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There are certain basic data about the patient that you must obtain
during your evaluation on her.
Age
Race
Maritial status
Parity
Occupation
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.
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,
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.
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.
Menstrual History:
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:
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
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:
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.
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).
10
Bivalve or
Cuscos
speculum
Sims speculum
11
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:
CONCLUSIONS
Taking a full relevant history and performing a proper examination is
the essence of good gynaecological practice.
CHIEF COMPLAINT;
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.
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.
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
2
ANATOMY OF
THE FEMALE REPRODUCTIVE ORGANS
14
External
Genitalia
Internal
Genitalia
VULVA
VAGINA
CERVIX
UTERUS
FALLOPIAN
TUBES
OVARIES
The reproductive system of the female (Fig. 1.1) may be divided into
the external and internal genitalia.
MONS PUBIS
15
Clitoris
Labial Majora
Labial Minora
Vestibule
Fourchette
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
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
External iliac
group
Deep femoral
group
Superficial
inguinal group
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
Blood supply of
vulva
drain
age
Accompany
arterial supply
Also via
vesical and
Internal
pudendal artery
Superfficial
external
pudedndal
artery
20
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.
21
Posterior
Fig. 1.6 Anterior and posterior relationship between the vagina and the pelvic
structures.
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.
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
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:
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
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
Ovarian artery
Uterine artery
Anterior branch of
internal iliac artery
Vaginal artery
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
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.
Ampulla
Interstitial
Isthmus
Infundibulum
Fig. 1.11 Anatomy of the fallopian tube
30
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.
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
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.
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
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.
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
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
38
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.
39
FALLOPIAN TUBE
UTERUS
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
Internal pudendal
artery
Superficial
external
pudendal artery
Dorsal
clitoris
artery
40
41
Obturator node
Obturator lymph node is larger in size.
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.
LYMPHATICS
Middle
third drain into internal
iliacDRAINAGE
nodes
OFthird
THE
Lower
drain into
superficial nodes
Para-aortic
External iliac
Obturator
inguinal
Superficial inguinal
Deep
Paracervical
nodes
Fig. 1.2 Lymphatics drainage of body of uterus and cervix.
5
THE URINARY TRACT OF THE FEMALE
- URETER, BLADDER AND URETHRA Common
artery
iliac
URETER
RECTUM
UTERUS
BLADDER
Fig. 1.1
URETER
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.
Psoas
muscl
e
URETER
Round
ligament
Uterine artery
Levator ani
Obturator
internus
muscle
Vaginal artery
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
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
Pelvic
division
URETER
Intramural
segment
Medial relations :
Right ureter related to the vena cava.
The duodeno-pancreas
Sigmoid colon
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
INTRAMURAL portion
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.
Trigone
Tunica serosa
Internal sphincter
Urogenital
diaphragm
Urethra
External urethra
sphincter
are
6
THE NORMAL MENSTRUAL CYCLE
FSH , LH
OVARIAN CYCLE
HORMONAL EVENTS
Feedback
mechanism
ENDOMETRIUM CYCLE
Estrogen
Progesterone
Fig 1.1
menstrual cycle.
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.
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
Fig. 1.2 Hormonal changes during the events of the menstrual cycle.
Soiral atterioke
Uterine gland
BL
FL = Functional layer
Fig. 1.3
BL = Basal layer
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.
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.
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.
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
UTERUS 1
UT
Fig 1.1 Double uterus (uterus didelphys) - congenital malformation of the genital
tract.
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.
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.
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).
Lower end of
Mullerian duct
Vaginal plate
( tissue of
sinovaginal
bulbs )
Urogenital sinus
Vagina canal
Hymen
Before canalization
canalization of the
plate
Fig. 1.3
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.
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
Degenerating
primary sex cords
20 weeks
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.
Organs
Origin
Normal development
Ovary
Fallopia
n tube
Remain separate
Uterus
Vagina
Labia
minora
Genital folds
Labia
majora
Genital swelling
Clitoris
Genital tubercle
Remains small
teratogenesis
genetic inheritance, and
multifactorial expression
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.
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.
Fig. 1.8 Uterus didelphys. Duplication of the uterus result from complete fusion of
the two Mullerian ducts.
Fig. 1.9 Uterus bicornis the most common abnormalities of the uterus which is the
result of partial fusion of the Mullerian ducts.
SEPTATE
COMPLETE
Fig. 1.10
PARTIAL
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.
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
1)
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).
Complications
Haematosalphinx
Haematometra
Haematocolpos
Imperforate hymen
Amenorrhoea.
Abdominal discomfort or pain which has a cyclical pattern.
Interference with micturition.
Bulging occluding membrane at the vaginal introitus.
Absence
UTERUS
Absence
Complications
Infertility
Menstrual disorders
Double uterus
Uterus unicornis
Uterus bicornis
Incomplete (partial)
canalization.
and
Rudimentary horn
Dysmenorrhoea
Septate uterus
Dyspareunia
Primary amenorrhoea
Hydrocolpos or hametocolpos
Haaematometra
Haematosalpinx
Sexual ambiguity
Sexual ambiguity
VAGINA
Absence
fusion
Failure of canailzation
Septate vagina
Failure of canalization.
Imperforate hymen
External genitalia
Fusion of labia
Clitoromegaly
(enlarge)
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
STAGE 1 (prepubertal)
STAGE 2 (9 13 years)
Areola enlarging.
STAGE 3 (10 14 years)
STAGE 1 (Prepubertal)
STAGE 2 (9 13 years)
Sparse
growth
of
long
pigmented hair along the labia
majora
Fig. 1.2
development.
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
External
organs
Internal
organs
wall thicken
stimulation.
as
the
result
of
estrogens
Hair growth
Voice
ABNORMAL PUBERTY
Abnormalities of puberty can occur as a result of problems at any
level of the hypothalamic-pituitary axis. Aberrations can result in,
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,
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
precocious puberty.
About 28% of sexual precocity
associated with congenital adrenal hyperplasia.
are
PSEUDOPRECOCIUOS PUBERTY
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.
9
DISORDERS OF MENSTRUATION
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
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
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)
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.
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.
Fig. 1.2 Testicular feminization. The external genitalia are female, but the patient
has a 46 XY karyotype and testes.
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 :
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.
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.
hypothalamus
anterior pituitary
ovary
uterus
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
it may reduce the size of small tumours. Small tumours can also be
removed surgically.
2. Hypothyroidism
The anterior pituitary gland loses its function and the production of
gonadotrophin, thyrotrophic and adrenotrophic ceases or
inadequate.
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
suppressed
and
to
follicular
Pathology :
Hormonal changes :
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:
Ovarian Failure
Secondary amenorrhoea from ovarian failure may occur. This include :
a).
a
b).
Premature menopause
(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
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.
Hyperprolactinaemia condition
Pituitary tumours, Drugs
Thyroid disturbances
Ashermans syndrome
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
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
adrenal
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
SECONDARY AMENORRHOEA
A patient who has previously menstruated
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.
-
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
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
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.
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.
-
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
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
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
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:
c) SURGERY
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
Intrauterine device
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)
Examination:
A careful pelvic examination with special attention to
detecting endometriosis, pelvic inflammatory disease,
pelvic masses or uterine enlargement should be made.
Investigations:
2. TO RELIEVE SYMPTOMS :
Analgesics
Symptomatic relief can be achieved with analgesic drugs
such as aspirin, codeine.
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.
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.
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
Blood dyscrasias
Endocrine disorders
Psychiatric disorders
as
hypothyroidism
(particularly
Anatomical causes
Traumatic causes
Infective causes
Hyperplasia of endometrium
Malignant causes
CONDITIONS
PATHOGENESIS
UTERUS
Congenital malformation Double uterus
Enlarge
increase
bleeding
TRAUMATIC
uterus
area
Traumatize
endometrium
interfere with
contraction
HYPERPLASIA
OF
ENDOMETRIUM
with
of
the
and
uterine
ENDOMETRIAL HYPERPLASIA
Thickened endometrial
tissue increases more
menstrual bleeding
NEOPLASTIC
GROWTH
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,
b)
c)
d)
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.
Fig. 1.4 Hysteroscope view showing the diagnosis of submucous and intracavitary
fibroids
TREATMENT
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
dysfunctional
Progestogens
to 12 days
stopping each
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.
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.
2. Anovulatory DUB
PRESENTATION
Dysfunctional uterine bleeding
reproductive age woman.
affects
about
9%
to
12%
of
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.
2.
3.
4.
5.
Hormonal therapy
Dilation and curettage
Endometrial ablation
Hysterectomy
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.
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.
PREMENSTRUAL SYNDROME
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.
Acne.
Backache
Bloating.
Fatigue
Headache
Sore breasts.
Weight gain.
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.
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
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
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
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.
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
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 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
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
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.
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.
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.
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:
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
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).
Treatment of trichonomiasis
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.
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)
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.
contraceptive use;
pruritus,
postcoital irritation, or
Investigations:
13
Fig 1.1
Acute salpingitis
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).
Fig. 1.2
Aetiology of salpingitis.
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
Pathways of
salpingitis
infection
of
Systemic upset
Pain
Recurrence
Infertility
Ectopic pregnancy
The
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
Tubo-ovarian mass
Table 1. Symptoms and signs of salpingitis
ASSESSMENT:
Gynaecological examination
laterally,
mobility,
Investigations
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
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
The
viable
endometrial tissue are
deposited
and
implanted
on
the
structures within the
pelvic
cavity,
e.g.
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:
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).
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
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.
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
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:
(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.
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
Progestogens
Danazol
Analogues of gonadotrophin-releasing hormone (GnRH)
Weight gain
Acne and oily skin
Hirsutism
Headaches
Deepening voice
Surgical Treatment
Surgery is usually reserved for women with severe endometriosis,
including adhesions and infertility. Surgical procedures can be
accomplished with laparotomy or laparoscopy.
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
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.
Types of retroversion:
can
be
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
Symptoms:
Uncomplicated retroversion of the uterus causes no symptoms.
Symptoms traditionally attributed to uterine retroversion include the
following:
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.
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:
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.
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
16
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:
First-degree prolapse
Second-degree prolapse
Third-deree prolapse
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:
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
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
Management
The management of prolapse may be operative or palliative (nonsurgical). The management of prolapse will depend upon:
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
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:
Prevention
Measures that may reduce the likelihood of prolapse include:
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
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.
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.
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.
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
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
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
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:
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.
.
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.
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.
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.
Uterine fobroids are poorly supplied with blood vessels and tend to
outgrow their blood supply. This causes some but not all of the
Recurrence abortion
Pre-term labour
Malpresentations
18
UTERINE POLYPS
Endometrial
polyp
Cervical
polyp
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
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
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
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:
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.
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
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
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
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:
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:
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:
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:
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
Hirsutism
o
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.
FOLLOW UP
Further Outpatient Care:
Complications:
PROGNOSIS:
The
chances
of
Background
Pathogenesis
Pathology
Clinical Features
Laboratory
evaluation
Treatment
Infertility
Hirsuitism
Oligoamenorrhoea
bleeding
Obesity
or
Dysfunctional
uterine
Complication
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
21
BENIGN TUMOURS OF THE OVARY
Cell of Origin
Functional
cysts
(follicular, Normal
follicle
theca-lutein, corpus luteum)
Serous cystadenoma
Mucinous cystadenoma
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
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.
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
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
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
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.
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
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,
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
Reproductive Period
Menopausal Period
mild,
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. 1.5 CIN 1 Basaloid neoplastic cells occupy not more than the lower third of
epithelium.
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.
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
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
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:
VIN 1
VIN 2
VIN 3
Site
Symptoms
Signs
Raised
or
flat,
leukoplakia,
hyperkeratotic, pigmented.
reddened,
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.
VAIN 2
VAIN 3
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
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
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
PATHOLOGY
The majority of cases of cervical cancer are squamous cell lesions, with
adenocarcinomas and adenosquamous lesions occurring less
frequently.
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
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.
including
combined
Clinical staging:
Lymphatics:
INVESTIGATIONS
Possible investigations include:
Intravenous pyelogram
TREATMENT
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.
cervical stenosis
cervical incompetence
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:
CHEMOTHERAPY TREATMENT:
Chemotherapy may be indicated in:
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%
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
30
Bladder,
rectum
metastases
10
or
Palliation
25
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
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.
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.
G1 - Well differentiated
G2 - Moderately differentiated
G3 - Poorly differentiated
Degree of
differentiation
Extension of cancer
1a
1b
G123
G123
1c
G123
2a
2b
G123
G123
3a
G123
3b
3c
G123
G123
4a
4c
G123
G123
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.
PROGNOSIS
This is determined by stage, grade, myometrial invasion and lymph
node involvement:
26
OVARIAN CANCER
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.
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.
Malignant teratoma
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.
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.
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.
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:
(5) diaphragm
(6) liver capsule
(7) pleural cavity
positive
o
o
o
o
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:
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.
27
VULVAL CARCINOMA
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.
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.
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
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.
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.
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
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.
Features
Pre-invasive carcinoma
IIa
Involvement of subvaginal tissues. Not extending to
parametrium
IIb
III
IVa
IVb
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.
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
Signs:
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).
Age (years)
Antecedent pregnancy
Interval
time
(months)
between end of antecedent
pregnancy
and
start
treatment
< 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
> 105
105
Brains
Total score for patient isn obtained by addition of score for each prognostic.
<4
5.7
5.8
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:
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
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.
PSYCHOSOMATIC FACTOR
Psychosomatic factors have been suggested but not proven as
causes for early miscarriage.
Threatened abortion
Inevitable abortion
Complete abortion
Incomplete abortion
Missed abortion
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:
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.
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.
INCOMPLETE ABORTION
Incomplete abortion occurs when part of the products of conception
are retained in the uterus. The features of incomplete abortion are:
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.
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:
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:
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
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:
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
Acute appendicitis
Pelvic Inflammatory disease
Ectopic pregnancy
Urinary tract infections in pregnancy
Vaginitis
Septic shock
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:
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
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
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
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
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?
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%)
In cervix
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.
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 :-
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.
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:
Amenorrhoea
Unilateral pain
Vaginal bleeding
Lower abdominal tenderness
Extreme tenderness in the lateral fornix on one side
Marked cervical excitation
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.
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:
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.
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:
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
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
Hydatidiform
uncommon
Hydatidiform
trophoblastic
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:
Signs:
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:
Snowstorm
on
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
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.
CLINICAL ASSESSMENTS
PREGNANCY TESTS
CONTRACEPTION
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
Development
reproductive
normal.
tract
of Congenital
or
developmental
is factors
Unusual
uterus
(e.g.,
congenitally small, or infantile, uterus)
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)
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.
Blockage
of
tube
by
compression or Kinking by abnormal
growth such as endometriosis and
neoplasm
Duration of infertility
of
actual
techniques,
Adequacy of erection
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.
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.)
Tubal
Hystrosalpingography or hysterography
Laparoscopic examination
Cervical
Physical examination
reaction
Who
Woman
Why
How
When
Information
Sought
Who
Why
How
When
of
mucus
ovulation
and
characteristics
Who
Woman
Why
How
When
Information
sought
Hormone Analysis
Who
Woman
Why
How
When
Information sought
Endometrial Biopsy
Who
Woman;
Why
How
When
Information
sought
Postcoital Test
Who
Why
How
When
Information
Sought
Hysterosalpingography
Who
Woman;
Why
How
When
Information
sought
Laparoscopic Examination
Who
Woman
Why
How
When
Information Sought
Who
Woman
Why
Information
Sought
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
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.
Ovulation induction
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.
Oocyte
Cytoplasma
B
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,
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.
Mechanism
Haemoperiteu
m
Clinical condition
Ruptured
ectopic
pregnancy
Rupture of endometriotic
cyst
Ruptured corpus luteum
or follicular cyst
Ruptured of endometriotic
cyst
Vascular
complication
Visceral
distension
Complication of
pregnancy
Miscarriage
Nongynaecologi
cal
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.
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
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
Fig. 1.1 Endometriosis involving the ovary as seen during laparscopic examination
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.
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.
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
Imaging Studies:
Ultrasonography
Barium
enema
sigmoidoscopy.
o
radiography,
colonoscopy,
and
Other Tests:
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.
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
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.
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
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:
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
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.
Medical management
In women under 40 years old, and in older women without organic
pathology, dysfunctional uterine bleeding may be treated with:
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
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.
NON-MENSTRUAL BLEEDING
Non-cyclical, patternless vaginal bleeding is often described as
metrorrhagia. A useful classification is as:
postcoital bleeding
intermenstrual bleeding
postmenopausal bleeding
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:
Examination:
Investigation:
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
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
Investigation:
All cases must be thoroughly investigated (except perhaps for
withdrawal bleeding which occurs at the expected time in menopausal
women taking HRT).
Treatment:
This is dependent on cause.
36
INCONTINENCE OF URINE IN WOMEN
ETIOLOGY
Urinary incontinence in women may be classified according to whether
it is urethral or extraurethral leakage (Table 1)
Urethral causes
Incompetence urethral sphincter
mechanism (stress incontinence)
Uninhibited detrusor activity (urge
incontinence)
Extraurethral causes
Fistula
-
Ureterovaginal fistula
Vesicovaginal fistula
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
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
URGE INCONTINENCE
Symptoms
Etiology
Bladder function
Normal
Abnormal
CLINICAL
ASSESSMENT
INCONTINENCE
OF
PATIENT
WITH
replacement, beta-mimetics,
diuretics, and ACE inhibitors.
sedatives,
muscle
relaxants,
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
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.
Grade 0 Continent.
Grade 1 - Loss of urine with sudden increases in abdominal
pressure, not in bed at night.
Laboratory Investigations:
Imaging Studies:
Cystourethrography
o
Intravenous pyelography
o
Other Tests:
Electromyography
o
Diagnostic Procedures:
Urodynamic studies
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.
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.
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:
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.
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:
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:
Postoperative care:
Postoperative care is similar for patients undergoing each of the
incontinence procedures.
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.
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
Osteomyelitis
Urogenital fistula
Rare
Nerve injuries
Voiding dysfunction
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
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.
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
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
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.
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)
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.
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.
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.
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
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
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.
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).
rate
in
typical
use
is
estimated
to
be
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
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
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
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
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
(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.
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:
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.
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
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.
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
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.
IMPLANT
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
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.
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.
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.
Abdomen
with gas
filled
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.
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.
and
the
minipill
Copper
T380
contraception
intrauterine
device
as
an
emergency
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.
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.
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
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
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.
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
41
GYNAECOLOGICAL PROCEDURES
COLPOSCOPY
DIAGNOSTIC PROCEDURES
The colposcopic evaluation must be performed thoroughly and
accurately, and this can be accomplished only if a systematic routine is
meticulously followed.
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
Squamous
epithelium
Columnar epitheliun
TZ
Acetowhite epithelium
Squamous epithelium
Transformation zone
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
Grade II
Grade III
The epithelium is
intensely acetowhite
The
vessels
regular
and
calibre
The
vessels
are
regular but or larger
calibre
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)
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.
Cuscos speculum
Ayres spatula
Pencil
Fixing jar
Glass slides
Cytobrush
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.
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
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.
Table 1. Interpretation of smear result recommended by the British Society for Clinical
Cytology
Cytology report
Explanation
Inadequate
Negative
Severe
dyskaryosis/
invasive carcinoma
Glandular
neoplasia
suspicion of glandular
or
Normal. Includes
changes.
or
simple
inflammatory
Source. Practical Guide for General Practitioner (14): Cervical screening (1992)
Austoker, J. and Macpherson, A. Cancer Research Campaign, Oxford Medical
Publications.
Descriptive diagnosis
Reactive changes
o Reactive cellular changes
o Inflammation
o Atrophy with inflammation (atrophic vaginitis)
Table 3.
Correlation between UK and Bethesda reporting systems: squamous
epithelial cell abnormalities
BETHESDA SYSTEM
ASCUS
LSIL
HSIL
BRITISH SYSTEM
Severe dyskaryosis
(CIN 3)
SQUAMOUS CELL
CARCINOMA
SQUAMOUS CELL
CARCINOMA
HYSTEROSCOPY
Fig.1.1
diagram
Schematic
showing
INDICATIONS
Diagnostic hysteroscope: investigated by hysteroscope:
The following
conditions
can be
Operating hysterscope:
An operating hysterscope can be used in the following condition:
cause
and
B): A submucous
myoma
Fig.1.3 Hysteroscopic view of the uterine cavity showing abnormal pathology of the
endometrium
CYSTOSCOPY IN GYNAECOLOGY
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
42
GYNAECOLOGICAL OPERATIONS
(Pre-operative assessment and Post-operative complications)
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
NURSING PREPARATIONS
1) Shaving: the vulva is usually shaved for major surgery but
shaving is unnecessary for minor surgery.
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.
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
Infertility investigation
Investigation for primary
or secondary
amenorrhoea
Unexplained pelvic pain
acute or chronic
Staging of endometriosis
Investigation of adnexal
or pelvic masses
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.
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.1.4 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
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.
Diaphragmatic hernia
Advanced malignancy
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
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
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
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.
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.
Cone specimen
Therapeutic conization
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.
Volsellum
Scalpel blade
Lateral suture to
reduce bleeding
Weighted speculun
Area of conization
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
for
the
the
on
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
2:
CIN lesion
3:
Administration
anaesthesia
4:
of
local
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.
A midline subumbilical or
suprapubic transverse incision
is made on the abdominal
wall.
Line of
incision
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.
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.
C
A
D
B
BLUNT
SHARP
Curette
Uterus
Retained
product of
conception
Volsellum
Curette
Speculum
Complications
following
anaesthesia
Laceration to the
cervix
Perforation of the
uterus
Haemorrhage
Injury
to
bowel,
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
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.
surgery of the tear is not feasible or where the general condition of the
patient indicates that hysterectomy is the quicker and safer procedure.
Round ligament
UTERUS
Fallopian tube
Ovarian pedicle
Division and ligation of the first pedicle (round ligament, fallopian tube and ovarian
pedicle)
Uterine artery
UTERUS
Left
Right
Division of the cardinal
ligament
UTERUS
CERVIX
Vaginal canal
Stump of cardinal
ligament
Stump of uterine artery
Stump of uterosacral
ligament
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
Postoperative complications:
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.
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
Cyst
Ovary
Ovary after
reconstruction
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
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)
ANTIBIOTIC
(e.g.
actinomycin-D,
bleomycin,
Class
Drugs
Common
application
gynaecological cancer
Antimetabolites
Methotrexate
5-FU
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
Plant alkaloids
Vinblastin
Vincristine
Etoposide
16)
Hormonal
Tamoxifen
Progestogen
(VP-
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.
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.
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).
44
RADIOTHERAPY IN GYNAECOLOGICAL
CANCERS
an
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.
CARCINOMA
PRINCIPLES
OF
THE
UTERINE
CERVIX:
MANAGEMENT
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.
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.
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
Treatment.
a) Remove foreign body with warm saline irrigation or
bayonet forceps. Obtain vaginal and urine cultures and
treats concurrent infection.
LABIAL ADHESIONS
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.
Investigations:
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:
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
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
Uterine curette
It consists of a blunt
and sharp end.
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
Hegars dilators
Ovum forceps:
This instrument is used to
empty the contents of the
uterus, such products of
conception or polyps.
Cervical
forceps
volsellum
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
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.
a): longitudinal
b): transverse
Right ovary
Left ovary
Bladder
Uterus
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.
DISORDERS
AND
ABNORMAL
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
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.
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
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
Fig.
1.10
Characteristic
appearance of a dermoid cyst:
ultrasound
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.
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.
Bladder
uterus
Fetal echo
Fig.1.15 Missed abortion the gestational sac is irregular in shape and absence of
heartbeat.
Fig.
1.16
Molar
pregnancy
(complete
hydatidiform mole). Numerous cysts can be
observed within the uterus
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
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.
Infertility
Congenital abnormality of the uterus
Intrauterine adhesions (Ashermans syndrome)
Abnormal uterine bleeding
Tubal surgery (pre- and postoperative)
Location of intrauterine devices.