism. The causes of
stress incontinence are as follows:
1) Obstetrical and other injuries A direct injury in the region of the
urethrovesical junction can lead to failure of the internal
sphincter. Childbirth is the commonest predisposing cause and it
may be assumed that the supports of the urethra and bladder
neck are damaged during delivery.
2) Post-menopause Stress incontinence may not make its
appearance till after the menopause when there is atrophy of the
smooth muscle components of the bladder neck and urethra.
3) Genital prolapse Although sphincter incompetent and urethral
atony are sometimes evidenced by urethrocoele, prolapse itself
does not cause stress incontinence.
4) Other predisposing causes include obesity, chronic cough,
abdominal tumours and urinary tract infections.
Pathophysiology: During episodes of stress incontinence, the
generated intra-abdominal pressure causes a coincident rise in
intravesical pressure. The rise in intravesical pressure is greater than

the rise in urethral pressure. Urethral resistance is overcome, resulting

in leakage. Leakage ceases when bladder pressure again falls below
urethral pressure.
Most cases of stress incontinence are believed to be related to damage
to the neuromuscular functioning of the pelvic floor, coupled with
injury, both remote and ongoing, to the connective tissue supports of
the urethra and bladder neck. Loss of intrinsic urethral tone also may
be involved in the pathologic picture. Neuromuscular damage to the
voluntary striated urethral sphincter is believed to be the main cause,
but mucosal atrophy, hypovascularity, and local scarring also may be
involved.
Two defects are thought to be involved in the mechanism of stress
incontinence. The first is that the proximal urethra has been displaced
downwards through the urogenital diaphragm. When the abdominal
pressure rises, as a woman sneezes, coughs or walking, the pressure it
is not transmitted to the urethra, with the result that the intravesical
pressure rises while the intraurethral pressure does not.
The second mechanism is that either because of defective
development of the supporting muscles, or damage to the bladder
neck support during childbirth, when the bladder is at rest its base is
funneled, not flat. This impairs the normal closure mechanism at the
urethro-vesical junction.
Diagnosis: The diagnosis of stress incontinence rests primarily on the
facts that the leakage of urine occur relatively small amount when the
woman laughs, sneezes or cough. The leak can be confirmed when
she is asked to cough when she has a full bladder.

URGE INCONTINENCE
Urge incontinence is the involuntary loss of urine associated with
strong desire to micturate. It can be divided into motor urgency
associated with uninhibited detrusor contracts and sensory urgency
due to irritative lesions in which the detrusor is stable. There may be a
background of anxiety, tension, depression, or occasionally lumbar disc
lesions or radical pelvic sugery.
Symptoms: The presenting symptoms include frequency, urgency and
urge incontinence. These tend to fluctuate in severity and are quite
often worse in the morning and better in the evening. Urine leakage
may be triggered by sudden movement and is commonly preceded by

desire to void which cannot be suppressed. The urine loss is large

amount and more prolonged that that encountered in stress
incontinence.
Signs: There are no special signs.
Pathophysiolog: In urge incontinence, the sphincter mechanism is
normal but is overpowered by abnormal activity of the bladder, the
detrusor muscle of which is hypertonic, oversensitive or outside the
voluntary control of the central nervous system. Ordinarily the patient
is continent but, once she experiences a desire to void, the bladder
escapes from inhibition and contracts so strongly that it opens its
urethral sphincters. So immediately after the urge the women has to
run to avoid an accident. If she is too late, the bladder empties itself
in part or whole.
Diagnosis: The diagnosis of urge incontinence rest primarily on the
facts that the leakage of urine occurs in relatively large amounts and is
heralded by a desire to void. Confirm of detrusor instability is by
urodynamic studies.

Table 2 - INCONTINENCE OF URINE IN FEMALE

STRESS INCONTINENCE

URGE INCONTINENCE

Loss of urine due to

Increase in intra-abdominal pressure,

e.g. coughing, sneezing, laughing

An involuntary bladder contractions

Symptoms

Symptoms include loss of urine with

cough, laugh, sneeze, running, lifting,
walking

Complaints of urgency, frequency,

inability to reach the toilet in time, up
a lot at night to use the toilet

Etiology

Caused by pelvic floor damage and

weakness or weak sphincter(s)

Over activity of the bladder detrusor

muscle due to multiple triggers

Bladder function

Normal

Abnormal

Amount of urine loss

Repeated and frequent small leak

Leakage of urine is relatively large

amount and prolonged

CLINICAL
ASSESSMENT
INCONTINENCE

OF

PATIENT

WITH

A woman presenting with a complaint of urinary incontinence requires

careful examination.
History
The clinical presentation of urinary incontinence can be varied in many
respects. Patient complaints may be minor and situational or severe,
constant, and debilitating. When obtaining a clinical history,
determining whether the problem is a social and/or hygienic problem
and the degree of disability attributable to the incontinence also is
important. In addition, the following points regarding the clinical
presentation should be sought when obtaining the history:

Severity and quantity of urine lost and frequency of incontinence

episodes
Duration of the complaint and whether problems have been
worsening
Triggering factors or events (e.g. cough, sneeze, lifting, bending,
feeling of urgency, sexual activity/orgasm)
Constant versus intermittent urine loss and provocation by
minimal increases in intra-abdominal pressure, such as
movement, changes in position, and incontinence with an empty
bladder
Associated frequency, urgency, dysuria, pain with a full bladder,
and history of urinary tract infections
Concomitant symptoms of fecal incontinence or pelvic organ
prolapse, such as pelvic pressure, feeling of protrusion, sacral
backache, vaginal splinting for bowel movements, chronic
constipation, urinary hesitancy, and poor stream
Coexistent complicating or exacerbating medical problems, such
as chronic cough, obstructive lung disease, diabetes, obesity,
connective tissue disorders, postmenopausal hypoestrogenism,
CNS or spinal cord disorders, chronic urinary tract infections, and
urinary tract stones
Obstetrical history, including difficult deliveries, grand
multiparity, forceps use, obstetrical lacerations, and large babies
History of pelvic surgery, especially prior incontinence
procedures, hysterectomy, or pelvic floor reconstructive
procedures
Other urologic procedures
Spinal and CNS surgery
Lifestyle issues, such as smoking, alcohol or caffeine abuse, and
occupational and recreational factors causing severe or repetitive
increases in intra-abdominal pressure
Medications, such as cholinergic or anticholinergic drugs, alphablockers, over-the-counter allergy medications, estrogen

replacement, beta-mimetics,
diuretics, and ACE inhibitors.

sedatives,

muscle

relaxants,

Many cases of urinary incontinence present as a gradually progressive

disorder. Progression from very mild symptoms to more severe and
debilitating urine loss may take many years. The patient may come to
medical attention only after experiencing a progressive worsening of
symptoms. In other patients, symptoms may appear suddenly and may
or may not be associated with a specific inciting event, such as
pelvic/urinary tract surgery, trauma, and genitourinary tract infection.
In these instances especially, associated symptoms such as pelvic
pain, urgency, frequency, dysuria, and hematuria may point to a
specific etiology.

Physical examination
A focused physical examination should be performed. The examination
is tailored somewhat in each case, based on the specifics of the
patient's incontinence complaint and pertinent medical and surgical
history. Each patient should have height, weight, blood pressure, and
pulse recorded. Obesity is an important contributor to stress
incontinence, and the presence of obesity may influence management
decisions. Urinalysis and culture tests should be sent.
The general physical examination is tailored to each individual
patient. Medical illnesses and comorbidities that may be contributing
to the overall incontinence disorder should be sought. Cardiac and
pulmonary evaluation can be important. The abdomen should be
examined for surgical scars, hernias, masses, and organomegaly. The
presence of hernias may indicate inherent connective tissue weakness,
a possible contributor to incontinence. Masses may contribute to stress
incontinence and, occasionally, may cause obstructed voiding with
resultant overflow incontinence. The back and costovertebral angles
should be inspected and palpated. Tenderness, deformity, or the
presence of surgical scars should prompt further investigation.
Because neurologic disorders can cause or exacerbate urinary
incontinence, a focused neurologic examination should be a part of
every incontinence evaluation. Much information can be gained from
simple conversation with the patient (e.g. mental status) and
observation of gait (e.g. CNS, spinal cord, peripheral nervous system
disease). Any abnormalities
should
prompt
more
in-depth
investigations. Strength, sensation, and deep tendon reflexes of the

lower extremities should be tested. Sensation of the perineum and

perianal area should be tested with a soft touch and light prick
The pelvic floor examination is an integral part of the incontinence
evaluation. In female patients, in particular, incontinence disorders
often coexist with pelvic floor relaxation. If a surgical approach to the
incontinence is chosen, other pelvic floor defects of significance can be
treated simultaneously. The examination begins with inspection of the
external genitalia and urethral meatus. Evidence of atrophy, such as
pallor and thinness of tissue, may indicate estrogen deficiency. A red,
fleshy lesion of the posterior urethra, a caruncle, may be another
indicator of urogenital hypoestrogenism. The suburethral area should
be inspected and palpated. A suburethral mass should raise suspicion
for a urethral diverticulum.
Other signs of a diverticulum might include tenderness and purulent or
watery discharge upon compression. Urethral and trigonal tenderness
also may indicate urethritis, urethral syndrome, or intersitial cystitis.
The vaginal mucosa should be inspected for pallor, thinning, loss of
rugae, and other signs of hypoestrogenism. If clinically suspected, a
fistula opening may be discovered during vaginal examination. At
times, pooling of fluid, exudate, or granulation tissue may indicate a
nearby fistula tract.
A detailed pelvic floor examination should be performed for signs of
pelvic organ prolapse. A systematic examination is conducted for
cystocele, rectocele, uterine or vaginal prolapse, enterocele, and
perineal laxity. A bivalve (Cusco) speculum should be used to visualize
the cervix or vaginal apex. With the patient straining maximally, the
speculum is withdrawn slowly, and any descent of the cervix or vaginal
cuff is noted. The speculum is then disarticulated, and a single blade
speculum (Sims speculum) examination is performed, inspecting the
anterior vaginal wall during straining with the posterior wall retracted.
Next, attention is turned to the posterior vaginal wall. The Sims
speculum is used to retract the anterior wall of the vagina, while the
posterior wall is examined during Valsalva maneuver. The presence or
absence of a rectocele should be noted. If a double bump is observed
when the patient strains, an enterocele may be present in addition to
the rectocele.
Next, the levator muscles are palpated, and the resting tone is noted.
Then, the patient is instructed to squeeze the examining fingers, and
the levator strength can be appreciated. A rectovaginal examination is
performed to determine the thickness of the rectovaginal septum. The
patient then is asked to strain. Tissue felt sliding through the

examining fingers may indicate an enterocele. Resting and squeezing

rectal sphincter tone is noted. As the rectal finger is withdrawn, the
external anal sphincter should be palpated between this finger and the
thumb. The absence or attenuation of this body of muscle indicates a
sphincter laceration

Stress testing
Stress testing should be performed with a full bladder. The patient is
asked to cough forcefully and repetitively. Alternatively, the patient
may perform a strong Valsalva maneuver. Urine loss directly observed
from the urethral meatus at the peak of the increase in intra-abdominal
pressure is strongly suggestive of stress incontinence.
Generally, the patient with stress incontinence displays immediate
urine loss of relatively short duration. A few drops to a squirt of urine
characteristically are lost. Delayed loss or prolonged loss raises the
question of stress-induced detrusor instability. If no urine loss is
observed, the test can be repeated. If more than mild pelvic organ
prolapse is present, reduction of the prolapse should be performed with
a a pessary, or the examining fingers during the stress test. Care must
be taken not to compress the urethra, regardless of which reduction
method is employed.
Positive stress test findings in the supine position with a relatively
empty bladder and with position change or other minimal increases in
intra-abdominal pressure raise the question of intrinsic sphincter
deficiency. Complex urodynamic testing would be indicated.

Grading urinary incontinence

The results of the history and physical examination provide the
informations that guide the ongoing evaluation. Part of the information
available at this point is an estimation of the degree of incontinence
experienced by the patient. In the 1970s, Stamey devised a grading
system based on the degree of incontinence. Such a system, as
outlined below, can prove to be useful in both the clinical and research
settings.

Grade 0 Continent.
Grade 1 - Loss of urine with sudden increases in abdominal
pressure, not in bed at night.

Grade 2 - Incontinence worsens with lesser degree of physical

stress.
Grade 3 - Incontinence with walking, standing erect from sitting
position, or sitting up in bed.
Grade 4 - Total incontinence occurs and urine is lost without
relation to physical activity or position.

Laboratory Investigations:

Urinalysis and urine culture

o

Urinary tract infections can cause or contribute to urinary

incontinence disorders in several ways. Local inflammation
can serve as a bladder irritant, causing uninhibited bladder
contractions. Endotoxins produced by some bacterial
strains can have an alpha-blocking effect on the urethral
sphincter, thereby lowering intraurethral pressures.

Postmenopausal women are especially susceptible to these

effects on the urethra and bladder. Hypoestrogenism may
enhance the effects. Urinart tract infections may present in
postmenopausal women without the classic symptoms of
irritation and pain. The predominant symptom in some
patients may be the onset or the worsening of urinary
incontinence.

Colony counts of less than 10 5 may be of significance in

postmenopausal women and should be treated. Evidence
of inflammation through urinalysis may be mild or entirely
lacking despite bacterial growth from a culture. Women
who are tested for urinary incontinence generally are
recommended to have a screening urinalysis, and
postmenopausal women also should have a urine culture.

Imaging Studies:

Fluoroscopy and video urodynamics

o

Fluoroscopic video urodynamics has become the

investigative technique of choice for incontinence in many
referral and research centers. This technique involves the
simultaneous display of real-time images of the bladder

neck and urethra and cystometric summaries of bladder,

intra-abdominal, and, in some cases, urethral pressures.
o

The precise placement of pressure transducers and a

constant understanding of their exact anatomic location is
one of the advantages of this technique. Another
advantage is the ability to fluoroscopically observe the
bladder neck area throughout bladder filling and during
stress maneuvers. Contrast material can be observed
entering the proximal urethra just before leakage; thus,
leak point pressure findings can be more precise. Cough
profiles and pressure transmission ratios can be
determined. The physical location of the transducer tip can
be observed during urethral pressure profilometry and
correlated with the pressure findings. Although probably
not necessary for the evaluation of straightforward stress
incontinence, video urodynamics can be a valuable
diagnostic tool in complex or confusing cases.

Cystourethrography
o

Antegrade or retrograde cystourethrography is a useful

adjunct to incontinence workups in situations where
urinary tract fistulas are suspected.

Voiding cystourethrography may reveal urethrovaginal

fistulas and urethral diverticula.

Intravenous pyelography
o

Intravenous pyelography (IVP) may be useful in defining

the course and caliber of the ureter preoperatively in cases
of stress incontinence and coexisting severe apical or
anterior vaginal wall prolapse.

An IVP also can help differentiate between ureterovaginal

and vesicovaginal fistulas. Finally, if suspecting ureteral
obstruction following incontinence surgery, an IVP is
indicated.

Other Tests:

Electromyography
o

Electromyography (EMG) is a type of neurophysiologic

testing. EMG studies have several potential roles in the
evaluation of patients with urinary incontinence.

Measurement of the striated muscle activity within the

urethral sphincter mechanism and nerve conduction times
in nerves supplying the sphincter mechanism and the
pelvic floor, is useful in the diagnosis of neurophatic
bladder disorders.

Diagnostic Procedures:
Urodynamic studies

If the diagnosis is still uncertain the woman should be asked to

attend urodynamic studies by uroflowmetry and cystometry.
Urodynamics is the study of hydrodynamics and muscle activity
for the purpose of defining the functional status of the lower
urinary tract. The ultimate goal of urodynamics is to aid in the
correct diagnosis based on pathophysiology.
Urodynamic studies should assess both the filling-storage phase
and the voiding phase of bladder and urethral function.
Urodynamic testing is expensive and requires specialized
equipment and expertise.
Before urodynamic testing, the urine should be free from
bacteria or evidence of inflammation.

Uroflowmetry
o

Uroflowmetry is a method of measuring urine volume passed per unit time. The
simplest method uses a stopwatch and a commode that is equipped to measure
urine volume. More complicated devices use the increasing weight of the urine
over time to determine flow rates. Note that flow rates are dependent on voided
volume. Uroflow studies should be performed with a minimum of 150-200 mL in
the bladder.

o Urine flow rates are a product of detrusor contraction strength,

urethral resistance, and, in some instances, the contribution of

abdominal straining. Normal flow curves are bell shaped and

display a rapid rise to peak flow (maximum flow rate exceeding
15 ml/s for a voided volume of at least 150 ml), a short duration
of peak flow, and a rapid fall.
o Decreased detrusor contractility, outlet obstruction, or a
combination of both may be responsible for low flows. In women,
aging by itself results in little or no drop in flow rates.
o Factors such as pelvic organ prolapse, stress incontinence,
increased parity, and, perhaps, hypoestrogenism are far more
predictive of decrease flow rates.
o Flow patterns generally do not point to a specific urodynamic
diagnosis, although some associations have been noted.
Detrusor instability often is associated with high flow rates,
although the opposite can be true. In patients with aging
bladders or in the early stages of neuropathy, detrusor instability
may coexist with detrusor hypofunctioning. Stress incontinence
sometimes is associated with low flow rates.

Cystometry
o Cystometry is a technique of assessing the filling phase of
bladder function. Much information can be gained during
cystometry, including the diagnosis of bladder instability,
sensory-urgency syndrome, sensory neuropathy, loss of
compliance, and determination of bladder capacities.
o In addition, leak point pressures and cough stress tests can be
performed during cystometry, and pressure-flow studies can be
performed if the cystometry catheters are left in place during
uroflow studies.
o The simplest forms of cystometry can be performed with a
catheter and syringe or manometer held 15 cm above the pubic
bone. This inexpensive and readily available method may be
adequate for screening in uncomplicated cases but may miss
subtle findings.
o Single-channel cystometry consists of recording isolated
intravesical pressures during filling with a single catheter. With
this method, increases in intra-abdominal pressure cannot
always be differentiated from increases in true detrusor pressure.
Multichannel cystometry is performed with a bladder catheter
and a second catheter to approximate intra-abdominal pressure.
The second catheter can be placed in the rectum or vagina. In
cases of severe pelvic organ prolapse, a rectal catheter may
perform more reliably.

o The summary consists of a vesicle pressure channel, an

abdominal pressure channel, and true detrusor pressure channel.
The true detrusor pressure channel, also called the subtracted
channel, is the bladder pressure minus the abdominal pressure.
Depending on the individual set up, additional channels may
accommodate simultaneous urethral pressure readings and
continuous EMG readings.
o Patient position during testing varies in the literature, but, most
commonly, the patient is sitting, semierect, or standing. The
catheters generally are calibrated so that zero corresponds to
atmospheric pressure. A complete cystometric evaluation
monitors the filling-storage segment and emptying segment of
bladder function.
o For clinical purposes, the emphasis often is on the filling-storage
segment. During filling, normally, detrusor pressure does not
rise. This finding reflects the compliance of the bladder. With
rapid filling rates, a small-to-moderate increase in pressure may
be noted. The 4 recognized cystometric phases of bladder
function are described below. The first 3 of these phases make
up the filling-storage segment of bladder function. The last phase
represents the emptying segment. The 4 phases are as follows:
1) Initial small increase in intravesical pressure at the
beginning of filling
2) Stable pressure that comprises the majority of the filling
phase
3) Terminal rise in pressure at bladder capacity representing
the limit of viscoelastic expansion: In a clinical setting, this
phase often is not reached due to patient discomfort.
4) Voiding phase with an inconsistently observed small
increase in intravesical pressure
o Bladder sensation and capacity can be measured during filling
cystometry. The first sensation is described as the volume at
which the patient first is aware of fluid in the bladder (reference
range of 50-150 mL). The second sensation (full) has been
described as the volume at which the individual normally would
consider voiding due to an urge sensation (reference range of
200-400 mL). Maximum capacity is when the patient is
experiencing pain and does not allow continued filling (reference
range of 400-600+ mL).
o Low bladder capacities can be observed with urinary tract
infections, sensory-urgency syndrome, interstitial cystitis,
detrusor instability, and stress incontinence. Increased capacity
can be observed with a neurogenic bladder.

o Low-compliance bladders are demonstrated through cytometry

by a slowly rising bladder pressure through all or most of the
filling segment. Compliance problems can be due to chronic
infection, fibrosis, cancer, radiation effect, and inflammation from
long-term indwelling catheters.
o Any bladder contraction during filling is considered abnormal.

Pad testing
Pad testing is a method of verifying, objectifying, and quantifying
incontinence episodes. Many different test protocols have been
described.
Short-term tests generally involve the subject drinking a known volume
of liquid or undergoing retrograde filling of the bladder. A preweighed
sanitary pad is applied. The individual is instructed to perform specific
activities such as coughing, running in place, bending and lifting, or
hand washing. The testing interval can range from 15 minutes to 2
hours. At the end of the test period, the pad is removed and weighed.
Long-term tests are conducted under normal living conditions for 24-48
hours. Each pad is preweighed and then weighed again after use.

TREATMENT
Innumerable methods, both surgical and medical, have been described
for the treatment of incontinent women.
URETHRAL INCOMPETENCE (STRESS INCONTINENCE)
In this distressing condition the aim is to either reduce the intraabdominal pressure (which can sometimes be achieved by loss of
weight, careful choice of recreational and social activities, and
treatment of upper respiratory tract disease) or increase in the
intrauretheral pressure by the following methods:

1. Strengthening the pelvic floor musculature through physiotherapy

and electrical stimulation.
2. Surgically restoring the proximal urethral to a position above the
pelvic floor so that it is compressed by sudden rises of intraabdominal pressure.
3. Elongation and at the same time narrowing the urethral lumen by
surgical or mechanical elevation.

Medical therapy for stress incontinence:

Medical therapy of stress urinary incontinence can include
pharmacology therapy, behavioral therapy, pelvic floor conditioning,
pelvic floor stimulation, bladder training, and treatment of medical
problems. Some experts recommend a trial of medical therapy before
considering surgical treatment. Others believe that if the incontinence
is severe and correctable by surgical means, a trial of medical therapy
is not mandatory and does not need to be performed if the informed
patient chooses to proceed directly to surgery.
Pharmacologic therapy:
Alpha agonists may improve symptoms of mild stress incontinence
by increasing intrinsic urethral tone due to effects on the urethral
sphincter.
Imipramine, which has both alpha-agonist and
anticholinergic effects, has been shown to have moderate efficacy (6071%) in treating stress incontinence. Imipramine appears to work by
increasing both urethral closure pressure and functional urethral
length.
Estrogen therapy may have several positive effects in patients who
are estrogen deficient with stress incontinence. Estrogen may increase
the density of alpha-receptors in the urethra. In addition, the
vascularity of the urethral mucosa is increased and the coaptive
abilities of the urethral mucosa may be augmented. Estrogen therapy
is used best as an adjunct to other medical treatments or surgery. As a
sole treatment modality for genuine stress incontinence, studies have
shown that estrogen therapy has either no or only marginal clinical
benefit. Local urogenital treatment provides more rapid and reliable
effects and may be especially helpful as a preoperative adjunct.

Pelvic floor rehabilitation:

Kegel exercises have been shown to improve the strength and tone
of the muscles of the pelvic floor. During times of increased intraabdominal pressure, tensing of these muscles tightens the connective
tissue supports surrounding the urethra. Thus, pressure transmission to
the urethra may increase, and the urethra compresses shut during
times of increased stress. The exercises consist of voluntary
contractions of the muscles of the pelvic floor. Because both fast-twitch
and slow-twitch muscle fibers are found in the levator ani complex,
both rapid contractions and slow contractions held for maximal
duration should be performed to achieve the best possible results.
The patient can confirm that she is using the correct muscles at home
by periodically performing the contractions during voiding with the
goal of interrupting the urinary stream. Approximately 6-12 weeks of
exercises are required before improvement is noted. Patients with
severe neuromuscular damage to the pelvic floor may not be able to
perform Kegel exercises even with proper instruction.
Vaginal cones are weighted devices designed to increase the strength
of the pelvic floor muscles. Typically, the cones are retained for 15
minutes twice a day, and the weight of the cones is gradually
increased. Although probably no more efficacious than properly
performed Kegel exercises, this method may be preferred by some
individuals.

Behavioral approaches:
Timed, frequent voiding can be employed to minimize incontinence,
especially if the bladder is kept empty before incontinence-producing
activities. Symptoms of urgency and frequency can develop over time
with this strategy due to decreased bladder capacity. Anticipatory
pelvic floor contractions can be taught to patients to cut down on
incontinence episodes. The patient is taught to perform a strong pelvic
floor contraction just before anticipated episodes of increased intraabdominal pressure, such as a cough or a sneeze. Modifying activities
occasionally can be a solution to incontinence-related specific
activities. For example, if a woman experiences incontinence only
during high-impact aerobics, substitution of another fitness activity,
such as swimming, may solve the incontinence problem.

Treatment of medical problems:

As previously discussed, disease treatment, including weight loss,

smoking cessation, control of asthma, and chronic constipation, may
minimize incontinence episodes. A few studies show significant
decreases in urinary incontinence in small cohorts of women
experiencing weight loss.

Surgical Treatment For Stress Incontinence

Surgical treatment of stress urinary incontinence is indicated if the
patient desires surgical correction, if the problem is perceived as a
significant social and/or hygienic problem, and the incontinence is
demonstrable and of a type that is amenable to surgery.
Procedures for stress incontinence, although varied in terms of
approach, share the common goal of stabilizing the bladder neck and
proximal urethra. Over 250 procedures, some of which are
modifications of older procedures, have been devised. Only a few
procedures have been shown to yield good result. Many others have
been disregarded due to poor long-term efficacy, technical difficulties
in performance, and/or unacceptable complication rates.

Preoperative details:
Selection of the surgical procedure
The success or failure of incontinence surgery largely depends on
selecting the appropriate procedure for the appropriate patient. A
correct diagnosis with knowledge of the pathophysiology in each
individual case is the cornerstone of planning good surgical therapy. A
patient history and a physical examination are helpful but should not
be relied upon exclusively when planning stress incontinence surgery.
Urodynamic studies can help narrow the diagnostic focus further but
are not perfect tests for various reasons. A large percentage of surgical
failures may be related to an incorrect or incomplete diagnosis. The
following are other factors that may influence the type of surgery
chosen and the specific approach:

The need to perform other indicated procedures: A vaginal

approach may be chosen if other vaginal pelvic floor repairs are
to be performed. An abdominal approach may be favored in
cases requiring abdominal exploration for other reasons.
Body habitus/obesity
Previous surgical approaches/failures, previous scars

Age and medical condition of the patient: A patient who is frail

may be less tolerant of a prolonged procedure, and an abdominal
approach may potentially result in more postoperative morbidity.
Experience and skill of the surgeon
Medical problems (e.g. chronic obstructive pulmonary disease,
chronic cough, chronic constipation)
Unexpected intraoperative findings or conditions

Preoperative preparation
Appropriate preoperative preparation of the patient may enhance the
positive results of a well-performed incontinence procedure. The
following are important points to be considered preoperatively:

Estrogen replacement therapy may enhance urethral, bladder,

and vaginal tissue integrity. Estrogen replacement can improve
surgical healing; augment the effect of the procedure on urethral
competency; and, ultimately, translate into better surgical
outcomes.
Replacement
therapy
should
be
continued
postoperatively.
Smoking cessation reduces chronic cough, improves the
condition of connective tissue, and enhances the effect of
endogenous or pharmacologic estrogen.
Treatment of contributing medical problems.
Weight loss in cases of obesity.
Good nutrition helps to maximize tissue integrity and to support
good healing. Vitamin C, in particular, may be important in
wound healing and connective tissue quality.
A preoperative commitment on the part of the patient to
decrease postoperative activity is vital; the patient cannot
engage in any heavy lifting or straining for at least 12 weeks.

A thorough discussion of risks, benefits, anticipated success rates, and

potential common complications should be undertaken. A discussion of
the possible need for prolonged postoperative bladder drainage is
important.
SURGICAL PROCEDURES
Primary suprapubic procedures are reported to have success rates of
80 to 90 percent. Among them are:
Anterior colporrhaphy with or without Kelly sutures have been
traditionally a gynaecological procedure. It is usually recommended
when the bladder neck descends more than 4 cm below the inferior

border or the pubic symphysis. This technique has advantage of a

low incidence of complications and it allows simultaneous correction
of other forms of uterovaginal prolapse. Unfortunately there is long
term recurrence.

Colposuspension by the Burch technique in which the bladder

neck and anterior vaginal wall are elevated by suturing the paravaginal fascia to the ipsilateral ileopectineal ligament.
An
advantage is that the bladder neck is elevated to a high level and
fixed to immobile structures such as the pubis symphysis.
Urethropexy
by
the
Marshall-Marchetti
and
Krantz
technique. Elevation of the bladder neck is achieved by suturing
the para-urethral and para-vesical tissues to the cartilage of the
symphysis pubis or periosteum of the pelvic ramus.
Suburethral sling procedures - Sling procedures of various types
are among the oldest and most successful procedures for
incontinence. In 1942, Aldridge described his classic rectus fascial
sling procedure. He developed strips of rectus fascia that were left
attached in the midline. These strips of fascia were tunneled
through the retropubic space and delivered to the suburethral area
that previously had been exposed via a vaginal incision. The strips
were sutured in the midline under the bladder neck.
Modern sling procedures are based on this procedure. Various
materials have been used, ranging from a host of permanent
synthetic materials, cadaveric donor fascia, and endogenous rectus
fascia to fascia lata and vaginal wall materials.

Tension-free vaginal tape

This technique uses a thin strip of Prolene mesh with barbed edges to
serve as artificial pubourethral ligaments. Both ends of the tape are
attached to sharp curved trocars. After minimal suburethral and
periurethral dissection is performed transvaginally, the trocars are
tunneled in the periurethral area, under the pubic ramus and through
the space of Retzius. The trocars are delivered through 2 small
transverse incisions just above the pubic bone.
The central body of the mesh should be located at the mid urethra,
although some experts believe that the final location usually is closer

to the proximal urethra and urethrovesical junction. When the sling

ends are visible through the abdominal incisions, they are grasped with
clamps, and the trocars are released. The plastic encasement then can
be released in the middle, and the 2 pieces can be pulled up and out
through the abdominal incisions. The plastic is intended to minimize
contamination of the mesh with vaginal bacteria and to aid in sliding
the tape into place. Cystoscopic inspection of the urethra and bladder
should be performed, looking for injury and foreign material.
To facilitate adjustment of sling tension, performing the procedure
under local anesthesia and sedation is recommended. The awake
patient is asked to cough repetitively, while tension on the sling arms is
increased until stress-induced leakage is eliminated. At this point, the
sling arms are trimmed flush with the skin and released, and the arms
retract below the skin level immediately. The sling is not sutured in
place.

Postoperative care:
Postoperative care is similar for patients undergoing each of the
incontinence procedures.

Bladder drainage is an essential aspect of postoperative care.

Drainage allows the bladder to rest while postoperative edema and
inflammation resolve. Most patients are able to void spontaneously
in 3-7 days. A few patients require drainage for several weeks.
Catheterization rarely is needed longer than 3-4 weeks.

Avoid increase intra-abdominal pressure - Straining and large

sudden increases in intra-abdominal pressure should be avoided.
Take measures to control chronic coughs and to avoid or treat
constipation. The patient should avoid lifting anything heavier for 12
weeks. The long-term success of the repair may depend partly on
the patient's lifestyle and activities.

Nutrition - Nutrition in the postoperative healing phase also may

affect long-term outcomes. Vitamin C especially may be important
in collagen formation, and supplementation should be provided
liberally. Estrogen may have a positive effect on the healing tissues
and should be replaced as indicated.

Follow-up care:
Follow-up care of patients after incontinence surgery consists of
surveillance for persistent or recurrent incontinence, voiding
dysfunction, and signs or symptoms of pelvic organ prolapse. If
postoperative incontinence or voiding dysfunction is identified,
complex urodynamic testing is indicated. Patients with foreign bodies,
such as synthetic slings, should be followed closely for infections,
erosion, and rejection.

COMPLICTIONS FOLLOWING INCONTINENCE SURGERY

Hemorrhage

Bleeding usually is from the perivesical venous plexus. The

obturator vascular bundle or an accessory vessel crossing the
Cooper ligament rarely may be injured.

Urinary tract injury

Bladder injuries are the most common.

Urethral injuries may be more common with the MarshallMarchetti and Krantz procedure.
Injury to the ureter usually is a kinking or angulation rather than
a transection or ligation. The ureter can be injured in any of the
retropubic procedures.

Urinary tract infection

Urinary tract infections especially are associated with

postoperative voiding difficulties with prolonged catheterization.
Bacteruria is related to the number of days of catheterization and
the type of catheter.
Most cases of colonization do not result in clinical infection, but
upper tract infection and urosepsis can occur, especially in
elderly and debilitated patients.

Wound infection
Risk factors for wound infection in incontinence surgery include
the use of artificial materials, length of procedure, medical
problems (eg, diabetes, steroid-dependent illnesses), and
concomitant vaginal hysterectomy.
Prophylactic antibiotics in the form of a single dose of a broadspectrum agent are efficacious in vaginal and retropubic
procedures.

Osteitis pubis

Inflammation of the pubic bone related to foreign body

placement (e.g. suture, bone anchors)
Usually self-limited, but can complicate MMK (2-4%) and needle
procedures
Rarely complicates Burch procedures and may be related to
misplacement of sutures

Osteomyelitis

Infection of the pubic bone

More severe and more rare than osteitis pubis

Urogenital fistula

Rare

Nerve injuries

Common peroneal, sciatic, obturator, femoral, saphenous, and

ilioinguinal injuries have been reported in association with
incontinence operations.
Many are related to hyperflexion and external rotation of the hips
in the lithotomy position. Compression injury can occur,
especially with the use of self-retaining retractors.
Direct surgical injury can occur rarely, such as an obturator nerve
injury during a retropubic urethropexy.

Voiding dysfunction

This may be manifest as a slow or poor urinary stream.

The more severe form may result in the inability to void due to
relative obstruction and the need for prolonged catheterization.
Abnormal uroflowmetry findings preoperatively indicating
Valsalva voiding and/or poor detrusor contractility may suggest
higher risk.

Other complications

Dyspareunia
Chronic suprapubic pain
Sinus tract formation

URGE INCONTINENCE
Medical management of urge incontinence (detrusor
instability)
Management options include pharmacologic, behavioral, and electrical
stimulation. These options may be tried sequentially, but combined
approaches often work best.
Idiopathic detrusor instability (i.e.
nonneuropathic) is more amenable to medical approaches than
detrusor hyperreflexia (i.e. neuropathic). The latter often may require a
more invasive surgical approach. Clinically significant improvement in
DI can be expected in approximately 80% of the cases using one or
more of the described medical approaches.

Pharmacological agents
Anticholinergic agents
The clinical and urodynamic effects of blocking cholinergic receptors in
the bladder are to increase bladder capacity, increase the volume
threshold for initiation of an involuntary contraction, and decrease the
strength of involuntary contractions. Propantheline bromide is an

anticholinergic agent that has been used to treat detrusor instability.

Propantheline commonly is prescribed in dosages of 15-30 mg every 46 hours. Typical anticholinergic adverse effects can be expected,
including dry mouth, constipation, dry eyes, blurred vision, orthostatic
hypotension, and increased heart rate. Patients with heart disease and
closed-angle glaucoma probably should avoid this agent. Improvement
rates in various studies generally have been approximately 50%.
Propantheline is no longer considered a first-line drug for DI due to
relatively poor efficacy and a high incidence of adverse effects.

Tricyclic antidepressants
These drugs have complicated direct and indirect effects on the lower
genitourinary tract. They possess both a central and peripheral
anticholinergic effect. Tricyclic antidepressants also are alphaadrenergic agonists and central sedatives. The resultant clinical effect
is bladder muscle relaxation and increased urethral sphincter tone. The
pharmacological effects make these drugs good choices for mixed
incontinence, nocturia, and nocturnal enuresis. Imipramine is the most
widely used tricyclic for urologic indications. The dosage range is 25
mg 2-4 times per day.

Musculotropic relaxants
Musculotropic relaxants depress smooth muscle activity directly but at
a site distal to the cholinergic receptor. Relaxants also may work, in
part due to anticholinergic and local anesthetic properties at the level
of the bladder. Oxybutynin is the prototype drug in this class. The
typical dosage is 5 mg 2-4 times per day. Adverse effects are related
mostly to the anticholinergic effects. Lower dosages, such as 2.5 mg 23 times a day, may be more appropriate for elderly patients.

Estrogen
Sensory-urgency symptoms in postmenopausal females, which are
common in patients with genuine stress incontinence and detrusor
instability, often respond to estrogen therapy. No studies demonstrate
the efficacy of estrogen in the treatment of detrusor instability.

Functional electrical stimulation

Functional electrical stimulation (FES) has been found useful in therapy
for both genuine stress incontinence and dtrusor instability. In addition
to increasing skeletal muscle tone and strength in the pelvic floor,
afferent stimulation of the pudendal nerve can result in reflex inhibition
of detrusor contractions. The 2 main modes of FES therapy are longterm stimulation and short-term maximal stimulation. Long-term
therapy requires the use of an intravaginal or intra-anal probe for
several hours a day. Low intensity, subthreshold stimulation is used.
Short-term maximal stimulation therapy was developed because it is
more practical, and high intensity stimulation may produce a better
inhibitory effect.

Behavior modification
Behavioral interventions are based on the assumption that cortical
control over a hyperactive micturition reflex can be established or
reestablished. Clearly, behavioral therapies can be successful in the
highly motivated patient in the short-term. Long-term efficacy is much
less certain, and relapse rates, when reported, have been high. In
addition to a highly motivated patient, this type of therapy requires a
dedicated team to provide support and reinforcement to the patient.
Biofeedback is a type of learning where the patient receives
information in the form of visual or auditory stimuli concerning a
physiologic function. The patient learns to control this normally
unconscious function. In the case of detrusor instability, the patient
learns awareness of the external striated urethral sphincter that may,
in turn, improve the urethrovesical inhibitory reflex. This therapy often
is combined with Kegel pelvic floor exercises.
Bladder training can be performed in a number of ways. Voiding diary
- The patient uses the chosen interval to void by the clock during
waking hours and void as needed at night. The interval is increased by
15 minutes per week until reaching a voiding interval of approximately
3-4 hours. Bladder training can be conducted with or without
simultaneous pharmacotherapy.

Intermittent catheterization

This type of management is most appropriate for patients with

detrusor hyperreflexia and functional obstruction. Many of these
patients have detrusor-sphincter dyssynergia and are at risk for
pyelonephritis and upper tract injury. Some patients with urge
incontinence and coexisting hypofunctioning detrusors may benefit
from self-catheterization.

OTHER FORMS OF URINARY INCONTINENCE

Overflow incontinence
There is often a history of extensive bladder neck surgery and
sometimes of pelvic irradiation. Overflow incontinence develops when
the intravesical pressure caused by passive distension of the bladder
exceeds the maximum intrauretheral pressure in the absence of
detrusor activity. It is associated with a high level of residual urine and
may be caused by either outflow obstruction due to surgical fibrosis or
an excessive elevation of the bladder neck. Overflow incontinence can
also arise subsequent to neurological damage, cauda equine lesions, or
diseases such as diabetes, tabes dorsalis, and poliomyelitis.
Mictirition is associated with hesitation, a slow stream, the passage of
infrequent small volumes of urine, and feeling of incomplete bladder
emptying.
Leakage usually occurs suddenly and without warning and is often
related to bending down or turning over.

Continuous incontinence
This severe type of incontinence is characterized by constant or near
constant leakage with no symptoms other than wetness. Generally,
this represents some significant breech in the storage capabilities of
the bladder or urethra. Urogenital fistulas are a classic example. A
nonfunctioning urethra can result in continuous leakage. Scarring and
fibrosis from previous surgery, partial urethral resection for vulvar
cancer, and urethral sphincter paralysis due to lower motor neuron
disease can cause the urethra to fail. In addition to being a possible
etiology for fistula, pelvic irradiation rarely results in bladder

noncompliance and continuous incontinence. Congenital malformations

of the genitourinary tract, such as bladder extrophy, epispadias, and
ectopic ureters, can result in total incontinence.
Treatment for incontinence caused by vesicovaginal fistula is by
surgery. The aim of surgery is to excise completely the fistula tract
and to close the bladder and vaginal defect in layers without tension.

37
SURGICAL INJURIES TO THE URETER

The anatomy proximity of the genital tract and urinary tract suggests
that a thorough understanding of pelvic anatomy is the cornerstone for
gynaecologic surgery. Familiarity with new urinary tract anatomy and
the various anomalies encountered in clinical practice will help prevent
urinary tract injury.

ANATOMY OF THE URETER

Common
iliac artery

Psoas
mus
cle

CI
CI

Ureter

EI
II

Rectum

EI

P.O.D
UTERUS

Uterine
artery

Bladder
The
entering
bladder

ureter
the

Uterine artery
crosses the
ureter
Ureteral orifice in the
bladder

Fig. 1.1 The anatomy and the course of the female ureter
(CI Common iliac artery; EI External iliac artery and I I Internal iliac artery)

THE COURSE OF THE URETER

The ureter is about 25 cm to 30 cm long (the left being a little longer
than the right) and has approximately equal abdominal and pelvic
compound.
In the abdomen, the ureter passes along the anterior aspect of the
psoas muscle to the pelvic inlet and crosses the iliac vessel at the

bifurcation of the common iliac artery (Figure 1.1). At the point where
the ureter crosses the iliac vessels, the abdominal portion of the ureter
becomes the pelvic ureter.
The pelvic ureter passes along the
posterior lateral pelvic wall, anterior to the internal iliac artery and
crosses the iliac artery and proceeds lateral to the uterosacral
ligaments to enter the base of the broad ligament. It courses beneath
the uterine artery approximate 1.5 cm lateral to the cervix at the level
of the internal cervical os. The ureter then passes medially over the
anterior fornix of the vaginal before entering the vesical trigone of the
bladder.
INJURY OF THE URETER
The injury to the ureter occurs most often during an abdominal
hysterectomy than a vaginal hysterectomy. Injury of the ureter occurs
more commonly when other pelvic disease, such as tuboovarian
abscess, ovarian neoplasm, endometriosis, or a broad-ligament
leiomyoma are present.
A large tumour filling the pelvis will displace it laterally; a tumour in the
broad-ligament may displace the ureter outwards and upwards. The
ureter may be embedded in malignant or inflammatory tissue, making
dissection almost impossible.
Places where ureter is commonly injured - The ureter may be
injured at one of the following site:
1) At the pelvic brim when the ovarian vessels are
ligated.
The ureter is most often damaged at this site during ligation
and division of the infundibulo pelvic ligaments, and care
must always be taken when carrying out this step to palpate
the bundle before applying the clamp.
2) At the region of the uterine artery (uterine artery cross
the ureter).
This is not a common site for the injury to the ureter, but it
must always be remembered that the normal anatomical
relationships may not apply in the presence of fibroids arising
from the lower part of the uterus. Endometriosis and chronic
pelvic infection may also distort normal anatomical
relationships and impair the normal motility of the ureter.
3) At the entry into the bladder.

This is by far the commonest site of injury in the abdominal

procedures and vaginal operation.
A clamped placed
alongside the cervix to include the cervical branch of the
uterine artery and the main attachment of the lateral cervical
ligament is usually responsible for the ureteric damage.
4) During removal of broad ligament tumours which displace
it from the normal position.
5) During peritonization of the pelvis.
Types of injuries to the ureters The types of injuries to the
ureters during surgery include ligation, transcetion, laceration, excision
of a portion of the ureter, and crush injuries.

The ureter is in a close

anterior relation to the
uterine artery.

Fig. 1.2 The most frequent site of injury is in the region of the uterine artery
(division of the uterine vessels) during abdominal hysterectomy.

PREVENTION OF INJURY TO THE URETER DURING SURGERY

The primary procedures in preventing ureter damage are precise
knowledge of the pelvic anatomy and specifically the course of the
ureter, adequate surgical exposure during operation and identification

of the ureter. Also, careful dissection of adherent masses and removal

of broad ligament leiomyomas before hysterectomy will reduce the
incidence of ureter damage.
Preoperative placement of a ureteral catheter has been recommended
for difficult cases
TREATMENT
Ureteral injuries recognized at operation:
Prompt intraoperative recognition of ureteral injuries and the
immediate surgical repair result in increased incidence of good renal
function, reduced ureteral complications, and reduced morbidity.
The ureter can be clamped, crushed, ligated or transected. The
management of these injuries depends principally upon their extend
and location.

Crushing and bruising by clamp or ligature:

When a clamp or suture is discovered on the ureter, it should be
removed immediately and the ureter is inspected carefully. If
ureteral peristalsis is present, no further treatment is necessary.
If the ureter is badly bruises or torn, the correct treatment is to
excise the bruised portion and re-anastomose.

Tears in the ureteral sheath can be repaired with chromic suture.

Division of the ureter:

If the ureter is transected, the mobility of the ureter and bladder
and the location of the injury dictate the type of repair. If possible,
a primary repair end-to-end anastomosis should be done. If more
than 3 cm of ureter been removed, the ureter can be re-implant in
the bladder wall. If the injury occurs in the upper or mid-portion of
the ureter, an ureteroureteral anastomosis is performed.

Ureteral injuries recognized postoperatively:

Unfortunately, most ureteral injuries are not recognized at the time of
surgery.
Clinical features:

1) Bilateral ligation: Occlusion of both ureters will result in anuria.

2) Unilateral ureteral injuries (bruises, ligated, transected or
tear): Often the patient is acutely ill for no reason, and at this
stage ureter damage should be considered.
Signs include
pyrexia, loin pain is hydronephrosis is developing, abdominal
pain, peritonitis and ileus if urine is leaking internally through
fistula.
Investigation:
The first step is an intravenous pyelogram (IVP). This will confirm the
presence of ureteric obsteruction.
Treatment:

Anuria without fistula Both kidney are involved, and the

treatment consist of decompression of the kidney and
establishment of renal drainage.
Fistula without obstruction The fistula should be repaired as
soon as possible.
Fistula associated with progressive renal damage - Renal
drainage must be established immediately, the site and extent of
the ureteric damage assess and definitive repair carried out.

38

BLADDER INJURIES
Bladder injuries are common complications following pelvic surgery,
i.e. abdominal hysterectomy or vaginal repair.
Fortunately, such
injuries heal rapidly if promptly recognized and appropriately repaired.
In carrying out abdominal hysterectomy great care must be taken
when dissecting the bladder off the anterior aspect of the cervix and
upper vagina. Even in seemingly uncomplicated cases, injury to the
bladder may occur.

Injuries to the apex of

the bladder
The apex of the bladder can
be lacerated or opened during
the course of an abdominal
operation. This type of injury
is commonly associated with
an anatomic distortion of the
bladder as a result of dense
adhesion
from
previous
operation or infections, uterine
tumour or endometriosis.
When
recognized
during
operation, the lacerated bladder is best repaired with chromic suture in
two-layer and postoperative decompression of the bladder by catheter
drainage is required for at least 5 to 10 days. A broad-spectrum
antibiotic should be given to reduce the chance of infection at the site
of the injury. In most cases healing will occur uneventfully, and the
bladder function will thereafter be unimpaired.

Injuries to the base of the bladder

Injuries to the base of the bladder base are more complicated, for
several reasons:
1) The bladder base are apt to be recognized.

2) Healing may be impeded because immediate operative field is

infected.
3) One or both ureters may be involved either the injury or repair.
The most common type of injury to the bladder base is a laceration
occurring during vaginal entry of the anterior cul-de-sac. Such an
injury is likely to be due to forceful blunt dissection by pushing down
the bladder base with a gauzed-wrapped finger. The site of injury is
usually in the midline.
Injury to the bladder base may occur during vaginal repair operations
and, as with abdominal hysterectomy, is most likely during the
dissection of the bladder off the anterior aspect of the cervix.
When the bladder base injury is recognized during abdominal or
vaginal surgery, a two-layer should be utilized and postoperative
urethral catheter drainage should be continued for at least 10 dmays.

39
CONTRACEPTION
Today, the voluntary control of fertility is of paramount importance to
modern society. Patients seek contraceptive for variety of reasons. The
effective control of reproduction can be essential to a woman's ability
to achieve her own individual goals as well as contribute to her sense
of well-being.
Many methods of contraception, of greatly varying efficiency, are in
used. The ideal method should be safe, without risk to health,
acceptable, inexpensive and should not interfere with the enjoyment of
coitus. A patient's choice of contraceptive method involves factors
such as efficacy, safety, noncontraceptive benefits, cost, and personal
considerations.

Methods of Contraceptions

Methods not requiring

medical consultation:
o Coitus interrruptus
o Condoms
o Rhythmn method
o Spermicides
Methods
requiring
medical consultation:
o Hormonal
contraception
o Intrauterine devices
o Occlusive
diaphragm/caps

Methods of contraception may be classified as the following:

Classification of methods of contraception

Methods Not Requiring
Medical Consultation

Methods Requiring Medical Consultation

Reversible Methods

Coitus interruptus
Safe
period
(Rhythm
method)
Barriers
method
(Condoms)
Spermicides

Reversible Methods

Hormonal
contraception
Occlusive diaphragm
or caps
Intrauterine devices

Permanent
Methods

Tubal ligation
Vasectomy

Table 1. Classification of methods of contraception

METHODS NOT REQUIRING MEDICAL CONSULTATION

COITUS INTERRUPTUS
Coitus interruptus involves withdrawal of the entire penis from the
vagina before ejaculation. Fertilization is prevented by lack of contact
between spermatozoa and the ovum. This method of contraception
remains a significant means of fertility control in the developing world.
Efficacy: Effectiveness depends largely on the man's capability to
withdraw prior to ejaculation. The failure rate is estimated to be
approximately 20 to 30%. Failures with methods are due to the escape
of spermatozoa into the vagina either because withdrawal is mistimed
or because premature escape of sperms occur before ejaculation is
some men.
Advantages: Advantages include immediate availability, requires no
devices, no cost, does not involve chemicals, and theoretical reduced
risk of transmission of sexually transmitted diseases (STDs).

Disadvantages: A high probability of pregnancy exists with incorrect

or inconsistent use.

SAFE PERIOD
Safe period is one of the most widely used methods of fertility
regulation, particularly for those whose religious or cultural beliefs do
not permit devices or drugs for contraception. This method involves
periodic abstinence, with couples attempting to avoid intercourse
during a woman's fertile periodaround the time of ovulation.
Techniques to determine the fertile period include the calendar
method, cervical mucus method, or the temperature method.

The calendar method:

The calendar method is based on 3 assumptions as follows: (1) A
human ovum is capable of fertilization only for about 24 hours after
ovulation, (2) spermatozoa can retain their fertilizing ability for only 48
hours after coitus, and (3) ovulation usually occurs 12-16 days before
the onset of the subsequent menses. The menses is recorded for 6
cycles to approximate the fertile period. The earliest day of the fertile
period is determined by the number of days in the shortest menstrual
cycle subtracted by 18. The latest day of the fertile period is calculated
by the number of days in the longest cycle subtracted by 11.

Fig.1.1 Calendar method

The cervical mucus method:

With the cervical mucus method, the woman attempts to predict her
fertile period by quantifying the cervical mucus with her fingers. Under
the influence of estrogen, the mucus increases in quantity and
becomes progressively more elastic and copious until a peak day is
reached. This is followed by scant and dry mucus, secondary to the
influence of progesterone, which remains until the onset of the next
menses. Intercourse is allowed 4 days after the maximal cervical
mucus until menstruation.

Fig. 1.2 Mucus method to determine fertile period.

The temperature method:

This was the first scientific method based on period abstience to be
developed. The end of the fertile period is predicted by use of basal
body temperature. Essentially, a woman records her temperature
immediately on waking each morning to get a basal reading. The basal
body temperature of a woman is relatively low during the follicular
phase and rises in the luteal phase of the menstrual cycle in response
so the thermogenic effect of progesterone. The rise in temperature can
vary from 0.2-0.5C. The elevated temperatures begin 1-2 days after

ovulation and correspond to the rising level of progesterone. By waiting

until three consecutive daily temperatures at the higher level have
been recorded, the woman can resume intercourse withy very little risk
of conception. This is because of the short life of the ovum.
Days of cycle

Shaded area shows period of raised temperature. The fertile period in this
cycle is from day 11 to 15 inclusive.
Fig.1.3 - Basal body temperature.
(Typical normal temperature range. Note how it is consistently higher after ovulation
until before the next menstrual period).

Efficacy: The failure

approximately 25%.

rate

in

typical

use

is

estimated

to

be

Advantages: No adverse effects from hormones occur. This may be

the only method acceptable to couples for cultural or religious reasons.
Immediate return of fertility occurs with cessation of method.

Disadvantages: This is most suitable for women with regular and

predictable cycles. Complete abstinence is necessary during the fertile
period unless backup contraception is utilized. This method requires
discipline. The method is not effective with improper use. A relatively
high failure rate exists. This method does not protect against STDs.

MALE CONDOM
The condom consists of a thin sheath placed over the glans and the
shaft of the penis that is applied before any vaginal insertion. It is one
of the most popular mechanical barriers. Among all of the barrier
methods, the condom provides the most effective protection of the
genital tract from STDs. Its usage has increased among all women of
reproductive age because of the concern regarding the acquisition of
HIV and STDs. It prevents pregnancy by acting as a barrier to the
passage of semen into the vagina
Efficacy: The failure rate of condoms is estimated to be about 14%.
This higher failure rates reflects the error of usage. Common errors
with condoms usage include failure to use condoms with every act of
intercourse and throughout intercourse, incorrect placement of the
condom on the penis, and poor withdrawal technique.
Advantages: Condoms are readily available and usually are
inexpensive. This method involves the male partner in the
contraceptive choice. Condoms are effective against both pregnancy
and STDs.
Disadvantages: Condoms possibly decrease enjoyment of sex. Some
users may have a latex allergy. Condom breakage and slippage
decrease effectiveness.

FEMALE CONDOM
The female condom is a polyurethane sheath intended for 1-time use,
similar to the male condom. It contains 2 flexible rings and measures
7.8 cm in diameter and 17 cm long. The ring at the closed end of the
sheath serves as an insertion mechanism and internal anchor that is
placed inside the vaginal canal. The other ring forms the external
patent edge of the device and remains outside of the canal after
insertion.
The female condom prevents pregnancy by acting as a barrier to the
passage of semen into the vagina. Simultaneous use of both the
female and male condom is not recommended because they may

adhere to each other, leading to slippage or displacement of either

device.
Efficacy: Efficacy trials are noted to be limited. Initial trials have
demonstrated a pregnancy rate of 15%.
Advantages: The female condom provides some protection to the
labia and the base of the penis during intercourse. The sheath is
coated on the inside with a silicone-based lubricant. It does not
deteriorate with oil-based lubricants. It can be inserted as long as 8
hours before intercourse.
Disadvantages: The lubricant does not contain spermicide. The
device is difficult to place in the vagina. The inner ring may cause
discomfort. Some users consider the female condom cumbersome. The
female condom may cause urinary tract infection (UTI) if left in vagina
for a prolonged period.

SPERMICIDAL AGENTS
Vaginal spermicides consist of a base combined with either nonoxynol9 or octoxynol. The actual spermicidal agent consists of a surfactant
that destroys the sperm cell membrane. Bases include vaginal foams,
suppositories, jellies, films, foaming tablets, and creams. These have to
be inserted into the vagina prior to each coital act. Use of spermicidal
agents also reduces the risk of infection by both viral and bacterial
STDs; however, clinical data on its efficacy on preventing the
transmission of HIV are limited. Nonoxynol-9 is toxic to the lactobacilli
that are part of the normal vaginal flora. Adverse effects include an
increased vaginal colonization with the bacteria Escherichia coli that
may predispose to bacteriuria after intercourse.
Spermicides prevent sperm from entering the cervical os by attacking
the sperm's flagella and body, reducing their mobility, and disrupting
their fructolytic activity, thereby inhibiting their nourishment.
Efficacy: Perfect use failure rate within the first year is 6%. Typical use
failure rate within the first year is 26%.
Advantages: The lubrication provided by spermicides may heighten
satisfaction in both partners. Another advantage is the ease of
application. Either partner can purchase and apply spermicide because
it is easily accessible, available over the counter, and inexpensive.
Applying spermicide requires minimal patient education. It augments

contraceptive efficacy of the cervical cap and diaphragm. Spermicides

produce no systemic adverse effects.
Disadvantages: Spermicides provide minimal protection from STDs.
Insertion may be uncomfortable for some couples. Vaginal irritation is
possible, and spermicide may cause allergic reaction.

METHODS REQUIRING MEDICAL CONSULTATION

DIAPHRAGM
The diaphragm is a shallow latex cup with
a spring mechanism in its rim to hold it in
place in the vagina. Diaphragms are
manufactured in various diameters. A
pelvic examination and measurement of
the diagonal length of the vaginal canal
determines the correct diaphragm size. It
is inserted before intercourse so that the
posterior rim fits into the posterior fornix
and the anterior rim is placed behind the pubic bone. Spermicidal
cream or jelly is applied to the inside of the dome, which then covers
the cervix.
It prevents pregnancy by acting as a
barrier to the passage of semen into
the cervix. Once in position, the
diaphragm
provides
effective
contraception for 6 hours. If a longer
interval has elapsed without removal of
the diaphragm, a fresh spermicide is
added
with
an
applicator.
After
intercourse, the diaphragm must be left
in place for at least 6 hours.
Fig.1.4 - Correct placement of the diaphragm

Efficacy: Effectiveness of the diaphragm depends on the age of the

user, experience with its use, continuity of use, and the use of
spermicide. The failure rate is estimated to be 20%.
Advantages: The diaphragm does not entail hormonal usage.
Contraception is controlled by the woman. The diaphragm may be
placed by the woman in anticipation of intercourse.

Disadvantages: Prolonged use during multiple acts of intercourse

may increase the risk of UTIs. Usage for longer than 24 hours is not
recommended due to the possible risk of toxic shock syndrome. The
diaphragm requires professional fitting. Poorly fitted diaphragms may
cause vaginal erosions. Diaphragms have a high failure rate. Use of a
diaphragm requires brief formal training. The diaphragm may develop
odor if not properly cleansed.

CERVICAL CAPS
The cervical cap is a cup-shaped latex
device that fits over the base of the cervix.
A groove along the inner circumference of
the rim improves the seal between the
inner rim of the cap and the base of the
cervix. Spermicide is needed to fill the cap
one third full prior to its insertion. It is
inserted as long as 8 hours before coitus
and can be left in place for as long as 48
hours.
A cervical cap acts as both a mechanical barrier to sperm migration
into the cervical canal and as a chemical agent with the use of
spermicide.
Efficacy: The effectiveness depends on the parity of women due to the
shape of the cervical os. The failure rate is 20% in the nulliparous
woman and 40% in the parous woman.
Advantages: It provides continuous contraceptive protection for its
duration of use regardless of the number of intercourse acts. Additional
spermicide, unlike the diaphragm, is not necessary for repeated
intercourse. The cervical cap does not involve ongoing use of
hormones.
Disadvantages: Cervical erosion may lead to vaginal spotting. The
cervical cap requires professional fitting and training for use. Severe
obesity may make placement difficult. A relatively high failure rate
exists. The women must have history of normal results on pap smears.

INTRAUTERINE DEVICES
The intrauterine device (IUD) is a highly effective method of
contraception. Many different devices have been introduced, but most

have now been withdrawn. The reason for withdrawal was due to the
series of litigations related to infections. The manufacturers withdrew
their product due to the decision that the cost of defending the
litigation suits was deemed too expensive.
Until today, only 2 types of IUDs available were the IUDs containing
copper and the progesterone-releasing form. In December 2000, the
FDA approved another form of IUD has been approved, the
levonorgestrel intrauterine system (LNG IUS, Mirena).
Millions of
women have used this form of contraception in the past decade with
great success.
The IUDs are produced in the form of T and 7 shapes. They are
made of plastic material, and they can be compressed (or straightened
out) to be inserted into an introducer for insertion into the uterine
cavity. When the device is placed in the uterine cavity it opens out, so
that it retained. All IUDs have nylon thread or tail which allow the
women to check that it is in place and for removal. The IUD is radioopaque and can be located by X-ray or ultrasound. Figure 1.3 shows
the IUDs that were still available.

Multiload

Copper 7

Nova T
Copper T

Mirena
Gynefix IUD
Fig.1.5 Different types of intrauterine devices

Description of IUD
The T-shaped progesterone-releasing IUD, which is placed into the
uterine cavity, is made of ethylene vinyl acetate copolymer. It contains
38 mg of progesterone and minimal amounts of barium sulfate for
greater visibility on x-rays. The vertical limbs are 36 mm long and the
horizontal arms are 32 mm wide. It has a pair of dark blue double
strings that hangs from the lower limb. Approximately 65 mcg of
progesterone a day is released from the progesterone form from a
reservoir in its stem. This is a sufficient amount of hormone to last for
400 days; therefore, this IUD must be replaced yearly.
The Copper T380 was introduced in 1988. The T-shaped IUD is made
of polyethylene with fine copper wire wrapped around the vertical
stem. The string is clear or white and hangs from the lower limb of the

IUD. This device consists of 308 mg of copper covering portions of its

stem and arms. Contraceptive effectiveness continues for 5 years,
after which time it must be replaced.
The LNG IUS (Mirena) is similar in shape to the Copper T380 in that it
also consists of a small T-shaped frame with a reservoir that contains
LNG, a progesterone. The IUS releases 20 mcg of LNG per day into the
uterine cavity for as long as 5 years. It consists of a polyethylene frame
with a cylinder containing a polydimethylsiloxane-levonorgestrel
mixture enveloping the vertical arm. The cylinder is coated with a
membrane that regulates the release of the hormone. This model also
is visible on x-ray.
The Gynefix is a frameless IUD, which has been designed to try and
overcome the problems of expulsion, heavy bleeding and increased
dysmenorrhoea associated withy the use of conventional, framed
devices.
It consists of six copper cylinders on a monofilament
polyprophylene thread. The upper end of the thread is anchored into
the fundal of the myometrium.

Upper end of the thread has

a knot which acts as a
anchor

Six copper cylinders

Fig.1.6 The Gynefix IUD

Mode of action
The IUDs cause a mild inflammatory reaction in the endometrium,
which becomes infiltrated with leucocytes and macrophages resulting
in endometrial suppression.. In addition tubal motility is increased.
Uterotubal fluid and

motility changes inhibit sperm migration.

Copper IUDs prevent pregnancy by incapacitating the sperms making
them dysfunctional for fertilization. The progesterone IUDs releasing
levonorgestrel prevent pregnancy in the same manner as the
progesterone-only pill. This IUD causes cervical mucus to be thicker in
consistency, thereby altering sperm migration.
Insertion
The insertion of IUD is more easily done during or immediately after
menstruation, when the cervix is less tightly closed. Insertion can also
be done at a postnatal examination or immediately after termination of
pregnancy.
Technique of insertion:
1) A pelvic examination is made to exclude any possible
contraindication, and to determine the position of the uterus.
2) The cervix is visualized with a speculum and swabbed with a sterile
cottonwool ball dipped in a disinfecting fluid.
3) The cervix is then steadied with a tenaculum.
4) A uterine sound is passed to confirm the direction and depth of the
uterine canal.
5) The IUD is then loaded in the introducer and passed into the uterine
cavity as far as the fundus.
6) The introducer is then withdrawn and the device is extruded into
the uterine cavity.
7) The thread is cut to leave only 3 cm visible.
Efficacy: The failure rate is 2% with the progesterone form, 0.6% with
the Copper T380, and of 0.1 % with the LNG IUS.
Advantages: The biggest advantage of IUD is that once the device
has been inserted there is nothing more for the woman or her husband
to do. IUDs produce no systemic side effects. Ectopic pregnancies are
reduced overall; however, the ratio of extrauterine to intrauterine
pregnancy is increased if conception does occur. Decreased menstrual
blood loss occurs with progesterone IUD. Decreased dysmenorrhea
occurs with progesterone IUD.

Complications:
(1)Perforation: Risk of uterine perforation is a rare event. When it
occurs it is usually at the time of insertion.
Most perforations
cause no symptoms and are only suspected when the tail of the IUD
cannot be felt and ultrasound scan or radiological examination
shows that it is outside the uterus.

Laparoscopy view
Fig.1.7 Perforation: The IUD is seen outside the uterine cavity

(2)Bleeding and menstrual loss: Following insertion of an IUD there

is almost always a certain amount of bleeding. Women should be
reassured that this is normal reaction to the insertion.
The first few menstrual periods after insertion may be heavier and
more prolonged than previously and this change may last
indefinitely, but does not usually become menorrhagic. However, if
bleeding is of any severity, causing anaemia, the device will have to
be removed.
The amount of increased bleeding associated with different devices
varies. Hormone-releasing IUDs decrease the amount of bleeding.

(3)Pain: Pain, usually in the form of uterine cramps, and occasionally

as low backache, may occur soon after insertion particularly if the
device is large. It is usually not severe. Increased dysmenorrhea
may occur with Copper T380.

(4)Expulsion: Spontaneous expulsion may occur, particularly during

menstruation and within the first year. Expulsion is more likely if
insertion is performed post-partum. Larger devices are more likely
to be expelled than smaller ones. Sometimes the woman is unaware
that expulsion has taken placed. Women are advised to feel for the
tail of the IUD after each period to check that it is still in position.

(5)Infection: Studies has shown that IUD user users run a higher risk
of pelvic inflammatory disease (PID) than women using other forms
of contraception. The risk of PID is higher not only immediately after
insertion, but also for as long as the device remains in place. IUDs
do not protect against STDs.
If PID occurs with an IUD in place, it should be removed once
adequate antibiotic therapy has been instituted.

(6)Ectopic pregnancy: Ectopic pregnancy may occur in women using

an intrauterine device. There is no evidence that the incidence is
greater than in the general population exposed to the risk of
pregnancy.

(7)Pregnancy with IUD in place: Rarely intrauterine pregnancy

occurs with a device in place.
The IUD may be expelled
spontaneously, or the tail may disappear into the uterine cavity as
the uterus enlarges. The risk of miscarriages is significantly greater
if the device is not removed. When pregnancy is detected in a
woman with an IUD in place, the device should be removed if the
tail is accessible. If the device is left in place there is slight risk of
intrauterine
infection,
preterm
labour
and
antepartum
haemorrhage, but most pregnancies are uncomplicated and the
device is delivered with the placenta.
Contraindications
IUDs, like other contraceptive methods, are not suitable for all women
at all times. Contraindications include,

history of previous PID

abnormal or distorted uterine cavity
undiagnosed genital bleeding
uterine or cervical malignancy
history of ectopic pregnancy
increase susceptibility to infection (leukemia, diabetes, valvular
heart disease, AIDS)
Wilson disease
known or suspected pregnancy
history of genital actinomyces
active cervical or endometrial infections.

Removal
Removal of IUD may be required for both medical and other
indications.
Medical indications:

Pregnancy
Acute inflammatory disease
Endometrial or cervical malignancy
Perforation or partial expulsion of the IUD
Abnormal excessive bleeding if affecting the health of the woman.

Other indication:

Copper-bearing and hormonal IUDs when their effective lifespan has

expired.

Follow-up care
Immediately post-insertion complications and long-term side effects
should be sympathetically managed. A six-weeks follow-up check is
advisable to discover if the woman is satisfied with the IUD, to assess
pain and to ensure there is no infection. It is important to ensure that
the device is in situ and not expelled, either partially or totally.
Following this visit, checks at three months, six months and yearly
thereafter, are advisable if they can be arranged.

HORMONAL CONTRACEPTION
ORAL CONTRACEPTION
Oral contraception is a substance or a combination of substances
(usually steroids) administered orally which prevent pregnancy. The
main forms of oral contraception include the combined oral
contraceptive containing both estrogen and progestagen (COC), the
progestagen-only pill (POP) and hormonal post-coital contraception
(POC). The latter is used in emergencies.

COMBINED ORAL CONTRACEPTIVE PILLS (COC)

The combined oral contraceptive pill (containing synthetic estrogen

and progestogen) was first introduced in 1956. Since its introduction
the dose of estrogen has declined significantly in the past 40 years.
This is to reduce the thromboembolic complications.
Formulation
The estrogenic component of COCs consisted of either ethinyl estradiol
or mestranol. Today, ethinyl estradiol is used in all preparations
containing 35 mcg or less of estrogen. The progestin component
consists of norethindrone, levonorgestrel, norgestrel, norethindrone
acetate, or ethynodiol diacetate. Recently, 2 new progestins have been
added, norgestimate and desogestrel.
The other major new development is the reduction in the dosage of
ethinyl estradiol to 20 mcg. The major impetus for this change is to
improve the safety and reduce side effects. However, little data exist to

indicate whether reduction of the estrogen dose is associated with a

decreased risk of serious sequelae. These lower doses are associated
with a decrease in the incidence of estrogen-related adverse effects,
such as weight gain, breast tenderness, and nausea.
The majority of the formulations have 21 hormonally active pills in a
constant amount followed by and interval of 7 days, when no tablet is
taken, or 7 placebo pills. Monophasic OCs has a constant dose of both
estrogen and progestin in each of the hormonally active pills. Phasic
combinations can alter either or both hormonal components.
Patterns of administration vary slightly with the different preparations.
The commonest regimen starts on the fifth a pill is taken each day for
21 days, i.e. at the same time each day. After the completing the 21
pills there is an interval of a 7-day interval during which no pills are
taken (unless placebo pill are included in the packet). During the
interval period withdrawal bleeding usually occurs, but even if it does
not the woman starts the next course of pills after 7 days.
If a woman misses 1 pill, she should take 1 tablet as soon as it is
remembered and the next one at the normal time. If more than 12
hours (especially with the first in the packet), continue but take extra
precautions for 7 days. If 7 days run into the next pack, the woman
should be advise do not have the pill-free interval and start the next
pack immediately. Women who have missed more than 2 consecutive
pills should be advised to use a backup method of contraception
simultaneous to finishing up the packet of pills until their next menses.

Mode of action
Ovulation is suppressed by imitating the feedback mechanism of
ovarian hormones on the pituitary and hypothalamus. Either estrogen
or progesterone alone is capable of inhibiting both follicle stimulating
hormone (FSH) and luteunising hormone (LH) sufficiently to prevent
ovulation. The combination of the 2 steroids creates a synergistic
effect that greatly increases their antigonadotropic and ovulation
inhibitory effect.
The combined pill has other actions which contribute to
effectiveness should break-through ovulation occur. These are:

its

1) prevention of the changes in the endometrium which are

necessary for successful implantation of the pregnancy;

2) inhibition of sperm progression through the cervical mucus (i.e.

they alter the consistency of cervical mucous and making it
hostile to the sperm);
3) interference with normal motility and secretion of the fallopian
tubes.

Efficacy: Failure rates are associated with individual compliance. With

perfect use the failure rate is 0.1%.
Beneficial Effects: There are a number of advantages I taking the pill.
COCs are used as treatment for menstrual irregularity because menses
is more regular and predictable. In the prevention of ovulation, COCs
can reduce and sometimes eliminate mittelschmerz. Women with
anemia secondary to menorrhagia increase their iron stores. Women
can manipulate the cycle to avoid menses during certain events, such
as vacations or weekends by extending the number intake days of
hormonally active pills or by skipping the placebo pill week. COCs
prevent benign conditions, such as benign breast disease, pelvic
inflammatory disease (PID), and functional cysts. Functional cysts are
reduced by the suppression of stimulation of the ovaries by FSH and
LH. Ectopic pregnancies are prevented by the cessation of ovulation.
COCs are noted to prevent epithelial ovarian and endometrial
carcinoma. Studies have noted an approximate 40% reduced risk of
malignant and borderline ovarian epithelial cancer. This protection
appears to last for at least 15 years following discontinuation of use
and increases with duration of use. This protection has not been
studied with low-dose COCs and/or in women with genetic ovarian
cancer syndromes. Use of COC is associated with a 50% reduction of
risk of endometrial adenocarcinoma. Protection appears to persist for
at least 15 years following discontinuation of use.

Disadvantages: Adverse effects include nausea, breast tenderness,

weight gain, breakthrough bleeding, amenorrhea, headaches,
depression, anxiety, and decreased libido. COCs do not provide
protection from STDs. Daily administration is necessary, and
inconsistent use may increase the failure rate. A few months of delay
of normal ovulatory cycles after discontinuation of COCs may occur.
Women who continue to have amenorrhea after a discontinuation
period of 6 months require a full evaluation.

Metabolic effects and safety

Venous thrombosis: The estrogen component of COCs has the

capability of activating the blood clotting mechanism. Use of lowestrogen COC is associated with a lower risk of thromboembolism
than in COCs with higher levels of estrogen. Although use of OCs
is not associated with a detectable hypercoagulable state for
most women, users at a greater risk for thromboembolism
include heavy smokers, women with high or abnormal blood
lipids, women with severe diabetes with damage to the arteries,
women with consistently elevated blood pressures, and women
who are obese.

Hypertension: COCs have a dose-related effect on blood

pressure. With the older high-dose pills, as many as 5% of
patients could expect to have blood pressure elevations of
140/90 mm Hg or higher. This elevation is believed to be
secondary to an estrogen-induced increase in renin substrate in
susceptible individuals. Although today's low-dose pills have
minimal blood pressure effects, maintaining a surveillance of
blood pressure is advisable.

Atherogenesis and stroke: Although androgens and a few of

the progestins actually may increase low-density lipoproteins
(LDLs) and decrease high-density lipoproteins (HDLs), past use of
COCs does not increase the risk of cardiovascular disease.
Limited preliminary data have demonstrated that COC use does
not lead to coronary atherosclerosis. In rare cases where
myocardial infarcts have been found, the cause has been noted
to be of thrombotic rather than of atherosclerotic etiology. In
general, a woman's habits are more significant than the use of
COCs in determining her risk for cardiovascular disease. The
patient who is sedentary, overweight, a heavy smoker,
hypertensive, diabetic, or has hypercholesterolemia is clearly at
risk.

Hepatocellular adenoma: These benign liver tumors have

been associated with use of COCs. Although these tumors are

histologically benign, their danger lies in the risk of rupture of the

capsule of the liver, leading to extensive bleeding and, possibly,
death. With the current low-dose OC combination, the risk for
liver tumors is much lower.

Cancer
o The association of COC use and breast cancer in young
women is controversial. The Collaborative Group on
Hormonal Factors in Breast Cancer performed the most
comprehensive analysis of breast cancer and OCC use as
reported in 1996. This group evaluated original published
epidemiological data from more than 20 countries. The
results demonstrated that current COC users, and those
who had used COCs within the past 1-4 years, had a
slightly increased risk of breast cancer. Although these
observations support the possibility of a marginally
elevated risk, the group noted that the COC users had
more breast examinations and breast imaging than the
nonusers. Thus, although the consensus states that COCs
can lead to breast cancer, the risk is small and the
resulting tumors spread less aggressively than usual.
Current thought is that COC use may be a cofactor that can
interact with another primary cause to stimulate breast
cancer.

The relationship between COC use and cervical cancer also

is quite controversial. A weak association may exist
between COC use and squamous cell cancer of the cervix.
Important risk factors include early sexual intercourse and
exposure to the human papillomavirus. The overall
consensus is that if indeed COC use increases the risk of
cervical neoplasia, it is a minimal risk. Thus, women who
use COCs should have annual Papanicolaou tests.

Contraindications
Contraindications to use include history of deep vein thrombosis,
pulmonary embolism, or congestive heart failure; cerebrovascular
disease or coronary artery disease; untreated hypertension; diabetes
with vascular complications; estrogen-dependent neoplasia; breast

cancer; undiagnosed abnormal vaginal bleeding; known or suspected

pregnancy; active liver disease; and age older than 35 years and
cigarette smoking.

PROGESTOGEN-ONLY PILLS (POP)

Progestogen-only oral contraceptives, also known as the minipill, are
estrogen-free oral contraceptives containing a microdose of
progestogen, either from the noresthisterone or levonorgestrel group.
The POP is taken regularly daily without break and regardless of
bleeding patterns. Fewer than 1% of users of oral contraceptives
utilize them as their sole method of contraception. Candidates for use
include
women who are breastfeeding and women with
contraindications to estrogen use. Two formulations are available, both
of which have lower doses of progestin than combined OCs. One
formulation contains 75 mcg of norgestrel. The other has 350 mcg of
norethindrone.

Mechanism of action
Progestogens in the dose used in the POP exert their main action on
cervical mucus, leading to the production of thick mucus with poor
sperm penetrability. As an adjunct to this, biochemical changes are
produced in the endometrium (reduction in the number and size of
endometrial glands, leading to an atrophic endometrium) making it
unfavourable for implantation. Also there is reduction in cilia motility
in the fallopian tube, thus slowing the rate of ovum transport.
Efficacy: The efficacy is less than that of combined oral
contraceptives. Failure rates vary between 1.5 to 3.0 percent. Serum
progestin levels peak approximately 2 hours after administration.
Within 24 hours, rapid distribution and elimination returns the level to
baseline. Greater efficacy is achieved with consistent administration.
Advantages: Due to the lack of estrogen, minimal evidence exists
that demonstrates the serious complications to which estrogen can
contribute (ie, thromboembolism). Noncontraceptive benefits include
decreased dysmenorrhea, decreased menstrual blood loss, and
decreased premenstrual syndrome (PMS) symptoms.
Fertility is
immediately reestablished after the cessation of Progestogen-only oral
contraceptives.

Disadvantages: The most significant disadvantage is the continuous

need for compliance with regularity of usage. Users need to be
counseled on the need for a backup method of contraception if a pill is
missed or taken late. A pill is considered late if ingestion occurs 3
hours after the established time of administration. If a pill is missed, it
should be taken as soon as possible, the next pill is to be taken at the
scheduled time. Backup contraception should be utilized for the next
48 hours. Adverse effects include nausea, breast tenderness,
headache, menstrual irregularities, and amenorrhea.
Indications for progestogen-only pill
Women for whom POP would be a good choice include:
1) Those who have side-effects with, or contraindication to, the
combined oral contraceptives.
2) The older age group.
3) Diabetic and obese women.
4) Women with hypertension.
5) Migraine sufferers.
6) Most importantly during lactation.

Contraindications to the progestogen-only pill

1) Any severe condition likely to be worsend by steroidal
contraception, such as past or current severe arterial disease or
current high risk for cardiovascular disease.
2) Undiagnosed genital tract bleeding can be confused with the
irregular bleeding on POPs and therefore investigations must
precede starting the POP.
3) Pregnancy has to be excluded.
4) Recent trophoblastic disease until hCG is undetectable in blood as
well as urine, since it may be the progestogen that increase the
likehood of chemotherapy being required.
5) Previous ectopic pregnancy.

INJECTABLE DEPOMEDROXYPROGESTERONE ACETATE

Depomedroxyprogesterone acetate (DMPA) is a suspension of
microcrystals of a synthetic progestin that is injected intramuscularly
for contraceptive purposes. Pharmacological active levels are achieved
within 24 hours after injection, and serum concentrations of 1 ng/mL
are maintained for 3 months. The contraceptive regimen consists of 1
dose (150 mg) every 3 months.
Mode of action: Most DMPA acts by the inhibition of ovulation with
the suppression of follicle-stimulating hormone (FSH) and LH levels and
eliminates the LH surge. This results in a relative hypoestrogenic state.
Single doses of 150 mg will suppress ovulation in most women for as
long as 14 weeks.
Subsidiary effects on luteal function, tubal function, endometrium and
cervical mucus all contribute to the high efficacy of this contraceptive
approach.
Efficacy: DMPA is an extremely effective contraceptive option. They
are usually associated with fewer than 0.5 pregnancies per 100
woman-years.
Advantages: DMPA does not produce the serious adverse effects of
estrogen, such as thromboembolism. Diminished anemia occurs.
Dysmenorrhea is decreased. Risk of endometrial and ovarian cancer is
decreased.
Disadvantages: The disadvantages of DMPA injections are:
1) The major disadvantage of using DPMA is that once given none of
its actions can be reversed for the duration of the activity of the
drug.
2) A disturbed menstrual pattern such as irregular bleeding, heavy
and prolonged.
3) Amenorrhoea in about 30 - 50% of women after one years of use.
4) Possible weight gain.

IMPLANT

In 1990 the use of levonorgestrel implants (Norplant)was approved for

contraceptive purposes. This method consists of 6 silicone rubber
rods, each measuring 34 mm long and 2.4 mm in diameter and each
containing 36 mg of levonorgestrel. The implant releases
approximately 80 mcg of levonorgestrel per 24 hours during the first
year of use, achieving effective serum concentrations of 0.4-0.5 ng/mL
within the first 24 hours. The rate of release decreases to an average
of 30 mcg/d in the latter years of use. Release of the progestational
agent by diffusion provides effective contraception for 5 years.
Contraceptive protection begins within 24 hours of insertion if inserted
during the first week of the menstrual cycle. The rods are inserted
subcutaneously, usually in the woman's upper arm, where they are
visible under the skin and can be palpated easily.
Mode of action: The mechanism of action is a combination of
suppression of the LH surge, suppression of ovulation, development of
viscous and scant cervical mucus to deter sperm penetration, and
prevention of endometrial growth and development.
Efficacy: The contraceptive efficacy of the method is equivalent to
that of surgical sterilization. Overall, pregnancy rates increase from
0.2% in the first year to 1.1% by the fifth year.
Advantages: The longevity of its effectiveness is an advantage. Its
effectiveness is not related to its use in regards to coitus. Exogenous
estrogen is absent. Prompt return to the previous state of fertility
occurs upon removal. No adverse effect on breast milk production
occurs.
Disadvantages: A minor surgical procedure is necessary for incision.
Difficulty in removal is a disadvantage. Menstrual irregularities are
common along with other adverse effects, including weight gain,
headaches, mood changes, hirsutism, galactorrhea, and acne.

Contraindications
Absolute contraindications include active thrombophlebitis or
thromboembolic disease, undiagnosed genital bleeding, acute liver
disease, benign or malignant liver tumors, known or suspected breast
cancer, and history of idiopathic hypertension.
Relative contraindications include heavy cigarette smoking, history of
ectopic pregnancy, diabetes mellitus, hypercholesterolemia, severe

acne, hypertension, history of cardiovascular disease, severe vascular

or migraine headaches, and severe depression.

Indications
Appropriate candidates are women who are postpartum or
breastfeeding, women who have difficulty with contraceptive
compliance, women in whom pregnancy is contraindicated due to
medical condition, and patients with contraindications for use of
estrogen.

SURGICAL CONTRACEPTION - STERILIZATION

Sterilization is considered an elective permanent method of
contraception. Although both female and male sterilization procedures
can be reversed surgically, the surgery is technically more difficult than
the original procedure and may not be successful. Success is noted to
be greater with tubal reanastomosis than with reanastomosis of the
vas deferens in regards to reversal of sterilization.

FEMALE STERILIZATION - Tubal Sterilization

Tubal sterilization is indicated for women who want a permanent
method of contraception and are free of any gynecologic pathology
that would otherwise dictate an alternate procedure. Tubal sterilization

is also indicated for women in whom a pregnancy could represent a

significant clinical and medical risk.
Pathophysiology: Tubal sterilization results in mechanically blocking
or interrupting the fallopian tubes to prevent sperm from fertilizing the
egg. The isthmic portion of the fallopian tube is the proper site for all
sterilization procedures that depend on tubal occlusion rather than on
removal of a tubal segment
Methods of Female sterilization or Tubal occlusion
Sterilization can be performed in the postpartum period with a small
transverse infraumbilical incision or during the interval period. In the
female, tubal sterilization or occlusion may be done through several
approaches. Sterilization during the interval period can be performed
with laparoscopy, laparotomy, or colpotomy. The methods of fallopian
tube sterilization include occlusion with Falope rings, clips, bands,
segmental destruction with electrocoagulation, or suture ligation with
partial salpingectomy.
MINILAPARAOTOMY TUBAL STERILIZATION
Minilaparotomy is defined as a laparotomy with an incision size smaller
than 5 cm. The operation can be performed through a suprapubic
incision in the interval after pregnancy and through a subumbilical
incision within the first 48 hours after delivery. At the present time, the
tubal occlusion methods most commonly used with this approach are
fimriectomy, Pomeroy or its modifications.
A 2- to 5-cm incision is made on the skin dissection is carried down to
the peritoneum, which can then be entered gently. With manipulation
and retraction, the tubes can be visualized and grasped with a Babcock
clamp. Often, the fallopian tubes can be palpated laterally and near
the fundus and then flipped anteriorly. The fallopian tube is walked
with Babcock clamps until the fimbriated end is identified. A major
cause of bilateral tubal ligation (BTL) failure is mistakenly ligating the
round ligament, falsely identified as the tube. After the BTL, the
minilaparotomy incision is closed in layers. Closure of the peritoneum
is optional. The fascia is closed with running 2-0 or 0 delayed
absorbable suture. Subcutaneous closure is optional, and the skin is
closed with 3-0 or 4-0 absorbable suture in a subcuticular manner.
Methods of Bilateral Tubal Ligation:

Pomeroy technique
This technique is the simplest and most commonly performed tubal
sterilization.
The mid portion of the fallopian tube is grasped with a Babcock clamp,
creating a loop, which is tied with 2-0 or 0 plain catgut suture, and
each limb of the tubal knuckle is cut separately. Specimens are
submitted to pathology. The endosalpinx at the cut ends may be
cauterized (optional). The ligation sutures are held while the tube is cut
to prevent retraction of the cut tubal stumps into the peritoneal cavity
before they can be adequately examined for hemostasis.

The original description consisted of a loop of tube ligated in the

middle with a double strand of 1-0 chromic catgut, followed by
resection of the top of the ligated loop. The rationale for this technique
is based on prompt absorption of the suture ligature with subsequent
separation of the cut ends of the tube, which then become sealed by
spontaneous reperitonealization and fibrosis. A resultant natural gap of
2-3 cm should occur between the severed proximal and distal
segments of the tube.
Many modifications of the Pomeroy technique have been described;
the most common involves doubly ligating each loop.
Failure rates are reported to be 1 case in 300-500 patients.

The fallopian tube is

identified

The middle segment of the

tube is ligated with catgut
suture and the knuckle is
cut.

The knuckle of the ligated

tube has been resected

Fig.1.8 Pomeroy method of tubal ligation

Parkland technique
The Parkland technique is a midsegmental resection similar to the
Pomeroy technique, except each leg of the loop is tied
separately. The Parkland technique was designed to avoid the
intimate approximation of the tubal cut ends, as occurs with the
Pomeroy technique, thereby eliminating the risk of secondary
adherence and subsequent recanalization. Failure rates are
reported to be 1 case in 400 patients.
Irving technique
The Irving technique is designed to be used in conjunction with
cesarean delivery.

Fig.1.9 Irving method of tubal ligation

A mesosalpingeal window is created beneath the tube approximately 4

cm from the uterotubal junction. The tube is doubly ligated with 0 or 00
absorbable suture and severed, with the sutures on the proximal end
left long. The proximal tubal stump may require mobilization by
dissecting it free from the mesosalpinx. A small nick is made into the
serosa on the posterior (or anterior) uterine wall near the uterotubal
junction. A tonsil or hemostat is used to deepen the incision, creating a
pocket in the myometrium approximately 1-2 cm deep. The 2 free ends
of the proximal stump ligature are then individually threaded onto a
curved needle and brought deep into the myometrium tunnel and out
through the uterine serosa. Traction on the sutures draws the proximal
tubal stump deep into the myometrial tunnel, and the sutures are tied.
The serosal opening of the tunnel is then closed around the tube with
fine absorbable suture.
An additional option is to bury the distal end of the tube between the
leaves of the broad ligament as originally described by Irving.
Failure rates are less than 1 case in 1000 patients.

LAPAROSCOPIC TUBAL STERILIZATION

Laparoscopy is instrumental visualization of the abdominal organs
through the abdominal wall using the laparoscope. Sterilization by this

method is made possible by the incorporation of operating accessories

in the instrument. Tubal occlusion is accomplished by electrocautery,
application of silastic rings, or application of clips.
Advantages include small incisions, rapid access to the fallopian tubes,
rapid recovery, and the ability to inspect intraperitoneal organs.
Disadvantages include the maintenance of fragile and expensive
equipment and the risks of vessel/viscera injury with needle
insufflation/trocar entry. Entry accounts for 30-50% of all laparoscopic
sterilization complications.

Abdomen
with gas

filled

Fig.1..9 Laparoscopy procedure

Electrocoagulation technique
Bipolar current is inherently safer than unipolar current because tissue
destruction is essentially confined to the area between and
immediately adjacent to the bipolar paddles.
The fallopian tube is identified and grasped at the mid isthmus region,
at least 2.5-3 cm laterally from the uterotubal junction, with the bipolar
forceps. The tube is tented up to ensure the forceps are not in contact
with any other structure (e.g. bowel, sidewall), and non-modulated
cutting current (cutting, not coagulation waveform) is applied in each
tube to create a 3-cm contiguous area of desiccation.
Electrocoagulation causes greater tubal damage, making tubal reversal
more difficult if the patient regrets her decision.

Mechanical techniques
(a) Falope (Yoon) ring technique
A non-reactive silicone rubber band measuring 3.6 mm in outer
diameter and incorporating 5% barium sulfate for radiographic
identification is used. The applicator consists of inner grasping prongs
and an outer double-barreled sheath.
The Falope ring is stretched around the base of the narrow sheath, and,
after the prongs grasp the narrow isthmic portion of the tube (at least
3 cm from the uterine cornu), approximately 2.5 cm of tube is pulled
into the barrel. The larger-diameter outer barrel then pushes the
dilated Falope ring over the knuckle of tube, and the ring constricts
back to its undilated state, with an inner diameter of 1 mm.
The loop of tube should clearly contain 2 complete lumens of tube.
Slowly advancing the entire applicator toward the tube while gradually
retracting the tongs and tube into the applicator and avoiding
excessive traction on the tube are important. Failure to do this can
result in mesosalpingeal hemorrhage and tubal laceration. This can be
treated with bipolar coagulation, or a Falope ring may be placed on
each transected end.

(b) Hulka clip technique

The clip is designed to be applied at a right angle to the isthmic portion
of the tube 2.5-3 cm from the uterotubal junction. When properly
applied, only 4 mm of tube and virtually none of the blood supply is
destroyed.
The clip consists of 2 toothed jaws of plastic joined by a stainless steel
hinge pin. The lower jaw has a distal hook. A gold-plated spring
maintains the clip in an open position. When completely advanced, the
spring closes and locks the jaw.
The Hulka applicator is 7 mm in diameter with a 3-ring configuration at
the upper end consisting of a central ring (designed to accommodate

the thumb for stabilization) and a pair of lower rings (to accommodate
the index and middle fingers and control the clip application
mechanism). The distal end of the applicator has a fixed lower jaw to
accommodate the clip. A mobile upper jaw, when retracted, permits
placement of the open clip and, when advanced, closes the clip. When
completely advanced, a central piston locks the spring.
Once the fallopian tubes have been identified laparoscopically and
deemed suitable for clip sterilization, the Hulka clip applicator is
introduced with the clip in the closed position, and the clip is opened
after the applicator is intra-abdominal in position. The hook of the
lower jaw is placed against the posterior mesosalpinx, the tube is
tented slightly upwards, and the clip is applied. The clip may be
opened and repositioned repeatedly until the correct position is
achieved, at which time the center piston is advanced to permanently
lock the clip and unseat it from the applicator. If the clip has not been
applied satisfactorily, a second clip is placed immediately alongside
the first.
The applicator is withdrawn from the abdomen and reloaded, and the
contralateral tube is treated in the same fashion.
Failure of the Hulka clip should not exceed 2-3 cases per 1000 patients.

(c) Filshie clip technique

This technique involves a 12.7-mm long clip of titanium with a silicone
rubber lining. The clip is applied laparoscopically with an applicator,
much like the Hulka spring clip, at right angles to the isthmus
approximately 2-2.5 cm from the uterotubal junction.
Initially, the clip occludes the tubal lumen by pressure. As tubal
necrosis occurs, the rubber expands to maintain blockage of the
lumen. The tube eventually divides, and the stumps heal closed. The
Filshie clip usually remains attached and is eventually covered by
peritoneum. Theoretically, because the silicone rubber of the Filshie
clip is able to expand and provide continuous pressure even when the
tube becomes ischemic, any residual tubal patency, such as may occur
with the spring clip, is prevented.

Fig.1.10 Laparascopic sterilization by means of Filshie clips (arrows)

Advantages of Female sterilization:

Female sterilization does not involve hormones. It is a permanent form
of contraception. No data indicate that change in libido, menstrual
cycle, or lactation occurs. Female sterilization usually is a same day
procedure.

Disadvantages of Female sterilization:

Female sterilization is a procedure that involves general or regional
anesthesia. It is permanent contraception, and patients may regret the
decision later. Sterilization does not protect the patient from STDs.

Sterilization involves all of the risks of surgery. It creates short-term

discomfort.

MALE STERILIZATION - VASECTOMY

Vasectomy involves incision of the scrotal sac, transection of the vas
deferens, and occlusion of both severed ends by suture ligation. The
procedure usually is performed under local anesthesia in an outpatient
setting. Complications include hematoma formation and sperm
granulomas. Occurrence of spontaneous resolution is rare. After
sterilization, remnant sperm remains in the ejaculatory ducts. The man
is not considered sterile until he has produced sperm-free ejaculates as
documented by semen analysis. This usually requires 15-20
ejaculations. Vasectomy prevents the passage of sperm into seminal
fluid by blocking the vas deferens.
Efficacy: The failure rate is determined to be approximately 0.1%.
Advantages: Vasectomy involves no hormones, it is permanent, it is
an outpatient procedure, it is quick, and risk from the procedure is
minimal.
Disadvantages: Patients may regret the decision later. Alternative
contraception is required until the ejaculate is deemed sperm-free.
Vasectomy does not prevent STDs. Short-term discomfort occurs.

EMERGENCY POSTCOITAL CONTRACEPTION

Emergency postcoital contraception is defined as the use of a drug or
device to prevent pregnancy after unprotected sexual intercourse.
A variety of different methods of emergency contraception have been
described., such as emergency contraceptive pills, the Copper T380
IUD, and the minipill emergency contraception method.
Candidates for emergency contraception include reproductive-aged
women who have had unprotected sexual intercourse within 72 hours
of presentation independent of the menstrual cycle. No known absolute
contraindications to any of these methods.

Emergency contraceptive pills (ECP)

emergency contraception method (MECM)

and

the

minipill

The emergency contraceptive pills

mode utilizes 2 combined
contraceptive pills, each containing 0.05 mg of ethinyl estradiol and
0.5 mg of norgestrel, ingested 12 hours apart for a total of 4 pills. The
first dose should be taken within the first 72 hours after unprotected
intercourse.
Only the progestin levonorgestrel has been studied for the use in
minipill emergency contraceptive method. The treatment schedule is 1
dose of 750 mcg levonorgestrel taken as soon as possible and no later
than 48 hours after unprotected intercourse and a second dose taken
12 hours later.
The mechanism action of either the emergency contraceptive pills or
minipill contraceptive emergency method is not clearly established. If
administered before ovulation, both methods may inhibit follicular
development and maturation, resulting in anovulation and deficient
luteal function. Treatment following ovulation may affect the
endometrium, thus inhibiting implantation. They also may affect tubal
transport of the sperm or ova. However, both menses and fertility
return with the next cycle.
Efficacy: Most studies cite an effectiveness rate of 55-94%. Several
factors complicate the calculation of a failure rate. Factors include
dependence on the patient's history of their last menstrual period and
day of exposure, effect of regular and irregular menstrual cycles on the
calculation of the estimated time of ovulation, the possibility of the
patient being pregnant, and the possibility that more than one
unprotected coitus has occurred during that period.
Disadvantages: Adverse effects include nausea and emesis, minor
changes in menses, breast tenderness, fatigue, headache, abdominal
pain, and dizziness. Ectopic pregnancy is possible if treatment fails.

Copper
T380
contraception

intrauterine

device

as

an

emergency

The Copper T380 IUD can be inserted as many as 7 days after

unprotected sexual intercourse to prevent pregnancy. Insertion of the
IUD is significantly more effective than either the emergency oral
contraception
regimen, reducing the risk of pregnancy following
unprotected intercourse by more than 99%.

FUTURE METHOD OF CONTRACEPTION

Many new contraceptive designs are under investigation to provide a
greater variety of contraception that have fewer side effects, are safer,
and are more efficacious.
One of the more exciting new developments is a hormonal
contraceptive method for men. The male birth control pill manipulates
steroid hormones to decrease spermatogenesis, as well as testosterone
secretion.
Newer methods of subdermal implants are on the horizon. Implanon is
a single-rod implant that is 4 cm long and 2 mm in diameter. It consists
of 68 mg of etonogestrel in an ethylene vinyl acetate copolymer core.
Etonogestrel is a biologically active metabolite of desogestrel.
Desogestrel is significantly more potent than levonorgestrel; a serum
concentration of 0.09 ng/mL can inhibit ovulation in most women.
Serum concentrations are adequate for contraception coverage for
approximately 3 years. In more than 10 different studies utilizing 4000
women-years of use, no pregnancies have been demonstrated.
The advantages it has as compared to the Norplant system include
higher incidence of amenorrhea and oligomenorrhea, decrease in the
incidence of frequent and prolonged bleeding, and a decrease in the
incidence of side effects such as weight gain, headache, and acne.
When the rod is removed, the return to fertility is rapid, with return of
ovulation within 3 weeks. Implanon was approved for usage in the
United Kingdom in 1999, it still awaits FDA approval in the United
States. Understanding of the long-term effects and overall safety data
are limited at this point.
Uniplant is also a single-rod implant system that consists of 55 mg of
nomegestrol acetate in a capsule that is 3.5 cm long and 2.4 mm in
diameter. Uniplant has been shown to be highly effective for as long as
1 year, with incidence and degree of menstrual irregularities similar to
those of Norplant.
Clinical studies are in progress for a biodegradable implant, Capnor, to
eliminate the necessity of implant removal. This is a single 40-mm rod
that contains levonorgestrel and maintains contraceptive protection for
1 year.
Biodegradable pellet implants containing norethindrone and
cholesterol currently are undergoing investigation. They dissolve within

2 years and release the norethindrone for 12-18 months. Insertion of

the pellets has been demonstrated to be simple; however, if the
patient wishes for removal several months later, removal has been
noted to be difficult.
The contraceptive vaginal ring is a new form of contraception that is
expected to be on the market in the near future. The actual design of
vaginal rings as a mode of contraception was first developed in the
1970s. The first rings studied were homogenous devices with the
steroid mixed uniformly through a polysiloxane matrix. The design was
abandoned because of a high initial release of drug with rapid decrease
of drug release thereafter. The vaginal rings can deliver progesterone
or progesterone/estrogen combinations. The combined ring is in the
most advanced development phase. It releases both norethindrone
acetate and ethinyl estradiol. The hormones are released slowly and
absorbed directly by the reproductive organs. Preliminary studies
demonstrate efficacy of prevention of pregnancy similar to oral
contraceptives with fewer side effects.
The vaginal sponge is made of soft disposable polyurethane foam that
contains the spermicide nonoxynol-9. It offers an immediate and
continuous presence of spermicide throughout a 24-hour period. The
polyurethane foam is designed to trap and absorb semen before the
entry of sperm into the cervix. Clinical trials have demonstrated an
efficacy rate of 89% and 91% for parous and nulliparous women
respectively.
Lea's Shield is a 1-size-fits-all diaphragm-like device is another new
method of contraception under investigation. This device consists of a
1-way valve that allows air to escape during placement, thus creating a
suction effect against the cervix. The unilateral direction of the valve
permits uterine and cervical fluids to be released into the vaginal
canal, but prevents sperm from entering.
A few potential methods of tubal sterilization are under investigation.
One of these new developments includes chemical scarring of the
fallopian tubes. The scarring is a result of a combination of phenol and
a thickening agent and phenol quinacrine that ultimately leads to
blockage of the tubes. Another non-surgical form of tubal sterilization is
by utilizing chemical plugs. A reversible chemical plug also can be
created by the injection of silicone into the fallopian tubes. The silicone
eventually hardens but can be removed later. Chemical scarring and
plugs are under investigation as potential methods of vasectomy as
well.

A pregnancy vaccine is one of the most controversial and exciting

forms of contraception under development. The pregnancy vaccine,
unlike anti-infective vaccines, stimulates an immune response against
one or more host-specific antigens. The targets of the immune
response are accessible to the immune system during a finite time
period, such as coitus (sperm antigens in the female), egg maturation
(zona pellucida antigens), or successful fertilization (chorionic
gonadotropin).

40
PALLIATIVE CARE OF THE PATIENT WITH
ADVANCED GYNAECOLOGICAL CANCER
INTRODUCTION
Cancer of the female genital tract is a significant cause of morbidity
and mortality worldwide. In Malaysia, ovarian cancer is the deadliest of
gynecologic cancers, ranking fifth among all causes of cancer death in
women. In Malaysia and in countries where Papanicolaou testing (Pap
smear screening) and treatment of cervical dysplasia are widely
implemented, ovarian cancer is responsible for more cancer deaths
each year than cancers of the uterine corpus and cervix combined.
Elsewhere, in the absence of effective screening and early intervention
programs, cervical cancer is a much more common cause of
gynecologic cancer death.
When potentially curative treatment options are unavailable or are
ineffective, the clinical goal changes from cure to palliation. The
various gynecologic cancers, although arising from anatomically
adjacent organs, have different natural histories. Symptoms of
progressive disease vary with the site of primary tumor origin.
Strategies to palliate disease progression are therefore tailored to the
complications caused by the particular combination of local invasion
and distant spread encountered with tumors arising from a given site
of origin.

CERVICAL CANCER
Cervical cancer tends to spread locally before it metastasizes to distant
organs. When cervical cancer is confined to the pelvis or regional
lymph nodes, it may be cured with radical surgery, chemoradiation, or
both. When patients with cervical cancer have distant metastatic
disease, the cancer is generally not curable. In this setting, any
treatment administered is of palliative intent. As always, palliative
treatment should be directed at symptom control. Patients with
advanced or recurrent cervical cancer may have any of the following
symptoms:

VAGINAL BLEEDING:
Available interventions to control vaginal bleeding include vaginal
packing, radiation therapy, embolization of the uterine arteries,
surgical resection, or arterial ligation. Vaginal packing is usually a
temporary
measure.
Potentially
helpful
approaches
include
transvaginal orthovoltage treatment, high-dose fraction teletherapy, or
brachytherapy.
Fulminant hemorrhage might require embolization of the uterine
arteries, a procedure performed in the interventional radiology suite. If
radiographically directed embolization is not available, laparotomy with
ligation of the uterine arteries or the anterior divisions of the
hypogastric arteries is another alternative. A desperate measure of this
intensity is not appropriate when widespread dissemination of disease
causing imminent threat to the patient's life exists, but carefully
selected patients may derive meaningful benefit. Symptomatic anemia
from blood loss can be remedied with blood transfusions once
cessation of bleeding is accomplished.

PELVIC OR BACK PAIN:

Pain is often a very disabling symptom of advanced or recurrent
cervical cancer. Regional nerve, muscle, and bone infiltration can cause
severe discomfort. Narcotic analgesics are a fundamental component
of cancer pain treatment. Recognizing that narcotics can be delivered
via many different routes is important. Agents may be prepared for
oral, rectal, vaginal, sublingual, intravenous, intramuscular, and topical
administration.
Unfortunately,
narcotics
are
associated
with
troublesome and common adverse effects that must also be

addressed. These include constipation, pruritus, nausea, drowsiness,

and skin rash. Because constipation is almost universal with increasing
doses of narcotics, a bowel stimulant should be prescribed
simultaneously.
Nonsteroidal
anti-inflammatory
drugs
(NSAIDs)
and
certain
antidepressant medications can often provide a favorable synergistic
effect when prescribed concurrently with narcotics, especially for pain
thought to be of neuropathic origin. When pain is directly attributable
to specific foci of disease, such as bone metastasis or para-aortic
lymph node recurrence, a brief course of palliative radiation therapy
yields substantial pain reduction in a high percentage of patients.

DEPRESSION
Anxiety and depression are common comorbidities in patients with
malignancy of any type. Although these responses are not
inappropriate in a patient diagnosed with a life-threatening condition,
recognizing them and initiating intervention are crucial. Unless these
conditions are adequately treated, patients might be noncompliant
with other important therapies. Furthermore, efforts to control pain are
particularly compromised. Fortunately, several effective medical
therapies are available for both of these conditions. In addition to
anxiolytics and antidepressants, supportive counseling, spiritual
counseling, and family support can help counter feelings of depression
and anxiety.

TRUE URINARY INCONTINENCE (caused by fistulas) OR FECAL

INCONTINENCE:
Advanced cervical cancer may cause urinary fistulas. Vesicovaginal
fistulas are more common; ureterovaginal fistulas are less common.
Constant leakage of urine is extremely disturbing to many patients.
Although not necessarily painful, fistulous drainage can have an
extremely negative impact on quality of life. Patients with fistulas may
often choose to avoid social and family encounters, ultimately
becoming housebound.
Palliation of fistulas may be surgically accomplished by creation of a
ureterointestinal conduit or by placement of bilateral percutaneous
nephrostomies to obstruct the ureters. Both procedures require an
external appliance and maintenance. Functional status and operative
risk should guide the selection of the means of palliation.

Although placement of nephrostomy tubes is a simpler procedure than

surgical diversion of ureteral outflow, it is not necessarily a better
choice for patients with a life expectancy of more than a few months.
One disadvantage of percutaneous nephrostomies is the relative ease
with which these tubes become kinked or dislodged. The tubes can be
a source of infection and must be exchanged every few months. The
use of external pads (diapers) to absorb drainage is the simplest option
of all. However, in this authors experience, unless the patient is
confined to bed for other reasons, this is a choice of minimal benefit for
most patients.
Occasionally, rectovaginal fistulas occur from primary tumor invasion
of the adjacent rectum. These fistulas more often result from radiation
injury or tumor recurrence. A diverting colostomy is the surgical
procedure of choice in someone with a limited lifespan. Diverting end
colostomy is associated with fewer long-term complications than loop
colostomy.
EDEMA OF THE LOWER EXTRIMITIES:
Edema may result from generalized anasarca from protein depletion
and malnutrition. Alternatively, edema may be localized to the lower
extremities as a consequence of lymphatic and/or venous obstruction
due to a large tumor burden in the lymph nodes. Symptomatic relief of
edema and leg discomfort may be obtained by the use of graded
compression stockings, elevation of the extremities, and administration
of diuretics. Physical therapists with training and expertise in
lymphedema management can facilitate fluid drainage with external
massage maneuvers.

VENOUS THROMBOSIS:
Deep venous thrombosis (DVT) may cause secondary edema. For DVT
developing for any other reason, anticoagulation is standard treatment
unless medically contraindicated. Conventional or low molecular
heparin is usually followed by oral warfarin. Prolonged anticoagulation
is typically necessary because DVT often recurs in terminally ill
patients with recurrent cancer. Anticoagulation prevents further
extension of the thrombus and promotes gradual recanalization of the
vessel as the thrombus is resorbed. At the same time, collateral
vessels enlarge to accommodate more flow, and the net result is relief
of extremity swelling and improved comfort for the patient. Because
anticoagulation might exacerbate hemorrhage from recurrent cancer in

the pelvis or elsewhere, vena caval filters are sometimes preferable to

prevent pulmonary emboli.

DYSPNEA FROM ANAEMIA OR PULMONARY INVOLVEMENT:

Dyspnea may be a symptom of anemia, pleural effusion, infection,
heart failure, or lymphangitic spread of cancer. Blood transfusions
rapidly ameliorate the dyspnea of anemia. Thoracentesis with
pleurodesis should improve the symptoms of a malignant pleural
effusion. Pneumonia and heart failure should be treated as in the
patient without cancer. Lymphangitic spread of cancer can cause
hypoxia and dyspnea. Both oxygen and narcotics ameliorate this
symptom.

NAUSEA AND VOMITING:

Progressive or recurrent cervical cancer may cause uremia secondary
to ureteral obstruction. Uremia may induce nausea, vomiting,
somnolence, confusion, and seizures. Untreated uremia is eventually
fatal. Death may be delayed if ureteral obstruction is relieved by
percutaneous nephrostomy or ureteral stents.
Nausea and vomiting can occur as a result of mechanical obstruction of
the small or large bowel. Metabolic derangements, such as uremia,
infection, or central nervous system metastases, can also cause
nausea. Vomiting from small bowel obstruction can be relieved by
small bowel resection and reanastomosis, bowel bypass, ileostomy,
percutaneous gastrostomy tube, or nasogastric tube. Colonic
obstruction usually occurs at the rectum or sigmoid. Transverse loop
colostomy is a fast and relatively easy way to circumvent vomiting
from this problem.
Metabolic causes of nausea and vomiting can be relieved by correcting
the metabolic imbalance. Hypercalcemia is an uncommon
paraneoplastic manifestation of metastatic gynecologic cancer.
Hydration,
diuretics,
steroids,
calcium-binding
agents,
and
bisphosphonates should be considered. Immediate symptomatic relief
of nausea may be obtained with the use of phenothiazines,

antihistamines, steroids, or 5HT-3 antagonists. Nausea and vomiting

caused by brain metastases can be improved by the use of radiation
therapy and steroids.

GASTROINTESTINAL COMPLICATION e.g. Diarrhoea

Diarrhea can also accompany advanced or recurrent cervical cancer.
While loose bowel movements are a frequent result of acute lower
gastrointestinal toxicity from pelvic radiotherapy, this effect nearly
always resolves within a few weeks after treatment is completed.
Agents that reduce diarrhea include anticholinergics and opiate
derivatives such as loperamide, codeine, diphenoxylate sodium with
atropine, and Kaopectate.
Occasionally, diarrhea remains a long-term adverse effect following
successful treatment of cervical cancer. A suspected contributing
influence is chronic mucosal change within the terminal ileum (where
bile acid reabsorption can be impaired), especially when patients
experience exacerbation with intake of fatty foods. Dietary
modification can be particularly helpful in this regard.

OVARIAN CANCER
Recurrent ovarian cancer is seldom curable. Second-, third-, or even
fourth-line chemotherapy is often administered in a palliative fashion,
both to diminish symptoms and to prolong life. When
chemotherapeutic options are exhausted or the adverse effects are not
worth the small potential for benefit, other means of palliating
symptoms of progressive ovarian cancer are necessary.
Ovarian cancer spreads regionally in the form of scattered deposits of
tumor on all surfaces in the peritoneal cavity. Morbidity and mortality
as a direct result of this process are far more common than symptoms
related to recurrence, specifically at the primary tumor site or in
distant extra-abdominal sites. Bowel obstruction is a common terminal
effect of progressive ovarian cancer.
Rectosigmoid obstruction in the face of progressive disease is best
palliated with a transverse loop colostomy. Often, a small incision at

the stoma site is all that is necessary to identify the dilated proximal
colon and to elevate it through the anterior abdominal wall. The stoma
starts to function immediately, and patients can eat and return to their
baseline functional status soon.
Small bowel obstruction is more challenging. Multiple areas of
partial small bowel obstruction are typically not amenable to surgical
correction. Tumor implants on the bowel surface and mesentery cause
adhesions and impede peristalsis. Infrequently, an isolated small bowel
obstruction can be managed with bowel resection and reanastomosis.
More commonly, palliation is achieved with a percutaneous
gastrostomy tube draining by gravity or with a nasogastric tube on
suction.
Ascites can result from widespread microscopic and macroscopic
tumor infiltration over the peritoneum, preventing absorption of
peritoneal fluid. This symptom can become quite troubling when
progressive disease is unresponsive to chemotherapy. Patients
complain of pain, early satiety, vomiting, fatigue, and shortness of
breath. Diuretics are of limited efficacy in relieving malignant ascites,
and relief is best obtained by repetitive paracentesis. The eventual
metabolic impact is depletion of albumin. However, the immediate
temporary improvement in patient comfort usually takes precedence
over long-term nutritional status for a patient who is terminally ill.
Anorexia seldom occurs without a component of bowel obstruction or
ascites. For anorexia without associated bowel obstruction, treatment
with megestrol acetate or steroids can stimulate appetite and lead to
an increased sense of well-being. Parenteral nutritional support might
be appropriate as a short-term measure perioperatively following relief
of bowel obstruction or other intervention. However, long-term
parenteral nutritional support is seldom an appropriate measure in a
patient with incurable malignant impairment of bowel function.
Constipation may be an adverse effect of narcotic analgesics or
colonic dysmotility from tumor involvement. Treatment options range
from behavioral changes to medicinal agents. When possible, an
increase in fluid intake and exercise helps, as does close attention to
bodily signals of defecation. More useful to the patient with cancer is
the addition of fiber, colonic stimulants, and laxatives to their regimen.
For narcotic-induced constipation, stool softeners should be
combined with stimulant laxatives such as docusate sodium tablets
and senna or bisacodyl tablets. Cascara, a liquid cathartic derived from
tree bark, is also useful. For patients with obstipation or for those in
whom the above measures are inadequate, enemas and suppositories

are
helpful.
Enema
choices
include
warm
tap
water,
phosphate/biphosphate, soapsuds, milk and molasses, and mineral oil.
Bisacodyl or glycerin suppositories are also useful. Saline laxatives
draw fluid into the intestine, causing distention and reflex peristalsis.
Saline laxatives include magnesium sulfate, milk of magnesia,
magnesium citrate, Phospho-soda, and sodium phospate. Prolonged
use of these agents may cause fluid and electrolyte imbalance.
Stimulant laxatives include senna, bisacodyl, cascara, castor oil,
phenolphthalein, and danthron. These drugs may ultimately contribute
to a loss of normal bowel function and cause laxative dependence, but
this issue is often unimportant in the palliative care setting. Lubricating
agents include oral ingestion of mineral oil. Prolonged use of mineral oil
may lead to malabsorption of fat-soluble vitamins. Lactulose draws
water into the intestinal lumen, softens stools, and increases
defecation frequency. Excessive use can lead to fluid and electrolyte
imbalance. Polyethylene glycol electrolyte solution is useful for
stimulating defecation with minimal fluid or electrolyte imbalance.
Fatigue or dyspnea secondary to anemia can be treated with blood
transfusions or erythropoietin. Transfusions provide immediate
improvement, whereas erythropoietin injections may take weeks to
improve fatigue and require at least weekly injections

ENDOMETRIAL CANCER
Endometrial cancer may recur regionally within the pelvis or in distant
sites including the lung, bone, and liver. Complications from pelvic or
intra-abdominal disease progression are managed according to the
general principles previously outlined for cervical or ovarian cancer.
Recurrence in other sites warrants symptom-driven intervention.
Parenchymal lung metastases are often asymptomatic until erosion
into a bronchus or blood vessel occurs. Centrally located recurrence in
the mediastinum or hilar regions can cause superior vena cava
syndrome or large airway compromise. Palliative radiotherapy and
endobronchial stents are available therapeutic options. Metastases to
the pleural cavity may cause effusions and subsequent dyspnea.
Thoracentesis may temporarily improve the pulmonary symptoms. For

recurrent effusions, thoracostomy tube drainage and subsequent

pleurodesis relieve the symptoms of pleural effusion.
Bone metastasis can cause severe pain, jeopardize the spinal column
or nerve roots, lead to fracture, and contribute to hypercalcemia. Focal
external beam radiation directed at metastasis can prevent and
alleviate impending spinal or nerve root injury. Fractures or impending
fractures of the femur require orthopedic surgical fixation to stabilize
the weight-bearing structure. Postoperative radiotherapy is then
applied to prevent dislocation of the implanted devices as a result of
continued tumor cell proliferation within the remaining bone.
Hypercalcemia may accompany bone metastases, either as a direct
consequence of bone destruction or as an indirect paraneoplastic
phenomenon. Common symptoms of hypercalcemia include malaise,
fatigue, obtundation, anorexia, pain, polyuria, polydipsia, dehydration,
constipation, nausea, and vomiting. Cardiac dysrhythmias and cardiac
arrest may result. Untreated hypercalcemia may progress to loss of
consciousness and coma. As with correcting uremia by relieving
bilateral ureteral obstruction, correcting hypercalcemia can prolong life
and relieve symptoms; however, the quality of life preserved should be
reasonable. Prolonging dying by extending a period of suffering is
usually not in the patient's or family's best interest, especially when
the alternative may be a relatively painless death.
Treatment of hypercalcemia with subsequent reversal of symptoms
rests in restoring volume, increasing calcium excretion, and inhibiting
osteoclastic release of calcium. Administration of intravenous fluids is
the first step. Once volume has been restored, treatment with loop
diuretics increases calcium excretion. Avoid re-creation of a dehydrated
state with overly aggressive diuretics. In the palliative setting, a
significant decrease in tumor burden is unlikely; therefore, other
agents must be used to correct hypercalcemia. Administering
bisphosphonates, calcitonin, mithramycin, or gallium nitrate inhibits
osteoclastic activity. Bisphosphonates are the most popular agent
because of their ease of administration, relatively long duration of
action, and effectiveness throughout multiple treatments.
Liver metastases are usually asymptomatic and are frequently
detected only after other sites of disease have become manifest. A
potential role exists for systemic chemotherapy for treatment of
pulmonary or hepatic spread of disease, but response rates are
generally low. No consensus standard regimen exists for metastatic
endometrial cancer.

Hepatic metastases can occasionally enlarge and cause pain from liver
capsule distention. Analgesics, regional nerve block, and whole liver
radiotherapy can provide palliative benefit. Brain metastases may
cause a wide range of cognitive or behavioral abnormalities. Systemic
corticosteroids and radiation are usually employed to lessen the effects
of brain metastasis. Neurosurgical resection followed by whole brain
radiotherapy is appropriate for patients with a solitary solid tumor
brain metastasis, good performance status, and minimal disease
outside the central nervous system.

VULVA AND VAGINAL CANCER

Vulva and vaginal cancer, as with cervical cancer, tends to spread
locally before widespread metastases occur. Accordingly, vulva and
vaginal cancers can cause many of the same problems of pelvic and
systemic disease progression as the other cancers already mentioned.
Palliative treatment strategies are similar to those previously outlined.
Additionally, because of their relatively more superficial site of origin,
complications may arise as a result of disease involvement of the
perineal region and inguinofemoral nodal chains
Rectal fistulas or anal sphincter involvement might warrant
consideration of diverting colostomy. Groin node involvement may
compress the femoral vessels and cause lower extremity edema.
Vascular stents can sometimes relieve obstruction and improve edema.
Ulceration of the skin by infiltrative tumor can be treated with
radiotherapy if the region has not been pretreated too heavily with
radiotherapy during an initial attempted curative treatment. Other
topical treatments for localized ulcers include zinc oxide and gel-based
wound dressings.

SUMMARY
Palliative care of the patient with gynecologic cancer requires attention
to many diverse issues. As with most incurable cancers, pain control is
the dominant issue. Patients paramount fear is dying with uncontrolled
pain, and health care providers must adequately address pain needs.
Judicious use of narcotics, radiation, and nonnarcotic pain remedies is
essential. Bowel obstruction and fistulas remain common problems
resulting from progressive gynecologic cancer. Surgical procedures are
often used to ameliorate these problems. The skills of the

interventional radiologist are also useful for palliation of urinary fistulas

and ureteral obstruction.
Palliative care of the patient with gynecologic cancer requires the
services of many different specialists. A treatment team that may
include a gynecologic oncologist, a radiation oncologist, a radiologist, a
pain specialist from hospice services, and/or a palliative care physician
when available provides optimal palliative care.

41

GYNAECOLOGICAL PROCEDURES
COLPOSCOPY

 COLPOSCOPY is a technique of viewing the cervix using a

stereoscopic binocular microscope with a low magnification to
determine the source of abnormal cells. It consists of:

Soaking the cervix with vinegar (acetic acid).

Looking with binocular magnification (10x).
Using a green filter, and frequently
Taking small biopsies of the cervix.

INDICATIONS FOR COLPOSCOPY

Colposcopic testing is indicated any time a malignant lesion or
precursor is suspected in the cervix, vagina, or vulva. As mentioned
earlier, the most common reason for performance of a colposcopy is in
the evaluation of a woman with an abnormal finding on a Pap smear.

DIAGNOSTIC PROCEDURES
The colposcopic evaluation must be performed thoroughly and
accurately, and this can be accomplished only if a systematic routine is
meticulously followed.

Position the patient as comfortably as possible in the lithotomy

position.

Carefully insert a speculum of the appropriate size. For patient

comfort, this program uses a thinly applied water-based lubricant
to the speculum blades. This should not distort the subsequent
evaluation in any way. Try to avoid any trauma to the cervix on
insertion or opening of the speculum. Normal columnar
epithelium and dysplastic epithelium can be very fragile, and
even minor trauma can cause enough oozing to obscure findings.
Inspect the vagina and cervix visually with the naked eye. Gently
remove any excess mucus or discharge with a large cottontipped applicator moistened with saline. Document any clinical
findings on inspection.
Liberally apply 3-5% acetic acid with a large cotton swab
saturated with the solution. This must be in place for at least 60
seconds prior to inspecting for changes. If evaluation takes more
than 3-5 minutes, acetic acid should be reapplied.
Position the colposcope and focus on the cervix with the desired
magnification.
Inspect carefully to ensure that the entire transformation zone
(TZ) can be observed. If the TZ is at the external os, the use of
an endocervical speculum can aid in the visualization. If the
entire TZ cannot be observed adequately, the evaluation must
be considered unsatisfactory. Cervical cone via loop
electrosurgical excision procedure (LEEP) or cold knife then
would be indicated.
Identify and document with drawings and description the
presence of any acetowhite lesions and their internal vascular
patterns. Use of the green filter at this point can improve the
ability to identify lesion margins and vascular patterns.
Biopsies should be obtained from all lesions with any potential
for invasion. Extensive experience is required before any
individual clinician can be comfortable not performing biopsies
on all acetowhite lesions. Specimens should be removed from the
instrument and placed in an appropriate fixative.

The speculum is removed, and patient instructions are provided.

Spotting and a light discharge can be anticipated. Coitus should
be avoided for 7-10 days, and a follow-up examination and
discussion of pathologic findings should take place in 1-2 weeks.

Many expert colposcopists also place Lugol solution (dilute iodine) on

the cervix after initial examination and before any biopsies are
obtained. This technique is based on the differential staining of cells
with different glycogen content with this solution. Normal mature
squamous cells have a high glycogen content and typically stain a dark

mahogany brown. Columnar cells and dysplastic cells have minimal

glycogen and tend to stain mustard yellow. This step can be helpful in
outlining lesions and the TZ if an excisional procedure such as a LEEP
cone is to be performed without colposcopic guidance.

NORMAL COLPOSCOPIC APPEARANCES

On the normal cervix three types of epithelium can be identified.
Normal squamous epithelium of the ectocervix
This
is
the
mature
and
native
epithelium.
At colposcopy, using
ordinary light, it appears smooth and
pink with distinct vascular markings at
low
magnification
(10x).
These
epithelium becomes more obvious by
inflammatory
changes,
and
in
pregnancy. It stains a mahogany colour
with Schillers iodine solution.
Fig.1.1 The normal cervix squamous epithelium

Endocervical epithelium
This is a mucus-secreting glandular
(columnar) epithelium and has a
glistening
red
papillary
surface
resembling small grapes which become
more whiter when treated with acetic
acid solution. Normally it is confined to
the endocervix. It may also be found
extending on to the ectocervix, when it
is referred
Fig.1.2 The normal cervix columnar epithelium

Transformation zone mestaplastic squamous epithelium.

The term transfomation zone is used to describe that part of the
cervix which at one stage in its life had been covered by columnar
epithelium, but subsequently changed to squamous epithelium by the
process of metaplasia.
This area contains areas of columnar
epithelium and metasplastic squamous epithelium of various stages of
maturity.
It also contains cervical crypt openings.
In the

premenopausal the transformation zone is usually wholly visible,

wheras in the postmenopausal woman it can be found in part or totally
in the endocervical canal.
Mature metaplastic squamous epithelium can be recognized by the
presence of crypt openings and branching vessels.
It is in this atypical areas of transformation zone that the invasive
lesion of squamous carcinoma of the cervix are thought to originate.
Such abnormal transformation zone is acetowhite and will exhibit
atypical appearance such as vascular punctation or mosaic.

Squamous
epithelium

Columnar epitheliun

TZ

Fig. 1.3 The normal cervix Transformation zone (TZ)

COLPOSCOPY OF THE ATYPICAL TRANSFORMATION ZONE

The atypical transformation zone is the area of the cervix whose cervix
limits defines cervical intraepithelial neoplasia.

Acetowhite epithelium
Squamous epithelium

Transformation zone

This is a focal abnormal

colposcopic appearance after
the application of acetic acid. It
is a transient phenomenon
associated
with
increased

nuclear density. It is the most commonly found of all abnormal

features associated with abnormal transformation zone but is not
diagnostic of CIN1. It may be found in association with Human
papillomavirus (HPV) infection, immature squamous metaplasia. In
general, the more intense the change, the more extreme the degree of
histological abnormality.

Vascular pattern
The view pattern and caliber of the subepithelial capillaries frequently
give a striking colposcopic appearance.
There are three clearly
identifiable types.
a): Mosaic
This
is
a
focal
abnormal
colposcopic appearance in which
the vascular patterns show fields
of
mosaic
within
the
transformation
zone.
The
capillaries appear parallel to the
surface, giving the characteristic
mosaicism pattern. The wider
the caliber and greater the
surface area enclosed, the more
likely a greater degree of
abnormality.

b): Punctation
The stromal capillaries produce a
stippled or punctate appearance
within the epithelium. The degree
of punctation may be fine with
evenly spaced loop capillaries of

narrow calibre with minimal intercapillary distance. In more marked

change, the course and caliber of the capillaries is altered, with coarsecalibre vessels resembling corkscrews. In general the more severe the
change the greater the degree of histological abnormality.

c): Atypical vessels

These vessels are frequently arranged in a haphazard way. New
vessels are formed and often demonstrate gross variation in caliber
and branching. At the extreme, the appearances of atypical vessels
are suggestive that early invasion of the stroma may have taken place.

Fig.1.4 The atypical transformation zone: highly atypical vessels.

Table 1. GRADING OF COLPOSCOPIC FINDINGS

Grade I

Grade II

Grade III

The epithelium is flat

and white

The epithelium is flat

but more wide

The epithelium is
intensely acetowhite

The
vessels
regular
and
calibre

The
vessels
are
regular but or larger
calibre

The blood vessel are

dilated and irregular

are
fine

There
are
many
atypical vessels

The
surface
are
uneven in contour
suggestive of early
invasion

COMPLICATIONS
Complications from colposcopic procedures are exceedingly rare.
Occasionally, bothersome bleeding can occur following biopsy. This
tends to be problematic only with procedures performed during
pregnancy or with large excisional procedures. Infection of biopsy
sites also is exceedingly rare, although it can occur following laser
ablation or LEEP procedures. The most worrisome complication is
inadequate or inaccurate evaluation leading to the missed
diagnosis of invasive cancer. This obviously can lead to treatment
delays and poorer outcomes. Another complication is the
overestimation of lesion severity by inexperienced practitioners.
This can put the patient on a treatment course that may not be
necessary and has the potential for adverse sequelae.

TREATMENT
Following accurate colposcopic evaluation of a cervical lesion,
appropriate treatment then can be tailored to the individual patient's
needs. Treatment options include conservative follow-up with cytology,
ablation with cryotherapy or laser, excision with LEEP or cold knife
cone, and hysterectomy for invasive lesions. Regardless of treatment
undertaken, plans for follow-up screening should be stressed to
evaluate for recurrent or residual disease.

CERVICAL SMEAR
(PAP SMEAR)

Fig.1.1 Technique for taking a cervical smear (1 and 2) Cervical

scrape,
(3) Spreading the scrapings on to the glass slide

Dr. Papanicolaou developed a technique for sampling the cells of

the cervix (Pap smear) to screen patients for cancer of the
cervix. This technique has proven to be very effective at not only
detecting cancer, but also the pre-cancerous, reversible changes
that lead to cancer.
So useful has the Pap smear become, it is considered an
essential part of women's health care. It is typically performed
annually in sexually active women of childbearing age, although
there are some important exceptions.
Because the Pap smear is a screening test, it can have both false positive and false
negative results. For this reason, it is important to have the test performed
regularly. It is not likely that the Pap smear will miss an important lesion time
after time.
In most countries, cervical screening is opportunistic and a cervical
smear is only available on request. In some developed countries, they
have organized screening programmes of three to five years.
CERVICAL CYTOLOGY

A cervical smear properly taken with an Ayre spatula contains variety

of cells, some of which have been exfoliated locally and trapped in the
cervical mucus, and others which have been detached forcibly by the
spatula from the region of the external os. A smear taken from normal
cervix may therefore contain:

Cells from original squamous epithelium of the ectocervix;

Cells from the columnar epitjelium of the endocervical canal;
Cells from the metaplastic epithelium of the transformation zone;
Cells from the other part of the genital tract, e.g. endometrial cells;
Leucocytes and red blood cells;
Commensal organisms; cervical mucus strands; and
Contaminations, e.g. spermatozoa.

Cells shed from the cervical epithelium

Four types of epithelial cells can be recognized in smear, i.e.
superficial, intermediate, parabasal and columnar.

Superficial cells these are shed from the surface of fully mature
squamous epithelium. They appear in the smear as large polygonal
squames with transparent cytoplasm which are stained delicate
pink. The nuclei of the superficial cells also reflect the maturity of
the epithelium.
Intermediate cells these are shed from the surface of
semimature squamous epithelium. These flat squames are only
slightly smaller than the superficial; cells. Intermediate cells are
less angular appearance and the nucleus size is larger. They
cytoplaqsm of the intermediate cell is normally more cyanophilic
and denser.
Parabasal They are found in atrophic smear such as those
obtained after menopause.
The cells are small with dense
cytoplasm and granular nucleus. The nucleus appear larger. The
cytoplasm is generally cyanophilic.
Columnar cells these cells are derived from the epithelium lining
of the emdocervical canal crypts. They may appear as a single cell
or as a sheet of cells.
Endocervical cells can usually be
distinguished from parabasal cells by their eccentric neuclei.

INDICATION FOR CERVICAL SMEARS

The indications for cervical smear test include the following:
1) As a method of screening programme for cervical pre-cancer and
early cervical cancer: The cervical smear is offered as method of
screening by most countries for preinvasive and invasive cancer of
the cervix. Each countries have their own screening programmes.
2) As an investigation of a woman suspected clinically of having
cervical cancer: A cervical is useful in patient have symptoms or
signs suggestive of cervical cancer such as postcoital or
postmenopausal bleeding.
3) As a follow-up procedure of patients following treatment of CIN:
Cervical smear are mandatory in monitoring patients who have
received treatment for CIN. This follow-up smears are able to detect
any evidence of residual disease after treatment and also to detect
any recurrence. The protocol for follow-up smears are three months
after treatment and then six months after treatment and then
yearly. After five negative smear the interval of cervical smear can
be extended as the general population.
Who needs cervical smear testing?
The answer is, every sexually active woman should be advised to have
a cervical smear. It is also recommended for women on hormonal
contraception methods.
At what age should cervical smears start?
It is generally recommended that woman who are have been pregnant
and delivered previously, who are on hormonal contraception and
women who are exposed to sexually transmitted diseases should their
first smear by 25 years old and rest of the women who are sexually
active should have their first smear at 30 years.
How often should a smear be done?
The first smear should be repeated ideally a year later to guard against
false-negative results. After that every 3 years is adequate for women
who have previously been fond normal. In the age group 35-45 a one
year interval is advisable.

When should cervical smear stop?

Cervical neoplasia changes are rarely seen after 60 years of age and so
regular smear testing of a normal woman could stop then.
THE PROCEDURE
Instruments required:
It is advisable to get ready the essential instruments for the cervical
smear procedure.
Fig. 1.2 Requirements for cervical smear

Cuscos speculum

Ayres spatula

Pencil
Fixing jar
Glass slides

Cytobrush

Taking the cervical smear

The woman lies on her back with her knees drawn up.
No bimanual examination should be done carried out before the
smear is taken.
The cervix is exposed with a Cuscos speculum preferably without
using any lubrication.
After the cervix has been exposed a scrape is taken from the
ectocervix and the full circumference of the squamous-columnar
junction with an Ayres spatula rotating through 360 movement
(Fig.1.1). For young, multiparous and premenopausal women the bilobed end of the spatula is used, while the tapered end of the
spatula is for postmenopause women.
Cytobrush is used when the os is stenosed, squamous-columnar
junction is high up in the endocervical canal.

Tapered end for menopausal

women

Bi-lobed end is for young

and premenopausal women

Fig.1.3 Choice of spatula for different age group of women

The materials from the end of the spatula are evenly spread over
the glass slide (Fig. 1.4). The name of the patient should been
written on the glass slide.
Direction of spreading the scrapping on the glass
slide

Patient name
Scrapings material on the glass slide
Fig. 1.4 Spreading the scrapings on the glass slide with the Ayres spatula

The specimen is then immediately fixed in a fixing jar containing

fixing fluid, usually 95% alcohol.
Alternatively, spray fixation

containing an aerosol agents and different mixture of alcohol can be

used for fixation.

Any cervical smear sent to a pathologist must be accompanied by

adequate information about the patient (such as her name, age,
details of any previous pregnancies, her menstrual cycle, method of
contraception used and also information about the state of the
cervix).

STAINING PROCEDURES
A modified Papinocolaou stain is used to stain the slide. The stained is
design to distinguish between the keratinized and non-keratinized
epithelial cells. Squames which contain keratin assume a delicate pink
colour, whereas the cytoplasm of non-keratinized cells is blue.

Fig.1.5 Cervical smear Mild dyskaryosis suggestive of CIN1. Note large squames
cell with enlarged nuclei of varying size.

COMMON ERRORS IN SMEAR PREPARATION AND PROCESSING

1. Insufficient material in the scrape.

2. Thick films with inadequate spread of material.
3. Material collected from the wrong site, e.g. scraping the posterior
vaginal wall instead of the cervix.
4. Use of slides which are insufficiently cleaned.
5. Air drying before fixation or during the staining procedures.
6. Insufficient fixation for too short times or use of too weak alcohols.
7. Incorrect staining.
Any one of these mistakes may seriously interfere with the correct
interpretation of the slides. Correct preparation, fixation and staining
of the specimens are fundamental steps in cytological investigation of
a woman. Even the most experience cytologist cannot achieve a
correct diagnosis when a faulty specimen is submitted to him.
WHAT CONSTITUTES AN ADEQUATE SMEAR?
An adequate smear should contain abundant squamous cells which are
evenly spread and well displayed. It should also contain evidence of
transformation zone sampling in the form of endocervical or immature
metaplastic cells.
THE SMEAR REPORT
Reporting the cervical smear can be either using the UK or Bethesda
system. Bethesda system differs from the UK system in that it
introduces several new categories of lesion, namely high-grade and
low-grade squamous intraepithelial lesions (HSIL and LSIL) and atypical
squamous (or glandular) epithelial of unknown significance (ASCUS or
AGUS).
TERMINOLOGY:
Mild dysplasia means the skin cells of the cervix are reproducing
slightly more quickly than normal. The cells are slightly more plump
than they should be and have larger, darker nuclei. This is not cancer,
but does have some pre-malignant potential in some women. Other
phrases that describe mild dysplasia include:

LGSIL (Low-grade Squamous Intraepithelial Lesion)

CIN I (Cervical Intraepithelial Neoplasia, Grade 1)

Many factors contribute the development of mild dysplasia, but

infection with HPV, (Human Papilloma Virus) is probably the most

important. Smoking tobacco products and an impaired immune system

also may contribute to this.
Mild dysplasia can come and go, being present on a woman's cervix
(and Pap smear) at one time and not another.

Moderate dysplasia means the skin of the cervix is growing faster

than it should and has progressed beyond the mild stage. A biopsy of
the cervix would show immature basal cells growing partway through
to the surface of the skin, without significant maturation.
Moderate dysplasia is important because there is a much greater risk
that these changes will advance, if untreated, into invasive cervical
cancer. For that reason, moderate dysplasia is known as a "high
grade" lesion, or "high grade squamous intra-epithelial lesion"
(HGSIL). Another synonym for this condition is "CIN II" (Cervical Intraepithelial Neoplasia Grade II).

Severe dysplasia means that the skin of the cervix is growing so

rapidly that the immature basal cells extend completely through the
skin thickness to the surface with any maturation. This is evidenced on
the Pap smear as many completely immature cells appearing on the
slide. This condition, a high grade intraepithelial problem, is also
known as "CIN III." (Cervical Intraepithelial Neoplasia, Grade III), or
"carcinoma-in-situ."
This is not cancer, but the only reason it isn't cancer is because the
immature cells have not started growing (invading) beneath the
epithelium into the underlying tissues. Because it is only one step
away from invasive cancer, this is a very dangerous condition requiring
treatment.
Treatment might consist of eliminating the dysplastic cells by freezing
them (cryosurgery), vaporizing them (laser), or shaving them off with
an electrified wire loop (LEEP). In some circumstances, more extensive
surgery in the form of a cervical cone biopsy is required to eliminate
the problem.

CIN (Cervical Intraepithelial Neoplasia)

CIN (Cervical Intraepithelial Neoplasia) is an older term that describes
the process of dysplasia. There are degrees of CIN:

CIN I is equivalent to mild dysplasia and low grade SIL

(Squamous Intraepithelial Lesion)
CIN II is equivalent to moderate dysplasia and represents a high
grade SIL
CIN III is equivalent to severe dysplasia, carcinoma-in-situ, and
is a high grade SIL.

SIL (Squamous Intraepithelial Lesion)

This is a general term for dysplasia.
Low grade SIL (LGSIL) includes mild dysplasia, HPV changes, and
CIN I. These are considered "low grade" because the risk of
progression to malignancy is small (10% or less).
High grade SIL (HGSIL) includes moderate dysplasia, severe
dysplasia, carcinoma in situ, CIN II and CIN III. These are considered
"high grade" because many of them (although not all) will progress
ultimately to invasive cancer of the cervix if not treated.

Table 1. Interpretation of smear result recommended by the British Society for Clinical
Cytology

Cytology report

Explanation

Inadequate

Negative

Borderline changes with or

without HPV change

Mild dyskaryosis with

without HPV change

Moderate dyskaryosis with

or without HPV changes

Severe dyskaryosis with or

without HPV changes

Severe
dyskaryosis/
invasive carcinoma

Glandular
neoplasia
suspicion of glandular

or

Insufficient cellular material, inadequate

fixation, smear consisting mainly of blood or
inflammatory exudates; little material to
suggest transformation zone has been
sample.

Normal. Includes
changes.

Cellular appearances that cannot be

describe as normal. A smear which there is
doubtful as to whether the nuclear changes
are inflammatory or dyskaryosis

Cellualar appearance consistent with origin

from CIN 1 (mild dysplasia)

Cellualar appearance consistent with origin

from CIN 2 (moderate dysplasia)

Cellualar appearance consistent with origin

from CIN 3 (severe dysplasia/carcinoma in
situ)

Cellualar appearance consistent with origin

from CIN 3, but with additional features
which suggest the possibility of invasive
cancer.

Celluar appearance suggesting precancer or

cancer in the cercal canal or the
endometrium

or

simple

inflammatory

Source. Practical Guide for General Practitioner (14): Cervical screening (1992)
Austoker, J. and Macpherson, A. Cancer Research Campaign, Oxford Medical
Publications.

Table. 2 Bethesda system

Adequacy of the specimen

o Satisfactory for evaluation
o Satisfactory for evaluation but limited by(specifyb reason)
o Unsatisfactory for evaluation .(specify reason)

General categorization (optional)

o Within normal limits
o Benign cellular changes (see descriptive diagnosis)
o Epethilial abnormality. (see descriptive diagnosis)

Descriptive diagnosis

BENIGN CELLULAR CHANGES

Infection
o Trichomonas vaginalis
o Fungal organism (e.g. candida)
o Herpes simplex viruses
o Bacteria

Reactive changes
o Reactive cellular changes
o Inflammation
o Atrophy with inflammation (atrophic vaginitis)

EPITHELIAL CELL ABNORMALITIES

Squamous cell
o Atypical squamous cells of undertermined significance quality
(ASCUS)
o Low-grade squamous intraepithelial lesion (LSIL) encompassing: HPV,
mild dysplasia/CIN 1
o High-grade squamous intraepithelial lesion (HSIL) encompassing:
moderate and severe, CIS/CIN 2 and CIN 3

Table 3.
Correlation between UK and Bethesda reporting systems: squamous
epithelial cell abnormalities

BETHESDA SYSTEM

ASCUS
LSIL

HSIL

BRITISH SYSTEM

Borderline nuclear change

Mild dyskaryosis (CIN 1)
Moderate dyskaryosis
(CIN 2)

Severe dyskaryosis
(CIN 3)
SQUAMOUS CELL
CARCINOMA

SQUAMOUS CELL
CARCINOMA

HYSTEROSCOPY

Fig.1.1
diagram

rigid hysteroscopy procedure resecting intracavitary fibroid.

Schematic
showing

Direct inspection of the interior of the cervical canal and uterus by

hysteroscopy is now a standard part of tge gynaecological
investigation.
Hysteroscopy uses a hysteroscope, which is a thin telescope, either
flexible or rigid, that is inserted through the cervix into the uterus.
Hysteroscopy procedure can be
performed as an out-patient or
in-patient procedure.
Modern hysteroscopes are so
thin that they can fit through
the cervix with minimal or no
dilation. Because the inside of
the uterus is a potential cavity,
like a collapsed air dome, it is
necessary to fill (distend) it with
either a liquid or a gas (carbon
dioxide) in order to see.

Fig.1.2 Flexible hysteroscope

Diagnostic hysteroscopy can be

done as an outpatient procedure

and usually a flexible hysterscope is used and uses a carbon diaoxide

as a filling medium. During diagnostic hysteroscopy the hysteroscope
is used to observe the endometrial cavity and to obtain an endometrial
biopsy.
Alternatively, the procedure may be performed during a short in hospital under general
anaesthesia, using a rigid scope and saline to distend the uterine cavity.

INDICATIONS
Diagnostic hysteroscope: investigated by hysteroscope:

The following

conditions

can be

Any abnormal uterine bleeding, such as intermenstrual bleeding,

persistent menorrhagia, postcoital bleeding or postmenopausal
bleeding
Suspected uterine malformation
Suspected Ashermans syndrome

Operating hysterscope:
An operating hysterscope can be used in the following condition:

To resect endometrial polyps or submucous or intracavitary fibroids.

Transcervical resection of endometrium (TCRE) or endometrial
ablation, under direct hysteroscopic vision in the treatment for
menorrhagia.

This is a view through a hysteroscope

examination.
It shows the inside of a uterus with two
intracavitary myomas on the back wall.
The upper portion of the photograph
shows the top of the uterus, which is
normal.
Fibroids
like
this
can
dysmenorrhea,
menorrhagia
bleeding between periods.

cause
and

A): Endometrial cancer

B): A submucous

myoma
Fig.1.3 Hysteroscopic view of the uterine cavity showing abnormal pathology of the
endometrium

Hysteroscopic submucous myoma resection

This procedure entails the introduction of a small telescope through the
cervix, thus allowing the inside of the uterus to be seen visually.
Protruding fibroids may then be shaved sufficiently to allow the
configuration of the uterine cavity to be returned to normal. This is
appropriate for those patients who wish to maintain their fertility, and
are having heavy or prolonged periods, as the possibility for conception
and uterine implantation will still exist.
COMPLICATIONS

Perforation of the uterus

Damage to the cervical sphincter, if dilatation is required.
Ascending infection

CYSTOSCOPY IN GYNAECOLOGY

Fig.1.1 Schematic representation of cystoscopy

Cystoscopy is one of the common gynaecological procedures, which gives a direct

inspection of the interior of the bladder. Cystoscopy involves passing a small diameter
cystoscope through the urethra into the bladder after the bladder is distended with
normal saline. Complications include infection and baldder perforation.

INDICATIONS
Cystoscopy is indicated in the following conditions:
To investigate the causes of haematuria.
Assessment of baldder neck.
Assessment for recurrent urinary tract infection.
To evaluate when suspected bladder abnormality (e.g. diverticulum,
fistula)
As a procedure for the staging of cervical cancer.

Fig.1.2
papilloma

Cystoscopic view showing bladder

42

GYNAECOLOGICAL OPERATIONS
(Pre-operative assessment and Post-operative complications)

Gynaecologic surgery forms the common procedures in the

gynaecological practice. Gynaecological operations may be broadly
divided into minor operations mainly performed by the vaginal route
and major operations performed by vagina or through the abdomen.
Dilatation and curettage (D&C) is the most common minor procedure,
which is performed for diagnostic or therapeutic reasons.
Hysterectomy is still the most common major operation.
The main reasons for gynaecological surgery are:
1) Diagnostic
and
therapeutic
procedures
for
menstrual
abnormality.
2) Correction of congenital abnormalities that infers with menstrual
function and/or fertility.
3) Treatment of chronic pelvic pain and endometriosis.
4) Treatment of benign and malignant tumours.
5) Repair of childbirth injuries sustained by the uterus and vaginal
and their supporting structure.

PREPARATION FOR GYNAECOLOGICAL OPERATION

The aim is to have the patient in the optimum and physical fitness,
which is essential for surgical procedures and adequate recovery
following surgical procedure.
COUNSELLING AND CONSENT
Every woman has their right to know about the extent and risks of any
planned surgical procedure. It is the responsibility of the doctor to give
an outline and further information about the intended surgical
procedure including the possible complication. After the surgery, the
woman should be told precisely what has been done and complications
which has arisen.
All patients should sign a consent form for the intended surgical
procedure after hearing the relevant explanation by a doctor, who
should also sign the form to acknowledge that everything has been
explained to the patient. This is a medico-legal document, which
includes the patient name, and the type of surgical procedure to which
she is about to consent. Any alternative and additional measures,
which may be performed if necessary, should also be included in this
consent form.

PRE-OPEARTIVE PREPARATION
HISTORY
A complete history is taken (see Chapter 1) with special attention to
any recent illness. The date of the last period should be note. The
possibility of pregnancy must be borne in mind. Note should be made
of any drugs being taking, especially ones which could affect the
outcome of the operation. These include corticosteriods, anti-diabetic
agents, drugs acting on the cardiovascular system, monoamine

oxidase inhibitor (MAOI), oral contraceptive pills, and antidepressant or

anticonvulsant.
CLINICAL EXAMINATION
A general examination is made to examine the heart and lungs and
estimate blood pressure. Examination of the abdomen and pelvic
organs follows. The lower limbs are inspected for varicose veins. The
patient undergoing elective surgery should be as fit as possible.
INVESTIGATIONS
Certain investigations should be performed:
1) Haemoglobin: An estimation of a haemoglobin is made in
every case before operations. It is unwise to carry out major
elective (except for an emergency) surgery with a haemoglobin
level below 10 gm percent.
2) Urine analysis: The urine is tested routinely for albumin and
sugar by dipstick analysis. If there is any suspicion of urinary
tract infection, a mid-stream urine specimen is sent for
bacteriological examination and culture and sensitivity,
especially if urogynaecological procedures are intended.
3) Renal function test: Blood urea, serum electrolytes and serum
creatinine may also be estimated if there is suspicion of renal
impairment.
4) Chest X-ray: An X-ray of the chest is taken if there is any doubt
about chest disease. Intravenous pyelogram is often done before
operations when the ureters may be involved as in Wertheims
hysterectomy.
5) Electrocardograph (ECG): An electrocardiograph is desirable
in patients with any suggestion of heart disease.

NURSING PREPARATIONS
1) Shaving: the vulva is usually shaved for major surgery but
shaving is unnecessary for minor surgery.

2) Bowel preparation: The lower bowel should be well emptied

by either an enema or by Dulcolax suppositories for major
surgery.
3) Diet: Patients should be starved from 12 mid-night prior to
surgery for an elective surgery.
4) Prophylactic antibiotic:
Prophylactic antibiotic may be
administered, depending on the operations and the surgeon
wishes.

POSTOPERATIVE CARE
During the first 12 hours after an operation the patient must be
carefully observed for the following:
Respiratory failure
Shock
Haemorrhage
Cardiac failure
After surgery the patient should be monitored and provide care as
follows:
Care immediately after surgery:
The patient should not be left unattended until she has recovered
consciousness.
The pulse rate and blood pressure should be recorded every
15 minutes for the first 2 hours and then every hour for the first
12 hours.
Pain must be relieved by adequate dose of analgesics such as
pethidine.
Addition of anti-emetic such as promazine or
promethazine can help to prevent post-operative vomiting.
Postoperative analgesia is given initially by injection and then
orally after 24-48 hours.
Monitoring for per vaginal haemorrhage - The patient
should be put on pad chart especially following hysterectomy to
monitor any per vaginal bleeding post-operatively.
Fluid and electrolyte balance This may be disturbed if too
much or too little intravenous fluid is administered. A strict input
and output fluid chart should be maintained in order to avoid
problem.

Day 1 to 2 post surgery:

If bowel sounds are present fluids may be allowed orally and the
intravenous infusion discontinued.
Catheter and any drain may be removed.
The patient is encourage to mobilize and sits out of bed. This
can minimize or prevent thrombophlebitis and deep vein
thrombosis.
Day 3 to 4 post surgery:
The haemoglobin is usually measured on day 3.
The wound is inspected for any infections.
Signs of infection
include redness, swelling, wound discharge and tenderness.
Fever may accompany the wound infection.
Day 5 post surgery:
Unabsorbable skin sutures or clips are removed from day 5
onwards.
A fit patient with no complications may leave the hospital.
Follow-up:
For major surgery a follow-up appointment is usually made at 6 to 8
weeks, so that patient can discussed any outstanding problems and a
clinical examination can be performed to confirm that all is satisfactory.
During the follow-up patient are given advice regarding resumption of
sexually activity and her social or household activities.
POSTOPERATIVE COMPLICATIONS
Postoperative complications may be grouped as follows:
HAEMORRHAGE:
Haemorrhage may either be primary, i.e. occurring during the
operation and requiring immediate transfusion; reactionary
occurring during the immediate postoperative period and generally
due to slipped ligature or a bleeding vessel in the vagina or cervix; and
secondary occurring 10 to 14 days after operation and generally
from the vagina or cervix but sometimes from the abdominal wound.
Treatment is by suturing the bleeding area and blood transfusion.

RESPIRATORY TRACT INFECTION

Chest infection is common in patients who smokes or in those with
other lung disease. Respiratory tract infections may also be due to
anaesthetic complications. Complications of a general anaesthesia
include sore throat, bronchitis, bronchopneumonia and massive
collapse of the lungs. Pulmonary infection is treated with antibiotics
URINARY TRACT
Retention of urine is usually encountered with any vaginal surgery
involving urethra and bladder neck. Treatment of retention of urine
consists in immediate catheterization.
Postoperative urinary tract infections are very common after
gynaecological operation.
The causative factors of urinary tract
infection are the catheter and some degree of retention of urine. Most
of the urinary tract infection after pelvic surgery fortunately remained
localized to the lower urinary tract and symptoms and signs are those
of cystitis. The symptoms include dysuria, frequency, and urgency. The
commonest causative agent is E.coli.
Some urinary tract infection is acute pyelonephritis and patient is very
ill with high fever, rigor and vomiting. The patient usually complaints
of lion pain and renal angle are tender to palpation.
A catheter specimen or a mid-stream specimen should be examined for
evidence of infection and suitable antibiotic given.
WOUND INFECTION
A wound infection is more likely to occur where the following
predisposing factors are found:
a large wound
a haematoma
surgery following infective source
Wound infection usually occurs from day 3 onwards post surgery. The
patient will have pyrexia and painful and redden wound, which may be
discharging.
Treatments consist in taking wound swab and
administrating antibiotic and also daily dressing of the wound.

WOUND DEHISCENE
This is one of the major complications. Wound dehiscence may partial
or complete.
Etiological factors may be pre-operative (diabetes,
malnutrition, irradiation, malignancy disease and obesity), operation
(surgical techniques mainly failure in haemostasis, infection control
and suturing) or post-operative (increased abdominal pressure, wound
haematoma and infection). The obvious sign is leakage of clear or
blood stained serum from the skin defect usually from day 4 onwards.
In complete wound dehiscence (burst abdomen) the abdominal
contents appear on the abdominal wall and this is a serious
complication because of the risk of peritonitis. This complication
requires wound toilet and immediate resuture. Superficial wound
dehiscence may be managed by applying a suture.
THROMBOEMBOLISM
Post-operative thromboembolism remains a dangerous and often fatal
complication of any operation.
Trauma, venous stasis, previous
thromembolism, consumption of estrogen (oral contraceptive pills),
prolonged bed rest, obesity and varicose veins are the known
predisposing factors. The risk of thromboembolism is higher with
abdominal hysterectomy.
The diagnosis of deep vein thrombosis is based on a combination of
symptoms of local pain and signs of fever, local tenderness and
swelling of the leg. Confirmation is by venogram or local Doppler
ultrasound.
Prevention of thrombosis and embolism consists in early movement,
avoidance of infection and prompt treatment of early cases. In high
risk group, it is wiser to offer prophylactic heparin i.e. 5,000 units of
subcutaneous heparin 2 hours prior to surgery and then repeated 8hourly until patient is mobile.
In established thrombosis heparin is given 10,000 units 6-hourly for 48
hours with an initial dose of 10 mg warfarin and 5 mg on the second
day then the subsequent dose is adjusted according to the
prothrombin time.

GYNAECOLOGIC LAPAROSCOPY

Umbilicus

Abdomen filled with gas

Fig.1.1 Laparoscopy procedure

The role of gynecologic laparoscopy has evolved from a limited surgical

procedure used only for diagnosis and tubal ligation to a major surgical
tool used to treat a multitude of gynecologic indications. Laparoscopy
has become one of the most common surgical procedures performed
by gynecologists for gynaecological investigation and treatment.

This procedure involves the passage of a fine telescope into the

abdominal cavity to allow inspection of the pelvic and abdominal
organs and some forms of treatment.
INDICATIONS
The indications for laparoscopy are classified into diagnostic and
therapeutic indications (Table 1).
Table 1. Indications for laparoscopy
Indications for Diagnostic
Laparascopy

Infertility investigation
Investigation for primary
or secondary
amenorrhoea
Unexplained pelvic pain
acute or chronic
Staging of endometriosis
Investigation of adnexal
or pelvic masses

Indications for Therapeutic

Laparaoscopy

Performing sterilization
procedure
Division of adhesions
Ventrosuspension of the
uterus
Aspiration of ovarian cyst
Removal of intraperitoneal
IUCD
Ovum pick-up for assisted
conception, e.g. IVF
Ablation of endometriotic
deposits
Laparoscopic assisted
vaginal hysterectomy

Diagnostic laparoscopy:
Frequently, the doctor needs to assess the pelvis for acute or chronic
pain, ectopic pregnancy, endometriosis, adnexal torsion, or other
pelvic pathology. Determination of tubal patency may also be an issue.
Usually, the camera lens is placed infraumbilically and a second port is
placed suprapubically to probe systematically and observe pelvic
organs. If needed, a biopsy specimen can be obtained to aid in the
diagnosis of endometriosis or malignancy
In the investigation for infertility, laparoscopy provided a more
accurate assessment of tubal patency than hysterosalpingoraphy. . If
tubal patency is a concern, use of a uterine manipulator with a cannula
allows a dilute dye to be injected transcervically to note whether there
is filling of the tubes and spillage of dye from the fimbria portions.

Laparoscopy is also commonly used in the evaluation of pelvic pain,

especially if ectopic pregnancy is suspected.
Laparoscopic view of normal internal reproductive organs

Laparoscope for diagnosis of pelvic pain

(a): Endometriotic nodule of the ovary

(b): Ectopic pregnancy

Patent tube spillage of blue dye noted at the fimbria portion

Fig.1.2 Indications for diagnostic laparoscopy

Therapeutic Indications:
Tubal sterilization
Trocar placement is similar to diagnostic laparoscopy. Bipolar
electrosurgery, clips, or silastic bands may be used to occlude the
tubes at the mid-isthmic portion, approximately 3 cm from the cornua.
Bipolar surgery desiccates the tube with 3 adjacent passes to occlude
approximately 2 cm of tube.

Fig.1.3 Therapeutic laparoscopic Sterilization: placement of Filshie clips to both

tubes.

Removal of intraperitoneal IUCD

When the OUCD has been located in the peritoneal cavity, it is grasped
by the Palmer biopsy forceps and gently freed.

Fig.1.4 Lippes loop IUCD which is located in the peritoneal cavity is removed by
laparoscopic procedure.

Lysis of adhesion
Adhesions may form due to prior infection, such as a ruptured
appendix or pelvic inflammatory disease (PID), endometriosis, or
previous surgery. Adhesions may contribute to infertility or chronic
pelvic pain. Adhesions may be lysed by blunt or sharp dissection.
Fulguration of endometriosis
Endometriotic lesions may be resected or ablated using coagulation
instruments. This has been shown to improve fertility and decrease
pelvic pain.
Treatment of ectopic pregnancy
Laparoscopy is the surgery of choice for most ectopic pregnancies. A
salpingostomy or salpingectomy may be used to remove the embryo
and gestational sac. Auxiliary instruments, such as pretied loops or
stapling devices, may be particularly well suited for the salpingectomy
Ovarian cystectomy
If a simple ovarian cyst sized 6 cm or larger persists for 2 or more
cycles in a premenopausal, nonpregnant female, a cystectomy is
indicated. This can be achieved using laparoscopy depending on the
cyst size and the likelihood of the presence of malignancy.
Ovarian cysts with septa, internal echoes, or solid tumors are not good
candidates for laparoscopy unless a benign cystic teratoma is a strong
possibility.
Postmenopausal cysts may also be removed by laparoscopy

Fig. 1.5 Laparoscopic ovarian cystectomy

Hysterectomy
Laparoscopic-assisted vaginal hysterectomy (LAVH). LAVH is the most
commonly employed and technically straightforward. Using 3-4 ports,
the peritoneal cavity is surveyed and lysis of adhesions is performed if
necessary. The infundibular or uteroovarian ligaments are occluded
and divided, depending on whether the ovaries will be removed. The
round ligament is cut in a similar fashion, and the uterovesical
peritoneum is incised. Depending on gynaecologist preference, the
proximal uterine blood supply is occluded and divided laparoscopically.
After the uterovesical peritoneum is incised, the gynaecologist may
also choose to laparoscopically incise the posterior cul-de-sac. The
gynaecologist then proceeds vaginally for the remainder of the case,
dissecting the vesicovaginal septum anteriorly to enter the anterior
cul-de-sac, ligating the uterine vessels, removing the uterus and
ovaries (if appropriate), and closing the vaginal cuff.

Oncologic procedures
Laparoscopy was originally used in oncology for second-look
procedures following surgical and chemical treatment of malignancy.
With time, staging, including peritoneal washes with biopsy, partial
omentectomy, and pelvic and periaortic lymphadenectomy, was
performed laparoscopically. Some oncologists believe the laparotomy
can then be avoided.

CONTRAINDICATIONS
For years, previous abdominal surgery and intestinal obstruction were
regarded as contraindications to laparoscopy because of an increased
risk of iatrogenic bowel perforation. Contraindications to laparoscopy
are summarized in Table 2.

Table 2. Contraindications for laparoscopy

Diaphragmatic hernia

Abdominal, umbilical hernia

Advanced malignancy

Chronic tuberculous peritinitis

In gynecology, the most commonly suggested contraindication is

hemodynamic instability resulting from ruptured ectopic pregnancy.
However, following appropriate fluid resuscitation, laparoscopy is a
safe approach.
Although few absolute contraindications exist for laparoscopy, several
risk factors are well appreciated.
Patient risk factors
Previous abdominal surgery
As far as laparoscopic complications are concerned, one of the most
important risk factors is a history of previous abdominal surgery. The
risk of adhesions of omentum and/or bowel to the anterior abdominal
wall after previous abdominal surgery is greater. Because laparoscopy
requires the insertion of sharp instruments into the abdominal cavity, a
reasonable assumption is that previous surgery would increase the risk
of bowel injury. Thus, strategies have been developed to decrease the
risk of bowel injury in patients with previous abdominal surgery.
The most common of these strategies is the use of an open technique
for laparoscopic trocar placement, as first advocated by Hasson. Open
laparoscopy techniques almost certainly decrease the risk of bowel
injury distant to the umbilicus.
Anaesthetic risk factors
Anesthesiologists are trained not only in the art of providing
anesthesia, but also to serve as consultants. This may be one of the
least-used assets available to modern surgeons. Prior to surgery,
discuss preparation of any patient with significant health problems with
an anesthesiologist. In complex cases, these patients should be seen
by an anesthesiologist for optimal preanesthesia preparation.

Heart disease
Preoperative evaluation should include a search for evidence of
underlying cardiac disease. With a positive history or physical
examination findings suggestive of cardiac disease, preoperative
evaluation by both a cardiologist and an anesthesiologist is extremely
important. Patients with ischemic heart disease who undergo
anesthesia may have decreased cardiac blood return coupled with an
increase heart rate that may result in infarction. Laparoscopicassociated metabolic acidosis, respiratory acidosis, and hypothermia
may result in arrhythmia in predisposed patients, thus increasing the
risk of ischemia even further. Also, the risk of arrhythmia increases
with distention of the abdomen, especially in patients who are
breathing spontaneously.
Finally, patients at risk for congestive heart failure should be evaluated
carefully prior to laparoscopy because a decrease in cardiac output
may be related to decrease venous return and increased peripheral
vascular resistance.

Pulmonary disease
Any patient with a significant history of pulmonary problems should be
evaluated by both a pulmonologist and an anesthesiologist prior to
laparoscopy.
Special care should be taken during laparoscopy in patients with
pulmonary disease. Hypercarbia and decreased ventilation associated
with laparoscopy may be especially deleterious in pulmonary patients
with chronic respiratory acidosis. In rare cases, pneumothorax and
pneumomediastinum have been described as complications of
abdominal insufflation. In patients with compromised pulmonary
function, even a small intravasation of carbon dioxide could result in
significant pulmonary decompensation

SURGICAL PROCEDURES

General techniques for laparoscopy

Anaesthesia:
General anaesthesia with relaxant, endotracheal intubation, and
assisted respiration is usual type of anaesthesia used.

Patient positioning:
Gynecologic laparoscopy procedures are usually performed with the
patient in the modified lithotomy position (by suspending the ankles in
the stirrups) to allow vaginal access for uterine manipulation. The
thighs is slightly flexed, no more than 90 from the plane of the
abdomen, to avoided nerve injury. The buttocks should be slightly over
the edge of the table, but the sacrum should be completely supported
by the table to avoid back strain.
Once the primary trocar is placed, the patient is usually placed in no
more than 25 Trendelenburg position to help keep the bowel out of
the pelvis.
Bladder catheterization:
Traditionally, complete emptying of the urinary bladder with a catheter
immediately prior to Veress cannula or trocar placement is performed
to minimize the risk of bladder injury. Some laparoscopists advocate
having the patient void immediately prior to entering the operating
room.
Induction of pneumoperitoneum and primary trochar insertion:
Fig. 1.6 Insertion of Verres needle

Pneumoperitoneum is achieved by
the insertion of a Verres needle.
When the Veress needle is placed
through the umbilicus and into the
peritoneal cavity, avoidance of both
the retroperitoneal vessels and the
intestinal tract is of paramount
importance. The patient must be in
the complete horizontal position (not
Trendelenburg). The abdominal wall is
elevated by manually grasping the
skin and subcutaneous tissue to
maximize the distance between the umbilicus and the retroperitoneal
vessels. An alternative method for elevation is to place penetrating
towel clips at the base of the umbilicus.
In persons of average weight, the lower anterior abdominal wall is
grasped and elevated and the Veress needle is inserted toward the

hollow of the sacrum at a 45 angle. In patients who are obese, a more

vertical approach, approximately 70-80, is required because of the
increased thickness of the abdominal wall. Without the vertical
insertion, the trocar would not be long enough to penetrate the layers
and enter the peritoneal cavity.
When correct placement of the Veress needle is established, it is
connected to the insufflation apparatus and delivery of carbon dioxide
gas is commenced. The intraperitoneal pressure should not rise above
30 mmHg. The gas should be allowed to flow until the abdomen is
reasonably distended but not tense (this usually requires about 2-3
litres of gas but need more if the abdomen is lax).
When the abdomen is considered adequately distended the gas is turn
off and the Verres needle is removed.

Trochar insertion
After a pneumoperitoneum has been achieved with a Veress needle,
the primary trochar with sleeve (most commonly 5 mm or 10 mm in
diameter) is inserted at a similar angle to the Veress needle with a
twisting motion. The trochar is removed and the laparoscope inserted.
The insufflator is connected to the laparoscope and the fibreoptic cable
is attached. The contents of the pelvis may then be viewed.

Fig. 1.7 Insertion of trochar and laparoscope, and viewing of the pelvic contents

If the pelvic contents are obscured by gut, increased Tredelenburg tilt

is used and the intestine is gently pushed upwards with the end of the
laparoscope. If the lens of the laparoscope becomes fogged it can be
cleared by gently wiping it against the parietal peritoneum.

Placement of secondary trochars:

Secondary trochars are required to perform most gynecologic
laparoscopy procedures, with the exception of some diagnostic
laparoscopies.
After
identifying
the
epigastric
vessels
by
transillumination and intraperitoneal observation, 1-3 secondary
trochars are placed, depending on the procedure and the number of
trochars required for the operation.
The trochars are placed either in the midline, 3 cm above the pubic
symphysis, or laterally, approximately 8 cm from the midline and 8 cm
above the pubic symphysis to avoid the inferior epigastric vessels.
Insertion of the trochar and removal of the sleeves are performed
under direct laparoscopic visualization while observing for signs of
hemorrhage. If the trochar is larger than 8 mm, the fascia is closed
with suture after removal of the sleeve to reduce risk of hernia.

COMPLICATIONS
Laparoscopy remains an intra-abdominal procedure. Therefore, it
shares all intraoperative and postoperative risks of laparotomy,
including infection and injury to adjacent intra-abdominal structures.
When
major
intra-abdominal
procedures
are
performed
laparoscopically (e.g. hysterectomy), the resultant postoperative pain
and morbidity are still significant. However, because a large abdominal
incision is unnecessary, the postoperative pain and morbidity are
always less significant than similar major surgery performed by
laparotomy.
In addition to the traditional risks of surgery such as infection and
generalized bleeding, laparoscopy is a technique that presents its own
unique complications.

Gas embolism
Because carbon dioxide is used to create the pneumoperitoneum in
laparoscopic procedures, gas embolization is an uncommon but very
serious complication. Embolization is usually caused by inadvertent
placement of the Veress needle into a major vessel prior to insufflation
of the abdominal cavity with carbon dioxide. Placement in the aorta or
one of its major branches allows carbon dioxide to escape into the
vessel, which produces temporary arterial occlusion. Usually, the
carbon dioxide is quickly absorbed from the artery. No serious results
have been reported secondary to arterial embolization. In these cases,
arterial bleeding is the major complication. On the other hand,
embolization of carbon dioxide into the venous system may be fatal
due to complete occlusion of the pulmonary artery by a large carbon
dioxide embolism.
To avoid this complication, the operator must verify intraperitoneal
placement of the Veress needle prior to insufflation. If results from one
of the following tests indicate malposition, the needle must be
repositioned.

Open the Veress valve and observe for the flow of blood from the
abdomen through the needle.
Aspirate with a syringe through the Veress needle.

Administer the hanging drop test by placing a drop of saline at

the open end of the Veress, then observe if the drop disappears
into the shaft as the abdominal wall is elevated.
Elevate the abdomen with the Veress valve closed, then assess
for a hissing sound as the Veress valve is opened. Alternatively,
the Veress needle may be attached to the insufflator with the
valve in the off position and the gas off. The abdomen is then
elevated with the valve open and a negative pressure reading
will be observed on the insufflation instrument.

Recognition and treatment of a large venous embolization must be

immediate. Clinical signs include decreased end-tidal carbon dioxide,
decreased oxygen saturation, a loud mill-wheel murmur, severe
hypotension, and possible cardiac arrest. Treatment includes
immediately stopping insufflation, removing the needle, placing the
patient in the left lateral decubitus position, administering 100%
oxygen, and giving cardiac support. The gas embolism may be broken
up with external cardiac massage, but definitive treatment is
placement of a central line for aspiration of the gas from the right side
of the heart and from the pulmonary vasculature.

Retroperitoneal major vessel injury

Laceration of major abdominal blood vessels is one of the least
common but most life-threatening complications in laparoscopy. These
injuries may occur during insertion of the Veress needle or the primary
trochar.
In theory, because the umbilicus usually lies over the bifurcation of the
aorta at the fouth lumbar (L4), the aorta and inferior vena cava are
avoided if one inserts the Veress or trochar through the umbilicus
toward the hollow of the pelvis. In patients who are obese, the
umbilicus may not lie over L4; therefore, palpation of the iliac crest,
which is lateral to L4, is a better assessment of the position of the
bifurcation.
When placing the Veress needle, the patient must be in the horizontal
position (not Trendelenburg), and the angle of entry varies depending
on patient weight. Immediate recognition of the injury is paramount to
patient survival. If blood flows from the open Veress needle or if the
patient's vital signs rapidly decompensate after Veress or trochar
insertion, prompt action must be taken. With a retroperitoneal
hemorrhage, the peritoneal cavity may not show signs of bleeding. If
major vessel injury is a possibility, notify the anesthesiologist in order

to place a central line and order blood products, make a midline

incision for good exposure, and immediately call a vascular surgeon.

Abdominal wall vessel injury

As laparoscopy has become more sophisticated, the placement of
numerous and larger accessory trochars lateral to the rectus muscles
has increased the risk of abdominal wall vessel injury. The primary
vessels injured are the epigastric vessels (inferior and superficial) and
the superficial circumflex iliac vessel. The inferior epigastric vessel
originates from the external iliac vessel, and the superficial vessel
originates from the femoral vessel. Damage can lead to abrupt and
significant blood loss, producing a hematoma or postoperative
hemorrhage.
The first step to avoiding injury is knowing the positions of these
vessels. Often, transilluminating the abdominal wall with the
laparoscope can see the superficial vessels. The inferior epigastric
artery cannot be transilluminated but may be seen intraperitoneally
beneath the peritoneum between the insertion of the round ligament
at the inguinal canal and the obliterated umbilical artery. Prior to
insertion of the lateral trochars, the operator should make an effort to
identify and avoid these vessels.
When an injury occurs, the operator must be prepared to control the
bleeding promptly. First, an attempt can be made to coagulate the
vessel with electrocautery. A more secure technique is to enlarge the
incision and selectively ligate the epigastric vessels, which lie just
below the rectus abdominus muscle adjacent to the peritoneum.

Intestinal injury
Both the small and large intestine can be injured during laparoscopy,
posing a life-threatening situation for the patient if unrecognized. If the
patient has had previous abdominal surgeries or a history of abdominal
infections, such as PID or a ruptured appendix, the risk of injury to
bowel adhered to the abdominal wall increases.
Thermal injury to the bowel is also a risk when using electrocautery,
particularly monopolar cautery, which can cause an arc of electricity to
the bowel. This injury can cause peritonitis if unrecognized, and it is a
life-threatening situation if not promptly treated.

If injury is recognized at the time of surgery, immediate action must be

taken to repair the damage. However, frequently, minor injuries are not
seen and manifest 24-48 hours after surgery. Counseling the patient
before surgery is of utmost importance. Patients should be aware of
symptoms that they must report, such as fever, chills, nausea and
vomiting, and abdominal pain. In addition, patient counseling should
include the risk of requiring a laparotomy and colostomy to repair
injuries.
Urologic injuries
Injury to the bladder or ureters can occur during trochar placement or
during the use of power instruments, stapling devices, or suturing
devices. The greatest challenge is recognizing that the injury has
occurred so that treatment can be performed in a timely manner.
Draining the bladder with a catheter prior to trochar placement is the
first step to preventing bladder injuries. Small retroperitoneal injuries
may be treated with Foley catheter placement for 7-10 days, but larger
or intraperitoneal injures must be repaired through a laparotomy.
Suprapubic, retroperitoneal, and transurethral drains may be used
depending on the operator and the injury. If bladder injury is
unrecognized at time of surgery, the patient may present with
diminished urine output, hematuria, or suprapubic pain.
Ureteral injuries can occur with any procedure involving
instrumentation near the ureters. Thermal injuries from laser or
cautery may not be apparent for days after surgery. When a surgeon
uses one of the power instruments, the operator must be aware of the
position of the ureter and avoid cautery in close proximity to the ureter.
If the ureter is ligated, the patient may present with flank pain
secondary to hydronephrosis. If the ureter is transected, the patient
may develop a urinoma or ascites and present 1-5 days
postoperatively with abdominal pain, fever, or leukocytosis.
Incisional hernia
Before trochar and sleeves larger than 5 mm were used, incisional
hernias were rare. However, larger ports have increased the number of
incisional hernias, allowing a small amount of bowel to become
trapped in the fascia. Therefore, fascial closure is recommended for
incisions larger than 5 mm. Umbilical closure is not required unless a
very large incision is made, such as with open laparoscopy. The patient
is counseled to not perform any heavy lifting or straining for 30 days in
order to minimize the risk of umbilical hernia.

CONIZATION OF THE CERVIX

Cone specimen

Fig.1.1 Cone biopsy

Conization is defined as excision of a cone-shaped or cylindrical wedge

from the cervix uteri that includes the transformation zone and all or a
portion of the endocervical canal. It is used for the definitive diagnosis
of squamous or glandular intraepithelial lesions, for excluding
microinvasive carcinomas, and for conservative treatment of cervical
intraepithelial neoplasia (CIN). Techniques for diagnostic and
therapeutic conization are virtually identical. The extent of excision
must be adjusted according to individual needs.
Conization can be performed with a scalpel (cold-knife conization),
laser, or electrosurgical loop. The latter is called the loop
electrosurgical excision procedure (LEEP) or large loop excision of the
transformation zone (LLETZ). Combined conization usually refers to a
procedure started with a laser and completed with a cold-knife
technique. Laser conization can be excisional or destructive (by
vaporization).

Each of these approaches has distinct benefits and disadvantages.

Cold-knife conization provides the cleanest specimen margins for
further histologic study, but it typically is associated with more
bleeding than laser or LEEP and it requires general anesthesia in most
cases. Laser procedures are of longer duration and, especially if lowpower density is employed, may "burn" the margins, thus interfering
with histologic diagnosis. The main advantage with this procedure is
that dots produced by the laser energy can be used to accurately
outline the exocervical margins. However, overall, the benefit of using
laser for conization may not justify the high cost of the procedure.
LEEP procedures have several advantages, including rapidity,
preservation of the margins for histologic evaluation, and virtual
bloodlessness. Moreover, one can perform LEEP procedures in the
office or in other outpatient settings.

INDICATIONS FOR CONE BIOPSY

Diagnostic conization
Diagnostic conization is indicated in the following situations:

Finding epithelial cell abnormalities, in particular high-grade

squamous intraepithelial lesions (HSIL) or low-grade squamous
intraepithelial lesions (LSIL) in the absence of gross or
colposcopic lesions of the cervix
Unsatisfactory colposcopy, defined as the examiners inability to
view
the
entire
transformation
zone,
including
the
squamocolumnar junction, in women with epithelial cell
abnormalities
Uncertainty regarding the presence or absence of microinvasion
or invasion following the diagnosis of CIN by directed biopsy
Finding CIN or microinvasive cancer during endocervical
curettage
Cytologic or histologic evidence of premalignant or malignant
glandular epithelium
Cytologic diagnosis inconsistent with histologic diagnosis based
on directed biopsy findings

Therapeutic conization

Therapeutic conization is currently the preferred modality to treat CIN

grades 2 and 3. All described approaches (i.e. cold-knife, laser, LEEP)
are equally effective.
Controversies exist as to the necessity of removing the entire
endocervical canal, including the internal os, in all cases. This approach
may increase the risk of cervical incompetence in women who desire
post-treatment pregnancy.
In addition to conization, CIN can also be treated by hysterectomy or
by other destructive methods, such as cryotherapy, laser vaporization
conization, or radical electrocoagulation. The decision to use
hysterectomy or conization is usually based on the grade and extent of
the disease, the patients age, the desire for childbearing, and the
history of recurrence after conservative management. Because
destructive methods such as cryotherapy yield no specimen for
histologic studies, their use should be limited to those women in whom
an accurate preoperative diagnosis has been established by directed
biopsy findings.

PROCEDURES
Cold-knife conization
Under adequate anesthesia, the patient is placed in a dorsal lithotomy
position and prepared and draped in the usual manner. A weighted
speculum is inserted into the vagina.
Inserting a black silk suture in the cervix at the 12-oclock position is
useful to help the pathologist orient the specimen.
For conization, sound the cervical canal to determine its length and the
position of the internal os. Paint the cervix with Lugol solution.
Conization is performed with a No. 11 blade, which should be pointed
toward the planned apex of the cone. The preferred approach is to
start the incision at the 3- or 9-oclock position and to cut posteriorly
first to avoid loss of visualization from bleeding. The exocervical
incision should include the entire transformation zone, with a 2- to 3mm margin. If deep endocervical extension of the lesion into the
endocervical canal is not present, the apex of the cone should end
approximately 1 cm caudal to the internal os. Deep extension may
necessitate excision of the internal os. Remove the cone specimen in
one piece, if possible.

Following completion of the conization, the endocervical canal is

curetted to help exclude the presence of residual lesions.
One should observe the operative site for a few minutes following the
procedure to look for excessive bleeding. Arterial bleeding can be
controlled by coagulation or by inserting lateral cervical figure-8
sutures (at 3-oclock and 9-oclock). Vaginal gauze pack is then inserted
leaving a 5-cm protrusion of the packing beyond the introitus eases
removal. The vaginal pack is removed 24 hours following insertion.

Volsellum

Scalpel blade
Lateral suture to
reduce bleeding
Weighted speculun

Area of conization

Fig. 1.2 Conization procedure

Laser conization
While laser conization is effective for treating CIN, it offers few
advantages
over
LEEP
or
cold-knife
approaches.
Potential
disadvantages include costly equipment and a possible coagulative
effect on the margins, which makes histologic evaluation difficult.
Gynecologists performing any type of laser surgery should attend
specific courses on laser physics, safety features, and operative
techniques. The use of lasers is confines to patients with definitive

diagnosis of CIN-2 or CIN-3 in whom a large lesion is close to the

vaginal fornix or extends into the vault.
The operation is performed with carbon dioxide laser, using a
colposcopic micromanipulator. The procedure is begun by outlining the
exocervical margins with 0.5- to 1-mm dots produced by laser energy
at a power setting of 20-50 W. A laser incision is then performed to
connect the dots and extended to a depth of 3-5 mm. Bleeders in the
raw stump can be coagulated.
One variety of laser conization is called vaporization conization. It
involves vaporization to a depth of 7 mm of the entire transformation
zone, including a 2- to 3-mm margin. To accomplish this procedure, a
spot size of 2 mm and a power setting of 25 W are commonly used. A
gauge must be used to determine the precise depth of the vaporized
area.
Because vaporization conization does not provide a specimen
histologic evaluation, it should only be used in cases in which
entire lesion is visible colposcopically and does not extend into
endocervical canal. Pretreatment histologic diagnosis based
directed biopsies is mandatory.

for
the
the
on

Loop electrosurgical excision procedure

LEEP (LLETZ) procedures use diathermy
current for excising all or selected areas
of the transformation zone. The thin wire
loop electrodes are insulated to prevent
thermocoagulative
artifacts;
consequently, the excised tissues are
preserved for histologic examination. The
author prefers to use pure cutting rather
than blended current because the cutting
current causes fewer thermal artifacts in
the excised specimen.
LEEP is a precise and inexpensive technique that results in less
bleeding than cold-knife or laser conizations. The author believes that
it has proven itself as the best approach to conization in the
overwhelming majority of patients. In rare patients with CIN, the size of
the transformation zone exceeds the size of the largest loop. In such
cases and in patients with vaginal fornix involvement, laser conization
may be a better approach. The equipment for the LEEP procedure

consists of a generator that creates high-frequency (350-1200 kHz)

low-voltage (200-500 V) electric current. The generator is connected to
an insulated thin wire loop, which is available in various sizes.
Most loop electrosurgical procedures can be performed under local
anesthesia in an outpatient setting. The patient is placed in a lithotomy
position and is attached to a grounding pad. An insulated speculum,
connected to smoke-evacuator tubing, is used to prevent electric
shock, which can occur if a noninsulated metal speculum is touched
inadvertently by an active loop. For local anesthesia, the author injects
2-5 mL of lidocaine with epinephrine at the 3-, 6-, 9-, and 12-o'clock
positions 1-2 mm beneath the surface of the cervical epithelium using
a 25-gauge spinal needle. The use of epinephrine (or dilute
vasopressin) is crucial to prevent intraoperative bleeding that could
obscure the field of vision. If a patient is unable to relax, a safer plan
may be to perform the procedure under general anesthesia because
accidental burns of the vaginal wall can occur in patients who move
during the procedure.
The loop size, usually 1.5-2 cm in
width and 0.8-1.0 cm in depth, should
be appropriate to remove the entire
transformation zone with a 3-mm
margin in one pass. In the first pass,
tissue is ablated to a depth of
approximately 1 cm. Using a 1-cm by
1-cm loop, more of the endocervical
canal can be excised in a second
pass from the crater base. Once the
cervix is adequately exposed, LEEP
procedures can be performed with extreme rapidity, usually in less
than 1 minute. The loop can be directed in a transverse direction (e.g.
from the 9- to 3-o'clock position) or anteroposteriorly. Following the
loop excision, the surface of the cervix appears raw. Larger bleeders
should be cauterized with a ball cautery tool.

Postoperative:
Following any method of conization, complete healing of the cervix
takes as long as 6 weeks. Intercourse and/or the use of vaginal
tampons during the early healing period may cause significant
bleeding and infections, and these activities should be restricted for at
least 2-3 weeks.

Follow-up care:
Conization sites usually heal in 6 weeks. Reexamination of patients 2
weeks postoperatively is useful to help determine whether restrictions,
such as coitus, can be lifted. A final postoperative examination is
recommended at 6 weeks. To ascertain the absence of residual or
recurrent CIN, Papanicolaou tests (Pap smears) should be performed
every 3 months during the first postoperative year and every 6 months
thereafter. A single follow-up Pap smear shows positive results in fewer
than 25% of women with residual disease.

COMPLICATIONS
Intraoperative and postoperative bleeding are the most common
complications of cervical conization. Both of these can be eliminated or
significantly reduced if the lateral cervical cerclage technique is
practiced. Intracervical injection of dilute epinephrine or vasopressin
into the cervix, contraindicated in patients with hypertension and those
with cardiac problems, reduces intraoperative bleeding but not delayed
bleeding, which usually occurs 7-14 days postoperatively in
approximately 2% of the patients who undergo cold-knife conization.
Delayed bleeding, uncommon after LEEP, may be managed
successfully in most women with the use of vaginal packing. Failure to
respond to packing necessitates resuturing of the operative area.
According to anecdotal reports, an emergency hysterectomy was
performed in rare patients in whom extreme intraoperative
hemorrhage was triggered by conization. Such a complication is
avoidable with the use of proper operative technique.
Cervical stenosis may occur in a few women. Inserting a rubber drain
following the procedure has a limited role in the prevention of this
often negligible complication. Cervical incompetence can result if the
apex of the cone involves the internal os. Women who become
pregnant after conization should be closely monitored for this potential
complication, which is treated with cerclage.
Both laser conization and LEEP generate smoke. Inhalation of smoke
may be dangerous for the operator because the smoke may contain

HPV particles. Therefore, the use of smoke evacuators is indispensable,

and wearing a mask during the procedure is recommended.

CONE BIOPSY PROCEDURE

LARGE LOOP EXCISION OF TRANSFORMATION ZONE CONE
BIOPSY
(LLETZ)

Wire loops of various

dimensions
1:

2:

CIN lesion

3:

Administration
anaesthesia

4:

of

local

LLETZ almost complete

Application of wire loop

CONE BIOPSY PROCEDURE

COLD KNIFE CONE BIOPSY

1:

2:

CIN lesion

3:

4:

Cone specimen

MYOMECTOMY
If the patient has fibroids and wishes to retain her uterus, the
individual fibroids may be removed. Myomectomy is a uterine sparing
procedure in which fibroid tumors are surgically removed from the
uterus. This procedure can sometimes be technically more difficult
(especially if the size of the fibroids are large) with a greater blood loss.
Myomectomy is indicated for women who,
4. are infertile.
5. want more children.

6. wishes to preserve their menstrual functions (refuse to undergo

hysterectomy).
Myomectomy may be accomplished using minimally invasive
technique ("laparoscopic myomectomy") or through a standard
conventional incision ("laparotomy").

An abdominal myomectomy is done through an abdominal

incision. An anterior incision is preferred to monimize the risk of later
adhesion of bowel to the uterine surfaces. At the operation, the
fibroids are shelled out of their capsules. It is generally advisable to
open the uterine cavity to exclude submucous fibroid or polyp. The
uterus is reconstructed with meticulous care for haemostatsis. After
myomectomy there is about 5 per cent risk of recurrence of the
fibroids.

A midline subumbilical or
suprapubic transverse incision
is made on the abdominal
wall.

The uterus, which, is greatly

enlarged by the fibroid, is lifted
through the incision. A blade,
electrocuting and coagulation
instrument or laser can be
used to make an incision into
the anterior wall of the uterus
uterus so the fibroid can be
removed.

Line of
incision

The fibroid is being separated

from the wall of the uterus
(myometrium).
It is very
important to do this in the
exact location between the
fibroid and the myometrium in
order
to
prevent
excess
bleeding.

This shows the fibroid almost

completely free from the
uterus. It is attached only at
the base. The blood vessels at
the base are being sealed with
an electrosurgical device.


The
uterus
is
being
reconstructed by suturing the
walls together with dissolving
suture. This is being done in
multiple layers to ensure a
precise repair.
It is important to ensure good
haemostasis.

The last layer of sutures is

placed, and the uterus is
completely restored.
The
uterus
is
sometimes
anteverted at the end of the
procudure by plication of the
round
ligaments
(ventrosuspension), this is to
prevent adhesions.

Specimen of the fibroids which

was
removed
during
myomemctomy

Fig. 1.1 Myomectomy procedures

The advantage of abdominal myomectomy is that large myomas can

be quickly removed. The surgeon is able to feel the uterus, which is
helpful in locating myomas that may be deep in the uterine wall. The
ability to touch the uterus facilitates repairing the uterus. The
disadvantage of an abdominal myomectomy is that it requires an
incision, so recovery is somewhat longer.

Laparoscopic myomectomy
Fibroids that are attached to the outside of the uterus by a stalk
(pedunculated myomas) are the easiest to remove laparoscopically.
Many subserous myomas (close to the outer surface) can also be
removed through the laparoscope.
Fibroids that are deep in the wall of the uterus, or submucous are most
difficult to remove laparoscopically. Although there have been
successful pregnancies after laparoscopic removal of deep or multiple
myomas, the real question is whether or not the uterus can be repaired
as well through the laparoscope as can be done through an abdominal
myomectomy.
The advantage of a laparoscopic myomectomy over an abdominal
myomectomy is that several small incisions are used rather than one
larger incision.
COMPLICATIONS OF MYOMECTOMY
1) Haemorrhage: Myomectomy is technically more difficult, with a
greater blood loss during the procedure. Bleeding can be controlled
by obliterating the dead spaces in the myometrium and carefully
closed for haemostatsis.
Prior to myomectomy, especially in larger myomas, the use of GnRH analogue (e.g.
Zoladex) for 2 to 3 months can minimized the haemorrhage.

2) Adhesions:
Adhesions of the bowel to the uterine surface
frequently occurs.
The used of anterior incision and
ventrosuspension of the uterus may minimize the risk of adhesions.
3) Recurrent myomas: After myomectomy there is about 5 per cent
risk of recurrence of the fibroids.

4) Rupture of myomectomy scar during subsequent pregnancy or

labour may occur but is very rare. Elective Caesarean is considered
if the uterine cavity is entered.

DILATATION AND CURETTAGE

(D & C)
A dilatation and curettage (D&C) is the most frequently performed
minor gynaecological operation and has a diagnostic and therapeutic
role. This procedure involves a dilatation to the cervix and curettage of
the uterus.
INDICATIONS FOR DILATATION AND CURETTAGE
The indications for D&C may be summed up as follows:
Diagnostic
Diagnostic indications include abnormal uterine bleeding, menstrual
disorders, postmenopausal bleeding, and postcoital bleeding. It is
indicated for investigation in malignant disease of the uterus in by
obtaining an endometrial biopsy for histological examination. A D&C
can also be used in cases of infertility to obtain an endometrial biopsy
for histological dating (i.e. proliferative or secretory phase of the
endometrium) and to exclude pelvic tuberculosis infection.
Therapeutic
Therapeutic indications include removal of retained products of
conception (ERPOC) following incomplete or missed abortion; for the
management of menorrhagia, irregular bleeding, where the cause is an
endometrial polyp.
It is used for drainage of pyometra or
haematometra and for removal of molar tissues in molar pregnancy
(hydatidiform mole).

THE PROCEDURES OF D&C

The steps of the D&C procedure are as follows:
1) The placed is anaesthetized and placed in the lithotomy position.
2) The external genital and vaginal are cleaned with antiseptic
solution.

3) The bladder is then catheterized.

4) A bimanual examination is carried out with special reference to the
position and size of the uterus.
5) A speculum (usually an Avuards speculum) is inserted into the
vagina.
6) The cervix is grasped with volsellum forceps.
7) A sound is passed gentle into the uterus; the uterine cavity is
measured and its directional noted.
8) The cervix is gently dilated with graduated (Hegar) dilators to not
more than 8 mm in diameter.
9) The uterine cavity is explored with sponge or polyp forceps to
remove any polyp or retained products of conception.
10) The uterine cavity is curetted systemically, i.e. using the blunt
end first then the sharp end: any irregularity such as submucous
fibroid is noted.
11) The curetting are sent to the laboratory for histological
examination.

C
A
D
B

Fig.1.1 Instruments used in dilatation and curettage.

(A)
(B)
(C)
(D)
(E)
(F)
(G)

Weighted (Auvard) speculum

Sims speculum
Volsellum
Uterine sound
Hegars dilators
Curette
Polyp foceps

BLUNT
SHARP

Curette

Uterus

Retained
product of
conception

Volsellum
Curette

Fig.1.2 Dilatation and curettage procedure

Speculum

COMPLICATIONS FOLLOWING D&C

The complications following dilatation and curettage occur during
anesthesia, grasping the cervix with the volsellum, sounding of the
uterine cavity, dilatation of the cervix and curettage. The complications
following a dilatation and curettage procedure are summarized in Table
1.
Table 1. Complications of Dilatation and Curettage
During D&C
procedure

Complications
following
anaesthesia
Laceration to the
cervix
Perforation of the
uterus
Haemorrhage
Injury
to
bowel,

After D&C procedure

Haemorrhage
Abdominal pain
Infections
Peritonitis if involve
perforation of bowel

Late Complications

Infections pelvic
inflammatory disease
Ashermans
syndrome leading to
secondary
amenborrhoea
Cervical
incompetence
leading to

bladder if perforation
of the uterus occurs
Damage to internal
cervical os sphincter
due to over-dilatation

midtrimester
miscarriage

HYSTERECTOMY

Hysterectomy strictly means removal of the uterus and can be

performed abdominally or vaginally.
When performed by the
abdominal route it may be:

Subtotal hysterectomy
Total hysterectomy
Wertheims hysterectomy

A subtotal hysterectomy means that the body of the uterus and the
cervix is left.
This procedure is technically easier than a total
hysterectomy. It is indicated when further dissection to free the cervix
might damage the rectum, bladder or ureter. Total hysterectomy is
the removal of the uterus and cervix. Wertheims hysterectomy is
performed for carcinoma of the cervix. It consists in the removal of the
uterus, tubes, ovaries, broad ligaments, parametria, the upper third of
the vagina and the regional lymph nodes.
In the absence of malignancy, or in younger patient (age less than 50
years) the ovaries are usually left.

INDICATIONS FOR TOTAL ABDOMINAL HYSTERECTOMY

Indications for total abdominal hysterectomy includes
1): Uterine fibroids: One of the commonest indications for the
removal of the uterus is the presence of uterine fibroid causing
excessive blood loss. Total hysterectomy is indicated if:

The fibroids are causing symptoms, such as heavy or prolonged

bleeding.
They are larger than 14 weeks pregnancy.
The diagnosis is in doubt.
The fibroids distort the uterine cavity and are likely to complicate a
future pregnancy.
The fibroid grows rapidly which might suggest malignancy change.
The fibroid is situated in the cervix which would complicate
childbirth.
Fibroid has undergone torsion.

2): Endometriosis and Adenomyosis: The accepted method of

treatment of endometriosis and adenomyosis that is unresponsive to
conservative medical treatment is hysterectomy, because the
operation cures menorrhagia and dysmenorrhoea which are likely to be
dominant symptoms of theses two conditions.
3): Intractable Menorrhagia and Dysfunctional uterine
bleeding: Total abdominal hysterectomy is indicated for intractable
menorrhagia and dysfunction uterine bleeding that is unresponsive to
medical measures.
4): Chronic pelvic infections: The first line of treatment for theses
patients is antibiotic therapy. If, in spite of this, a residual, painful
mass persists, associated with menorrhagia, low sacral backache,
congestive dysmeorrhoea and dyspareunia hysterectomy may well be
considered, especially if the uterus is enlarged and fixed in the
retroverted position.
5): Malignant conditions: Total abdominal hysterectomy can also
be performed for malignant disease such as microinvasive carcinoma
of the cervix, stage I carcinoma of the uterus, or ovarian cancer or
fallopian tubes cancer.
6): Caesarean hysterectomy:
Hysterectomy is required for a
complete rupture of the uterus during labour, where conservative

surgery of the tear is not feasible or where the general condition of the
patient indicates that hysterectomy is the quicker and safer procedure.

TOTAL ABDOMINAL HYSTERECTOMY PROCEDURES

The steps of the operation are as follow:
1) Abdominal incision When the hysterectomy procedure is simple
and without any pelvic pathology, a low transverse (Pfannenstiel) is
usually employed. If extensive exposure is required, a subumbilical
midline incision is made.
2) Ensuring good exposure of the operating area The abdominal
contents (i.e. intestines) are packed out of the pelvis, and the
patient is placed in a modified Tredelenburg position.
3) Division and ligation of the pedicles Three pedicles are divided and
ligated in as follow:

First pedicle: Division of the fallopian tubes and round ligament

and the ovarian pedicles.

Second pedicle: Division and tying off of uterine arteries.

Third pedicle: Division of cardinal and uterosacral ligaments.

4) The anterior peritoneum (utero-vesical fold) is incised. The lower

peritoneum flap is pushed down with a free wet swab to mobilize
the bladder from the cervix and upper vagina. The posterior
peritoneum is divided and pushed down onto the vagina.
5) The vaginal is entered with a stab incision anteriorly just beyond the
cervix and the incision are carried round posteriorly on both sides to
remove the uterus and its pedicle in toto.
6) Angles of the vaginal vault: Angle clamps are applied to angles of
the vaginal vault. The angles of the vaginal vault are then sutured,
achieving haemostasis and anchorage of the vault to the cardinal
ligament.
7) Closure of the vaginal stump with interrupted sutures.
8) The pedicles on each side are then ligated to the suture at the angle
of the vaginal vault.

9) Closure of the pelvic peritoneum: The pelvic peritoneum is then

closed over the bladder, rectum and vaginal vault.
10)

The abdominal walls are closed in layers.

Round ligament

UTERUS

Fallopian tube
Ovarian pedicle

Division and ligation of the first pedicle (round ligament, fallopian tube and ovarian
pedicle)

Uterine artery

UTERUS

Stump of the first

pedicle

Division and ligation of the second pedicle (uterine artery)

Left

Right
Division of the cardinal
ligament

UTERUS

Division and ligation of the third pedicle (cardinal ligaments)

CERVIX
Vaginal canal
Stump of cardinal
ligament
Stump of uterine artery
Stump of uterosacral
ligament

The vaginal is opened

Vaginal vault closed

with interrupted
suture

Anterior and posterior peritoneum

flaps
Closure of the pelvic peritoneum:
bladder, rectum and vaginal vault.

The pelvic peritoneum is then closed over the

End of total abdominal procedure

COMPLICATIONS OF HYSTERECTOMY
Intraoperative complications:

Bleeding:
The most common intraoperative complication of
abdominal hysterectomy is bleeding, from the ovarian pedicle,
uterine pedicle or the vaginal angles.
To overcome these
complications all main pedicles ovarian and uterine must be firmly

secured by double ligature so that there is no risk of any vessel

escaping the ligature pedicle to cause bleeding and a subsequent
haematoma.

Ureteric injury: Injury to the ureter is the most serious complication

of hysterectomy and usually occurs during a difficult dissection for
pelvic inflammatory disease, endometriosis or pelvic malignancy. The
most common site of injury is just lateral to the cervix; the second
most common site is beneath the infundibulopelvic ligament. The
ureter can be clamped, ligated or cut. It is important to identify the
ureter before ligating and incising the infundibulopelvic ligament.
Unrecognised injury to the ureter may lead to ureterovaginal fistula
and patient will present with leak of urine through the vagina.
Bladder injury: Intraoperative injury to the bladder can occur and
usually occur during the opening of the abdomen or when the bladder
is dissected off from its attachment. If bladder injuries are recognized
during operation, it should be repaired immediately. If a bladder
repair is necessary, 7 to 10 days of postoperative continuous bladder
drainage with a Foley catheter is necessary for optimal healing.
Intestine injury: Injury to the intestines can occur, particularly
during a difficult dissection of adhesions to large or small bowels. If
the serosal or seromuscularis of the bowel has been torn or damaged,
the defect must be immediately repaired.

Postoperative complications:

Bleeding: When postoperative haemorrhage occurs, bleeding is

from the vaginal angle can be identified and controlled vaginally. If
bleeding is sufficient to cause hypotension, laparotomy may be
required to ligate the bleeding vascular pedicle.
Wound infections: Wound infection usually occurs about 5 days
postoperatively and is associated with redness, tenderness, swelling,
and increased warmth around the wound. Treatment will requires
systemic antibiotics, drainage the discharge and wound care.
Urinary tract infection: Urinary tract infection can occur at any
time in the postoperative period. Urine for microscopy and culture
should be obtained on any patient with postoperative fever.
Wound breakdown:
Would disruption, with evisceration of
intestine, is generally heralded by a profuse serous discharge from
the wound 4 to 7 days postoperatively.

Thrombophlebitis: Thrombophlebitis is a known complication with

pelvic surgery and if the patient the patient is immobilized. It is
manifest by fever and leg swelling or pain usually 7 to 10 days
postoperatively.

VAGINAL HYSTERECTOMY
Vaginal hysterectomy avoids an abdominal scar and is associated with
minimal postoperative discomfort.
INDICATIONS
Vaginal hysterectomy may be performed provided that the uterus is
mobile and not larger than 12 weeks gestational size; there are no
adhesions; and ovarian disease is not suspected.
The most common indications for vaginal hysterectomy is uterine
prolapse with or without associated cystocoele, enterocoele or
rectocoele.

CONTRAINDICATIONS
The contraindication include a uterus larger than 12 weeks in size, the
presence of genital tract malignancy, previous abdominal surgery where
bowel has become adherent to the uterus anduncertain ovarian
pathology.

TECNIQUE OF VAGINAL HYSTERECTOMY

The principles of this operation are similar to those for the abdominal
hysterectomy except the main pedicles (ligaments and vessels) are
clamped and ligated in the reverse order.
The steps of the operation are as follow:

Position of the patient - The patient is placed in the lithotomy

position.

Adequate exposure of the operating area - The operating is

adequately exposed by placing a weighted speculum in the vagina
and placing two lateral sutures to labial.
Making an incision on the at the cervicovaginal junction A
circumferential incision is made at the c ervicovaginal junction and
the posterior cul-de-sac is entered. An index finger is introduced in
the cul-de-sac to ensure that there are no adhesions.
First pedicle - The uterosacral and cardinal ligaments are identified,
clamped, cut and tied separately.
Separating the bladder from the cervix The bladder is separated
from the cervix to expose the anterior peritoneal reflection. The
anterior peritoneal cavity is entered anterior.
Second pedicle The uterine vessels are identified and cut and
ligated.
Third pedicle After the division and ligation of the uterine vessels
are achieved the uterus is pull down to expose the utero-ovarian
pedicles, round ligaments which are clamped, cut and tied. The
uterus is then removed in toto and the ovaries are inspected for any
pathology.
Closure of the pelvic peritoneum The peritoneum is closed in a
purse-string fashion.
Steps in preventing vault prolapse and enterocoele - Each cardinal
ligament is sutured against the vaginal vault on either side to protect
against the vaginal vault to prevent against vaginal vault prolapse.
The uterosacral ligaments are vied in the midline to prevent a
subsequent enterocoele.
Closure of the vaginal cuf - The vaginal cuff is closed with interrupted
absorbable suture.

COMPLICATIONS
The complications of vaginal hysterectomy are similar to that of the
abdominal
hysterectomy.
Immediate
complications
include
haemorrhage due to slipping of the ligature from the main pedicle. The
late complications include haematoma, infection of the vaginal vault,
thrombophlebitis and postoperative fever.

OVARIAN CYSTECTOMY
OVARIAN CYSTECTOMY means the removal of ovarian cysts from
the substance of the ovary either by shelling out or by clean dissection,
and in which the healthy ovarian tissue is left behind. This procedure is
essentially conservative and is particularly for innocent cysts and
tumours and is carried out in women below 40 years of age.
TECHNIQUE OF OVARIAN CYSTECTOMY

The scalpel blade is used to incise the ovarian surface in the

transition zone between the recognizable ovarian cortex and the wall
of the cyst.
The incision is made until the plane of cleavage is found.
The tumour or cyst is then enucleated or dissected out from the
capsule.
Once the cyst is enucleated, the ovary is carefully reconstructed
taking care not to leave any dead space.
Cyst capsule

Cyst
Ovary

(a): A transverse incision is made on

cyst to
the surface of the ovarian capsule
capsule

(b): Dissecting of the ovarian

separate the cyst from its

Ovary after
reconstruction

(c): Reconstruction of the ovary

43
THE ROLE OF CHEMOTHERAPY IN
GYNAECOLOGICAL CANCER
Modern chemotherapy has radically altered the outlook for some
women with gynaecological malignancies. The prognosis for women
with gestational trophoblastic disease and nonepithelial tumours has
been dramatically improved effective chemotherapy. In epithelial
ovarian cancer cisplatin based chemotherapy regimens produce high
response rates and possibly improved survival. Progress in other
gynaecological tumours has been less dramatic.
PHASE OF THE CELL CYCLE
Every dividing cell may exist in a number or distinct phases.

G0
G1
S
G2
M

- quiescent, resting (non-dividing) phase

- prereplicative phase
- DNA replication
Proliferative
- postreplicative phase. Preparation for cell division
phase
- mitosis

CHEMOTHERAPUETIC AGENTS USED IN THE TREATMENT OF

GYNAECOLOGICAL MALIGANCIES
Modern chemotherapeutic regimens for the treatment of gynaecologic
malignancies utilize a wide variety of agents with different chemical
properties and mechanism of action. Chemotherapeutic agents act
primarily by disrupting nucleus DNA, thus inhibiting cellular division.
CLASSIFICATION
Chemotherapeutic agents are often classified either by their chemical
origin or by the phase of cell cycle when they are active.
Chemical of origin this include:
Antimetabolites
Alkylating agents
antitumour antibiotic
Plant alkaloids
Hormonal agent
Many of these drugs interfere with cell replication by blocking
nucleotide synthesis and thus preferentially act on dividing cells. Thus

not only are malignant tumours affected, but the following normal
tissues may be damaged:
Bone marrow (red cell, leucocyte and platelet formation)
Gonads (production of germ cells)
Gastrointestinal tract
Skin (particularly the bases of the hair follicle)
Phase of cell cycle - Chemotherapeutic agents may be into two
categories according to their mode of action relative to the cell cycle.
1) Cycle-specific agents such as alkylating agent and cisplatinum,
which exert their damage at any phase of the cell cycle. They may
damage resting phase as well as cycling cells, but the latter are
more sensitive.
2) Phase-specific agent are phase specific and act only at certain
phase of the cell cycle. Example include: - hydroxyurea and
methotrexate, which acts primarily during the S-phase bleomycin,
which acts in the G1 phase vinca alkaloid, which acts on the M
phase.
THE COMMON AGENTS USED IN GYNAECOLOGY
ANTIMETABOLITES
The antimetabolites are structural and chemical analogs of naturally
occurring substances in the metabolic pathways leading to synthesis of
purines, pyrimidines, and nucleic acid. In most cases, they are Sphase-specific agents that are most effective in rapidly growing
tumour. Because of cycle-specific mechanism of action, efficacy of
metabolite is dependent on duration of exposure. Therefore, long
exposure is often more effective.
The metabolites may be classified into:
Purine analogs e.g. 6-mercaptopurine
Fluorinated pyrimidines 5- Fluourouracil
Ribonucleotide reductase inhibitor hydroxyurea
Folic acid antagonists methotrexate.
ALKYLATING AGENTS (e.g. cyclophosphamide, melphalan, cisplatin,
carbaplatin, chlorambucil, thiotepa)

The alkylating agents are chemical compounds.

They possess
positively charge alkly groups that are able to bind to negatively
charge sites on DNA. The mode of action of alkylating agent is by
inhibiting cell replication by forming covalent bonds with bases in
nuclear DNA and bind to guanine bases in opposite strands of the DNA
double helix and thus prevent strand separation prior to DNA
replication. DNA alkylation most commonly at the N-7 position of
guanine.
ANTITUMOUR
doxorubicin)

ANTIBIOTIC

(e.g.

actinomycin-D,

bleomycin,

Antitumour antibiotics are class of chemotherapeutic agents that are

generally derived from micro-organism. Most of these agents produce
cytotoxic effect resulting in inhibition of DNA transcription and DNA
translation. In general they are cell-cycle non-specific.
PLANT ALKYLOIDS (agents derived from plants)
Several useful cytotoxic agents are derived from plants. A common
theme in the cytotoxic activity of these agents is disturbances of
normal assembly, disassembly, and stabilization of intracellular
microtubules. Microtubules are present in all eukaryotic cells and play
a critical role in cellular transport and maintenance of cell shape.
The vinca alkaloids, epipodophyllotoxin, and texanes are naturally
occurring substances isolated from the plant.
Vica alkaloids e.g. vincristine, vinblastine
Epipodophyllotoxin e.g. etoposide (VP-16)

Class

Drugs

Common
application
gynaecological cancer

Antimetabolites

Methotrexate
5-FU

Gestational trophoblastic tumour,

cervival carcinoma

Alkylating agents

Cyclophosphami
de

Epithelial
ovarian
cancer,
gestational trophoblastic disease
Cervical
carcinoma,
Epithelial
cancer of ovary
Cervical
and
endometrial
carcinoma.
Epithelial
ovarian
cancer, Germ cell cancer of the

Melphalan
Cisplatin
Carboplatin

in

Chlorambucil
Thoptepa

ovary,
getational
trophoblastic
disease and cervical and vulva
cancer.
Epithelial
ovarian
cancer
and
gestational trophoblastic disease.
Epithelial ovarian cancer.

Antitumour
antibiotic

Actinomycin D
Bleomycin
Doxorubicin

Gestational trophoblastic tumours

Cervical vcancer and vulva
Epithelial ovarian cancer, Cervical
and endometrial carcinoma

Plant alkaloids

Vinblastin
Vincristine
Etoposide
16)

Germ cell tumour, gestational

trophoblastic
Germ cell tumour, gestational
trophoblastic
Epithelial
ovarian
cancer,
gestational trophoblastic, germ cell
tumour, sarcoma

Hormonal

Tamoxifen
Progestogen

(VP-

Epithelial ovaraian cancer

Table 1. Classification of common used chemotherapeutic agents for gynaecologic

malignancies.

HORMONAL AGENTS
Hormonal therapy is used for the treatment of endometrial and breast
cancers. These agents may be broken into two classes: progestational
agents and estrogen antagonist.
Commonly used progestational
agents include megestrol acetate, medroxyprosgesterone acetate
(Provera) and hydroxyprogesterone. Tamoxifen citrate is a commonly
used antiestrogen.

CHEMOTHERAPY IN GYNAECOLOGIC CANCER

EPITHELIAL CARCINOMA OF THE OVARY
Chemotherapy in advance disease:
Adjuvant therapy after surgery has become the mainstay of treatment
of patients with advanced disease. Following completion of surgical
cytoreduction, majority of the patient with advanced (Stage III or IV)

disease will required chemotherapy. A number of chemotherapeutic

drugs are active against carcinoma of the ovary.
Platinum based compound generally platinum based compound
(cisplatin and carbaplatin) has been regarded as the most active and
most important cytotoxic agent in the treatment of advanced ovarian
cancer. These two agents appear to be therapeutically equivalent.
Carbaplatin has causes less nephrotoxicity and neurotoxicity and
appears to have an advantage.
Alkylating agents The alkylating agents also have activity against
ovarian cancer.
Melphalan and cyclophosphamide are the most
commonly employed member of this class.
Other agents active against ovarian carcinoma include the doxorubicin,
hexamethylmelamine, 5-Fluourouracil, methotrexate, mitomycin C,
prosgestins and tamoxifen.
Chemotherapy in limited disease:
Patient with limited (Stage I or II) disease should be classified as either
high risk or low risk for recurrence base on the pathological features of
the disease.

For low risk patient Total hysterectomy, bilateral salpingooophorectomy, omentectomy is therefore the treatment of choice.
For high risk patients, the use of adjuvant chemotherapy is
appropriate.
Best result is obtained with platinum based
chemotherapy.

Chemotherapy in recurrent disease:

Patient who are sensitive to platinum base agent should receive
platinum based combination chemotherapy (paclitaxel followed by
ciplastin).
For those who are resistant to platinum based agent, choice of drugs
should focus on those with demonstrated activity again resistant
disease (paclitaxel, i8fosfamide, hexamethylmelamine, tamoxifen, and
5-Fluorouracil).
ENDOMETRIAL CARCINOMA

$Endometrial carcinoma is the most common invasive malignancy of

the female genital tract.
The only currently defined role for
chemotherapy is in patient with primary Stage IV or recurrent disease
not amenable to control with surgery with or without radiotherapy.
Active systemic agents include progestins, tamoxifen, doxorubicin, the
bplatinum compounds and paclitaxel.
Candidates for progestins or tamoxifen include those with disease
positive for estrogen and progesterone receptors.
For women who hadve grade 3 or receptor negative disease, or who
are no longer response to hormonal therapy, chemotherapy should be
considered. The common one are cisplatin/doxorubicin.
CARCINOMA OF CERVIX
Chemotherapy has a defined role in two situations:
1. the management of advanced (Stage IVB), or recurrent disease
2. the management of locoregionally advanced (Stage IIB, III or IVB)
disease in conjunction with radiation.
Chemotherapy should be considered in two situation: (1) advanced or
recurrent disease as the primary treatment and locoregionally
advanced disease in combination with radiotherapy. In advanced or
recurrent diseases single agent cisplatin remain the best choice. In
locoregionally advanced disease, combination of radiation and
concomitant hydroxyurea is reasonable.
OVARIAN GERM CELL CANCER
Ovarian germ cell carcinoma account for only 5 percent of all ovarian
cancer. Chemotherapy treatment is dictated by the extend of disease
and completion of single resection. For patient with Stage IV or
incomplete resected neoplasia, systemic therapy is the treatment of
choice.
The optional regimen appears to be a combination of
bleomycin plus etoposide plus cisplatin (BEP).
For patient with completely resected Stage I, II, or III disease, the need
for adjuvant therapy is determine to some extend of histology. For
patient with immature teratomas grade 1, no further treatment

required. For all others, adjuvant treatment with BEP for 3 cycles
should be considered.
For patients unable to take BEP, enhanced results are reported with
vincristine, actinomycin D and cylophosphamide (VAC).

GESTATIONAL TROPHOBLASTIC DISEASE

Chemotherapy has a definite role in the management of patient with
gestational trophoblastic disease. In those with nonmetastatic and low
risk, single agent chemotherapy consists of methotrexate or
actinomycin D is recommended. Patient with high risk metastases
disease required combination chemotherapy, with MAC or EMA-CO.

44
RADIOTHERAPY IN GYNAECOLOGICAL
CANCERS

Fig.1.1 - Intracavitary brachytherapy radiation. Anteroposterior view of

intrauterine tandem and vaginal ovoids used for low dose rate brachytherapy.

an

Gynecologic cancers were among the first malignancies treated with

ionizing radiation more than a century ago. Today, radiation therapy
remains an essential component of both the primary nonsurgical
management and adjuvant postoperative treatment of selected
malignancies arising in the female reproductive tract.
Primary radiotherapy can provide a chance for cure for women with
unresectable locally advanced disease or for women with medical risk
factors that contraindicate primary surgical therapy. Unfortunately, for
women with distant metastatic disease at presentation, disease cure is
unlikely. Palliative radiotherapy frequently can improve a patient's
quality of life when used for the relief of symptoms. Although adjuvant
radiotherapy is used commonly for advanced or metastatic cervical
and endometrial cancer, it is employed infrequently as adjuvant
therapy for ovarian cancer.
In this chapter, clinical indications and common techniques for
radiation therapy in the management of common gynecologic cancers
are described.

RADIATION PRINCIPLE
When living matter absorbs radiation energy, ionization of biological
molecules occurs. Ionization is the result of radiation energy ejecting
one or more electrons from an atom. Ionizing radiation as used for
treatment is either electromagnetic or particulate.

Electromagnetic radiation
X-rays and gamma rays are identical electromagnetic radiation in the
mode of production. X-rays produced by bombardment of an anode by
a high-speed electron beam. Gamma rays result from the decay of
radioactive isotopes, such as cobalt 60 (60Co).
X-rays and gamma rays consist of a stream of photon (energy), which
penetrates tissue and at high acceleration have sufficient power to
break chemical bonds, which lead to biological changes and can result
in the death of the cell hence their use in treatment of cancer.
Particulate radiation
Particulate radiations consist of moving particle of matter. Their
energy consists of kinectic energy of the moving particle. The
particles vary greatly in size and include,
neutrons (no charge)
protons (positive charge)
electrons (negative charge)
The commonly used particulates are electrons. They may be delivered
from linear accelerator, the beam of electron being directed into the
patient without first striking a metal target and producing x-ray.
Particulate radiations penetrate tissues and produced ionization.

MODALITIES OF RADIATION THERAPY

In general there are two types of radiation techniques:
Teletherapy Is external irradiation when the tumour is at a long
distance from the source of the ionizing radiation. In teletherapy, rays
are directed through the skin onto the deep structures from an external
source, such as supervoltage X-ray machine. The radiations are
delivered by Cobalt-60 machine or Linear accelerator.
Linear
accelerators, which have higher range of energies (4 to 20 MeV) are
widely used for the treatment of gynaecological cancer.
Teletherapy is used to treat large volumes such as those required for
carcinoma of the cervix where the volume includes the tumour itself,
the parametria and regional lymph nodes. The aim of teletherapy is to
deliver a homogenous dose to the tumour volume while giving a low
dose to surrounding normal tissue.

Brachytherapy In brachytherapy the radiation source either

intracavitary or interstitial therapy is place either within or close to the
target tissue (e.g. in the vaginal and cervical canal).
a) Intracavitary Radiation - Intracavitary therapy is suitable for
treating small tumour volumes, particularly in the treatment of
cervical cancer, stage II endometrial cancer, and vaginal cancer.
The energy sources used are radium-226 and caesium-137 (137Cs).
Caesium is currently used because it produces nom toxic gases.
There are different types of applicator which are used (Fig. 1.2) to
delivered this energy source. All applicators, which are use, should
be afterload, which means that they are placed in the patient and
their position are checked by x-ray (Fig. 1.3) before the radioactive
radium or cesium is loaded into the applicator.

Fig. 1.2 Applicators for intracavitary radiation

applicators for
(A): Vaginal cylinder; (B): Uterine tandems, and
view)
(C) : Vaginal colpostats (ovoids)

Fig. 1.3 Placement of

intracavitary radiation (X-ray

The correct placement of the applicator is critical if the tumour is to

receive the maximum dose and the surrounding tissues the
minimum dose.
The commonest methods of giving intracavitary radiation for
gynaecological cancers is with Manchester system in which a single
uterine tube containing 137Cs is passed through the cervix so that
the inferior margin is flushed with the external cervical os and
smaller tubes (vaginal ovoids), contained 137Cs are inserted into the
lateral fornices.

Uterine tubes (tandems)

Cervix
Vaginal ovoids
Vagina

Fig. 1.4 Intracavitary brachytherapy radiation Manchester system

a) Interstitial brachytherapy In some areas, treatment of small

tumours with sparing of normal tissues can be best carried out
by insertion directly into the tumour of radioactive sources as
needle (Fig. 1.5). An example is the insertion of radioactive
needles for early cases of vaginal carcinoma.

Fig. 1.5 Radioactive needle used in interstitial brachytherapy radiation

THE ROLE OF RADIOTHERAPY IN GYNAECOLOGIC

MALIGNANCIES

RADIOTHERPY FOR ENDOMETRIAL CARCINOMA

When hysterectomy is medically contraindicated, primary radiotherapy
can offer 5-year disease-specific survival rates of 80-90%, approaching
those achieved with surgery.
Whole pelvic external beam radiotherapy (XRT) and intravaginal
brachytherapy (IVB) commonly are used as adjuvant postoperative
therapy for patients with stage I disease.
Whole pelvic XRT may be administered through a 4-field setup
involving parallel opposed anteroposterior (AP), posteroanterior (PA),
right lateral, and left lateral fields.
IVB may be administered with either a low dose rate (LDR) or high dose
rate (HDR) afterloading device. The HDR technique has become very
popular because of its convenience as a well-tolerated outpatient
regimen.
For stage II endometrial carcinoma, either preoperative or
postoperative radiotherapy may be administered. The goals of the
preoperative treatment are to facilitate hysterectomy by reducing
tumor bulk and clearing microscopic infiltration from the upper vaginal
mucosa. Pelvic XRT may be combined with brachytherapy in this
setting.
For stage III-IV disease, patients are treated with combinations of pelvic
XRT, whole abdominal radiotherapy and intravaginal brachytherapy..

CARCINOMA
PRINCIPLES

OF

THE

UTERINE

CERVIX:

MANAGEMENT

Comprehensive radiotherapy for stages IIA-IVB cervical cancer involves

both external beam treatment and brachytherapy. Initial external beam
fields encompass a clinical target volume that includes the primary
tumor and adjacent areas at risk for direct occult invasion or regional
lymph node metastases. The field borders usually are similar to those
for endometrial cancer with particular attention to coverage of the
posterior extent of disease. Brachytherapy involves the temporary
placement of intrauterine tandem and intravaginal ovoid that are
afterloaded with radioactive material. Brachytherapy may be
performed in the form of either HDR or LDR applications.

CANCER OF THE VULVA AND VAGINA

A): VULVA CANCER
For clinical stage I-II lesions, postoperative radiotherapy is indicated
when pathologic evidence of inguinal node metastasis or close (<8
mm) margins of resection around the primary site is present. For
limited ipsilateral nodal involvement with no pathologic nodal
involvement identified by contralateral dissection, the external beam
fields often are reduced to cover only the hemipelvis.
Using the proper technique for effective radiotherapeutic treatment of
the groin node regions is important. The region of concern is located
anterior to the ischium, and it is desirable to avoid an excessive
radiation dose to the femoral neck. Available options include a wide AP
(anterior-posterior) photon field prescribed to the depth of the external
iliac artery as it crosses the inguinal ligament, supplemented by a
narrower PA (posterior-anterior) field to ensure adequate coverage of
the pelvic nodes. Alternatively, electrons may be used for some or all
of the inguinal node region coverage, but the energy must be carefully
selected to achieve a sufficiently deep distribution of radiation dose to
the full nodal area.
For stage III-IVA disease, the management strategy is tailored to the
individual. Brachytherapy also can be used to provide boost treatment
to the primary site in selected cases.
B) VAGINAL CANCER:
For stage I-II lesions, partial or total vaginectomy followed by
postoperative radiotherapy sometimes is feasible. However, primary
nonsurgical treatment usually is preferable. For stage I-IVA disease,
combined-modality treatment with radiotherapy and concurrent
cisplatin chemotherapy likely is more beneficial than radiotherapy
alone because the biologic behavior of vaginal cancer is expected to
be similar to that of cervix cancer. Following elective regional external
beam treatment to fields in doses similar to those used for vulvar
cancer, tailored interstitial brachytherapy generally is necessary to
administer potentially curative radiotherapy doses to the primary site.
OVARIAN CANCER

The current regimen for adjuvant therapy following surgery is

combination chemotherapy with cisplatin and paclitaxel. Whole
abdomen radiotherapy has been used, but its popularity has waned in
view of the more favorable toxicity profiles of current chemotherapy
regimens. Techniques for whole abdomen radiotherapy have included
AP/PA field treatment to the entire peritoneal cavity in doses of 25-30
Gy in fractions of 1-1.5 Gy. Maintaining kidney doses of less than 20 Gy
and whole liver doses of less than 30 Gy is advisable. Boost treatment
to the pelvis and paraaortic lymph nodes may be combined with whole
abdomen radiotherapy to give total doses of 45-50 Gy to these regions.
Palliative radiotherapy frequently is offered to patients who have
focally symptomatic recurrences of ovarian cancer. For painful or
hemorrhagic pelvic masses refractory to chemotherapy, radiotherapy
provide a helpful reduction in symptoms for most patients.

COMPLICATIONS FOLLOWING RADIOTHERAPY

The dose of radiation is limited by the tolerance of normal tissue.
Large single fractions of radiation causes more damage than multiple
small fractions for the same total dose.
Normal tissue reactions occur both early and late. Early reaction takes
place during or immediately after a course of radiotherapy but
recovery is usually rapid. Late reactions occur from 12 months
onwards, and are permanent and usually slowly progressive.
Skin, bowel and bone marrow are particularly subceptible to acute
reactions during treatment. Tissue which divide slowly, such as kidney,
show late reaction.
Acute complications:
Acute complications to radiation include the following pathologic
changes:

SKIN Erythema may follow by dry desquamation, or with more

severe damage, by moist desquamation. The basal cells are usually
spared allowing the skin to grow.
GASTROINTESTINAL MUCOSA Cells in the intestinal mucosa are
replaced every 3-6 days. The changes include:

a) Proctosigmoiditis, manifested by tenesmus, diarrhea, and

passage of blood and mucus in the stool.
b) Enteritis, manifested by nausea, vomiting, diarrhea and colicky
pain.

BONE MARROW is very sensitive to radiation. Bone marrow

depression is manifested by changes in the haematological
components.

Chronic complications:
Chronic complications occur 1 year onward after completion of
radiation and are characterized pathologically by the following
changes:
1) Internal thickening and obliteration of small blood vessel
(endarteritis)
2) Fibrosis
These changes may be slowly progressive over several years.
Common chronic complication of radiation include the following:
Radiation entheropathy (Large bowel complications):
a) Proctosigmoditis, manifested by pelvic pain, tenesmus, alteration
in bowel habits, anorexia and weight loss.
b) Ulceration, manifested by rectal bleeding.
c) Rectovaginal fistula, manifested by passage of stool through the
vagina.
d) Rectal or sigmoid stenosis, manifested by progressive large
bowel obstruction.
Vaginal vault necrosis
This is associated with severe pain and tenderness of the vaginal vault, and
haemorrhage may occur. The condition may mimic recurrent cancer.
Urologic injuries They may include,
a) Haemorrhagic cystitis, which may necessitate frequent blood transfusions.
Cystoscopy confirms the diagnosis.
b) Vesicovaginal fistula, in which the patient complaints of constant leakage of the
urine.
c) Ureterovaginal fistula, also manifested by constant leakage of the urine.
d) Ureteric stenosis, manifested by progressive hydronephrosis.

45
PAEDIATRIC GYNAECOLOGY
Gynecology of infancy and childhood is often neglected, primarily
because problems are uncommon before the onset of puberty;
however, when such problems arise, they must be appropriately
evaluated. If child abuse is suspected, document the examination
carefully and report to the appropriate authorities. Consultation with a
specialist in pediatric gynecology may be helpful in cases with legal
ramifications.

COMMON GYNAECOLOGICAL DISORDERS OF INFANCY

AND CHILDHOOD
Gynaecological disorders of infancy and childhood can be group into:
(1) congenital anomalies, (2) genital trauma, (3) infections, (4)
pubertal disorders, and (5) tumours.

CONGENITAL ANOMALIES
IMPERFORATE HYMEN
An imperforate membrane usually situated immediately above the
hymen occludes the lower part of the vaginal. An imperforate hymen
can be detected in the newborn infant on clinical examination or by
observation of mucocolpos (collection of fluid within the vagina).
Inspection of the vulva usually reveals a bulging membrane.
If
undetected in early infancy, the condition will remain unapparent until
puberty, when it may present with haematocolpos and haematometra.
Correct diagnosis permits the imperforate hymen to be treated
properly by simple incision of the membrane and release of the
retained fluid. The optimal time to excise the membrane is when the
tissue is estrogenized, either in the newborn period or at the time of
thelarche.

The imperforate hymen may be associated with anomalies of the renal

tract.

GENITAL TRAUMA
VULVAR LACERATIONS
Vulvar lacerations occur when a child falls on a pointed object or is
injured with a foreign body. Because of the painful condition it is best
to repair all vulvar laceration under general anaesthesia.
The
laceration should be irrigated, all bleeding vessels identified and
ligated, and the edges of the wound closed.
VULVAR HAEMATOMAS
The most common cause of vulvar haematoma in children is straddle
injuries. While ridding a bicycle, or falling from or on to furniture the
child sustains blunt trauma to the vulva. The majority of the injuries
are to the labia.
A child with a vulvar haematoma present with a swollen, ecchymotic,
tender labial lesion.
A small labial haematoma can generally be managed conservatively
with ice packs and pressure dressing. Enlarging haematoma causing
considerable pain, and/or obstructs the urethra may require evacuation
and ligation of bleeding vessels under general anaesthesia.

INFECTIONS
VULVOVAGINITIS
This is most common gynaecological disorder of the childhood. The
most common complaint with vulvovaginitis is of irritation of the vulva,
vagina or both.
They may present with discomfort and vaginal
discharge.
The risk of vaginal infections in young girls prior to puberty is increased
by a thin vaginal mucosa, an exposed introitus, the close proximity of
the vaginal opening and anal orifice, and poor perineal hygiene. The
unestrogenized vaginal mucosa is very thin and easily susceptible to
infection should bacteria gain access to the vagina. Failure of the

labial minora to develop prior to puberty leaves the vaginal introitus

relatively unprotected by labial fat pads and pubic hair. The anatomic
proximity of the opening of the vaginal canal to the anus facilitates
exposure to fecal bacteria. The most significant is the failure to
instruct young girls in proper perineal hygiene.

Causes There are several possible etiological factors

concerned. Many cases of the childhood vulvovaginitis are due
to infection. These include:
Nonspecific polymicrobial infection secondary to poor hygiene or
foreign body, contact irritation from soaps, etc.
Primary
infections
(Candida,
Gardnerella,
Trichomonas,
gonorrhea, syphilis, herpes, etc.), lichen sclerosus et atrophicus
may also occur.
Pinworms (Enterobias vermicularis). May cause vulvovaginitis;
rectal itching common; frequently have vaginal pain.
Diaper dermatitis (primary contact irritant dermatitis). Caused by
irritants in urine, producing red, papulovesicular, shiny rash
sparing skin folds; may fissure.
Neoplasms are rare.

Symptoms: Vaginal discharge is the cardinal symptom of

vulvovaginitis. Soreness, pruritus, burning, and dysuria may be
present.
Examination: An attempt should be made to examine the
vagina of every child with prepubertal vulvovaginitis. Simple
inspection of the vulva will show whether there is considerable
soreness or not. The vulva is usually redden and may be swollen,
and gentle separation of the labia will reveal a small amount of
discharge present.
Microscopic examination of vaginal secretions, urine analysis,
and possible vaginal cultures. Recurrent or refractory infections
of foul-smelling, bloody discharge require vaginoscopy to exclude
foreign body or tumor.

Treatment.
a) Remove foreign body with warm saline irrigation or
bayonet forceps. Obtain vaginal and urine cultures and
treats concurrent infection.

b) Treat specific infections: Candidiasis: is treated by

using topical antifungal creams (nystatin, miconazole, or
clotrimazole) for 7 14 days. Recurrent vaginal yeast
infections may be treated with oral nystatin. Bacterial
vaginosis and Trichomonas vulvovaginitis: may be
treated with metronidazole 35 to 50 mg/kg/day up to 750
mg divided TID for 7 days. Pinworms are treated with
mebendazole (vermox) one 100 mg chewable tablet and
therapy is repeated in 2 weeks. Gonorrhea infection in
prepubertal are treated with regimens appropriate for their
body weight (a single intramuscular injection with
ceftriaxone 125 mg or azithromycin 10 mg/kg per oral.
c) Suspect sexual abuse if bacterial vaginitis, trichomonas,
gonorrhea, or chlamydia is present. Sexually transmitted
diseases in childhood are treated with regimens
appropriate for body weight.
d) Treat with good hygiene and protection with zinc oxide or
white petroleum jelly as well as frequent diaper changes
allowing skin to dry fully. Treat secondary infections caused
by Streptococcus, Staphylococcus, or Candida organisms.
e) Educate about perineal hygiene: The child should be
instructed that following urination and defecation she
should wipe away from the vulvovaginal area. A parent
may have to supervise the child until it is certain she is
practicing proper perineal hygiene. The underwear should
be changed frequently.
f) Estrogen cream: If a specific etiology is not found,
persistent vulvovaginitis is treated with estrogen cream
applied locally to the vulva for no more than 3 weeks. The
estrogen thickens the vaginal mucosa, making it more
resistant to infection.

LABIAL ADHESIONS

This is a simple condition not uncommon in the young, in which

the labial minora becomes adherent to each other, usually from
behind, forwards, leaving a tiny opening through which the urine
is passed.
The line of adhesion is quite thin and almost
translucent in early cases but becomes firmer and thicker as
times goes by. This condition may be mistaken for absence of
the vagina.
Labial adhesions are usually the result of local inflammation and
chronic irritation due to hypoestrogenized vulvar tissue.

Most commonly children with labial adhesions are asymptomatic

but may interfere with urination leading to dysuria and recurrent
vulvar and vaginal infections.
The need of treatment is based on the patients ability to void
spontaneously.
As long as the child can urinate without difficulty, and is free of
urinary tract symptoms, there is no need to initiate therapy. The
patient and parents should be counseled that in most cases the
labial separate spontaneously in early puberty as the
concentration of endogenous estrogen increases.

If labial adhesions cause problem in micturition or recurrent urinary

tract infections, active treatment must be started.
Improved
personal hygiene and the topical application of estrogen cream to
the labia once or twice a day for 7 to 10 days, which will lyse
adhesions and resulting in separation of the labia. Once the labia is
separated, the estrogen cream is continued for another 7 days so
that the new edges of the labia have a chance to reepithelialize.
This reduces the chance that the labia will fuse again when the
estrogen cream has been discontinued.
Use surgical intervention only as a last resort.

PUBERTAL DISORDER
PRECOCIUS PUBERTY
Abnormalities of puberty can occur as a result of problems at any level
of the hypothalamic-pituitary axis. Precocious puberty is defined as a
premature initiation of either sexual development and/or menstrual
bleeding before the age of 8 years.
The precocious puberty is classified into, (1) true complete precocious
puberty, and (2) incomplete pseudoprecocious puberty.

True complete precocious puberty

This is the most common form of sexual precocious puberty, which
is initiated by premature maturation of the hypothalamic-pituitaryovarian axis resulting in total ovarian function with ovulation before
the age of 9. Children with complete precocity are able to conceive.

Incomplete pseudoprecocious puberty

In this condition, only the secondary sexual developments occur

without evidence of ovulation.
Causes of precocious puberty - Precocious puberty may occur in
the following conditions:

Idiopathic or constitutional is probably the most common form

of true precocious puberty. This condition may occur in families
where there is a history of early onset of puberty in other family
members (i.e., constitutional).
Abnormalities in central nervous system such as
craniopharyngioma, a hamartoma, suprasellar cyst or teratoma.

McCune-Albright syndrome consists of caf-au-lait skin spots,

multiple disseminated cystic bone lesions (polyostotic fibrous
dysplasia), and precocious puberty.
Primary hypothyroidism - may be associated with precocious
puberty.
In such cases, TRH (thyroid releasing hormone) is
elevated, which in turn elevates TSH, FSH, and LH.
Ovarian tumours - An increased level of sex steroid production
can be a cause for precocious puberty and may be associated with
ovarian tumours. The most common ovarian tumours that produce
estrogens are the granulosa-thecal cell tumours. Excess estrogen
production produces breast growth and vaginal bleeding, along with
skeletal maturation. A luteoma, a small tumour that produces both
estrogen and progesterone, may produce pseudosexual precocity.
Adrenal tumours are not common, however, an adrenal
carcinoma may secrete estrogen and may be the cause of
precocious puberty.
Drug ingestion particular estrogens may be the cause of
precocious puberty.

Clinical features of precocious puberty

Precocious puberty is associated with accelerated growth; accelerated
osseous maturation also occurs, resulting in ultimate short stature.
Also sexual precocity is associated with early sexual maturation and
development.

Evaluation of precocious puberty

The importance of evaluating a child with sexual precocity is to identify
the possible causes, which may be life threatening, such tumours of
the central nervous system, ovary or adrenal.

Enquiry about the presence of similar conditions in other family

members.
The chronologic order of sexual development should be elicited.
The growth record should be checked to determine the onset of
increase in height velocity, and the degree of correlation
between height and weight measurements.
Enquiry should be made about any central nervous system
symptoms, such as headaches or seizures.
History of sex steroid ingestion, particularly estrogens should be
asked.
A history of encephalitis, meningitis, and cranial trauma can be
important factors in such cases.

Physical examination will consist of:

Historical findings A detailed history is required.

Measurement of height and weight.

Thorough description of secondary sexual development.
The skin must be examined for acne, hair distribution and
growth, and abnormal pigmentation.
Neurologic examination is essential if there is central nernous
system involvement. These nerologic examinations will include
the assessment of the visual fields and optic discs.
An abdominal and pelvic examination must be performed.
The inspection of the external genitalia may show evidence of
estrogenization.
If vaginal bleeding is present, examination of the vagina may
reveal whether there is any abnormality, including a foreign
body.

Investigations:

A thyroid function test is important if there are any symptoms or

signs of hypothyroidism.
Laboratory evaluation includes estimation of serum FSH, LH,
testosterone and estradiol.
The measurement of DHEA-S , and 17-alpha-hydroxyprogesterone may be valuable if congenital adrenal hyperplasia
is suspected.
Radiological examination of the left hand-wrist will usually define
the skeletal age.
Radiological examination of the long bones should be done if
there is any suspicion of McCune-Albright syndrome.
A CT scan of the brain, with particular emphasis on the
hypothalamic and sellar regions, is the most sensitive
radiological means of identifying a CNS tumours associated with
sexual precocity.
Ultrasonic examination will reveal ovarian and adrenal tumours.

Treatment:
Management of precocious puberty depends on the accuracy of
diagnosis. The treatment goal in true precocious puberty is to stop
the growth process so that patients ultimate height will be
protected. Also the aim of the treatment is to suppress
menstruation, ovulation and fertility.
Principal of treatment:

Suppression of menstruation Treatment with progesterone,

preferably those without androgen or estrogen activity, will
suppress the menstrual cycle. Alternatively, medroxy-progesterone
acetate (MPA), Depo-Provera, Cyproterone acetate is effective in
suppressing ovarian function and menstruation.
Cyproterone
acetate usage is limited by side-effects, the most important of
which is adrenal suppression.
Suppression of breast development can be achieved with the
usage of medroxy-progesterone acetate (MPA). MPA in doses of 100
200 mg intramuscular weekly or biweekly is the treatment of
choice. MPA stops breast development and menses. Danazol, a
2,3-isoxasol derivative of 17-alpha-etinyl-testosterone is a weak
androgen, effectively stops menstruation and breast development.
To prevent short stature - GnRH agonist has been successfully
used in the treatment of precocious puberty patients.
This

treatment delays the closure of the epiphyses so that the patients

ultimate height will be protected. GnRH agonist treatment will also
eliminates the menstrual periods and inhibits the development of
the secondary sexual characteristics.

Psychological support and counseling - Children with sexual

precocity have a physical appearance that outstrips their
psychosexual maturation. Thus many have severe psychological
disturbances, are shy and withdrawn. Therefore, it is important to
provide psychological counseling and support for the patient and for
her family.

Specific treatable condition - When a specific treatable condition

is identified, treatment is directed against the condition.

CNS tumours may be treated surgically.

Hypothyroidism is treated with thyroxine
Congenital adrenal hyperplasia is treated with glucocorticoids or
mineralocorticoids.
Adrenal and ovarian tumours are treated surgically.

OTHER DISORDERS
VAGINAL BLEEDING IN PREPUBERTAL CHILD
Vaginal bleeding is a frequent and distressing complaint in childhood.
Although it will most often be of benign etiology, more serious
pathology must be ruled out.
Vaginal bleeding in the newborn is the most often physiologic as a
result of maternal estrogen withdrawal, which occur at 3 to 5 days
after delivery. No treatment except reassurance of parents.
Bleeding disorders should be considered in this age group. Precocious
puberty and vulvovaginitis may present with vaginal bleeding.
When vaginal bleeding is present, it is necessary to assess the vagina
and rule out foreign body or vaginal tumour (sarcoma botryoides). It is
important to ensure that the bleeding is originating in the vagina.
Finally trauma or child abuse must always be considered.

URETHRAL PROLAPSE

Prolapse of the urethra results in the urethral mucosa protruding

through the external urethral orifice as an annular reddish in colour.
The tissue may be friable or even necrotic and becoming painful.
Urethral prolapse is usually noted after sudden increase in
intraabdominal pressure from crying, coughing or straining.
Support of the distal urethra is in part estrogen-dependent and
prolapse of the urethra may be related to hypoestrogenism.
Children with prolapse of the urethra may complain of vulvar pain,
bleeding, or dysuria.
Diagnosis is usually made by recognizing the urethral orifice in the
center of the mass. Passage of the catheter into the urinary bladder
will confirm the diagnosis.
Prolapse of the urethral usually responds to nonsurgical treatment.
Treatment with sitz baths, topical application of estrogens cream
and antibiotic creams has been successfully used to reduce the
edema and return the prolapse urethra tissue to its normal
anatomic location.
If urinary retention is present or lesion is large and necrotic, surgical
excision may be required.

RARE BUT SERIOUS GYNAECOLOGICAL DISORDERS OF

INFANCY AND CHILDHOOD

SARCOMA BOTRYOIDES (embryonal carcinoma of vagina).

These rare tumours develop in young infants (< 3 years) and clinically
presents as bloody vaginal discharge with polypoid growth, which may
look like a cluster of grapes.
The tumour arises from the connective tissue of the vaginal wall and
tends to form polypoidal mass of reddish haemorrhagic tissues, which
may fill and protrude from the vagina.
A vaginal sarcoma botyroides infiltrates locally into the pelvic tissues
and has a poor prognosis. Survival rare but improving with use of
combination chemotherapy and radical surgery.

OVARIAN TUMOURS
Symptoms include pain, mass, pressure; may cause vaginal bleeding or the precocious
development of secondary sex characteristics if hormonally active. Requires complete
evaluation by experienced gynecologist

46
GYNAECOLOGICAL INSTRUMENTS
Cuscos or bivalve speculum
This consists of two blades fixed
GYNAECOLOGICAL SPECULUMS
together by a hinge at the vulva
end of the instrument.
It is made in various sizes
It is also made of disposable
plastic form
It is used to gives an excellent
view of the cervix and vaginal
wall.

Sims speculum
Sims speculum is a retractor for
the vaginal wall.
It
consists of two concave
blades of different sizes, with a
handle connecting them
It gives a good view of the
cervix and vaginal walls.
Helps to display vesicovaginal
fistula

Auvards speculum
This is a weighted speculum.
It is used in the dilatation and
curettage procedure.
It gives a good view of the
cervix and vaginal walls

INSTRUMENT TO OBTAIN ENDOMETRIAL SAMPLING

Uterine curette
It consists of a blunt
and sharp end.

It is used for the

removal of the products
of
conception
and
obtaining endometrial
biopsy.

INSTRUMENT TO DETERMINE THE AXIS OF THE UTERUS AND THE

LENGTH OF THE UTERINE CAVITY

Uterine sound
It is a graduated piece
of instrument usually
in cm.
It is used to determine
the
length
of
the
uterine cavity.
It is used to determine
the axis of the uterus

INSTRUMENT TO DILATE CERVICAL OS

Hegars dilators

Various sizes of the dilators, such

as size 6, 7, 8, 9, 10.
The size is graduated in mm.
Hegars dilators are used to dilate
the cervical os.

INSTRUMENT FOR EMPTYING THE CONTENTS OF THE UTERUS

Ovum forceps

Ovum forceps:
This instrument is used to
empty the contents of the
uterus, such products of
conception or polyps.

INSTRUMENT FOR SECURING THE CERVIX

Cervical
forceps

volsellum

This volsellum serves to

steady and fix the whole uterus during dilatation and curettage. If necessary two pairs of
forceps can be placed side by side to give a firmer hold.
INSTRUMENTS FOR TREATMENT OF UTERINE PROLAPSE

Ring pessary

Hodge pessary
The pessaries are used to support the prolapsed
uterus
Pessaries are indicated in the following:
Patients wish
Medically unfit for surgery
While waiting for surgery
During pregnancy
Childbearing not complete

Shelf pessary
INSTRUMENTS FOR DILATATION AND CURETTAGE

INSTRUMENT FOR LLETZ PROCEDURE

(Large loop excision of transformation zone)

Various sizes of a LLETZ loop

LLETZ procedure for the management of CIN (cervical intraepithelial
neoplasia) has become extremely popular because it is safe, quick and
easy to perform.
A diathermy generator delivers the excision
technique of LLETZ.

47
IMAGING IN GYNAECOLOGY
There are multiple imaging diagnostic modalities, such as ultrasound,
radiological examination, computed tomography (CT) and magnetic
resonance imaging (MRI) that can be utilized in the evaluation of
gynaecological conditions.
Ultrasound scanning and radiological examination is the principal
imaging techniques, which is routinely used in the management of
gynaecological conditions. Others imaging modalities in gynaecology
such as CT (computerized tomography) scanning and MRI (magnetic
resonance imaging) are complementary techniques which may provide
additional information in certain gynaecological conditions, such as in
assessing the spread of cervical and uterine carcinoma.

ULTRASOUND EXAMINATION

The
use
of
ultrasound
in
gynaecological has become widespread. Its high patient acceptance
and relatively low cost make it applicable as an initial means for
assessing many gynaecological disorders. Ultrasonic diagnostic
electronic scanning equipments have been improved remarkably in
performance and image quality. Nowadays, ultrasound examination
may either be performed using the transabdominal approach in which
the uterus and adnexae are imaged through a distended urinary
bladder or using transvaginal sonography (TVS), in which the probe is
inserted into the vagina for detailed imaging of the uterus and ovaries.

Fig. 1.1 Transvaginal ultrasound examination

Transabdominal ultrasound scanning is typically performed with a

linear transducer operating at 3.5 MHz. However, anatomic detail
using transabdominal approach may be limited by subcutaneous and
pelvic fat, which increases artifact and scattered the incident
ultrasound beam.

The transvaginal sonography provides more detailed evaluation of the

uterus and adnexae than transabdominal scanning. This is because of
its close proximity to the pelvic organs.

Purposes of diagnostic ultrasound in gynaecology

Ultrasound examination helps in the differential diagnosis of many
benign and malignant conditions, allows assessment of response of
treatment and also this examination helps in the management of an
infertile couple.
In generally, the purposes of ultrasound examination include:
1) To determine the position, size and malformation of the uterus.
2) To evaluate an endometrial image the presence of intrauterine
obstacles and myometrium tumour.
3) To diagnose the presence of tumour in the pelvic and abdominal
cavity.
4) To study the size, form and character of the tumour.
5) To identify the presence of fluid in the pelvic and abdominal cavity.
6) To identify the presence of retroperitoneal tumour and swelling of
lymphnode.
7) To determine the position and size of the ovary, and the number and
size of ovarian follicles.
8) To study the vascular system and irregularity in the pelvic cavity.

THE NORMAL ULTRASOUND IMAGES OF THE PELVIC

ORGANS
UTERUS
On ultrasound examination the uterus and cervix can be visualized in
longitudinal and transverse planes.
Endometrial image

a): longitudinal

b): transverse

Fig.1.2 Ultrasound image of a normal adult uterus

The uterine muscle is of a uniform grainy texture around a central

endometrium. A nulliparous normal uterus is about 7.5 cm average
length (range 7-10 cm), whereas the multiparous uterus is a bout 9 cm
average length (range 9-11 cm).
After menopause, the uterus gradually atrophies and the uterus
resumes an infantile size and shape

Endometrium image: The image of the normal endometrium can

be recognized as a long ellipsoid with a strong echo in the uterus,
surrounded by the low-level echo layer.
In most women of childbearing age, the endometrium varies
according to the phases of the cycle. The endometrium can be
observed from the later half of the proliferative phase until the
secretory phase.
In the menstrual phase, the normal endometrium is 3 to 5 mm thick
with mildly echogenic texture. As the endometrium develops in the
periovulatory period, a triple layer texture (Fig. 1.3) can be seen
with thickness ranging from 5 to 8 mm. The outer echogenic layer
represents the basalis whereas the inner layer is the functionalis.
The central echogenic interface is refluxed cervical mucus. In the
secretory phase (Fig.1.3), the endometrium becomes diffusely
echogenic and up to 12 to 14 mm in thickness.

Mid-cycle of the menstrual

The endometrium is recognized as
a typical three layer

The secretory phase

The endometrium can be often
displayed to the level of thickness
as indicated in the image during a
secretory phase.

Fig. 1.3 The morphology of a normal endometrial image on ultrasound scanning

After menopause the uterus becomes smaller and the endometrium

becomes thinner and should always be < 5mm in thickness.
OVARIES
By careful scanning, the ovary can be clearly displayed as a
lozenges-shaped structured lateral to the uterus (Fig. 1.3). The
visualization of the ovary can be used to confirm the disappearance
of ovarian follicles (ovulation) or to determine that the tumour does
not originate from the ovary.
During the menstrual cycles the growth of the follicles can be
monitored.

Right ovary

Left ovary

Fig.1.4 Ultrasound image of a normal ovary

Bladder

Uterus

Fig.1.5 Ultrasound image of the ovary showing ovarian follicle (F)

FALLOPIAN TUBES
Normal fallopian tubes cannot be seen by ultrasound. The fimbrial
ends of the tubes can only be seen if there is fluid collection as in
hydrosalpinx.

CLINICAL APPLICATIONS OF ULTRASOUND IN

GYNAECOLOGY
Ultrasound examination helps in the differential diagnosis of many
benign and malignant conditions, allows assessment of response of
treatment and also this examination helps in the management of an
infertile couple.
EVALUATION OF MENSTRUAL
UTERINE BLEEDING

DISORDERS

AND

ABNORMAL

The ultrasound examination has an important role in the evaluation of

a peri- or postmenopausal women presenting with menstrual disorders
or with unexplained uterine bleeding. Ultrasound examination can
suggest the presence of abnormalities of the endometrium
(hyperplasia, polyps, intracavitary fibroids), myometrium (fibroids,
adenomyosis) or ovaries (functional cysts, polycystic ovarian disease).
In the management of postmenopausal women with abnormal uterine
bleeding, transvaginal ultrasound has a major role in determining
which patients should undergo endometrial biopsy. An endometrium
less than 5 mm is typical of atrophic endometritis, whereas one greater
than 6 mm may represent a variety of abnormal pathology.

DIFFERENTIAL DIAGNOSIS OF PELVIC MASS

Transabdominal and transvaginal ultrasound examination provides a
means to evaluate the location, and internal consistency of pelvic
mass. The differential diagnosis of the pelvic mass (e.g. uterine
fibroids, ovarian cysts or hydrosalpinx) can usually be made by
ultrasound examination.
A general outline of diagnostic considerations according to location and
internal consistency is shown in Table 1.
Physiological cysts demonstrate a smooth wall and no internal
septations. Their location is within the ovary. On the other hand, the
presence of a papillary excrescence or irregular and thickened internal
septations usually is associated with ovarian tumours.

Internal consistency
Location

Cystic

Complex

Solid

Ovarian

Physiological cysts
Neoplastic cyst

Dermoid cyst
Neoplastic cyst
Haemorrhagic cyst
Tuboovaraian
abscess

Metastases
Solid
ovarian
tumour
Fibroma

Adnexal

Paraovarian cyst

Endometrioma

Tubal tumour

Extraovarian

Hydrosalpinx

Uterine

Developmental
cyst

Degenerating
fibroid

Pendunculated
fibroid

Table 1. Differential diagnosis of pelvic mass by ultrasound appearance

Uterine fibroid
Uterine fibroid can be suspected when the uterus is seen to be
irregularly enlarged with areas of increased and decreased
echogenicity.
The position (i.e. subserous, intramural, submucus,
cervical) and size of the fibroids can be documented.

Fig. 1.6 Intramural uterine fibroid

Subserous and intramural fibroid These are often diagnosed from the
swelling of the entire uterus or the uneven outline of the uterine wall.
The distinction between a myoma node and a normal endometrium is
sometimes possible.
Submucous fibroid As it protrudes in the uterine cavity, the diagnosis
may become possible by a deformed endometrial image or by means
of the observation through the space made between the symmetrical
endometium.

Uterine muscle
Endometrium
cavity

Fig. 1.7 Ultrasound showing submucous fibroid (F).

Ovarian cyst and tumour

The appearance of the ovarian tumours, i.e. benign or malignant, can
be studied by careful ultrasound examination. In certain ovarian
tumours the appearance may be so characteristic that a specific
diagnosis can be made on ultrasound examination alone.
Benign ovarian tumour:
a) Serous cystadenoma
Ultrasound often shows a unilocular cyst that may
contain thin septae.
The wall of the tumour is even and thin.

b) Mucinous cystadenoma
The mucinous cystadenoma usually appear as a multiloculated cyst.
The septum is thin and an abnormal protuberance of tumour wall
and septum is not recognized. The wall of the tumour is even and
thin.

cyst

cyst

cyst
septum

Fig.1.8 Mucinous cystadenoma multiloculated, thin and smooth wall and thin
septum

c) Dermoid cyst
Sometimes the dermoid tumour presents as a complex adnexal
mass, with clusters of highly reflective dense echoes within the
lesion (Fig. 19).

Hairball

High amplitude solid portion

Fig.1.9 Dermoid cyst. Ultrasound showing

a complex appearance

Fig.
1.10
Characteristic
appearance of a dermoid cyst:

ultrasound

(M) solid material containing fat and

hair
(F) fluid
(T) - tooth

Malignant ovarian tumour:

When thick irregular septae or solid nodules are present, a malignant
cystadenocarcinoma should be suspected.
Sonographically, it is
generally recognized as being solid or partially solid and it indicates a
saw-toothed or papillary protuberance from the cyst wall (Fig. 1.11)
Solid portion
Cystic

Papillary protuberance
from the cyst wall

Fig. 1.11 Ovarian carcinoma: On the whole this is a cystic tumour and a solid portion
which protrudes from the wall. The periphery of the solid portion is saw-toothed and
irregular. This pattern is typical adenocarcinoma of ovary.

EVALUATION OF PELVIC PAIN

Transvaginal ultrasound has an important role in evaluating patients

with pelvic pain. The transvaginal ultrasound can demonstrate certain
causes of acute pelvic pain (e.g. ectopic pregnancy, haemorrhagic cyst
or torsion of the ovarian cyst) and chronic pain caused by ovarian
endometriosis or pyosalpinx.

INFERTILITY MANAGEMENT
Transvaginal ultrasound provides important information in the
evaluation of the infertile couple. This includes the observation of
ovarian follicular growth and ovulation as well as evaluation of the
thickness and texture of endometrium.
In the investigation and treatment of infertility, ultrasound examination
offers the following contributions:
1.
2.
3.
4.

To assess the anatomy of the pelvic organs.

To monitor the development and evolution of ovarian follicles.
To evaluate the endometrium
To guide oocyte retrieval (follicular aspiration) and in vitro
fertilization-embryo transfer.
5. To avoid the development of ovarian hyperstimulation
syndrome.
Follicular monitoring:
During ovulation induction with clomiphene citrate of human
menopausal gonadotrophin, transvaginal ultrasound is used to monitor
the development of ovarian follicles.
This is usually performed
beginning at day 7 of the patients cycle, preferably on a daily basis.
The ovarian follicle can be recognized as small round or oval cyst. The
number of follicles and their relative size can be determined, with
mature follicles measuring between 18 and 20 mm and favourable
endometrial thickness in the periovulatory period between 7 and 11
mm. The multilayered appearance has been associated with higher
rates of implantation. Ovulation is taught to occur when fine echoes
are seen in the mature follicle.

Fig. 1.12 Day 11 of cycle - Ovulation induction with human menopausal

gonadotrophin. Transvaginal ultrasound scanning showing multiple matured follicles.

ULTRASOUND IN THE MANAGEMENT OF EARLY PREGNANCY

PROBLEMS
Beside quantitative hCG, transvaginal ultrasound has an important
role in the evaluation of bleeding and pain in early pregnancy which
can be due to miscarriage and ectopic pregnancy. The ultrasonic
diagnosis of miscarriage is given by judging an embrional of fetal death
inside the uterus.
Ectopic pregnancy:
In women with an ectopic pregnancy, the
endometrial cavity is usually empty. Transvaginal ultrasound provides
an accurate means for detection of ectopic pregnancy. On transvaginal
ultrasound, this condition should be suspected in presence of a round
structure separate from the ovary in patients in whom an intrauterine
pregnancy cannot be detected. The tubal ring is an indication of an
unruptured ectopic pregnancy. Other ultrasound features of ectopic
pregnancy are:

An adnexal mass suspicious of haematocoele.

Free fluid (blood) in the pelvis.

Bladder
uterus

Fig.1.13 Gestational is displayed

outside the uterus as shown in this
ultrasound image

Colour Doppler sonography may provide an additional means of

diagnosis of ectopic pregnancy. The colour Doppler sonography shows
a vascular area with no specific waveforms. If an area of high-velocity,
low impedance flow is seen in the adnexae, separate from the ovary
this increases the suspicious for ectopic pregnancy.

Fig.1.14 Ectopic pregnancy: Transvaginal Colour Doppler ultrasound showing

vascularity of tubal ring of an unruptured ectopic pregnancy.

Missed abortion: The diagnosis of a fetal death (missed abortion) is

given on the facts that a fetal heartbeat cannot be detected after 8

weeks of pregnancy. The impression such as the degeneration and

irregular outline of gestational sacs are an important reference as an
indicator of fetal death.

Fetal echo

Fig.1.15 Missed abortion the gestational sac is irregular in shape and absence of
heartbeat.

Hydatidiform mole: In the case of complete hydatidiform mole, the

gestational sac and the fetus cannot be recognized and many small
cysts are displayed in the uterine cavity. Ultrasound appearances of a
hydatidiform mole are diagnostic with the typical snowstorm
appearance.

Fig.
1.16
Molar
pregnancy
(complete
hydatidiform mole). Numerous cysts can be
observed within the uterus

A partial hydatidiform mole is generally difficult to distinguish from a

missed abortion.

Blighted ovum: If there is a gestational sac with no embryo is seen than a blighted
ovum should be suspected.

COMPUTED TOMOGRAPHY
(CT SCANNING)
This imaging modality provides excellent soft tissue imaging compared
to standard radiography. It provides an accurate method of assessing
solid tumours.
Carcinoma of the cervix: CT scans provide better information than
ultrasound on the parametrial spread of cervical cancer and in
particular lymphnode metastasis.
Carcinoma of the ovary: CT scanning may provide information of
the nature of the pelvic mass. Retroperitoneal lymph nodes, common
sites for metastasis may be visualized. The CT scan may be useful in
assessing the response to chemotherapy.

Solid ovarian
tumour

Fig.1.17 CT scan showing a large solid ovarian tumour - fibroma

MAGNECTIC RESONANCE IMAGING

(MRI)

ROLE OF MAGNETIC RESONANCE IMAGING IN THE EVALUATION

OF GYNAECOLOGIC DISEASE
Magnectic resonance imaging (MRI) is an excellent modality for
secondary evaluation of a variety of pelvic disorders. MRI is considered
the next step in the imaging assesement of benign disease of the
uterus and adnexa and is becoming the primary imaging modality for
evaluating gynaecologic malignancies.
The mulriplanar imaging
capability of MRI and superior soft tissue contrast and large field of
view offer distinct advantages over both ultrasonography and
computed tomography (CT) in the assessment of gynaecologic
abnormalities.
MRI employs radiofrequency in the presence of magnectic field to
create cross sectional images of the body.
MAJOR CLINICAL INDICATIONS
Although ultrasonography remains the initial modality used in
evaluating clinically suspected gynaecologic disease, MRI can offer
supplemental diagnoctic information in cases of suboptimal or
equivocal ultrasound examination and in patients in whom there is
discrepancy between sonographic findings and physical examination.
The most common indications for the use of MRI in gynaecologic
disease include the following:
1) Congenital anomalies of the genital tract.
Precise diagnostic classification for counseling and treatment
options.
Presurgical planning.
2) Leiomyomas (fibroids)
Precise delineation of number, size, and location.
Help with selection of the type of surgery: myomectomy versus
hysterectomy.
Differentiation between leiomyomas and adenomyosis.

In selected patients before and after hormonal treatment, or

uterine artery embolization.
3) Adenomyosis
Diagnosis
Distinguishing between adenomyosis and leiomyoma
4) Pelvic malignancies
Staging primary tumours. MRI is the primary imaging modality
cancers of the endometrium, cervix, and vagina.
Detection of recurrent disease.
Secondaries malignancies.
Detection of the spread of pelvic cancer - MRI is probably more
effective in assessing parametrial spread of cervical cancer than CT
scanning. MRI has been shown to be more effective in detecting the
depth of myometrial invasion in cancer of the endometrium. MRI is
able to detect small deposits of peritoneal endometriosis.
Ovarian pathology A number of ovarian lesions have charactreristic
MRI features. MRI can accurately differentiate benign from malignant
ovarian lesions.

Dermoid cyst

Fig.1.18 MRI of the pelvis showing dermoid cyst.

Functional cysts of the ovary (e.g. follicular cysts and corpus luteum
cysts) appear on MRI as smooth, well circumscribe, rounded lesions
with a thin wall.
Cystadenomas on MRI are typically unilocular or multilocular cystic
masses with thin walls and septa. The cyst fluid may be of variable
signal intensity depending on its proteinaceous contents.
Teratomas - On MRI, cystic teratomas are well-defined, heterogenous
masses. They characteristically contain some component of fat, which
is isointense to subcutaneous fat on the images. Fluid-fluid or fat-fluid
levels are commonly present (Fig. 1.18).
Ovarian carcinoma appears on MRI as both solid and mixed solid/cystic
masses. The lesions are generally heterogeneous signal intensity.
They are characterized by irregular margins, thick walls (>3 mm),
septa thicker than 3 mm, and nodular internal septations, and area of
necrosis. Spread of disease to the abdomen may be manifested by
ascites, peritoneal implant, omental cake, or mesenteric disease.
Adenomyosis MRI is the examination of choice in the evaluation of
suspected adenomyosis.
The accuracy of MRI in distinguishing
adenomyosis from leiomyomas has been reported as high as 90%.
Although MRI can accurately diagnose diffuse adenomyosis, the
differentiation of a focal adenomyoma from a leiomyoma may be
difficult.

RADIOGRAPHY HYSTEROSALPINGOGRAPHY (HSG)

Hysterosalpingography is the radiological delineation of the uterus and
fallopian tubes. Contrast media introduced into the uterine cavity
through the cervical os outlined the inner cavity of the uterus, depicts
the lumen of the fallopian tubes, and determines the patency of the
tubes. The procedure is monitored by fluoroscopy, and the images are
recorded on film radiography.
Hysterosalpingography is most commonly used in the diagnostic
evaluation of infertility. Thisstudy is also useful in the diagnosis and
treatment planning of many gynaecological problem such as an
abnormal uterine bleeding, intrauterine adhesions or congenital
anomalies.
Indications of hysterosalpingography include:

Infertility
Congenital abnormality of the uterus
Intrauterine adhesions (Ashermans syndrome)
Abnormal uterine bleeding
Tubal surgery (pre- and postoperative)
Location of intrauterine devices.

Fig.1.19 Hysterosalpingography showing bilateral hydrosalpinx with no free

intraperitoneal spill