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 LIST OF CONTRIBUTORS

Staff members of the department of Ob GYN - Cairo University

ln alphabetical order

. Abdelhamid Attia Mahmoud Salem

. Adel Farouk Moaataz Elsherbiny
. Ahmed Abdelmeguid Mohamed Abdelhady
. Ahmed Mahmoud Mohamed Abolkassem
. Akram El adawy Mohamed lhab
. Alaa El Ebrashy Mohamed Momtaz
. Ashraf Younis Mohamed Osman
. t'...1Essam Abolfotouh Mohamed Aly
. Fadel Shaltout Mohamed lismail,
. Fouad Abohamila Mona Fawzy
. GamalAbdelsamaei Mostafa Abdelbar
. Gamal Eid Moustafa Abdelhamid
. GamalYoussef Moustafa Metwally
. Hany El Didiy Nadin Alaa
. Hazem Ashamawy Omar Abdelaziz
. Hesham Badawy Omayma ldris
. Hesham Mourad Reham fouad
. Inas Abdelhamid Salah Sanad

. lsmail ElEsseily Samah Abolgheit

. Khaled Abdekmalek Sameh Zaki
. Khaled Rasheed Sherif Khattab

' Magdy lbrahim Sherif Negm

. Maha Mosaad Somaya hassan
Prefoce to the filth Edition
Hello dear students.

This is the 5th edition. our book is now 15 years old, but is even growing younger, as
we are keen to update the information within in accordance with the latest studies
in our field. You will find in the current edition, in an appealing form, full of
illustrations whether in the book itself or on the adjoining CD.

This edition, in its final version, met my vision into upgrading the book into the
digital mobile platform. so that you, can study anywhere and any place you go, make
it on the road, in the coffee shop, or club.

In addition I asked our active editorial board to add quick response codes (QR)
alongside each chapter to link to external sources for optional further reading and
explanatory videos. This will help broaden your vision on the topic for better
understanding the facts and make it easier for you to accumulate the knowledge and
retain the information in accordance with scientific fact stating that the brain
assimilates knowledge more readily in a picture form.

Thanks to the enthusiasm and perseverance of the editorial board, headed by Prof.
Khaled Rasheed, and the valuable contribution of the faculty members of the
department in Cairo University, this edition in its final version met my expectations,
and I hope it will meet yours as well.

r o oo$esft is a valuable addition to our department's efforts to upgrade our

education standards to meet and hopefully surpass the most recent education
advances worldwide.

This book will be a valuable learning tool for both our undergraduate students as a
requirement, as well as for our postgraduate students as a baseline for further
reading sources.

I hope you make good use of this rich source of medical information both in your
undergrad education and in your practice later on in your career

Abdel Maguid Ramzy

Heqd of deportment of Obstetrics and Gynaecology 2078-2079
Foculty of medicine, Coiro University
 CONTENTS

Page

BASIC GYNEACOLOGY
1. Gyn. History and Examination L

2. Anatomy of the Female Genital Tract 9

3. Development of the Female Genital Organs 27

GYNAECOLOGIC EN DOCRI NOLOGY

4. The Menstrual Cycle an Associated Disorders 35

5. Puberty and its Disorders 47

6. Menopause and Associated Disorders 51

7. Amenorrhoea 57

8. Hirsutism 69

9. Chronic Anovulatory Disorders and PCOS 79

FEMALE GENITAL TRACT INFECTIONS

10. Female LGT Infections 81

11. Female UGT Infections 92

12. Sexually Transmitted Diseases 100

GENERAL GYNAECOLOGY

13. Infertility and Assisted Reproduction 108

14. Contraception and Family Planning Lzt

15. Benign Conditions of the Vulva and Vagina 133

15. Pelvic Organ Prolapse L4t

17. Perineal Lacerations 153

18. Urinary Incontinence 158

19. Abnormal Uterine Bleeding L7t

GYNAECOLOGIC ONCOLOGY

20. Uterine Leiomyomas L79

21. Endometriosis and Adenomyosis L9L

22. Screening for Premalignant Lesions of FGT 199

23. Endometrial Carcinoma and Uterine Sarcoma 205

24. lnvasive Cancer of the Cervix zts

25. Malignancies of the Vulva and Vagina 223
 U,
26. Non Neoplastic Ovarian Swellings 227
27. Benign Ovarian Neoplasms 234
28. Malignant Ovarian Neoplasms 244

DIAGNOSTIC PROCEDURES AND OPERATIONS IN GYNAECOTOGY

29. lmaging Techniques in GYN 256

30. Endoscopy in GYN 262
:
31. Differential Diagnosis In Gynaecology 266
r Uterine polypi
r DD of a Pelvi-abdominal Masse

. DD of an Adnexal Swelling

' DD of a mass in the pouch of Douglas

' Gynaecologic causes of Acute Abdomen and chronic pelvic pain

32. Operative Gynaecology And postoperative Complications 273

\,

\-./.

\-,

\,
 Gynaecologic History
Gyn aeco I og i c Exo m i n otio n

Commonly used Diagnostic lnvestigotions

GYNAECO LOG I CAL H ISTORY

The most important evidence is always provided by the history given by the patient or one of
her attending relatives. In many cases a provisional diagnosis can be reached before starting
detailed physical examination.

1. PERSONAL HISTORY:
- Patient's name, age, address, occupation, marital status, gravidity and parity

- Special habits of medical importance

2. COMPLAINT:
Complaint is best written in the pafient's own words as; excessive vaginal bleeding, pelvic pain,
painful intercourse, progressive abdominal enlargement, mass filling or protruding from the
vagina, excessive vaginal discharge, vaginal itching or burning sensation, low back ache, swelling
of lower limbs, etc...

3. PRESENT HISTORY:
) Analysis of the onset, course, and duration, of the present complaint.
) Ask about symptoms relevant to, or associated with, the present complaint.
D Ask about symptoms related to other body system affection as; urinary, GlT, cardiac,
pulmonary, neurologic, etc...

4. PAST HISTORY:
A) Medical Disorders:
Y Systemic diseose: hypertension, diabetes mellitus, cardiac, renal, or liver disease.
Y Endocrine disorders: especially thyroid and adrenal disorders.
Y Blood dyscrasios: as ITP & von Willebrand disease (VWD).
B) Drugs and Medications: as ongoing medical or hormonaltherapy.

C) Surgical Procedure:

Y Gynaecologic & Obstetric procedures; D&C, CS, Myomectomy, Hysterectomy, Laparoscopic

a nd hysteroscopic procedures.
Y Relevont Surgical procedures: as pelvic surgery (appendicitis, peritonitis, pelvic masses) and
bariatric procedures (gastric banding, and sleeve operations)
Y Other Surgical procedures; thyroidectomy, breast lumps, cholycystectomy, etc...
 Gy na e colog i c h isto ry an d Exo m i n a ti o n

5. MENSTRUAL HISTORY:
- Age ot menorche.' normally 1L-13 years
- Cyclic pattern: normally every 25-32 days (mean 28 days)
- Duration of bleeding; normally 3-5 days.
- Amount;30-50 ml/cycle, changing 2-3 blood soaked diapers/day.
- Chardcter of bleeding; usually dark in colour with no or minimal clots.
- Dysmenorrhoea: Menstrual pain and its relation to the onset of bleeding.
- Last menstruol period (LMP).' calculated from L" day of onset of menses.

6. OBSTETRIC HISTORY:
t Previous pregnancies ond deliveries in sequence of their occurrence.
- Durotion of each gestation (term, preterm, or abortion)
- Route of eoch delivery: vaginal delivery (VD), or caesarean section (CS)

- still born (SB), or neonatal death (NND).

The condition of the newly born: living,

- Complications related to pregnancy, delivery, and puerperium; as gestational diabetes,

hypertension, haemorrhage and sepsis.
t Previous obortions:
- Durotion of pregnoncy ot occurrence of eoch qbortion (1" or 2no trimester)
- Method of termination (spontaneous, medical, or surgical termination).
- Post-abortive complicotions (bleeding, sepsis, infertility, etc...)
t The Obstetric Code:The obstetric history can be described for simplicity by either;

- The 4 digit code (0000)i _

Y First 3 digits: stand for duration of pregnancies (term, preterm, & abortions).
D lhe 4'h digit: stands for number of living offspring.
- The Gravidity / Pority code (G0/P0):
Y Grovidity describes the number of pregnoncies, including the current pregnancy if
present (term + preterm + abortions)
F Parity stands for number of previous deliveries (term + preterm).
. lf present pregnancy is ongoing: establish LMP, EDD, and complaints related to each trimester.

7. COITAL HISTORY: Particularly in cases of infertility.

- Frequency of sexual intercourse (times /week)
- Associated symptoms; as presence of dyspareunia (painful intercourse).
- Husbands age, occupation, and any previous investigations for male infertility, previous
marriage and children .

8. CONTRACEPTIVE HISTORY:
Methods used, by both partners, duration of its use, and time of its termination.

9. FAMITY HISTORY:
Inherited diseases, genetic disorders, and hereditary malignancies
 Gynaecology

GYNAECOLOGIC EXAM INATION

1. GENERAT EXAMINATION:
- General medical examination; measurement of the Pulse, temp, and B.p.
- Gait, height, weight, and body mass index (BMl) = weight kg /height in meter square
- Hair distribution and development, of the secondary sexual characters.
- Breast examination is an important part of any gynaecological examination.
- Inspection of the back: for spina bifida, hair tuft, severe kyphosis, or scoliosis.

2. ABDOMINAL EXAMINATION: bladder should be empty

t lnspection.'abdomen exposed from costal margin till symphysis pubis;
- Abdominal masses, scars of previous operations, pigmentation, etc...
- Hernia orifices, and divarication of the rectii muscles (during straining)
t Palpotion ol oll abdominal guadronts
- 9 quodronts; (right and left hypochondruim, right and left lumbar, right and left iliac fassa,
hypogastrium, umbilical, and suprapubic regains)
- quodrants; (right and left upper quadrant and right and left lower quadrants)
4
- Palpation for enlarged liver, spleen, renal, abdominal, and
pelviabdominal masses.
t Percussion of the obdomen:
Normally there is resonance in the centre due to
air in intestinal loops.
Tumours show uniform dullness all over the
- Moderate ascites shows central resonance ( ith dull
flanks (fluid). Shifting dullness will occur w ned on
her side with upper flanks becoming resona ascites
to more dependent parts and intestines floa
Tense ascites gives generalized dullness (fluid
everywhere)' ,,g 1-1: 4 quodronts of the
3. BREAST EXAMINATION obdomen
Breast examination is an integral part of a comprehensive
gynaecologic examination. lt is an important method for both
screening for benign and malignant breast tumours, and diagnosis of
breast conditions as a breast lump, fibrocystic breast disease,
mastitis, breast abscess, and galactorrhoea.
A) Inspection: with patient in upright position, for contour,
symmetry, skin changes or nipple retraction.
B) Palpation: with patient in upright then supine position, of
Fig 1.-2: Breast exomination

hand.

patient's arm is supported.

C) Investigations in case of presence of a suspicious lesion include:

BRCA gene positive women) \

 Gynoecologic history ond Clinicol Evoluotion

4. LOCAL EXAMINATION
- Patient's attendance is by itself considered consent for a pelvic examination. However
presence of a third party (a female relative or a nurse), is ethically important.
- The patient's bladder must be empty, and only disposable gloves should be used.
- lnstruments used are either disposable or should be sterilized by dutocldving, to avoid the
risk of transferring infecting vaginal organisms from one woman to another.
- The patient is examined locally while lying down in the lithotomy position (see fig1-1)

Fig 1-3: Lithotomy position Fig 1-4: lnspection of the vulvo

A. lnspection of the Vulva and Perineum:

- The vulva: is inspected for anatomical abnormalities, swellings, tumours, warts, or ulcers,
together with presence of abnormal vaginal discharge or bleeding.
- The externol urethrol meotus: for any redness, discharge, or presence of urethral caruncle,
- The perineum: for old lacerations, and the presence of piles around the anal orifice.
- lnspection while stroining: for presence of genital prolapse and stress incon-tinence.

B. DigitolVoginal Palpotion (PV):

The index finger is inserted into the vagina first, and as the
patient relaxes, it is followed by the middle finger, and together
slope gradually deeper in the vagina following its direction (upwards
and backwards). As the fingers are withdrawn, the following
structures are palpated :

- The cervix: noting its size, consistency, mobility, direction, and

level. Presence of lacerations, hypertrophy, dilatation, and any
descent on straining, or any contact bleeding.
- The voginol wolls: palpated for any mass, ulcer, or fistulous Fig 1-5: PV Examinotion

opening,
- The bladder ond urethra; can be palpated through the anterior
vaginalwall.
- The rectum and pouch of Douglas: can be palpated through
the posterior vaginal wall.
- Bartholin's glonds: are palpated to detect any swelling.
- The condition of the levators ani muscles; can be determined
by two fingers in the vagina, and the thumb on the perineum. Fig 1-6: Bimanuol Exominotion
Ask the patient to cough and feel the muscle as it contracts.
 Gynaecology

C. Bimonual Pelvic Examinotion:

The index and middle fingers of the right hand are placed in the anterior vaginal fornix, while
the left hand is placed flat on the abdominal wall.
1. Examination of the Uterus:
The vaginal fingers of the right hand should push the cervix upwards, rotating the fundus
forwards' The abdominal hand is placed below the umbilicus and gradually moved lower
suprapubically until the fundus is caught and pressed against the fingers of both hands in the
anterior fornix, in AVF uterus, or at the posterior fornix in RVF uterus.
2. Examination of the Adnexae and Vaginal Fornices:
The fingers of the vaginal hand move towards one lateral fornix with the abdominal hand
following, trying to gently squeeze the adnexa to palpate any masses, swellings, or elicit
tenderness. The same procedure is then repeated in the other lateral fornix.
3. Examination of the Pouch of Douglas:
The vaginal hand is moved to the posterior fornix, while the abdominal hand follows trying
ao reach the vaginal fingers behind the uterus suprapubically

.
) Uterine Size, Shape, Consistency, and Contour: the uterus is a pear shaped organ with
firm consistency, and smooth outer contour. lt normally measures nearly 7.5 X 3.5 X 5.5
cm in Long/AP/Transverse, diameters. lt may be felt with difficulty in women with
marked trunk obesity.

) Uterine Position: The uterus is commonly Anteverted flexed (AVF) in position, with the
external os pointing towards the posterior fornix. In nearly 20% of cases the uterus is
retroverted flexed (RVF), with the external os pointing towards the anterior fornix,
F Uterine Tenderness and Mobility: The uterus is slightly tender when squeezed between
the two hands' lt is normally mobile, but might be fixed with adhesions or pelvic masses.
D Presence of Adnexal Tenderness, Fullness, or Masses:
- The normal tubes are never palpable even in the very thin patient, while the normal
ovaries can be felt in the thin patient, in absence of pelvic tenderness.

- Presence of adnexal tenderness, fullness, or masses (cystic or solid), is always

abnormal, and should raise suspicion for presence of pelvic pathology as; plD, ectopic
pregnancy, and tubo-ovarian masses.

) Evaluation of vaginal discharge:

- The amount and character of vaginal discharge, if present, are noted on the
examining fingers while being withdrawn outside the vagina at the end of vaginal
examination.
 Gynoecologic history ond Clinicol Evoluation

D. Speculum Examinotion :
Inspection of the cervix and vaginal walls is achieved by the aid of a vaginal speculum. The one
commonly used is the self retaining Cusco's bivalve speculum, which is inserted directly without
rotation (remember that the vagina is wider from side to side than from front to back).
The cervix is inspected to detect ectopy, laceration, polyp or ulceration.

j. Opening to view cervix 2. lnside vagino 1. At the introitus

Fig L-7: Speculum exominqtion

E. Rectol Examinotion (PR)

Rectal examination is indicated in:

1-. Examination of virgins.

2. In cancer cervix; to detects extens-ion to parametrium along the uterosacral ligament.

3. In cases of prolapse: to detect presence of rectocele and exclude presence of enterocele.

4. Cases with complete perineal tears if diagnosis is not sure by inspection alone.
5. Cases with mass in Douglas pouch.
6. Cases with postmenopausal bleed-ing (piles, cancer rectum).

7. Any patient complaining of rectal symptoms.

Fig L-8: PR examination

 Gynaecology

COM MON LY USED DIAG NOSTIC I NVESTIGATIONS

IN GYNAECOLOGY
A) DTAGNOSTTC |MAG|NG PROCEDURES

1. UTTRASONOGRAPHY (US): see imaging in gynoecology

US may be performed transabdominally (TAS) or transvaginally (TVS),
either in a two
dimensional scan (2D US), or more recently in a three dimensional scan (3D
us). lt is the most
often diagnostic tool used in both obstetrics and gynaecology, with a very
high degree of
accuracy and safety.
2. CT and MRI:
Computerized axial tomography (CT) and magnetic resonance imaging (MRl)
may confirm US
findings, in addition to assessment of lymph node affection in gynecologic
malignancies. They
have generally a limited place in gynaecology compared to US.
3. HYSTEROSALPTNGOGRApHy (HSG): see imoging in gynoecology
HSG is performed via injection of a radio-opaque dye into the uterine cavity, using a special
cannuf a, to examine the uterine cavity, and to detect tubal paten cy (see also infertility).

B) DTAGNOSTTC ENDOSCOPY pRocEDURES

1. COLPOSCOPY:
Examination of the cervix and vagina via special magnifying lens instrument
allows detection of
cervical esions at the squamo-columnar junction (see premolignant lesions
f
CtN).
2. HYSTEROSCOPY:
Insertion of a special endoscope via the cervical canal, with a light source
and video camera,
allows inspection of the endometrial cavity and tubal orifices, together with performing
some
operative procedures (see endoscopy in gynoecotogy).
3. LAPAROSCOPY:
Insertion of a special endoscope through the abdominal wall, under general
anaesthesia, with a
light source and a video camera, allows visualization and inspection of
the pelvic organs,
together with performing some operative procedures (see endoscopy in gynoecotogy).

c) oFFtcE DTAGNOSTTC PROCEDURES

1. VAGINAL SWAB:
For obtaining vaginal discharge for culture and sensitivity using cotton
bud stick
2.PAP SMEAR:
For obtaining cells from the endocervix and ectocervix, using cytobrush
and wooden
spatula, stainad by papanicolau stain for early detection of premalignant
and
malignant cervical lesions.
3. OFFICE ENDOMETRIAL BIOPSY:
For obtaining cells from the endometrial lining using endometrial pipelle
instrument
for histopathological examination.
 Gynaecologic history ond Clinicol Evaluotion

EXAMTNATTON UNDER ANAESTHESIA (EUA)

When pelvic examination is difficult or impossible, examination will be made easier with
relaxed patients abdominal wall and vaginal introitus yielding better data for diagnosis.

LAPAROTOMY:
Sometimes the diagnosis is so much in doubt to the point that justifies opening the abdomen to
visualize the internal genital organs. lt is not justifiable to do this, however, unless it is

reasonably certain that some organ requires surgical attention.

c) LABORATORY TESTS

- HORMONAL ASSAYS
Y Chorionic Gonadotrophins: urinary hCG, serum B-hCG
Y Pituitory Gonodotrophins; serum FSH & LH.
Y Other Pituitory Hormones:serum PRL, TSH, GH, & ACTH
Y Ovorion Hormones: serum E2, PRG, Inhibin, AMH, &Testosterone.
Y Adrenal Hormones: DHEAS, serum Cortisol.
- TUMOUR MARKERS
> cAL25

Y CEA: Carcino Embryonic Antigen

- lJnits ol Meosurements in Hormonal Assay

Test Unit

FSH & LH mlU/ml

PRL nglml
PRG nglml
E2 pglml

T3,r4 ngldl
FT3 pglml

FT4 neldl
T nglml
 The vulva The ureter
The vagina The uterine ligoments
The uterus The cervicol ligaments
The fallopian tubes The pelvic floor muscles
The ovary The perineum

I. ANATOMY OF THE VULVA

Mons publs

Frenrrlum of clltorls glrnd orlflae

Hart s line

Vulvar yestabul€ Lablum majus

Lablum mlnue
Eanholin's gland
Vaglna
{greater vestlbuli r gtand}

Poiterlor
i Badholln's gland orlllce

Anus Hymenal rl.1g

Fig. 2-1: The vulva

female external genital structures are collectively called the vulva and consist of:

l.MonsVeneris: lsthepadoffatoverlyingthesymphysispubisandcoveredbyskin&hairs.
2. Clitoris:

- The clitoris is an erectile cavernous structure situated below the symphysis pubis. lt is
homologous to the penis in the male, and is formed of a smallglans and a body (formed of two
corpora cavernosa).

- The glans is a sensitive structure and is covered by the folds of clitoris that are the biforked
anterior end of the labia minora (prepuce above and frenulum below the glans).

3. Labia Majora:
- They are the outer two skin folds, raised by underlying fat, and passing back from the mons
veneris to the perineum. The outer skin is covered by hairs while the inner medial surface is
smooth, hairless and contains sebaceous and sweat glands.

- They are homologous to the scrotum in the male, and contain fat and Bartholin's gland.
10 Anqtomy of the Female Genitol Troct

4. Labia Minora:
- These are two thin folds of modified skin situated medial to the labia majora.

- Theyvaryinsize,arelargerinchildren,andcontainlooseconnectivetissuedevoidoffat
- The labia minora are very vascular and become turgid during coitus.

- Anteriorly: they divide into two folds (prepuce and frenulum of glans).

- posteriorly: they meet to form the fourchette that is separated from the hymen by a

depression known as the "fossa navicularis".

5. Vestibule:

- The vestibule is the area between the inner aspects of the labia minora and the fourchette.

- lt is continuous posteriorly with the vaginal opening (vaginal orifice or introitus).

- Structures that open in the vestibule: L.The urethra. 2. The vagina 3. Bartholin's glands duct.

6. The Hymen:

- The hymen is a membrane, situated about 2 cm deep to the vestibular orifice it demarcates the
external from the internal genital organs, and partially closes the vaginal orifice.

- lt is formed of connective tissue covered by stratified squamous epithelium on both sides.

- The hymen is usually torn by the first intercourse unless the opening is unusually large or the
hymen itself is elastic. Further lacerations occur on repeated intercourse.

- Remnants of the hymen in parous women are called "carunculae myrtiformis".

o Types of hymen:
- lt is usually perforated and according to the shape of its opening; it may be; crescent, annular,
fringed, cribriform, or bi-perforate'

- Rarely the hymen may be imperforate resulting in accumulation of the menstrual blood in the
vagina after puberty resulting in crypto-menorrhoea with haematocolpos (see amenorrhea)

Defloroted Bi-perforate. Cribriform lmperforate

Virgin

Fig. 2-2: Types of hymen

 Gynaecology 11

\J 7. Bartholin's Glands: (Greater Vestibular Glands):

- Bartholin's glands are bilateral compound racemes glands situated deep in the labia majora, at
v the junction of its posterior and middle thirds
\_, - They secrete mucus during sexual excitement to act as a lubricant.

v - lts duct is 2 cm long and opens between the hymen and the labium minus.
- lf the duct is obstructed it may form a vulvae swelling (Bartholin's cyst, or abscess).
v' - The gland is rarely a site for a Bartholin's gland tumour (see swellings of the vulva).

v 8. Vestibular bulbs: Oblong masses of erectile tissue that lie on each side of the vaginal introitus

v 9. The urethra and external urethral meatus:

- In the female the urethra is a tubular structure, 4 cm in length, extending from the bladder neck
\!- to the external urethral meatus that opens in the vestibule anteriorly below the clitoris.
v 10. Skene's duct:
- Two blindly ending para-urethral tubules which open in the floor of the urethra, few millimetres
from the external urethral meatus.

N.B.: The vaginal orifice is bounded anteriorly by the vestibule, inferiorly by the fourchette, and
v laterally by the labia minora and is partially closed by the hymen in virgins.

BLOOD SUPPLY AND LYMPHATIC DRAINAGE OF THE VULVA

v ArterialSupply:
v a) Internal pudendal artery: One of the two terminal branches of the anterior division of the
internal iliac artery that ends as the dorsal artery of the clitoris.
v b) Branches from the femoral artery, supply the anterior part.
v c) Superficial and deep external pudendal arteries,

v Venous Drainage:

\v - The veins draining the vulva form a venous plexus from which veins accompany their
corresponding arteries. Veins draining the clitoris join vaginal and vesical venous plexuses
\v Lymphatic Drainage of the vulva
\_ - From the skin and appendages, to the superficial inguinal lymph nodes, to the deep inguinal
and femoral lymph nodes of which the lymph node of Cloquet drains the clitoris directly.
v - From the former superficial group, lymphatic channels pass to the deep pelvic nodes including;
the external iliac, common iliac, then para-aortic lymph nodes.
\r
NERVE SUPPLY OF THE VULVA

- The vulva is supplied mainly from the pudendal nerve (S 2,3 & 4\.
\!- - Additional sensory nerves are supplied from; the llio-inguinal nerve (11), the genital branch of
genito-femoral nerve (Lt,2), and the posterior cutaneous nerve of the thigh.
v
12 Anatomy of the Femole Genitql Tract

II. ANATOMY OF THE VAGINA

The vagina is a fibro-muscular tube that extends upwards and backwards from the vulva to the
uterus forming an angle of 60ffiwith the horizontal plane. lts mucous (skin) is elevated into folds
or rugae allowing the vagina to be distended during labour.
Vaginal Length: Theanteriorwall is8-gcmandtheposteriorwall isIO-1.1.cmlong.
Vaginal fornices: The cervix projects in the upper blind end of the vagina that forms a pouch
(vaginal pouch) around the cervix and is divided into four fornices: two lateral, anterior and
posterior (deeper) fornices.
External iliac vessels

- Oblurator vessels and nerve

Cardinal ligament

Obturator inlernus m.
Levator ani

Pudenal vessels and nerves

lschioreclal tossa
Urogenilal.diaphragm (deap.
trans. pennear m. encroseol
lschiocavernosus m.
Bulbocavernosus m.

Fig 2-3: Anatomy of the vagina

ANATOMICAL RELATIONS OF THE VAGINA

o Anteriorly: trigone of the urinary bladder in the upper 1/3
and the urethra in the lower 2/3.
. Posteriorly: Peritoneum of the pouch of Douglas in the
upper 1/3, the ampulla of the rectum in the middle 1,/3, and
the perineal body in the lower 1/3.
. Laterally:
Lower end: Bulbocavernosus muscle, vestibular bulb, and
Bartholin's gland.
1 cm above orifice: urogenital diaphragm

- 2% cm above the orifice: levators ani muscle with the

Fig 2-4: Anterior snd loteral relotions
pelvic fascia above it.
of the vagina
- The lateral fornix gives attachment, to the lower part of
the cardinal ligaments.
- The ureters pass through the cardinal ligaments 1 cm lateral to the vagina.
 Gynaecology 13

VAGINAL SUPPORTS:
. Ligaments attached to the upper vagina:
- Pubocervical ligament anteriorly
- Mackenrodt's ligament laterally,
- Uterosacral ligament posteriorly.
Levators ani muscles: pubo-vaginalis part of
pubococcygeus
-Longitudinal
fold
. Triangular ligament and the perineal membrane. ,r
H-shapc
. Vaginal fascia: Connective tissue fascia that condenses
anteriorly forming the vesico-vaginal fascia and Fig 2-5: H shaped vaginol cut section
posteriorly forming the recto-vaginal fascia.

Iound --?
tordirrol

l+vrrior Anl
flut<h Dcep lrarrver*e
Ferineel tlustle

trhiopublc
Iomur
lshlotqr.emous
turle

lound
Ligol|renl

Fiq 2-6: Vaginal supports

BLOOD SUPPLY AND LYMPHATIC DRAINAGE OF THE VAGINA

l. Arterial supply:
a.The vaginal artery (from internal iliac artery) is the main blood supply to the upper vagina
b.Additional branches to the lower vagina from:

- Middle rectal artery (from internal iliac artery)

- Inferior rectalartery (from the internal pudendal artery, of the internal iliac artery)
ll. Venous drainage:
Veins form the vaginal plexus connect with the plexuses around the bladder and the rectum and
drain into the internal iliac vein by veins that accompany their corresponding arteries.
I4 Anatomy of the Female Genital Tract

lll. Lymphatic drainage of the vagina

- The upper 1/3 follows lymphatic drainage of the cervix (see later)

- The lower 1/3 drains to the inguinal lymph nodes.

- The middle 1/3 drains in both upper and lower directions. J

NERVE SUPPLY OF THE VAGINA: \-.
The pudendal nerve gives sensory fibres to the lower vagina

APPLIED ANATOMY

1. Vaginal Prolapse:

Weakness of the vaginal supports (ligaments, fascia and muscles) may lead to descent of anterior
vaginal wall (cystocele or urethrocele), descent of posterior vaginal wall (rectocele or enterocele), v
or descent of the vaginal vault after hysterectomy (vault prolapse).
2. The posterior fornix:

The posterior fornix offers a

passage to the pouch of Douglas for performing culdoscopy, 'r
culdocentesis and for drainage of a pelvic abscess.

3. The lateral fornix:

The ureters lieL-2 cm lateral to it so that it may be injured during clamping the angle of the vagina
J
in hysterectomy operation.
4. Pudendal nerve block:
Transvaginal injection of a local anaesthetic solution around the pudendal nerve as it passes around
the ischial spine gives a local anaesthesia sufficient for minor operations on the vulva and vagina, J
and has been used for low forceps operations in obstetrics.
 Gynaecology l5

III. ANATOMY OF THE UTERUS

trllopl.n tubo

mirus

Fig 2-7: Anatomy of the uterus

The adult uterus is a pear shaped hollow muscular organ measuring around 7.5 x 4.0 x 2.5 cm
in the longitudinal, transverse, and antero-posterior diameters. lt is slightly larger in the multipara
than in the nullipara. The uterus is divided into:
1. The corpus uteri:
- The corpus uteri include;the body that lies above the internal os, the cornu, which is the area
of insertion of the fallopian tubes, and the /undus which lies above the insertion of the tubes.

- Three structures are attached to the cornu; the round ligament anteriorly, the Fallopian tube
centrally, and the ovarian ligament posteriorly (collectively known as the adnexa).
2. The isthmus:

- lt is an area 4-5 mm in length that lies between the anatomical internal os above, and the
histological internal os below. lt is lined by low columnar epithelium and few glands.
- The isthmus expands during pregnancy forming the lower uterine segment (10 cm in last
trimester).
3. The cervix:

- The cervix is the elongated lower part of the uterus measuring

2.5-3.0 cm.

- lt is divided by the vaginal attachment into supravaginal portion

above, and vaginal portion (portio-vaginalis) below.
-- InLmal c
- The cervix - body ratio is 2/1, at birth, 1,/1, at puberty, and 1,/2 in
adu lts.

- The cervical canal is the cavitythat communicates above with the Fig2-8:Cervixtobodyratio
uterine cavity at the internal os and below with the vagina at the
external os.
- The external os is round in nullipara and slit shaped in multiparous.

- The cervical mucosa has two ridges (anterior and posterior) from which transverse ridges
radiate to form the arbour vitae uteri (racemose glands).
t6 Anatomy of the Female Genitql Trqct

The position and direction of the uterus

- The uterus is kept in an anteverted anteflexed position (AVF) with the external os lying at the
level of the ischial spines, by the support of the cervical ligaments, endopelvic fascia, and pelvic
floor muscles (levators ani).

- Anteversion: The angle between the axis of the cervix and that of the vagina is usually a right
angle (90 d).

- Anteflexion: The angle between the axis of the body of the uterus and that of the cervix is
usually an obtuse angle,

Anatomical relations of the body of the uterus:

- Anteriorly: The bladder and vesicouterine pouch.
- Posteriorly: The pouch of Douglas.
- Laterally: The broad ligament on each side.
N.B.: At the base of the broad ligament the uterine artery crosses above the ureter 1,/2 an inch
lateral to the internal cervical os.

Fig 2-9: Lateral relotions ofthe uterine body ond cervix

Anatomical relations of the supravaginal cervix:

o Anteriorly: the urinary bladder, and pubocervical ligament.

. Posteriorly:The pouch of Douglas, and attachments of the uterosacral ligaments.

o Laterally: the cardinal ligament, the uterine artery and the ureter.
N.B.; about 2 cm lateral to the internal os the ureter is crossed by the uterine artery, the ureter
being below the artery (like the water under the bridge).

Histology of the uterus

1. Endometrium: (mucosa)The endometrium is modified mucosa that contain glands &stroma

- Lined by simple cubical or columnar epithelium.

- lt shows cyclic changes with the menstrual cycle under the influence of ovarian hormones;
oestrogen and progesterone (see physiology of menstruation).
 Gynaecology l1

2. Myometrium (musculosa); formed of 3 layers;

- Outer longitudinal muscle layer

- Middle layer of interlacing criss-cross muscle fibres surrounding the blood vessels (its
contraction controls blood loss during menstruation and after labour)
- Inner circular muscle layer which is well developed over tubal openings and isthmus uteri.
3. The perimetrium (the peritoneal covering):

- Anteriorly: The peritoneum is firmly attached to the fundus and body till the isthmus where it
becomes loose and is reflected on the superior surface of the urinary bladder forming the
vesicouterine pouch.
- Posteriorly: The peritoneum is firmly attached to the fundus, body, cervix, and posterior vaginal
fornix then is reflected on the pelvic colon forming the Douglas pouch.
- Laterally:At the sides of the uterus, the anterior and posterior peritonealcoverings blend as the
anterior and posterior layers of the broad ligaments.
Histology of the cervix:
A) Endocervix: Lined by simple columnar epithelium with compound racemose glands or crypts
that is liable to chronic infection. lt secretes alkaline cervical mucus.
B) Muscle layer: Outer longitudinal and inner circular muscles.(2 layers only)
C) Ectocervix: Formed of stratified squamous epithelium covering the outer portion of the cervix.
The junction between squamous and columnar epithelium at the external os is either abrupt or
it may form a transitional zone 1-3 mm known as the transformation zone.

Ovadil adaly lol

Mry

Tubal b.urchs8
O€6an bEnclps

Ovary Cut d
u€|tr- perlffi

tnqim olex6 and win

Intenal ilirc
UledG artery 8rl€fy
Vagiml a.lery b6ncfi ol uterim an6
ard vgtn
VagiGl brErch ot ulstB en6r],

VagimlwsFloxG Inl€ru| engry

Postdlor Yid Vagrm - - -i-

Fig 2-10: Blood supply of the uterus

Blood Supply and lymphatic drainage

l. Arterialsupply:
The uterine arteries form the main supply of the uterus. They arise from the anterior division of
internal iliac artery and run medially towards the isthmus, in the base of the broad ligament,
crossing above the ureter 'J./2 an inch lateral to the supravaginal cervix.
At the level of the internal os each artery gives an ascending and a descending branch, with their
contralateral fellows they form the circular arteries which supply the uterus and the upper cervix.
l8 Anotomy of the Female Genital Troct

a) The ascending branches pass upwards in a tortuous manner parallel to the lateral border of the
uterus between the 2 layers of the broad ligament to end by anastomosing with branches of the
ovarian arteries near the uterine cornu.

b) The descending cervical branch supplies the lower cervix.

- The main branch, along its length, divides into anterior and posterior coronary arteries that
surround the uterus circumferentially, thus the uterus is least vascular in the midline.
- The coronary arteries give rise to the radial arteries that penetrate the myometrium to end as
the basal arteries supplying the endometrium.
N.B.; the tortuous course of the uterine artery allows for increase in the size of the uterus without
overstretch of the artery (no ischaemia).

Fig 2-11: The Uterine ortery

ll. Venous drainage:

Starts as a plexus between the 2 layers of the broad ligament (Pampiniform plexus) that
communicate with the vesical plexus and drains into the uterine and ovarian veins.
lll. Lymphatic drainage:
- Fundus: To the para-aortic lymph nodes via ovarian vessels.
- Cornu: To the superficial inguinal lymph nodes via lymphatics of the round ligament.
- Body: To the internal then external iliac lymph nodes via the uterine vessels.
- lsthmus: As that of the cervix.
- Cervix:Two groups of lymphatics:
o Primary groups: Paracervical, parametrial, obturator, internal and external iliac nodes.
. Secondary groups: Common iliac, para-aortic, and lateral sacral lymph nodes.
Nerve supply of the uterus
- The cervix and body are relatively insensitive to touch, cutting and burning.
- The cervix is sensitive to dilatation and the body is sensitive to distension.
- Parasympathetic innervations are received form 52,3, 4,
- Sympathetic innervations from T5 and T6 (motor) T10, TL1, T12, and LL (sensory). Both reach
the uterus through branches of inferior hypogastric plexus.
 Gynaecology I9

IV- ANATOMY OF THE FALLOPIAN TUBE

Intetstirlal part Istl,mus Ampulla Infirndibulun

I cm long and 2 straight
cm long, S cm long, thin 2 cm long. The
very natrow and cord-like. walled and terminal expansion,
(less than 1 mm)- 1 mm diameter. convoluted. with fimbrial
processes
which h€lp
to attract
the ovum.

Fig 2-12: The Follopiqn tube

The Fallopian tubes are two tortuous tubes that lie in the free upper part of the broad ligament.
They blend medially with the cornu of the uterus, while laterally their free outer end curves
backwards towards the ovary.
The lumen of the Fallopian tubes communicates between the uterine and the peritoneal
cavities. Each tube is about 10 cm in length and is divided into four parrs;
1.Interstitial part (1 cm): lt is the part that pierces the uterine wall. lts lumen is very narrow, and
has no peritoneal covering and no outer longitudinal muscles.
2' lsthmus (2 cm): lt is the straight, narrow, thick walled portion just lateral to the uterus.
3. Ampulla {5 cm}: lt is the widest, tortuous, and thin walled outer part.
4.Infundibulum (2 cm): lt is the trumpet shaped outer end that opens into the peritoneal cavity
by the tubal ostium. The ostium is surrounded by fimbriae, one of which is long and directed
towards the ovary (fimbria ovarica). The fimbriated end is free and turns backwards towards the
ovary.
Tubalfun$ions:
The major functions of the Fallopian tubes include ovum pick up, at the time of ovulation, by
their free fimbrial end, transport of the ovo through the tubal lumen, by their peristaltic and ciliary
movements, and production of secretions necessary for capacitation of the sperm and nutrition of
the ova during their journey, by their lining cells.
Anatomical relations:
The Fallopian tubes lie in the free upper part of the broad ligament, bounded obove by loops of
intestine, and below bythe broad ligament and its contents. Mediolty they blend with cornu of the
uterus while laterally they are bounded by the lateral pelvic wall. The ovaries lie posterior and
inferior to the Fallopian tubes at each side.
20 Anqtomy of the Femole Genitol Troct

Histology of the Fallopian tubes

a. Mucosa (endosalpnix); Arranged into 4-5 main longitudinal ridges that give rise to subsidiary
folds or plicae. lt is lined by columnar partially ciliated epithelium.
b. Muscle layer: Outer longitudinal and inner circular involuntary smooth muscles. lt is thick at the
isthmus and thin at the ampulla.
c. Serosa: The extrauterine part is covered by peritoneum in the upper margin of the broad
ligament.
Blood supply and lymphatic drainage
f. Arteriaf supply: Each Fallopian tube is supplied by branches from both the uterine ortery, and the
ovorian ortery. That is why gangrene is rare to occur in the tube unless completely twisted.
ll. Venous drainage:
Right ovarian vein drains directly into the IVC
- Left ovarian vein drains into the left renal vein.
lll. Lymphatic drainage: to the para-aortic lymph nodes directly via ovarian lymphatics.
Nerve supply of the Fallopian tubes
Sympathetic and parasympathetic fibres (Sympathetic fibres arise from T11 and T12).
Applied anatomy
Tubal oain is referred to the tubal points which lie on the lower abdominal wall L/2 an inch
above the midinguinal points.

V. ANATOMY OF THE OVARY

The ovary is an almond shaped organ lying in the fossa ovarica on the lateral pelvic wall,
measuring 3 x2x L.5 cm. lt is the only organ in the abdomen that is not covered by peritoneum. lts
surface is pearly white and corrugated by the effect of the monthly ovulatory activity that leaves
surface gyrii indentations,
lrtEttd hd
During the child bearing period its main function is olthTuh ldil|!
production of ova and sex hormones, after menopause
it atrophies and diminishes in size. The ovaries and the
Fallooian tubes are included in the term adnexa.

Ovarian attachments:
The ovary is fixed in the pelvis by three attachments:
lnfirdbdum
1. The mesovorium; A peritoneal fold that suspends
lllddd
0,rdan
the ovary to the back of the broad ligament. l!ilrab olilorsgri
dd Papohton Epoophc!n
2. The infundibulopelvic ligoment: suspends the
upper pole of the ovary to the lateral pelvic wall Fig 2-1j: Attachments of the ovory
and carries the ovarian vessels, nerves and
lymphatics.
3. The ovarian ligament:attaches the lower pole to the cornu of the uterus.

Anatomical relations:
The ovary is bounded mediolly by the Fallopian tube, loterol/y by the lateral pelvic wall. Superiorly
ond anteriorly itis surrounded by the small intestine, and inferiorly by the ovarian fossa where the
ureter and the internal iliac vessels pass.
 Gynaecology 21

Histology of the ovary pnma/y ovw g

/\
btood | \
The ovary is subdivided into; Cortex, wb pfimqrdtrl

medulla, and hilum. \

fol'icle

1. The medulla: The central core of the

ovary surrounded by the cortex and
continuous with the hilum. lt is formed of
connective tissue.
2. The cortex: The outer active part of the
ovary that produces hormones and
oocytes. lt is formed of:

- The surfoce epithelium: A single layer €dy Bpus

of cuboidal cells, called the germinal --

lutem
-

Fig 2-14: Histology of the ovary

epithelium, covering the free surface
of the ovary (NB: no peritoneal covering).

- Connective tissue stroma: Composed of dense connective tissue containing the oocytes.
lt is
condensed on the surface to form the tunica albuginea.
3' The hilum: ls the site of attachment of the mesovarium that
carries blood vessels, nerves and lymphatics entering and
leaving the ovary.

Blood supply and lymphatic drainage

l. Arterial supply:
a. Ovorian qrtery: Arises from the dorta at the level of L2
and passes through the infundibulopelvic ligament.
b. Ovarian bronch from the uterine ortery; which
anastomose with the ovarian vessels at the broad
ligament.
ll. Venous drainage: l
The ovarian veins accompany the arterial supply, and join
.," rrrrirZ ri"ini." '-"' Ei
Fig2-t5: Blood supply of the ovary
lll. Lymphatic drainage:
Lymphatic drainage of the ovaries is directly to the para-aortic lymph nodes via the ovarian
vessets.
Nerve supply of the ovary
The ovary is insensitive except to squeezing on P,V examination. lt is supplied
by sympathetic
and parasympathetic nerves (T1o and T11) that accompany the ovarian vessel.

Applied anatomy
Removal of the ovary (ovariotomy or ovariectomy) needs the application of 6
ciamps, two on
each pedicle (mesovarium, infundibulopelvic, and ovarian ligaments) and cutting in
between to free
the ovary completely and remove it.
22 Anqtomy of the Femole Genitol Tract

VI. ANATOMY OF THE PELVIC PART OF THE URETER

The ureter is a narrow muscular tube, abqut 25 cm in length. lt runs retroperitoneal from the
kidney to the urinary bladder. lts wall undergoes peristaltic movement to propel urine downwards.

Fallop an
tube

Uterus t
Round
- ligament

Uterine
artery

- Ut€rine
vetn

Fig 2-1.6: Blood suPPlY of the ovorY

. At the pelvic inlet: The ureter enters the pelvis above the bifurcation of the common iliac artery
anterior to the sacroiliac joint.
. In the pelvis: lt runs downwards lying in front of the internal iliac artery.
- At the base of the broad ligament it runs medially and forwards through the parametrium
till it reaches about 1 cm lateral to the supravaginal cervix where it passes below and at right
angle to the uterine artery (i.e. the artery crosses over the ureter)'
- The ureter then passes forwards through the ureteric canal in the upper part of the cardinal
ligament, closely related to the lateral vaginal fornix, to enter the trigone of urinary bladder.
Blood supply of the ureter
The ureter is supplied throughout its course by branches from the internal iliac artery, the
uterine artery, the inferior vesical artery, and the vaginal artery.
Applied anatomy - Sites of ureteric injuries during hysterectomy:
On clamping the infundibulopelvic ligament where the ureter passes below ovarian vessels.
- On clamping the uterine arteries as it passes below the uterine artery 1 cm lateral to cervix.

- During clamping the vaginal angles and the parametrium 1.0 cm lateral to vaginal vault.
N.B.: Avascular necrosis of its wall may occur due to cutting of its blood supply during dissection of
the parametrium in Wertheim's operation.
N.B.: lschaemic necrosis of the ureter may occur due to exposure of the ureter to overdose of
irradiation in treatment of cancer cervix.
 Gynaecology ZJ

VII. THE UTERINE AND CERVICAL LIGAMENTS

Ligaments attached to the uterine fundus and body on each side include; the broad ligament,
the round ligament, and the ovarian ligament. These ligaments being soft, lax, and easily
stretchable, play a very limited or almost no role in the pelvic support of the uterus in contrast to
the strong, tough cervical ligaments.
Round
Frllop dn
A)THE BROAD UGAMENT: Epoopnolon lagament
trrbe

The broad ligament is a double Ovsrisn

lig0nent
sheet of peritoneum that extends Utg.ine
from the lateral wall of the uterus to ansry

8road,
the lateral pelvic wall. lts outer upper ligamont
part forms the infundibulopelvic
ligament in which the ovarian vessels
traverse there way to the ovary. Fig 2-L7: The broad ligament

Contents of the broad ligament:

- The round ligament, the ovorian vessels, the uterine vessels, the ureter, pqrdmetriql tymphatics
and lymph nodes, sympathetic ond parasympothetic nerves, porometrial pelvic cellular tissue
and foscia.

- Embryological remnants of the Wolffian ducts

- Hydatid cyst of Morgogni: A pea sized thin wotted cyst attoched to the
fimbrial end of the tube.
- Koblet's tubules: Blind tubules lying on the outer qspect of the ligament
- Epoophoron: Tubules lying between the ovory ond the tube.
- Poroophoron: Tubules lying between the ovary and the uterus.
- Gortner's duct: Runs in the broad ligoment porallet to the tube then downwards lateral to the
uterus then anterolateral to the vagino.

Applied anatomy; Remnants of Wolffian duct may undergo cystic dilatation giving rise to:
. A paroovarian cyst that lies in between leafs of the broad ligament.
o Gortner's duct cyst in the anterolateral wall of the vagina.
B} THE ROUND LIGAMENT:

This is a fibromuscular ligament attached to the uterine cornu. lt FslloDian tubo

runs downwards and forwards in between the two leafs of the broad
ligament to enter the inguinal canal via the internal inguinal ring and
comes out of it at the external inguinal ring to be inserted in the upper
part of the labium majus. lt pulls the uterus forwards and help keeping it Round
lig6m€nt
in an anteverted position.
. Applied anatomy; Lymphatics accompanying the round ligament li{*ff'
drain the cornu of the uterus to the superficial inguinal lymph
Fig 2-18: Attachment of
nodes.
the round ligament
c) THE OVARTAN LTGAMENT:
It is a fibromuscular ligament that attaches the inner lower pole of the ovary to the cornu of the
uterus. lt plays no role in pelvic support of tne uterus.
.,4
Anotomy of the Female Genital Troct

THE CERVICAL LIGAMENTS

The cervical ligaments are condensed thickening of the pelvic cellular tissue, that lies between
the pelvic peri-toneum above and the levators ani below and radiates outwards from the cervix to
reach the pelvic walls. These strong ligaments, that contain few smooth muscle fibres, act as the
chief support of the uterus and pelvic structures

Pubis Symphysis pubis

Obturator mcmbrane
Obturator intcmus rhuscle
ani muscle
Panrcical spacr-

Vesicovaginal spacr ligament

Advcntitia of ngina parictal pelvic
fascia (infraanal)
Fomix
-Cadiml ligament
(tranlrrsr ccrvical.
Mac*enrodt s)
Retrdraginal spacc Obturator fascia
Utcrosacral parietal pelvic
fascia (supraanal)
Cocqqeus mttsc,lc-
Presacral spac!

Sacnrm

Fig 2-19: The cervical ligaments

Three pairs of ligaments can be distinguished, which extend from the suprdvoginol port of the
cervix ond upper part of the vqgind to the pelvic walls:
A. Mackenrodt's ligaments (The cardinal ligaments of the cervix): spread out on either side from
the lateral surface of the cervix and vagina, in a fan-shaped manner, and are inserted in the
lateral pelvic wall.
B. Utero-sacral ligaments: From the posterior aspect of the cervix and vagina, backwards
surrounding the rectum, below the utero-sacral folds of peritoneum, to become inserted in the
third piece of the sacrum.
C. Pubo-cervical ligaments: extend from the anterior surface of the cervix and vagina, forwards
beneath the bladder and surrounding the urethra, to the posterior surface of the pubis.

Round

=-Transvers
ceruiel
ligament

Fig 2-20: Attqchments of the cervicol ligoments

 Gynaecology 25

VIII. THE PELVIC FLOOR

The pelvic floor consists of all tissues lying between the pelvic cavity and, the surface of the
vulva and perineum. lt includes the pelvic peritoneum, extraperitoneal fat and cellular tissue, the
levators ani and their fascial coats, the triangular ligament (urogenital diaphragm), the perineal
muscles and their aponeuroses, subcutaneous fascia and fat, and finally skin.
The levators ani muscles together with the fascia which covers their upper and lower surfaces are
collectively called the pelvic diaphragm. In the midline, the pelvic floor is pierced by the urethra, the
vagina and the rectum.

Fig 2-21: Levqtors oni muscles

THE LEVATORS ANI MUSCLE:

A. The ischiococcygeus par! arises from the spine of the
ischium and spreads out in a fan-shaped manner
backwards and upwards to be inserted into the front
ofthe coccyx.
B. The iliococcygeus arises from the "white line" on the
lateral Wall of the pelvis, directly from the pelvic
fascia, and passes backwards and inwards, to be thpfFt
inserted partly into the tip of the coccyx and also into
the raphe, which passes from the rectum to the tip of
coccyx.
PuhWfd
C. The pubococcygeus muscle is the most important of
the three muscles: Fig 2-22:

- lt arises from the back of the pubic ramus and passes backwards to be inserted, partly into
the tip of the coccyx and into the raphe which passes between the rectum and the coccyx.
- The pubococcygeus sends fibres to the urethra (pubourethralis), to the vagina (pubo-
vaginolis), and rectum (puborectalrsl to blend with their intrinsic muscles, giving them
muscular support.
- The innermost fibres of the pubococcygeus muscle decussate in between the vagina and the
rectum. The decussating fibres divide the opening in the pelvic floor into urogenital hiatus
and rectal hiatus. During perineorrhaphy suturing these fibres together is vital to reduce the
dimension of the urogenital hiatus
26 Anatomy of the Femole Genitql Trqct

Applied anatomy
- The uterus is kept in its normal anatomic position (anteverted anteflexed with the external
cervical os at the level of the ischial spines) by the traction of the cervical ligaments, the round
ligament, and the support of the pelvic floor muscles and fascia.
Loss of the anteverted position will bring the uterus in the axis of the vagina facilitating its
prolapse through the vagina with chronic increase in intra-abdominal pressure.
- Weakness of cervical ligaments is the major predisposing factor for pelvic organ prolapse,
whether being due to congenital weakness, repeated child birth trauma, or menopausal
atrophy.
- Loss of the pelvic floor muscle and fascial support mostly occurs due to repeated child birth
trauma and inadequate repair of the pubococcygeus part of the levators ani during childbirth.
- Success of surgical techniques in treatment of genital prolapse depends in its major part on the
proper repair of the cervical ligaments, fascial defects and the pubococcygeus muscle.

IX. THE PERINEUM

The perineum is the area between the vaginal orifice and the anus. lt covers the perineal body
and is characterized by a less hairy skin with less subcutaneous tissue.

{:r*ffB t*.i att'

tffiffir
Frr&'flor"t*r
tthfi#
svr#r#l
rfl'|ffi
hrfrirlF',6l|
GmrflFcl
&sdy
(,;lfirr'hp

fikfr+atfl n3fiftF
A*xra

Fig 2-23: The Perineol Body

THE PERINEAL BODY

The perineal body is the wedge of tissue that lies between
the posterior vaginal wall in its lower third, and the anterior wall
of the anal canal. lts apex is at the lower end of the recto-vaginal
septum at the point where the rectum and posterior vaginal wall
come in contact. lts base is covered by perineal skin between
vaginal orifice and the anus. lt is the point of insertion of the
superficial perineal muscles, bounded above by decussating fibres
of the levator ani muscles where they meet together between
posterior vaginal wall and the rectum.
 5e x u o I d iffe re nti a ti o n

Deve I op m e nt of th e gen ita lo rgo n s :

Ovo ri e s-F a I I o pio ntu be s- lJte ru s-Va g i no

SEXUAL DI FFERENTIATION
Genetic sex is determined at the moment of conception by the presence or absence of a y chro-
mosome. Until week 6 development it is the same in all fetuses, after week 6 it will guide subse-
quent fetal development into either male or female.

Mesonephric
duct

\
Mesonephric
/ swelling
Primitive gonads

- Coelomic epithelium

- -- Gr,

Fig 3-1: Migration of primitive germ cells

GONADAT DIFFERENTIATION

o At the sixth week of fetal life, gonads are capable of differentiating into either testis or ovary.
- The indifferent gonad is formed of a cortex and medulla of mesenchymal tissue with some
primitive cells called the sex cord cells.
- Primitive germ cells (primordial cells) migrate from the wall of the yolk sac towards the de-
veloping gonads. Subsequent differentiation depends on the presence or absence of a y
chromosome.

1. TESTICULAR DIFFERENTIATION :

In males (XY), a gene present on the Y chromosome known as testicular differentiation factor (TDF)
produces a protein called H-Y antigen which is the signal for testicular differentiation.

27
8 DevenWnent af Fennale Genitol Orgons

Afitlheserenhrrcck:
- Teslitrk trffiirn omrrs wllpre sex cord cells migrate taking with it many germ cells
to tlhe gomndall medulllla whift erqpamds on expense of the cortex-
- lllhre gE m clb willllfomnn ttre spernmatogonia while the sex cord cells will form the Sertoli
@lllls, hodhr of tlhenn wiillllfornm tlhe senfdfielous tubules.

Afrdh'ee*fihuoek
- Lctrft d fonnnratiiorrn omruns ftorm local mesodermal differentiatio n.

2. OVARIAN DIFFERENTIATION:
llm fefinalles (XX)), albsemre of tlhe Y chnonrosome with subsequent absence of the TDF and H-Y anti-
for ovrarriiarn diiffenenntiation of the gonads.
germ wiillll alllb'rru

- qg d@miimates wltniile the medulla shrinks.

llllne

- Ser od ds sunnournd ffie arriving dividing germ cells (primary oocytes) to form the pri-
Irmordihll folllliidles. Oocytes not surrounded by these sex cord cells will die (what occur in
1l-turrner qpndronne)-

- Tlh€ rrcfiila mow rqress into a small area containing Leydig cell like cells called hilar cells
arnd tllrc rnulhrolb nrnedrullla is now called the hilum.

DIFFERENTIATION OF INTERNAL GENITALIA

Alnnf;tAlE
- secrete Miillerian duct inhib-
I-estifrqurllan Sertollii celllb
iironyfador (mD|Fl tlhat inhibits Miillerian develop-
-- Para-
rmsrnt (start at 61- days and completed at 80 days meBonephiic
9roove
fuu6)" I
I

- ttljnnden tltle effiect of testicular testosterone, the I

I
becomes
Wolffialr drurct develops to form the vas deferens I
I
anrd tJlrc serniinal vesicles, while Mullerian (para I
*
nnesonrreplhnric) ducts atrophy. - P!r!-
mo90nophric

- Tlne effieat of MDIF and testosterone is local duct

/ Masonephric
affiectiirngtlhe side of the secreting gonad only. duct

\ Megoneohtos
q ilTHE FEMALE:
- Ahsene of MDIF, due to absence of Sertoli cells,
wlllll alllow the Mfllerian duct to develop forming
tlhe Fallopian tubes, uterus, cervix and the upper
4l5atrthevagina.
- lln ahsence of testosterone, the Wolffian duct will Fig 3-2: Development of the Mullerian
regress and is represented in the female adult by (pora mesonephric) duct in the female
the Gartner's duct.
 Gynaecology 29

DIFFERENTIATION OF THE EXTERNAL GENITALIA

External genitalia start to develop from the urogenitatsinus (part of the primitive
cloaca) about the
LO'h week of gestation. The basic parts of the primitive (undifferentiated) externalgenitalia are:
1. A medial pair of swellings called genital folds.
2. A lateral pair of swellings called genital swellings.
3. A central swelling called genital tubercle.
In the male: (in presence of androgens)

- The genital tubercle enlarges markedly forming the penis

- The gen-ital folds fuse to become the penile part of the male urethra.
- The genital swellings enlarge, fuse and form the scrotum.
In the female (in absence of androgens);

- The genital tubercle enlarges slightly and becomes the clitoris.

- The genital folds become the labia minora.
- The genital swellings enlarge to form the labia majora.
Factors needed for normal sexual differentiation:
L. Normal sex chromosomal pattern (XX in the female and Xy in the male).
2. Normal testicular functioning (producing androgens) is needed for male development.
3. In the female ovarian function is not needed for sexual differentiation.
4. Responsive male end organs for testicular testosterone.
tdQF"r*St|{r
iiti$ fi#laa hAird.
il tleOae* gOr
il Lrbsddtr|trgr

On'frtsglFr
.H

Efrri t|aia {ricr

ttfia laat-
Htdtft
hi
tllrb n|D
Llr|ll !*r
&rnA
riFlae.{n
!6tr6 ,{F
'l
*ryt E
ffi
30 Development of Female Genitol Orgons

DEVELOPMENT OF THE FEMALE GENITAL ORGANS

Development of the female genital organs begins at the fifth week of intrauterine life. Two
structures participate in the developmenU
THE UROGENITAT RIDGE (UGR): situated in the middle line of the posterior abdominal wall of the
embryo, and includes three important structures;
1. The genital ridges; medially that give rise to the ovaries.
2. The Wolffian ducts; situated lateral to the genital ridges. They undergo atrophy in females.
3. The Mullerian ducts; situated lateral to the Wolffian ducts. They give rise to the Fallopian
tubes, uterus, and the upper 3f4'n'of the vagrna.
THE UROGENITAT SINUS (UGS): caudally, gives rise to lower L/4'n of the vagina and the vulva.

A) DEVELOPMENT OF THE OVARTES

The ovaries develop from the genital ridges at the level of the 10th - 11th dorsal (thoracic) verte-
brae and descend later on to the pelvis.
The germ cells, that give rise to the ova, develop in the yolk sac then migrate to the genital
ridge. Failure of its migration gives rise to streak gonads.
- The genital ridge is attached to the inguinal region by a fibro-muscular band called the guber-
naculum that runs in the inguinal canal. The gubernaculums becomes shorter pulling the ovary
down to the pelvis and attaches to the uterus posteriorly forming the ovarian ligament and
anteriorly forming the round ligament

Developmental anomalies of the ovary:

- Aplasia: complete absence is extremely rare and leads to primary amenorrhoea.
Hypoplasia: underdevelopment may lead to amenorrhoea, oligomenorrhoea or hypomenor-
rhoea due to ooor secretion of ovarian hormones.
- Streaks gonads (ovarian dysgenesis): the ovaries are represented by con-nective tissue bands
leading to primary amenorrhoea (see amenorrhoea -Turner's syndrome).
- Accessory ovary: has no harmful effect.

B} DEVELOPMENT OF THE FALLOPIAN TUBES

The fallopian tubes develop from the upper parts of the Mullerian ducts after their canalisation.

o Developmental anomalies of the Fallopian tubes Gubsrnaculum

of ovary
(ovarlan llgamcntl
1. Aplasia: complete absence of the tubes. This will be
associated with absence of the uterus and upper
3f 4th' of the vagina.
Falloplan or
2. Hypoplasia: the tube is thin, and tortuous. lt may utoflno tube
lead to infertility or ectopic pregnancy. a
Degcneratlng ,z/
*!-l----
mcconcohrlc Milllerian
3. Accessory ostium: may lead to ectopic pregnancy. duct lbccomr3 tub.rclc
4. Tubal diverticulum: may lead to ectopic pregnancy. Gartn€r's ductl - \\
Urogenital
rlnuB

Fig 3-4:
 Gynaecology a1
JI

c) DEVELOPMENT OF THE UTERUS

The uterus develops from the middle part of the Mullerian ducts after their fusion and canali-
sation. Uterine anomalies may be due to failure of Mullerian duct development, failure of fusion of
both Mullerian ducts, or failure of their canalization.

t) tMpRopER MULtER|AN DUCT DEVETOPMENT

1. Uterine aplasia: complete absence of the uterus (rare anomaly). Cases will present after puberty
with primary amenorrhoea and well developed secondary sexual characters.
2. Uterine hypoplasia: small solid uterus with no cavity, or small infantile uterus with a body to cer-
vix ratio of I: 2. Cases will present after puberty with primary amenorrhoea, oligomenorrnoea,
infertility, or rarely recurrent pregnancy loss (RpL)

il) tMpRopER MULtERIAN DUCT FUSTON AND CANAUZATTON

L' Arcuate uterus: broad fundus with a depression from outside. lt is of no clinical significance
2' Subseptate uterus: the uterine cavity is divided by a longitudinal incomplete median septum
starting at the fundus downwards not reaching the isthmus.
3. Septate uterus: the uterine cavity is divided by a longitudinal complete median septum extend-
ing from the fundus to the isthmus, not reaching the cervix.
4. Bicornuate uterus: the uterine body is divided into two horns, both attached to one cervix, join-
ing one vagina.

l,ormal ulefus Subs€gtete uterus Arcuate ul€rus

Bicolnuale uterus Bicornuate uterus Unicornuate ulerus

Oouble cervix

Bico.nuale uterus Ul€rus didelphys Cervical atresia

Budincntary horn S€ptate vagina

Fig 3-5: Anomalies of the uterus

)z Development of Femole Genitol Orgons

5. Bicornuate uterus with double cervix (pseudo-didelphys); two uterine bodies (2 horns) each
attached to a cervix (2 cervices) attached to each other and both open together in one vagi-
na.
6. Uterus didelphys: there are two separate uteri (two bodies & two cervices) with two vaginae
(separated by a longitudinal septum). -
7. Rudimentary horn: one horn of the uterus is well developed, but the other is rudimentary.
8. Unicornuate uterus: One Mullerian duct is well developed forming a well canalized Fallopian
tube connected to one horn of the uterus opening into the cervix and vagina. The other Mulleri-
an ducts failed to develop with absent other tube, and second uterine horn.
9. Cervical atresia; lmproper canalization of the cervical canal may lead to cervical atresia with en-
trapment of menstrual blood after puberty leading to haematometra and haematosalpinx (false
amenorrhoea or Cryptomenorrhoea).

COMMON CLINICAL PRESENTATIONS OF UTERINE ANOMALIES:

a. Primary amenorrhoea: in cases with uterine aplasia, hypoplasia, and cervical atresia.
b. Severe dysmenorrhoea: in cervical atresia, and non communicating rudimentary horn
c. Primary infertility: in cases with uterine aplasia, hypoplasia, cervical atresia, and less commonly
with septate and bicornuate uterus.
d. Recurrent pregnancy loss (RPL) in first trimester; may be associated with infantile uterus, sep-
tate uterus, and rarely bicornuate uterus
e. RPL in second trimester: due to incompetent isthmus associated with septate and less com-
monly bicornuate and unicornuate uterus
f. Preterm labour, malpresentations, and dysfunctional labour: may occur with septate and bi-
cornuate uteri.
g. Cervical atresia may present with; primary amenorrhoea, spasmodic dysmenorrhoea, haema-
tometra, haematosa lpi nx, endometriosis and infertil ity.
h. Pregnancy in a rudimentary horn is a type of ectopic pregnancy that can cause rupture uterus.

D) DEVELOPMENT OF THE VAGINA

The upper 3f 4rh'of the vagina develops from the lower parts of the Mullerian ducts after their
fusion and canalisation, while the lower 1/4'n develops from the urogenital sinus.

DEVELOPMENTAT ANOMATIES OF THE VAGINA:

1. Aplasia of the vagina:

- lt usually affects the upper 3f4'h'of the vagina while the lower l-/4th develop giving rise to a
small vaginal pouch.

- After puberty, they will present by 1ry amenorrhoea as the uterus is usually absent too. lt may
also present with dyspareunia and 1ry infertility after marnage.
Operative correction of the vagina aims at allowing sexual intercourse. Mc Indoe's operation
(creation of a new vagina) can be done using a skin graft taken from the thigh with its blood
supply and innervation, situated between the rectum posteriorly and the urethra and urinary
bladder anteriorly over a mould, thus fashioning a new vagtna.
 Gynaecollogy ti

2. Transverse vaginal septum:

- Results from improper fusion behween the urnogen'rtall sftnus arnd the Nlulllierrfran dlucts- After pu-
berty these cases will present with 1ry amenornhea, andiswere dysnrnennorrr.lhoea, whiile tlhe 2rry
sexual characters are normally developed.
- Entrapment of menstrual blood will! lead to lhaerrnatoeolipos, lhaerrmatonnretra, amd liaten lniaerna-
tosalpinx. Backflow of hlood into perritonealicavfty nxay aause pelvic emdormetrr.iosis
- Diagnosis is by history, general and F.R, exannirnation, and r^rhrasonography.
- Treatment is by surgical excision of the septunn.
3.lmperforate hymen:
- Occurs due to improper canalization of the urogenital slnus.
- After puberty, clinical presentation wiMnclude 1ry annenonrhea and sevene dysrnenonnhoea,
with nonmal 2ry sexual characters. By time haematocolpos will develiop, th,at rnay extend to
haematornetl'a, and haernatosalplnx ln rare cases.
- Diagnosis is hy hlstory, generalN and F-R. exarni,xatiotx, inspectlon of the vu,]va,and hymen.
- Treatrnent is by cruciate incision of the irnperforate fryrnen under anaesthesla

Inpufrute RstAnadrncnntnJA

Iryneu lwrwymowrlto
>lL

Afrbronvwular
ndnvnneconrcd
6,14,w0t
byqtunnus
cptlhclium
thv crl

Fig 3-5: Hoemotocolpos ond haemotometra Fig 3-7: lmperforote hymen

4. longifrtdinal vagi nal septu m:

Occurs due to improper fusion of the two Mullerian ducts.

Clinically it may lead to dyspareunia and is treated by surgical excision of the septum.
N.B.; Both transverse vaginal septum and imperforate hymen are common causes for false
amenor-
rhoea or Cryptomenorrhoea (see amenorrhoea).
o Oinical presentation vaginal anomalies:
Amenorrhea, dysmenorrheal, dyspareunia, and infertilW.2ty sexual characters are preserved.
Haematocolpos leading to a pelvlc nlass.
Rarely Urinary symptoms as retentfon of urine are associated with large haenlatocolpos.

I
34 Development of Female Genital Orgons

E) DEVELOPMENT OF THE VULVA

1. The genital tubercle forms the anterior boundary of the urogenital sinus and gives rise to the
clitoris.
2. The inner and outer genital folds lie lateral to the urogenital sinus and give rise to the labia mino-
ra and majora respectively.

NB: In males, the genital tubercle develops into the penis and the inner and outer genital folds fuse
to develop into the penile urethra and the scrotum respectively.

THE WOLFFIAN REMNANTS IN THE FEMALE

Infemales, the Wolffian ducts undergo atrophy leaving remnants that lie between the two lay-
ers of the broad ligament and in the antero-lateral wall of the vagina. These remnants are:

1. Hydatid cyst of Morgagni lateral to the tube.

2. Koblet's: tubules in the outer part of the broad ligament.

3. Epoophoron: between the ovary and the tubes.
4. Paroophoron: between the ovary and the uterus.
5. Gartner's duct: that run in the broad ligament parallel to the tubes then descends downward par-
allel to the uterus then in the antero-lateral wall of the vagina.

NB: Gartner's duct may undergo cystic dilatation in the broad ligament giving rise to parovarian cyst
or in the antero-lateral wall of the vagina giving rise to Gartner's duct cyst.

Fig 3-8: Wofffian duct remnonts in the female

 The Hypothalomus Theendometrialcycle
The Pituitory glond Dysmenorrhea
The Ovorian cycle The Premenstruo I Sy n d rome

OVERVIEW
The average menstrual cycle lasts for 3-7 days (mean 5 days), recurs every 21-35 days (mean 28
days), with an average blood loss of about 30-50 ml/cycle. The first few cycles following menarche
and those in the few years prior to menopause are usually irregular mostly due to anovulation.
Along their lifetime from puberty to menopause women will have around 4(X) menstrual cycles.
Each cycle represents a complex interaction between the hypothalamus, pituitary gland, ovaries
and the endometrium.

THE HYPOTHALAMUS
The hypothalamus is a small neural structure situated at the base of the brain above
the optic chiasma and below the third ventricle. lt is connected to the pituitary gland.

Hypothelamus

Mammillary body

Fig. 4-1: The hypotholomus and pituitary glond

Hypothalamic Releasing Hormones

Releasing hormones are small peptides characterized by having short half-lives of few minutes
due to their rapid degradation. They are released in minute quantities in a pulsatile manner, ano
reach the anterior pituitary via the hypothalamic portal circulation.

Biologically active concentrations of these factors are locally restricted to the anterior pituitary
gland with very low concentrations in peripheral circulation rendering them undetectable in serum.
Levels of their corresponding pituitary hormones are measured as markers for their presence ano
activity.

35
36 The Menstruol Cycle ond Associates Disorders

Hypothalamic releasing hormones include:

L. Gonadotrophin-releasing hormone (GnRH): lt is a decapeptide produced by the arcuate nucle-
us in the hypothalamus and is responsible for synthesis and release of pituitary gonadotropins
(FSH and LH).

2. Thyrotropin-releasing hormone (TRHI; regulates secretion of TSH

3. Corticotrophin-releasing hormone (CRH); stimulates the release of ACTH.
4. Growth hormone-releasing hormone (GHRH); stimulates the release of GH
5. Prolactin inhibiting factor (PlF or dopamine); it inhibits production of prolactin (PRL) J
THE PITUITARY GLAND
The pituitary gland lies at the base of the brain, below the hypothalamus within a bony cavity
known as the sella turcica. lt is divided into two major portions:

A. The Anterior Pituitary Gland (adenohypophysis)

It consists of an anterior lobe (pars distalis), an intermediate lobe, and pars tubalis which sur-
round the neural stalk. lt is derived from the ectoderm, and is indirectly connected to the hypothal-
amusthrough the hypophyseal-pituitary portal system which represents a major route of transport
of hypothalamic releasing factors to the anterior pituitary gland.
The anterior pituitary serves primarily in the producton of six trophic hormones produced .J
through five hormone producing celltypes:
1. FSH and LH (gonadotrophins) produced by cells known as Gonadotrophs. FSH and LH are glyco-
proteins responsible for the process of growth, maturation and rupture of Graafian follicles
(ovulation), and maintenance of corpus luteum function.

2. TSH (thyrotropin stimulating hormone) produced by cells known as thyrotrophs.

3. ACTH (ad reno-cortico-troph ic hormone) produced by Adrenocorticotrophs.

4. GH (growth hormone) produced by cells known as somatotrophs.

5. PRL produced by cells known as lactotrophs.

Pituitary hormones are all stimulated and controlled by hypothalamic releasing hormones
(GnRH, GHRH, TRH, and CRH) with the exception of PRLwhich is under chronic inhibition by prolac-
tin inhibiting factor (PlF). Consequently damage to the pituitary stalk will result in hypopituitarism
for FSH, LH, GH, ACTH, and TSH, but with an associated increase in PRLsecretion.

B. The posterior pituitary gland (neurohypophysis):

The posterior pituitary (neurohypophysis) consists of the posterior lobe (pars nervosa), and the
neural stalk (lnfundibulum). lt is derived from neural tissue and is in direct continuity with the hypo-
thalamus and CNS.
The posterior pituitary serves primarily in the transport oxytocin and vasopressin
(antidiuerteic hormone ADH) along neuronal axons from the supraoptic and paraventricular nuclei
of the hypothalamus to their release into the circulation.
I

Gynaecology JI

THE OVARIAN CYCLE

lhrov*lun and
blood wa$la

Gorminal I Verlcuhr l&erfi.'r)

/

eprlhelrurhi'.+..
Gprlhelruln I . "" folllcL
Primortlirl
lollrclo.
1 i .l _ fl__-x
\ Anfrum
Ooclna

F.llucldr
$
Thoc.
fiolllcull

Ovubr.d
oocytr

{rl r lutaum op|ng

a llrr|J|n

Fig 4-2: historogy of the ovary ot different phases of ovorion

cycre

The foetal ovary contains a maximum number of 7 million primordial follicles at mid-
gestation' The number then declines sharply reaching 1.5-2.0
million at birth, then declines grad-
ually to reach around 4oo.ooo primordial follicles at puberty. Throughout
the menstrual cycles
ovarian follicles become gradually exhausted untilthey become
depleted by the time of the men-
opause.

The ovarian cycle is divided into follicular phase, and luteal phase,
separated by ovulation.

A. FOLTICULAR PHASE:
This phase lasts from the l't day of menses till ovulation. lt is
of variable length (mean 14 days).
Graafian follicles grow and mature under the influence of follicle
stimulating horn.ron" FSH. They
produce increasing amounts of E2, which lead to proliferative
changes in the endometrial glands.
1. THE PRIMORDIAT FOLtICtE

Each primordial follicle consists of a single oocyte, arrested in

the diplotene stage of the pro-
phase of the first meiotic division, surrounded by a
single layer of flattened cells (granulosa cells)
and cells of the ovarian stroma (theca cells).

2. THE PRE-ANTRAL FOTLICLE

FSH stimulates growth of several primordial follicles, the

oocytes grow and the granulosa cells
multiply to become multilayered cuboidal shape, thus changing into preantral
a follicle.
38 The Menstruql Cycle ond Associotes Disorders

THE TWO-CELL, TWO-GONADOTROPHIN hypothesis oI oestrogen production

A) Within theca cells; LH stimulates conversion of
cholesterol to androgens, which are then trans-
ported from theca cells to granulosa cells
B) Within granulosa cells; FSH stimulates rror.ti- | \
=
zation of androgens into oestrogens by the L_f
"n-
zyme aromatase.
o Oestradiol (E2) the chief ovarian oestrogen;
- Enhances the induction of FSH receotors
on granulosa cells.
Acts synergistically with FSH to increase
LH receptors in the granulosa cells.
o Androgens produced within the theca cells;
- At low levels enhance aromatization and
hence increase oestrogen production.
- At high levels inhibit aromatization and
Fig 4-3 : Two-Cell, Two-Gonqdotrophin
produce follicular atresia.
Hypothesis
CONTROL OF STEROIDOGENESIS:
Apart from FSH, LH, oestrogen and androgens, some autocrine and paracrine mediators play an
important role in the process of folliculogenesis as:
A. Inhibin: A peptide produced by granulosa cells that attenuates FSH production and enhances
LH-induced androgen synthesis, thus the dominant follicle can continue development and
other follicles undergo atresia.
B. Activin: A peptide produced by granulosa cells PRIilORDIAL iltT Lttu&E
rNf 00c1lt
and the pituitary gland that augments FSH pro- FOLLICLE tJLOtr Cflls
40pm _-_ ", -,_ 0ls€reir LtrirAf
duction, an action almost directly opposite to
:s-*6f,riUL03l (ttl3
that of inhibin. PRIUARY
--..- . .FULLT Cnofr oocllt
FOLLTCLE
C. Growth Factors: As Insulin like growth factor lO0pm *"_.-_. __t0f,1 ptLLuetor

(lGF), fibroblast growth factor (FGF), and epi-

dermal growth factor (EGF), may all help en-
hanced resoonsiveness to FSH.
SfCOilDARY
FOLLICLE
SELECTION OF THE DOMINANT FOLLICLE rurLr Gnotl oocttt
2OOpm ,tslrpflvt Trccl
During folliculogenesis a dominant follicle is se-
lected to continue growth, maturation, and ovu- Y*CA CIIENil
-E strtir Lrllrrf
lation. Other follicles will be arrested and later 5rtr0r0 3fcF[l-
uc cfl.rl
become atretic. - lilrRur

- The selected follicle is characterized by having EARLY -

- 8L000 vf,sstL
l0ll PttLliclDr
the highest number of FSH receptors in its granu- TERTIARY fuaLl 6n0ll
FOLLICLE OCCYIE
losa cells, having the most efFicient aromatase 40Opm TUTIIPLE TAYTFi O'
activity, the highest concentration of FSH in- CflrrULo:l CtLLg

duced LH receptors, the greatest amounts of E2 rHtcr lllt*ll

and inhibin produced, and thus requiring the
least FSH and LH levels to complete maturation. Fig 4-4: development of the primordial to mo-
ture follicle
 Gynaecology 39

3. THE PREOVULATORY FOLLTCLE (MATURE GRAAFTAN FOLLtCtE)

The oocyte is pushed to one side of the follicle, secretes clear gelatinous material around itself
forming the zona pellucida. Simultaneously the theca cells become differentiated into theca interna
and theca externa around the multiple layered granulosa cells.

B. OVULATION
Late in the follicular phase, FSH results in production of increasing amounts of oestradiol (E2)
by the dominant follicle, and induces LH receptors on the granulosa cells. High E2 levels exert a
positive feedback effect on the pituitary gland, with release of LH rapidly and in increasing
amounts.

- LH induces luteinization of granulosa cell in

the dominant follicle so that progesterone (p) starts
to be produced. (P) Amplifies (E2) induced positive feed back on LH secretion leading to an LH
surge.

Ovulation occurs approximately 35 hours after the onset of the LH surge and about 12 hours
after the LH peak.

- oocyte release is facilitated by FSH, LH, and (P) induced activation of collagenase enzyme that
breaks down the follicle wall, preparing for its rupture.

Resumption of meiosis occurs during the process of ovulation, with oocytes progressing from
prophase I through metaphase ll.

Fitu itcr ry tl orrnertes

Fo_l_lic lc- rf t mu_lcrrl rrg

]lorrnorre (Fg}|l - ."'Ll-ha[ftf orrrrcr]r

Cycle Doys
Fig 4-5: Diogrom showing LH surge

C. THE LUTEAL PHASE

- The luteal phase extends from the time of ovulation till the onset of menstruation, and is fairlv
constant lasting for about 14 days.

- Corpus luteum (CL) formation: After ovulation, and under the influence of LH, the granulosa cell
of the ruptured follicle undergoes luteinization. These luteinized granulosa cells, plus the sur-
rounding theca cells, capillaries, and connective tissue, form the CL. The luteinized cells of the CL
have a vacuolated appearance associated with the accumulation of a yellow pigment (lutein)
where the name CL is derived.
40 The Menstruol Cycle ond Associates Disorders

The CL, in response to the continuous pituitary LH stimulation, will produce copious amounts of
Progesterone (P) and smaller amounts of (E2) and little inhibin leading to decreased FSH & LH
production hence the initiation of new follicular growth in the luteal phase will be inhibited.
Progesterone produced by the CL will lead to secretory changes in the endometrium, which is
necessary to prepare the endometrium for implantation of the embryo
Fate of the CL: The duration of the luteal phase is fairly constant in most women being around
14 days. The life span of the CL is around 9 days after which it undergoes luteolysis and becomes
replaced by the avascular corpus albicans.
. fn absence of pregnancy; the CL undergoes apoptosis and cease to produce (P) bV 12-Ia
days after ovulation. Gonadotrophin inhibition is released and FSH starts to rise
. In presence of pregnancy trophoblastic production of human chorionic gonadotropins
(hCG) will maintain (P) secretion from the CL until placental steroidogenesis is established
about the 8th week of gestation
As the CL dies, E2, P, and inhibin levels decline and the pituitary gland becomes released from
the negative feed back effect of these hormones. FSH levels start to rise, cohorts of follicles
which happen to be in the preantral stage are rescued from atresia, and a new ovarian and men-
strual cycle is now initiated.

Hormonal Patterns in the Menstrual Cycle

Pltu,llary tlqrrnone Cyale

Oviri€n Cycl€

$let lfor|'ron,e Cycl€

ryotCyol.
Endomslrlsl Cyclc
Fig 4.6: hormonol patterns in the Fig 4-7: H-P-O axis showing positive and negotive
menstruol cycle feedbock of hormones (P4: progesterone,
E2:oestradiol)
 Gynaecology 4l

Levels of feed-back to the hypothalamus

a. The long feedbock loop, from ovarian hormones (oestrogens and androgens).
b. The short feedbock loop, from the pituitary hormones (FSH & LH).
c. The ultro-short feedbock loop,from the hypothalamic releasing factors.

Positive and Negative feed back loops

o Low levels of E2 have an inhibiting effect on LH (negative feedback), whereas high E2 levels
stimulate LH production (positive feedback).
o Low levels of P have a positive feedback effect on FSH & LH and share in the production of an
LH surge prior to ovulation. High P levels present in the mid-luteal phase inhibit LH & FSH
con-
sequently inhibiting growth of primordial follicles in the luteal phase thus producing a nega-
tive feedback effect.

THE ENDOMETRIAL CYCLE

Changes in the endometrium in response to ovarian hormones throughout the menstrual cycle
are divided into three phases; proliferative phase, secretory phase, and menstruation.

1. THE PROLIFERATIVE PHASE

- The proliferative phase of the endometrium coincides with the follicular phase of the ovarian
cycle, and is characterized by both glandular and stromal growth.

- lt starts with shedding of the endometrium at menstruation, and continues under the effect of
ovarian oestrogen produced by the maturing follicles till ovulation occurs.

- The epithelium lining the endometrial glands changes from a single layer of low columnar cells
to pseudo-stratified epithelium with frequent mitoses, and the stromal component of the en-
dometrium also expands rapidly.
- The endometrial thickness grows from 0.5 mm at the end of menstruation to about 5-g mm at
the end of the proliferative phase.
Time ol ovulatron
PitUrl.ry
hffmoaros
(hypoPhlrsisl

Ovadan holmoocs
.twifiO the c]El6

Cyctical oycnls
in ths wafy
O
Unrip6 Rsg.Esion ot
tolticla co{pG luleum

Rlsc In leml'G6tur€
ChanOG ln body
tcmpeEluro dwing
th€ ct|ct€
(.to m6t toveta)

lrlerlnc mucoca

Fig 4-8: the endometrial cycle

42 The Menstrual Cycle ond Associates Disorders

2. THE SECRETORY PHASE

The secretory phase of the endometrium coincides with the luteal phase of ovarian cycle, and is
characterized by endometrial glandular secretory activity. lt starts shortly after ovulation and con-
tinues, under the effect of P and E2 produced by the CL, till menstruation starts.

- Progesterone inhibits oestrogen induced cellular proliferation restricting the depth of endo-
metrial thickness, while endometrial glands continue to grow leading to increased tortuosity of
both glands and spiral arteries in order to fit in the endometrial layer.

- In the early secretory phase; shortly after ovulation, vacuoles containing subnuclear intracyto-
plasmic granules appear in glandular cells. These vacuoles progress to the apex of the glandu-
lar cells and their contents are released into the endometrial cavity.

- In the mid-secretory phase; peak secretory activity occurs at the time of implantation, seven
days after the LH surge (mid luteal phase), with associated stromal oedema. Within the endo-
metrium large granulated lymphocytes predominate, which may play a role in regulating
trophoblastic invasion during implantation if pregnancy occurs.

- In the late secretory phase; progesterone induces irreversible decidualization of the stroma. The
surrounding stroma cells display increased mitotic activity and nuclear enlargement. Three dis-
tinct zones of the endometrium can be seen:
a. The basdl portion (bosolis): represents thb basal 25% of the endometrium, which is retained
during menstruation and shows few changes during the menstrual cycle.
b.The mid-portion (spongiosum): composed of oedematous stroma, glandular tortuosity and
secretions.

c. The superficiol portion (compactum): composed of decidualized stromal cells.

Co$-d
greadr

t*G|..stad
g|lq€r

6-3-ffir
Fig 4-9: the endometrium a) postmenstruol b) proliferative c) secretory
 Gynaecology 43

3. MENSTRUATION
Menstruation is the cyclic shedding of the superficial and intermediate layers of the endometrium
in response to progesterone withdrawal after CL demise.

A) Endometrial shedding:
- Premenstrual sharp and rapid decline in P & E2 levels result in coiling and vasoconstriction of
the endometrial spiral arteries, with ischaemia to the functional portion of the endometrium
(superficial and intermediate layers)

- Vasoconstriction is initiated and controlled through the action of prostaglandin F2 alpha

(PGF2-a), endothelin-1 (ET-l) a nd platelet-activati ng factor (pAF).

Haemostasis:

- Achieved by vasoconstriction of spiral arteries, and increased platelet aggregation,

Enhanced fibrinolysis with breakdown of blood clots minimizes endometrial scarring and
clot formation.

Regeneration and Repair:

- Within 2 days from the onset of menstruation the surface epithelium begins to regenerate
under the influence of follicular phase oestrogen.

- Angiogenesis (new blood vessel formation) and endometrial regeneration lead to complete
cessation of bleeding within 5-7 days from the start of menstruation

CERVICAL MUCUS CHANGES DURING THE MENSTRUAL CYCLE

The physical and chemical properties of the cervical mucus vary in relation to the changing
oestrogen and progesterone levels in the follicular and luteal phases of the menstrual cycle.
In the follicular phase, cervical mucus becomes more profuse, watery, and less cellular, to al-
!- low for easier sperm penetration at the time of ovulation (peak oestrogen effect).

v After ovulation and throughout the luteal phase, cervical mucus becomes scanty, viscid, and
more cellular, and less ready for sperm penetration (peak progesterone effect)

Cervical mucus changes in the menstrual cycle

Follicular phase (oestrogen effect) Luteal phase (progesterone effect)

r Profuse r Scanty

r Decreased viscosity (thin-watery) o Increased viscosity (thick-viscid)

o Decreased leucocvtes o Increased leucocvtes

o Positive Ferning test . Negative Ferning test

o Positive Spinbarkeit test (threads 7-10 cm) . Negative Spinbarkeit test (threads 3-4 cm)
44 The Menstruql Cycle and Associqtes Disorders

o Ferning test: Microscopic examination of a drop of cervical mucus left to dry for 10 minutes
on a glass slide in the follicular phase will reveal an arborizing palm leaf pattern, due to its
high sodium chloride and potassium content in response to a high oestrogenic levels (+ve
test). In the luteal phase the arborizing pattern is lost giving a negative test.
. Spinbarkeit test is positive when the cervical mucus can be drawn between two slides into
threads stretching up to 10 cm due to high mucus content in response to high oestrogen lev-
els

Vaginal Epithelial Cellular changes during the menstrual cycle

The vaginal epithelium is composed of basal, intermediate, and superficial (mature) cells.

. In the follicular phase under oestrogenic effect superficial cells predominate

. In the luteal phase progesterone causes shedding of more intermediate cells

N.B.; Maturation index calculates the ratio of basal, intermediate, to superficial cells on vaginal
cytology

Cytology of the vaginal epithelium in different phases of the menstrual cycle

Follicular phase vaginal cytology Luteal phase vaginal cytology

. Superficial cells with non rolled edges . Intermediate cells with rolled edges
o Eosinophilic cytoplasm . Basophilic cytoplasm
. Pyknotic nucleus . Vesicular nucleus

o Few lymphocytes . Many lymphocytes

o Maturation index 0-30-70 r Maturation index 0-70-30

DYSMENORRHOEA
DEFINITION
Dysmenorrhoea is defined as pain and cramping during menstruation that interferes with
normal activities, and requires the use of medications to control the symptoms. Pain may
range from mild discomfort, to severe pain that causes some patients to be bedridden for 1-3
days each month.
INCIDENCE
Dysmenorrhoea affects 45-9O% of women in their reproductive age with variable degrees
of severity. Almost 5O% of women will suffer significant pain, with LO% of these become inca-
pacitated during the first few days of the cycle.
CLASSIFICATION

(endometriosis, fibroids, adenomyosis, PlD, cervical stenosis).

 Gynaecology 4)

PRIMARY DYSMENORRHOEA
Primary Dysmenorrhoea is almost always associated with ovulatory cycles, with no obvi-
ous orgontc couse.
Aetiology
v
-Mostly results from increased levels of endometrial prostaglandins (pGLs)
-Additional psychologicalcomponent may be involved in some patients
-The condition usually spontaneously improves after term pregnancies and deliveries
Diagnosis
- Age; usually occurs in younger women <20 years of age
Pain; occurs on the 1't or 2nd days of ovulatory cycle
- Associoted symptoms; nausea, vomiting, and headaches
- Physical examinotion; reveals no obvious abnormalities or pelvic pathology
- Pelvic US; reveals normal uterus, ovaries, and adnexa.
Treatment
!- 1'. Non steroidal anti-inflommatory drugs (NSAlDs): this is the first and most important
line of treatment (aspirin, lbuprofen, ketoprofen, and naproxen). They are taken
at on-
set of menses, continued for 1-3 days then taken as needed.
2. Combined oralcontroceptive pills (CoCs): oCPs are the second line of treatment
in cases
which do not get adequate pain relief with the use of NSAIDs alone, or cannot tolerate
their side effects.
SECON DARY DYSM ENORRHOEA

Secondary dysmenorrhoea may occur in both ovulatory and anovulatory cycles.

Aetiology
Symptoms are 2ry to an identifiable cause, such as endometriosis, uterine leiomyomas,
cervical stenosis, pelvic adhesions, and plD.
Diagnosis
- Age; women are commonly middle aged (30-35 years)
- Pority; it occurs in both parous and nulliparous women
- Poin; starts few days before menses and gradually decreases by onset of menses.
lt is
dull aching or colicky suprapubic pain commonty associated with low back ache that
v usually occurs after severalyears of relatively painless menstruation.

v - Physicol exomination; may detect sizable uterine or adnexal masses

- Pelvic US; may diagnose smaller utenne myomas, ovarian endoemtriomas, and tubo-
ovanan masses
- Laparoscopy; for diagnosis of endometriosis, pelvic adhesions, and plD.
Treatment
- Medicattreotment: to control pain via NSAIDs

- Hormonal treatment.'OCP, Gestagens, and GnRH agonists (see endometriosis)

Surgicol treotment: for larger myomas, endoemtriomas, and tubo-ovarian mass
46 The Menstrusl Cycle and Associates Disorders

THE PREMENSTRUAL SYNDROME

The premenstrual syndrome (PMS) describes a group of physical and/or emotional

changes that constantly occur and recur in the luteal phase of successive cycles, severe
enough to interfere with the patient's regular life style.
Symptoms and changes include; headache, weight gain, bloating, breast tenderness,
mood fluctuation, restlessness, irritability, anxiety, depression, and fatigue.
Symptoms should occur in the 2 weeks prior to menstruation (luteal phase), with at least
a 7 day symptom free interval in the first half of the menstrual cycle.
The highest incidence of PMS occurs in women in their late 2O's to early 30's.
Up to 8O% of women will report uncomfortable symptoms in the premenstrual period.
However in only s-LO% symptoms will be severe enough to interfere with daily activities. In
almost 50% of severe PMS cases an underlying psychiatric disorder can be elicited.
Aetiology
The causes of PMS are not completely understood.
- PMS may be due to the interaction between the neurotransmitter serotonin and cyclic
changes in ovarian steroids.
- PMS is more pronounced in genetically and psychologically susceptible women.
- Although women with PMS have normal levels of E2 & PRG, they may have an abnormal
response to normal hormonal changes.
TREATMENT
Treatmentof PMS is based on alleviating symptoms with special consideration to the psy-
chological aspects of PMS,They include;
t. Selective serotonin reuptake inhibitors have demonstrated reasonable efficacy in treating
both physical and mood symptoms in women with severe PMS, taken as daily oral tablets
throughout the menstrual cycle.
2. Changes in the life style: as regular exercise, balanced diet, avoid premenstrual
stress, eliminate caffeine, cigarette smoking, and alcohol ...etc
3. Calcium 600 mg BlD, Vitamin D 8OO lU/day, Vitamin 86 (100 mg/day), & Magnesium
20 mg/day), all may slightly improve PMS symptoms in many women.
4. OCP: may improve some cases as it minimizes fluctuations in ovarian steroids.
 Normol puberty Disorders puberty
- Definition - Precocious puberty
- Pathophysiology - Deloyed puberty
- Clinical monifestotions

PUBERTY
DEFINITION
Puberty is the period of life that marks the normal physiologic transition from childhood to
sexual and reproductive maturity (physical, mental, sexual growth).

During puberty the hypothalamus, pituitary gland, and ovaries undergo a maturation process
that ultimately leads to the complex development of secondary sexual characters involving the
breast, sexual hair, and genitalia, in addition to a limited acceleration in physicalgrowth.

Normally, pubertal changes start by the age of 8-9 years, and is completed by the age of L2-'J.4
years culminating by the onset of menses and acquiring the reproductive capacity.

PATHOPHYSIOLOGY OF PUBERTY

- In childhood hypothalamic Gn RH is centrally suppressed mostly via control by a gene in the Gn

RH nucleus.

- At initiation of puberty single nocturnal spikes of Gn RH start to occur, and gradually increase in
frequency becoming night and day over a period of 1,-2 years, until the normal adult frequency
is achieved.

- Pituitary FSHsecretion starts in response to pulsatile GnRH stimulation, resulting in stimulation

of follicular development, oestrogen production, appearance of secondary sexual characters,
and finally the onset of menstruation with the establishment of ovulatory cycles.
- other factors as leptin play an important role in the initiation of puberty
CLINICAL MANIFESTATIONS OF PUBERTY

1'. Growth spurt: first sign of puberty to occur with a peak growth velocity at age of LL years,
is the
followed by a slower growth rate until cessation usually by age of 15 years, where closure of
bone epiphysis occurs in most girls as an effect of increased oestrogen levels.

2. Thelarche: (Breast Development): The breast grows in phases (5-stages) under the effect of
oestrogen. This starts by growth of the body of the breast (budding), followed by pronounceo
areolar development and ends by full breast development, where the breast tissue grows to
become confluent with the areola (fig 5-1 Tanner stages of breast development).

3. Pubarche: Growth of pubic hair occurs under effect of ACTH and androgens. pubic hair growth is
classified into (S-stages) according to degree of distribution (fig. 5-2 Tanner stages of pubic hair
growth).

4. Menarche: This is the onset of first menstruation. lts average age in Egypt is 12.5 years.
5' Axillarche: growth of axillary hair, appears later also under effect of androgens.

A-
+/
48 Puberty snd its Disorders

TANNER STAGES OF PUBERTAL GROWTH I

Pubertal cascade starts usually by growth spurt, followed by breast devel-

opment, pubic hair, menarche, and finally axillary hair. Tanner had classified t
physical stages of puberty into 5-stages depending on the degree of breast de-
velopment and distribution of pubic hair.

Stages of breast development

Fig 5-2: Tanner Stoges of

Fig 5-1: Tanner Stages of the Breost pubic hair

DISORDERS OF PUBERTY
I. PRECOCIOUS PUBERTY
Precocious puberty describes appearance of secondary sexual characters before 8 years of
age, with or without onset of menstruation. Besides the psychological impact of the syndrome, ear-
ly oestrogen production will carry the risk of short stature from early epiphyseal bone closure.

A) rsosExuAl PRECOCTOUS pUBERTy (rpcp)

The secondary sexual characters are in agreement with genetic and phenotypic sex
1. True IPCP: (GnRH dependant, possibly be associated with ovulation)
. Constitutional: due to idiopathic premature activation of the gene in the GnRH cell, leading to
early FSH production, and early onset of ovarian E2 secretion (74% of cases).
. Organic: due to CNS lesions that impede neural signals that normally inhibit GnRH release in
childhood
a. Tumours; craniopharyngioma, adenoma, glioma, etc....
b. Infections; meningitis, encephalitis, etc...
c. Malformations; hydrocephalus, empty sella syndrome, hamartomas, etc....
d. Head trauma
2. Pseudo IPCP: ( GnRH independent, not associated with ovulation)
a, Oestrogen secreting ovarian tumours(granulosa theca cell tumours)
b. Primary hypothyroidism; elevated TSH may induce FSH production
c. Exogenous oestrogen intake

B. HETEROSEXUAL PRECOCTOUS pUBERTY (Hpcp)

The secondary sexual characters are in disagreement with genetic and phenotypic sex,

a. Androgen secreting tumours (virilizing ovarian or adrenal neoplasia)

 Gynaecology 49

b. Congenital adrenal hyperplasia (CAH)

-
c. Exogenous androgen intake

C. ISOLATED PREMATURE PUBERTAL EVENTS

lsolated pubertal events may occur, as premature menarche only, or premature thelarche only,
v etc, without other oestrogen induced pubertal events or advancement of bone age. Such condi-
tion is usually benign and does not usually necessitate treatment.
DIAGNOSIS OF PRECOCIOUS PUBERTY
r HistorY and Physical examination: Age, height, growth spurt, breast development, and hair dis-
tribution, according to Tanner stages of pubertal development.
L.
o Hormonal assays:
\v
- Pituitary gonadotropins (serum FSH & LH)

v - Thyroid function tests (TSH, T3, & T4) to exclude 1ry hypothyroidism.

' Radiological investigations:

v
X-ray to the wrist of the non dominant hand to determine bone age.
'-
- CT & MRI for brain tumours and intracranial masses.
- Pelvic ultrasound for exclusion of ovarian tumours or cvsts.

v MANAGEMENT OF PRECOCTOUS PUBERTY

The chief goal at therapy aims at slowing down accelerated growth and inducing regression of
secondary sex characters through reducing pituitary and ovarian hormones, thus avoiding prema-
ture epiphyseal closure which predisposes to short stature.
a. ldiopathic PCP: long acting GnRH agonists willsuppress pituitary FSH & LH, and ovarian E2,
halting the progression through puberty. Treatment is continued until an appropriate age
\v has been reached for resumption of pubertal development.

b. Functioning ovarian tumours are surgically removed

c. Primary hypothyroidism is treated with thyroid replacement therapy (Eltroxin)

d. Adrenal tumours are treated with surgery or irradiation

.- II. DELAYED PUBERTY
v Puberty is considered delayed if no secondary sexual characters are noted by the age of 13-1-4
years, or if menses is still absent by the age of 15-16 years. Delayed puberty affects almost 3% of
adolescents. Causes, diagnosis and management are discussed in primary amenorrnoea.

Aetiology
A. Hereditary Factors:
These may account for about tO-2O% of cases. Constitutional delay may run in families mostly
due to delayed activation of the GnRH pulse generator.

B. Chromosomal abnormalities, genetic, and autoimmune disorders:

50 Puberty snd its Disorders

These may be present in up to 50% of cases. The ovaries, or gonads, are non-functioning and
unable to respond to gonadotropins, leading to markedly elevated FSH & LH levels
(hypergonadotrophic hypogonadism). Examples include Turner syndrome (45 X), premature
ovarian failure, autoimmune ovarian failure, and gonadal dysgenesis.

C. Pituitary and hypothalamic tumours and severe illness:

These conditions account for IO-15% of cases with delayed puberty. The ovary is normal howev-
er there is lack of production of hormonal stimulation from the hypothalamus, leading to low
FSH & LH levels (hypogonadotrophic hypogonadism). Examples include Kallmann syndrome
(isolated GnRH deficiency), and hypothalamic suppression by stress, severe disease, and malnu-
trition.
D. Pituitary tumours and lesions:

Prolactinomas and empty sella syndrome; induce hyperprolactinaemia which suppresses GnRH
pulses, while tumour invasion by craniopharyngiomas suppress Pituitary gonadotrophins
( hypogonadotroph ic hypogonadism ).

E. Congenital Mullerian agenesis or dysgenesis: absent or hypoplastic uterus, in presence of normal

ovaries will result in primary amenorrhea with normal development of 2ry sexual characters
(euogonadotrophic hypogonadism).

DIAGNOSIS AND INVESTIGATIONS

See examination and investigations for Precocious puberty and primary amenorrhoea

TREATMENT FOR DELAYED PUBERTY

Treatment for delayed puberty depends on the cause of the problem. Often, when the underlying
cause is treated, puberty proceeds normally.

. lf the delayed puberty is due to heredity, no treatment is usually necessary.

. In some cases, treatment may involve hormone therapy to stimulate the development of
secondary sexual characteristics (combined oestrogen progesterone therapy), or surgery to
correct an anatomical problem.
. In gonadal dysgenesis with a Y chromosome present gonadectomy should be performed for
the risk of neoplastic changes in the gonads
 Perimenopquse
Menopouse
Postmenopause
Hormone theropy in menopause
Prevention and monagement of Osteoporosis

PERIMENOPAUSE
Climacteric is the phase of the aging process during which a woman passes from the
reproductive to the non-reproductive stage (Figo definition).

I The Perimenopause, also known as the menopausal transition, refers to the part of
the climacteric before the menopause (2-8 years prior to the FMP), in which there is
transition from normal ovulatory cycles to permanent amenorrhoea of menopause.
- This period is characterized by irregular menstrual cycles together with some of
the symptoms associated with the menopause as; hot flushes, night sweats, and
mood swings.
- During this period, inhibin-B secretion from granulose cells falls due to diminished
follicular number, and as result FSH levels rise, and PRG levels become low.
- Ovarian E2 secretion is preserved until late perimenopause

MENOPAUSE
Menopause is the final menstruation that occurs at the end of climacteric. lt is defined by 72
months of omenorrheo after the finol menstrual period (FMP), in the absence of any other
pathological or physiological cause.

Menopause occurs due to depletion of ovarian primordial follicles due to their consumption since
menarche (the adult ovary at puberty contains around 400.OOO primordial follicles).

I Natural Menopause: occurs due to intrinsic ovarian failure that usually occurs between
45-55 years with a median age of 51 years. lt is characterized by complete, or near
complete, ovarian follicular depletion, with subsequent cessation of ovarian estrogen (E2)
secretion.

. Induced Menopause: menopause can be artificially induceo;

- Surgicolly; as after bilateral oophorectomy
- Ablotion of ovorion function; as pelvic irradiation or systemic chemotherapy
- Medically; during the use of long acting GnRH agonists in the management of
endometriosis.

5l
52 Menopause and Associated Conditions

r Premature Menopause occurring at an age 40-45 years may be either;

o) Premature ovarion insufficiency (POI): due to congenitally deficient number of ovarian
follicles at puberty, leading to their early exhaustion at a relatively young age.
- ldiopathic: no underlying etiology
- Gonadal dysgenesis: as in cases of mosaic turner syndrome (46XX/45XO)
b) lnduced: surgical, irradiation, or chemotherapy before the age of 45 years

ENDOCRINE CHANGES CHARACTERISTIC OF MENOPAUSE

- Decreosedserum inhibin-B levels that started at the perimenopause.
- Marked increose in serum FSH & LH levels.
- Marked and persistent decreose in Ovarian E2 levels
- Decreose in sex hormone binding globulin (SHBG)
- lncreosedfree testosterone (FT) levels
- Persistent production of ovarian testosterone (T).

Hypothalamus

= No gonadal estrogen

Bone

rl
Fig 6-1: Changes in both the ovary and the hypothalamus contributing to changes ofthe menopause

CHANGES IN BODY SYSTEMS ASSOCIATED WITH MENOPAUSE

Changes in the menopause start in the climacteric period, and continue gradually and
persistently after cessation of menstruation. They are almost all related to estrogen deficiency,
and are therefore gradually progressive and time related.

- The vagina becomes smaller, thinner, with gradual loss of its rugae, decreased
vascularity, and increased vaginal PH. Vaginalsmears become atrophic.
The pelvic ligaments become weaker predisposing to pelvic organ prolapse (POP).
The uterus becomes smaller in size. lf myomas are present they undergo atrophy.
The endometrium becomes thin and atrophic (< 5 mm thickness)
The cervix becomes gradually flushed with vaginal fornices, and the squamo-columnar
junction migrates higher in the endocervical canal.
The urethra and blodder mucoso show loss of elasticity, bladder dysfunction, and
to relaxation in the weak pelvic ligaments).
stress incontinence (due
 Gynaecology 53

The Breasts become gradually smaller and flabby with progressive fatty replacement
of breast tissue and atrophy of active glandular elements.
The skin shows gradual decrease in thickness and collagen content.
lncreased facial hair and androgenic alopecia in response to increased androgens
Gradual changes in cognitive function and mood swings.
Decreased mineral bone density leading to osteoporosis (see later)
Nervous and Psychologicol chonges

CLINICAL FEATURES OF THE MENOPAUSE (Symptoms & Signs)

Most menopausal manifestations are secondary to the chronic low serum E2 levels
characteristic of the menopause.
Symptoms usually start gradually in the perimenopause, increase sharply after FMp, and
extend years into the menopause.
In almost 50% of women menopausal symptoms will be severe enough to call for
gynaecologic consultation and or treatment.
Menstruation may stop abruptly, however the FMP is more commonly preceded by a period of
oligomenorrhoea in the late Perimenopausal period.

1. Vasomotor Symptoms (VMS); Hot flushes & Cold sweating

- Hot flushes: are recurrent waves of heat over the chest, neck, and face, followed by cotd
sweoting' A flush may last for 1-5 minutes, and may be associated by palpitation,
dizziness or headaches.
- Flushes affect at leost 50% of menopausal women but with variable grades of severity.
- Flushes start in the perimenopause and become more aggressive in the menopause.

- Flushes result from inappropriate stimulation of the thermoregulatory centres in the

hypothalamus with vasodilatation of the skin over the head, neck, and chest, causing a
skin temperature rise although core body temperature does not change.
2. Nervous and psychological symptoms: Anxiety, irritability, mood changes, insomnia, and
lack of concentration, are common although with variable oegrees.
3. G.l.T. symptoms: ccnstipation, abdominal distension, and tendency to weight gain
4. Dyspareunia: due to vaginal atrophy, dryness, and senile vaginitis.
5' Urinary symptoms: as frequency, dysuria, and stress urinary incontinence, may occur alone
or in association with pelvic relaxation and genital prolapse.
6' Tendency towards pelvic organ prolapse (POP): uterine and vaginal prolapse occur more
frequently due to weakness and atrophy of pelvic and cervical ligaments.
7' Androgenic manifestations: increased facial hair and baldness affect women variablv.
8. Symptoms related to osteopenia and osteoporosis (see later)

DIAGNOSIS OF MENOPAUSE
54 Menopouse and Associoted Conditions

Deformity of
vertebrae

Thinned bone
(loss ot calcium)

Fig6-2: Osteoporotic changes in menopause

MANAGEMENT OF THE MENOPAUSE

- Reossurance about the physiological nature of the menopausal symptoms

- Education for healthy life style; Calcium rich diet, suitable exercise, and avoid smoking.
- Symptomotic treatment for some menopousal symptoms; Sedatives, tranquilizers, or
antidepressants on individual basis whenever needed.
- Periodic tesfs for early detection of premalignant and malignant lesions including;
Mammography, TVS, Pap smear cytology, and colposcopy.
- Diagnosis, prevention, qnd tredtment of osteoporosis (see later).
- Hormone therapy (HT)in selected cases with severe menopausal symptoms (see later).
REMOTE HEALTH HAZARDS RELATED TO MENOPAUSE

cAR Dt OVASCU LAR SYSTE M CH AN G ES ( CVS )

. Pothogenesis: Oestrogen deficiency may lead to hypercholesterolemia with increased LDL
and decreased HDL (reversed LDL/HDL ratio).
t Clinicol manifestations: reversed LDL/HDL ratio may predispose to ischaemic coronary
heart disease (ICHD), myocardial infarction (Ml), atherosclerosis, hypertension (HTN), and
cerebrovascular strokes.

osrEoPoRosts
t Definition.' Osteoporosis is a disorder characterized by decreased bone mineraldensity
leading to compromised bone strength with increased risk of bone fractures.
. Pothogenesis;Oestrogen deficiencyresults in accelerated bone mineral calcium
loss, and increased activity of osteoclasts (bone destroying cells), affecting mainly
the vertebrae, femoral neck, distal radium, and the calcaneum.
t Clinicol manifestations.' bone demineralization is usually a silent disease that manifests years
after menopause with; decreased height, increased curvature of the spine, silent fractures of
the vertebrae, or fractures of the hip and long bones on exposure to mild trauma
 Gynaecology 55

t Risk foctors: premature menopause, heavy smoking, lack of exercise, low body weight,
together with hereditary and genetic factors (white race).
t Diagnosrs;by X-ray bone densitometry (DEXA).
t Prevention of osteoporosis:
intake or 1500mg dairv

- - ;ffi:i;#:,'J;:;'''"
- Healthy life style; including weight bearing exercises, stop smoking, and avoid long term
corticosteroid thera py.
t Treatment of osteoporosis:
A) Drugs that slow bone breakdown during bone remodeling
- Biphosphonotes: orally once per week, decrease non vertebral fractures.
- Colcitonin; nasal spray increase the vertebral bone mass and reduce fractures risk.

'' ":'?;'""i,Til1:l;:r::::'J"ff:i::::;Tffli1
- and non vertebral fractures.
decreasesve*ebra,

C) Hormone Therapy (HT)

- Hormone Theropy (HT): although effective in prevention and management of

osteoporosis, is rarely used as a primary therapy, except in cases which need HT for
control of menopausal flushes, or in cases of premature menopause.

: ::';'#:oo:"'fifi:,-":;:::'.y"r::::'::iti.'ffi,i;i;"1':",il';':"u,o,,Jf/3;,,!':":
uterus. lt is approved for prevention of osteoporosis but may induce hot flashes,
- Phyto-oestrogens: plant substitutes that have a weak oestrogen action

THERAPY lN MEN.PAUSE
: rypesorHormon",:r:ltoNE
A) Oestrogen + Progestin therapy (Combined HI/: where a progestin is added to avoid
oestrogen induced endometrial hyperplasia (EH) and possible endometrial carcinoma.
B) Oestrogen only theropy (ET):suitableforwomen who have undergone hysterectomy (no
risk for oestrogen induced endometrial hyperplasia or carcinoma).
Benefits of Oestrogen in the Menopause
L. lt reduces menopausal symptoms as; hot flashes, sleepiness, and mood disorders
2. Treats vaginal dryness and atrophy which may cause dyspareunia and senile vaginitis
3. Prevents or reduces the risk of osteoporosis during the period of therapy
Risks of Hormone Therapy
- Small but significant increase for CVS disease, stroke, and venous thromboembolism

- Small but significant increase in the risk of breast cancer

Endometrial cancerrisk: with prolonged oestrogen only therapy (> 5 years).
56 Menopquse ond Associated Conditions

Indications of HT in menopause
- Menopausal symptoms affecting the patient's life style and psychologicalcondition
- Premature menopause (idiopathic or surgically induced), till age of natural menopause.
- Prevention of osteoporosis in high risk cases. The effect is limited to the period of HT.
Contraindication to the use of HT
a. Undiagnosed abnormal bleeding from the genital tract
b. Known or suspected breast cancer, or oestrogen dependent neoplasia
c. History of DVT, stroke, or thromboembolic disease
d. Active liver disease
Commonly used schedules for HT
r Continuous Combined E/PRG therapy: daily oraltablets throughout duration of therapy (1-
2 years). Nowithdrawal bleeding expected.
r Cyclic Combined E/PRG therapy: daily oral oestrogen tablets for 3 weeks, PRG added last12
days. Treatment stopped for one week in which withdrawal bleeding is expected.
r Oestrogen only therapy (ET): daily oral doses, sub-dermal implants, or transdermal
patches are used for patients with absent uterus (after hysterectomy).
r Oestrogen vaginal cream preparations: for local application in cases of vaginal atrophy
Types of Hormones used

0.625 mg/day or oestradiol valerate t-2 mg/day.

include mastalgia, mood changes, PMS like symptoms, weight gain, etc...

Key Points
- Menopouse is the permanent cessotion of menstruotion that affects oll women ot oges ronging 45-55
years, due to exhoustion or depletion of ovorion follicles.

- Perimenopouse describes the few yeors prior to menopquse in which some of the feotures ond symp-
toms of menopquse stqrt to be clinicolly evident
- Premqture menopause describes cessation of menses < 40 yeors of oge
- Symptoms ond clinicol features characteristic of menopause qre qll reloted to lock of ovorion E2 pro-
duction, qnd its effect on vorious body systems
- Changes in body systems due to menopause moy offect the vagino, cervix, uterus, endometrium, ovo-
ries, skin, breosts, psychiotric & C /t ond skeletol systems.
- Symptoms of menopause include: cessqtion of menstruation, hot flushes, insomnio, irritobility, weight
gain, mood swings, depression, onxiety, voginal dryness, dyspareunia, loss of libido, ond susceptibility
to skeletal froctures, ond tendency to POP.
- Remote health hazards related to menopause include: CVS chonges ond osteoporosis

- Diognosis of menopause is based on; history, symptoms, qnd hormonol assays reveoling elevoted FSH
& LH levels together with decreased E2.

- Management of menopouse includes; reossurqnce, educotion, changes of life style, prophylaxis and
monagement of CVS problems ond osteoporosis.
- HT in menopause is reserved to selected coses, ond is moinly directed towords treatment of acute
symptoms of menopause, and prophylaxis ogoinst osteoporosis.
- HT should be corefully monitored, to guard ogqinst long term complicotions of its use.
 - Physiologic omenorrhoeq Gu ideli nes i n mo nage me nt
- Pathologic Amenorrhoea Hyperprolactinaemio
- Clinicol qssessment

DEFINITION
The term amenorrhoea describes absence or cessation of menstruation,
it may be eitner;
A. Primary Amenorrhoea; Menstruation has never occurred before
B' Secondary Amenorrhoea: Cessation of menstruation after a period of regular
cyclic bleeding
r N.B.: primary amenorrhoea should be investigated in all females if:
- Menses delayed >14 years of age in absence of developed 2ry sexual characters
- Menses delayed >16 years weather 2ry sexual characters has started development
or not
CAUSES OF AMENORRHOEA
A. PHYSIOLOGIC AMENORRHOEA
1'. Before puberty: due to absence of pituitary FSH / LH stimulation
2. After menopduse.' due to exhaustion and depletion of oocytes in the
ovaries
3. During pregndncy: due to continuous production of oestrogen and progesterone
4. During lactation: high prolactin levels interfere with LH surge and cause anovulation
B. PATHOLOGIC AMENORRHOEA
1" outflow Tract Disorders; imperforate hymen, transverse vaginal septum, and cervical
atresia
2. Uterine Disorders: as Mullerian agenesis, androgen insensitivity, and Asherman,s
syndrome
3. Ovorian Disorders: as Turner's syndrome, premature ovarian failure, and pCOS
4' Pituitary Gland Disorders: pituitary adenomas, empty sella syndrome, pituitary insufficiency
5' Hypothalamic and CNS Disorders.' as GnRH deficiency, psychiatric disorders, rapid
weight
loss, excessive exercise, drug induces, hypothalamic tumours and infiltrative
disease
6. Endocrine Disorders: as hypothyroidism, hyperthyroidism and Cushing,s syndrome

COMMON CAUSES OF PRIMARY AND SECONDARY AMENORRHOEA

PRIMARY AMENORRHOEA SECONDARY AMENORRHOEA

lmperforate hymen
- Polycystic ovary syndrome (PCOS)
Transverse vaginal septum
- Hyperprolactinaemia
Turner syndrome (45 XO)
- Thyroid disorders
- Mullerian agenesis (46 XX)
- Drug induced (OCps - GnRH agonists)
- Androgen insensitivity (46 Xy)
- Rapid weight loss
- Congenital GnRH deficiency
- Stressful exercise
- Kallman's syndrome
- Asherman syndrome
- Premature ovarian failure (pOF - pOl)

57
58 Amenorrhoea

I. OUTFLOW TRACT DISORDERS

These disorders describe cases with obstruction of the menstrual flow at the level of the; hy-
men, vagina, or cervix. Such cases present with 1ry Amenorrhoea usually at a young age, with nor-
mal development of their 2ry sexual characters.
Because menstruation occurs but is not revealed this type of 1ry amenorrhoea is commonly
known as false amenorrhoea or cryptomenorrhoea.

A) IMPERFORATE HYMEN:
lmperforate hymen is a congenital anomaly in which the hymeneal orifice is absent. The condi-
tion may affect up to 0.1% of the newly born females, and is the commonest cause for crypto-
menorrhoea.
- Pathogenesis.. at puberty, menstruation will start, but blood will accumulate behind the imper-
forate hymen leading to;
Y Hoematocolpos; blood entrapped and accumulating inside the vagina
Y Haematometra; in long standing cases blood will extend to the uterine cavity
D Hoematosalpinx; blood collecting in the fallopian tubes retrograde from the uterus
- Clinicol Presentotion; young girls with 1ry amenorrhoea and well developed 2ry sexual charac-
re rs.

- Symptoms; lower abdominal pain synchronous with the timing of the menstrual period.
- Signs:
Y tnspection and palpotion of the lower obdomen; may reveal a suprapubic bulge only if
the haematocolpos is large enough to extend upwards to the suprapubic region.
Y tnspection of the vulva & voQino: hymeneal orifices are absent, and if haematocolpos is
large the hymen will bulge at the hymeneal ring with a slight bluish colour.
Y PR Exominotion: a sizable haematocolpos can be easily palpated by PR examination

- Speciol lnvestigation; pelvic ultrasound is the gold standard in diagnosis.

- Treatment.. once diagnosed, surgical cruciate incision is performed dividing the imperforate

\'fi'

Fig 7-7: lmperforote hymen with haematocolpos Fig 7-2: Tronsverse vaginol septum site from
ond hoemotometrq qbove downwards
 Gynaecology 59

B. TRANSVERES VAGINAL SEPTUM

One or more transverse vaginal septae may be congenitally present at any level between the
hymeneal ring and the cervix leading to occlusion of the lower, middle, or upper segment of the
vagina. The condition is rare, but is the 2nd most common cause for cryptomenorrhoea.
Clinicol Presentationj cryptomenorrhoea as seen with imperforate hymen (see above)

- Diagnosis: haematocolpos diagnosed by US, while hymen, if present, is apparently normal

Treqtment: surgical excision of the transverse seprum.
C. CERVICAL ATTRESIA
Congenital cervical atresia is a very rare condition, in which there is failure of canalization of the
cervical canal as a part of Mullerian dysgenesis.
Clinicol Presentation.' picture of cryptomenorrhoea as seen with imperforate hymen (see
above)
Diagnosis: Pelvic US reveals marked haematometra, absent cervix, and no haematocolpos.
- Treatment: is difFicult and controversial. Cervical reconstruction and canalization is attempt-
ed, but with poor results, and if fails hysterectomy may be the only option.

II. UTERINE ABNORMALITIES AND DISORDERS

Uterine causes of amenorrhoea are not uncommon, they include
) Complete or Partial Mullerian Agenesis (congenital)
F Complete Androgen Insensitivity Syndrome CAIS (congenital)
F Asherman Syndrome (acquired)

A) MULLERTAN AGENESTS (coMPLETE or PART|AL)

(Mayer Rokitansky Kauster Hausser Syndrome):
v These are females (46 XX karyotype) with congenital genetic defect that resulted in failure of
!. development of the Mullerian structures (the uterus, cervix, and upper vagina).
- Aetiology; possibly due to an unwanted intrauterine exposure to anti-mullerian hormone
(AMH), with failed development of the Mullerian ducts.

- lncidence; Mullerian agenesis may occur in 1:4000 female births and accounts for almost
20% of cases with 1ry amenorrhoea (2nd common after Turner syndrome)
v - Clinicol Presentqtion; 1ry amenorrhoea with normal 2ry sexual characteristics. Such cas-
es have normal ovaries, as the gonads develop from the genital ridge, and are capable of
v producing normal amounts of E2 due to an intact hypothalamic-pituitary-ovarian axis.

- PV Examinotion (if not virgin): reveals a blind ended short vagina, with absent cervix ano
urerus.

- Pelvic U5; reveals absent uterus, and upper vagina, with normal ovaries.

- Karyotyping: ablood sample for genetic study reveals a 46 XX chromosomal pattern

- Monogement; a short vagina can be managed surgically by lengthening the vaginal canal
through vaginoplasty as with Mclndoe procedure
- I N.B.: Associated urinary tract and skeletal anomalies are common associations
60 Amenorrhoea

B. COMptETE ANDRpGEN tNSENStTtVtTY SYNDROME (CA|S)

(Testicular feminization Syndrome) :

These are male subjects (46

XY karyotype) with an X-linked inherited recessive disorder that
render them androgen resistant due to a defect in peripheral androgen receptors.
These male subjects fail to develop testosterone dependent male sexual characteristics, inspite
of normal male testosterone levels. They therefore develop phenotypically as females. They
present by \ry amenorrhea, female external genitalia, and a blind ended vagina.

- tncidence: rare, but is 3'd common cause of 1ry amenorrhoea after Mullerian agenesis.
Pathogenesis; male gonadal tissue may be present in the labia or inguinal canal, but inca-
pable of spermatogenesis. The presence of a Y chromosome, and Mullerian inhibiting
factor (MlF) leads to failure of Mullerian system development (uterus, cervix and upper
1/3 vagina).

- Management:
) Gonadectomy must be performed in such patients as they carry a 20% risk of gonado-
blastoma, however treatment is usually deferred until after puberty.
F Creation of a neo-vagina surgically via Mclndoe procedure if the patient rquires, as
such cases are reared as females.
I N.B.: Hormone therapy in the form of oestrogen preparation will help keeping the external
female appearance, and prevent accelerated bone loss (osteoporosis)

C. ASHERMAN'S SYNDROME (lntrauterine Synaechae)

Asherman's syndrome describes acquired intrauterine adhesions which prevent endometrial
proliferation, leading to 2ry amenorrhoea.

- Aetiology; Endometritis (post abortive, puerperal, IUD induced, or T.B), or iatrogenic via
vigorous curettage during D&C procedures especially with surgical evacuation.

Clinical presentation; 2ry amenorrhoea following endometritis or curettage

Diagnosis: both HSG and hysteroscopy are excellent diagnostic tools.

Treatment: Lysis of adhesions best under vision via hysteroscopy, or through D&C like pro-
cedure. This is followed by cyclic combined EST/PRG therapy for at least 3 cycles to restore
endometrial regeneration.
 Gynaecology 61

III. OVARIAN DISORDERS

A) TURNER SYNDROME: (Gonadal Dysgenesis)
In Turner syndrome achromosomal defect occurs in
which an X chrornosome will be missing (45-XO) and the
ovaries will be replaced by fibrous tissue (streak gonads).

- lt is the commonest cause of lry

lncidence..
amenorrhoea, being responsible for 3O/o of cas-
es

- Clinical presentation: 1-ry amenorrhoea with phe-

no-typic characteristics including; low hair line,
short stature, webbing of the neck, increased car-
rying angle at the elbow, Cardiac anomalies as; co- &ownspors(nwr)
arcitation of the aorta.

- Pathogenesis; Absence of the Y chromosome

will allow for normal development of Mullerian
elements (the vagina, uterus, and fallopian tubes), Fig 7-3: Features of Turner syndrome
however at puberty the streak gonads fail to produce enough E2, inspite of elevated FSH
and LH levels, leading to 1ry amenorrhoea.

Treatment: HRT, in the form of cyclic combines EST/PRG will induce regular cycles, ano
preserve the 2ry sexual characters, and act as prophylaxis from bone osteoporosis.

N.B.: In some cases with a mosaic karyotype (45X0/46XX), spontaneous menstruation and
in some cases pregnancy might occur (2%-5% of cases), but most cases will develop prem-
ature ovarian failure (POF) and premature menopause.

B) PREMATURE OVARIAN FAtIURE OR |NSUFFtCtENCY (pOF or pOt)

Premature ovarian failure occurs due to early exhaustion of ovarian primordial follicles before
the age of 40 years leading to premature menopause.
- Aetiology:
F ldiopathic; associated with autoimmune ovarian destruction
) Karyotype abnormalities; as loss of a small portion of the X chromosome
) Viral infections; as mumps
) Induced; by radiation therapy, chemotherapy, or surgical removal
- Clinical Presentation; Premature menopause (2ry amenorrhoea with high FSH & LH levels)

- Treatment; cases of POF should be offered HRT (combined EST/PRG)to avoid hazards and
complications of premature menopause (see chapter G)
) Resistant Ovary Syndrome: 2ry amenorrhea with high FSH and LH levels may occur
when viable ovarian follicles fail to respond to pituitary gonadotropins due to a defect
in their FSH/LH receptors. In few cases the condition is temporary and some may ovu-
late and conceive.
62 Amenorrhoeo

c) poLYcYcilc ovARY SYNDROME (PCOS)

PCOS describes a syndrome characterized by chronic anovula-

tion, and hyperandrogenism, in association with morphologic and
histological changes in the ovaries. lt is the commonest cause for 2ry
amenorrhoea due to pathologic anovulation.
Clinicol Presentotion: 2ry amenorrhoea or oligomenor-
rhoea, in association with one or more of hirsutism, infer-
tility, and obesity.
Diagnosis: Fig 7.4 US picture of PCO
Y Pelvic US; characteristic picture with increased size and
volume, dense'stroma, and peripherally arranged equal size small follicles (necklace
or string of pearls appearance).
b Hormonal profiles: show abnormally reversed FSH/LH ratio (elevated LH level > 2
times FSH), together with elevated total and free Testosterone levels, and increased
DHEAS (hyperandrogenism).

D N.B.: Some cases show increased insulin resistance and hyperinsulinaemia.

Treatment: according to the patient's complaint, (see details in chapter 8 PCOS)

IV. ANTERIOR PITUITARY GLAND DISORDERS

A. PITUITARY ADENOMAS: (see hyperprolactinaemia)

Hyperprolactinaemia, by itself, is responsible for up to 20% of cases of 2ry amenorrhoea. lt
acts via its effect on suppression of GnRH and LH surge inducing a state of chronic oligo-ovulation,
anovulation, and finally 2ry amenorrhoea.
Prolactinomas are the commonest cause for hyperprolactinaemia, and the most common pitu-
itary cause for 2ry amenorrhoea. They are classified histologically as either;
Y Microodenomas (< 10 mm in size): these are the commonest, and are usually associat-
ed with moderate elevations in serum PRL levels.

D Mocroodenomos (>10mm in size): are relatively rare, and are associated with high
serum PRL levels and possible signs of increased intracranial tension (lCT).

- Diagnosis ond Treatment: (see hyperprolactinaemia)

B. EMPTY SELLA SYNDROME:

The condition refers to enlarged sella turcica that is not entirely filled with pituitary tissue.

- Pothogenesis; lt occurs mostly due to a defect in the diaphragm sella that allows cere-
brospinalfluid (CSF) pressure to enlarge the sella.
I P rese ntotion ; 2ry
Cli n ica a menorrhoea or ol igohypomenorrhoea with hyperprolacti-
naemta
Diognosis: MRI or CT scan is the mainstay in its diagnosis.
 Gynaecology 63

: c. PrrurrARY rNsuFFrcrENcY
Pituitary insufficiency will result in diminished FSH and LH secretion, leading to a
v state of chronic anovulation with hypogonadotrophic amenorrhoea. Causes are rare but
include;
'v ) Sheehan's Syndrome: (anterior pituitary necrosis following severe postpartum haemor-
v rhage)
) Simmond's Disease.
F Radiation necrosis, pituitary infarctions, and non-lactotrophic adenoma
v F Infiltrative lesions of the pituitary gland, such as lymphocytic hypophysitis.
v Y Management; according to the cause, but generally HRT with combined EST/PRG is suita-
ble. Induction of ovulation can be attempted using FSH/hCG preparations, but clomi-
phene citrate is contraindicted due to inability of the pituitary to produce FSH and LH.

: Hypo,ha,am c and .,1;lll,T:::il:3::l:l::l:::1"

frequency with it consequences of Low FSH &
decreased GnRH pu,se
LH production, absent LH surge, low E2 levels, and
\- chronic anovulation (hypogonadotrophic amenorrhoea). Common causes include;
A. CONGENITAL GnRH DEFICIENCY:
\_
Congenital GnRH deficiency is a rare condition that presents with 1ry amenorrhoea in asso-
ciation with infantile sexual development (hypogonadotrophic hypogonadism).
Kallmann's syndrome describes congenital GnRH deficiency in association with an-
osmia dueto congenitalfailure of neuronal migration of olfactory placode in the nose.
Treotment: HRT with combined EST/PRG therapy is essential to help preservation of
2ry sexual characters, uterine size, and attempt to induce uterine withdrawal bleed-
ing. In cases with normal size uterus and responsive endometrium, induction of ov-
ulation may be attempted using FSH/LH/hCG protocols.
v
B. PSYCHIATRIC DISORDERS:
v !. Emotionolly stressful events: as family problems, work, study, travel, death or severe ill-
ness may cause 2ry amenorrhoea in some women.
2. Pseudocyesis; (falsepregnancy): is a rare condition that may occur in emotional women
v extremely desirous of pregnancy. The etiology is unknown but appears to be a voluntary
alteration of hypothalamic function. Prolactin levels may be elevated enough to cause
v galactorrhoea.
v 3. Anorexia nervosd: may affect I% of young women. Bulimia (induced vomiting) may be pre-
sent in 50% of cases
C. RAPID WEIGHT LOSS AND EXCESSIVE EXERCISE:
v 1,.RapidondExcessiveweight loss;aminimum of 20% of bodyfatbyweightisrequiredfor
initiation of menarche and maintenance of menses. Rapid weight loss (below 20% of ideal
body weight) may cause 2ry amenorrhoea
2. Excessive stressful Exercise: is usually associated with increased circulating endorphins and
may cause 2ry amenorrhoea in female athletes as marathon runners, ballet dancers, etc...,
especially those with markedly decreased body fat.
64 Amenorrhoea

D. DRUG-INDUCED AMENORRHEA:
1'. GnRH Agonists; the use of long acting GnRH agonists will induce initial stimulation of
GnRH for a short period, followed by a longer suppression of FSH & LH due to a down regu-
lation receptor effect. A state of 2ry amenorrhoea is induced, which is useful in treatment
of cases with severe endometriosis, some cases of severe AUB, and to reduce the size of
large uterine myomas prior to surgery if necessary.
2. Progestins,' continuous synthetic progesterone therapy will prevent endometrial shedding,
and inhibit GnRH pulses, leading to delay in the cycle and 2ryamenorrhoea. Normal menses
is resumed after stopping therapy.
3. Combined EST/PRG therapy: continuous therapy will also prevent endometrial shedding
and inhibit GnRH pulses as long as therapy continues. Post pill amenorrhoea may occur in
1% of women after long use of combined OCPs, due to chronically decreased gonadotropin
levels. The condition is self limiting, and normal menses is usually spontaneously resumed
in 2-6 months.
4. Androgenic drugs as Danazol (formerly used in treatment of endometriosis) induces
atrophic endometrial changes by its androgenic and progestational effects.
5. Anti-psychoticsondtri-cyclicanti-depressants(stimulateprolactinsecretion)

E. HYPOTHALAMIC TUMOURS AND INFILTRATIVE LESIONS (rare):

- Craniophoryngioma: is associated with visual field defects, and calcification on X-ray
Lymphomo, Langerhans cell histiocytosis, ond sarcoidosis: can result in decreased GnRH
secretion, low or normal serum FSH and LH, and amenorrhoea.
I N.B.: Most women will have 2ry amenorrhoea with one or more neurologic symptoms as
severe headaches, change in personality or marked mood changes.

VI. ENDOCRINE DISORDERS

Some endocrine disorders may be severe enough to cause hypothalamic pituitary ovarian dis-
turbances, leading to transient 2ry amenorrhoea, which is managed by correcting the endocrine
disorder
L. Hypothyroidism: TRH is usually elevated which results in an elevated serum PRL levels.
2. Cushing's Syndrome: increased adrenal activity leads to a hyperandrogenic state.
 Gynaecology 65

CLINICAL ASSESSMENT IN A CASE OF AMENORRHOEA

!- - Proper history taking to differentiate between 1ry and 2ry amenorrhoea.

v - Exclusion of physiologic amenorrhoea (pregnancy, lactation, and menopause)

- General examination including development of 2ry sexual characters

v - Local examination including inspection of the vulva, PV and Bimanual examination if possible

- Pelvic US; for evaluation of the proper development of the uterus and the ovaries

v - Hormonal assays including pituitary hormones (FSH, LH, and PRL), Ovarian hormones (E2 and
PRG), ovarian androgens (Total and free Testosterone), Thyroid hormones (TSH, T3 & T4), ad-
renal androgens (DHEAS).
- Genetic studies and karyotyping may be required to confirm diagnosis in some cases.

A. PRIMARY AMENORRHOEA with Non-Developed 2ry Sexual Characters

v r Exclude delayed puberty: history, clinical examination, FSH, LH, & E2 assays.

v r Exclude Turner syndrome (Gonadal Dysgenesis)via:

F Physicalfeatures suggestive of Turner syndrome (see before)
) Pelvic US for presence of a small uterus and streak gonads
F Elevated FSH & LH levels (Hypergonadotropic hypogonadism)
F Echocardiography for associated cardiac anomalies
F karyotyping (45 XO abnormality) to confirm diagnosis and exclude mosaic Turner cases

B. PRIMARY AMENORRHOEA with Well-developed 2ry Sexual Characters

r Exclude Cryptomenorrhoea due to imperforate hymen or transverse vaginal septum via;

v F Local examination including PR examination

F Pelvic US revealing haematocolpos and haematometra
!;
Differentiation between Mullerian Agenesis and Androgen Insensitivity syndromes

Mullerian Agenesis Complete Androgen

Mayer Rokitansky Syndrome (MRS) I nsensitivity Syndrome (CAIS)
- Karyotype -XX _XY
- Gonads - Ovaries - Testicles (inguinal)
Uterus - Absent - Absent
- Vagina - Short vaginal pouch - Absent or small dimple
- Axillary/pubic hair - Present - Absent/sparse
- Associated anomalies - Renal, skeletal, and deafness - Absent
- Reproduction - Possible oocyte retrieval - Not possible
- Surgical interventions - Vaginoplasty only if short - Vaginoplasty & Gonadec-
_ EST HRT poucn romy
- Not required - Required for appearance
and osteoporosrs
66 Amenorrhoeo

CASES OF SECONDARY AMENORRHOEA

r History and Symptoms:
- Cessation of menstruation after a period of regular menstrual cycles (2ry amenorrhoea)
- Menopausal symptoms and hot flashes in POI & POF
- Headaches and visual field limitation in pituitary adenomas and brain tumours
- Galactorrhoea in cases of Hyperprloactinaemia and pituitary hyperplasia
- Psychiatric disorders and antidepressant drugs
- Hormonal treatment of endometriosis; as OCPs, gestagens, Visanne, & GnRH agonists
- Drug addiction and drug abuse; as with opioids
- History of post abortive sepsis or endometritis following repeated curettage (Asherman
syndrome)
r General Examination: Obesity, hirsutism and signs of hyperandrogenism in cases with PCOS
r Breast Examination: Galactorrhoea in cases with Hyperprloactinaemia
r Hormonal Assays:
- Elevated Serum FSH & LH: in cases with POI or POF
- Abnormal FSH/LH ratio in PCOS

- Elevated serum PRL in Hyperprloactinaemia and Galactorrhoea

- Elevated serum androgens and DHEAS in some cases with PCOS
- Elevated E2 and/or testosterone levels in cases of suspected functioning ovarian tumours
- Thyroid function tests for severe hypothyroid and hyperthyroid disorders
r Pelvic US:
- Increased ovarian volume and characteristic necklace appearance for PCOS
- Small uterus with atrophic endometrium and ovaries in POI and POF
- Ovarian swelling in cases of functioning ovarian tumours (granulosa theca and Sertoli-
Leydig)
r CT and MRI:
- For diagnosing prolactinomas, empty-sella syndrome and craniopharyngioma
r Exclude Asherman's syndrome: TVS, saline infusion sonography, hysterography, and hyster-
oscopy
r Exclude psychiatric disorders: as anorexia nervosa, and severe depression

GUIDELINES IN THE MANAGEMENT OF A CASE OF AMENORRHOEA

The goal for treatment in amenorrhoea is to restore regular menstrual cycles, preserve fertility,
and maintain development of 2ry sexual characters, and allow for satisfactory sexual life in married
women.
1. Treatment of the Underlying Cause of Amenorrhoea: examples include

- lnduction ol ovulation in cases with PCOS and chronic anovulation (Clomiphene and HMG)

- Tredtment of hyperprolactinaemro (Brompcryptine and Cabergoline)

- Hormone replacement therapy (HRT) in POF (oestrogen or combined oestrogen/

progesterone)

- Treotment of severe thyroid disorders (Euthyrox or Thiouracil)

 Gynaecology 6l

2. Surgical treatment in Amenorrhoea:

Relief ol outflow tritct obstruction' hymenotomy or excision of a transverse vaginal septum

Reconstruction of a neo-vagina.' in cases of vaginal agenesis to allow for sexual intercourse

Gonadectomy; in patients with a Y containing gonad, gonadectomy is performed once diag-
nosis is genetically confirmed to avoid the risk of malignant transformation into gonado-
blastoma. However in cases with androgen insensitivity syndrome (testicular feminization)
gonadectomy can be postponed till puberty is complete to allow for normal bone growth.
Such cases will require long term HRT to improve 2ry sexual development and avoid exces-
sive bone loss and asteooorosis.

Trans-sphenoid resection or gammo knife: in some cases with pituitary macroadenoma

and craniopharyngioma

- Loporoscopic Ovorian Drilling (LOD): in some cases of PCOS resistant to medical induction
of ovulation or susceptible to severe forms of ovarian hyperstimulation (OHSS) when
treated medicallv.
HYPERPROLACTINAEM IA AND GATACTORRHOEA

Prolactin is a polypeptide hormone secreted by the lactotrophic cells of the anterior pituitary
gland. lts secretion is controlled by hypothalamic Prolactin inhibiting factor (PlF) known as dopa-
mine, lt is the hormone responsible for initiation and maintenance of lactation in females.
Hyperprolactinaemia; elevated serum Prolactin levels (N: 2.9-29 ng/ml.)
Galactorrhoea; refers to the continuous extrusion of milk from the nipples in the absence of
recent pregnancy or lactation. lt is almost always secondary to hyperprolactinaemia.
AETIOLOGY
1.. Physiologic cctuses: During pregnancy and lactation.
2. Drug induced: Phenothiazine derivatives, Reserpine, psychotropic drugs,
Metclorpramide, and oestrogens. These drugs act by reduction in hypothalamic secretion
of dopamine (PlF).
3. Primory hypothyroidism: due to persistently elevated TRH levels.
4. Prolactin secreting pituitary odenomos (Prolactinomas);
F Microadenomas (tumours < 10 mm) are a common cause for hyperprolactinaemia.
F Macroadenomas (tumours > 10 mm) are rare; may be associated with symptoms
and signs of increased intracranial tension (headache, vomiting, and diminution in
the field of vision).
5. Hypotholamicdisorders:
) Severe stress and psychological conditions.
F Hypothalamic tumours (craniopharyngioma); cause damage to hypothalamus, or
compression on the pituitary stalk interfering with production of prolactin, or
transport of dopamine.
 Amenorrhoea

CLINICAL PICTURE
Hyperprolactinaemia may clinically present by one or more of the following;
a. Mastalgia (breast pain and tenderness), with or without galactorrhoea
b. Menstrual disorders (irregular cycles, 2ry amenorrhoea); due to chronic anovulation
c. Infertility; due to anovulatory dysfunction (PRL interferes with GnRH pulses and with ovari-
an sensitivity to pituitary gonadotrophins).
DIAGNOSIS
1. History: of breast pain (mastalgia), and breast milky secretions (galactorrhoea), with or with-
out menstrua I disturbance a nd/or inferti lity.
2. Clinical Examination: gentle pressure on the nipples results in extrusion of milky secretion.
3. Diagnostic Investigations:
Y Laboratory: elevated serum PRL levels (N: 2.9-29 ng/ml).
r N.B.: markedly elevated levels of PRL > 100 ng/ml suggest PRL secreting adenomas.
) C.T scan and MRI: in cases of persistently high serum PRL levels, or in cases with signs of
increased intracranial tension suggestive of brain tumours.
TREATMENT
a. Stop medications that may cause hyperprolactinaemta.
b. Treat primary hypothyroidism by thyroid hormone replacement therapy (e.g.; Eltroxin)
c. Drugs used for treatment of hyperprolactinaemia (dopamine agonists)
Y Bromo-ergo-cryptine:2mg(1.-2 tablets daily, until normal PRL levels restored).
Y Lisuride hydrogen moleote: O.2mg (1-2 tablets daily, until normal PRL levels restored)
Y Cabergoline:0.5 mg0,l2 tablet twice weekly for 4 weeks, until normal PRL levels re-
stored).
d. Treatment of pituitary adenoma:
Y Medicol treqtment: using dopamine agonists; the primary treatment for most cases.
is
'D Trons-sphenoidol surgery, or Gomma Knife techniques: are reserved to cases with failure
of response to medical treatment, or Macroadenomas with CNS pressure symptoms.

Key Points in Amenorrhoeo

t. Primary omenorrhea moy occur either due to outflow troct disorders, uterine developmental or acquired
conditions, chromosomal qbnormalities, Gonodol or Mulleriqn agenesis, centrql hypothalamic disorders,
or e ndocri ne d isorde rs.
2. Physicot exqmination for the development of 2ry sexuol chorocters, integrity of external genitalia, pres-
ence of the uterus ond gonads by IJS and hormonol qssays are the key points for proper diagnosis, ond
mqnqgement.
3. In qbsence of uterus and presence of breosts, koryotype will differentiqte between Mullerion ogenesis
(46XX), ond testiculor feminizotion (46XY).
4. Secondary omenorrhoes is mostly due to onovulotory disorders nomely PCOS, hypothalamic dysfunction,
or hyperprolactinoemia, whenever pregnoncy hqs been excluded. Ashermonn ond Sheehan syndromes
qre,rore couses
5. Pituitory FSH and LH levels will differentiote between hypergonodotrophic ond hy- pogonodotrophic
amenorrheo, while proloctin levels will exclude hyperproloctinaemio.
6. Treqtment of omenorrhoeo is specific to the couse, ond may include hormone replacement theropy, in-
duction of ovulotion, treotment of hyperprolactinaemio, correction of thyroid and odrenol disorderS.
7. Surgicol treatment includes correction of outflow trqct disorders, creotion of neovogino ,and Gonodecto-
my in cases with Y chromosome disorders.
8. Hyperproloctinqemiq is o common cause of 2ry qmenorrhoeo treqted medically by dopamine ogonists in
the vast mojority of cases.
 - Hirsutism

DEFINITIONS
. Hirsutism; Excessive growth of ondrogen dependent sexuolharr (present on the upper lip, chin,
inner thighs, limbs, chest, abdomen and pubic triangle).
. Hypertrichosis; Excessive growth of ondrogen independent hair (as in the forearm and legs)
. Virilization; is hirsutism associated with other signs of hyperandrogenism such as; increased
muscle mass, cliteromegaly, temporal baldness, and voice deepening.
CLASSIFICATION
1. Mild: fine pigmented hair affecting the face, chest, abdomen and perineum.
2. Moderate: coarse pigmented hair affecting same areas as in mild cases.
3. Severe: coarse pigmented hair affecting the face (complete beard), tip of nose, ear lobes, chest,
abdomen, and perineum.
AETIOLOGY
1. ldiopathic: increased hair follicles sensitivity to normal female androgen levels
- Increased receptor activity in the skin, or
- Increased activity of the enzyme 5 alpha reductase (responsible for conversion of T into DHT
which has a more potent action than T).
2. Adrenal gland causes:
- Congenital adrenal hyperplasia (partial or complete 21 hydroxylase deficiency...,).
- Adrenal tumours: secrete DHA, DHAS, and rarely Testosterone.
3. Ovarian causes:
- PCOS, hyperthecosis, and stromal cell hyperplasia (increased ovarian androgens).
- Androgenic ovarian tumors as sertoli lyedig cell tumor, adrenal rest tumor, hilar cell tumor, and
gonadoblastoma. (increased testosterone prod uction )
4. Mixed ovarian & adrenal hyperandrogenism: (30-40% of cases)
- Increase ad rena I prod uction of a nd rogen leads to inhibition of follicu la r matu ration & induction
of premature atresia with increased production of ovarian anorogen.
5. Pituitary gland:

- Cushing's syndrome due to increase production of ACTH.

Acromegaly due to increased production of GH.
6. Androgenic drugs: Rarely, long term use of drugs with androgenic side effects (as Danazol in en-
dometriosis) may cause hirsutism and virilizing effects.
INVESTIGATIONS OF A CASE OF HIRSUTISM
a. Hormonal assays
L. Plasma T level (n= 0.2-0.8 ng/ml),levels > 2 ng/ml suggest androgen secreting tumor.
2. Free T level (n= !-3% of total T) it is a good index for androgenicity.
3. DHAS (n= 1500-2500 ng/ml), levels > 9000 ng/mlsuggests adrenar tumour.

69
70 Hirsutism

b. Radiological investigations:
- CT or MRI on the pituitary gland.
- IVP and abdominal US for adrenal tumor.
- Pelvic US, for PCOS, and virilizing ovarian tumours.
TREATMENT OF HIRSUTISM
A combination of hormonal suppression of hair growth and mechanical hair removal offers the
most complete and effective treatment for patients with hirsutism. Once terminal hair has been
established withdrawal of androgen does not affect the established hair pattern
1. Elimination of specific causes

- Removal of androgen secreting ovarian or adrenal tumours

- Elimination of drugs suspected to contribute to the abnormal hair growth
- Treatment of Cushing syndrome, thyroid disease, or hyperprolactinaemia
2. Hair removal techniques
- Shaving, tweezing, waxing, and use of depilatories, performed at repeated intervals
Bleaching is effective for mild hair growth
- Permanent destruction of hair follicles by electrolysis or by laser is reasonably effective.
3. Suppression of androgen synthesis

- Oral contraceptive pills (OCPs), containing combined low dose E and P, decrease ovarian an-
drogen production, increases SHBG, and decrease free T levels. Progestins may also inhibit 5-
alpha reductase activity
- Corticosteroids (dexamethazone 1-5 mg/dayl; induce suppression of adrenal androgen pro-
duction in severe cases of CAH. Long term side effects include osteoporosis, diabetes mellitus,
and avascular necrosis of the hip.
- Spironolactone is an aldosterone antagonist used frequently as a diuretic that also inhibits
5alpha reductase and variably suppresses ovarian and adrenal synthesis of androgen
- Cypretorone acetate is a potent progestin and antiandrogen that inhibits LH and decreases
androgen levels. lt is used for 10 days each cycle. Diane 35 is an OCP that uses cypretorone
acetate as a progestin and is widely used in treatment of hirsutism in females that request -
contraception.
4. Androgen receptor blockers

- Androgen receptor blockers inhibit binding of DHT to androgen receptors thus directly inhib-
iting hair growth. When combined with OCPs or progestins further benefit may be obtained.
- Cimetidine: competes with androgen at the receptor site. Dose: 300mg 5 times daily.
Key Points in Hirsutism

L. Hirsutism is mostly idiopathic in the maiority of coses.

2. It moy be one of the androgenic monifestations of PCOS, or otherwise secondory to endocrine disorders in
the pituitary, thyroid, or odrenol glonds
3. Diognosis is bosed on clinical exomination for the site, density, ond charocter of the hoir
4. Loborotory investigations oim qt meosurement of testosterone qnd DHEA levels, together with exclusion of
adrenal, thyroid, ovorion, or pituitory contribution.
5. Pelvic tJS, MRl, qnd CT ore useful in excluding ovorion, odrenol & pituitory tumours.
6. Treotment of hirsutism includes; eliminotion of the couse, suppression of ondrogen synthesis, use of on-
drogen receptor blockers, qnd mechanicol removol by depilation.
 Chronic anovulotion
Polycystic Ovary Syndrome (pCOS)
Luteal phase defect (LPD)
Ovorio n Hy pe r-sti m ulation Synd rom e (O H SS)

ANOVULATION
Ovulatory menstrual cycles are characterized by being regular, rhythmic, occurring at predicta-
ble intervals due to the fixed span of its luteal phase (about 14 days from ovulation to onset of the
next menses). Anovulatory cycles on the other hand are commonly prolonged, irregular, and unpre-
dictable, due to the variations in the follicular phase duration in absence of regular follicular growth
and maturation.

Anovulation, whether spontaneous or induced, sporadic or chronic, is the commonest cause for
menstrual irregularities and secondary amenorrhoea in women, especially at the premenopausal
and child bearing periods.

AETIOLOGY OF CHRONIC ANOVULATION

Anovulation is caused by failure or disturbance of hypothalamic-pituitary-ovarian axis it will

therefore have the same aetiology as amenorrhoea excluding uterine and vaginal causes (see physi-
ology of the menstrual cycle Ch 4 and amenorrhoea chapter 7).

WHO CLASSIFICATION OF OVUTATORY DYSFUNCTION

I GROUP 1: Hypothalamic / Pituitary Failure (Hypogonadotropic Hypogonadism): as in Kallman
syndrome, Sheehan's syndrome, pituitary tumours, stress or exercise induced amenorrhoea
' GROUP 2: Hypothalamic I Pituitary Dysfunction (Eugonadotropic Hypogonadism): as in poly-
cystic Ovary Syndrome (PCOS)
I GROUP 3: End Organ Failure (Hypergonadotropic Hypogonadism): as in primary ovarian In-
sufficiency (POl) formerly called primary ovarian failure (POF), and Turner syndrome

PATHOLOGICAT CAUSES OF OVULATORY DYSFUNCTION:

1. Hvpothaf amic causes: (decreased GnRH putse frequency ond amptitude)
a. Functionol disorders;
- Emotionalstress in its severe forms, especially if associated with psychic disturbances
- Exercise; when excessive and under stress as with athletic training and competition
- Marked weight loss reachin gto <20% of ideal body weight . e.g.; onorexia nervosa
- severe psychological disturbances; including depression, and pseudocyesis
b. Organic lesions;
- Brain tumours, cystic malformations, and infiltrative brain disease
- Excessive scarring; after brain surgery, or irradiation.
c. Congenitol disorders;
- Kallmann's syndrome; anosmic primary amenorrhoea with absent Gn-RH

l1
l2 Chronic Anovulotory Disturbonces Pcos And Luteql Phase Defect

2. Pituitarv Causes: (disturbed FSH & LH production)

a. Pituitory adenomos:
- Prolactinomas (prolactin secreting adenomas); causing hyperprolactinaemia, are responsible
for >9O% of pituitary causes for anovulation. Microadenomas < 10 mm are far more common
than macroadenomas >10 mm
b. Empty sello syndrome; causing hyperprolactinaemia (see amenorrhoea)
c. Pituitary insufficiency; as occurs in Sheehan syndrome or Simmond's disease (see amenorrhoea)

3. Ovarian Causes:
a. Polycystic ovdry syndrome (PCOS); is one of the commonest causes for anovulation encountered J
especially in infertile females. Patients will present by 2ry oligomenorrhoea, with or without signs of
hyperandrogenism. PCOS is characterized by an abnormal LH/FSH ratio > 2:1- (see later in PCOS).
b. Premature ovorion failure, insensitive ovary syndrome, ond gonadal dysgenesis; due to absence
or resistance of ovarian follicles to FSH stimulation. These conditions are characterized by high men-
opausal levels of FSH & LH with low serum E2 levels
c. Bilateral surgicol removol, or destruction, of the ovaries by irradiation.

4. Endocrine Disorders:
- Thyroid disorders; as hypothyroidism
- Adrenol disorders; as Cushing's disease (adrenal hyperplasia)

5. Drug induced effect:

OCPs; decrease FSH production, inhibit Gn-RH, and LH surge
- Progestin theropy ond androgenic drugs os Donozol in endometriosis treatment.
- Gn-RH ogonists; for suppression of FSH and LH as in treatment of endometriosis.
- Drugs that induce hyperproloctinoemio; e.g.; psychotropic agents, etc.
- Antihypertensive drugs;(reserpine and alpha methyl dopa), opiates and barbiturates.
- Chemotheropeutic ogents; are some times followed by a transient period of anovulation
DIAGNOSIS OF CHRONIC ANOVULATION

CLINICAL PRESENTATION
1. Amenorrhoea or oligomenorrhoea (mostly 2ry, rarely 1ry amenorrhoea)
2. Infertility whether primary or secondary
3. Dysfunctional uterine bleeding (DUB), e.g.; metropathia heamorrhagica
4. Hirsutism which may rarely be associated with signs of virilization.
DIAGNOSIS OF ANOVULATION
A. History: suggestive of irregular cycles, with periods of 2ry amenorrhoea or oligomenorrhoea
is strongly suggestive of anovulatory dysfunction, but not diagnostic.
B. Symptoms: Absence of symptoms suggestive of ovulation, as primary dysmenorrhoea,
midcycle pain, or spotting, is only assumptive but not reliable in diagnosis of anovulation.
C. Test for detection of ovulation (see later).
 Gynaecology /)

TESTS FOR DETECTION OF OVULATION

1. Basal body temperature charts (BBT):
A daily record of the patient's oral temperature is taken in the morning just before rising
from
bed in two or three successive cycle. A temperature rise is expected to occur in the
luteal phase of
ovulatory cycles due to progesterone induced thermogenic effect. These charts although
cheap and
easily applicable, yet have the disadvantage of being easily biased by other factors
that mav cause
any rise in BBT throughout the month.

- ovulotory cycles show a biphasic BBT chart with a rise in temp (0.2-0.3 C) in the luteal
phase of the cycle. This temperature rise declines few days before the
next cycle.
- Anovulatory cycles will show a flat monophasic BBT chart due to absence of thermogenic
progesterone therma I effect.

Fig. 8-1: Biphosic BBT

2. Ultrasound monitoring of ovulation (Folliculometry):

Serial TVS scans, in the follicular phase, allow monitoring growth, maturation,
and ovulation
(rupture of dominant follicles at a mean diameter of 1-8-24 mm), and tracing
early CL formation.

Fig. 8-2: Preovulotory follicle by TVS

74 Chronic Anovulotory Disturbqnces Pcos And Luteal Phase Defect

3. Mid luteal serum progesterone assay (MLSP): meosured by RIA;

MLSP is performed 7 days after ovulation, or day 21, of the cycle (maximum CL activity).

- Levels <5 ng/ml suggest anovulation

- Values >10 ng/ml suggest ovulation with adequate CL function.

- Levels 5-9 ng/ml suggest ovulation but with inadequate CL function (LPD)

4. Premenstrual endometrial biopsy (PEB):

without cervical dilatation as an office procedure, using a small caliper
PEB can be performed -
cannula (Pippele), or under general anaesthesia if cervical dilatation is mandatory (see D&C opera-
tion). PEB done 2-3 days prior to menstruation will reveal either;
- Secretory endometrium, in ovulatory cycles due to progestational effect of the CL.

- Proliferotive endometrium, in anovulatory cycles.

- Poor secretory changes, in cases of LPD
r N.B: Urinary LH kits can detect the timing of LH surge that immediately precedes ovulation -

TREATM ENT OF ANOVU LATION

Induction of ovulation can be achieved using oral drugs as Clomiphene Citrate, Tamoxi-
fen, Cyclofenil, Letrozole, or lM injection of human Pituitary Gonadotropins or Human Chori-
onic Gonadotropins. lt can also be achieved surgically via laparoscopic ovarian drilling (LOD)
in special cases
A) MEDTCAL tNDUCTION OF OVULATION
1. CLOMIPHENE CITRATE: (Oral tablets)
Clomiphene Citrate (CC); is a non-steroidal compound closely related to diethyl stilbosterol (DES),
but has no estrogenic effect on short term use.
- Mode of oction: lt competes with endogenous E2 for its hypothalamic receptors leading to
their blockage. The hypothalamus reacts by increasing its pulsatile release of GnRH to com-
bat this artificially induced hypo-oestrogenic state.

- Increased GnRH pulse frequency and amplitude increases pituitary FSH production, which
directly stimulates follicular growth and maturation leading to production of increasing
amounts of E2 levels.
- Markedly elevated E2 levels will exert a positive feedback on LH stimulating a strong LH surge
(after CC has been stopped), finally leading to the release of one or more of the mature oo-
cytes (ovulation).
, Dosoge:50 mg oral tablets, twice daily for 5 days starting day 3, 4 or 5 of menstruation. Dose
can be increased up to 200 mg/day (4 tablets)

- tndicotions; CC is the first line of treatment in onovulatory conditions with normql FSH pro-
duction and intact hypothalamic pituitary axis as in cases of PCOD, and post pillamenorrhea.
- Success rdtes: CC is successful in induction of ovulation in around 85% of cases.
 Gynaecology 15

- Side effects:
Vasomotor flushes, nausea, headache, and visual disturbances
Increased risk of twin pregna ncy (1,0%), and of multifetal pregnancy (1%)
Ovarian hyperstimulation (OHSS), grade l-ll, with mild pelvic pain and discomfort
Anti-estrogenic effects on the endometrium may cause LPD, and on cervical mucous
may cause hostile cervical mucous only repeated use.
o Tamoxifen: is a weak anti-oestrogen (used in treatment of oestrogen receptor positive breast
cancers after mastectomy) that acts by a mechanism similar to cC.
Dosage: 10-40 mg daily orally (1-4 tablets) for 5 days starting from the 2nd day of cycle.
. Cyclofenil: lt is a compound chemically related to CC with a weak oestrogenic effect.
- Dosage: 400 mg twice daily, orally, for 5 days starting 5th day of the cycle.
. Letrozole:
Letrozole is an aromatase inhibitorthat blocks conversion of testosterone to oestrogen, lead-
ing to increased pituitary FSH, and stimulation of follicular growth. .
2. PITUITARY GONADOTROPINS (FSH & LH DERIVATIVES): (repeated l.M. injections)
A' Human menopausal Gonadotrophins (HMG): derived from urine of menopausal women. lt
contains 75 lU FSH + 75 tU LH.
B. Purified Urinary FSH; derived from urine of menopausal women and contains only one lU of
LH (75 lU FSH + one lU LH). They are more suitable for cases with high endogenous LH as those
of PCOD, to minimize possibility of severe OHSS, and in IVF/|CS| protocols (see assisted repro-
duction in infertility).
C. Synthetic FSH; containing no LH is prepared by recombinant DNA technology, used mostly in
IVF/|CSI protocols in same indications as purified urinary FSH.
o Mode of oction of gonodotrophins;direct stimulation of growth and maturation of ovarian pri-
mordial follicles, with production of increasing amounts of E2.
. lndications:
- CC resistant cases
- Cases with hypogonadotrophic anovulation (low FSH / LH levels)
- In lCSl/lVF/ET protocols to stimulate growth of multiple follicles.
- Purified and synthetic FSH are suitable both for cases with high endogenous LH (as pCOS),
and in lcSl protocols to help retrieval of largest number of oocytes.

' Dosage: repeated l.M. Injections given from mid-follicular phase of the cycle until complete fol-
licular maturation. Doses are repeated with TVS monitoring of follicular growth to avoid the
complications of severe OHSS (see laterl.
. Side effects: Same as those with CC however;
OHSS is more frequent especially severe forms (grade lll-lV OHSS).
Marked increased risk of twin and multifetal pregnancy (1,0-30%)
- No adverse effects on cervical mucous or endometrium
76 Chronic Anovulotorv Disturbonces Pcos And Luteql Phqse Defect

3. HUMAN CHORIONIC GONADOTROPINS (hCG): (single l.M. injection)

. Preporotion and oction: hCG is prepared from urine of pregnant women. lt has a strong LH ac-
tion that induces an artificial LH surge leading to ovulation & oocyte release
. lndication; to assist ovulation especially in CC or HMG induced cycles.
o Dosage ond timing:2 ampoules 5000 m/lU each, given by l.M. injection as one shot after full
oocyte maturation (size of dominant follicle > 18 mm by TVS).
. Side effects: OHSS, especially if given after HMG (see later)
4. GONADOTROPTN RELEASTNG HORMONE (GN RH)ANALOGUES:
. Preporqtion.'GnRH agonists are synthetic decapeptide forms of GnRH, given either by
repeated S.C. injection or as a nasal spray.
o Dosage & Mode of action: In small repeated doses they act as GnRH thus increasing FSH produc-
tion, and inducing follicular maturation. In larger doses (long acting preparations), they induce
initial FSH stimulation, followed by down regulation of hypothalamic receptors, with consequent
suppression of FSH & LH production.
. lndications: They are used mostly in IVF & lCSl protocols to prevent premature ovulation via LH
suppression, allowing for timed retrieval of maximum number of eggs.
5. COMBINED THERAPY
. CC/HMG/hCG: Adding CC to HMG/hCG has the benefit of minimizing the dose of HMG thus re-
ducing both the cost and chanced for OHSS.
o GnRH/HMG/hCG is used in practice in various doses and different protocols of stimulation espe-
cially in IVF/ICSl stimulations protocols.
5. ADJUVANT DRUGS USED TO ASSIST IN INDUCTION OF OVULATION:
A. Bromocryptine:0.2 mg 1-2 tablets daily, or Cabergoline:0.5 mg t/2tablet twice weekly in
cases of hyperprolactinaemia (see amenorrhea)
B. Metformin: 500-800 mg daily in cases with insulin resistance (see PCOS)

C. Thyroid extract: Eltroxin 50-150 ug daily in cases of hypothyroidism

D. Corticosteroids: in cases of Addison's disease, adrenogenital syndrome, and PCOS

B)SURGTCAL PRODECURES USED FOR TNDUCTION OF OVULATION

. Loparoscopic Ovarian drilling (LOD): LOD is a procedure in which a diathermy needle is used to
make multiple small punctures in the surface of the ovary via laparoscopy
- Elfect of drilling: LOD may decrease ovarian androgen environment resulting in spontaneous
ovulation, or at least minimize doses of CC/HMG required for stimulation.
lndicotions: LOD is reserved to selected PCOS cases that are resistant to stimulation or may
require large doses of HMG with high costs and increased risk of OHSS.
- Disodvantages: The use of LOD is hindered by its time limited effect on ovulation (3-6
months), and its potential for creating ovarian and peritubal adhesions.
 Gynaecology 71

POLYCYSTTC OVARY SYNDROME (PCOS)

In 1935 Stein and Leventhal described a group of patient showing cystic changes in their ova-
ries in association with amenorrhea, hirsutism, obesity, and infertility.
PCoS is the more recent description of the syndrome which is characterized by 2 or more
of:
Chronic anovulation; presenting clinically by 2ry amenorrhoea or oligomenorrhoea
- Hyperandrogenism; (hirsutism, elevated serum LH, and increased free Testosterone levels)
- Characteristic ultrasound morphology; increased ovarian size and volume, with peripherally
arranged small follicles in a dense stroma (necklace appearance).

The pet ipherolly arranged multiplesmall Enlarged ovaries v:ilh pearlv white sntooth strrfnce os
/b I I ic I es (Neckl ace a ppea rctncel see n dtt r i n g la ptt ros to 1:r,t

Fig. 8-3: PCOS

PREVALENCE AND AETIOLOGY:

- PCOS may affect up to 5-10% of women in the reproductive age.
- lt is the commonest ovarian cause for 2ry amenorrhoea, chronic anovulation, and infertility.
The exact aetiology of PCOS remains unclear however a familial background is suggested with a
special gene related to its development.
PATHOGENESIS OF PCOS
PCOS is characterized by a triad of; high LH, high serum androgen, and high plasma insulin:
A. High LH:
- Aetiology: it is due to increased LH pulse and frequency. lt is manifested by an abnormally high
LHIFSH ration (> 2:1).
- Effect: it stimulates secretion of androgen by ovarian theca cells, and inhibits aromatase en-
zyme responsible for conversion of ovarian androgen into oestrogen, resultin g in increosed
ovorian androgen.
B. Hyperandrogenaemia :
- Aetiology: it is due to stimulation of theca cells (by both high LH and high insulin levels), togeth-
er with inhibition of aromatase enzyme
- Effect: excess ovarian androgen leads to;
L. Atresia of developing follicles leading to anovulation and amenorrhoea
2. Hyperandrogenaemia; high serum androgen
3. Hirsutism
4. Excess androgen is converted in fat cells into oestrone (peripheralconversion). This results
in acyclic increase in oestrone which leads to
- Increased pituitary LH, and suppression of FSH
Unopposed oestrogen leads to endometrial hyperplasia or carcinoma
78 Chronic Anovulotory Disturbonces Pcos And Luteal Phase Defect

C. Hyperinsulinaemia:
- Aetiology: PCOS may be associated with peripheral insulin resistance disorder leading to hy-
perinsulinaemia.
- Effect: hyperinsulinaemia leads to;
1. Increased sensitivity of ovarian theca cells to LH, thus increasing LH induced androgen
production by the ovaries
2. Decreased aromatase enzyme activity leadingto excess ovarian androgen production
3. Decreased production of SHBG leading to increased free androgen substrate.

DIAGNOSIS OF PCOS
A. Clinical presentation:
- 2ry amenorrhea, oligomenorrhoea, and or infertility (chronic anovulation)

- Hyperandrogenism (Hirsutism affecting face, chest and inner thighs)

- Obesity with tendency to abnormal glucose tolerance.

- DUB may occur in cases with chronic anovulation associated with endometrial hyperplas-
ia.

B. Laboratory investigations:
- Elevated LH levels with normal FSH lead to an abnormal LH/FSH ration of >2,

- Elevated levels of plasma E1-, androstenedione (AD), and free Testosterone (FT).
- Hyperinsulinaemia due to associated increased insulin resistance.

C. Uftrasound diagnosis: (Adam's criteria)

- The ovaries are increased in size and volume.

- The ovaries show central dense stroma surrounded by small follicles (2-10 mm in diame-
ter) peripherally arranged giving the characteris|.c neckloce oppeoronce.
- No dominant or mature follicles are present due to chronic anovulation.

- US picture of PCOS may be encountered in up to 25% otherwise normal females.

D. Laparoscopic appearance: Enlarged ovaries with thick capsule, and absent gyrii due to ab-
sence of ovulation stigma on ovarian surface (oyster shell ovory), see Fig 8:2

Fig. 8-4: PCOS by TVS Fig. 8-5: PCOS by Loporoscopy

 Gynaecology 79

LONG TERM RISKS OF PCOS

v
1. Increased risk for diabetes mellitus, obesity, hyperlipidaemia, and cardiovascular disease.
2. Increased risk of endometrial hyperplasia (EH); due to increased oestrogen effect on the endo-
metrium unopposed by progesterone.
v 3. Increased risk of endometrial carcinoma if atypical EH develops.

MANAGEMENT OF PCOS
v 1. Weight reduction; In obese females a reduction of 5-tO% of body weight, reduces insulin and
androgen and improves response to therapy, and may by itself re-establish ovulation.
2. Hormone therapy: In cases with menstrual disorders as amenorrhoea or DUB;
v a.Cyclic gestagen therapy for 10 days every cycle (day 1,6-25), to induce a regular 28-30
days cycle (e.g. medroxy progesterone acetate 10 mg per day)
b'Combined OCP (day 5-25), to establish regular cycles in cases not requesting pregnancy
v. 3. Induction of ovulation for infertility (see details in treatment of chronic anovulation).

v :,:iliiil:::J:':,rffi,::'','i?;1:l:?'#y,:""ffffi'il::,1";"-",ili;l*il;J;::
the least risk for ovarian hypertstimulation syndrome (OHSS).
v
- Human MenopausalGonadotropins (HMG); given as repeated lM injections, is effective in

_ ffi:;il:':::::"#Hl#1,fi:1,'JL]1.0".,
compared to HMG due to their minimal or absent LH content.
have,ower incidences of oHSS

- lM injections; can be used tofacilitate rupture of follicles when they reach maturity
hCG
4' Insulin sensitizing drugs (metformin 500 mg/day orally) improve insulin sensitivity, thus decreas-
ing hyperinsulinaemia and androgen levels. Such drugs also increase sensitivity of PCO to endoge-
nous FSH and drugs like CC, and may by itself establish ovulatory cycles.
5. Corticosteroid therapy to suppress ACTH production in case of adrenal hyperandrogenism.
5' Surgical treatment via laparoscopic ovarian drilling (LOD); aims at decreasing ovarian androgen
production. However, adhesion formation is an unfavorable side effect of surgery.
v
7. Hirsutism: Cypretorone acetate, laser depilation, or electrolysis (see later for details)

Key Points in PCOS

1. PCOS is the commonest cause of pathologic 2ry amenorrhoea occurring in 5-IO% of females.
2. Besides menstrual disorders it may present with infertility, hirsutism, and obesity.

3. Diagnosis of PCOS is based on combination of clinical, laboratory, and US criteria.

4. Menstrual irregularities are management by hormonal therapy (gestagens or combined OCps),

while anovulatory infertility is managed by induction of ovulation.
5' Weight reduction in obese patients, and insulin sensitizers as metformin, play an adjuvant role in
improving response of patients to various ovulation induction protocols.
6' Surgical treatment by LOD should be reserved to highly selected cases resistant to all other stim-
ulation protocols, to avoid ovarian destruction and creation of peri-ovarian adhesions.
80 Chronic Anovulotory Disturbonces Pcos And Luteol Phose Defect

ovARtAN HypER-STtMULAT|ON SyNDROME (OHSS)

OHSS is an iatrogenic disorder that describes the occurrence of ovarian multicystic enlargement
secondary to the use of drugs for induction of ovulation, namely HMG/hCG. lt is classified into four
grades according to severity of symptoms.
. Mild forms (Grades l-ll);
- These cases may be associated with variable degrees of ab-
dominal pain and distension, oedema, mild ascites, hypoten-
sion, and oliguria.
- Cases are managed by rest, reassurance, follow up, and symp-
tomatic treatment
o Severe forms (Grades lll-lV); Fig 8-5 OHSS Grade ll
- These cases may be associated with fluid shift from intravas-
cular to extravascular compartment leading to severe ascites, pleural effusion, hypoalbumi-
naemia, electrolyte imbalance, haemoconcentration and changes in blood coagulability with
tendency to DIC and increased risk of pulmonary embolism.
- These life-threatening cases are best managed by hospitalization, restoration of fluid and
electrolyte imbalance, use of anticoagulants and sometimes tapping for aspiration of ascites.
Diuretics are avoided as they will increase haemoconcentration with risk of thrombosis.
- Prevention of severe OHSS could be achieved by both carefulTVS monitoring of HMG doses
during stimulation, and withholding hCG injections in cases with Gr ll-lll hyperstimulation.
LUTEAL PHASE DEFECT
Luteal phase defect (LPD); is a condition in which the endometrium shows poor secretory
changes in the luteal phase of ovulatory cycles. These cycles are characterized by either low proges-
terone levels in the luteal phase, or short luteal phase duration (<11- days interval between ovula-
tion and menstruation), or both.
Sporadic LPD may occur in isolated cycles in normally ovulating women while recurrent LPD may
be a cause of infertility in 3-4% of cases. The incidence is much higher in cases with recurrent first
trimesteric abortion.
Aetiology
a. Inadequate follicular phase FSH production or inadequate FSH/LH ratio at time of ovulation.
b. Hyperprolactinaemia (decrease FSH and blunted LH surge)
c. Prolonged use of CC for induction of ovulation (decreased endogenous FSH release)
Diagnosis
Biphasic BBT chart showing a short luteal phase
- Low midlutealserum P levels (5-10 ng/ml)
- Dated PEB showing secretory changes with a lag > 2 days behind that for a normal cycle
Treatment
- Progesterone support throughout luteal phase using oral or vagi-
naltablets
- Repeated hCG injections in the luteal phase to stimulate CL pro-
gesterone secretion
- Bromocryptine or Cabergoline for cases with elevated serum PRL
levels
- Drugs used to stimulate super ovulation (CC/HMG/hCG)
 N atu ral defe nse mechq nisms Cervicitis
Predisposing Foctors Voginol discharge
Vaginitis

VAGINAL FLORA AND VAGINAL PH

r Vaginal flora (ecosystem) of a normal asymptomatic reproductive age woman incluoes;

Y Multiple oerobic or focultotive species

D Obligate anoerobic species. Ratio of anaerobes to aerobes is approximately (10:1).
I Nonpathogenic bacteria; normally inhabit the vagina without causing infection include;
Y Group B streptococcus
Y Escherichiq coli. ond
Y Lactobacilli.
I Lactobacillus acidophilus is the dominant bacterium in a healthy vagina. They play a critical role
to maintain the normal vaginal environment through:
Y Production of loctic acid responsible for acidic vaginal environment (PH: 3.8-4.5).
Y Lactic ocid and hydrogen peroxide produced are toxic to anaerobic bacteria.
I Glycogen content of vaginal mucosa provides nutrients for vaginal flora, especially lactobacilli,
thus maintaining an acidic vaginal PH.
N.B.: Decreased glycogen content of vaginal mucosa will result in diminished acid production,
leading to a rise in vaginolPH that becomes alkaline (pH: G.5- 7.0).

Common voginol FLORA

Aerobes
F Gram positive: Lactobacillus spp, Diphtheroids, Staphylococcus aureus, Group B
streptococcus, Enterococcus faeca I is.

F Gram negative: E. coli, Klebsiella spp, Proteus spp, Enterobacter spp, Pseudomonas spp

Anaerobes
F Gram positive: Peptostreptococcus, Clostridium, Lactobacillus spp, Gardnerella vaginalis
) Gram negative: Bacteroides spp, Bacteroides fragilis, Fusobacterium spp
) Yeast: Candida albicans, Candida tropicalis, Torulopsis glabrata

8l
82 Femole Lower Genital Tract lnfections

NATURAL DEFENSE MECHANISMS AGAINST GENITAL TRACT

TNFECTTON (GTr)
A. Vaginal PH: The slightly acidic vaginal PH acts as an unfavorable medium for many pathogenic
organisms. Changes of vaginal PH towards alkaline environment, renders the vaginal epithelium
more vulnerable for infection.

B. Vaginal epithelium: the thick stratified squamous epithelium lining of the vagina is protective
against pathogenic organisms and toxic substances. Normal oestrogen levels further protects it
against atrophic changes.
-
C. Cellular and Humoral immunity play a role in normal vaginal defense mechanisms

FACTORS THAT PREDISPOSE TO VAGINAL INFECTIONS

1. Alterations in the normalVaginal PH:

- Menstruol blood flow; results in a more alkaline vaginal PH

- Vaginol douching; unnecessary routine vaginal douching alters vaginal PH

- Decreosed oestrogen; as in childhood and menopause, may lead to lowered prevalence of

lactobacilli leading to decreased glycogen content and higher vaginal PH

- Sexual intercourse; may lead to higher vaginal PH due to the alkaline PH of the semen
2. lmbalance between vaginal bacterialflora and Candida species

- Recent treotment with brood spectrum antibiotics

3. Decreased resistance of vaginal epithelium

- Atrophic voginal epithelium: as in childhood and menopause.

- lntroduction of new orgonisms; as with STDs that alter vaginal microbiology.

- Foreign bodies; as vaginal tampons, IUD threads, and neglected pessaries in cases of POP.

4. Suppression of immune system: as with HIV infections, autoimmune disorders, corticosteroid

therapy, and diabetes mellitus, may all result in recurrent vaginal infections especially
Candidiasis.

COMMON TYPES OF VAGINITIS

Vaginitis, with or without vaginal discharge, is one of the commonest complaints encountered
in gynaecologic practice. lt commonly occurs in different periods of women's life:

a. ln the child bearing period:

F Bacterial vaginosis (BV).
F Candida vaginitis (CV).
F Trichomonas vaginalis (TV).
b. In childhood: as Vulvovaginitis of childhood.

c. In menopausalwomen: as Senile or Atrophic vaginitis.

 Gynaecology 83

VAGINITIS IN THE CHILD BEARING PERIOD

. 1. BACTERIAL VAGINOSIS
Bacterial vaginosis (BV) is the commonest bacterial vaginal infection encountered in
gynaecologic practice (previously known as non-specific vaginitis and Gardnerella
vaginitis).
It is also the commonest cause for non-irritant, malodorous vaginal discharge encountered
in women attending routine gynaecologic and obstetric clinics.
r AETIOLOGY AND CAUSATTVE ORGANTSMS
Anaerobic bacteria normally found in the vagina including:
F Gardnerella vaginalis (GV)
D Bacteroides species and Mycoplasma hominrs.
I BV represents a state of unexplained alteration of the normalvaginalflora, where;

- Anaerobic organisms markedly increase in concentration (thousands of times)

- Hydrogen peroxide producing lactobacilli markedly decrease (or even disappear)
- The vaginal PH rises, ranging 4.7-7.O (alkaline pH).
I Anaerobic bacteria produce enzymes that break peptides to amino acids and amines, resulting
in
its characteristic discharge and odour.
r BV is not sexually acquired hence the sexual partner does not need to be treated.
CtINICAL PICTURE (symptoms & Signs)
r Asymptomatic in 50% of women.
r Vaginal discharge is the commonest symptom. lt is
usually profuse, thin, homogenous, non-irritant, s" uSmg
malodorous discharge that is adherent to vaginal I

stippling of
walls. lt may be yellowish grey or white in colour.
cYtoplssm duo
r Characteristic fishy amine smell is especially to sdherent
noticeable around the time of menses or following coccobacilli
sexual intercourse.
Fig 10-L: Clue cells in BV
DTAGNOSTTC tNVESTIGAT|ONS (AMSET CRtTERtA)
1' Microscopic examination of a saline wet preparation of vaginal secretions; reveal
characteristic clue cells which are vaginal epithelial cells heavily coated with bacteria
obscuring its borders (fig.L1-1.). The positive predictive value for this test in diagnosis of BV
reaches almost 95%
2. Addingto%KOHtoafreshsampleof vaginal secretionsreleasesvolatileaminesthathavea
characteiistic fishy odour (whiff test).
3' Vaginal PH > 4.5: results from diminished acid production due to markedly decreased
number of lactobacilli.
N.B.: Trichomonas vaginalis infection may be also associated with anaerobic overgrowth,
increased
pH, and release of volatile amines, therefore women diagnosed with BVshould
have no microscopic
evidence of Trichomoniasis.
N.B.: Cultures from a vaginal swab yields mixed anaerobes and a high concentration
of Gardnerella
vaginalis (GV). However GV con be grown from over 5o% of women with normol voginal flora,
therefore its presence olone is not diagnostic of BV.
84 Femole Lower Genitol Troct lnfections

TREATMENT OF BV (CDC 2010)

Oral Preparations:
- Metronidazole tablets: 500 mg twice a day for 7 daysx,
intravaginal Preparations:
Metronidozole gelvaginally: 0.75%, one full applicator (5 e) daily for 5 days, OR
Clindomycin cream voginally:2%o, one full applicator (5 g) daily 7 dayst
During Pregnancy:
- Voginol Clindamycin may be used from first trimester throughout pregnancy.
- Orol Metronidozole may be used in 2nd and 3'd trimesters safely.
f Clindomycin cream is oil-based ond might weoken latex condoms and diaphragms for 5 days ofter
use.
N.B.:
r Cure rates in non-pregnant women with BV will reach up to 80-90% at one week.
r Recurrent infection may occur in up to 30% of treated women within 3 months, especially those with
heterosexual contacts.
I Women with BV are at increased risk for: second trimester abortion, preterm labour, endometritis, and
pelvic inflammatory disease (PlD).
r Screening for BV should be offered for women with a history of idiopathic preterm labour or second
trimester abortion. Treatment for positive cases is best initiated before a new pregnancy is allowed.

2. CANDIDA VAGINITIS
Candida vaginitis CV (Candidiasis or Moniliasis) is the second most common causes for child
bearing period vaginitis. lt is responsible for almost 30% of cases presenting with vulvovaginitis in
gynaecologic clinics. lt flourishes in acidic media, and is rarely transmitted during sexual
i ntercou rse.

Candida albicans
on the vaginal walls

Fig1,0-2: Candlda albicans on the vaginalwalls Fig 10-3: Candlda albicans vaginal discharge
 Gynaecology 85

AETIOLOGY AND CAUSATIVE ORGANISMS

v

cases. lt is a normal inhabitant of the bowel and peri-anal region. Almost 30% of women
may have vaginar coronization with no symptoms of infection.

enc.ountered in < 20% of cases. They are usually resistont to stondard ontifungat treatment
'egrmens.

PREDISPOSING FACTORS FOR SYMPTOMATIC INFECTION

A. Changes to a more acidic vaginal pH:
- During pregnoncy and long term use of OCPs: due to increased glycogen content of
vaginal epithelium, allowing for more production of lactic acid by lactobacilli.
- Routine vaginol douching in absence of infection
!
-During the use of some voginal Spermicidalsas a method for long term contraception.
\v B. Decreased host immunity:

infection.
C. Altered vaginal microbiology:
During long term use of ontibiotics or chemotheropy, thus disturbing the balance
between different types of bacterial inhabitants and vaginal flora.
D. Increased local warmth and moisture: as with tight clothing, nylon underwear, and
bathing
suits.
CLINICAL PICTURE (Symptoms & Signs)
lntense pruritus with itching and progressive scratching is usually the main symptom.
v Voginal burning sensation that may cause discomfort and dyspareunia
vaginal dischorge; scanty thick white discharge (cottage cheese discharge)
Dysurio may be an associated symptom in some cases
- The vulva may be red and swollen, sometimes showing the classic satellite lesions
The vagino may show patches of scantv, adherent, cottage-cheese discharge

DIAGNOSTIC I NVESTIGATIONS
- Vaginal pH may be normal or slightly acidic (< 4.5)
Wet mount microscopic examination with saline and tO% KOH; reveals hyphae or

itiiilyi*?,:xllft i::'ff :ff Jff ,:JffI:HI:J,:1'J,':lTl?ito".

TREATMENT OF VAGtNAt CANDtDtAStS (CDC 2O1O)
r Oral preparations: "1:?f
- Fluconozole; single oral dose 150 mg, for treatment of uncomplicated cases
r Intravaginal preparations
-
Butoconazole 2% cream 5 g daily for 3 days, OR
-
Clotrimazole 2% cream 5 g daily for 3 days, OR
-
Miconozole 4% cream 5 g daily for 3 days, OR
-
Tioconozole 6.5% ointment 5 g as a single application, OR
-
Butoconazole29/o 5 g for 1 day, OR,
-
Terconazole 80 mg vaginal suppository, one suppository for 3 days
I During pregnancy; intravaginal treatment for CV is considered safe throughout pregnancy.
86 Femole Lower Genital Trqct lnfections

N.B.:
I Cure rates of > 80-90% are expected within one week of treatment
I Routine treatment of sexual partners is not recommended, except in recurrent infection.
I Recurrent infection: (5% of cases), may be due to:
- Infection with non albicans strains (C. tropicalis & T. glabrata)
Sexual transmission from male partner
lmmunocompromized hosts; as pregnancy, DM, HlV, or chemotherapy treatment
- Treatment of recurrent cases: Prolonged and repeated courses of vaginal and oral
therapy.

3. TRICHOMONAS VAGINALIS VAGINITIS

Trichomoniasis is the 3'd most common cause for vaginitis, accounting

for almost 25% of cases presenting with vulvovaginitis accompanied by
vaginal discharge. lt is a multifocal infection that involves the vaginal
epithelium, Skene's glands, Bartholin gland and urethra.
AETIOLOGY AND CAUSATIVE ORGANISM
) Trichomonas vaginalis (TV): an ovoid, motile, flagellated protozoon,
with 4 anterior flagellae and an axostyle, which traverses its body to end
in a spike. lt is slightly larger than a leucocyte (20mm length & 10mm
width).
F Sexual transmission:ln70% of cases TV can be recovered from male
partners, hence it is considered a sexually transmitted disease (STD)

CLINICAL PICTURE (Symptoms and Signs)

- Asymptomoticin 25% - 50% of women.
- Vaginal discharge: Copious, yellow or green, frothy, offensive. Fig 10- 4: Flagellated
- Vulvolirritation causing vulvitis and pruritus organism in TV
- Speculum examination: reveals vaginal or cervical punctuate
haemorrhagesin 25% of cases also known as strawberry spots.

DIAG NOSTIC I NVESTIGATIONS

- Vaginal pH: is usually weak acidic (5.0 - 6.0)
- Saline wet mount preparations: of the vaginal discharge reveal numerous leukocytes and
highly motile flagellated trichomonadsinT0% of cases
- Cultures: are sensitive in diagnosis, but are not widely used as they need special media which
are not easily available in many laboratories.
- Pap smear: Trichomoniasis may be noted on Pap smear screening for cervical neoplasia, with
a sensitivity approaching 60%.

TREATMENT (CDC 2010)

Metronidazole: 2 g orally in a single dose, OR

Tinidozole: 29 orally in a single dose
During Pregnancy: Oral Metronidazole can be used after 1't trimester
The male sexual partner should be promptly treated by oral Metronidazole re-infected.
Recurrent and resistant infection necessitates searching for reinfection. lf reinfection is ex-
cluded, the patient can be treated with metronidazole 50Omg twice daily for 7 days.
 Gynaecology 87

CHILDHOOD VAGINITIS
Childhood vulvovaginitis is rare, however may occur mostly due to decreased vaginal wall
resistance secondary to low oestrogen levels and low vaginal pH.

RISK FACTORS
- Poor hygiene; leading to Infection by pathogenic organisms.
- Foreign bodyintroduced inside the vagina, usually accidentally.
- Pinworms (Enterobius vermicularis), may reach the vagina from anus as they migrate
by
night, causing intense pruritus and itching by night.

CAUSATIVE ORGANISMS:
F Bacterial infection: E. coli, streptococci, staphylococcus aureus, ano gonococci
F CV and TV (rare causes).
CtINICAL PICTURE (symptoms and signs)
- vaginal discharge: which is pururent, foul odour, and sometimes bloody
- Pruritus vulvae: itching, scratching, pain, and sometimes dysuria
DIAG NOSTIC I NVESTIGATIONS
- Culture and sensitivity of discharge to choose the appropriate antibiotic
- U.S. and f or X-ray to detect foreign body
- Investigations to detect Enterobius vermicularis and oxyuris worms.

TREATMENT
L. Local cleanliness with diluted antiseotics
2. Systemic antibiotics according to culture and sensitivity of discharge.
3. Treatment of Enterobius and oxyuris worms,
4. Removal of foreign body in the vagina under anaesthesia

ATROPHIC VAGINITIS
Atrophic vaginitis occurs due to loss of the normal protective thickness of the vaginal
epithelium associated with decreased oestrogen levels. lt is often seen in postmenopausar
women
(senile vaginitis), but can be seen in breast feeding women.

The vaginal epithelium becomes thin, the amount of glycogen content decreases,
and pH
becomes alkaline. The vagina becomes pale with predominance of parabasal cells.

CtINICAL PICTURE (Symptoms and signs)

- Leucorrhoea, pruritus, vaginal burning, tenderness, and dyspareunia
- Speculum examination shows atrophic vagina, inflamed walls, and sometimes discharge
that may be offensive if secondarV infected.
DIAGNOSIS
- Vaginal PH is usually low < 4.5, while in menopause it should be >4.5.
- Vaginal infection is usually not identified on wet mount preparation
TREATMENT
- Systemic antibiotics; according to culture and sensitivity,in 2ry infected vaginal discharge
- Intravaginal oestrogen cream administered every night for 2 weeks, then once weekly.
- Systemic hormone therapy (HT): is given only if otherwise medically indicated for
treatment of menopausal symptoms (as hot flashes) or osteoporosis.
88 Female Lower Genitql Troct Infections

ACUTE AND CHRONIC CERVICITIS

1- ACUTE ENDOCERVICITIS
Acute endocervicitis describes acute inflammation of the endocervical glands and
underlying tissues, mostly secondary to infection by sexually transmitted pathogens.
AETIOLOGY AND CAUSATIVE ORGANISMS

insertion, puerperal, post-abortive, or post-operative infection (D&C procedures).

CLINICAL PICTURE (symptoms and signs)
- Vaginoldischarge: Mucopurulent discharge, backache, dyspareunia, and sometimes mild
fever
- On speculum examination,'the cervix is red swollen with mucopurulent discharge.
- On bimanuol examination' marked tenderness on moving the cervix
DIAGNOSIS
-
Culture and sensitivity of the discharge for appropriate antibiotic therapy
TREATMENT (CDC 2010)
- Azithromycin t g orally in a single dose, OR
- Doxycycline IO0 mg orally twice a day for 7 days.
N.B.: Consider concurrent treatment for gonococcal infection if prevalence of gonorrhea is
high in the patient population under assessment.
coMPUCAT|ONS
1,. Chronic Cervicitis: high tendency for chronicity due to the racemose (branching) nature of
the cervical glands, and lack of cyclic shedding of cervical mucosa
2. Spread of the infection to the upper genital tract, may lead to pelvic inflammatory disease
(PrD)

2- CHRONTC CERVtCtflS
Chronic cervicitis describes chronic inflammation of the endocervical glands. lt usually
occurs as a common sequel of acute Cervicitis.
CLINICAL PICTURE
. Symptoms:
-
Voginol discharge: mucopurulent offensive discharge in association with endocervicitis
-
Bockache due to spread of infection along the uterosacral ligament
-
Dyspareunia due to parametrial infection if present
-
Dysmenorrhoeo due to pelvic congestion
-
Contactbleeding in some cases in association with congestion and cervicalerosion
-
lnfertility due to infected hostile cervical discharge
-
Frequency of micturitfon due to cystitis caused by lymphatic spread
r Signs on Speculum examination:
- Mucopurulent offensive discharge coming out from the cervix (Endocervicitis)
- Cervical erosion (see loter)
- Chronic hypertrophic cervicitis: the cervix becomes swollen and hyperaemic.
- Mucous polyp: reddish pedunculated small polyp protruding from the endocervical canal,
due to hyperplasia of the endocervical epithelium
- Nabothian cysts: small blue or yellowish cysts within the substance of the cervix, projecting
on the portio-vaginalis. lt represents distended cervical glands with secretions due to
blockage of their ducts.
 Gynaecology 89

DIAGNOSIS
1. Culture and sensitivity of the discharge.
2' Exclusion of malignancy by vaginal and cervical smear in cases of suspicious cervix.
TREATMENT (CDC 20101
oral or vaginal antimicrobials according to the causative organism (clinical and lab
screening).

CERVICAL EROSION
Cervical erosion (ectopy) is a bright red area around the external os due
to replacement of
the stratified squamous epithelium of the ectocervix with the endocervical columnar
epithelium,
which is thin and shows the underlying blood vessels.

AETIOTOGY
1. chronic cervicitis: The infected cervical discharge from the
endo- cervix produces a devitalized denuded area of the
stratified squamous epithelium around the external os.

endocervix grows to cover the denuded area on the

ectocervix.

from the ectocervix grows under the columnar

epithelium leading to blockage of the ducts of cervical Fig L0-5: Cervical erosion
glands and formation of retention (Nabothian) cysts.

2. Congenital erosion: Persistence of the intra-uterine condition where the

columnar
epithelium covers an area on the ectocervix (very rarely seen after puberty).
3. Hormonal erosion: Excess oestrogen (as during pregnancy and with oral contraceptive
use)
causes growth of columnar epithelium replacing the stratified squamous
epithelium.
CLINICAT PICTURE
I SYMPTOMS
- Voginal discharge: excessive mucoid in nature.
- contoct bleeding: manifested after douching or intercourse.
- Symptoms of chronic cervicitis if complicated by associated infection (mucopurulent
foul
discharge, backache, dysmenorrhoea, dyspareunia, etc...)
I SIGNS
- Voginal examination; velvety sensation and occasional contact bleeding,
- Speculum exominotion; reveals flat erosion (red flat area), or papillary Jrosion (red
area
with raised folds) or follicular erosion (red are with glandular distension).
DIAGNOSIS
- Vaginal and cervical smears exclude malignancy
TREATMENT
- Hormonal erosion: require no treatment except if they persists for more than 3
months,
- Antimicrobials to treat associated infection as in chronic cervicitis (mainly
c.trachomatis and N. Gonorrhea): cDC recommendations (2010)
- Azithromycin 19 orally single dose O
- Doxycycline 100mg orally twice daily for 7 days. Followed by should be offered
after
treatment since recurrence and re_infection is not rare.
- Resistant or recurrent infections are mainly treated by repeated antibiotic
courses.
Destruction.of cervical tissue by cauterization, cryotherapy, or laser is not commonly
done nowadays.
90 Femqle Lower Genitql Troct lnfections

VAGINAL DISCHARGE

Normally the vagina and the introitus are kept moist with minimal discharge that may
occasionally stain the underclothes by one or two drops. The discharge consists of fluid
formed from as a transu- dation from the vaginal walls, desquamated epithelial cells, bacteria
(mainly lactobacilli), together with mucus secreted mainly from cervical glands.

Normal vaginal discharge is characterized by being white in colour, semi fluid in nature,
small in amount, with a slightly acidic PH (3.8-4.5).
. Sources of Normal Vaginal Discharge:

Vaginal discharge is formed from vaginal transudate and exfoliated cells, endocervical
glandular secretions and exfoliated cells, vulval secretions from Bartholin glands (thin alkaline
mucus during sexual intercourse), micro-organisms and their metabolic products.
. Characters of Normal Vaginal Discharge:
Normal vaginal discharge is characterized by being clear in colour, semi-fluid in nature,
with little or no smell. lts PH ranges from 3.8-4.5 (acidic), and its amount<0.5 ml/day.
(For details on DD of vaginal discharge see lower genital tract infections and vulvovaginitis).

LEUCORRHOEA
This is the term used to describe the excessive white non infected voginal dischorge due
to excess of the normal secretion or transudation of the cervix, vagina, and Bartholin's gland. lt
may be related to:
. Physiologic causes: mostly related to oestrogen effect with increased vascularity and
associated pelvic congestion; as in puberty with onset of menstruation, at the
preovulatory and the premen- strual phases of the menstrual cycle, and during
pregnancy.
. Pathologic causes: Associated with pelvic congestion; as in pelvic inflammatory disease
(PlD), fibroids, pelvic, and adnexal masses.

ABNORMAL VAGINAL DISCHARGE

a, Coloured offensive discharge: bacterial vaginosis & trichomonas vaginalis
b, Muco-purulent discharge:e.g.;chroniccervicitis
c. Purulent offensive discharge: septic abortion, puerperal sepsis, foreign body in vagina,
ne- glected pessary, pyometra, pelvic abscess evacuating vaginally, and infected
neoplasms as sub- mucus fibroid polyp, endometrial, cervical, and vaginal cancers,

d. Blood stained (sanguineous) discharge: atrophic vaginitis, vaginal and cervical ulcers,
cervical erosion, fibroid polyp, and malignancies of the vagina, cervix, and
endometrium.
e. Serous (watery) discharge: Intermittent hydrosalpinx, and urinary fistula.
 Gynaecology 9l

.- THE CLINICAL APPROACH FOR A CASE OF VAGINAL DISCHARGE

A. History & related conditions:

- Age at onset of symptoms; childhood, childbearing period or menopause.

- Recent use of systemic or local antibiotics
v - Previous or recurrent vulvovaginal infections.
- Vaginalhygienic practices e.g.,frequency of repeated and routine douching.
- Menstrual history: reration of discharge to menstruation.
v - obstetric history: relation of discharge to recent pregnancy, delivery, or abortion
- Contraceptive history:Use of vaginalspermicidals, diaphragms, and hormonal rings
- Sexual history: relation of intercourse to vaginal discharge and associated symptoms

v B. Symptoms & associated conditions

v - character of discharge,its amount, consistency, colour, and odour
: - Associated burning sensation in the vulva and vagina (the commonest symptom)

! - Presence of itching or pruritus; that may be intense and distressing to the patient

C.Signs on examinationof the vulva and vagina

v. - The vulva; is inspected for associated vulvitis, or Bartholinitis

- The vagina and cervix; are inspected using a dry sterile speculum, for white plaques in
cases of cV, strawberry cervix in TV, and grey frothy discharge in BV
v - Milking of the urethra through the vagina to detect gonorrhoea

- Bimanual examination to exclude uterine or adnexal masses.

D. Laboratory diagnosis

Wet mount preparations and microscopic examination; reveals clue cells in BV, hyphae
in CV, and flagellated trichomonads in TV.
v - Addition of to% KoH; may revealfishy amine odour in cases of BV.

!- - Vaginal swabs for culture, will reveal other bacterial causes for vaginitis pap smears
may
reveal trichomonas vaginalis

- Biopsy from suspicious vaginar or cervicar urcers or tumours.

- X-ray may reveala vaginal foreign body in infants with resistant and recurrent vaginitis.
TREATMENT:
- Treatment of the cause e.g. trichomonas, moniliasis or neoplasms.
- Genital hygiene including vaginal douching when necessary, propertreatment of first
attack and adequate treatment of repeated or recurrent infection.
 I Acute PID
I Chronic PID
I Chronic specific FGTI

PELVTC TNFLAMMATORY DISEASE (PlD)

Pelvic inflammatory disease (PlD) is an infection of the upper reproductive tract organs.
The fallopian tube is the most common and most important organ affected hence PID is common-
ly used to describe acute salpingitis and/or salpingo-oophoritis. PID is usually caused by bacterial
pathogens ascending from the lower to the upper female genital tract.

DEFINITIONS AND TYPES

A. Acute PID: acute infection ascending from the cervix, to the tubes and ovaries.

B. Chronic PID: chronic pelvic in-

Pelvic peritonitis rian ahs,cess
fection that can follow an acute
episode of PlD, or may occur as a
sequel to an inflammatory pelvic
lesion or genital T.B.

N.B: PID may be silent, occurring with

asymptomatic or mildly symptomatic
pelvic infection. lt is usually diagnosed
only when the sequelae of tubal dam-
age is found later, as with formation of
fine peritubal adhesions detected at
laparoscopy. Fig 1l-l:

1- ACUTE PELVIC INFLAMMATORY DISEASE (PlD)

MICROBIOLOGY OF PID
Acute PID is a polymicrobial infection that may be caused by;
F Neisserio gonorrheo: a Gram negative diplococcus, recovered from the cervix in27%to8O%o,
and from the fallopian tubes from 1,3%to 18% of cases with PlD. lt is the most common cause
for acute salpingitis.

Y Chlomydio trachomatis; Chlamydial antibodies are found in 20%to 40% of women with histo-
ry of PlD, although C. Trachomatis does not by itself cause an acute inflammatory response.
N. gonorrhea and C. trachomatis may coexist together in 25%to 40% of cases of PlD.

Y Endogenous bacterio; which may be:

o Aerobic as E.coli, Streptococcus species, bacillus proteus, and Klebsiella.
o Anoerobic as Bacteroides fragilis, and Peptostreptococcus.

92
 Gynaecology 93

ROUTES OF INFECTION:
1. Ascending infection from endocervicitis (namely gonorrhoea! & chlamydial) by transluminar
spread leading to endosalpingitis.

2. Direct or lymphatic extension from inflammatory GIT conditions as; appendicitis, colitis, and
diverticulitis (whether aerobic or anaerobic bacteria). Puerperal infection spreads along peri-
tubal lymphatics leading to interstitial or perisalpingitis.
3. Rarely the tubes may be affected by blood borne extension from pulmonary T.B.

RISK FACTORS

' 'o'11?,on'1,":::::i,{::Jffi":;ZX:::':'^i:^"st risk ror inrection representing armost 85%or

cases, mostly occurring in the age group ranging from 25-35 years.
Women with multiple sexual partners have a 3 fold risk for PID than a single partner.
- Use of intrauterine contraceptive device (IUCD) has been associated with an increased
incidence of PID especially in the period following its insertion.
c Factors associated with decreased risk for plD
- Barrier methods for contraception; as the male condom, the female diaphragm, sponge,
and contraceptive gel-foams, all decrease the risk of STDs and plD.
- Oral contraceptive pills (OCPs); are associated with significantly low incidence of plD,
probably through its effect on regular endometrial shedding, decreased menstrual flow,
and its progestational effects on the cervical mucus rendering it less penetrable by bacteri-
al patho- gens.
o Factors Iacilitating ascending infection:
- Menstrual periods: due to degenerating endometrium, retrograde menstruation, and cer-
vical mucous changes.2/3 of acute PID cases begin just after menses
- Sexual intercourse: bacteria may be pushed into the cervix during intercourse, and ascent
to the uterus assisted by associated uterine contractions.
- latrogenic procedures: as D&C operations, IUD insertion, hysterosalpingography (HSG),
hysteroscopy, and during dye tubal patency testing in laparoscopy.

PATHOLOGY OF ACUTE SALPINGO-OOPHORITIS

Infection is usually bilateral, however unilateral infection is possible.

1. Endosalpingitis; with congestion, oedema, and destruction of tubal luminalcells, cilia, and
mucosal folds. lt is either catarrhal or suppurative

2. Interstitial salpingitis and perisalpingitis; due to extension of infection to the tubal muscu-
laris and serosa. Infection also spread by direct extension to the tubal ostea and abdominal
cavity.

. Oophoritis; may occur with development of micro-abscesses on ovarian surface

4. Pelvic peritonitis; may occur either by direct extension from the tubal lumen laterally, or
by lymphatic spread.

5. Chronic PID; see later

94 Femole Upper Genital Tract lnfections

REMOTE SEQUETAE AND COMPTICATIONS OF PID

Medical complications may develop in one out of 4 cases of acute PlD.
1. Tubal obstruction and infertility: such risk correlates with the severity and the number of
PID episodes. lt reaches up to 11o/o after one episode, 23 o/o after 2 episodes, and 54%
after the third eoisode.
2. Ectopic pregnancy: the rate increase 10 fold in women with PlD. Approximately 50% of
tubal ectopic pregnancy is thought to result from tubal damage caused by PlD.
3. Chronic pelvic pain: develops in almost 20% of women with acute PlD, sometimes associat-
ed with dyspareunia.

4. Mortality: Rarely occurs, only in neglected cases with septic shock and ruptured tubo-
ovarian abscess

CLINICAL PICTURE (Symptoms & Signs)

A. History: recent IUD insertion, D&C procedure, recent delivery or abortion, or recently per-
formed HSG for infertility, in a young sexually active woman.
B. Symptoms: Symptoms often start in the postmenstrual period. Women with chlamydial
PID usually have clinically milder disease than those with gonococcal PlD. Symptoms are
generally non-specifi c including:
- Acute lower abdominal pain is the most common symptom
- Fever, headache, and malaise
- GIT symptoms; as nausea and vomiting.
- Increased vaginal discharge, and sometimes vaginal bleeding.
DIAG NOSTIC I NVESTIGATIONS
1. Examination of Cervico-vaginal discharge:
- Grom stain: isuseful in diagnosis of N. gonorrhoea although alone may miss up to half of
cases and does not diagnose C. trachomatis.
- Testing for Chlomydiol and gonorrheal ontibodies; presence of antibodies will help in di-
agnosis in cases where clinical symptoms are suggestive of acute PlD.
2. Blood tests:
- lncreosed WBCs (Leucocytosis); is not accurate for diagnosing acute PlD.
- lncreased ESR; is a non-specific finding although elevated in >75% of PID cases (good sen-
sitivity but low specificity).
3. Ultrasound:
- Findings may be normal or non-specific.
- TVS to exclude ectopic pregnancy, uterine myomata, and ovarian swellings.
4. Laparoscopy:
- Laparoscopy is considered the gold standard to confirm the diagnosis whenever in doubt
or in cases with poor response to parentral antibiotic therapy aft.er 48-72 hours of initi-
ating treatment.
- Laparoscopy will reveal; tubal serosal hyperemia, tubal wall oedema, and purulent exu-
dates from the fallopian tubes pooling in the cul-de-sac.
5. Culdocentesis:
- Aspiration of purulent fluid in the pouch of Douglas may assist diagnosis and antibiotic
selection after culture and sensitivity, yet its use is limited by its associated pain, and ten-
dency for secondary infection.
6. Testing for HIV and STDs: should be offered to all women diagnosed as PlD.
 Gynaecology 95

CDC Criteria for Diagnosis of Acute ptD (2015)

Treatment for PID should be initiated in sexually active young women if one or more of the
following minimum clinical criteria are present on pelvic examination:
o Cervical motion tenderness or uterine tenderness or adnexal tenderness.
' One or more of the following additional criteria can be used to support a diagnosis of plD:
. Oral temperature >38.3"C
. Abnormal cervical mucopurulent discharge or cervical friability
' Presence of abundant numbers of WBC on saline microscopy of vaginal fluid
o Elevated erythrocyte sedimentation rate
. Elevated C-reactive protein and
' Laboratory documentation of cervical infection with rV. gonorrhoeoe or C. trochomatis.
Laparoscopic Evidence of PID:

- Peri-tubel adhesions, peritonitis, pelvic abscess and tubo-ovarian comolex

DIFFERENTIAL DIAGNOSIS FOR ACUTE PID
1. Ectopic pregnancv
2. Torsion or ruptured ovarian cyst
3. Degenerating fibroids
4. Endometriosis and ovarian endometriomas.
5. Inflammatory bowel disease; as appendicitis and diverticulitis
TREATMENT OF ACUTE PID
Empiric treatment is immediately started whenever minimal diagnostic criteria are met with
in women with high risk factors. The primary goal of therapy is to eradicate bacteria, relieve
symptoms, and prevent adverse sequelae especially tubal damage.
o Rest in bed
o Analgesics and antipyretics are important to alleviate pain and fever.
o Antibiotic treatment

CDC antibiotic regimens (2010)

A. lM regimen is indicated in mild-moderate cases of acute PlD. The recommended drugs are:
Ceftriaxone 250 mg lM single dose PLUS
Doxycycline 100 mg orally twice a day for 1-4 days
WITH or WITHOUT
Metronidozole 500 mg orally twice a day for 14 days
B. lV regimen is used in severe PID cases, which require hospitalization. lV regimens are continued
f or ar 24-48 hours after clinical improvement then oral treatment is continued
to comolete 14
days. The recommended drugs are:
Cefotetan 2 g lV every 1-2 hours OR
Cefoxitin 2 g lV every 6 hours pLUS
Doxycycline 100 mg orally/12 hours

o lf no improvement occurs within 72 hours of start of standard treatment, the patient should
be hospitalized (if not) for further investigations and surgical treatment may be indicated.
o lf the woman is using an IUCD, it should be removed but after starting the antibiotic cover.
o Evaluation and treatment of male partner is essential.
96 Femole Upper Genital Troct lnfections

Treatment of Tubo-Ovarian Abscess (TOA):

A. Medical:
- Clindamycin 900mg lV/8 hours + Metronidazole 500 mg lV/8 hours + Doxycycline 1O0mg
orally/!2 hours (triple therapy).
the patient's condition worsens or does not
B. Surgical: Considered in severe cases whenever
improve within T2hours of treatment, or whenever diagnosis is not definitive.
- Laparoscopy:
Y Diagnostic loporoscopy confirms diagnosis whenever in doubt
Y Operotive laporoscopy may assist drainage or for performing unilateral salpingo-
oophorectomy.
- Laparotomy: To perform drainage, or salpingo-oophorectomy.
- Vaginal drainage rarely done is selected cases of localized TOA.

2- CHRONTC PELVTC TNFLAMMATORY DTSEASE (PtD)

Chronic PID is an ill-defined term including all sequelae of acute PID either with complete res-
olution of microbial load leaving residual fibrosis or incomplete bacterial resolution leaving chronic
inflammatory pathology affecting the upper genital organs and the surrounding structures.

AETIOLOGY
1. Sequelae of acute PID (inadequate treatment or neglected cases)
2. TB starts as chronic disease (however it is betterto be a separate entity).

PATHOLOGY
1. Hydrosalpinx: sequelae of acute catarrhal salpingitis. The tube is retort shaped, thin walled,
transparent, containing serous fluid, with no or minimal surrounding adhesions.
2. Pyosalpinx: sequelae of acute suppurative salpingitis. The tube is thick walled, containing pus,
and surrounded by dense adhesions.
3. Chronic interstitial salpingitis.
4. Tubo-ovarian cyst: communicating between hydrosalpinx and ovarian cyst
5. Tubo-ovarian abscess: connecting between pyosalpinx and ovarian abscess

CLINICAL PICTURE (Symptoms & Signs)

A. Symptoms

- History of acute PID

- Dull aching lower abdominal pain
- Lower Backache; especially sacral
- Pelvic congestive symptoms; as vaginal discharge, and menorrhagia
- Secondary dysmenorrhoea: due to pelvic congestion and/or tuba-ovarian mass
- Chronic pelvic pain
- Infertility (primary or secondary) due to tubo-peritoneal factor whether associated with
dense adhesions or tubal occlusion.
B. Signs: Adnexal swelling; usually bilateral, tense cystic, tender, fixed, with fixed RVF
 Gynaecology 97

DIAGNOSTIC I NVESTIGATIONS
- Pelvic ultrasonography (TAS I TVS): to detect adnexal masses
- Diagnostic Laparoscopy: to confirm the nature of adnexal mass
- For TB (see loter)
DIFFERENTIAL DIAGNOSIS:
- Pelvic endometriosis, or pelvic malignancy.
- Other non gynaecologic causes of chronic pelvic pain
TREATMENT OF CHRONIC PID
- Antibiotics are used only in acute exacerbations or when bacterial existence is diagnosed.
- Symptomatic treatment for pain (analgesic), inflammation (NSAID) and congestion (anti-
congestives).
- Infertile patients; are best advised for lCSl/lVF procedures since tubal surgery (salpingolysis
or salpingostomy) have poor prognosis.
- Elderly patients and cases resistant to medical treatment that have completed their family
may benefit from surgery with total abdominal hysterectomy and bilateral salpingo-
oophorectomy (TAH-BSO).
N'8.: Surgery in cases with chronic PID carry a high risk for intestinal and ureteric injury due to asso-
ciated dense adhesions.

TUBERCULOSTS OF THE FEMALE GENTTAL TRACT (TB)

Tuberculosis (TB) is a chronic granulomatous disease caused by Mycobacterium tuberculosis.

Female genital TB is always secondary to a lesion elsewhere in the body, most commonly the lungs,
and less commonly the bones and urinary tract. Spread of infection through the genital tract is
mainly hematogenous, via the blood, or less commonly through the lymphatics. 95% of female gen-
italTB is due to human strain.

PATHOLOGY:
A. Sites affected: The tubes are affected in almost all cases of genital T.B.; the endometrium will
be involved in up to 80% of cases, and the ovaries in nearly 20-30%.
B. Macroscopic picture:
1. The tube:
a. Endo-salpingitis:
- The tube is thickened and tortuous, commonly with patent fimbrial end. The tube may
be filled with caseous material forming a TB pyosalpinx, and may be matted with the
ovary forming a TB tube-ovarian abscess.
- T.B pyosalpinx is characterized by eversion of fimbriae (tobacco pouch appearance),
presence of external tubercles, and scarce adhesions to the surroundings.
- During healing by fibrosis some ectopic endosalpinx is driven within the muscle wall in
the region of the isthmus producing "salpingitis isthmica nodosum".
b. Perisalpingitis: The serosa of the tubes, ovaries, uterus, intestines and wall of Douglas
pouch are all studded by multiple tubercles.
c. lnterstitiol solpingitis:There is thickening and nodularity of the tubes.
98 Female Upper Genital Troct lnfections

2. The Endometrium:
- Tuberculous follicles may be found in the endometrial stroma especially in the 2nd half
of the cycle therefore for diagnosis an endometrial biopsy should be performed pre-
menstrual
- Intrauterine synechiae may develop due to destruction of surface epithelium and fibro-
sis lead to partial or complete obliteration of the uterine cavity by adhesions resulting in
Asherman's syndrome.

3. The ovaries:
- Peri-oophoritis
- Oophoritis with foci of caseation
4. Other rare sites:
a. Vulvar ulcerative lesions; the vulva may be affected especially in children, leaving an ulcer
with undermined edges that may lead to fibrosis and scarring of the labia.
b. Cervical ulcerative lesions; that can be misdiagnosed as cancer cervix.

C. Microscopic picture:
- Tuberculous follicle; is the characteristic lesion, with central Langhan's giant cells, sur-
rounded by epithelioid cells, then a coat of round cell infiltration.
- Caseation, from the center outwards may occur, due to coagulative necrosis, with for-
mation of necrotic structureless material surrounded with epithelioid and round cells.
Caseous material may soften and liquefy forming cold abscess
- Fibrosis or even calcification may occur from the periphery inwards.

CLINICAL PICTURE (Symptoms & Signs)

A. Symptoms:
o Early cases are usually asymptomatic.
o More advanced disease will usually present with infertility associated with symptoms and
signs suggestive of PID with or without menstrual disorders.
1. Infertility: genital TB may be the underlying cause in almost s-LO% of infertile women
mostly due to; tubal destruction, peritoneal adhesions, or endometrial synechiae.
2. Chronic pelvic pain associated with low grade fever, is a common presentation.
3. Acute lower abdominal pain with high fever may occur if 2ry infection develops on top
of a TB pyosalpinx.
4. Abnormal bleeding may occur from ulcerative lesion in the endometrium.
5. 2ry amenorrhoea or oligomenorrhoea may occur in about 10% of cases due to intrau-
terine synechiae, and/or ovarian destruction.
B. Signs

- Most cases are normal on gynaecologic examination.

- A Tender, fixed, adnexal swelling, with low grade fever, especially in an infertile patient
with no previous history of pelvic infection, should be strongly suspicious for TB
- Genital ulcerative lesions: with serpiginous margin and undermined edges, characteristic
of TB, may develop on the vulva and cervix, with later scarring or sinus formation.
 Gynaecology 99

DIAGNOSTIC I NVESTIGATIONS
1. Chest x-ray to look for evidence of pulmonary TB
2. Plain x-ray pelvis: may detect calcification at tubal sites or pelvic nodes, in chronic cases.
3. Ultrasonography: may detect solid adnexal masses with scattered calcification.
4. H.S.G: (not done if active T.B or 2ry infection is suspected to avoid flaring up infection): usual-
ly diagnosis of TB is made retrospectively when a HSG is performed for infertility. HSG charac-
teristic findings are:
- The endometrial cavity may be normal, or may be small showing linear filling defects due
to intrauterine synechiae.
- The tubes are usually affected showing beading, pipe-stem appearance, and terminal
block with sacculation (Hydrosalpinx).
5. Endometrial Biopsy:
- An endometrial biopsy is usually divided into 2 parts one for histopathology (formalin pre-
served) and the second for microbiology (saline preserved).
- PEB (premenstrual endometrial biopsy) obtained from the uterine fundus and cornu and
subjected to histopathologic examination is strongly suggestive.
- Bacteriologic examination (the acid and alcohol fast organism stains by Zeal-Nelsen stain),
bacterial cultures, and animal inoculation are more conclusive in some cases. Recentlv pCR
can be used as a specific test for diagnosis of TB
5. Laparoscopy:
- Usually indicated to confirm abnormal HSG findings suggestive of TB in an infertile patient.
- Performedalsoinpresenceofanadnexal masssuspiciousofTBdetectedonpelvicexami-
nation or ultrasonography.
- Biopsies are taken from serosal tubercles and suspicious lesions for bacteriologic and path-
ologic examination, together with culture from peritoneal fluid in the pouch of Douglas.
N.B.: Tuberculin test is good negative test for exclusion of the disease rather than for establishing
the diagnosis.
GUIDELINES IN THE TREATMENT OF FEMALE GENITAT TB
o Even in the absence of symptoms, the disease always calis for active treatment.
o General treatmenU for anaemia and malnutrition and to increase the general resistance.
o Antituberculous drugs: The treatment should last for 1g-24 months.
-
Rifampicin, LN.H. (isonicotinic acid Hydrazide), Ethambutol, or pyrizinamide.
o Surgical treatment: Indicated only in cases of:
1. Adnexal mass not responding to medical treatment.
2. Recurrent endometrial T.B, one year after treatment.
o Post-operative antituberculous treatment is mandatory.
 - Bacterial STDs - Virql STDs
t Gonorrhoea . HSV
t Chlqmydiq Trqchomotis . HPV
t Chancroid I HIV
t Gronuloma lnguinale - Syphilis
- Lym phog ronu loma vene reu m

Sexually transmitted diseases (STDs) are infections acquired principally through sexual con-
tact or sexual intercourse. They are among the most common encountered infectious diseases.
Urinary tract infections (UTl) may be triggered by sexual intercourse although the organism is
colonizing the woman beforehand. They are thus not considered as STDs.

RISK FACTOR FOR STDS

Young sexually active females especially< 25 years of age

- Multiple sexual partners
- Lack of sexual hygiene
- Previous or present infection of one STD increases the risk for other STDs

CAUSATIVE ORGANISMS FOR STDS

F Bacterial: N. Gonorrhea, C. Trachomatis, H. ducreyi (Chancroid), Klebsiella (Granuloma ingui-

nale), and Gardnerella vaginalis (Bacterial vaginosis).
F Viral: Human papilloma virus (HPV), Herpes simplex virus (HSV), Human immune deficiency
virus (HlV), Molluscum contagiosum, and Hepatitis B virus (HBV)
F Spirochetes: Syphilis.
F Protozoons: Trichomoniasis (see LGT infections chapter 10)
F Ectoparasites: Pediculosis pubis, and scabies

BACTERIAL SEXUALLY TRANSM ITTED DISEASES

1. GONORRHEA
Gonorrhea is an STD caused by the Gram negative diplococci Neis-
seria gonorrhea, a bacterium species that involves infection of columnar
and transitional epithelium primarily causing gonococcal endocervicitis.
The vagina is not involved being lined by squamous epithelium (except in
childhood).

,'
P THOEOGY," -

;f " Plimary sites of infection include: the cervix (endocervicitis), ure-

.;. tlrra (urethritis) and BartLrqlin gland (bartholinitis)
. .'n Secpndary sites of infection include pelvic inflammatory disease
' '.' (PlD) (see
female upper genitol troct infections Chopter 1L).

Fig l2-I :

100
 Gynaecology 101

o Other sites of infection:

In women: oropharynx (pharyngitis), and the rectum (proctitis).
In the new born: Eye (ophthalmitis), and joints (arthritis).
- In men: Urethra (urethritis), prostate (prostatitis), and epididymis (epididymitis).
CLINICAL PICTURE (Symptoms & Signs)
A. Frequently asymptomatic
B. In symptomatic cases; symptoms usually appear 2 to 5 days after exposure, but may be de-
layed for up to 30 days. They include;
- Mucopurulent cervical discharge; as occurs in acute cervicitis.
- Lower abdominal pain, anorexia, and fever if plD develops
- Dysuria may occur in both men and women if there is associated urethritis and cystitis.
- Symptoms of bartholinitis may occur if infection of Bartholin gland occurs
- Symptoms of pharyngitis and proctitis may be present and should be looked for.
- Disseminated gonococcal infection (< 3% of cases); may cause arthritis, endocarditis, and
septicaemia.
- Other sequelae of infection include; infertility, and chronic pelvic pain.
DIAGNOSTIC INVESTIGATIONS
A. Gram stains: shows Gram negative diplococci within polymorph nuclear leucocytes (pNLs).
However presence of vaginalflora can yield false positive results, therefore it is considered a
good negative test if NO gram (-ve) diplococct are seen.
B. Culture on Thayer-Martin medium; besides being highly accurate, it is suitable for use for
specimens obtained from various body sites as the cervix, rectum, and oropharynx.
C. Nucleic acid amplification test (NAAT): this test uses nucleic acid sequence unique to a spe-
cific organism for identification. NAAT has a sensitivity of 96.7% in endocervical specimens.
TREATMENT
Gonococci are fragile organisms that rarely develop resistance to commonly used antibiotics.
Treatment of uncomplicated cases is usually sufficient trough single dose therapy:

cDC regimens for treatment ol uncomplicated N. Gonorrhoea (zolo)

A- Uncomplicated genital, urinory and rectal infections:
Ceftriaxone 250 mg lM in a single dose
PLUS
Azithromycin 19 orally in a single dose
OR
Doxycycline 100 mg a day for 7 daysexcluded
o No test of cure is required.
' Sex partners within 60 days of appearance of symptoms should be evaluated and treated for
gonorrhea and chlamydia
B- Disseminated gonococcal infections.'ceftriaxone L g lM or lV every 24 hours then cefixime
4oo
mg orally twice daily to complete 7-L4 days of treatment

SEQUETAE OF UNTREATED GONORRHEAL INFECTIONS

o Ascending infection may lead to salpingitis and tubal damage that may predispose to infertili-
ty and ectopic pregnancy (see plD).
o In the new born exposure during vaginal delivery, from an infected mother with endocervici-
tis, may cause ophthalmitis, blindness, or serious sepsis.
o In males, it leads to urethritis, prostatitis, epididymitis and repeated transmission to the fe-
male.
t02 Sexu o I ly T rq n sm itte d D i se o se s

2. CHLAMYDIA TRACHOMATIS
Chlamydia trachomatis is the second most commonly reported STD in many countries. lt is an
obligatory intracellular Gram negative bacterium that causes chlamydial genital infection.
Chlamydia grows only intracellular as do viruses. They attack only columnar epithelial cells
causing mild inflammatory reaction usually localized to the infected area without deep tissue inva-
ston.

Rf SK FACTORS: See risk factors for STDs

PATHOLOGY
o Primary sites for infection: include the endocervix and less commonly the urethra
- Chlamydial endocervicitrs; Infection usually starts as endocervicitis, causing mucopurulent
discharge milder or similar to that seen with gonorrhea.
. Secondary sites for infection: include upper genital infection (PlD)
- Chlamydial endosalpingitrs; ascending infection occurs insidiously and may later cause
PID.
. Co-infection with N.gonorrhea is common, and susceptibilityto HIV is 3 folds increased.

CLINICAL PICTURE (Symptoms & Signs)

. Asymptomatic in almost 75% of cases
. Symptomatic cases may present with:
- Mucopurulent endocervicitis: mucopurulent discharge, with oedematous and hyperaemic
cervtx.

- Symptoms of urethritis and pyurio: in association of negative urine culture is highly sug-
gestive in sexually active women.

- Fever ond lower obdominolpoin suggest PID; which may occur in up to 40% of women
with untreated chlamydia. Infection is more insidious and protracted than that seen with
gonococcal PlD.
DIAGNOSTIC I NVESTIGATIONS
A. Microscopic examination of endocervical secretions following saline preparation typically re-
veals 20 or more leucocytes by HPF.
B. Culture: from endocervix is a highly specific technique although expensive, and results are
difficult to standardize, thus limiting its use.
C. Nucleic acid amplification tests (NAAT): This sensitive test amplifies organism-specific nucleic
acid sequences using polymerase chain reaction (PCR). Endocervical sampling in women has
sensitivity of 85% and specificity of 99%.

TREATMENT

CDC regimens for tredtment of uncomplicoted coses of urethritis ond cervicitis (2010)
Azithromycin: I g orally once (4 tablets 250 mg each), suitable during pregnancy
OR
Doxycycline: 100 mg orally twice daily for 7 days (not used in pregnancy)

. Abstinence from sexual intercourse for 7 davs from treatment start.

o Test of cure is not recommended
 Gynaecology 103

SEQUEIAE OF UNTREATED CHtAMyDtAL tNFECT|ON

- Ascending infection may lead to chlamydial salpingitis and tubal damage that may predis-
pose to ectopic pregnancy and infertility (see plD).

- During labour the vaginally delivered neonate may develop chlamydial conjunctivitis in
50% of cases and late onset pneumonitis in IO%. Premature delivery and postpartum en-
dometritis are also associated problems.

3. CHANCROID
Chancroid is a genital ulcerative disease, caused by the Gram negative coccobacillus Haemoph-
ilus ducreyi. The disease is generally rare, but may occur as outbreaks of infection.
Epidemiology: Trauma facilitates entry of coccobacilli into the vulval mucosa with an incubation
period of 3-5 days. Co-infection with HIV is common, while associated syphilis or herpes is found in
1,0% of cases.
Clinical picture: Lesions begin as small papules that later break into painfulgenitalvulval ulcers in 2-
3 days that may be accompanied with inguinal lymphadenopathy.
Diagnostic investigations: Cultures and PCR for chancroid are not readily available in many centers.
Probable diagnosis is made when painful genital ulcers are present without evidence of herpes, or
syph ilis.
Treatment (CDC 2010):
- Azithromycin: 19 orally once OR
- Ceftriaxone 250mg lM single dose.
4. GRANULOMA INGUINALE
It is a genital ulcerative disease, caused by a gram negative bacterium Klebsiella granulomatis.
Epidemiology: The disease is endemic in some countries as India and Africa.
Clinical picture: Painless friable ulcerative genital lesions with inguinal swelling but without lym-
phadenopathy.
Diagnostic investigations: Scrapings from the ulcers show pathognomonic cells known as Donovan
bodies.
Treatment (CDC 2010):
- Doxycycline tOO mg orally twice a day for at least 3 weeks and until all lesions have completely
healed OR
- Azithromycin 1' g orally once per week for at least 3 weeks and until all lesions have completely
healed.

5. LYMPHOGRANULOMA VENERUM
Lymphogranuloma venereum (LGV) is caused by C. trachomotis serotypes 17, L2, ond 13, producing
local and regional ulcerations and destruction of genital tissues.
Epidemiology: LGV is a rare disease that is endemic in some parts of Africa and India.
Clinical picture: Primary genital ulcers appear 3-5 weeks after exposure and resolve spontaneously.
2 to 6 weeks later tender 2ry unilateral inguinal lymphadenopathy develops that can break into ul-
cers.
Diagnostic investigations: Complement fixation tests with titers >1/64 indicate active infection.
Treatment (cDC 2010): Doxycycline 100 mg orally twice a day for 21 days.
r04 Sexually Transmitted Diseoses

VI RAL SEXUALLY TRANSMITTED DISEASES

1. HERPES SIMPLEX VIRUS
Herpes simplex virus (HSV) is a double strand DNA virus of two main types:

fected saliva. lt is responsible for facial and oropharyngeal infections like herpetic gingivo-
stomatitis and the common cold sore or fever blister.

new born during vaginal delivery. lt is responsible for genital herpes and neonatal infec-
tions, and has been linked epidemiologically with carcinoma of the cervix.

CLINICAL PICTURE (Symptoms & Signs)

- The first attack: is the most severe with pain, vulvitis, Lymphadenopathy, and discharge. lt
occurs after an incubation period of around 21- days, and is manifested by multiple painful
anogenital vesicles or painful ulcers with erythematous base that usually resolve after 3-4
weeKs.
- Subsequent attacks: are normally shorter and less severe.

DIAG NOSTIC I NVESTIGATIONS

- Cultureofserumcollectedfromvesiclesbyaspirationorbyswabbingbaseoftheulcer.
- Serum anti-HSV antibody levels are increased with both type-1, and type-2 infection.

TREATMENT
- Treatment is mainly supportive with analgesics
- Treatment of any associated secondary infection.
- First attack: Acyclovir 400 mg orally three times a day for 7-10 days. Treatment can be ex-
tended if healing is incomplete.
- Subsequent attacks: Acyclovir 400 mg orally three times a day for 5 days.

2. HUMAN PAPTLLOMA VrRUS (HPV)

The genital virus in this double stranded DNA family is responsible for a variety of mucocuta-
neous genital lesions, commonly resulting in genital warts (condyloma accuminata). HPV is also as-
sociated with female LGT cancers especially cervical intraepithelial neoplasia (ClN).
EPIDEMIOLOGY:
. Types of HPV: HPV types 6 and 11 are the usual causes for visible external warts. HPV types
16,L8,3L,33, and 35 have all been strongly associated with CIN and with externalgenital
squamous intraepithelial neoplasia

. Prevalence: In the USA 50% to75% of sexually active men and women acquire HPV at some
time of their lives. HPV are associated with other STDs in almost 25% of cases.
. Mode of transmission:
- Contoct with infected male pdrtners: yield a risk of 60-80% for contracting genital
warts, with an incubation period (lP) ranging from 6 weeks to 18 months (mean 3
months).
- Mqternalto fetoltransmission; very rare (1:1000), through transplacental, intrapartum,
or postnatal routes. Foetal affection may cause neonatal and juvenile respiratory papil-
lomatosis.
 Gynaecology r05

CLINICAL PICTURE (Symptoms & Signs)

- Asymptomatic: genital HpV are frequently asymptomatic.
- Skin lesions (genital warts or condylomata acuminate): appear on the vulva and peri-anal
region as warty like, scattered and multifocal lesions. Secondary infection will result in an
irritating itchy sensation.
DIAGNOSIS OF HPV
- Direct inspection: easily diagnose overt warts. Biopsy is rarely required, only if in doubt.
- Pap smear test: demonstrates the pathognomonic koilocytes or hallo cell exfoliated from
the cervix, designated as low-grade squamous intra-epithelial lesions (LSIL).
- Colposcopy: on staining with !% acetic acid lesions appear as flat, small, acetowhite areas,
with vascular punctuation or mosaicism.
- HPV DNA test: is a diagnostic procedure that uses a small plastic spatula to collect material
from the cervix and vagina. This sample allows identification of !4 high risk types of HpV,
including HPV 16 & HPV 18.

TREATMENT OF EXTERNAT CONDYLOMAS (CDC 2010)

- Podofilox 0.5% solution or gel administered by the patient
-Destruction: using cryotherapy, Podophyllin resin IO%-25%, Trichloroacetic acid (TCA) or
Bichloroacetic acid (BCA) 80%-90% or surgical removal.
- Barrier contraception is advised during treatment.
TREATMENT OF HPV RELATED PRECANCEROUS CONDITIONS (CDC 2O1O)
- Destruction of abnormal cells via colposcopy using laser ablation or cryotherapy.
- Surgical excision by Loop electrode excision of the transformation zone (LEETZ)
N.B: Recurrence and relapse are common in immune-compromised patients, and whenever treat-
ment of infected male partners is neglected.
N.B: Vaccination against HPV was introduced in the USA in 2006. lt is recommended in young girls,
years before starting sexual activity. This will hopefully decrease infection and subsequent develop-
ment of ClN.

3. HUMAN tMMUNODEF|C!ENCY VTRUS (HtV)

HIV was first identified in 1981 as a retrovirus that causes acquired immunodeficiency syn-
drome (AIDS). The syndrome is responsible for severe deficiencies in cell mediated immunity, lead-
ing to unusual opportunistic infections, malignancy, and eventually death.

HIV has a variable and long asymptomatic latent period that ranges from2 months to17 years
in which patients are asymptomatic carriers. The mean age at diagnosis of AIDS infection is around
35 years.

EPIDEMIOLOGY
' HIV is worldwide. Men are affected more than women, but prevalence in women seems to be
increasi ng.

' Most of infections are caused by HIV type l. HIV type ll is rare and less virulent.
. Modes of transmission:
- Horizontal transmission: from one sexual partner to another through micro-abrasions
of the mucous membranes or through skin penetration by needles.
- Vertical transmission: from an infected mother to the fetus by trans-placental route.
 06 Sexuallv Trq nsmitted Diseases

HIGH RISK POPULATIONS INCLUDE:

Male homosexuals and bisexuals and female heterosexual consorts of infected men
- Intravenous drug users, recipients of infected blood, or concentrated blood products
- Infection with other STDs
- Neonates born to infected women
CtINICAL PICTURE (Symptoms & Signs)
1. Asymptomatic: 80% of HIV infected cases remain asymptomatic for around 10 years
2. Initial HIV exposure: fever, sweats, headache, pharyngitis, myalgia, and arthralgia.
3. AIDS is the final stage: with associated generalized lymphadenopathy, Kaposi sarcoma, op-
portunistic infections, malaise, diarrhea, and weight loss.

DIAG NOSTIC I NVESTIGATIONS

1. ELIZA screening: for individuals at risk detects > 95% of patients within 3 months of infec-
tion.
2. Western blot analysis: Confirmatory test for ELIZA positive cases.
3. Viral load testing for HIV plasma RNA: if acute retroviral syndrome is suspected.

TREATMENT (CDC 2010)

1. lmmediate medical care and referral to soecialized centers.
2. Prophylaxis for opportunistic infections by vaccination against pneumococcal infection, Hep-
atitis B, measles, and haemophilus influenza B.
3. There is now a great development in antiretroviral therapy as well as vaccination against HIV
that helped in reducing the disease prevalence and improved prognosis.

SYPHILIS
Syphilis is a systemic STD caused by the spirochete Treponema pallidum.
EPIDEMIOLOGY:
. After the introduction of Penicillin treatment regimens, by the
second half of the 20th century, the disease showed a sharp de-
cline in prevalence in most developed countries. However, the
last 2 decades have shown an increase in the incidence of infec-
tion concomitant with the rise in the incidence of HlV.
. Modes of transmission: syphilis can be transmitted either by Fis 12_2;
Treponema pallidum
A. Direct contact with an infected lesion. or contact with infected blood
B. Intrauterine verticaltransmission from mother to fetus (congenital syphilis).
o Once the organism reaches circulation, there is a rapid systemic spread via the blood and
lymphatics to reach different organs.
CLINICAL PICTURE (Symptoms & Signs)
L. Primary syphilis: the initial lesion is a painless, ulcerated, hard chancre, usually on the exter-
nalgenitalia, although vaginal and cervical lesions may be detected. The lP ranges from 1-0-90
days. The primary lesion usually resolves in 2-6 weeks.
2. Secondary syphilis: in untreated patients this chancre is followed in 6 weeks to 6 months by a
secondary or bacteremic stage with infection of the skin and mucous membranes that usually
resolve in 2-6 weeks.
 Gynaecology 107

- Mucous patches; maculo-papular rash of the palms, soles, and mucous memoranes.
- Condyloma latum (moist flat confluent plaques), and generalized lymphadenopathy.
3' Tertiary syphilis: will affect approximately 33% of untreated patients with multiple organ in-
volvement. This is a non-contagious but highly destructive phase of syphilis.
- Aortitis (the basic lesion); with endarteritis, aortic aneurysm, and aortic insufficiency.
- Tabes dorsalis, optic atrophy, meningovascular syphilis, and gummatous lesions (gummas
are nodular lesions characterized by granulomatous inflammation that may occur in any
organ).
4. Congenital syphilis: due to materno-fetal transmission may cause still birth, nonimmune hy-
drops, jaundice, infant hepatosplenomegaly, and skin rash. ldentification of and treatment of
pregnant women with diagnosed syphilis is the mainstay of prevention for congenital syphilis.
N.B.: Latent infection may occur in infected individuals with no clinical manifestations of the disease

DIAG NOSTIC I NVESTIGATIONS

. Dark field examination: of fresh specimens obtained from tissue exudates and mixed with
saline detects spirochetes in the primary and secondary stages of the disease.
. Serologic tests: In primary disease serology may be negative until individuals have enough
time to mount an immune response. In secondary and tertiary syphilis serologic test are help-
ful in diagnosis,
l-. Non treponemal tests: Rapid Plasma Reagin (RPR) and Venereal Disease Research Labora-
tory (VDRL) measured in titers, usually correlate with disease activity. These tests may give
false positive results being positive in a variety of other medical conditions.
2. Treponemal antibody tests: Fluorescent Treponemal Antibody Absorption (FTA-ABS) and
T. pallidum Particle Agglutination (TP-PA) can remain positive for life although may turn
negative with early treatment. These tests are specific and used to confirm the diagnosis

TREATMENT (CDC 2010)

A. Early disease; primary, secondary, early latent and asymptomatic recent contacts:
- Benzathine penicillin G 2.4 million units lM in a single dose
- Doxycycline L00 mg orally twice daily for 2 weeks in non-pregnant patients with penicillin
allergy
B. Late disease: late latent syphilis or tertiary syphilis (not including neurosyphilis)
- Benzothine penicillin G 2.4 million units lM every week for 3 weeks
- Doxycycline L00 mg orally twice daily for 4 weeks in non-pregnant patients with penicillin
allergy
C. Neurosyphilis:
- Aqueous crystolline penicillin G 1,8-24 million units/day lV infusion for 10-14 days.
- ln pregnant or penicillin sensitive cdses: Penicillin desensitization.
D. Congenital syphilis: infants and children with history of inadequate maternal treatment
- Eorly diseose: Aqueous crystalline penicillin G 5O.OOO unit/kg tM single dose up to the
adult dose.
- Late diseose: Aqueous crystalline penicillin G 50.OOO unit/kg lM up to the adult dose every
week for 3 weeks.
' All patients should be evaluated clinically and serologically at 6 months, 1 year and 2 years (for
latent & tertiary cases.
 Male Infertility Coitol dysfunction
Female infertility U nexploined nfertility
I

Assisted Reproduction

OVERVIEW
Infertility (or subfertility) is the term that describes failure of a couple to achieve conception
after one year of regular sexual intercourse, without using any method of contraception.
Almost L5% of couples may suffer infertility after thefirst year of marriage. Problems may be
foundeitherin thefemale(50-60%) orinthemalepartnerG0-aO%1.Inabout25%of casesprob-
lems will be found in both partners at the same time.
Fecundability is the monthly probability of pregnancy among fertile couples. lt ranges around
20-25% per cycle with unprotected intercourse.
The cumulative pregnancy rates increase by time to reach up to 50% in 6 months, and up to
85% after one year of regular marital life.
r Infertility may be either primary or secondary;
Y Primory infertility: pregnancy has never been achieved before.
Y Secondory infertility; history of previous one or more pregnancies, but failure to con-
ceive again.
Investigations for infertility should be carried out on both the male and the female partners,
and should cover all the possible factors that may be responsible for delaying pregnancy in each of
them.
In the female, investigations include ovarian, uterine, tubal, peritoneal, and cervical factors.
In the male, evaluation always starts by a semen analysis, and if abnormal further tests and
clinical evaluation will be considered.
Pregnancy can be achieved in nearly 50-60% of infertile couples after performing thorough
investigations, and receiving appropriate medical and or hormonal treatment for both partners.
Assisted reproductive techniques (ART), will be indicated in cases with severe male factor,
severe tubal and peritoneal factors, and in some cases of unexplained infertility, ART includes;
Y lUl: Intra Uterine Insemination
Y |VF-ET:lnVitroFertilization&EmbryoTransfer,inwhichlntraCytoplasmicSpermlnjec-
tion (lCSl) is the most commonly applied technique

FACTORS RESPONSIBLE FOR I NFERTILITY

r Male factor (30-40%)
r Female factor (50-60%)
r Coital dysfunction
r Unexplained InfertilitV OO-15%l

108
 Gynaecology 109

MALE INFERTILITY
It is estimated that 2% of mendemonstrate issues with their seminogram. The male is respon-
sible alone for up to 40% of infertility cases, and should be evaluated separately and thoroughly in
every couple presenting with infertility, before going into invasive female investigations.

AETIOLOGY

A) Abnormal Spermatogenesis

L. lncreosed Scrotal temperoture: (scrotal temperature should be 1oC less than body temperature):
- Undescended testes
, u;r"un:";::::r1r, in micro-deretion orthe y chromosome
L- 3. Drug lnduced: as anti-hypertensive drugs, anti-epileptics, psychotropic agents, prolonged
antibiotic ad m in istration, a nd chemothera peutic agents

B) Failure of Sperm Transport through the Vas deferens:

1'. Bilateral Epididymeol Obstruction; Gonorrheal inflammation is the commonest cause.
2. Bilateral Vas Ligation:
F Intended: as in male sterilization.
F latrogenic: rarely faulty ligation during bilateral inguinal hernioplasty operations
3. lmmotile Cilia Syndrome: All sperms are immotile.
C) Failure of (due to ejacutatory dysfunction):
,Til::rfrosition:
- Premature ejaculation
- Retrograde ejaculation, and an-ejaculation

DIAGNOSIS OF MALE FACTOR

v. A) History:
Related operative procedures: repair of inguinal hernia or varicocele.

- iiHl**,"#iili1:.T*xffilh:"i-;:n:""
- Chronic drug intake; as antihypertensive, antiepileptic, psychotropic drugs, etc...
B) Clinical Examination:
- To exclude: undescended testicles, testicular masses, and small testes.
To detect: the presence of hydrocele, and/or varicocele, and their extent.

C) Special Investigations:

_ ';ffi[fTi:':;iJ;:f ff;::ffi1,i:".'.il:l:5'*i:."1
cou rse.
:111H.'ff:x',i:::
2. Hormonol assay:FSH, LH, prolactin, Testosterone,
3. Doppler US; on the testicles to detect varicocele
4. Testiculor biopsy: to differentiate between defective spermatogenesis and obstructive
disorders
5. Chromosomal studies;to diagnose genetic disorders
110 lnfertility and Art

cRrrERrA FOR NORMAL SEMEN ANALYSIS (WHO 2010)

Parameter Normal Criteria

Volume 2 ml or more
Count 15 million / ml or more
PH 7.2-7.8
Motility 50% or more with forward progressive motility
Morphology 30% or more with normal morphology

Term Definition
Aspermia Absence of semen
Azoospermia Zero sperm count
Oligospermia Count < 15 million / mr
Asthenospermia <50% with forward progressive motility
Teratospermia >70% abnormalforms

MANAGEMENT OF MALE INFERTILITY

lmprovement in poor semen parameters may take from 3-6 months of appropriate therapy
A. Stop smoking (to improve oxygenation).
B. Use of Multivitamins and Antioxidants, are thought to improve sperm count and motility.
C. Treat erection disorders; using medications (as Viagra), or synthetic prosthesis.
D. Shift to other types of antihypertensive and psychotropic drugs if they were a cause.
E. Hormonaltreatment: CC & HMG are useful in cases of defective spermatogenesis.
F. Surgicaltreatment:
- Ligation of varicocele: may improve sperm count and motility in some cases.

Artificial prosthesis: in some erection disorders

G. Assisted Reproductive Techniques (ART): see later for detoils
a. lntrauterineinsemination (llJl): lt is indicated in cases with;
> Mild oligospermia
D Coital dysfunction and erection disorders.
) Unexplained infertility.
b.ln-Vitro Fertilization qnd Embryo tronsfer (|VF/ET): suitable for
> Mild male factor or
) Unexplained infertility (see details in ART).
c. lntro Cytoplosmic Sperm lnjection (lCSl/ET): suitable for severe male factor as
F Severe oligoasthenospermia.
)Obstructive Azoospermia; sperms recovered directly by testicular sperm aspiration.
N.B.: Cases with genetic disorders & obstructive ozoospermio carry the poorest
prognosrs.
 Gynaecology tll

FEMALE INFERTILITY

: are responsible alone for delayed conception in nearly 5O% of cases. Anovulation,
Females
tubal damage, and peritoneal adhesions are the most frequently encountered causes. Uterine
and endometrial factors are less common, while cervical factor is rare. ln LO-LS% of cases no
identifiable cause will be reached in either partner referred to as unexplained infertility.
v
FACTORS CAUSING FEMALE INFERTILITY
1. OVARIAN FACTOR
Anovulatory disturbance is the most commonly encountered factor for female infertility being
the primary cause in almost 40% of cases, including;
a. PCOS: the most common cause of anovulation in the childbearing period
b. Hyperprolactinaemia.' due to stress, drug induces, or pituitary hyperplasia and/ or adenomas
c. Severe thyroid disorders (hyper and hypo thyroidism)
d. Premature ovorion foilure and insufficiency (POF & POI)
e. Severe stress, exhausting exercise, and rapid excessive weight loss
f . Drug induced: OCPs, GnRH agonists, gestagens, chemotherapy, opiates, barbiturates, etc...

I Luteal phase defect (LPD): due to inadequate progesterone sufficiency causes failure of im-
plantation and recurrent early pregnancy loss (see chapter 8)
I Age of the female is the single most important factor in anovulatory infertility, where fertility
declines rapidly after the age of 35 years and mor sharply after the age of 40 years
I N.B.: See amenorrhoea and chronic anovulatory disturbances ( chapters 7 and 8)

II. TUBAL AND PERITONEAL FACTORS

Tubaland Peritoneal factors may be responsible for almost 3O%of female infertility.

_ "n"':"i:';?,n":i:trtr;ily,:::";';:i'l#o.,,,,.tion and / or peritubar adhesions

Y lmpaired oocyte or embryo tronsport; due to tubalobstruction.
D Tubal epithelioldamage; with absent nourishment to the oocyte during transport
1. Salpingitis, Salpingo-oophoritis, and Pelvic Peritonitis: causing tubal damage & pelvic
adhesions
STDs: Gonococcal and Chlamydial infections causing endosolpingitis.
Puerperal and post abortive infections: lymphatic spread casing perisolpingitis
Chronic specific infections as T.B. : causing interstitial solpingitis
- Chronic non specific infection especially if it leads to tubo-ovorion obscess.
- Extension from appendicitis, ruptured gall bladder, perforated peptic ulcer.
Sepsis following pelvic surgery.
2. Mechanical Obstruction: causing compression, stenosis, or overstretching of the tubes
Large multiple ISM & SSM.
Large ovarian and adnexal masses
3. SurgicalTrauma (latrogenic): leading to direct tubal damage or peritubal adhesions
Salpingectomy (ectopic pregnancy), tubal ligation (for sterilization), or tuboplasty
Gynaecologic surgery; after myomectomy, and ovarian cystectomy.
Pelvic surgery; as during surgery for intestinal obstruction and appendectomy.
4. Pelvic Endometriosis: extensive disease may cause pelvic and peritubal adhesions.
It2 lnfertility ond Art

III. UTERINE AND ENDOMETRIAL FACTORS

Uterine and endometrial factors may be responsible for tO-t5% of female causes of infertility,
mostly via the following mechanisms;
-
D lmpairment of blastocyst implantation within the endometrial cavity
D Bilateral cornual obstruction of tubal ostea
F Interference with transport of sperms through the endometrial cavity
1. Congenital Uterine Anomalies:
Septate and Bicornuate uterus (infertility and or RPL)
- Uterine hypoplasia and or aplasia (amenorrhoea and infertility)
2. Uterine Leiomyomas: especially large and multiple ISM and SMM
3. Uterine Polyps: SMF polyps or endometrial polyps.
4. Intrauterine Synechae predisposed to by;
- Over curettage of basal endometrial layer (Ashermann's syndrome)
- Acute septic endometritis (puerperal, post abortive sepsis, and IUD associated)
Chronic specific infections (e.g.; T.B. endometritis)

IV. CERVICAL FACTOR

Abnormalities of cervical mucus that affect its amount, quality, and constituents may impair
sperm transport through the cervical canal making it incapable of fertilization, via the following
mechanisms i --
- Changes in physical and chemical properties, e.g.; scanty amount or increased viscosity

- Infection and presence of pus cells, e.g.; acute and chronic endocervicitis

- Presence of anti-sperm antibodies in cervical mucus

Destruction of mucus secreting glands; by conization or excessive cauterization

Elongation of cervical canal by a cervical fibroid may rarely be an underlying factor

I NVESTIGATIONS FOR FEMALE INFERTILITY

In the apparently normal couple, investigations for infertility do not usually start before 6
-
monthsto l yearof regular maritallife without contraception. Earlier investigations may be start-
ed whenever;
Y Age of the female partner is above 35 years
) History reveals marked menstrual disorders
F History strongly suspicious of uterine, tubol, or peritoneal pothology
F Suspicion of a severe mole factor especially in older age males.
Female evaluation usually starts by a detailed history, generaland local examination, pelvic
US, and a hormonal assay. lf no apparent cause was revealed, and the male semen analysis was
normal, then more invasive tests as HSG, hysteroscopy, and Laparoscopy will be required to evalu-
ate uterine, tubal and peritoneal factors.
ln t0-I5% of cases investigating both partners by standard tests may not reach a cause, a con-
dition known as unexplained infertility (see later)
 Gynaecology 113

I. ASSESSMENYT OF ANOVULATORY DYSFUNCTION

1'.Basal Body Temperoture ( BBT) Chart: reveals absence of a biphasic BBT chart
2.US monitoring of ovulation: serial TVS revealing inadequate growth of follicles and failure of
ovulation
3.Urinory LH kits: reveal absence of an LH surge at mid-cycle
4.Mid-luteslserum PRG.'revealing low levels < 5 ng/ml in anovulation and < 10 ng/ml in LPD
S.Premenstuql endometrisl biopsy (PEB): done as office procedure using a suction Pipelle or
Novak curette revealing proliferative endometrium in the premenstrual period instead of se-
cretory endometrium.

II. ASSESSMENT OF UTERINE AND ENDOMETRIAL FACTORS

1. PELVIC ULTRASOUND (US): see imaging in gynaecology
TAS and TVS are considered the gold standard in evaluation of uterine and endometrial fac-
tors. Introduction of 3D US and Saline Infusion Sonography (SlS), has improved the accuracy of US
diagnosis:

SMM, SMF polyp, and endometrial polyps (3D US & SIS).

Intra uterine adhesions (SlS)

Associated adnexal masses (TAS & TVS)

2. HYSTEROSALPINGOGRAPHY (HSG): see imaging in gynaecology

HSG entails injection of a radio-opaque dye within the endometrial cavity through
the cervical canal, to visualize the endometrial cavitv and the
fallopian tubes.
HSG is considered the gold standard in infertility evaluation as
it allows diagnosis of;

unicornuate uterus.

terine adhesions

site, nature, and bilaterality

the post dye injection control film. Fig 13-1: HSG showing normal
uterine covity with no filling de-
3. HYSTEROSCOPY: see imaging in gynaecology fects, ond bilateral tubol potency

Office hysteroscopy, done as an outpatient procedure, allows direct visualization of the

uterine cavity, using an optic lens, a light source, and a distending medium (saline, or glycine).
Minor surgical procedures can be also performed via hysteroscopy.
tt4 lnfertility and Art

III. ASSESSMENT OF TUBAL AND PERITONEAL FACTORS

1. HYSTEROSATPINGOGRAPHY (HSG): see imaging in gynaecology

HSG done to investigate uterine and endometrial factor at the same time is considered a
cornerstone in investigating tubo-peritoneal factors (see before).
r Normal HSG:
- Bilateraltubal patency; normaltubal caliber and free spill of the dye
- Absence of significant pelvic adhesions; free dispersion of the dye in the pelvis.
r AbnormalHSG:
- Unilateral or bilateral, distal or proximaltubal obstruction.
- Presence of hydrosalpinx; distal tubal obstruction with dye filled sacculation.
-Suspected pelvicadhesions; loculation of the dye in the pelvis in controlfilm.
r AdvantaBes of HSG in Infertility
F Easy to perform and does not require general anaesthesia or operating theatre
F lnvestigates both uterine and tubal factors at the same time.
) Accurately detects the site of tubal obstruction (cornual, proximal, distal, etc...)
> High suspicion in diagnosis of T.B. endometritis and T.B. salpingitis.
) lmproves pregnancy rates in the first 3 months in cases of unexplained infertility
r Disadvantages and Complications associated with HSG: generally rare, but may in-
clude
F Allergic reactions with shock and collapse
) Infection; causing flaring up of endometritis, salpingitis, and rarely peritonitis.
F Oil embolism and oilgranuloma.
B. LAPAROSCOPY AND DYE INJECTION: see endoscopy in gynaecology

Laparoscopy allows direct visualization of the pelvic peritoneum, pelvic organs, and external
surface of the fallopian tubes through an optic lens and a light source, introduced via
the umbilicus.
Injection of methylene blue dye through the cervix, allows for observing its spillage through
the fimbrial ends of fallopian tubes to ensure tubal patency, and evaluate its ciliary function.
The procedure is performed under general anaesthesia.

r Advantages of laparoscopy in infertility;

adhesions.

PlD, and T.B. peritonitis.

metriomas.

vic adhesions, treatment of pelvic and ovarian

endometriosis, and ovarian drilling in PCO.
Fig L3-2: Diognostic laparoscopy
 Gynaecology 115

IV. ASSESSMENT OF CERVICAT FACTOR

A. Assessment of the physical properties of the cervical mucus

Preovu latory Postovulatory

- Thin , profuse, and watery
- Thick and sconty
- Acellulqr ond Alkaline - Cellulqr
- Positive thread test (stretch 6-10 cm) - Negotive threqd test (threods breok < 6.0 cm)
- Mqximum Ferning when dried under microscopy - Minimol Ferning when dried under microscopy

B. The Post Coital Test (pCT): rarely performed nowadays

!- Examination of the cervical mucus 6-l-0 hours after intercourse, at time of ovulation, to
assess the number of living and dead sperms and presence of leucocytes, affecting sperm
motility within the cervix (normally> 20 progressively motile sperms / HpF)
- An abnormal PCT may point to hostile cervical mucus, or presence of antisperm antiboo-
v ies, yet its value has been recently questioned being of limited prognostic value.

HORMONAL ASSAYS COMMONLY REQUIRED FOR INFERTILTTY

- serum FsH & tH (day i.-3 of cycle): abnormal LH/FSH ratio in pcos
Urinary LH assays: positive urinary LH denotes impending ovulation (24 hours)
v Mid lutealSerum PRG: usually day 2t of the cycle (> 1Ong/ml denote ovulation)
Serum PRL: (N: 2.a-2a ng/ml); high levels denote hyperprolactinaemia
Serum androgen levels: (total and free T, DHEA) in cases with hirsutism and PCOS.
Thyroid function tests: (TSH, T3, T4) to detect major thyroid disorders

Coital dysfunction may prevent penetration and deposition of male sperms into the vagina. lt may
also affect the frequency and efficiency of sexual intercourse
v a' Superficiol Dyspareunia: painfulor difficult coitus at the levelof the vulva and lower vagina.
b. Vaginismus.' violent reflex spasm of levators ani, gluteus muscle, and adductors of the
thigh on any attempt at intercourse.
c. Male Erectile disorders: as impotence, and premature ejaculation, etc...
N.B.: Effluvium seminis of the seminal fluid from vagina after inter-
(excessive escape
course) is a common complaint that does not really affect or delay fertility.
_
UN EXPLAIN ED I N FERTI LITY
v Unexplained infertility is a diagnosis of exclusion. lt may be present in almost 15% of
infertile couples when all standard male and female infertility investigations fail to detect a pos-
sible cause. Almost 60% of these couples will conceive within 3 years without treatment.

Possible Contributing Factors

- lmmunological and psychological factors
Defective sperm fertilization capacity
.- - Decreased ovarian reserve: decreased number and quality of oocytes (day 3 FSH level > 10
mlU/ml, and low AMH < 1ng/ml).
Occult cervical infection.
l16 lnfertility qnd Art

MANAGEMENT OF FEMALE INFERTILITY

After the cause of female infertility has been apparently revealed, treatment will be initiated
according to the cause discovered.

INDUCTION OF OVULATION FOR ANOVULATORY INFERTILITY

A. ORAL DRUGS (for details see chapters 7,8)
L. Clomiphene citrate (CC): is the drug of choice for anovulatory infertility. lt acts by blocking E2
receptors and inducing pituitary FSH production stimulating follicular growth and maturation.
lt is given in a dose of 5O-2OO mgldaily/5 days starting day 3, 4, or 5 counted from the 1't day
of the LMP.
2. Tamoxifen: a weak anti-oestrogen that acts by blocking E2 receptors as CC, with increased pi-
tuitary stimulating follicular growth and maturation. lt is given in a dose of tO-4O mg/
FSH
daily/5 days, staring day 3, 4, or 5 counted from 1" day of LMP.
3. Letrozole: an aromataze inhibitor that blocks conversion of testosterone to osterogen, leading
to increased pituitary
FSH production and stimulation of follicular growth and maturation.

B. I.M. GONADOTROPHINS
1. Human MenopausalGonadotrophins (HMG): repeated doses each containing (75 lU FSH and
75 lU LH) given according to the size of growing follicles by US and / or serum oestrogen levels
2. Purified HMG: repeated doses each containing (75 lU FSH and 1 lU LH), suitable for PCOS cases
with high endogenous LH to avoid severe OHSS
3. Synthetic HMG: repeated doses each containing (75 lU FSH), suitable for cases of PCOS and for
protocols of induction in IVF / lCSl cases to induce controlled stimulation of multiple follicles
for recruitment
C. Human Chorionic Gonadotrophins (hCG):
5000-10000 lU if hCG are given lM as one shot to facilitate rupture of mature Graaftian follicles
as evidenced by US size > 20 mm or high oestrogen levels. lnjection is withheld if a large number of
follicles has reached maturity and > 20 mm size to avoid severe OHSS in cases not undergoing lCSl
procedures.
D. SURGICAL INDUCTION OF OVULATION
This can be achieved through laparoscopic ovarian drilling (LOD), a procedure in which small
punctures are made within the ovary using a diathermy needle. lt is assumed that this may de-
crease intra-ovarian androgens resulting in spontaneous ovulation.
lndications; PCOS cases that are either CC or HMG resistant, or easily develop OHSS

Side effects ond limitotions.'The use of LOD is hindered by;

.f. lt's time limited effect on ovulation (3-6 months).
..'. lt's potential for creating ovarian damage compromrsrng ovanan reserve.
.i. lt's potential for creating periovarian, and peritubal adhesions (tubo-peritoneal factor).

ADJUVANT DRUGS USED IN ANOVULATORY INFERTILITY:

D Druqs for Hypeproloctinoemia:
- Bromocriptine: 2.5 mg, 1-2 tablets daily, or
Cabergoline: 0.5 mg, 1/2 tablet twice weekly, until PRL levels drop to normal
 Gynaecology 111

Y lnsulin Sensitizers: Metformin:500-1000 mg daily in cases with insulin resistance

(see PCOS)
Y Thyroid extract: Eltroxin 50-150 ug daily in cases of hypothyroidism
Y Corticosteroids: in cases of adrenal insufFiciency and some cases of pCOS.
N.B.: A combination of drugs can be used for induction of ovulation according to different pro-
tocols that may use ORAK drugs only or in Combination with lM HMG and hCG. in addition
to one or more of adjuvant drugs.
N.B.: Patients with class 2 & 3 obesity will benefit from significant weight reduction before
starting protocols of induction, this will help in better follicular stimulation with lower doses
and combinations of drugs and less side effects and OHSS.

MANAGEMENT OF TUBAL AND PERITONEAL FACTORS

Tubal occlusion can usually be anatomically corrected by various surgical techniques however
restoration of tubal function 2ry to tubal damage could not be easily achieved.
a. Laparoscopic Procedures:
F Lysis of Peritoneal Adhesions (Adhesiolysis): Lysis of mild thin inflammatory peritubal and
periovarian adhesions, using Diathermy cauterization or Laser ablation, can be successfully
achieved via laparoscopy. lt improves ovum pick up mechanism and may restore fertilitv
as long as tubal function and patency are ensured.

F Excision & Ablation of Pelvic Endometriosis: small peritoneal and ovarian endometriotic
implants, may be easily laparoscopically excised or fulgurated using Diathermy or Laser,
with good results.
B. Laparotomy for Tuboplasty:
The role of laparotomy for performing tuboplasty procedures, as fimbrioplasty and neosalpin-
gostomy, has largely diminished in the last decade in favour of much better success rates for lCSl
procedures. When indicated it should follow strict microsurgical techniques with complete haemo-
stasis and minimal tissue handling. Results are not encouraging as post operative adhesions are
common, and initial occult tubal damage is already present in the majority of cases.

MANAGEMENT OF UTERINE FACTOR

7) Operative hysteroscopy can deal successfully with many uterine abnormalities in infertility;
D Hysteroscopic Septoplasty: resection of uterine septum (septate uterus)
Y Hysteroscopic Polypectomy: excision of endometrial polyps
D Hysteroscopic Myomectomy: excision of certain types of SMM and SMF polyp
Y Hysteroscopic Adhesiolysis: division of thin intrauterine synaechiae.
2) Myomectomy via Laparotomy or laparoscopy; indicated in large leiomyomas causing infertility

MANAGEMENT OF CERVICAT FACTOR

- Treatment of the cause; as chronic cervicitis, hostile cervical mucus, removal of polyps
- Use of oestrogen ond mucolytic drugs to improve cervical mucus physical properties

- lntrauterine lnseminotion IUI: injection of processed semen directly within the endome-
trial cavity bypassing the cervix.
118 lnfertility ond Art

5. MANAGEMENT OF UNEXPLAINED INFERTILITY

Reevaluation of both partners and obtaining more recent investigations.
- Further tests, not previously performed, as diagnostic laparoscopy and hysteroscopy.
- Serum Chlamydia antibodies, and cervical mucus assessment.
- Super ovulation induction protocols with purified HMG under TVS guidance.
Repeated lUl, for at least 3 cycles, may improve the chances of conception'
IVF & lCSl procedures are the last resort, but with best prognosis.

ASSISSTED REPRODUCTIVE TECHNIQUES

Assisted reproductive techniques (ART), describe the use of advanced technologies to
facilitate or assist oocyte fertilization. The commonly used techniques nowadays include:
F Intrauterine insemination (lUl)
F In-Vitro Fertilization and Embry Transfer (|VF/ET)
F IntraCytoplasmic Sperm Injection (lCSl).
r. rNTRA UTERTNE TNSEMINATION (lUl)
lUl entails intrauterine injection of processed male semen into the uterine cavity through
the endocervix at the time of ovulation. Semen is processed before injection, where high quali-
tyspermatozoaare mixedwith an enriched media (Ham F10) to ensure maximum sperm activity.
lUl is indicated in cases with coital dysfunction, male factor as erection disorders or mild oli-
gospermia, female cervical factor, or cases with unexplained infertility.
Success rates for lUl are limited, reaching almost 15% conception rates after at least 3 trials
within 5 months duration.

II. IN-VITRO FERTILIZATION AND EMBRYO TRANSFER IVF-ET

IVF involves incubation of female oocytes with male spermatozoa in the
US guided retrieved
laboratoryto facilitate their fertilization. The resultant embryos are transferred back intothe uterus
(ET).
OVUM PICK UP

-{
o

>

Fig 1.3-j: IVF-ET

ilr. TNTRACYTOPLASMIC SPERM INJECTION (lCSl)

lCSl: is a micromanipulation techniquethat differs from IVF in that a sperm is injected direct-
ly into the cytoplasm of the oocyte to enhance fertilization. It is the orocedure of choice com-
monly performed almost replacing older IVF procedure.
 Gynaecology 119

lndications for IV F/ I CS I Procedures

a) Severe tubo-peritoneal factor with tubal damage and/ or extensive tubo-peritonealadhe-
stons.
b) Failed adhesiolysis and/ or tuboplastyprocedures.
c) Severe male factor: as severe oligoasthenospermia, and Azoospermia.
d) Uexplained infertility:especially after repeated failed lUl.
Steps and Techniques in IVF/ICSI Procedures
7. Pituitory down-regulotion: daily S.C. or intranasal doses of Gn RH agonists are essential
to prevent natural LH surge during follicular stimulation as this may result in follicular rup-
ture before egg retrieval.
2. Ovorian stimulation.' controlled ovarian stimulation by daily lM FSH injection to induce
multiple follicular growth and maturation. Injections are continued for 1.'J.-14 days until the
leading follicles reach 18 mm in diameter by TVS.
3. Ovulation trigger: by hCG: in order to induce an artificialLH surge
4. Oocyte retrieval: egg collection: is performed via US guided transvaginal needle aspiration of
mature oocytes (larger than 18 mm in diameter), 24 hours after hCG ovulation trigger.
5. Laboratory sperm-egg fertilization: idts
a.ln IVF: 100,000-2OO,OOO sperms are incubated with retrieved ."n'n"n-
oocytes, 4-6 hours after collection, in a special container to al- , f i c',np
low spontaneous fertilization. u '
b.ln lCSl: a sperm is injected directly into the cytoplasm of the ,.
.i
metaphase ll oocyte through the zona pellucida under a special ' ,ou."u
e!'rri ion'hl
inverted phase microscooe
c.Oocytes are transferred to a fresh culture medium and exam- Fig 1j-4: ICSI
ined for fertilization and cleavage by the presence of 2 pro-nuclei.
6. Embryo transfer (ET): trans-cervical transfer of the embrvos into the uterine cavitv is
carried out 2-3 days after oocyte retrieval.
7. Luteol phase support:administration of progesterone to assist blastocyst implantation
and avoid premature shedding of the endometrium is started after ET and continued
for 2 weeks. lf serum B- hCG revealed a positive test 2 weeks after ET, progesrerone
support will be continued throughout the first trimester of pregnancy.
Success Rates oI IVF / lCSl Procedures
I Success rates in lCSl procedures are higher than lVF, reaching around 25-40%.
. Success rates depend largely on
Maternal age
- Quality of oocytes retrieved
Quality of embryos fertilized
- Presence of pelvic pathology as endometriosis or plD.
- The protocol chosen for stimulation, technique performed in oocyte retrieval and
embryo transfer, and the control on media used for oocyte/embryo incubation
Com pl icoti o ns of lVFfl CSI Proced u re s
1-. Allergic reaction to ovulation induction agents
2. OHSS with its complications (see OHSS in treatment of anovulation CH 8)
3. Trauma during oocyte retrieval: as vaginal haemorrhage, injury to major pelvic ves-
sels, or injury to adjacent uterine, tubal, or intestinal organs.
4. Pelvic infection related to the procedure of oocyte aspiration.
5. Complications of ART pregnancies as; increased incidence of abortion, ectopic preg-
nancy, M FP, and a slight increase in some congenital anomalies.
120 lnfertility ond Art

Gn RH Analogues in IVF/|CS| Protocols:

r GnRH agonists are synthetic decapeptide forms of GnRH.
- Route of administration: repeated S.C. injection or nasal spray.
lndications: used mostly in IVF/ICSl protocols to suppress endogenous FSH & LH
through their down regulation receptor effect, thus preventing premature ovulation,
and allowing maximum egg retrieval.
r GnRh antagonists: are gaining popularity now in the protocols of IVF/|CS| procedures. This is
due to the fact that is shorter in duration, safer in cases who more prone for OHSS
(including cases of PCOS), and cheaper in terms of using less medications. GnRH antagonists
are used as well in cases running on GnRh agonist protocol and who develops signs of im-
pending OHSS. lts value is that it almost immediately shuts down the endogenous FSH and
LH production thus preventing the development of OHSS.

Key points in lnfertility

- tnfertility is a problem of a couple, therefore history, examinotion, investigotions, and counseling
should include both portners.
- lnfertility moy be due to male factors, female factors, or o contribution of both
- lnvestigations for infertility usually stort at leqst 6 months ofter unprotected regular sexuql inter-
course unless history is suggestive of a significont male orfemole problem.
Fast track diagnosis ond monagement is essentiql in women over 35 years of age and in women
with baseline FSH > 10 ngl ml indicating compromisedovarion reserve.
- Female foctorsfor infertility include; ovorian, tubal, peritoneal, uterine, and cervicol factors
- Treqtment of onovulatory infertility carries the best prognosis. Success rates in induction of ovula-
tion moy reqch about 80-90%, with pregnancy rates opproaching 70-80%.
, lnduction of ovulotion usually starts by CC alone, CC/hCG, or CC/HMG/\CG. lt should be performed
under TVS monitoring to qvoid the serious complication of OHSS.

Mony uterine factors ore surgically correctable vio hysteroscopy or loporotomy as polypectomy. Septo-
plosty, and myomectomy

- Treotmentof mildtubo-peritonealfactors moy have success ratesreachingaround j0%.

- Severe tubal domoge or extensive odhesions carry poor prognosis even after surgery
- lUl is usually offered to cqses of mild mole foctor, suspected cervical factor, or unexplained infertil-
ity, before attempting at IVF or lCSl.
Success ratesfor ICSI are approoching 25-40% in most centres.
Best prognosis is achieved in younger femoles, with absent pelvic pathology, ond those with mild
mole factor or unexplained infertility.
- lCSl seems to be the only hope for coses with severe male foctor or severe tubol damoge
 - Physiologic controception - Hormonol contraception
- Barrier controception - Femqle sterilizqtion
- lntrauterine contraceptive device - Controception during lactotion
- Emergency postcoital controception
OVERVIEW
Family Planning is practiced by many couples aiming at spacing pregnancies and choosing
the proper time for conception and childbirth.
Delaying conception is usually a temporary need for most couples, however permanent con-
traception may be required either because of an already completed family, or due to the presence
of severe chronic medical disorder that may complicate or be complicated by pregnancy.
An ideal method for contraception should be cheap, readily available, easy to use, with mini-
mal side effects and complications, and with maximum efficiency in protection from unwanted
pregn an cies.

Finally the best contraceptive method is one that has no or minimal effects on the future fe-
male fertility, once the couple decided planning for a new pregnancy, i.e. reversible contraception.
Temporary contraception; can be achieved via physiologic methods, barrier methods, chemi-
cal methods, lUCDs, and hormonal methods.
Permanent contraception; can be achieved in the female via tubal ligation, or hysterectomy,
while in the male permanent sterilization is achieved via bilateral surgical ligation of the vas def-
erens.
Occasionally, an urgent contraceptive method may be required whenever a coital relationship
has occurred in absence of a suitable protection, in an attempt to minimize the risk of unwanted
pregnancy.

PHYSIOLOG IC CONTRACEPTION
Physiologic or natural methods for contraception are easy, cheap, readily available methods
with reasonable efficiency, but are not reliable when used alone. Combining more than one method
will very much improve the efficacy without additional costs or hazards.

1. COITUS INTERRUPTUS
Withdrawal and ejaculation outside the vagina during intercourse is one of the oldest most
com mon ly practiced methods for contraception.
Efficacy of this method is not high, as in some cases the pre-ejaculatory fluid may contain
sperms capable of fertilization. lt is best coupled with the safe period method.

2. THE SAFE PERIOD

Intercourse is totally prevented, or protected (by a condom or coitus interrupted) at the
time of expected ovulation (day 10-1s of a28 days cycle), while allowed forthe rest of the month
without protection methods. This method is suitable only for intellectual couples, with regular
cycles.

121
122 Controception ond Family Plonning

Efficacy is good, and is improved when coupled with additional methods that allow for more
accurate prediction of ovulation as the BBT chart and urinary LH tests.

3. LACTATION
During lactation, at least 60 % of females will experience amenorrhoea, anovulation, and oli-
go-ovulation during the first 6 months of the puerperium, due to elevated prolactin levels.
r Efficacy: is not high (nearly 50% protection if used alone), duetothefactthatsome
women may resume ovulation at variable unpredictable periods of time. Efficacy is im-
proved by adding other methods as barrier, spermicidals, and coitus interruptus.

BARRIER CONTRACEPTION
These methods work by physically or chemically preventing sperm egg interaction.
To be effective barrier methods need to be used correctly and consistently with every act
of sexual intercourse. Correct use requires motivation, skills and, communication between part-
ners.

Advontoges of Barrier Methods Disadvantages ol Barrier Methods

- Easy to initiate and discontinue Difficult to use consistently ond correctly
- No systemic side effects May interrupt sexual activity ond pleasure
Some req u i re po rtne r's po rti ci p oti o n
- No elfects on future fertility Less effective thon other modem methods
- No effect on lactotioon
- Failure rates < L0/HWY
- Some moy prevent transmission of STDs

1. MALE AND FEMALE LATEX CONDOM

Latex condoms, used by the male, are the most widely used barrier contraceptive method all
over the world. The female latex condoms are not widely available in many countries.

- Efficocy: high pregnancy prevention rate reaching up to 97% which is additionally increased
when used with spermicidal creams, coitus interruptus, or the safe period.
- Advqntoges; high efFiciency, ready availability, easy use, cheap price.
- Medicol benefits: prevention of STDs (as HIV & HPV), HCV, and treatment of premature ejacu-
lation.

- Disadvontoges: rarely becomes torn, or slips out, thus losing protection

'-r
*

, 14=7: Male condom Flg 14-2: Spermlclde cream

 Gynaecology 123

2. SPERMtCt DES (NONOXYNOL-9)

spermicides inactivate sperms deposited in the vagina during intercourse.
- Forms: vaginaltablets, creams, gel, or sponge applied 30 minutes before intercourse.

- Efficocy: failure rates reach up to 30 /HWY if used alone however tney are more
effective when used with condoms or vaginaldiaphragms.
- Disodvantdges: spermicidals may cause allergic vaginitis in some women.

INTRA-UTERINE CONTRACEPTTVE DEVTCE (tUCD or tUD)

The IUD is the most commonly used method in nationalfamily planning programs, in develop-
ing countries, due to its high efficacy and long term duration of use.
The IUD is made of a polyethylene material that is Barium Sulphate coated to render it radio-
opaque on X-ray.
The stem is usually covered with a thin Copper (Cu) wire, but may also contain silver or gold.
Progesterone impregnated lUD, as the Levo-Norgestrel Releasing Intrauterine System (LNG-
IUS) have been introduced in the last decade, with increased efficiency, and excellent control of
uterine bleeding. They are nowadays commonly used in treatment of DUB.
The limbs of the IUD emerge from its upper stem. They are usually plain, but in some lUDs
may be covered by copper bars. The limbs serve as an anchor holding
the device properly at the fundus of the uterine cavity, avoiding its ex-
pulsion during menstruation.
Two nylon threads are attached to its lower stem and protrude
out of the cervix. They serve as markers for its presence and at the
same time facilitate IUD removal by simply pulling on the threads out-
wards.
IUD is the preferable method for long term contraception especial-
ly for multiparous women after completing their family. lt is generally
suitable for most women except those with irregular cycles, menorrha-
gia, DUB, and those with uterine or pelvic pathology as uterine septum,
leiomyomas, and PlD.
Fig. I4-3:

MECHANISM OF ACTION: (not completely understood)

A) Interference with Blastocyst lmplantation, rendering the endometrium unsuitable, via:
Y Locol foreign body inflammatory responses
Y Increased local endometrial pGL production
Y lnhibition of Carbonic anhydrase ond Alkaline phosphotose activity (Copper tUD)
Y lnduction of atrophic endometrial chonges (LNG-tUS)
B) Interference with Sperm Motility rendering them incapable of fertilization.
Y lnhibits sperm motility through the endometrial covity ond foltopian tubes
Y lnduces and antisperm phagocytic activity(Cu ilJD)
D Toxic effect on sperms inhibiting its copability of fertitizotion(cu tuD)
Y Produces thick cervical mucus interfering with transcervical sperm penetrotion (LNG-tUS)
t24 Controception ond Fomily Plonning

TYPES OF IUDS:
L. Copper medicated IU-D: (Cu T 380) is the most commonly used type with a surface area of
the copper 380 mm'. lt lasts effectively for 6-8 years then changed by a new device.
2. Copper+Silvermedicated IUD (Nova T): Cu T 200 IUD in which silver is added to minimize
fragmentation of copper.
3. Progesterone medicoted IUD: (LNG-lUS Mirena IUD) with sustained release of levo-
norgestrel 35 ug/day. lt acts effectively for 3-4 years then changed by a new device.

IUD INSERTION:
A) Timing of Insertion:
- Best inserted by end menstruation to ensure a slightly dilated cervix, absence of
of
pregna ncy, and minima I post-insertion bleed i ng.
- ft can be inserted 4-6 weeks after delivery, or 3-4 weeks after an abortion.
B) Technique of insertion:

The contraceptive device is composed of a polythene lUD, an insertion tube and a plunger rod.
- A preliminary US is performed to ensure the size and direction of the uterus, and to ex-
clude myomas, polyps, and adnexal masses.

- Cusco speculum is introduced into the vagina with the patient in the lithotomy position.

- The anterior lip of the cervix is grasped by a multiple toothed Volsellum

- A uterine sound is passed through the cervix to reassure uterine length and direction.

- The IUD is launched in the insertion tube which is gently passed through the cervical
canal reaching just short of the uterine fundus.

- Withdrowol Technique: the plunger rod is used to fix the IUD near the fundus, while
the insertion tube is gently rotated and withdrawn back releasing the limbs of the IUD
with the T arms spreading towards each uterine cornu (see diagram)
- The long IUD threads are then cut 2 cm from the external os.

ru
rE
ru stt&
$D
w
m

Fig 14-4: IUD insertion

 Gynaecology t25

C) Follow up after insertion:

- Periodic follow up visits after IUD insertion are recommended to ensure its proper
v fitting.
- Threads can be felt on PV examination, or seen on speculum examination.
v
- TVS or TAS is generally the best method to reassure proper IUD fitting within the uterine
cavity.
v
- Dealing with associated side effects or complications (see later).
ADVANTAGES OF IUD:

- - Single choice method, with a long term protection (6-8 years).

- lt does not affect lactation, in recently delivering women.
- lt does not affect or interfere with sexual intercourse
\* - Very low failure rate: 0.5/HWY {Hundred Women Yearly).

\/ PROBLEMS AND COMPLICATIONS ASSOCIATED WITH IUDS:

v 1. Abnormal Uterine Bleeding AUB:
a) Post Insertion Bleeding:
Mild bleeding, or spotting, may occur in the first few days following insertion. Bleeding usu-
ally stops spontaneously, but if persists use antifibrinolytics and venotonics.
b) Menorrhogia:
> Heavy menstrual bleeding (HMB) is common in the first few cycles following IUD insertion,

Aetiology: mostly due to increase PGLs production, or increased fibrinolytic activity.

'v Copper IUD increases blood loss by almost 35%in many women.

'!-
Ttlffi:r urcrin" and pelvic pathotogy;by ctinicat examination and petvic US

menstrual blood loss, and hence can be used as an alternative in cases who
intractable bleeding with the use of regular cu IUD'
: c) Metrorrh"n;::"'"0
lrregular intermenstrual bleeding is usually associated with anovulatory dysfunction, pelvic
L infection, or partial expulsion of an lUD.
-* Management:

15th every cycle for 2-3 cycles. (See DUB).

126 Controception ond Fomily Plonning

2. Pelvic Pain:
During insertion: cramping pain is common due to forcible insertion. Give NSAIDs
After insertion: possibly due to incorrect placement. Check position and replace properly
Backache: due to pelvic congestion, or chronic cervicitis.
- Acute Abdominol poin:

3. Pelvic Infection:
Chronic cervicitis and cervical erosions; are more common in presence of an lUD.

PID is more common in presence of IUD s; the threads of an IUD may facilitate ascend-
ing infection, especially with STDs, causing endometritis and salpingitis

4. Vaginal Discharge:
Increased watery cervical discharge, due to pe lv ic congestion.

- Mucopurulent discharge may occur in chronic cervicitis.

F Management: treat the cause
5. Expulsion of an IUD:
Spontaneous expulsion may occur usually in the first few cycles after insertion due to;
- Intermittent uterine contractions especially during menstruation, or
- Misplacement at the time of insertion.
) Management: In both cases IUD should be removed and correctly re-inserted.
5. Perforation:
Perforation mostly occurs at the time of insertion.
- Symptoms: sharp stabbing or colicky pelvic pain, together with persistent vaginal bleed-
Ing.

- Signs: the threads will not be felt by the patient, nor seen by speculum examination.
- lnvestigafrons: TVS will fail to detectthe IUD within the uterine cavity, while a plain X-
ray will reveal its presence in the pelvic cavity.
Y Monogement (see later in missed IUD).
PREGNANCY ON IUD:
Failure rates for lUDs are very low < 0.5 /HWY. Most pregnancies occur when the IUD is
displaced downwards intracervically, leaving the rest of endometrial cavity unprotected.
F Management of pregnancy with IUD:
* lf threads ore visible; IUD removed, pregnancy continues with an abortion rate 25%
* lf threads are not visible; IUD is left in place, pregnancy continues with an abortion
rate of around 50%, with higher incidence of septic abortion.
 Gynaecology 127

IUD & ECTOPIC GESTATION

IUD prevents intrauterine but does not prevent extra uterine pregnancV to the same extent.
Incidence of ectopic gestation may be slightly increased especially in the presence of plD.
Management (see ectopic gestation)
MANGEMENTOF MISSING IUD THREADS:
lf IUD threads are not felt by PV nor seen at speculum examination, a TVS should be performed
to confirm the presence or absence of the IUD within the uterine cavity, and exclude pregnancy
a) lf IUD is intrauterine; leave it in place if there is no other indication for removal.
b) lf IUD is not detected by TVS; a plain X-ray to the abdomen and pelvis is performed:

may be inserted if the patient asks for one.

dominal or pelvic cavity. Such cases are managed by removal of the IUD via lapa-
roscopy or laparotomy, as its presence will provoke an inflammatory reaction
leading to peritoneal, omental, and intestinal adhesions, and / or injury.
CONTRAINDICATIONS FOR THE USE OF IUD:
1.. Undiagnosed vaginal bleeding
2. Uterine anomolies that interfere with proper insertion (as septate or bicornuate uterus).
3' Uterine pothology that interferes with proper insertion or cause complications
(leiomyomas, polyps, and adenomyosis).
4. History of PID; as IUD may provoke or aggravate plD.
5. History of ectopic pregnoncy; relative contraindication for fear of higher incidence of
repeat ectopic gestation.

HORMONE METHODS FOR CONTRACEPTION

Hormone contraception methods are among the most commonly used methods for con-
traception used around the world, owing to its very high efficiency and its ease for its administra-
tion or its discontinuation.
HORMONAL CONTRACEPTION :

A'OESTROGEN PROGESTOGEN CONTRACEPTION: OCPs, Vaginal rings, and dermal patches

B'POGESTERONE ONIY CONTRACEPTION; POPs, lM injectables, subdermal implants, and LNG-
IUS

I. COMBINED HORMONE CONTRACEPTION

MODE OF ACTION:
This type of hormone contraception contains a combination of an oestrogen and a gestagen in
the form of oral pills, vaginal ring, or adhesive dermal patches. They exert their contraceptive effect
through the following mechanisms;
1. oestrogen: Inhibits ovulation via suppression of GnRH, FSH, LH, and LH surge.

h e i r contraceptive effect through;

2. Gestagen: synthetic progesterones exert t
- Endometriol changes unfavourable for implontation:due glandular atrophy and stromal
oedema.
t28 Contraception and Family Plonning

- Cervical mucus changes resulting in thick cervical mucus hostile to sperm penetration
- Altered tubal motility and secretions; unfavourable for oocyte transport

- lnterference with ovulation; through FSH & LH suppression (but less than oestrogen)
N.B.; In addition to its contraceptive effect, gestagens also result in;
Excellent cycle control; due to cyclic endometrial shedding.
v
Prevent oestrogen induced endometrial hyperplasia.

TYPES OF COMBINED HORMONE CONTRACEPTION

A. Cambined Oral Contraceptive Pills COCs: contain a combination of;
r Oestrogen (Ethinyl Oestradiol EE:30 ug), and
r Gestagen (synthetic progesterone) that may vary from;
Y 2'd generatron: Levo-norgestrel and Norethisterone
Y 3rd generatron; Desogestrel and Gestodene
Y 4th ge ne rotlon; Drospi renone
Monophasic COCs;
Contain same EE/PRG content in every pill, started Day 3-4 from 1" day of LMP and taken
once dailyfor 21 consecutive days, then stopped for one week allowing for withdrawal bleeding
(menstruation), then restarted for a new cycle. Monophasic pills are commonest form of COCs r
with greatest popularity.
Biphasic & Triphasic COCs;
Contain different E E / P R G content in two phases or three phases, i.e. not all the pills in each
pack contain the same EE/PRG content. There are no proven benefits for a biphasic or a tri-
phasic COCs over monophasic pills hence their use has not gained enough popularity.
B) Vaginol Controceptive Ring VCR:
The ring is introduced vaginally by the patient by the end of the menstrual period, left for
3 weeks then removed followed by a 7-day ring free period, to allow for menstruation. The
mode of action of VCR is similar to that for the COC pills without the need for daily intake
owing to its slow hormone release that is readily absorbed from vaginal mucosa, giving an
additional benefit of bypassing the first hepatic absorption.
C) Contraceptive Adhesive Skin Potches:
The contraceptive patch is applied to the skin of the abdomen, buttock, or thigh, started on
the 3'd or 4th day of menses, changed on the same day every week for three consecutive weeks,
followed by a 7-days patch free interval to allow for menstruation.
ADVANTAGES OF COMBINED HORMONE CONTARCEPTION (mainlyCOCs):
7. Controceptive benefits of COCs
- Most effective method of contraception 0.1-1/HWY. lf pregnancy occurs it is said that it
is rather patient failure than method failure.
- Excellent cycle control, especially in patients with previously irregular cycles.
- No long term adverse effects on fertility, with rapid recovery after pill discontinuation.
- No effects on sexual intercourse compared to coitus interruptus, spermicidals, condoms,
and calendar methods for the safe period.
 Gynaecology t29

2. Non contrcrceptive benelits of COCs:

v - Treatment of DUB.
\_ - Postponing next menstruation (delaying an expected cycle).

\r - Treatment of spasmodic dysmenorrhoea.

- LessriskforPlD,functional cystsoftheovary,endometrialcarcinoma,andepithelialovariancancer.
\-, DISEASE RISK ASSOCIATED WITH THE USE OF COCS

Disease Relative risk

7. Lschoemic Coronory Heart Diseose (ICHD sliehtlv increased risk
2. lschoemic stroke 2fold increased risk
3. Venous thrombo-embolism VTE 3-5 fold increased accordins to tvpe of sestasen
4. Breqst concer small increase in risk on prolonged use (time related)
5. Cervicsl concer small increase in risk on prolonged use (in smokers)
6. Epitheliol ovqrion concer 50% decreased risk lasting for a long period after stopping
7. Endometriol cancer 50% decreased risk lasting for short period after stopping
8. Colorectol cancer slightlv decreased risk

! SIDE EFFECTS OF OCPS:

1'. Spofting: mostly due to inappropriate hormone content of the pill. In such cases shift to
\/ other preparation with higher dose of gestagen in the following cycles.
. 2. Breakthrough Bleeding: inter-menstrual bleeding during the course of pill taking. lf per-
sists more than 3 cycles, then shift to higher hormone content pills .
'\- 3. Hypomenorrhoea: lt is common with OCP as gestagens cause glandular atrophy. Pills
should be stopped if the symptom is unacceptable by the user.
v 4. Amenorrhea: during intake or after stopping the pills, is managed by excluding pregnancy,
inducing withdrawal bleeding by gestagens, and shifting to another non hormonal methoc.
\J 5. Thrombo-embolic Disorders: increased due to increased platelet adhesiveness, increased
\r level of factor ll, Vll, lX, and X. The risk for DVT and pulmonary embolism is increased
from 4 to 6folds if OCP were not stopped at least 4 weeks before surgery.
'\r 6. Hypertension (HTN):increased incidence in predisposed patients after prolonged use.
7. Diabetes mellitus(DM);impaired carbohydrate metabolism may predispose to DM, an d
\-' in diabetic patients will lead to difficult glycaemic control.
.\r 8. Liver: transient impairment of liver functions is not uncommon, with increased hepatic
cholestatsis, higher incidence of gall stones, and rarely benign hepatocellular adenoma.
\J- 9. Effect on Lactation: decreased milk production & quality protein, only with COCs.

\* OTHER MINOR SIDE EFFECTS:

\J a. Ndusea and vomiting: may be encountered in the first few cycles.
b. Migraine headoche: if severe needs discontinuation and shift to non-hormonal method.
v c. Irritability ond depressive mood: shift to lower progestogen content pills.
d. Weight goin: usually minor, mainly due to salt and water retention.
\-/ e. Breast tenderness, and enlargement: shift to lower E/p pills
f . Acne: may worsen during OCP intake..
\v
g. Skin pigmentotion: Chloasma similar to pregnancy due to increased pigment deposition.
\-- h. Change in Libido: decreased sexualdesire may rarely occur in some women.
r30 Contraception and Fomily Plonning

i. Vagindl Discharge: Leucorrhoea may occur due to associated cervical congestion.

j. Eye Symptoms: corneal oedema, contact lens wearers suffer from blurring of vision & cor-
neal irritation. Reported cases of transient optic nerve ischaemia, and transient blurring of
vision. The previous conditions call for the pills to be stopped

CONTRAINDICATIONS FOR USE OF OCP

Absolute Contraindications Relative Contraindications

t. Thrombophlebitis or thromoembolic disease. 1. Su pe rficiol th rom boph le bitis.
2. History of DVT. 2. Varicose veins.
3. Coronory heart disease. j. Migroine headoche.
4. Cerebrovasculor occidents or strokes. 4. Hypertension.
5. Liver diseose (impaired function). 5. Diobetes mellitus.
6. Malignancy of the female genitol system. 5. History of liver diseose.
7. Abnormol bleeding from the genitol tract. 7. Gqll blodder stones.
8. Benign or malignant liver disease. 8. Age >35 years.
9. Suspected or known carcinoma of breost or 9. History of: Pre-eclampsia, Diabetes with pregnon
history of benign neoplasms of the breost. cy, Cholestasis with pregnctncy.

II. PROGESTOGEN ONLY CONTRACEPTION

A) PROGESTOGEN ONLY PrLrS (POPS)

In POP each pill contains the same amount of gestagen (levo-norgestrel, norethisterone, or
desogestrel), administered orally, daily, around the same time every day, without a pill free
interval irrespective of menstrual cycle.
r Indications:
Although POP are suitable for most women, they are most often used by women for whom
a COC is contraindicated (e.g,; breast feeding women, hypertension, age above 40, women
who smoke regularly, and those who commonly get severe migraine headaches especially
with aura).
r Mode of Action:
POP affects mainly the cervical mucus rendering it thicker preventing sperm penetration. lt
has an atrophic endometrial effect, together with inhibiting of ovulation in only 60% of
cases.
I Side Effects:POP have minimal side effects compared to COC, but are generally associated
with higher incidence of menstrual irregularities, and ectopic pregnancy.

B) PROGESTOGEN ONLy TNJECTABLE CONTRACEPTTON

The most commonly used i njectable progestogen is composed of depot medroxy-
progesterone acetate (DMPA), given lM every 12 weeks.
r Mode of Action:
It acts mainly through inhibition of ovulation. lts main advantage is the convenience of its
3 monthly dose.
r Side Effects:
Vaginal spotting is common in the first few months, while up to 7O% of women will have
amenorrhoea at the end of the first year.
 Gynaecology 131

c) SUBDERMAL PROGESTAGEN tMPLANTS

A subdermal implant is made from a non-biodegradable
polymer which contains an active slow release progestogen
formulation and is about the size of a matchstick.
r Application & Mode of Action:
It is placed subdermally by a special introducer, and will
provide contraception for almost 3 years, mainly via inhibi- Fig 14-5: Subdermol implonts

tion of ovulation.
r Side Effects:
About 20% of women will have amenorrhoea within three
months, while up to 50% will have frequent or prolonged
cycles,
r Advantages:
lmplants are not associated with significant weight chang_
es, mood changes, or loss of libido, but their side effects
cannot be easily dealt with owing to their prolonged slow
hormone release. Fig 14-6: Tubol Ligation

FEMALE STERILIZATION
Female sterilization is a permanent method for contraception that entails surgicalocclu-
sion of both fallopian tubes to prevent egg fertilization.
r Indications:
- lts use should be reserved only to those cases with medical or surgical diseases or
conditions that contraindicate pregnancy, and necessitate pregnancy termination if it
occu rs.
- lt should not be advised for cases who just need to limit their family number.

r Techniques for tubal occlusion:

Y Laparoscopy: using clips, rings, or bipolar diathermy (commonest method used).
D Ldparotomy: using delayed absorbable sutures, performed via a mini-laparotomy inci-
sion, or more often during repeat CS procedure,

r Side Effects:
Some cases may suffer pelvic congestion (post ligation syndrome), leading to
heavy menstrual bleeding, and pelvic pain.

MALE STERIIZATION
r Surgical: via ligation of the vas deferens. The most commonly practiced method
r Medical: Gossypol (the male pill), inhibits spermatogenesis. Not commonly available,

/F
132 Controception and Family Plonning

CONTRACEPTION FOR LACTATING FEMALES

During lactation around 40-60% of females will experience amenorrhea and anovulation in
the 1st few months, mostly due to the anti-gonadotrophic effect exerted by the markedly ele-
vated PRL levels. However, lactation alone is not considered reliable as a method of contracep-
tion, as it is difficult to predict when ovulation will be restored.
Methods used:
1. IUD: is an ideal method as it gives long term contraception without interference with lacta-
tion.
2. Progestogen only injectables: DMPA: 150 mg LM./3 months are suitable in most cases.
3. Progestogen only pills (POP): daily administered in the same time, without pill free inter-
vals, regardless presence or absence of menstruation,are a good alternative to injections
4. Barrier Method: male and female condom and diaphragm are suitable especially with
back-up methods as spermicidals or coitus interruptus.
5. Spermicidal gel or foam: used in cases with infrequent intercourse (husband travelling, etc.)
6. Physiologic Methods: Coitus interruptus is a popular method widely practiced. The safe period
is not always suitable due to the high incidence of menstrual irregularity with lactation.

EMERGENCY OR POST COITAL CONTRACEPTION

It is the use of methods to prevent pregnancy after an unprotected intercourse has occurred
whenever no method has been previously used, or a method did not function properly, such as a
torn condom,ora missed pill.
Options for Emergency Contraception
f UD f nsertion within 24-48 hours of unprotected intercourse
OCPs: started immediately after intercourse 4 tablets (2 tablets /1,2hrs).
> POP high dose pills regimen; Each oraltablet contains 0.75 mg of levo-norgestrel. The
first tablet should be taken within 72 hours after unprotected intercourse, and the
2nd dose tablet is taken L2 hours after the first one.
F COCs regimen: Each dose should contain at least 0.1 mg of EE + 0.5 mg of levo-
norgestrel (i.e.; 4 tablets of the standard low-dose COCs taken together). First dose
must be taken within 72 hours after unprotected intercourse, with a repeat dose 12
hours after first dose.
- Low-dose COCs = 4 pills per dose
- High-dose COCs= 2 pills per dose
r Side Effects: include, nausea, vomiting, headaches, dizziness, fatigue, breast tender-
ness, irregular bleeding and spotting.
 BENIGN CONDITIONS OFTHE VULVA BENIGN CONDITIONS OF THE VAGINA
- Pruritus Vulvae - Voqinol discharge
- Epitheliol disordersof the vulva - Vaginol infections (voginitis)
- Vulval ulcers - Voginol swellings
- Vulvor swellings
OVERVIEW
Most women will present to the gynaecologic clinic, once or more in their lives, complaining
from different diseases and conditions affecting the vulva and the vagina. Among these the
common- est are diseases affecting the skin all over the body, infections, and non neoplastic
cysts. Benign neoplasms and premalignant lesions are less common, while malignant tumours of
the vulva and vagina are among the rarest in the female genitaltract.

BENIGN CONDITIONS OF THE VULVA

Pruritus vulvae, pain, discharge, and swelling are common manifestations of vulvar diseases.
Proper diagnosis of many vulvar conditions is often delayed because of a tendency for most physi-cians
to treat the symptoms without reaching a specific diagnosis which requires;

Prrn.rrd
fril

tlrrrul

fi|tr

Normal vulvo

Fiq.75-1: Fig.75-2:

133
t34 Benign Conditions of the Vulvo and Vogina

A. Careful historytaking for:

- The use of topical irritants; as soaps, perfumes, local cream or gel, and nylon tight-fitting
underclothing, especially in patients with known allergy to other conditions
Medicaldisease that may manifest by vulvar conditions; as with diabetes mellitus,
Chron's disease, atopic sensitivity, and psoriasis.
- Urinary conditions; as genito-urinary fistula (GUF) that may cause continuous dribbling
of urine through the vagina.
Faecalfistula; following a complete perineal tear, episiotomy, or intra-vaginal irradiation.
Previous or recurrent vulval condition; and its response to previous medications, or
therapeutic measures

B. Proper examination of the vulva:

t. lnspection of the vulva with the patient in the lithotomy position, with proper exposure,
good light, and sometimes with a hand held magnifying lens for smaller lesions.
2. Vaginal speculum examination; in cases with vulvitis secondary to vaginal discharge, or in
lesions that may extend intothe vagina and cervix as with HPV.

C. Special investigations:
Biopsies from suspicious lesions obtained using Keye's punch biopsy under local
anesthesia, and subjected to histopathologic examination.
- Colposcopy with 5% acetic acid or toluidine blue may be an aid to localize best sites for
biopsy.

D. Examination of Inguinal lymph nodes: The draining lymph nodes of the vulva
(superficial inguinal LN.) should be examined on both sides.
!
N.B.; the clinician should always examine the patient for a systemic disease

PRURITUS VULVAE
Pruritus means a sensqtion of itching, usuaHy arousing the desireto scrotch. Pruritus vulvee
properly refers to vulval irritation for which no lesion is defined, however it is commonly used
in practice to describe this upsetting symptom regardless of whether or not a cause is found.
Pruritus should be distinguished from burning sensation commonly described by many
women. lt may be clinically divided into;
A. Pruritus associated with vaginaldischarge (8O%l:

Trichomonas vaginalis and Candida albicans are the commonest vaginal infestations asso-
ciated with pruritus, They account for at least 80 per cent of all cases.

B. Pruritus without vaginal discharge l2o%l:

Generolized pruritus: as in cases of Jaundice, diabetes mellitus and Uraemia.
- Allergy and drug sensitivity: Skin sensitivity to various chemical constituents of toilet J
preparations such as soaps, bath salts and antiseptics may explain some cases, Rarely
idiosyncrasy to chemical or rubber contraceptives is present.
Skin diseoses not specific tothe vulva: as scabies and seborrhoeic dermatitis.
- Chronic epitheliol dystrophies.. as lichen sclerosus.
 Gynaecology 135

- Parositic infestations of the rectum: oxyuris worms may migrate forward to cause vulval
itching.
Rectol incontinence.' may also cause intense pruritus.
Urinory incontinence.' True urinary incontinence as in WF and UVF with continuous dribbling
of urine may cause severe vulvitis and pruritus in long standing cases.
Corcinomq of the vulva
Psychog e n i c (neu rodermatitis)

ldiopathic pruritus.

EPITHELIAL DISORDERS OF THE VULVA

A variety of terms have been applied to disorders of the vulvar epithelium that produce
a
number of non-specific gross changes. The term vulvar dystrophy has been replaced
by the classifi-
cation proposed by the internationalsociety for the study of vulvar disease (ISSVD)
The Terminology Committee presented a new classification of the benign,non-infectious
vulvar
dermatoses

The table below summarizes the most recent terminology changes (2014)

tssvD 1986 lssvD 2004 LAST 2012

Flat condyloma or HpV LSI L
VIN 1 effect
VlN, usualtype HSIL
VIN 2 a.VlN, warty type
b.VlN, basaloid type
VIN3 c,VlN, mixed
(warty/basaloid) type
Differentiated VIN Vl N, d ifferentiated type

NON.NEOPLASTIC EPITHELIAL DISORDERS OF THE VULVA

A. LICHEN SCTEROSUS ET ATROPHICUS:
Incidence: This is the commonest condition found in the elderly women complaining
of vulval itch-
ing but may also be seen in children and youngerwomen.
Aetiology: The cause is not known but it is associated with autoimmune
disorders.
Symptoms: ltching is prominent or is the main presenting complaint
signs: In early lesions the skin may be reddish or of normal colour, later on it
looks thin with a wrinkled surface and white shiny plaques. lf left untreated
the contour of the vulva slowly disappears and labial fusion may occur.
\
\'
Microscopically: there is hyperkeratosis, flattening of the rete pegs, and a \,
:\
zone of a homogenized pink staining collagenous appearing tissue
beneath the epithelium. Lichen sclerosus is often associated with foci of both
hyperplastic epithelium and atrophic changes.
Fig 75-3:
Premalignant potential: lt is uncertain if lichen sclerosus leads to vulvar can-
cer. VIN and lichen sclerosus can coexist in the same patient. Approximately 4%
of women with li-
chen sclerosus develop invasive cancer.
Treatment: Topicalapplication of corticosteroid creams or ointment offers the best resutts.
136 Benign Conditions of the Vulva and Vogina

B. SQUAMOUS CELL HYPERPLASIA:

The term is applied to lesions of epithelial thickening and hyperkeratosis with no specific
cause. The lesion may have a dusky red appearance when the degree of hyperkeratosis is
slight. At other times well defined white plaques may be seen. Lichenification is seen frequent-
ly, while fissures and excoriation, as a result of chronic scratching, may be present. Hyperplas-
tic lesions are best treated by localapplication of corticosteroids.

VULVAR ULCERS
Most vulvar ulcers are benign however any persistent ulcer should be biopsied to exclude
malignancy. Vulvar ulcers may be:
- Traumatic e,g. infected tear or episiotomy
- Syphilitic ulcer (painless)
- Tuberculous ulcer (painful)
- Herpetic ulcer (multiple and very painful) -
- Chancroid, lymphogranulomo venerum, and granulomo inguinale are rarely encountered
ulcers related to infection with STDs.
- Behcet's disease; (multiple recurrent vulvaland oralulcers)
- Corcinomo ulcer (everted edges, indurated base and floor with necrotic tissues)

VULVAR SWELLINGS
A swelling or a mass of the a mass protruding from
vulva should be differentiated from
the vulva, as cystocoele, rectocele, uterine prolapse, large fibroid polyp, inversion of the uterus,
and Gartner cyst. Vulvar swellings may be non neoplastic, or neoplastic (benign or malignant).

Classificotion of vulvar swellings

Non neoplastic swellings Neoplastic swellings

1.. Congenital T.Benign tumours
2. Retention cysts o. Cystic tumours
- Bortholin duct cYsts b. Solid tumours
Sebaceous cyst - Lipoma
- Epidermal inclusion cyst Fibromo
- Hydrocele of the conal of Nuck Squamous cell popillomo
3. Endometriomo - Hydrodenoma
L. Troumotic lesions Nevus
2. Circulatory disorders Coruncle
3. I nflommotory conditions - Granulomotous caruncle
- Others: neurofibroma
2.Malignant tumours
 Gynaecology t31

NON-NEOPLASTIC SWELLINGS OF THE VULVA

1. Congenital: Hypertrophy of the clitoris

2. Retention cysts: These are the result of blockage of ducts of glands:

A. Bqrtholin's duct cysf; Bartholin cyst is the commonest vulvar swelling. lt is actually a cyst of
the duct and not of the gland. lt contains mucoid fluid and is lined by transitionalepithelium.
Clinicolly it appears as a cystic swelling of variable sizes in the posterior part of the labium rna-
jus' Secondary infection leads to a painful Bartholin abscess, which is tense, tender, sur- round-
ed by vulvar redness, swelling, and oedema.
Treatment is by marsupialization to create a new opening between the duct wall and the
skin. This line of treatment is preferableto excision as it is easier, associated with less bleeding and
shorter convalescence, togetherwith preservation of the function of the gland. A penrose drain or a
small word catheter may be left for a few days to guard against closure of the tract and recur-
rence of the cyst.

Bartholin duct cyst Marsupiaalization of the cyst

Fig 15-4:

B. Sebaceous cyst: sebaceous cysts usually present on the hairy region of the labium majus, as mul-
tiple small cysts that contain whitish cheesy sebaceous material. The cyst may become infected
and cause pain. lf painfulthey can be surgically removed.
C. Epidermol inclusion cyst:

- Troumatic inclusion cysts; may occur from viable stratified squamous epithelium buried be-
neath either skin or mucosa, which will proliferate and desquamate forming an inclusion cyst.
They are commonly seen following episiotomy scars and rarely with circumcision scar
(clitoridalcyst).
- Congenitol inclusion cysts; may rarely originate from embryonic tissue destined to become
epithelium which remains in the dermis, or from pilosebaceous ducts that become occluded.
- Treotment; Small asymptomatic cysts may need no treatment, but if they are large annoying to
the patient or become infected they can be removed surgically under local anaesthesia.
D' Hydrocele of the canal of Nuck: During development, the round ligament (which is inserted in
the labia majora) is normally accompanied by a peritonealpouch called the canal of Nuck which will
be normally obliterated later on. Rarely if not obliterated, a cystic collection of serous fluid will
accumulate in this pouch forming cystic mass.
138 Benign Conditions of the Vulvo ond Vagina

it forms an elongated translucent swelling in the upper part of the labium majus
Clinicolly:
and may extend to the inguinal canal. Sometimes it can be emptied by pressure on lying
down if it communicates with the peritoneal cavity and it may be associated with inguinal her-
n ta.

Treotment: Excision of the sac and dealing with any inguinal hernia,
E. Endometrioma: An endometrioma may arise from either a metaplastic change, or through an
embolic origin from the uterus.
Clinically: lt is small bluish cyst containing altered blood and lined by endometrial epithelium
that increases in size and becomes tender during menstruation.
Treqtment: lf painful or annoying it may be surgically ex-
cised.

F. Troumatic Vulvar haematomas; Vulvar haematomas may occur secondary to vaginal birth trau-
ma associated with extensive vulval and perineal injury in absence of proper ligation of
the bleeding vessels, lt can also occur due to direct trauma as in car accidents or fall from a
height, or following female circumcision.

Clinically; the haematoma tends to spread widely becauseof the loose tissue structure at
the region of the vulva, forming a large, raised, diffuse, tense, tender area with bluish red
discolora- tion.
Treatment: Mild cases are managed conservatively by cold ice pack compresses, while large
extending haematomas will require surgical incision, evacuation of the haematoma, and liga-
tion of the bleeding vessels.
G. Swelling due to circulatory disorders:

Varicose veins; Usually occur during pregnancy as tortuous dark blue soft structures in one
or both labia, which become prominent on standing and empty on lying down. Treatment is
by ex- cision or injection of sclerosing agents.
Oedema: lt can be the result of a wide variety of systemic and local causes such as nephritic
syndrome heart failure and allergic reactions Oedema is usually diffuse and characterized
by pallor of the skin and pitting on pressure with the finger.
H. lnflommatory conditions:

Non specific inflammatory vulvitis; results in a diffuse swelling that surrounds the area of
the inflammation due to congestion and oedema.
Specific inflammatory conditions; may result in localized lesions, such as Bartholinitis, Bil-
ha rzia !

condyloma, syphilitic condyloma lata, or viral condyloma accuminata

(HPV).
 Gynaecology r39

BENIGN NEOPLASMS OF THE VULVA

A) Cystic tumours
Benign cystic tumours of the vulva are very rare, and are always benign. lf large they are
removed by simple surgical excision.
B) Solid tumours
- Lipomo: is found rarely. lt arises from the subcutaneous tissues of the vulva and usuallv
becomes pedunculated and dependent with growth. Treatment is by excision.

Fibroma: is also uncommon but present as a pedunculated tumour like a lipoma but is
firmer. lt arises from the fibrous tissue of the round ligament and the vulvar connective
tissue. Treatment is by excision. These tumours on occasion become sarcomatous.

Squamous cell papilloma is usually a single small lesion, formed of papillae of stratified
squamous epithelium, covering a core of vascular connective tissue the clinician has to
differentiate it from: condylomata accuminata caused by HPV virus which are usually mul-
tiple, fibroepithelial polyps which are small, sessile, or pedunculated pieces of redundant
skin, and Bilharzial papillomata.

Hydradenomo; lt is an unusual lesion that originates from the apocrine sweat glands. lt ap-
pears as a small nodule on the labium or the interlabial sulcus. Diagnosis and treatment
is by exci- sional biopsy. The Hydradenoma is not malignant, although on histologic exami-
nation the papillary nature of the tumour may be mistaken for an adenocarcinoma.

Nevus: Pigmented nevi occur on the vulva as they do else where, but functional activity,
which carries a risk for subsequent malignant transformation is more common in this lo-
cation. Excisional biopsy should be performed on all pigmented lesions on the vulva so
that tissue can be sent for histologic evaluation. These lesions should not be treated by
cryosurgery or laser therapy as histologic examination is essential.

Coruncle: A small tumour arising from the posterior part of the lower end of the ure-
thra. lt is composed of a very vascular stroma, almost like a haemangioma, usually infect-
ed and covered with squamous or transitional epithelium. The caruncles are red in corour
because of their vas- cularity and are extremely sensitive. The patient is usually an elderly
woman complaining of dysuria and bleeding. Treatment is by excision and histological ex-
amination although malignant change is rare. The base of the tumour on the urethral mu-
cosa should be cauterised.

Gronulomotous coruncle; lt is a chronic infection of the periurethral tissue. lt is called a

caruncle but it is not neoplastic and is often symptomless. Granulomatous caruncle is
often seen, while a true caruncle is uncommon. Treatment if needed is by cautery ano
there is a tendency to recurrence. Infection in this area must involve the paraurethral
gland network and complete cure is difficult. A search should be made for a vaginal or
bladder source of the infection.

Other tumours include haemangioma and neurofibroma.

t40 Benign Conditions of the Vulvo ond Vagino

VAGINAL CYSTS
1. Cysts of vestigialstructures:
Wolffion (Mesonephric duct): The majority of vaginalcysts arise from Gartner's duct.They lie
on the lateral or anterolateral wall of the vagina from the lateral fornix downwards. They are
variable in size.The lining is a single layer of cuboidal epithelium.
Mullerion (Pora-mesonephric duct): Rare, may be up near the cervix
2. Endometriotic cysts
3. Epidermoid cyst;implantation dermoid mainly due to obstetric laceration orepisiotomy.

BENIGN VAGINAL NEOPLASMS

Benign Neoplasms of the vagina are rare. Some are paravaginal rather than vaginal, in
that they arise in tissues in the paracolpos.

Common vaginal neoplasms include: Papilloma, Angioma, Fibroma, and Lipoma.

Clinically they may be sessile or pedunculated.
Diagnosis; is by digital vaginal examination and naked eye speculum examination. Pelvic
ultrasound, CT scan and MRI can all also diagnose larger swelling if vaginal examination is
not accessible (example in virgins)
Treatment; surgical excision if large or infected.

KEY POINTSEY POINTS

Leucorrheq is a term thqt describes excessive normal voginal dischorge.

tnfected discharge moy be mucopurulent, purulent, or songuinous. lt moy occur secon-

dory to vaginitis, cervicitis, endometritis, or tumours of the cervix, vogino or endometrium.
Vulvol itching is the most common vulvol comploint. lt is most commonly secondory to vulvo-
vaginal Candidiqsis, Trichomonql infections, or lichen sclerosus et atrophicus'
Pruritus vulvqe refer to the intrqctable vulval itching in obsence of a defined lesion, strong steroid
creoms ore effective in relieving the symptoms
 Utero-vaginal Prolapse

Uterine Displacements

Uterine Inversion

PELVTC ORGAN PROLPASE (POP)

Pelvic organ prolapse (POP) refers to descent of one or more of the pelvic organs below
their normal anatomical positions, downwards through the vagina.
POP occurs in nearly t2-30% of women, however the incidence significantly increases by
both age and repeated vaginal deliveries, due to progressive weakness of pelvic supports.
The anteverted anteflexed position of the uterus results in a forward tilt towards the symphy-
sis pubis that helps in preventing it's downwards descent during increased intra-abdominal
pressure (as during straining, chronic cough, and constipation, etc...).

SUPPORTS OF THE PELVIC ORGANS

The uterus and other pelvic organs are kept in normal anatomical positions by their surround-
ing fascia, ligaments, and muscles. The main supports of pelvic organs include:

A) Endopelvic Fascia: including vaginal, cervical, perivesical, and rectal fascia.

B) Pelvic Ligaments: condensations of the endopelvic fascia into strong ligaments attached to
the cervix form the main support of the uterus and pelvic organs.
D The Mockenrodt's ligaments; the most important support of the uterus. lt spreads from
the lateral pelvic walls, passes medially to be inserted in the supravaginal part of the
cervix and upper vaginal vault (see anatomy).
D The uterosocral ligaments: spread from the sacrum posteriorly to the back of the su-
pravaginal part of the cervix.

D The pubocervicol ligoment: spreads from the back of symphysis pubis anteriorly to the
front of the supravaginal part of the cervix.
C) Pelvic floor muscles: most important are the levators ani muscles with its 3 parts;

D The pubo-coccygeus.'the most important part of the muscle support

Y The ischio-coccygeus

D The //io-coccygeus
D) Additional support of pelvic organs is also provided by the perineal body, perineal muscles
and their innervations.

N.B.: See onotomy of pelvic fascia ond ligaments chapter 2 for

figures and details

t41
142 Pelvic Organ Prolopse qnd Uterine Displocements

TYPES OF PROLPASE
A) VAGINAL PROLAPSE:
1. Anterior compartment:
) Urerthrocele: descent of urethra + uppermost 2-3 cm of attached vagina
F Cystocele: descent of the urinary bladder + upper 2/3 of anterior vaginal wall
F Cysto-urothrocele: full vaginal length + bladder and urethra
2. Posterior compartment:
D Rectocele: middle 1/3 of posterior vaginal wall + rectum
) Enterocele: upper t/3 of posterior vaginal wall + small bowel loops
3. Central compartment (Apical):
) Utero-vaginal prolapse: uterine descent wit inversion of the vaginal apex
F Vault prolapse: descent of the blind ended vaginal apex after hysterectomy
BLAODER UTERUS

CERVIX VAGINALAPEX

RECTUM

PROLAPSE
VAGINA

ANUS

Fig 16-1: Cystocele

Rectocele

Rectum bulges
into the vagina

Fig 16-2: Rectocele

 Gynaecology 143

B) UTERTNE PROLAPSE
In uterine prolapse descent of the uterus is judged by the level of the cervix, where the exter-
nal cervical os normally lies at the level of the ischial spines.

1" Degree: The cervix descends downwards through the vagina, but the external os does
not reaching the introitus (hymenal ring).
2no Degree: The externalos reaches or slightly protrudes outside the introitus
3'd Degree: The whole uterus except the fundus descends outside the introitus

Procidentia: The whole uterus including the fundus descends outside the introitus.

--yrlrp rys !,
pr,l;i:;

- - F, :(;r:r

Pxriidr,rtliir ol lll( ilt$ils.Il(l \xf lilil

Fig 16-3: Degrees of uterine prolopse

RISK FACTORS FOR POP

Weakness of the pelvic organs support (fascia, ligaments and muscles), is the main predispos-
ing factor for PoP. Risk factors for weak pelvic organ support incrude;

A)CHTtDBtRTH TRAUMA:
Damage to the pelvic supports during vaginal birth trauma is the most frequently encountered
risk factor for POP. This might be due to overstretch of the cellular tissue and damage to the
muscular innervations. lt is aggravated by the following conditions;
D Difficult labour with oversized fetus andf or prolonged 2nd stage
F Short intervolsuccessive deliveries without appropriate involution periods.
Y Direct pelvic floor injury as in perineal lacerations without prompt repair
B) MENOPAUSAT ATROPHY:
Older menopausal women are at higher risk for POP due to degenerative changes in pelvic
supports secondary to prolonged oestrogen deficiency. Risk increases by increased age.
c) coNGEN|TAL WEAKNESS:
POP may occur in some women in a young age and in absence of childbirth trauma. This will
mostly attributed to congenital weakness in pelvic fascia, ligaments, and muscles. lt may be
associated with poor innervations (as in spina bifida), or generally poor mesenchyme with as-
sociated abdominal wall hernia, rectal prolapse, and or visceroptosis.
t44 Pelvic Orgon Prolapse and Uterine Displocements

D) IATROGENIC WEAKNESS:
This might be induced by improper technique for supporting vaginal vault during abdominal or
vaginal hysterectomy, hence increasing the risk for vaginal vault prolapse.

N.B: Precipitating Factors: chronically increased intra-abdominal pressure as occurring in chronic

cough and constipation may act as an important precipitating factor for POP, especially in elderly
high risk women. And unless properly managed it will act as a major cause for recurrence of the
prolapse after surgical treatment.

ANATOMICAL CHANGES ASSOCIATED WITH LONG STANDING PROLAPSE

in cases of prolonged vaginal prolapse be-
1. Vaginal skin Keratinization: everted vaginal skin
comes thickened, and white with keratin, being exposed to air and trauma. J
2. Vaginal and cervical ulcerations: may occur at the most dependent part of the vagina or
v
cervix as a result of congestion and circulatory changes rather than friction with the
thighs (decubitus ulcers). v
3. Cervical hypertrophy: due to chronic congestion and associated cervicitis.
4. Supravaginal elongation of the cervix; due to stretch on the Mackenrodt's ligament.
5. Descent of the base of the bladder with stretching of the urethral sphincter; may lead to v'
frequent desire to micturate and associated stress incontinence.
6. Kinking and compression on the ureters; in severe degrees of utero-vaginal prolapse,
may cause back pressure changes in the form of hydroureter and even hydronephrosis. v

CLINICAL PICTURE OF GENITAL PROLAPSE --

AlcoMMoN SYMPTOMS
In general mild cases with minimal degrees of utero-vaginal prolapse are asymptomatic. The
more severe degrees of POP may be associated with one or more of the following symptoms; v
1. Sensation of pelvic heaviness; especially towards the end of the day that improves or
disappears by rest.
2. A mass filling the vagina or protruding from the introitus; that may be felt by the pa-
tient on straining or squatting, and disappears by lying down on the back, or by reduction.
3. Low backache; is common in cases of uterine prolapse. Pain is dull aching, or dragging, that
radiates to the thighs and legs. lt is stimulated by prolonged walk, hard work, or heavy
weight lifting. Pain is usually relieved or decreased by rest and lying down on the back. Pain
is explained by marked traction on uterosacral ligaments by the prolonged uterine descent.
4. Urinary symptoms: are common in the presence of a cvstocele,as;
Y Frequency of micturition by doy; due to mechanical irritation of the trigone.
Y Frequency may develop by night (nocturio); due to residual urine cystitis.
F Stress urinory incontinence SU/(escape of urine during cough or straining).
Y Inobility to complete micturition unless the anterior vaginal wall is reduced upwards
and supported by the patient's fingers, to empty residual urine in a bladder pouch.
5. Rectal symptoms: as heaviness and difficulty when trying to defecate in cases of recto-
cele.
6. Pelvic congestion symptoms: in the form of Dysmenorrhoeo and Leucorrhoeo:
 Gynaecology t45

B)StGNS ON CUNTCAL EXAMTNATTON

1. GENERAL EXAMINATION
Chest and Abdominal examination are essential to rule out causes for chronic increase in intra-
abdominal pressure, as chronic cough, hepato-splenomegaly,ascites, pelvic masses, etc...

2. LOCAT EXAMINATION:
Local examination of the prolapsed mass is performed with the patient in the lithotomy position
while maximum straining:
A) Inspection: to detect
F Type of prolapse (vaginal, or utero-vaginal)
) Degree of uterine prolapse if present (r",2n0, or 3'd degree or procidentia).
F Presence of skin changes or decubitus ulcers
F Associated patulous introitus
B) Digital Palpation:
F PR examination to test for extent of rectal involvement in rectocele
F Test for levators ani function and strength by pressing index and middle fingers on peri-
neal body muscles.
F Test for complete procidentia by being able to approximate the index and thumb fingers
above the fundus of prolapsed uterus
C) Diagnosis of associated conditions; as
D Suprovoginol elongation of the cervix: using a uterine sound measure
} Stress Urinory lncontinence (SUt): by asking the patient to cough during examination to
detect involuntary escpe of urine through urethra (see sUl chapter)
Y Test for enterocele; via eliciting impulse on cough, and or gurgle sensation at the vaginal
vault. Combined PV & PR examination may add to accuracy of diagnosis.

DIFFERENTIAL DIAGNOSIS OF POP

A. Cystocele and Rectocele: are differentiated from cysts of anterior and posterior vaginal walls,
as inclusion dermoid cysts, which are usually small in size, cystic, tense, slightly tender, and
non-compressible or reducible.
B' Urethrocele: should be differentiated from urethral diverticulum, which on compression will
lead to discharge of urine or pus via external urethral meatus
C. Uterine prolopse: should be differentiated from swellings protruding from the vulva as; large
fibroid polyp, and chronic inversion of the uterus.
PREVENTION OF POP
r Adequate spacing of deliveries to allow proper involution.
r Avoid marked obesity and excessive rapid weight gain
I Avoid bearing down in the 1't stage of labour before full cervical dilatation
r Avoid difficult and prolonged labour especially in the 2nd stage
I Avoid damage to perineal muscles and pelvic fascia by proper episiotomy performance, wnen
indicated, and proper technique of repair
I Proper treatment of chronic cough and constipation, with prompt management of pelvi-
abdominalswellings.
146 Pelvic Orgon Prolapse ond Uterine Displacements

MANAGEMENT OF POP
The choice of treatment for genitalprolapse depends on several factors including;
F Type and degree of prolapse

) Acceptance and readiness for surgicaltreatment.

A) NON SURGTCAI MEASURES

t Pelvic floor exercise (Kegel exercises): may delay the need for sur-
gery in mild cases.
. Pessdry tredtment: is only a temporary option aiming at tempo-
rary reduction of the prolapsed organs until the patient is ready
for surgery, or in cases where surgical intervention poses unac-
ceptable risks on the patient's health.

SURGICAL TREATMENT FOR POP

Fig 1-6-4: Pessory treot-
Surgicaltreatment is the only curative approach for moderate and ment for uterovoginol
severe cases. prolpose
1. ANTERIOR COLPORRHAPHY:
For repair of the anterior vaginal wall and associated cystocele.
The anterior vaginal wall is opened and vesicovaginal fascia dissected.
The bladder is pushed upwards to its normal position
The fascial defect is repaired and plicated by interrupted delayed absorbable sutures.
Excess vagina is removed and vagina packed with gauze for compression haemostasis
t Associated urethrocele is managed by extending vaginal dissection to periurethral fascia
and its plication
r Associated stress urinary incontinence is managed by either;

ii:ir.!! '-"'
t]'.1. ,fl' r li! 'j li
'=ii';

Fig 16-5: Anterior colporrhophy for cystocele

 Gynaecology t41

2) POSTERTOR COLpOpERtNEORRHApHy
For repair of posterior vaginal wall prolapse and associated rectocele
The posterior vaginal wall is opened and rectovaginal fascia dissected
- The rectum is pushed downwards to its normal oosition.
The fascial defect is repaired and closed by interrupted delayed absorbable sutures
- The Perineal body is reconstructed and pubococcygeus muscle approximated at the four-
chette.
Excess vagina is removed and vagina is packed with gauze for compression haemostasis

Fig 16-6: Posterior colpoperineorrhophy

3. CLASSICAL REPAIR
- Cases of cysto-rectocele are best managed by anterior colporrhaphy + posterior col-
poperineorrha phy.
Associated 1-" degree uterine prolapse is managed by shortening of Mackenrodt's ligament
and their plication infront of the cervix.

4. MANCHESTER (FOTHERGtLTS) OPERAT|ON

Cases of 2no degree uterine prolapse with marked supravaginal elongation of the cervix are
best managed by amputation of the vaginal portion of the cervix and shortening of the
Mackenrodt's ligament.
Associated cystorectocele is managed by classical repair.

Fig 16-7: Manchester operotion

148 Pelvic Orgon Prolapse qnd Uterine Displocements

5. VAGINAL HYSTERCTOMY AND FASCIAL REPAIR

1,. Indicated in perimenopausal and postmenopausal patients with marked uterovaginal pro-
rapse.
2. A circumferential incision is performed around the cervix at cervico-vaginal junction.
3. Dissection of the anterior and posterior vaginal walls from the surrounding fascia
4. Clamping the uterosacral and mackenrodt's ligaments
5. Ligation and division of uterine arteries and ovarian artery at the infunbulo-pelvic
lihgamen, followed by removal of the uterus (hysterectomy).
6. The vaginal vault is supported by plication to the cardinal and uterosacral ligaments.
7. Anterior colporrhaphy and posterior colpo-perineorrhaphy are then completed.

SURGICAT REPAIR FOR ENTEROCELE

1,. Extending dissection of posterior vaginal wall to reach the posterior fornix
2. The peritoneal hernial sac is identified, excised at the neck, and peritoneum closed.
3. Approximation of the uterosacral ligaments will guard against recurrence of enterocele.

SURGICALPROCEDURES FOR REPAIR OF VAGINAL VAULT PROLAPSE

L. Abdominal sacro-colpopexy: The vaginal vault is sutured posteriorly to the sacral prom-
ontory using non absorbable suture material, via a laparotomy incision.
2. Vaginal sacrospinous ligament fixation: The vaginal vault is sutured to the sacrospinous -
ligament at one side via vaginal approach.
3. Vaginal Mesh repairs: recurrence of prolapse after surgical correction may occur with up
to 30% of cases requiring a second operation within 5 years. Recurrence may be due to
the weak connective tissue even before the original operation was performed. Mesh
augmented pelvic floor repair is gaining more interest recently aiming at improving tissue
strength and support.
4. Le Fort's operations: The procedure aims at obliteration of the vagina, except for two
small channels on either side through which the normal cervical discharges can escape
Rectangular flaps are excised from the anterior and posterior vaginal walls the raw are-
as are sutured together. The procedure is reserved for the very old, flail, non sexually
active patient, unfit for lengthy surgical procedures.
 Gynaecology 149

RETROVERSTON FLEXTON OF THE UTERUS (RVF)

ANATOM ICAL CONSI DERATIONS :

o Anteversion: The uterus is almost at right angle to the vagina, with a slight forward curve.
o Anteflexion: The body of the uterus is bent forwards upon the axis of the cervix.
o Retroversion: The longitudinal axis of the uterus is directed backwards.
o Retroflexion: The body of the uterus is curved backwards upon the axis of the cervix

SIID il*Gf,ff

Fig. 75-8: RVF uterus

r50 Pelvic Organ Prolapse qnd Uterine Displacements

AETIOLOGY OF RVF

A. Congenital RVF: ls the most common type, normally present in about IO-20% of women, lt
gives no symptoms and requires no treatment. The uterus is usually mobile RVF.

B. Acquired RVF: may occur secondary to a large fundal myoma pushing the uterus backwards,
pelvic adhesions as in endometriosis or chronic PID pulling the fundus posteriorly. The uterus
is usually fixed RVF

C. Puerperal retroversion; may occur due to increased weight of the uterus and laxity of pelvic
ligament support after delivery, and may lead to subinvolution of the uterus.

SYMPTOMS
1. No symptoms: RVF is asymptomatic, being accidentally encountered in majority of cases.
2. Dyspareunia, low backache, and pelvic congestive symptoms (as dysmenorrhoea and leucor-
rhoea) may occur especially in cases with fixed RVF due to endometriosis or PlD.

DIAGNOSIS OF RVF
a. On bimanual examination: The posterior lip of the cervix is felt before the anterior, with the
external os pointing directly forwards, while the body of the uterus is felt through the poste-
rior vaginal fornix instead of the anterior fornix (when the uterus is AVF).
b. On speculum examination: the cervix is seen pointing towards the urethra and symphysis
pubis. lf a uterine sound is passed gently it goes downwards and backwards.
c. Pelvic ultrasound: both TAS and TVS can accurately diagnose RVF or AVF uterus

TREATMENT OF RVF
1. NO TREATMENT: most RVF cases are asymptomatic and require no treatment.

2. Symptomatic cases: mostly in the form of low back ache, dysmenorrhoea and dyspareunia,
are usually secondary to the pre-existing pathology as; endometriosis, chronic PlD, and cervi-
cal erosions. These are treated according to the management of the primary cause.

3. Prophylactic measures against RVF include:

- During abdominal myomectomy: Plication of round ligaments to keep the fundus anteri-
orly.

- During operations for uterine prolapse; shortening of the Mackenrodt's ligaments in

front of the cervix anteriorly will restore the normal AVF position of the uterus.
to keep the
Pessary test: The uterus is corrected, and a Hodge smith pessary is inserted
uterus in the corrected position. The patient is re-examined after one month, if her
symptoms were relieved, this means that symptoms were due to retroversion.
 Gynaecology 151

INVERSION OF THE UTERUS

Inversion of the uterus is a very rare condition in which the uterus is partially or completely
turned inside out. lt may be either;
o Acute puerperal inversion; may be encountered as a complication of the 3'd stage of labour
due to forcible traction on the placenta (see obstetrical complicotions of j'd stage of tabour).
o Chronic inversion; may occur as a sequel of a neglected or overlooked acute puerperal inver-
sion, or secondary to dragging of the uterine fundus by a suomucus myoma.

/a
ui,
VUreter I
I
I

Fig 16-9: lnversion of the uterus

Pathogenesis and degrees:

Inversion of the uterus starts with a depression or cupping of the uterine fundus which does not
reach the cervix (1't degree). lt then continues downwards to reach, or protrudes from, the cer-
vical canal (2nd degree). Finally the whole uterus is inverted and may protrude through the in-
troitus (3'o degree).
Symptoms: cases may present with deep pelvic pain associated with vaginal bleeding or bloody dis-
charge, with or without a mass filling the vagina

Signs: Bimanual pelvic examination may reveal fundal cupping and a mass protruding through cer-
vix' Speculum examination may show a red mass is seen in the vagina resembling a fibroid polyp.
Ultrasonography may help confirm the diagnosis
152 Pelvic Organ Prolapse and Uterine Displocements

Differential Diagnosis
1. A fibroid polyp protruding through the cervix. Here
the uterus is felt normally bimanually (no cupping),
there is an external os and a uterine sound can be
introduced normally.
2. A mass protruding in the vagina e.g. uterine Prolapse
or sarcoma or a cauliflower cancer cervix Differentiat-
ed by the presence of the cervix; bimanual examina-
tion and sounding.
TREATMENT OF CHRONIC UTERINE INVERSION
Surgical correction of chronic inversion; either by an
abdominal approach, through a posterior incision in
the cervical ring and upper vagina, or via a vaginal
approach which is more difficult and rarely done.

Surgical removal of the uterus by Hysterectomy; is

indicated in postmenopausal women. Either a total Fig 16-10: Chronic lnversion of the uterus

abdominal or a vaginal hysterectomy may be per-

formed.

Key points in POP

- The genital orgons ore kept in their normol anotomical positions by the pelvic ligoments, foscio, ond pelvic
floor muscles.
- The primory couse of genital prolopse is weakness of the supporting structures of the uterus and vogino,
usuolly os a result of childbirth trqumo.

- POP could be either vaginol, or uterovoginol prolopse, ond moy include other orgons as the blodder, rec-
tum, or bowel.

- Symptoms of prolapse ore generally non specific. Cystocele and lJrethrocele ore commonly associated with
urinary symptoms. Rectocele has less morked symptoms.

- tJterine prolopse is mostly associoted with bockqche towards the end of the doy, aggravoted by octivity
and relieved by lying down and rest.

- Clinical exqminotion reveols a moss filling or protruding from the vogino on straining

- tn mild coses conservotive approoches moy be sufficient

- Pessory treatment is only o temporary opprooch for relief of symptoms until surgery becomes feasible, or in
the extremely morbid patient ot very high risk for surgery.
- Surgical treqtment by repair of the fascia ond restorotion of uterine position is the mainstoy of treatment in
moderote ond severe coses,
- The choice of the surgical procedure and sound surgical techniques ore crucial for the success of primory
surgery and for ovoiding recurrences.
 Perineol locerations

Old complete perineol teor

Rectovoginol fistula

PERINEAL LACERATIONS

Adduc{or longus muscle

lscfiloca\rernosus
muscle

I or ramug Superficial transv€rss

of bchium pedneal muscle

Fchlel
lube.o6ity

Pudendal
w6gels

nal ana
cter
Gluteal marimus
muscle

Fig. 77-1: Anqtomy of the Perineal Body

ANATOMY OF THE PERINEAT BODY

The perineal body is the pyramidal shaped mass of tissue wedged in be-tween the vagina and
the lower part of the rectum. lt is composed of the following layers from without inwards.
1. Skin and Subcutaneous fat

2. Superficial perineal muscles: the external anal sphincter, the bulbocavernosus (sphincter vagi-
nae), the transversus perinei, and the ischiocavernosus. All except the ischiocavernosus have
one insertion in the central part of the perineal body.

3. The decussation of the levator ani muscles (deep perineal muscles) be-tween the vagina and
rectum forms the apex of the perineal body.

r53
t54 Perineol Lacerqtions Foecol Incontinence ond Rectovoginql Fistulq

CAUSES OF PERINEAL TACERATION

A) Bad management of the 2nd stage of labour: (the commonest causes)
Allowing premature extension of the foetal head before crowning.
Lack of adequate perineal support during delivery of the foetal head.
Instrumental delivery without an adequate episiotomy
B) Inadequately performed episiotomy in association with;
Delivery of malpositions and malpresentations associated with larger diameters of the deliv-
ered head, as in cases of direct occipito posterior (face to pubis), face mento-anterior, and
after-coming head in breech deliveries.
The use of instrumental delivery as the forceps or the vacuum extractor.
Rigid perineum (as elderly primigravidas, and previous perineal scars)
Narrow subpubic angle (displacing the head posteriorly with excessive perineal stretching)
C) Rapid delivery of the head through the birth canal; as in precipitate labour
D) Severe oedema of the vulva with friable easily torn tissue (as in pre-eclampsia).
E) Rarely; Direct external trauma as with fall from a height, car accidents, or defloration injuries.

DEGREES OF PERINEAL TEARS:

1. First degree tears: involving the skin and superficial perineal muscles.
2. Second degree tears: Levotor oni muscle is involved as well, but the anal sphincter is intact.
Both the above types are included under the term incom-plete tears.
3. Third degree tears (Complete perineal tear): the anterior portion of the sphincter ani exter-
nus muscle is involved. The rectalwall may be torn leading to prolapse of the rectal mucosa.

Bulbocavemosus m.

Suprrffciel
trifhsva13€
prrinrel m.

lntrmsl
rnel
sphinctrr
R.€trl
muco6a

Fig.17-2: Degrees of Perineol Teors

 Gynaecology t))

COMPTICATIONS OF PERINEAL TEARS:

1. Postpartum haemorrhage, due to bleeding from lacerations.
2. Infection may occur in the laceration site (puerperal sepsis).
3. Patulous vaginal introitus with unsatisfactory sexual function.

4. Incomplete tears; may predispose to genital prolapse (due to loss of pelvic floor support).
5. Complete tears may lead to Incontinence to stools and flatus due to division of the sphincter
ani muscle' After sometime, some patients will learn to contract the levator muscles and can
control the passage of solid faecal matter, but remains incontinent to liquid stools and flatus.
6. Residual rectovaginal fistula.

7. Dyspareunia from a tender scar in the vagina.

PREVENTION OF PERINEAL LACERATIONS

L. Proper management of 2nd stage of labour, by maintaining flexion of the foetal head until
crowning occur, then allowing for slow delivery of the head in between uterine contractions.
2. Episiotomy, when the perineum threatens to tear and routinely with instrumental deliverv.

MANAGEMENT OF PERINEAT LACERATIONS

Every perineal tear, however, small, should be repaired. Primary suture is possible if done
within the first 24 hours lf the case is seen later than that, it is considered as a septic wound, and
left to heal by granulat-ion, Repair in such cases is postponed until all signs of infection have disap-
peared, usually 3-6 month later.

The post-operative care after perineorrhaphy will be described later. lt aims at keeping the
wound DRY AND CLEAN to encourage healing by primary intention.

A) Recent 1't and 2nd degree perineal lacerations:

1. The levator ani is approximated by at least three interrupted sutures.
2. Superficial perineal muscles and fascia are approximated with interrupted sutures.
3. The vagina and skin are finally sutured as in an episiotomy repair.
B) Recent 3'd degree perineal lacerations

- The rectal wall; is sutured in 2 layers by delayed absorbable type of sutures, first continuous
then interrupted sutures not going through the rectal mucosa. The sutures should extend
well above the apex of the laceration.

- The anol sphincter; the cut ends of the anal sphincter are identified and sutured
t56 Perineol Locerqtions Foecol Incontinence qnd Rectovaqinal Fistula

OLD COMPLETE PERINEAL TEAR

Definition and aetiology:
An old complete perineal tear is a 3'd degree perineal laceration that has occurred usually during
childbirth but was missed at the time of delivery or improperly sutured and repaired.
Symptoms and clinical presentation:
- The wound will heal by granulation tissue leaving an ugly scar with a weak anal sphincter
leading in some cases to incontinence for stools or flatus or both.
Many patients will be able to regain control over the passage of hard stools, but remain in-
continent to flatus, and usually complain of persistent leucorrhoea.
Signs on clinical examination:
a. A defect is noted in the perineol body, extending to the anal opening.
b. lf the rectal wall is also torn, the bright red colour of the rectal mucosa is apparent in the
lower part of the defect.
c. On eoch side of the anus a small shallow pit is seen in the skin. These two dimples indicate
the site of the cut retracted ends of the anal sphincter.
d. Absence of the normal corrugations oround the anus, except posteriorly.
e. A finger introduced in the onus will confirm absence of sphincter control if the patient is
asked to contract her muscles.
Pre-operative Prepa ration
The patient is admitted to hospital 3 doys before the operation, during which:
1-. A purge is given to empty the bowel, with daily cleansing enema and vaginal douches.
2. The patient is kept on a non-residue fluid diet (free of milk).
3. Intestinal antiseptics (as neomycin or streptomycin) are started orally 3 days preoperatively.
Operation for old complete perineal tear:
- An H-shaped incision is made in the skin, with the horizontal limb of the H at the junction of
the rectum with the vagina and the two vertical limbs; at the site of the two dimples
- The incision is deepened to expose the various structures of the perineal body, and the vagina
is seoarated from the rectum.

- The rectal wall and the cut ends of the anal sphincter are repaired as mentioned before in the
management of recent 3'd degree perineal laceration
- A posterior colpo-perineorrhaphy is then performed following the steps described in treating
rectocele. The vagina is packed tightly, and a urinary catheter is inserted until the pack is re-
moved.
Postoperative Aft er-ca re :
- The vulva is regularly washed with antiseptic solutions then dried (at least 3 times daily).
- The low residue diet is continued, as well as the intestinal antiseptic.
- Antibiotics against wound infection (systemic and possibly local creams or gel).
- The vaginal pack is removed after 24 hours.
- On the fifth night the patient is given oral purgative solutions (as 50 ml. castor oil) in order to
lubricate the stools. After that the patient is given daily oral laxatives and stool softeners to
avoid constipation.
N.B.; in the event of subsequent pregnancy, o postero-lateral episiotomy should be done before de-
livery of the head to ovoid recurrence of the lacerotion
 Gynaecology 151

RECTO-VAGINAL FISTULA

AETIOLOGY

1. Congenital recto-vaginalfistulae are very rare.

2. Traumatic RV fistula:
a.Obstetric trouma: the commonest cause of a recto-vaginal fistula is badly healed, complete
perineal tear: the lower part of the tear heals satisfactorily, but the upper part breaks down
due to sepsis or bad technique in suturing, resulting in a communication between the two pas-
sages.

b.Surgical trdumo: as injury to the rectum during posterior colpo-perineorrhaphy (in treatment
of a rectocele), or during vaginal hysterectomy.
c.Other rore causes; include defloration injuries, and ulceration of an ill-fitting neglected pessary.
3. Inflammatory conditions: as following rupture of a peri-rectal or peri-anal abscess.
4. Malignant RV fistula may occur due to direct extension of malignant disease from the cervix,
vagina, or anterior rectal wall.

5. Post-irradiation fistulae are frequently seen as complications of radium treatment. They are
always associated with symptoms of severe proctitis.

SYMPTOMS
a.Large RV-fistulae: are associated with loss of voluntary control over passage of faeces and
flatus, in addition to persistent leucorrhoea, due to the associated 2ry vaginitis.
b.Small RV-fistula: the patient's may complain only of involuntary escape of flatus, which she
feels as coming from the vagina

TREATMENT
The treatment of non malignant RV-fistulae is essentially surgical. Preoperative and postoperative care
of the patient are crucial for the success of the procedure, and they generally follow same rules as that de-
scribed for old complete perineal tears.

A) Fistulas in the lower third of the vagina:

- Are managed by cutting the remaining bridge of tissue below the fistula, thus converting the fistula into
a complete peri-neal tear (Ldwson Tait's operation/. The tear is now sutured in lavers, in the same
manner and order described under repair of complete tears.

B) Fistulas in the middle third of vagina:

- May be closed in the same manner for dealing with vesico-vaginal fistulae (see chapter).
- An alternative procedure is to start the operation as in perineorrhaphy for rectocele and to extend the
dissection ofthe recto-vaginal septum upwards above the fistula. The hole in the rectum is then closed.
and the operation continued as a perineorrhaphy.

C) Fistulas in the upper third:

- High recto-vaginal fistulas are usually surrounded by dense fibrosis, and are difficult to close vaginally.
They are usually best dealt with by an abdominal (trans-peritoneal) operation
 - Anatomy of the urinary blodder Genito-urinary fistula
- Control of micturition - Vesico-vaginal fistula

- U reth ral i nco nti ne n ce - Uretro-vaginal fistula

ANATOM ICAL CONSI DERATIONS

r The detrusor muscle of the urinary bladder is composed of a meshwork of muscle fibres
that allows for reduction in all of its diameters when it contracts. lt has a rich cholinergic
parasympathetic supply (S: 2, 3,4).
r The urethra is a 3-5 cm long thin-walled muscular tube that opens in the vestibule of
the vagina. The urethral smooth muscle fibres are innervated by sympathetic fibres (T10,
rt, t2).
r The internal urethral sphincter (involuntary) is formed by a thickening of the detrusor
muscle at the vesico-urethral junction.
r The external urethral sphincter (voluntary) is a skeletal muscle that surrounds the
urethra as it passes through the urogenital diaphragm.
r The urogenital diaphragm is part of the muscular portion of the pelvic floor that pro-
vides a stable base on which the bladder neck and proximal urethra rest

ul€thral sphincter

Pelvic floor-
urethral sphincter
urcthral oritice

Fig 78-7: onatomy of the urinary bla r

CONTROL OF MICTURITION
During rest accumulation of urine in the bladder activates stretch receptors in its wall
causing reflex relaxation of the detrusor muscle and contraction of the external ure-
thral sphincter.
- When about 200 ml of urine have accumulated, impulses are sent to the brain and one
begins to feel the urge to urinate.
- Activation of the micturition center in the pons signals parasympathetic neurons that
stimulate contraction of the detrusor muscle and relaxation of the internal urethral
sph i ncter

158
 Gynaecology 159

URINARY INCONTINENCE
DEFINITIONS
I Continence of urine; is the ability to hold urine at all times except during voiding. To
achieve this intra-urethral pressure (IUPR) is normally always kept higher than intra-
vesical pressure (IVPR).
I Incontinence of urine; is the involuntary leakage of urine that is objectively demonstrable.
CLASSIFICATION AND TYPES OF FEMALE URINARY INCONTINENCE
A) Urethral incontinence:
l-. Stress urinary incontinence (SUl)
2. Urge incontinence (detrusor over activity DO)
3. Retention with overflow
4. Nocturnal enuresis
5. Urethro-vaginal fistula
B) Extra-urethral incontinence:
- Genito-urinary fistulas (GUF), apart from urethro-vaginal type

UrC€ Arrct'now

Fig 18-2: Types of urinary incontinence

STRESS URtNARY TNCONTTNENCE (SUt)

DEFINITIONS AND INCIDENCE
I SUI describes the involuntary escape of urine through the urethra during suddenly in-
creased intra-abdominal pressure, as during cough, sneeze, or laughter.
r lt may be encountered in around;
- 5% of females < 45 years,
- tO% of females between 45 - 60 years,
- >30% in women over 65 years of age.
I Urodynamic stress incontinence UDSI: is the term used when SUI is confirmed
with objective urodynamic testing.
r Temporaryincontinence may sometimes occur in some conditions as;
) Following vaginal delivery, especially if difficult with prolonged second stage.
) During long periods of immobilization as in old bed-ridden patients
) In association with severe urinary tract infection (UTl)
) As a side effect of some medications
 60 Urinory lncontinence

AETIOLOGY AND RISK FACTORS

a) Weakness of pelvic floor muscles and supports:

- Congenitol (rare): occurring in young and nulliparous women with no risk factors.

- Childbirth trouma: due to overstretching of the pelvic floor muscles and the endopel-
vic fascia, with damage to its nerve supply, especially after prolonged and difficult de-
liveries.

- Postmenopousol: due to atrophic changes affecting pelvic fascia 2ry to oestrogen defi-
ciency.
b)Anterior vaginalwallprolapse: due to descent of the bladder neck and proximalurethra.
c) Chronic increase in IAPR: marked obesity, chronic lung disease, or chronic constipation,
may precipitate the condition in women with weak pelvic floor musculature and or vaginal
prorapse.

PATHOPHYSIOTOGYOF SUI

- The bladder neck and proximal urethra are normally situated in an intra-obdominal
retropubic position resting on the pelvic floor muscles and supported by the pubo-
urethral ligaments.
- This position allows equaltransmission of IAPR to the bladder and the proximal urethra,
maintaining a persistently higher IUPR over the IVPR.
This difference in pressure gradient results in urethral closure and continence even with
abrupt increases in the IAPR, except during voiding.
- Descent of the bladder neck and proximal urethra below the symphysis pubis, due to
damage to the levators ani muscles or the pubo-urethral ligaments, will make them no
longer intra- abdominal organs, and will result in unequal tansmission of IAPR to the
bladder and urethra.

- During sudden increase in IAPR the IVPR will exceed IUPR and urine will involuntary
escape through the urethra leading to SUl, which is limited to the period of increased
IAPR, as during cough, sneezing, or laughing.

- The patient neither the desire to void nor the control on voiding.

SYMPTOMS
l-. Involuntary leakage of urine through the urethra during coughing orsneezing, etc...
2. Symptoms of associated prolapse as heaviness and mass filling vagina may be present.

SIGNS AND TESTS ON CLINICAL EXAMINATION

1) Cough stress test: eliciting involuntary escape of urine through the urethra during cough
while the bladder is partially filled and the patient in an erect or better lithotomy position.
2) Bonney's test:
- With the patient in lithotomy position, perform a cough stress test to elicit a positive SUl.

- The bladder neck is then elevated gently by the index and middle fingers of the
examiner's hand, placed in the vagina on each side of the urethra without compress-
ing it (as if trying to correct mild vaginal and bladder neck descent).
 Gynaecology t61

The patient is asked to cough or strain agatn;

) lf no urine escapes during cough; then bladder neck descent is the cause, and
surgical repair will be successful.
F lf urine escapes during increased IAPR then weakness of bladder neck will be the
cause.
3) The Q-tip test: to detect mobility of the urethro-vesical junction on straining (see Fig. L7:41.
More than 30 degree mobility during straining indicates a hyprmdolie urthrove si-
ca ljuctu in
4) Presence of genital prolapse: should be always excluded in cases of sUl

.4

,, o I

Fig 18-3: Bonney's test Fig 18-4: Q-tip test

URODYNAMIC TESTS FOR DIAGNOSIS OF SUI

A special catheter with a sensor probe is introduced to the bladder through the urethra to allow
performing cystometry, uroflowmetry, and urethral pressure profile.

Porameters of Normal Bladder Function on and

Detrusor pressure filling: < L5 cm H2O
Absence of detrusor controctions
- First desire tovoid: 1-50-200 ml
Capocity: strong desire 400-600 ml
- No leakage during cough
Uroflowmetry: rate of urine flow through urethro; N =L5 ml/sec
- Residuol urine after voiding: < 50 ml

r Uretheral pressure profile: traces intraurethral pressure along urethral length, and al-
lows tracing urine leakage during lApR changes. It can confirm presence of SUI in cases
where clinical examination is not reassuring.
t62 Urinary lncontinence

DIAGNOSIS OF SUI BY URODYNAMIC TESTS

7. Cystometry: will reveal
) involuntary leakage of urine through the urethra during increased IAPR

F Absence of detrusor contractions during filling cystometry.

2. Urethral pressure profile: will reveal
F increased IVPR > IUPR during straining
F Decreased functional urethral length (length of urethra closed by IUP).
I N.B.j After confirmation with urodynamic studies the term urodynamic stress incontinence
UDSI will be used instead of the clinicalterm SUl.

PREVENTION OF SUI
a. Avoid prolonged second stage of labour and minimize child birth trauma.
b. Pelvic floor exercises especially in the puerperium, or after pelvic surgery
c. Avoid marked obesity and overweight.
d. Treatment of chronic cough and constipation especially in the post menopausal period
MANAGEMENT OFSUI
A. CONSERVATIVE MEASURES for Mild coses:
Mild SUI may show some improvement via;
7. Pelvic floor muscles strengthening exercise:
F Active pelvic floor muscle training (PFMT) known as Kegel exercises
F Passive electrical pelvic
floor muscle stimulation.
2. Scheduled voiding: to minimize amounts of urine in the bladder.
3. Oestrogen therapy: vaginal cream in cases of menopausal atrophy may improve urethral
blood flow and increase alpha adrenergic receptor sensitivity.
4. Pessdry treatment: in some cases of vaginal prolapse may improve associated
SUI,

B. SURGICAL TREATMENT for Moderote and Severe Coses:

Surgery is the gold standard in treatment of USl. The aim of
surgery is the permanent correction of proximal urethral and
bladder neck descent, by their elevation back to their normal
retropubic intra-abdominal position, thus restoring the balance
between IVPR and IUPR.

T.KELLY'S PERIURETHRAL FASCIAL PLICATION SUTURES:

It is a vaginal procedure in which periurethral plication
of fascia is performed along the course of a cysto-
urethrocele repair via anterior colporrhaphy procedure
(see genital prolapse).

- lt is a simple procedure associated with a 60-70%

success rate but unfortunately will fall to only 30% after 5
yea rs
 Gynaecology t63

2. BURCH COLPOSUSPENSION OPERATION:

It is an abdominal procedure in which the upper
vagina, (at the level of the urethrovesical junc-
tion and upper third of the urethra), is plicated
on each side to the iliopectineal ligament (Cooper
ligament) by 2-3 interrupted non absorbable su-
tu res.
Burch colposuspension is
considered the gold
standard procedure with success rates of 9S%o after
1 year, and nearly 75% afLer 1_5 years follow up.
Recently the procedure has been performed lapa-
roscopically.
Burch procedure and poravoginal repair
suspend the urethro and blqdder to correct
stress incontinence qnd cvstocele
3. THE SLING PROCEDURES.
Fig 18-6: Burch Colposuspension
a) Tension-free Vaginal Tape (TVT):
TVT is performed using synthetic mesh like tape introduced vaginally, on each side of the
proximal urethra, passing just below it acting as a sling, then each end of the tape is pushed
upwards to be pulled out through the abdominal wallto which it is finally fixed.
- TVT has a high success rate up to 9O%o, with the advantage of a simple technique that
requires a shorter stay in the hospital (1 day), and can be performed under local anes-
thesia.
b) Trans-Obturator Tape (TOT):
- TOT is performed using a synthetic mesh-like tape (similar to TVT), introduced vaginally, pass-
ing from one obturator foramen to the other, piercing the obturator diaphragm, and forming
a sling below the proximal urethra, with the distal tape pulled out through small groin inci-
sions at the level of clitoris.
- TOT is simpler than TOT with less complications, performed with regional anesthesia as an
outpatient procedure, with success rates approaching TVT.

4. PERIURETHRAL INIECTION OF COLLAGEN.

This is a short term treatment because long term success results are <30%o after 5 years

il1i

Fig 18-7: TVT Fig 18-8: TOT

164 Urinary lncontinence

URGE INCONTINENCE

DEFINITIONS AND INCIDENCES

Urge incontinence describes involuntary leakage of urine through the urethra before
starting to void when the bladder is partially full, posing difficulty in postponing urination urg-
es.

Urge incontinence is usually associated with detrusor overactivity (DO), which is an urody-
namic observation characterized by involuntary detrusor contractions during the bladder filling.
Urge incontinence is the second most common cause of female urethral incontinence, and ac-
counts for 30-40% of cases.

AETIOLOGY
- ldiopathic (most common).
- Local bladder irritation (e.g. infection, stone, ulcer, polyps).
- In association with a neuropathy as in; DM, DS, spinal cord or brain lesions.

CLINICAL SYMPTOMS
Urgency: sudden desire to void.
Frequency: urination 7 or more times a day.
Nocturia: awaking from bed more than once at night to void.

INVESTIGATIONS for DIAGNOSIS of DO

1. Cystometry: to measure IVPR and trace detrusor systolic filling contractions. DO will be
diagnosed whenever studies reveal detrusor pressure filling > L5 cm H20 due to increased
systolic contractions with failure to inhibit detrusor contractions during cystometry.
2. Midstream Urine Examination: to exclude cystitis and to perform culture and sensitivity
if pus cells are high.
3. Cystoscopy and IVP: may be needed to exclude intravesical pathology (stone, polyp, etc.)

TREATMENT
a. Bladder training exercises; tends to increase the interval between voids. lt is time con-
suming and requires cooperative patients,
b. Anticholinergic drugs: to reduce the vesical oressure and increase the bladder
volume (e.g.; detrusitol 2mg twice daily)
 Gynaecology r65

GEN ITO.U RI NARY FISTU LAS

Genitourinary fistulas are abnormal communications between the urinary organs
(bladder, ureter, and urethra), and the genital organs (uterus, cervix, and vagina). Tney are usu-
ally associated with continuous leakage of urine through the vagina (true incontinence).

ANATOM IC CLASSI FICATION OF G E N ITOU RI NARY FISTU LAS

GENITAL ORGANS URINARY TRACT
Ureter Blodder Urethro
Vagina Uretro-vaginal Vesico-vaginal Urethro-vaginol
Cervix U retro-cervical Vesico-cervicol U rethro-cervicol
Uterus U retro-uterine Vesico-uterine U rethro-uterine

OVERVIEW AND INCIDENCES:

The incidence of GUF has been sharply declining in the t- t a*er$r.lda f,|sat
last 3 decades due to effective preventive approaches. f. $ede.d.rd irhd|
+ tFrltarwr{laat ltfrd.
+ itqiorae*nd hrh*r
Necrotic fistulas, related to childbearing trauma, are
now considered rare, so as necrotic fistulas occurring 2ry
to pelvic irradiation.
Traumatic fistulas have also declined due to better
training and better surgical techniques, although are still
more common than necrotic fistulas nowadays.
In general vesico-vaginal fistulas (VVF) and uretro-
vaginal fistula (UVF) are the most common types of GUF
encountered in gynaecologic practice. Other types are ex-
tremely rare.
Fig 18-9: Common types of GIJF
AETIOLOGY OF GUF

Traumatic fistulas: due to direct injury to urinary organs, as that occurring during pelvic
surgery, crash accidents, or rarely the use of certain obstetric instruments during delivery.
b. Necrotic fistulas: 2ry to ischaemic necrosis to parts of urinary organs as that occurring
with prolonged and obstructed labour, pelvic malignancies, and pelvic irradiation therapy.
r66 Urinory lncontinence

vESrco-vAcr NAL FTSTULA (VVF)

OVERVIEW AND AETIOLOGY

VVF have long been considered as the commonest type of GUF encountered in gynaecologic
practice. In the majority of cases it occurred due to ischaemic necrosis 2ry to prolonged compres-
sion of thefoetal head againstthe bony pelvis, in cases with undiagnosed cephalopelvicdispropor-
tion (CPD).

The incidence of necrotic VVF has markedly declined due to better obstetric practice with more
liberal use of cesarean section (CS) operation in cases with CPD replacing difficult instrumental de-
livery.

WF may still occur due to direct traumatic injury during CS and hysterectomy operations, as
well as the faulty use of the obstetric forceps procedures.
WF may rarely occur due to invasion of vaginal and bladder walls in gynaecologic malignancy,
or 2ry to irradiation necrosis in the management of vaginal, cervical, or endometrial cancer.

SYMPTOMS and CLINICAL PRESENTATION

1. Complete Urinary lncontinence:
- Continuous leokage of urine from the vogino in a patient with a history of a recent delivery,
pelvic surgery, or pelvic irradiation is the main presenting symptom.

- Loss of the desire to void urine, due to absence of bladder filling, is the rule especially when
the fistula is large and in a low position.

- ln necrotic fistulas; Incontinence may present days or weeks after a difficult delivery, or
months after pelvic irradiation.

- ln traumatic fistulas; leakage of urine starts almost immediately after gynaecologic pelvic sur-
gery, CS, or urologic procedures.

2. Partial Urinary Incontinence:

- lnterrupted leokoge of urine with occosional desire to micturate; may occur in some cases
with a small VVF situated high in the bladder, enabling the patient to retain some of the
urine in her bladder. This type should be differentiated from UVF.
3. Pruritus and vulvitis:
These may occur secondary to prolonged irritation of vulval and vaginal skin with the continu-
ously leaking urine.

4. Cystitis & UTI:

UTI may complicate prolonged or neglected cases, due to ascending infection from the vulva. Pye-
lonephritis is a serious complication which may be the major cause for morbidity in such cases.
 Gynaecology t67

SIGNS ON CLINICAL EXAMINATION

a. With the patient in Sims, position:
Inspection of the anterior vaginal wall is performed using Sims' vaginal speculum, to vis-
ualize fistulous opening and detect urine leakage from VVF orifice.
b. With the patient in lithotomy position:
Digital palpation of the anterior vaginal wall is performed to detect the site, size, of VVF
and surrounding scarring and fibrosis.
,tt",
.d t.?
SPECIAL I NVESTIGATIONS

7. Retrogradecoloured dye injectioninto the bladder:

$ .*, J**
"t
Retrograde injection of 200 ml. of coloured dye
(methylene blue or indigo carmine) into the bladder is per-
"#
formed via a urethral catheter. Coloured dye will be seen
dribbling from the fistulous opening at the anterior vaginal wall
using Sim's speculum,

2. Intrdvenous pyelography (lvp):

to evaluate the amount of 18-10: sims' position for exomi-
Fig
IVP is helpful residual urine
the bladder, delineate the course of the ureters, and exclude notion of GUF
ureteric fistulae. Cysto-urethrography helps to exclude urethral fistulas and delineate
he fistu-
lous track to the vagina
3. Cystoscopy & Urethroscopy:
- cystoscopy; visualizes VVF and determines their relation to the ure-
teric openings in the bladder. lt can also exclude multiple VVF,
ureteric fistula, and can reveal any associated bladder pathology.

- Urethroscopy: mav exclude associated urethrovaginal fistula

PREVENTION OF WF: Fig 18-11: Sims' speculum

a. Avoid prolonged and obstructed labour by prompt diagnosis of cpD.
b. Use of CS instead of difficult forceps procedures.
c. Proper surgical technique in pelvic surgery to avoid bladder or ureteric injuries.
d. lmmediate intraoperative repair of bladder or ureteric injuries once diagnosed .

MANAGEMENT OF VESICO-VAGINAL FISTULA

A. CONSERVATIVE MANAGEMENT

- In case of a necrotic fistula, detected few days after a difficult labour, an indwelling silicone
catheter is introduced through the urethra and left for a period of 4-6 weeks, to divert the
flow of urine away from the fistula, prevent bladder distension, and allow wound healing.
Surgical repair is usually postponed for 3-6 months until oedema subsides and tissue
involu-
tion is complete, where surgery becomes easier and safer, allowing for better dissection and
healing.
Spontaneous closure of a small VVF may be achieved in some cases with comolete
healing of the tear, or failing this, it will be left much smaller in size.
r68 Urinory lncontinence

B. SURGICAL TREATMENT

- Surgical anatomical repair is the gold standard in management of VVF.

The first attempt for fistula repair carries the best prognosis. Repeated trials for repair are
less successful due to the extensive fibrosis left after each attempt.
Proper postoperative bladder drainage is crucial to success of surgery

Pre-operative Preparation
Proper assessment of the site and size of the fistula, with exclusion of multiple sites, or
associated ureteric fistula via performance of cystoscopy and lVP.

- Protection of the skin of vulva and vagina from continuous irritation by dribbling urine, via
use of indwelling catheters, vaseline or zinc oxide ointments.
- Culture and sensitivity of urine is done and if pathogenic organisms are found, the
patient is given the appropriate antibiotic until the urine is sterile.

OPERATIONS FOR VISCO-VAGINAL FISTULA

7. VAGINAL Flop-splitting operation (dedoublement):

- This approach is suitable for low fistulos accessible voginally

A circulor incision is made around the margin of the fistula

Dissection ond mobilizotion of the voginol wall from the bladder

over an area 2.0 cm around the fistulous opening.

- Closure of the blodder in 2 layers of interrupted sutures going

through the muscle wall only, not piercing the mucous membrane
making the closure water-tight.
Closure of the vagina by interrupted sutures going through its
Fig L8-12: SmqllVVF
whole thickness.

- Droinage of the blodder;via insertion of a rubber urethral catheter to avoid bladder disten-
sion, which will strain the stitches.
2.ABDOMINAL Repair of VVF:
High and recurrent fistulos may be better approached by abdominal repair through a

transverse suprapubic incision, and a retroperitoneal approach.

- This approach may also be more suitable in cases with large fistulas especially those
near the ureteric orifices.
Post-operative Care:
1. The bladder should be kept constantly empty to avoid any tension on the sutures, via en-
suring a patent catheter and avoid its occlusion by debris or blood clots.
2. The catheter is never removed before 10-14 days.

N.B.: In cases with successful repair of VVF, pregnancy should be avoided for a period of 1 year
after operation, and at full term delivery by CS is mandatory to avoid complications of vaginal
delivery on pelvic floor and recurrence of fistula.
 Gynaecology 169

URETERO.VAGINAL FISTU LA
This variety of fistula nearly always occurs as a result of injury to the ureter during gynae-
cologic operations as hysterectomy but may also develop following a difficult delivery by
C.S.
Symptoms:
- Incomplete urinary incontinence; the bladder fills normally from the intact ureter, and the
patient voids normally with a preserved sensation of bladder filling and desire to micturate,
while the urine continuously dribbles through the vagina from the affected ureter at the
site
of UVF.
Inspection by Sims' speculum:

- The fistula is always small and situated high up in the vagina lateral to the cervix.

Investigations:

- uvF can be differentiated from vvF by the methylene blue test.

- Cystoscopy shows a normal bladder with presence of the ureteric efflux on only one side.
Prevention:

- Preoperative identification of ureteric course through an lVp.

- Preoperative placement of ureteric catheters in cases with abnormal ureteric course or

large pelvic tumours

- Intra-operative proper anatomical identification of the ureter during pelvic surgery.

Surgicaltreatment:
- Abdominal re-implantation of the ureter into the bladder.

URETHRO-VAGINAL FISTU LA
This rare type of fistula may be caused by obstetric childbirth trauma or gynaecologic
surgical trauma (as in procedures for correction of vaginal prolapse or sUl).
Symptoms:
- The patient will be continent all through, with normal sensation of bladder fill-
ing and preserved desire to micturate
- During voiding; splashing or double stream of urine through the urethra and vagina
occurs.
Diagnosis:
- Direct visualization by passage of a urethral catheter through the defect, or
- Urethroscopy.
Treatment:
- Insert a catheter splinting the urethra once injury detected and leave itfor 2 weeks
for spontaneous healing with excellent results.
- Surgical reconstruction of the urethra and closure of the defect in old cases.
t70 Urinary Incontinence

Key points
- l-)rinory incontinence is a stressful condition thot has a negotive impact on the potient's life style

- tJrethrql incontinence in theform of StJt orDO may affect upto20%of femote populotion,qndisnow-
odoys far more common thon extra-urethrql incontinence cqused moinly by GUF.
- Diagnosis of SUt is bosed mostly on clinicql dota although exclusion of or differentioting from DO is
best ochieved through urodynomic studies.

- The definitive treatment of moderote or severe coses of SUI (or UDI) is essentially surgicol, using either
Burch fixotion procedure, or more recently Tape Colposuspension with high rotes of success (>9}%ofor
the first 5 years). Recurrence rates ore relotively low.

- DO is usually monoged through physiotheropy, blodder training, ond qnticholinergic medicqtions.

- Extraurethral incontinence is mainly coused by GUF, occurring mostly due to either obstetric or gynoe-
cologic complications. The most common forms include VVF qnd UVF.

- The diagnosis of GUF is essentially q clinicol one, bosed on proper history toking, vaginal examinotion
(using Sims' speculum), and performing speciol investigotions to locqte the site of the fistulo ond its
relotion to the blodder or ureters.
- Surgery is the mainstoy in the monogement of GUF. lt can be performed os o primory repoir ot the
time of occurrence, or postponed for 8-12 weeks until resolution of tissue oedema.
- WF issurgically treoted through removol of the fistutous troct, debridement, qnd closure of the blodder
and voginol walls in layers by interrupted sutures without tension. UVF will require implantation of
the cut ureteric end into the blqdder wall.

- In GIJF the Lst attempt ot surgical repoir alwoys gives the best prognosis. Recurrent fistulo is more diffi'
 - Menorrhagia postmenopausal Bleeding
- Metrorrhagia - Dysfunctional Uterine Bleeding
- Contact bleeding _ Management of AUB

The normal menstrual cycle is characterized by cyclic shedding of the endometrium

that
occurs every 21-35 days (mean 28 days), with a duration of 3-5 days and an average
blood loss of
30-50 ml/cycle.

Abnormal uterine bleeding (AUB) describes abnormal patterns of uterine bleeding

other than
that occurring in a normal menstrual cycle.

PATTERNS OF AUB
o Menorrhagia (Heavy Menstrual Bleeding HMB): excessive
bleeding during menstruation
o Metrorrhagia (intermenstrual Bleeding IMB): significant bleeding
in between cycles

' Meno-metrorrhagia: bleeding includes both HMB and IMB (acyclic irregular bleeding)
o Postmenopausal Bleeding (pMB): vaginal bleeding after
menopause.
o Contact bleeding (CB): bleeding on touching the cervix (e.g.: post-coital
bleeding)
o Other abnormal bleeding patterns of the menstrual cycle:

Y Hypomenorrhoeo: scanty menstrual flow usually of short duration

Y oligomenorrhoeo: infrequent menstrual cycles (duration > 35 days between cycles)
Y Oligohypomenorrhoea.' infrequent cycles with scanty flow or short duration
D Polymenorrhoeo: frequent menstrual cycles recurring every < 21days (normal
flow)
Y Polymenorrhagia: frequent HMB recurring every < 2L days

CAUSES OF AUB (F|GO 201U

A. STRUCTURAL CAUSES: referred to as pALM

1-. Pregnancy complications: as abortion, ectopic pregnancy, and hydatidiform

mole
2. Polyps: endometrial and endocervical polyps
3. Adenomyosis: myometrial myohypertrophy due to intramyometrial endometriosis
4. Leiomyomas: benign myometrial tumours
5. Malignancies: endometrial and cervical carcinomas, and functioning ovarian
tumours

17l
172 Abnormal Uterine Bleeding Dub And Endometrial Hyperplasia

B. NON STRUCTURAL CAUSES: referred to as COEIN

1-. Coagulation disorders: as ITTP and Von-Willebrand disease
2. Ovulatory dysfunction: as chronic anovulation in PCOS
3. Endometrial hyperplasia: see later
4. latrogenic causes; as anticoagulant therapy, IUD induced bleeding and OCP break
through bleeding
5. Non-classified aetiology: as systemic hypertension, capillary fragility, severe thyroid
disorders, chronic liver disease and renal failure.

CLASSIFICATION OF AUB ACCORDING TO AGE GROUPS

1. Childhood and Adolescence bleeding
2. Childbearing period bleeding
3. Perimenopausal bleeding
4. Postmenopausal bleeding

MENORRHAGIA
Menorrhagia also known as heavy menstrual bleeding (HMBI, is the term used to
describes excessive blood loss during menstruation that exceeds > 80 ml in amount and/
or >7 days in duration, or both. HMB occurs more frequently in association with benign
rather than malignant conditions.

coMMoN CAUSES OF MENORRHAGIA (HMB):

. Leiomyomos: especially larger intramural and submucus leiomyomas (see
leiomyomas)
. Adenomyosis: in association of symmetrical uterine enlargement and myoypertrphy
. Endometriot polyps; due to increased surface area of endometrium
. Endometrial hyperplosio (EH): especially mild forms of simple EH (Dysfunctional
menorrhagia)
. lntrauterine contraceptive device (lUD): non-hormonal and Cu lUDs
. Systemic disease and coagulotion disorders: as hypertension & ITTP'

EVATUATION OF THE AMOUNT OF MENSTRUAL BLEEDING:

1. Number of blood soaked diapers changed daily
2. Duration of menstrual bleeding
3. Presence of large blood clots and associated anaemia
4. Affection of the patient's general condition and her life style.
r N.B.: A scoring system is available to evaluate the amount of bleeding within each
diaper or tampoon changed daily, being light, moderate or completely soaked. The
amount of blood loss can be more accurately calculated using such scoring symptoms.
 Gynaecology 173

METRORRHAGIA
Metrorrhagia describes significant intermenstrual bleeding (lMB) occurring spontaneously
not in relation to the time of menstruation.
Significant IMB may be associated with various benign conditions, but is more also
commonly associated with hormonal disturbances, premalignant lesions, and malignancies of
the uterine body and cervix.
coMMoN CAUSES OF METRORRHAGTA (lMB)

- Non hormonallUD: one of the commonest causes in childbearing period (Cu T).

- Combined oCPs (COCCs), and Gestagen only pills (POPs): may cause breakthrough bleeding
and intermittent spotting.

- Leiomyomas: ulcerated submucus fibroid polyps

- Hyperplastic adenomatous endometrial polyp
- Endometrial and endocervicol carcinomas, and oestrogen producing ovarian tumours

PERIM ENOPAUSAL BLEEDING

Perimenopausal bleeding describes AUB occurring in elderly women, commonly > 40 years
of age, before their actual menopause. lt may occur in the form of Menorrhagia, Metrorrhagia,
or Meno-metrorrhagia.
Although the underlying aetiology is usually functional or benign, yet malignant neoplasms
should be thoroughly excluded, before treatment is initiated.

COMMON CAUSES OF PERIMENOPAUSAL BLEEDING

- Anovulotory DUB is the most common cause (see later)

- IUCD or OCPs induced bleeding

- Leiomyomas and Adenomyosis
- Endometriol and endocervicol polyps
- Endocervical carcinomo, and less commonly endometrial cancer and functioning ovarian
tumours.

POSTM ENOPAUSAL BLEEDI NG

Postmenopausal bleeding (PMB) describes vaginal bleeding that occurs ij menopausal

women after complete cessation of menstruation. Women are usually > 45 years of age, with
high serum FSH levels >30 mlU/ml. In PMB bleeding may be uterine, cervical, vaginal, or vulvar,
i.e.: not only limited to AUB
PMB is always abnormal, and although in most cases the underlying etiology is benign, yet
premalignant and malignant lesions should be thoroughly looked for and excluded in every
case.
t74 Abnormal Uterine Bleeding Dub And Endometriol Hyperplasia

COMMON CAUSES OF PMB:

- lotrogenic; as with hormone replacement therapy in menopause (HRT)

- Benign conditions: atrophic vaginitis, atrophic endometritis, vulvar dystrophies, endometrial

and endocervical polyps (most common causes).

- Premolignant lesions: EH, and high grade CIN lesions

- Gynecologic malignancies.' endometrial, cervical, vaginal, and vulvar cancers, and oestrogen
producing ovarian tumors (most serious causes).

- Systemic disease as hypertension and ITTP

CONTACT BLEEDING
Contact bleeding (CB) describes bleeding that occurs on touching the cervix. lt usually
presents as post coital bleeding that can occur also following PV or speculum examination.
ln most cases the underlying cause is a benign, inflammatory, or traumatic lesions, .?
however CB in perimenopausal and postmenopausal women is largely related to cervical cancer,
and should thoroughly looked for and excluded in such age groups, and even in younger high risk
population (see cancer cervix).
COMMON CAUSES OF CB:
- Benign cervical lesions: mucous polyps and cervical erosion (most common)

- Premalignant cervical conditions: High grade CIN lesions (common in high risk cases)

- Vaginal causes: severe Trichomonas vaginitis, or menopausal atrophic vaginitis.

- Vaginal trauma: as friction and defloration injuries.

DYSFUNCTIONAL UTERIN E BLEEDING

Dysfunctional uterine bleeding (DUB) describes AUB that occurs in absence of recognizable
pelvic pathology, systemic disease, blood dyscrasias, or pregnancy. lt is a diagnosis made by
exclusion more commonly occurring in Perimenopausal women and in late childbearing period,

DUB occurs most commonly in association with chronic anovulatory disturbances causing
endometrial hyperplasia (EH) in response to continuous oestrogen (E2l effect on the
endometrium unopposed by progesterone (PRG).

EFFEcToFANoVULAT|oNoNENDoMETR|ALVAscULARHoMEoSTAS|S:
The secretory endometrium in ovulatory cycles contains high levels of the potent
vasoconstrictor prostaglandin p2 - (PGL F2 -l which causes endometrial ischemia on PRG
withdrawal allowing for complete sloughing of the superficial and intermediate layers of the
endometrium, and control of the amount and duration of blood loss during menstruation.
In cases with anovulation, continuous estrogen (E2) stimulation in absence of PRG will cause
the proliferative endometrium to outgrow its blood supply, breaks down, and sloughs resulting in
irregular bleeding. The associated low levels of PGL F2 - will make the endometrium less efficient
in controlling the amount and duration of menstrual bleeding.
In cases with chronic anovulation, as in PCOS, prolonged estrogenic effect on the
endometrium unopposed by PRG will predispose to endometrial hyperplasia (EH) which will result
in excessive irregular type of AUB, and may predispose to endometrial carcinoma (EC).
 Gynaecology | /J

ENDOMETRTAT HYPERPLASTA (EH)

Endometrial hyperplasia (EH) is a pathologic entity that describes an increase in size and
number of irregularly proliferating endometrial glands, leading to abnormal endometrial thickness
and increased tendency for bleeding. This condition has long been known as metropathia
haemorrhagica.
Hyperplasia of the endometrium occurs in response to prolonged oestrogenic effect on the
endometrium in absence of an adequate counteracting progestational effect. lt occurs more
frequently in;
- Chronic anovulation: as in PCOD and delayed menopause

- Obesity: due to peripheral conversion of androgen (Androstendione) into oestrone (E1)

- Exogenous oestrogen therapy: as in menopausal oestrogen replacement therapy ERT

- Oestrogen secreting ovarian tumours: as feminizing granulosa theca cell tumours.

I N.B.: EH are commonly associated with leiomyomas, adenomyosis, and endometrial
carcinoma

PATHOLOGIC TYPES OF EH
A. Simple EH; cystic endometrial glandular dilatation with disparity in size (oestrogen effect) and
no evidence of secretory activity (PRG effect), giving it a Swiss cheese appearance
microscopically.
B. Complex EH.' new endometrial glands will be formed with resulting increase in number and
crowding with minimal intervening stroma (back to back orrangement microscopically/.
MALIGNANT POTENTIAT FOR EH
The presence of nuclear atypia (abnormal mitosis, hyperchromatosis, and increased nuclear
cytoplasmic ratio) will raise the malignant potential of EH, especially in complex EH, and increases
the risk for progression to endometrial adenocarcinoma as follows;
7. Simple EH without atypia: < 7%
2. Complex EH without otypia: < 3%
3. Simple EH with otypia:8% (rare)
4. Complex EH with otypia > 25%

EVALUATION AND MANAGEMENT OF A CASE OF AUB

Careful History: for exclusion of pregnancy, medical disorders, endocrine disorders, systemic
disease, and iatrogenic causes as use of ocp, lUD, and anticoagulant therapy.

Bimonual pelvic exomination: to exclude uterine leiomyomas, adenomyosis, and adnexar

masses

Speculum examination,' to exclude cervical polyp, erosion, ulcer, mass, or associated vaginal
pathology.

PAP smeor test.'to exclude high grade intracervical lesions (ClN)

Pelvic U5; to exclude uterine, endometrial and adnexal pathology.
t76 Abnormol Uterine Bleeding Dub And Endometriol Hyperplosio

- Laborotory tests and hormonol qssoys: for exclusion of suspected liver disease, endocrine
disorders, and blood dyscrasias (as lTP, & von Willebrand disease).

- Office hysteroscopy; is beneficial for diagnosis of small endocervical and endometrial lesions

- D&C biopsy: is the gold standard in diagnosis of endometrial hyperplasia (EH) in cases with DUB

- MRI & CT scan: are beneficial in presence of an adnexal mass or suspected malignancy

KEY POINTS IN DIAGNOSIS OF AUB:

r Menorrhagia: is usually caused by benign conditions as leiomyomas, adenomyosis and DUB.

r Metrorrhagia: is mostly associated with SMF polyps, endometrial polyps, EH, and uterine
malignancies -
r DUB: occurs in absence of clinically detectable pathology hence endometrial biopsy is mandatory
for exclusion of EH. TVS will usually reveal abnormal endometrial thickness.
r PMB: TVS will pick up cases with endometrialthickness > 5 mm with higher risk of EH or EC

r In CB: speculum examination, PAP smear, colposcopy and biopsy from suspicious lesions are
mandatory to exclude cervical cancer in suspicious and high risk cases

TREATMENT OF A CASE OF AUB

Treatment of AUB is a treatment of the cause. lt starts by controlling the primary attack of
bleeding, then identifying the possible primary cause, followed by immediate treatment of the
specifi c underlying etiology,

In many cases of more than one aetiology may be present, as with leiomyomas, adenomyosis,
EH, ClN, and suspicious adnexal masses, in such cases treatment starts bythe most probable
primary cause.
Treatment of anemia, systemic diseases, endocrine disorders, and blood dyscrasias, should be
initiated once diagnosis of any of these conditions is established.
Treatment will largely depend on the severity of AUB, weather primary or recurrent, previous
treatment if present, together with the patient's age her desire for further fertility, and the final
diagnosis of the primary aetiology.

A) DURING AN ACUTE ATTACK: control of an attack of HMB can be achieved via;

Y Antifibrinolytics: as Tranexamic acid, 500 mg t.d.s. orally, can control heavy bleeding by
converting plasminogen into plasmin, to inhibit fibrinolysis, and stabilize clots.

F Non-Steroidal Anti-inflommotory Drugs (NSAlDs): as Mefanimic acid 500 mg two to three

times daily orally, decrease amount of menstrual flow by up to 50% through decreased PGL
synthesis, leading to decreased vascular dilatation and restoration of endometrial
homeostasis. They also minimize pain and help to control bleeding.

> D&C operotion: to stop bleeding and obtain endometrial biopsy to exclude EH
 Gynaecology t]7

B) HORMONAL TREATMENT:

Hormonal treatment aims at correction of unopposed oestrogenic effect of anovulation and

inducing timed endometrial shedding to induce regular cycles of average amount of bleeding.

v 1. Cyclic Combined oestrogen / progesterone: e.g.; OCP for 21 days /month (day 3-24 of the
cycle). These regulate endometrial ripening and shedding inducing regular cycles with
v reduced menstrual flow. Treatment is usually extended for 3 successive cycles.

2. Cyclic Gestagens: oral tablets 10 mg daily for 14 days /month (day 1,0-24 in each cycle for 3
cycles).

from an IUD is an effective method for inducing hypomenorrhoea in cases of severe recurrent
DUB in absence of large myomata, complex EH, and EC.
.- HOW DO GESTAGENS CONTROT AUB ANd CORRECT ENDOMETRIAL HYPERPLASIA
v a. Counteract oestrogen induced mitotic effect on DNA level, thus preventing EH.

v b. Stabilize the endometrium and prevents its overgrowth, so that an organized sloughing will
occur after PRG withdrawal.

c. lmproves PGL imbalance restoring endometrial homeostasis (see DUB).

v d. Restores cyclic endometrial shedding leading to cyclic controlled bleeding.

v c) suRGtcAL TREATMENT:

- D&C for control of acute attack, and obtaining biopsy to exclude EH and EC. lt is indicated in
v cases with severe bleeding especially in presence of abnormal endometrial thickness or

- Cauterization of an endocervical polyp or a cervical erosion

- Cervical Conization (LEEP procedures): in cases of CB with high grade intraepithelial lesions
v (HG tL)

- Endometrial ablation: in some cases with recurrent DUB and failed hormone therapy in
absence of EH
v - Abdominal Myomectomy for larger myomata causing AUB in young women desiring to
preserve fertility. lt is usually performed via laparotomy, but can also be performed by
v laparoscopy in selected cases

v - Hysteroscopic Myomectomy or Polypectomy for small submucus leiomyomas, and/or

endometrial polyps

- Hysterectomy.' abdominal, vaginal, or laparoscopic hysterectomy should be reserved only

r for cases with;

cervical lesion (ClN 3), suspicious adnexal masses or failed hormonal; therapy.

:
hormone therapy.
178 Abnormal Uterine Bleeding Dub And Endometriol Hyperplosia

ENDOMETRIAL ABLATION:
Endometrial ablation is a procedure that aims at destroying the majority of endometrium, thus
controlling blood loss. lt carries an overall 90% success rates in reduction of HMB. The majority of
cases will experience a state of hypomenorrhoea or even 2ry amenorrhea, however IO-20% of
cases may experience irregular spotting or recurrent AUB.

The procedure may be appropriate for cases with persistent DUB in premenopausal women
with failed HT, in absence of EH, large myomata, uterine malignancy, or suspicious adnexal
pathology.

Endometrial Ablation can be performed via Hysteroscopic endometrial resection,

Hysteroscopic laser ablation, or intrauterine hydrothermal balloon. Cases with recurrent AUB after
ablation are best managed by hysterectomy.

Key Points in AUB

- AUB is the commonest couse of genital tract bleeding in the females

- AUB is usuolly secondory to an identifioble pelvic orgonic lesion or systemic diseose summqrized in
the abbreviation PALM COEIN

- Bleeding moy be in the form of Menorrhogio, Metrorrhogio, Contact bleeding, ond Postmenopou-
sal bleeding,

- Diagnosis of AUB is bosed on thorough history, physicol examinotion, and special investigations as:
U5, Ct/MRl, Hysteroscopy, loporoscopy, ond Laborotory tests

- DUB describes AUB in absence of an identifiable organic lesion or systemic disease.

- DUB mostly occurs in post-pubertol and premenopousol periods qnd is commonly ossocioted with
chronic qnovulqtion

- DUB is diognosed only ofter exclusion of all orgonic ond systemic cquses of AUB
- Treatment of AUB includes:
- Medical treotment: hoemostatic drugs & NSAlDs, to control ocute bleeding
- Hormonql treotment: Estrogen/PRG/LNG-IUD, to induce regular cycles
- Surgicol treotment: Polypectomy, Myomectomy, hysterectomy, ond endometriol ablation in select-
ed cqses

- ln PMB all efforts should be mqde to exclude premalignont or malignant lesions in FGT.
 - Uterine Leiomyomas - Uterine polyps

UTERINE LEIOMYOMAS
OVERVIEW

Uterine leiomyomas are the commonest benign tumours of the female genitalorgans.
They
arise from a single muscle cell within the myometrium, and are popularly known
as myomos or
fibroids.
Myomasare detectable in almost 20% of women inthechitd beoring period,and in upto
50%
of uteri examined at qutopsy.
Tumours usually grow slowly in size over many years, and have a very tow malignant poten-
tial. They will mostly pass unnoticed, due to their slowly progressive course, and will be diag-
nosed only when they reach a large size or produce significant symptoms, or
discovered acci-
dentally during routine gynaecologic examination.
Small leiomyomas with no or mild symptoms are commonly managed conservatively
through
careful follow up, and regular observation.
Large and symptomatizing leiomyomas are usually managed by surgical removal
whether alone,
or together with the uterus, according to the patient's age, her need for fertility preservation,
tu-
mour size, and the severity of associated symptoms.

Pedunculated
3ub€€rosal

Fig 20-1: Sites of Leiomyomos

179
180 Uterine Leiomyomos

RISK FACTORS
1. Pority: more common in nulliparous and low parity women.
2. Hereditaryfactors: m o re in women with positivefamily history (mother & sister).
3. Racial foctors: more common in dark races than in white and yellow races.
4. Obesity: more common in women with higher body mass index (BMl).

Co m m o n ly o ssoci ate d co nd iti o n s :

Y Follicular cysts of the ovary
D Endometriosis and adenomyosis
Y Endometriol hyperplasia (EH)and rarely endometrial carcinoma (EC).
AETIOLOGIC FACTORS: (exact etiology is unknown)
A. Abundant Oestrogen Environment: Leiomyomas are oestrogen dependent as evidenced by;
Leiomyomata appear only in the childbearing period.
No new tumours develop before puberty or after menopause.
- Increase in size occurs during pregnancy as well as during oestrogen therapy.
- Decrease in size and atrophy occur in conditions of oestrogen deficiency as during meno-
pause, or during GnRH agonist therapy.
Commonly associated with endometrial hyperplasia and or endometriosis.
B. Growth Factors:
Increased production of Epidermal Growth Factor (EGF).
Decreased production of Growth Inhibiting Factor (GlF).
N.B.: both may act synergisticallywith E2 to induce growth of myoma.
C. Genetic Factors:
- Forty percent of leiomyomas show cytogenetic abnormalities, suggesting a genetic role
in the pathogenesis of leiomyomas due to gene mutation

PATHOLOGY OF LEIOMYOMAS

7. Site Of Myomos:
a. Corporeal Leiomyomas: up to 95y" of leiomyomas develop within the myometrium
of the uterine body. They are usually multiple, and of variable size. They are classi-
fied according to their relation to the uterine mucosa (endometrium) into:
Y tnterstitial Myomas (lSM): within the centre of the myometrium
) Subserosal Myomos (SSM): raising the peritoneal covering of the uterus, the serosa, exter-
nally. lt may acquire a pedicle forming a pedunculoted SSM, or burrow within the leaves of
the broad ligament forming a 2ry broad ligamentary myomo (BLM)
Y Submucosol Myomas (SMM): indenting the endometrial lining, and encroaching on the en-
dometrial cavity. lt may acquire a pedicle forming a SMM polyp
b. Cervical Leiomyomas: represe nt < 5%" of uterine myomas, and are usually solitary.
Y From the portio-vaginalis: growing downward to project into the vagina, and may reach the
introitus, and protrude outside the vulva.
Y From the suprovaginol cervix: growing upwards in the true pelvis, in relation to the urinary
bladder, ureters, rectum, and broad ligament.
c. Broad-ligament Myomas (BLM): rare, representing < t%o of leiomyomas.
 Gynaecology l8r

D 1ry BLM: or true BLM, arising from muscle fibres within the broad ligament and not connect-
ed to the uterus

Y 2ry BLM: SSM that grow externally from the side of the uterus to burrow within the anterior
and posterior leaves of the broad ligament, The myoma is thus connected to the uterus ei-
ther directly or through a pedicle.
2. size: variable size, ranging from size of a pea-nut to that of foetal head.
3. Shape: rounded or spherical in shape

4. Number.'corporeal myomas are usually multiple, whereas cervical and BLM are usually single
5. Consistency: firm except of degenerated where it may become soft, cystic, or hard (see later)
6. Cut Section: Leiomyomas are well circumscribed tumours characterized by;

- Whorled appearonce.' due to interlacing bundles of muscle cells with fibrous tissue
- Paler than rest of myometrium: due to poorer vascularity.

- Pseudo-capsule: myomas are surrounded by a false capsule formed of compresseo nor-

mal myometrium (capsule does not belong to the tumour).
- The blood vessels: lie in the capsule and send radial branches towards the centre. This ex-
plains why calcifications occur in the periphery, while degeneration occurs at the centre
(poorer blood supply).

- Fibroid polyp: when a submuous fibroid attains a pedicle and protrudes into the cavity
forming a SMF polyp, the capsule usually ruptures and retracts. The fibroid polyp receives
blood supply from vessels in the pedicle.

Fig 20-2: Cut section in Fig 2O-j: SMF Polyp

hysterectomy specimen

7. Microscopic appeoronce:
- Leiomyomas consist of smooth muscle cells arranged in bundles, intermixed with fibrous
connective tissue.
- Vascular structures are few, and mitosis is rare.
- Celluldr leiomyomas: are tumours with mitotic counts of 5-10 per 10 consecutive high
power field (HPF) that lack cytological atypia. They are not considered malignant.
182 Uterine Leiomvomas

PATHOLOGIC CHANGES IN MYOMAS

1. Atrophy:
- lt is the commonest change occurring inthe menopause.
- lt occurs due to decreased blood supply 2ry to oestrogen deficiency.
- Also occurs during puerperium, and during long term treatment with GN-RH agonists.
- Clinically:atrophy is associated with diminished size which is usually silent and poinless.

2. Hyaline degeneration:
- This is the commonest change in the child beoring period.
- lt mostly occurs in the centre of the tumour due to diminished voscularity.
- Microscopicolly: the whorled appearance is lost, and the tumour tissue is replaced by v
homogenous structureless material staining pink with eosin.
- Clinicolly: tumours become generally sofiin consistency, however if increase in size occurs it -
may render the myoma tense cystic rather than soft. These changes may be associated
with mild to moderate dutt oching poin.
3. Cystic degeneration:
- Cystic changes in myomas are only rarely encountered in clinical practice
- lt occurs due to the absorption of liquefied hyaline materialatthecentreof myoma
- Microscopicolly: The cavity is lined by remnants of unabsorbed hyaline material.
- Clinicolly.'the tumour becomes soft and cystic, with mild dullaching pain.
4. Red degeneration: (Necro-biosis):

- lt is the commonest change during pregnancy, possibly due to;

) The tumour may outgrow its blood supply, or
) Kinking of the blood vessels due to rotation resulting from rapid uterine growth,or
) Increased tendency to thrombosis associated with pregnancy.
- lt reflects a state of incomplete necrosis from which the tumour is capable of recovery.
- Thrombosis of capsular vessels results in ischemio and release of a lipoid toxin,leading -
to intravascular hoemolysis and diffusion of blood pigments giving the tumour a red col-
our.
- Clinicolly; myomas become enlarged, tender, with ocute pelvic poin and mild pyrexia.
- Management: is essentially conservative by rest and analgesics as NSA|Ds.
5. Fatty degeneration: Deposition of fat within the muscle cells. lt is a precursor of calcification.

5. Calcification:
- Calcification is commonin long standing myomas and in menopause,
- lt occurs due to deposition of calcium phosphate and carbonate along the blood vessels
- lt is either peripheral giving an "egg shell" or diffuse giving a "womb stone" appearance
on plain X-ray or U.S.
7. Necrosisi ,
- Commonlyoccursat the tip of a SMF polyp due to poor blood supply.
- lt also occurs followingtorsion of pedunculated SSM.
8. Infection i J
- Occurs at necrosed tip of SMF polyp projecting into the uterine cavity, cervix or vagina.
- May occur during puerperium, or as spread from nearby infected organ as appendicitis.
 Gynaecology 183

C OMPLICATIONS OF LEIOMYOMAS
v
A' Torsion of o pedunculoted S S M , or rarely torsion of the whole uterus.
v B' Rupture of o surface vein of SSM leading to intraperitoneal heamorrhage.
C. lncorceration or impoction of a SSM in the pelvis especially during pregnancy.
\,
MALTGNANTTRANSFORMATTON rNTO LETOMYOSARCOMA:
\-,
t lncidence: Leiomyosarcoma is very rare occurring in only 0.2% -O.S% of myomas.
' '""1':::f:iff:,r'
: :::::,:";,wth without evidence or degeneration
- Tumours that first appear, or increase in size, in the menopause
- Tumours that present with postmenopausal bleeding (pMB)

:v . ,",,"',iioffi;^:::ili;:il:,ilT#:T'1,";:ilJ,sh
haemorrhage and capsular invasion leading
in co,our, rriab,e, with areas or
to difficult enucleation (non-encapsulated).
v t Microscopically: diagnosis is based on a mitotic count (1O mitotic figures per 10
HPF), with frequent ceilurar atypia and coagurative necrosis.
\_r'
EFFEcrs oF LEroMyoMAs on the uterus and pelvic organs
\_-
- Uterine enlorgemenf which may be symmetrical or asymmetrical according to
its site.
v - Distortion of the endometriol cavity;in cases of SMM and SMF polyp.
v -Displacement in uterine position; in large myomas (fundal, BLM and cervical myomas).

\- - lncreased vasculority ond venous congestion; occur with multiple and large myomas.
- Pressure on urinary btadder; leading to frequency of micturition.
\- - overstretching on urethro; by large cervical myoma may cause retention of urine.
\-'. - Compression on the ureters; by large cervical and BLMs may cause ureteric, back-
pressure with associated hydroureter and hydronephrosis.

CLINICAL PICTURE
'v I Age: Leiomyomas are more prevalent among age groups ranging 35-45 years
I Parity: more prevalent among infertile patients, nulliparous and low parity population
v
I NO SYMPToMS:
\- of
- The majority solitory and small fibroids ore asymptomatic, especially SSM
\v, and lSM.
- The nearer the fibroid to the endometrial cavity, the more will be the chances of
being symptomatic, even if they are relatively small (as in small SMM and SMF pol-
vp).
r84 Uterine Leiomyomos

SYMPTOMS OF LEIOMYOMAS

One or more of the following symptoms may be present in multiple o r large fibroids;

1) Abnormal Uterine Bleeding (AUB)

a. Menorrhogio: this is the commonest presentation for myomas in almost 30% of cases. lt
occurs mostly with S M M a n d large multiple lSM. Excessive bleeding may be due to;
F lncreased surface area of the endometrium.
) Mechanical interference with uterine contraction.
F Associated EH, and/or hormonal imbalance due to chronic anovulation.
F Increased myometrial vascularity; including venous congestion and engorgement.
b. Metrorrhagia: may be due to
) Sloughing in the tip of a SMF polyp
) Associated disturbed pregnancy
) Sarcomatous changes in a myoma or coincidental uterine carcinoma.

Fig 20-4: Engorged tip of SMF polyp Fig 20-5: Different sites of uterine myomas (concelled)

2) PELVIC PA|N

Fibroids are painless unless complicated, types of pain include:

- Dull aching pain: as hyaline degeneration and infection of SMF polyp.

- Acute obdominal pain: in red degeneration, and torsion of a pedunculated SSM

- Colicky pelvic pain: as with extrusion of a SMF polyp through the cervix
- Dysmenorrhoeo; congestive or spasmodic dysmenorrhoea: as with SMF and SMF polyp.
- Pain due to common associoted conditions: as endometriosis.

3)PRESSURE SYMPTOMS

- Frequency of micturition ond dysurio due to pressure on the urinary bladder

- Retention of urine due to stretching and pressure on the urethra by large cervical myo-
ma

- Referred back ond thigh pain, 2ry to pressure of myomas on pelvic nerves.
 Gynaecology 185

4)TNFERTtL|TY
Uterine leiomyomata are an associated cause for infertility in only s-t}% of cases, and are
reported as a sole cause for infertility in < 3% of cases. Mechanisms that may cause infertil-
ity include:
- Interference with implantation due to distortion of uterine cavity; as in SMM.
- Tubal obstruction may be caused by multiple ISM and/or bilateral cornual fibroids.
- Interference with sperm motility via the cervical canal: as in large cervicar myomas.
5) OTHER SYMPTOMS
. Pregnancy Complications
Recurrent pregnancy loss (RPL), preterm labour (PTL), dysfunctional labour, malpresenta-
tions, obstructed labour and post partum haemorrhage.
t Leucorrhoeo
Due to pelvic congestion, or infected fibroid polyp (associated foul discharge)
. Progressive Abdominal Enlargement
Huge myomas will arise in the pelvis and rise gradually above the pelvic brim, when the
patient may present w it h progressive abdominal enlargement, with or without pressure
symproms.

SIGNS ON CLINICAL EXAMINATION

No specific signs on general examination except for those of pallor if anemia is present

A) ABDOMTNAL EXAMTNATTON:
- Large myomas will be felt abdominally if the uterus enlarges above the pelvic brim, as a
central firm mass, with bossy irregular contour, that is usually non tender, of limited mobility,
and dull on percussion.
- The upper border is felt by the ulnar border of the examiner's left hand. lt mav sometimes
reach up to the umbilicus, or higher.
- The lower border is not usually felt by the examiner's other hand as the mass is pelvi-
abdominal.
B) LOCAL EXAMTNATTON:
t PV exomination; may detect cervical myomas and SMF polyp protruding through the cervix
t Bimonuol exdmination'will detect uterine enlargement, which may be firm with bossy con-
tour, non tender, and with restricted mobility.
' Speculum examination; may visualize cervical myomas and SMF polyp protruding through
the cervix.

DTFFERENTTAL D|AGNOSIS (DD):

- Lorge fibroid must be differentiated from other causes of pelviabdominal swellings.
- SMM or ISM from other causes of symmetrical enlargement of the uterus.
- Calcified myomo; from other causes of a calcified p e lv ic shadow on plain X-ray.
- SMF polyp; from other causes of a mass protruding from the cervix uteri.
r86 Uterine Leiomyomas

SPECIAL INVESTIGATIONS
1. Ultrasonography (U.S.) :
U.S. is considered Ihe gold standard in the diagnosis of uterine leiomyomata.
F Assessment of the site, size, number, and relation of myomas to the endometrial cavity.
F lt is also valuable in detecting adnexal pathology and excluding pregnancy complications.
F Saline infusion sonography (SlS), is sensitive in diagnosis of SMM and SMF polyps.

2. MRI and CT scan:

Both MRI and CT scan are diagnostic but are not superiorto US, which is cheaper, easier, and
more readily available.
3. Hysterosal pingography (HSG) :
HSG is valuable in diagnosis of SMM that appears as a filling defect. lt is also important for
testing tubal patency in patients complainin g of infertility.
4. Hysteroscopy:
Hysteroscopy is considered the gold stondard in diagnosis of small endometriol polyps,
SMF polyps, and SMM.
5. Laparoscopy:
Laparoscopy is a valuable tool in differential diagnosis of complex odnexal mosses.

MANAGEMENT OF UTERINE LEIOMYOMAS

l-. Conservative Approach: regular follow up without treatment
2. Medical treatment of associated symptoms: to control pain and bleeding
3. Hormonal treatment: to control amount of bleeding and size of leiomyomas

4, Minimally invasive procedures in selected cases:to avoid surgical approach

5, Definitive Surgical treatment:

a. Myomectomy: via laparotomy, laparoscopy, or hysteroscopy

b. Hysterectomy: via laparotomy, laparoscopy, or vaginal route

1. CONSERVATIVE APPROACH:

- Periodic follow up: every 6 - L2 months is appropriate for asymptomatic small leiomyomas

- During pregnancy: myomata are managed conservatively until delivery as a rule.

- DuringCS.'someleiomyomascanberemovedduringCSespeciallythoseatthesiteoftheuter-
ine incision

- Rarely torsion of a moderate size pedunculated subserous leiomyoma during pregnancy may
cause acute abdomen necessitating urgent laparotomy and myomectomy, regardless the ges-
tational age.
r N.B.: Conservative approach is abandoned whenever a leiomyoma reaches a large size or re-
sults in severe uncontrollable symptoms as severe pain, pressure symptoms or severe bleed-
Ing.
 Gynaecology t87

2. MEDICAL TREATMENT:
To control moderate bleeding and pain through oral or lM drugs as;

a' Nonsteroidal Anti-inflommotory drugs (NSAlDs/; these drugs act by inhibiting pGL syn-
thesis and restoration of PGL / Prostacyclin ratio. They are used to minimize menstrual
pain and bleeding.

b' Haemostatic drugs as Tranexamic acid: that act as fibrinolytic agents to controlAUB.
c. Venotonic drugs as Daflon 500: that act by improving vascular tone and decrease pelvic
venous congestion.

N.B.: Medical treatment has no place in cases with severe AUB that affects the patient,s
general condition and causes severe anaemia that requires parenteral iron therapy
or blood
transfusion.
3. HORMONAL TREATMENT:
To minimize menstrual blood flow and regulate withdrawal bleeding or induce 2ry amenor-
rhoea
a, Gestagens.' as oral norethisterone acetate 5 mg 2-3 times daily for 2 weeks throughout
days !O-24 of the cycle to induce regular cycles every 28 days with minimal pain and
bleeding (see mode of action and doses in AUB, DUB and endometrialhyperplasia).
b. GnRH Agonists: Long acting GnRH agonists (e.g. Leuprolide acetate 3.75 mg lM on
monthly intervals for 3-6 months), results in suppression of pituitary gonadotropins in-
ducing a state of severe oestrogen deficiency (medical menopause), leading to 2ry amen-
orrhoea, with reduction in the size and vascularity of leiomyomas. Hormonal treatment
is only temporary as it is expensive, induces unpleasant menopausal like symptoms,
and
finally leiomyomas return to pretreatment size within 6 months of stopping GnRH thera-
py. GnRH therapy may help preparing the patient for further more definitive treatment.

N.B.: Medical and hormonal treatment are commonly used in combination with each other.

4. MINIMALLY INVASIVE PROCEDURES

Several modalities have emerged in dealing with intermediate size symptomatizing leiomyo-
mas in an attempt to avoid a definitive surgical intervention as myomectomy and hysterectomy.
lmproved results of treatment are achieved with more use of such modern techniques that require
advanced equipment, proper training and above all proper selection of cases suitable for such
less
invasive modalities.

A. Uterine Artery Embolization (UAE)

B. Laparoscopic Myolysis
C. MRI-guided High llequencyUltrasound (HtFU)

5. DEFINITIVE SURGICAL TREATMENT

Surgical removal of leiomyomas is the only definitive treatment for these benign tumours.
) Myomectomy: removalof leiomyomas with preservation of the uterus
) Hysterectomy: removalof the uterus including leiomyomas
188 Uterine Leiomyomos

1. Uterine Artery Embolization (UAE)

t The procedure: The uterine artery or its branches are occluded by injection of gel foam
pledgets, through a catheter introduced via the femoral artery, thus depriving the tumour
from its m a in feeding vessels le a d in g to shrinkage in size, atrophy and necrosis of leiomyo-
mas.
t Advontages; The procedure is relatively safe. lt results in 60% reduction in size of myomas,
with controlof menorrhagia in up to 90% of cases within 8-L2 weeks from performing the pro-
cedure.
t Disodvontages: The main disadvantage is significant postoperative pain (like red degenera-
tion),the need for skilfultrained radiologyteam, and limitations related to the size and num-
ber of myomata that could be managed successfully by this procedure. UAE may not be also
suitable for patients seeking future fertility.

C.atl}G(".

FfffJ."it

Fig 20-6: Uterine Artery Embolization

2. Laparoscopic Myolysis
t The procedure: Laparoscopic myolysis using laser or coagulation current, or cryo-
myolysis using a -180 C probe.
t Advantages: persistent decrease in size of myomas
t Disadvantages: effective only in small and SSM which are mostly non symptomatizing. More
studies are needed to substantiate its role in management of leiomyomas, patient selection
and long term adverse effects.

3. MR!-guided High ftequency Ultrasound (HIFU)

t Theprocedure:Thisisa relativelynewtreatmentoptionthatusesultrasoundgeneratedheat
to cause cell death. Fibroids are localized by MRI and heat from a phased array ultrasound
transducer is directed towards the myoma to produce protein denaturation.
t Advantoges.'decrease in size and improvement in symptoms may occur in up to 60% of cas-
es.
 Gynaecology 189

INDICATIONS OF SURGICAL REMOVAL OF LEIOMYOMAS

a. Large size leiomyomas > 14 weeks pregnancy forming a pelviabdominal mass
b. Leiomyomas causing severe AUB affecting the patient's general condition
c. Leiomyomas causing recurrent abortion, infertility, or interfering with a planned lCSl procedure
d. Any growth in size of a leiomyoma during menopause (suspicious of malignancy)
e. Rapid growth of leiomyomas or rapid recurrence after myomectomy (suspicious of malignancy)
f. Submucus fibroid polyp protruding from the cervix (Lausing excessive bleeding and foul odor
discharge)
g' Cervical and broad ligament leiomyomas of intermediate size that may cause ureteric compres-
sion

MYOMECTOMY
Myomectomy is performed whenever surgical removal of leiomyomas is mandatory while the
patient is young in age, desirous for further fertility, or seeking preservation of her menstrual
cycre.

a. Abdominal myomectomy: the standard procedure performed via laparotomy to remove large
size myomata, especially if multiple in number or recurrent.
b. Laparoscopic myomectomy: for removal of intermediate size leiomyomas of limited number
(< s)

c. Hysteroscopic myomectomy or polypectomy: for removal of SMF polyp or solitary small sub-
mucus leiomyomas < 5 cm in size totally projecting in the endometrial cavity.
r For details on indications, contraindications, technique and complications of myomectomy see
gynaecologic operations and procedures chapter 32

HTSTERECTOMY
Hysterectomy is performed whenever surgical removal of leiomyomas is mandatory in presence
of multiple or large tumours are present in an elderly patient that has completed her family and
not desirous for further childbearing, or whenever malignancy is suspected or patient is meno-
pa usal.
a. Abdominal hysterectomy: the standard procedure performed via laparotomy, suitable

b. Vaginal hysterectomy: suitable in cases with intermediate size leiomvomas with associ-
ated uterine and pelvic organ prolapse (pOp)
c. Laparoscopic Hysterectomy: is gaining increased popularity in cases with benign inter-
mediate size tumours, whenever proper equipment and training skills are available.
I N.B.: for details on indications, contraindications, techniques, and complications of hys-
terctomy, see gynaecologic procedures and operations chapter 31.
190 Uterine Leiomvomos

KEY POINTS IN LEIOMYOMATA

- Fibroids qre the commonest benign tumours of the femole genital tract, they ore usually multiple,
ond run a very grodual progressive courset being clinicolly detectable in olmost 20% of women.
- The aetiology of leiomyomoto is unknown. However its growth is oestrogen dependent.
- Myomoto qre liable to 2ry pathological changes thot may offect their clinicol presentotion including;
hyaline, cystic, fatty, ond red degeneration. ln oddition to colcification, atrophy, necrosis and molig-
nant changes.
- Very small myomqs ore not clinicolly detectable, and ore usually non-symptomotizing, being inci-
dentally discovered during routine pelvic U.S. scan. They usually require no treotment.
- Lorger myomqs ore usuolly symptomotic, qnd qre diagnosed clinicolly during a bimonuol pelvic ex-
amination ond confirmed by pelvic ultrosonography.
- Large symptomatic fibroids ore surgicolly treoted by hysterectomy or myomectomy occording to the
patient's age ond pority, her desire for future fertility, and according to the size qnd number of myo-
mata and their risk for recurrence or molignant transformation.
- Alternqtive endoscopic techniques for hysterectomy ond myomectomy (vio laporoscopy ond hyster-
oscopy), myolysis, and selective uterine qrtery embolizotion, ore generolly reserved to corefully se-
lected cases, whenever the skills and experience with such procedures qre svailable.
- Some special types of myomata os cervical and broad ligomentary myomotq, ond uterine polypL
are qssociated with somewhat different clinical presentotion and may require further investigotions
and different types of treotment
 Endometriosis
Adenomyosis

ENDOMETRIOSIS
OVERVIEW
Endometriosis is the presence of endometrialglands and stroma outside the endome-
trial cavity. lt is a chronic disease that affects women of different ethnic and social groups.
lt is estimated to be present in almost LO%in women in their childbearing period, in around
20%of women with chronic pelvic pain, and in almost 30%of women with infertility.
Like the true endometrium, it responds to cyclic hormonal changes and bleeds at menstrua-
tion producing pelvic pain, and in some cases pelvic adhesions causing subfertility.
The severity of symptoms does not necessarily correlate with the extent of the endometrio-
sis. Advanced lesions may be sometimes silent while mild disease may cause significant pain.
Laparoscopy is the gold standard for diagnosis, and is the only method for staging the dis-
ease in order to plan treatment.
Management of endometriosis is individualized for each case based on the extent of the
disease, the severity of symptoms, and the need for preservation of fertility.
Management includes conservative approach, medical and hormonal therapy, and finally
surgical interventions which may be either conservative or extirpative.

Umbilicus
5i id colon'
Appendir
Ovary
Round
Eroad
ligarnent
tigdm€nt
Ul+ro-3ocral Bladder
ligamentg
Cervir
Rectu|n

Cul-d+sac

Recto-Yaginal
seplus

E Comrnon sites
Uncorlnon iilos

Fig 21-1: Sites of Pelvic Endometriosis

191
192 Endometriosis And Adenomyosis

RISK FACTORS:

SITES OF ENDOMETRIOSIS
a. Pelvic (Common sites): the ovaries, pelvic peritoneum, fallopian tubes, and uterosacral liga-
ments
b. Extro pelvic (Rare sites): anywhere in the body as far as the lungs, brain, breast, and umbilicus.

THEORIES FOR AETIOLOGY AND PATHOGENESIS

Several theories have been proposed about the etiology of endometriosis, but no one theory
can explain its occurrence in multiple different sites.
L. Sampson's theory of Retrogrode Menstruofion: suggests that viable endometrial tissue is
transported through the fallopian tubes during menstruation, resulting in intra-abdominal
pelvic implants. This theory exploins only pelvic endometriosis
2. Halban's theory ol Lymphatic Spread: proposes that endometrial tissue is transported via
fymphatic system to various intraperitoneal sites, where it grows ectopically. lt does not ex-
plain distanf sites of endometriosis as the diaphragm, breast, lungs and brain.
3. Meyer's theory ol Coelomic Metdpldsio.' proposes that multipotential cells in peritoneal tis-
sue undergo metaplasia transformation into functional endometrial tissue.
4. Theory ol Altered lmmune Response: women with endometriosis may have an altered im-
mune response that makes them less likely to recognize an attack of ectopic endometrial
implants, leading to reduction in immunologic clearance of viable endometrial cells from the
pelvic cavity (reduced natural killer cells and macrophage activity). '-
PATHOLOGY
A. Pelvic Endometriosis: appears as multiple small dark red or brown small cystic lesions,
containing altered blood, and lined by endometrial tissue. Theygive a naked eye appear
ance of burned match-head spots.
B. Ovarian Endometriosis: is present in one of two forms
t. Superlicial Lesions:
- Tiny dark red or brown lesions with adhesion formation (powder burns)
- Considered as part of pelvic endometriosis
2. Deep lesions: (ovarian endoemtriomos or chocolate cysts):
- One or more cysts seated deep within ovarian tissue.
- They are usually of moderate size, filled with dark altered blood and surround-
ed by adhesions.
Cysts are lined by endometrial tissue (glands and stroma)
Histologic examination reveals haemosiderin laden cells and endometrial stro-
ma, that characterize the lesions as endometriosis.
r N.B. Free endometriotic implants; grow on surface epithelium supported by endome-
--
trial stroma with or without glands, and are usually sensitive to hormonal stimulation
and suppression.
 Gynaecology 193

v
cLrNrcAL PrcruRE
v Many cases may remain asymptomatic for a long period of time, until accidentally discov-
ered during laparoscopy or laparotomy performed for different indications not related to endome-
v triosis.

SYMPTOMS IN ENDOMETRIOSIS
Symptoms when present are only suggestive as they are not specific to endometriosis.
v Symptoms do not necessarily correlate with the severity or extent of the disease;
) Marked pelvic disease may be silent
) Small endometriotic pelvic implants may produce significant symptoms.
) The same applies for ovarian endometriomas.
The 2 major clinical presentations of endometriosis are pain and/or infertility

A) PAIN:
-v I Dysmenorrhoea:
- 2ry dysmenorrhoea is one of the commonest clinical presentations.
Pain starts few years after a period of normal non painful menstrual cycles.
It starts during menstruation, and increases rapidly due to distension of ectopic endo-
metrial glands with blood without having an exit.
\v Pain decreases gradually towards the end of the cycle due to absorption of blood within
the endometriotic implants.
v r Chronic pelvic Pain:
- Diffuse or localized chronic pelvic pain, > 6 months, is strongly suggestive of endo-
does not often correlate with the severity of the disease.
,
v "r;;::ff;is.although
Deep dyspareunia may be secondary to endometriotic implants of the uterosacral
ligaments, pouch of Douglas, ovarian endometriomas, or due to associated fixed RVF
uterus.
Mechonism ol pain in Endometriosis
) Distension of ectopic endometrial glands by active bleeding within a closed space.
\r F Release of inflammatory mediators (PGLs and Cytokines) from superficial lesions.
F lrritation of pelvic nerves, or involvement by adhesions in deep lesions.
!
B) tNFERTTLITY:
v Endometriosis will be discovered at laparoscopy in up to 30% of infertile females, however in
many cases it may be an association rather than a cause.
v r Moderate to severe endometriosis; may compromise fenility through creating pelvic adhe-
v sions, which may be peritubal or periovarian, impairing ovum pick up.
I Mild endometriosis; may affect fertility through inducing luteal phase defect, and in-
\v creased tubal phagocytic macrophage activity on the sperms

v. c) OTHER SYMPTOMS:
r GIT symptoms: pain during defecation, intestinal cramps, and rarely cyclic rectal bleeding
v r Urinary symptoms: dysuria, frequency, and rarely cyclic haematuria
I Distant metastases: symptoms according to organ involved (brain, lungs, and umbilicus)
194 E nd o metriosi s An d Ad e n o m yos i s

SIGNS IN ENDOMETRIOSIS
r General Examination: no general specific signs for endometriosis
r PV and Bimanual Examination: only in extensive endometriosis
- The uterus may be fixed in AVF or RVF position
- Tender palpable nodules on uterosacral ligaments and pouch of Douglas
- Endometriomas (chocolate cysts); may be palpated as tender tense cystic fixed ad-
nexal masses in non obese patients

SPECIAL INVESTIGATIONS
A) Laparoscopy:
Diagnostic Laparoscopy is the gold standard in diagnosis and staging of endometriosis.
Laparoscopy is indicated in cases of chronic pelvic pain, infertility, and unresolved adnexal
masses.
Laparoscopy allows direct visualization of endometriotic implants, and performing biop-
sies for confirming visual diagnosis.

(powder burn lesions) on peritonealsurfaces, surrounded by adhesions.

crescences.

Fig 27-2: Pelvic endometriosis by Loporoscopy

B) Ultrasonography and MRI

Small endometriotic lesions are not visualized with pelvic US
MRI may detect larger implants and deep seated ones
Both US and MRI are sensitive in diagnosis of endometriomas even if small in size

c) cA-12s
CA-125 is a cell surface antigen found on coelomic epithelium (Normal 5-35 u/ml)
It shows slight to moderate increase in levels in many cases of endometriosis, but is not a
specific marker
It is a useful marker for response to treatment in cases with initially elevated levels

of Endometriosis
Classifi cation
During laparoscopy the extent of classic lesions, ovarian involvement, and presence of
adhesive disease is classified and graded according to the American Society of Reproductive
Medicine (ASRM).
 Gynaecology 195

v
Differential Diagnosis
'J a. Causes of chronic pelvic pain; PlD, lrritable bowel syndrome, ureteric pain, etc...
b. Endometriomas from other causes of adnexal masses: haemorrhagic ovarian cyst, dermoid
cyst, tubo-ovarian complex, pelvic malignancy
v Course of the Disease
r The disease is usually progressive in 30-60% of cases.
v r Prolonged periods of amenorrhea are associated with remarkable improvement of
symptoms.
I During pregnancy, lesions tend to enlarge during the first trimester then regress.
I Recurrence of endometriosis after surgical excision will recur in up to 20% of cases. Recur-
rence is less after extirpative surgery, and also with postoperative periods of amenorrhoea

tv MANAGEMENT OF ENDOMETRIOSIS
Management of endometriosis is planned according to several factors including; age of the
v patient, severity of symptoms, future reproductive plans, and extent of the disease at laoaros-
copy.
EXPECTANT MANAGEMENT:
Expectant management is appropriate for young patients, with minimal symptoms and minimal
- signs. The goal of expectant management is;

V MEDICALTREATMENT:
Medical treatment is indicated in cases with marked symptoms and minimal signs. Treatment is
v based on the observation that symptoms of endometriosis improve during pregnancy and meno-
pa use.
v 1. Combined OralContraceptive pills (COCs):
- Aim: induces amenorrhoea with a pseudo pregnancv state
- Mechonism.' amenorrhoea, pseudo-decidualization, and atrophy of ectopic endome-
trium.

: - as weigh, gain, b,oa,ing, headache,

etc..
'v "iii;ilxi,,;::i:::?:::"#H:#:il::j$
2. Synthetic progesterone (Gestagens):
- Aim: induces amenorrhoea with a pseudo pregnancv state
- Mechanism: pseudo-decidualization, followed by atrophy of ectopic endometrium
- Doses: continuous gestagen treatment for a 6-9 months course
FNor- ethisterone ocetote; 5.0 mg orally, 2_3 times daily.
v D Dienogest: 2.0 mg oral tablets, once daily, effectively controls pain.
YDepot Medroxy Progesterone ocetote (DMPA):150 mg lM injections, every 3 months
- Disodvontoges; side effects as bloating, weight gain, headaches, and breakthrough
bleeding.
v 3. Long acting Gn RH agonists
- Aim: induces amenorrhoea with a pseudo menopause state.
- Mechonisrn.' menopause like hyopo-oestrogenic state, with atrophy of ectopic endome-
.- trium' lt starts with an initial FSH stimulation, followed by down regulation of receptors
with suppression of FSH and LH, and consequently decreased oestrogen levels.
- Doses: Depot forms given lM monthly or every 3 months for 6-9 months
t96 Endo metriosi s And Ad eno myos i s

Disadvantoges: hot flushes, vaginal dryness, and accelerated bone loss

-
- Adverse effects may be minimized by the use of low dose oestrogen (add back therapy)
N.B.: Danazol a testosterone derivative that produces high androgen, low oestrogen environment
and 2ry amenorrhoea is no more in use due to its marked irreversible androgenic side effects on
prolonged use.
c) suRGlcAL TREATMENT OF ENDOMETRIOSIS:
Surgery is the best choice in cases with pelvic adhesions and / or larger endometriomas.
1.. CONSERVATIVE SURGERY:

) Excision, fulguration, or laser ablation of all visible lesions

) Lysis of pelvic peritubal and periovarian adhesions.
) Excision of sizable endometriomas (> 4.0 cm)
Conservative surgery can be achieved via either;
a. Loparoscopy: is the gold standard for conservative surgical approach. lt is suitable for the
infertile patients aiming to restore normal anatomy with creating minimal postopera-
tive adhesions.
b. Laparotomy: is reserved for the severe cases with extensive adhesions or large endo-
metriomas.
r N.B.: Preoperative hormonal treatment by a 3-months course of GnRH may reduce vascu-
larity and nodular size, facilitating surgery and improving the prognosis.
2. EXTIRPATIVE SURGERY:
TAH BSO is the procedure usually performed in elderly patients, with extensive dis-
&
ease, and no desire for fertility. lt has limited place and limited indications.
Oestrogen replacement therapy (ERT) is recommended in the relatively young patient
to relieve associated menopausal symptoms.
ERT carries only a small risk of inciting growth of small residual endometriosis while
if the ovaries were preserved recurrence rate will be high with a 15-40% chance to
reoperate.
. Summary for Treatment Options for a case of Endometriosis:
) Minimal lesion + desire for fertility: conservative surgery + assisted reproduction -

) Endometrioma > 4.0 cm: Excision and laser ablation via laparoscopy, or laparotomy
) Extensive lesion + no desire for fertility+ elderly: TAH-BSO + excision and ablation of im-
pla nts

MANAGEMENT OF Endometriosis Associated Infertility

a. Conservotive loporoscopic surgery:
- Diagnosis and staging of endometriosis

- Ablation of endometriotic implants, and lysis of adhesions

- Excision of larger sized endometriomas > 4.0 cm.

- Evaluation of tubal and peritoneal factors of infertility

b. Suppression of menses; using GnRH agonists for 6 months postoperative, OR
c. Active management ol infertility: via;
- Controlled ovarian stimulation
- Assisted reproductive techniques (ART) including; lUl and lCSl procedures.
 Gynaecology 197

ADENOMYOSIS
Adenomyosis is the presence of endometrial glands and stroma deep within the myome-
trium. lt has been formerly considered as internal endometriosis however it is now looked upon
as a separate pathological entity, affecting primarily multiparous women in their late thirties and
early forties.

AETIOLOGY

The aetiology of adenomyosis is unknown

- Theories postulate that it may be due to growth of endometrial glands deeply between
muscle fibers of the myometrium in presence of abundant oestrogen environment.
Adenomyosis is associated with smooth muscle hypertrophy around the ectopic glands.

PATHOLOGY

A. Diffuse type: the uterus is symmetrically enlarged, globular in shape, with a firm con-
sistency reflecting myometrial thickening generally affecting the fundus but may also
involve either or both uterine walls.
B. Localized type: adenomyosis may be localized at an area very similar to uterine leio-
myomata, which may coexist in the same uterus (adenomyoma). Unlike the myoma lo-
calized adenomyosis is not encapsulated
t The cut surface may have a whorl-like or granular trabecular pattern with small
yellow or brown cystic spaces containing fluid or blood.

CLINICAL PICTURE

A) SYMPTOMS

Severely increasing 2ry dysmenorrhoea and /or Menorrhagia are the chief symptoms.
I Spasmodic dysmenorrhoea: is due to contractions provoked by premenstrual swelling
and menstrual bleeding
I Menorrhagia is due to increased uterine size and endometrial surface
area

B) SIGNS on BIMANUAL EXAMINATION

I Symmetrically enlarged uterus which is sometimes tender especially in the premen-

strual period (Halban's sign).
c) sPEctAt tNVEsTtcATtoNS
I Ultrasonography (TAS/TVS/3DUS): will reveal thickened myometrium, sometimes
associated with localized areas of different echogenicity somewhat similar to leiomyo-
mas.
r Magnetic resonance imaging (MRl); gives excellent images of the myometrium
with areas of adenomyosis and is being regarded as the investigationof choice.
198 Endometriosi s And Ad e no myos is

TREATMENT OPTIONS:
Dysmenorrhoec, can be managed by NSA/D (see endometriosis).
Menorrhagio can be managed by

AUB)

- Hysterectomy is the treatment of choice in cases of severe perimenopausal

bleeding not responding to medical or hormonal treatment. Hysterectomy is also
the only way to establish the diagnosis with certainty.

Key points in Endometriosis

- Endometriosis is present in olmost 10 % of women in their child bearing period, but is

more prevalent in cases of severe dysmenorrhoeo, chronic pelvic pain ond infertility.

- Severe forms moy result in odhesive disease forming peritubol adhesions or moy offect
the ovory resulting in endometriomas

- Clinicol exominotion is usually inconclusive however in severe cqses it may reveol on adnexol
swelling, o fixed RVF uterus ond or tender nodules in pouch of Douglas.
Laporoscopy is the gold standard for diagnosis ond stoging of endometriosis
Elevoted CA-L25 moy act qs o morker for follow up rather thon for primary diognosis

- Manogement is occording to severity of the diseose ond its effect on fertility. lt may be
either; expectont, medical, surgical, or combined.

- Medical therapy does not dissolve odhesions or eliminote endometriomos, it is therefore

not suitable for coses presenting with infertility

- Laparoscopic adhesiolysis, fulgurotion of endometriol implants, and excision of endometrio-

maq is the treatment of choice for infertile coses.
Adjuvant postoperotive medical theropy moy by used including ovarion stimulation to os-
sist ovulation in mild coses, or ovarian suppression to induce periods of amenorrheo in
severe cases, leading to olleviation of symptoms ond otrophy of ectopic implonts.
 Cervical lntroepitheliol Neoplasia (CtN)
Vaginal lntraepitheliol Neoplosio (VAIN)
Vulvor lntroepithelial Neoplosia (VlN)

cERVtCAL tNTRAEptTHEL|AL NEOpLAStA (CtN)

BENIGN SQUAMOUS METAPLASIA:
Both the squamous cells (covering the ectocervix) and the columnar cells (lining the endocer-
vix) come from immature reserve cells present at the squamo-columnar junction SCJ (the junction
between the ectocervical squamous epithelium and endocervical glandular epithelium).
The immature reserve cells at the SCJ continuously generate both squamous cells and colum-
nar cells by metaplasia throughout the female's life.
The SCJ changes its place by age, moving slowly continuously towards the internal cervical os;
Y During childhood; it is at the outer edge of the external os
Y During the reproductive life; it moves slightly inwards few millimeters within the external os
) In postmenopausal women; it moves further inwards to be placed inside the cervical canal.
The Transformation Zone (TZ): is the area where squamous metaplasia occurs. lt lies be-
tween original SCJ and the new SCJ.

OiginrlSCJ

Fig 22-1: Transformotion zone TZ

ABNORMAT METAPLASIA AND CIN

Continuous exposure of reserve cells at the TZ to carcinogenic factors, as viral DNA may lead
to the production of atypical cells (through atypical metaplasia) or dysplasia (disordered growth)
which might progress by time to preinvasive or invasive cervical cancer.
r Cervical Intraepithelial Neoplasia (ClN): describes the presence of atypical cells inside the
cervical epithelium without invasion of the basement membrane.

r99
200 Screening For Premalignant Lesions Female Lower Genitol Troct

RISK FACTORS FOR CIN:

l.Abnormal sexual activity:

- Early age at first sexual intercourse (the transformation zone being near to external os).

- Multiple sexual partners (subject cervical epithelium to variable foreign proteins).

2.Viral sexually transmitted diseases:
A. Human Papilloma Virus (HPV):
High-risk HPV types include !6, 18, 3L, 33, 35, 45, & 58, and account for nearly 95o/o of
precancerous lesions worldwide.
In almost 7O-8O% of women exposed to genital HPV, the infection is transient, and
cleared by the immune system in L-2 years.
lf the virus remains present for several years, in patients with low immunity and repeat-
ed exposures, cervical intraepithelial neoplasia (ClN) may develop.
B. Herpes Simplex Virus type ll (HSV-2):
- HSV-2 DNA and messenger RNA sequences have been found in cervical cancer cells.
They may also increase the likelihood of HPV infection'
3. Low socioeconomic standards and poor hygiene (chronic irritation).
4. Cigarette smoking. (By-products in cigarettes may concentrate in cervical epithelium,
with depletion of Langerhan's cells that assist in cell mediated immunity).
5. lmmuno-suppression (HlV infection, or immunosuppressant drugs used in organ transplant).
6. Genetic predisposition: some cases, which develop cervical cancers, have never been exposed
to HPV, HSV ll, or other risk factors. Such cases are genetically determined.

PATHOLOGY:
The term CIN describes a spectrum of intraepithelial atypical (dysplastic) changes occurring
within the squamous epithelium of the ectocervix that carry a premalignant potential. These chang-
es include:
1-. Cellular atypia: characterized by production of abnormal cells with:
a. Large nucleus with increased nucleo-cytoplasmic ratio.
b. Hyperchromatism, increased mitotic figures, and abnormal mitosis.
2. Architectural atypio: means abnormal cellular relations and arrangement characterized by:
a. Increased cellular proliferation and increased amount of immature cells.
b. Disparity in the size and shape of cells (pleomorphism), Loss of polarity and loss of stratifica-
tion.
 Gynaecology 201

Histological Grading of clN (according to its premalignant potential);

t ClNT: dysplasticcellsoccupythebasal onethird (7/3lofthethicknessof thesquamousepi-
thelium. Cells of the upper 2/3 show normal stratification and maturation.
t CIN ll: dysplastic cells occupy one half (l/21 of the thickness of squamous epithelium. Cells of
the upper 1/2 show normal stratification and maturation.
.\-/ t CIN lll: dysplastic cells occupy the full thickness of the squamous epithelium, without inva-
sion of the basement membrane. CIN lll & in situ carcinoma are grouped in one category.

Basement
membrane
HPV effect

Fig 22-2: Histologic grading of CtN

Natural History of CIN

lf untreated, CIN-1 may undergo spontaneous regression, remain stationary, or will slowly
progress (throughout a period of 7-10 years) through grades ll, lll, preinvasive cancer, or finally in-
vasive cervical cancer.

DIAGNOSIS OF CIN
- CIN usually affects women in younger age groups (25-45 years).
- lt is usually asymptomatic.
- Diagnosed through routine screening of high risk women by the Pap smear test (see later).
- Suspicious Pap smears are confirmed by colposcopy and biopsies from abnormal areas (see
later).

7. CERVICAL PAP SMEAR Test:

- The Pap smear test is based on cytologic examination of
cells shed from both the ectocervix and endocervix.
- lt is performed using a cytobrush to wipe cells from the
endocervical canal and from the surface of the TZ of the
ectocervix.
- Cells obtained are spread on a glass slide fixed by ethyl
alcohol and stained by Papanicolaou stain.
- The test is done as an office procedure with an accuracy
rate up to 95%.
Fig 22-3: Pap smear test
202 Screening For Premalignant Lesions Femqle Lower Genitol Trqct

r Interpretation of a Pap smear:

1,. Negotive (no atypical cells).

2. ASCUS (Atypicol squamous cells of undetermined significonce); this indicates cells that are sug-
gestive but do not fulfil the criteria for squamous intra-epithelial lesions (SlL). For its evalua-
tion, testing for HPV, repeat cytology, and colposcopy, are required.
3. lSfls (Low grode squomous intra-epithelial lesions)concomitant with CIN l.
4. HSILs (High qrade squamous intro-epithelial lesions)concomitant with CIN ll & CIN lll.
5. Squomous cell carcinomo,
6. Atypicol glandulor cells.
7. E n d oce rvi ca I Adenoca rci noma.

,f
a-a, o
a .,

Fig 22-4: Normql Pap Smeor Mild dysplosia Severe Dysplasio

r Frequency of cervical cytology screening (screening protocol):

- High risk population; are screened annually within 3 years from onset of sexual activity.
- Low risk population; (age of >30, with 3 consecutive annual negative pap smears) should be
screened every 3 years.
- Low risk women over the age of 70; (with 3 negative Pap smears in the last decade) can con-
sider discontinuation of Pap testing at the physician's advice.

- Colposcopy allows inspection of the TZ with a magnification

up to 20 times after applying 3%-5% acetic acid solution.
- Colposcopic directed biopsies are performed from areas of
abnormal epithelium (aceto-white areas, punctuation, ffio-
{'''
saicism, leukoplakia, and Schiller's iodine negative areas)
with accuracy of 85%- 95%.
- Endocervical curettage is performed to rule out dysplasia
Fis 22-5: *:',?:'^":':Txamination
when the TZ in the cervical canal is not properly visualized in
oI the cervtx
presence of an abnormal pap smear.

TREATMENT of CIN (based on colposcopic obtained biopsies);

7. Low grade lesions (LSlLs - CIN 7):
a. Conservative treatment' (treat infection and repeat smear within 12 weeks);
- 70% will show spontaneous regression

- Only 15% may progress to high grade abnormality.

b. Destruction of obnormal cells ot TZ if the lesion persists in repeated smears;
- Ablation using CO2 laser.
- Cauterization by heat or electro-cautery.
 Gynaecology 203

2. High grcrde lesions (HStLs - CIN il-il\):

HSILs are managed by excision of abnormal cells at the TZ since they are more likely to pro-
gress to preinvasive or invasive cancer if neglected or inadequately treated. Excision is per-
formed via;
a. Cold knife conization: is the gold standard as it yields an adequate pathologic specimen with
clean margins. However postoperative bleeding, infection, cervical stenosis, and cervical in-
competence, are major complications of this simple procedure.
b. Loop Electrosurgical Excision Procedure (LEEP): a hot metal wire loop is used to excise a
wedge of cervical tissue at transformation zone (TZ). lt has the drawback of yielding a smaller
pathologic specimen with charred margins, but is associated with less postoperative
compli-
cations than cold knife conization.
c' Total abdominal hysterectomy (TAH) in older patients with resistant disease and those not
desiring fertility.
Follow Up After Treatment: Despite the efficacy of techniques in treating CIN yet recurrence is
still common and follow up by annual Pap smears is recommended for around 10 years.

f "q\*.

Fig 22-6: Diathermy destruction of CtN Fig 22-7: Cold knife excision of TZ

vAGtNAL tNTRAEptTHEL|AT NEOPLAS|A (VAtN)

It is an uncommon premalignant lesion of the vagina which is usually asymptomatic. lt may be
associated with neoplasia at other genitaltract sites as VIN and clN,
Diagnosis:
. Pap smear; showing abnormal vaginal epithelial cells.
o Diagnosis is confirmed by colposcopic examination of the vaginal epithelium with guided
biopsies from suspicious areas.
Treatment: individualized weather through;
1. Laser destruction (ablation) of the affected area under colposcopic guidance, or
2. Local surgical excision of suspicious area, or
3' Topical chemotherapy using 5-flurouracil vaginal cream for multifocal lesions.
204 Screening For Premolignont Lesions Femqle Lower Genitol Trqct

vULVAR TNTRAEPTTHELIAL N EOPLASIA (VlN)

VIN is defined like CIN as presence of atypical (dysplastic) cells within the vulvar epithelium
without invasion of the basement membrane.
VIN is classified after the International Society for the Study of Vulvar Diseases (ISSVD) 1986
into three degrees namely; VIN l, ll, and lll (like CIN). ln 2OI2 terms were changed into LSIL and HSIL
like ClN.
Although VIN seems to have low malignant potential. lt commonly occurs in younger age
where almost half of the cases are younger than 41 years. Spontaneous regression of VIN | & ll is
well reported.
DIAGNOSIS:
Symptoms: t/3 of cases are asymptomatic, however VIN often presents as pruritus vulvae.
Signs:
- Lesions are often raised above the surrounding skin with a rough surface.

- Colour is variable: whitish due to hyperkeratinization, red due to thinning of epithelium, or

dark brown due to melanin deposition in the epithelial cells.
- Lesions are often multifocal, that is why wide excision is mandatory.

- Painting the vulva with 5% acetic acid will result in VIN areas turning white and mosaic or
punctuations will be visible by the N.E., hand lens or colposcopy. Biopsies are taken from
acetowhite areas to rule out invasive cancer.

TREATMENT:
o The youth of many patients, the multifocal nature of the disease, and the discomfort and mu-
tilation of surgical wide excision, makes it necessary to be cautious and conservative to avoid
making the treatment worse than the disease.
. Asymptomatic cases especially < 50 years of age are managed conservatively, with repeated
biopsies to exclude progression of the disease.
. Symptomatic cases are treated by topical steroids for 3-6 months to relieve symptoms.
o lf the lesion is small; excision biopsy is enough (both diagnostic and therapeutic).
o Wide and multifocal lesions: skinning vulvectomy with or without skin graft is performed.
o Follow up and re-biopsy are essential to detect invasive disease among those who relapse.
Repeated treatments are commonly required.

N.B: Paget's disease: (adenocarcinoma in situ):

o lt is an uncommon condition similar to that found in the breast. ln almost 1./3 of cases there is
an associated adenocarcinoma in the apocrine gland, and in 2O%o concomitant cervical cancer
may be present.
. Pruritus is the presenting complaint.
o Often presents as a red crusted plaque with sharp edges.
. Biopsy is confirmatory.
o Treatment: is by very wide local excision usually including total vulvectomy, because unlike
VIN lllthe histologic extent of Paget's disease is frequently beyond the visible lesion.
 Endometrial Corcinoma
Sorcomo of the Uterus
G estotio n a I Cho rioco rci no mo

ENDOMETRIAL CARCINOMA
OVERVIEW
Endometrial carcinoma (Ec) is now considered the most common gynaecologic malignancy.
The rise in the incidence of EC, noted in the last decades, is expected to continue due to
the pro-
longed life span of women in general, together with the more liberal use of hormone therapy
in
the management of menopause.
EC is also described as the most curable gynaecologic cancer owing to the fact
that most
cases are diagnosed at an early stage, and when offered the proper treatment women
with stage I
disease will have a 5 year survival rate exceedingg5%.
oestrogen induced endometrial hyperplasia (EH), unopposed by pRG forms the most im-
portant background in development of EC.
Non oestrogen dependant EC is a much less common type of the disease, but is more
aggres-
sive and carries poorer prognosis than oestrogen dependant type.

RISK FACTORS FOR EC

Nulliparity (absent periods of amenorrhoea during

pregnancy and lactation)
Lote menopouse age > 55 years (long period of
anovulatory premenopausal cycles)
PCOS (chronic anovulation results long periods of E2
unopposed by PRG)
Marked Ohesity (increased peripheral conversion of
androgen to EL in adipose tissue)
Unopposed oestrogen therapy (as oestrogen re-
placement therapy in menopause ERT)
Long term Tomoxifen theropy (in treatment of oes-
Fig 23-1: Endometrial corcinoma
trogen receptor positive breast cancer)
o Atypical endometrial hyperplasia EH (see DUB)
o oestrogen producing ovarian neoplosm (e.g.; granulosa theca cell tumour)

N.B.: Long term use of OCPs is usually associated with a decreased risk of EC by nearly
50%, due to
the effect of Gestagens in protection from endometrial hyperplasia (EH).

zu)
206 Endometriol Cqrcinoma And Uterine Sqrcomo

Premolignont potentiol of various types of EH (WHO clossification)

Tvpe of EH Prosressionto EC

. Simple EH 1%
. Complex EH 3%
. Simple EH with otypio 8%
. Complex EH with otypio 29%

PATHOTOGY OF ENDOMETRIAL CARCINOMA

A. Gross Pathology

B. Microscopic Histopathology
Adenocorcinomo: is the commonest pathologic type of EC, and carries best prognosis.
Adenooconthomo: is an adenocarcinoma with areas of benign squamous metaplasia. lt
carries same prognosis as adenocarcinoma.
-
Adenosquomous: is an adenocarcinoma with areas of malignant squamous carcinoma. lt -
carries poorer prognosis than adenocarcinoma and adenoacanthoma.
- Primory sguomous cell corcinoma, papillory serous carcinomo ond clear cell carcinomo
are particularly aggressive but fortunately very rare types of endometrial carcinoma.
C. GRADING OF THE TUMOUR
Tumour grade is determined by both the degree of abnormality of the glandular architecture, -
and the degree of nuclear atypia.
- Well dilferentioted tumour (Grode t/; normally looking glandular epithelium with < 5%
solid structure. They are slowly invasive and carry the best prognosis.
Moderotely difierentiated tumour (Grade ll); glandular structure admixed with papillary
and occasional solid areas < 50%. lt is more aggressive and carries intermediate prognosis.
- Poorly difierentioted tumour (Grode lll)); the structure becomes predominantly solid, with
minimally identified glandular epithelium. The tumour is highly aggressive with early deep
myometrial invasion and generally poor prognosis.

PATTERNS OF SPREAD OF EC
l-. Direct Spread: primary mode of spread

pian tubes and implant on the ovaries, omentum, and peritoneal surfaces
2. Lymphatic Spread: Occurs later than direct spread

The risk of LN involvement increases with increased grade of tumour, depth of myometrial
invasion and stage of the disease. Spread occurs through;

ometrial invasion.
 Gynaecology 207

3. Vascular Spread: occurs late usually with higher grade tumours.

) Metastases to nearby intra-pelvic organs
) Distant extra-pelvic metastases rarely occurs (liver, lung, brain & bones).

Para-aotlic
fympft
glands t Faracayaf
2 Precaval
3 ln|eraofiocaval
4. Pro8orth
5. Para-aortic
6 Right suprahrlat
Pelvic 7. LEfl suprahilat
lyrnph I Righl iliac
glancls 9. Lell iliac
lO Inlefilrac
11 Bight gonadal vein
12 Lell gonadal vein

Fig 23-2: Lymphotic spread of EC

CLINICAL PICTURE
EC usually presents as AUB in postmenopausal women, with added risk to those who are
nulliparous, obese, diabetic and hypertensive.
SYMPTOMS:
1'. Post-menopausal bleeding,' is the commonest presenting symptom in cases with EC.
2. Metrorrhogia; perimenopausal women present with AUB, which is-recurrent and profuse
even after medical or hormonaltreatment.
3. Other symptoms: offensive vaginaldischarge, menstrualcramps, and deep pelvic pain.

SIGNS ON TOCAL EXAMINATION:

o. Bi mo n uo I Exo minotion :
-The uterus may be normal or slightly symmetrically enlarged in size
Consistency is usually softer than expected in a menopausal uterus.
The adnexae may be free, or may show a solid ovarian neoplasm, or metastases.
b. Speculum exominotion; is important to exclude;
Cervical mass or ulcer (in cases of cervical involvement)
Foul odor cervical discharge (in cases of pyometra)

SPECIAL INVESTIGATIONS

1-. Transvaginol Sonogrophy (rufl:

lncreased endometriol thickness in postmenopausal women above the cut-off value of
5.0 mm is strongly suspicious of EH. Thicker endometrium > 10 mm correlates with EC.
Associated uterine lesion as myomas, polyps, haematometra, or pyometra.
Associated odnexal mosses: as ovarian neoplasms
208 Endometriol Carcinoma And Uterine Sorcomo

2. Froctionol Curettage (FC):

FC the gold standardmethod for diagnosis of EC.
An endocervical biopsy is first obtained before cervical dilatation
Full curettage of the endometrial cavity (isthmus, anterior and posterior walls,
fundus, and uterine cornu). This is important to confirm the diagnosis of EC, its
histologic type and grade, and for detection of spread to the cervix.
3. Pap Smear Test:
- A pap smear has an accuracy of <5OTo in diagnosis of EC, hence considered unreliable
when compared with endometrial biopsy.
4. Other lnvestigations:
r Preoperativework Up including;
) Chest X-ray to exclude lung metastases.
F Abdominal US to exclude liver metastases, abdominal masses, and ascites.
F CT scan for pelvis and abdomen, may point to LN involvement
> MRI is sensitive in assessment of depth of myometrial invasion if present.
FIGO STAGING OF ENDOMETRIAL CANCER 2018: (Simplified SURGICAL STAGING)

:lGO Stage Stage Description*

The cancer is growing inside the uterus.

The cancer is in the endometrium (inner lining of the uterus) and may have grown
A
less than halfway through the myometrium
The cancer has grown from the endometrium into the myometrium. lt has grown
B
more than halfway through the myometrium.

The cancer has spread from the body of the uterus and is growing into the cervical
tl
stroma. But it has not spread outside the uterus.
ill The cancer has spread outside the uterus.

The cancer has spread to the outer surface of the uterus (the serosa) and/or to the
A
fallopian tubes or ovaries (the adnexa).
B The cancer has spread to the vagina or the parametrium

The cancer is growing in the body of the uterus.

iltc1
It has also spread to pelvic lymph nodes, but not to para-aortic lymph nodes
The cancer is growing in the body of the uterus. lt has also spread to the para-aortic
iltc2
lymph nodes.

IV The cancer has spread to other organs

IVA The cancer has spread to the inner lining of the rectum or urinary

The cancer has spread to inguinal (groin) lymph nodes, the upper abdomen, the
VB
omentum, or to organs away from the uterus, such as the lungs, liver, or bones

FIGO: lnternational Federotion of Gynoecology and Obstetrics

N.B.: Endocervicalglandular involvement is considered stage I disease
 Gynaecology 209

MANAGEMENT OF ENDOMETRIAL CARCINOMA

Following surgical staging the treatment will depend upon several factors including; the
stage of the disease, which is the most important factor, the histologic type and grade of the
tumour, and the patient's age and general health.

STAGE I:
A. Surgery
r An exploratory laparotomy with total abdominal hysterectomy and bilateral salpingo-
oophorectomy (TAH-BSO) is the gold standard treatment, performed in all patients, un-
less there are absolute medical contraindications.
r Peritoneal washings are taken with normal saline for cytological examination.
I Pelvic lymphadenectomy is performed on high risk cases including those with serous,
v clear cell, or grade 3 histology tumours, and in cases with stage lB (either outer half my-
ometrial involvement or cervical glandular extension).
B. Radiation Therapy
v I Cases of adenocarcinoma stage la or b, grade 1&2, can be followed without adjuvant radio-
therapy.
: r High risk cases, with serous or clear cell carcinoma, any grade 3 tumour, or with one posi-
tive pelvic node, should receive external beam pelvic radiation.
r Cases with multiple pelvic LNs of para-aortic LN involvement should receive extended field
radiation (pelvic and abdominal)
r Patients medically unfit for surgery may receive radiation therapy alone. A combination of
.v intracvitary plus external beam radiation, with an overall S-year survival rates 20% lower
than those treated with TAH-BSO.

C. Hormone Theropy
v r EC rarely occurs in women < 40 years of age. These tumours are usually early stage, and
low-grade, and there is frequently a desire to preserve fertility and avoid hysterectomy.
I High dose medroxyprogesterone acetate (200 mg twice daily) for 3-6 months will reverse
the changes in about 2/3 of cases. Recurrences are common.

STAGE II:
r When the cervix is involved, a radical hysterectomy with pelvic lymphadenectomy will be
the procedure of choice in surgically fit patients (see cancer cervix).

v MANAGEMENT OF ADVANCED STAGES (stage ilt & lV):

For advanced disease treatment should be individualized. lt may include a combination of;
v t TAH-BSO if possible as palliative therapy for bleeding, pain, & other pelvic symptoms.
t Radiation therapy: extended external beam irradiation
t Chemotherapy: combination of Cisplatin and Doxorubicin has been recently studied ei-
ther alone or in combination with radiotherapy with encouraging results.
RECURRENT DISEASE
More than 80% of recurrences occur within the first two years of treatment.
+ - The vaginal vault is the primary site for recurrent disease

.; Other sites include; the pelvis, upper abdomen, or distant metastases.

210 Endometrial Corcinoma And Uterine Sorcomq

- The Treatment of recurrent disease depends on the site and extent of recurrence.

- Progestagens may help only in well differentiated tumours containing oestrogen receptors.
- Radiotherapy and/or chemotherapy may be tried in less differentiated tumours.
- Limited surgery is rarely indicated for residual disease.

SARCOMA OF THE UTERUS

I.EIOMYOSARCOI\NA

Leiomyosarcoma is rare tumour that usually arise in the uterine myometrium, grows rap-
idly even in the menopause, invades into the myometrium, or through the capsule of leiomyoma
and spreads rapidly directly to adjacent organs, or early via blood stream metastases to reach dis-
-
tant organs.

- Malignant transformation in a benign leiomyomas is rare occurring in<O.2%.

- Endometrial stromal sarcoma; is rare, arising in the stroma of the endometrium.

r Macroscopically: cut surface shows areas of hemorrhages and necrosis.
r Microscopically: Spindle shaped or rounded cells, many of them being pleomorphic, with
little stroma and primitive blood vessels.
r Histological diagnosis of malignancy depends on the number of mitoses per high power
field (HPF), Patients with >10 mitosis per 10 HPF are regarded as having malignant dis-
ease.

CLINICAL PICTURE:

r Symptoms: AUB especially in perimenopausal or menopausalwomen.

r Signs: No specific signs, where most cases are diagnosed accidentally only after surgical re-
moval at hysterectomy. Leiomyosarcoma is highly suspected in the following situations;
) Rapid growth of myomas at any age

F Any growth of myomas after menopause

) Rapid recurrence after myomectomy
F Absence of plane of cleavage during myomectomy.

TREATMENT

r TAH BSO is the treatment of choice, followed in many cases by external radiotherapy.
r In general the prognosis is poor, except for early cases of leiomyosarcoma arising in a
myoma without associated blood stream spread.
 Gynaecology 2tl

GESTATIONAL CHORIOCARCI NOMA

Choriocarcinoma is a rarely occurring yet highly malignant tumour arising from tropho-
blastic epithelium, invading the endometrium and myometrium of the body of the uterus. lt is
characterized by its early metastases to the lungs, liver, and brain.
I Gestational Trophoblastic Neoplasia (GTN): is the term that collectivelv describes a soec-
trum of interrelated trophoblastic tumours, including:
a. Benign lesions: as complete and partial hydatidiform moles,
b. Invasive mole: a benign lesion that invades and metastasize
c. Malignant lesion: gestational choriocarcrnoma.
Most GTN cases will run a benign course with their disease remitting spontaneously.
Malignant and even metastatic disease can be effectively cured with chemotherapy.

- Serum B-hCG is a sensitive tumour marker for GTN which allows accurate diagnosis, risk clas-
sification, and follow up assessment during and after treatment.
N.B.: Non-gestational choriocarcinoma are exceedingly rare occurring as a part of ovarian germ
v cell neoplasms that do not arise in the uterus (see ovarian neoplasms).

INCIDENCE:
- Gestationol choriocarcinoma exhibits a geographic distribution similar to that of hydatidiform
, mole with an incidence of 1in 30,000 to 1in 5O,OOO pregnancies in the UK and USA, being 10
times more common in south east Asia, especially in older women with low socioeconomic
standards.

v > 50% of cases will develop following evacuation of a molar pregnancy

> 25% following abortion and
v > 25% following term pregnancy
> 5% following an ectopic gestation.
PATHOLOGY:
r Gross Pathology:
The tumour appears as a friable haemorrhagic nodular mass arising in the body of the
uterus, first invading the endometrium, projecting into its cavity, then extending to invade
the myometrium.
The ovaries may be enlarged showing multiple theca-lutein cysts
r Microscopic pathology:
! The tumour is comprised of sheets of anaplastic cytotrophoblasts and syncytiotrophoblast
cells with prominent haemorrhage, necrosis, and vascular invasion.
Unlike molar disea se, chorionic villi are characteristicolly obsent in choriocorcinomo.

SPREAD OF CHOROIOCARCINOMA:
r Haematogenous spread: early and widespread blood borne metastases to various sites,
namely to the lungs (80%), the vagina (30%),liver (10%), CNS and brain (10%)
r Direct spread: Malignant cells may directly invade the myometrium.
2t2 Endometriol Corcinomq And Uterine Sorcoma

DIAGNOSIS:

r Symptoms:
Persistent vaginal bleeding that continues for > 6 weeks following molar evacuation, abor-
tion or term pregnancy.
r Signs:

- Bimanual vaginal examination may reveal a slightly symmetrically enlarged uterus that
may be soft in consistency.
In cases with vaginal metastases, a soft haemorrhagic nodule may be seen within the vagi-
na.

SPECIAL INVESTIGATIONS:

1. Elevated serum B-hCG levels:

Persistently high B-hCG levels after evacuation of a molar pregnancy, in absence of a new
pregnancy, is the gold standard in diagnosis of gestational choriocarcinoma.

- Biopsy is not needed to establish diagnosis and start treatment, in presence of such a highly
specific tumour marker.
low risk cases primarily according to the serum B-hCG lev-
Cases are classified as high risk or
el, hence treatment is planned based on such levels.

2. TVS may show the following:

Slightly symmetrically enlarged uterus with absence of intrauterine gestational sac.

A small mass within the endometrial cavity that may extend to the myometrium

- Colour Doppler indices to the mass may be suggestive of malignancy (low Rl and high di-
astolic flow due to associated neo-vascularization)

- Bilateraltheca lutein cysts of the ovaries in association with elevated B-hCG levels
3. MRI: confirms the lesion and help in evaluation of intramyometrial invasion if present

4. C.T. scan may be required to exclude metastases in lungs, liver, and brain.

5. D&C Biopsy operation:

Biopsy will reveal anaplastic trophoblastic tissue with absence of villous pattern.
- Histological diagnosis of choriocarcinoma is not essential to confirm diagnosis or to start
chemotherapy, in presence of a specific tumour marker as B-hCG

CLASSIFICATION OF PATIENTS PRIOR TO TREATMENT

Risk Classification is based on severalfactors including;

Patient's age and B-hCG levels

Type of antecedent pregnancy (hydatidiform mole, abortion, or term pregnancy),

- Tumour size, site of metastases, number of metastatic lesions.

- Prior response to chemotherapy if previously given.

 Gynaecology ar t
ztJ

Patients are classified after investigations completed into 2 categories;

a. Non metastatic choriocarcinoma

b. Metastaticchoriocarcinoma; which is further divided inro;

D Low risk cases
> Hiqh risk cases
TREATMENT OF CHORIOCARCINOMA:
A. CHEMOTHERAPY:

Chemotherapy is indicated in all cases of gestational choriocarcinoma. lt is considered the

mainstay of treatment even in cases which may require surgical treatment (see later).

1. Single Agent Chemotherapy:

Y Methotrexate (MTX);
MTX is single agent drug of choice for non metastotic and metostatic low risk cases, with
complete remission rates of 60-80%.
MTX is given as 50 mg dose lM every 48 hours / 4 doses.
- MTX /
Folinic acid regimen: where folinic acid is taken orally 30 hours after MTX injection,
to minimize side effects of MTX
- cycle regimen is repeated after L4 days till a negative B-hcG is obtained.
Side effects of MTX include; nausea and vomiting, stomatitis and GIT ulcers, myelosup-
pression, hepatotoxicity, nephrotoxicity, and alopecia.
) Actinomycin: is also an effective single agent chemotherapy

2. Combined Agents Gemotherapy:

> MTX, Etoposide, and Actinomycin: is the combination of choice for metastatic hiqh risk cas-
for cases resistantto MTX single agent chemotherapy.
es, and
) Follow up after Chemotherapy:
Follow up by repeated serum B-hCG is recommended after chemotherapy is completed
until negative B-hCG levels are achieved for 3-6 months.
B. SURGICAL TREATMENT:

Surgery via a TAH in choriocarcinoma is reserved only for selected cases including;
Elderly, multiparous, high risk cases (>40 years age).
Cases resistantto combination chemotherapy (failure of achieving negative B-hCG)
- cases complicated by severe haemorrhage, perforation, or infection
TAH is usually preceded and followed by chemotherapy : MTX 10 mg given at day of
operation and continued postoperatively for 4 to 5 days to prevent the risk of dissemi-
nation and development of distal metastases.
- There is no need to remove the ovaries as ovarian metastases is rare and can effectively
be treated with MTX.
214 Endometrial Cqrcinomo And Uterine Sqrcoma

PLACENTAL SITE TROPHOBLASTIC TU MOU R

It is an uncommon variant of choriocarcinoma
It consists predominantly of intermediate trophoblasts

Human placental lactogen (HPL) is the tumour marker

They are insensitive to chemotherapy

Hysterectomy is the most efticient treatment for conformed cases

KEY POINTS
- Endometriol cqncer is the most common and most curoble gynoecologic cancer.
- More thon 75% of coses are qdenocorcinomo occurring in postmenopousol women, meon oge 60
yeors.
- Prolonged exposure to unopposed oestrogen is the most common risk foctor.
- Other important risk foctors include obesity, chronic onovulotion, Iote menopouse, ERT, ond EH.
- Postmenopousol bleeding is the most common presenting symptom, which moy be ossocioted with
offe n sive vo g i n o I d i sch o rge.
Premenopousol metrorrhogia is the second most common presentation.
Screening for EC using PAP smeors will miss>25% of coses.
TVS showing an abnormolly increosed endometrial thickness especiolly in the menopouse is a good
predictor for the diseose.
- The gold standord for diognosis of EC is on endometrial biopsy obtoined by FC under GA, which de-
fines the pothologicol type ond grode of the tumour present.
- The extent of the disease, the prognosis, ond the need for odjuvant rodiotheropy ore all determined
upon surgicol stoging of the diseose.
- The gold standord treotment is surgery vio TAH-BSO.
- Associsted pelvic lymphodenectomy may improve the prognosis and survivol rotes in cases with deeper
myometriol invasion.
- The overoll 5 yeor survival is > 80% in stage I ond >80% of recurrences occur within the first 3 yeqrs.
 P re- i nva sive ca rci n o m o Ce rv ica I stu m p co rci n o m o
lnvosive corcinoma Re cu rre nt ce rv i ca I co nce r

OVERVIEW

Carcinoma of the cervix is the second most common cancer of the female genital tract (after
endometrial carcinoma), and is also the most preventable one.
The introduction of the Papanicolaou screening test (Pap smear) resulted in early diagnosis of
increasing number of cases with premalignant lesions (ClN), with a concomitant decline in occur-
rence of preinvasive and Invasive disease.

A further decline is expected to occur in the coming decades with the introduction of efficient
vaccination against genital HPV, which is considered the primary premalignant condition predispos-
ing to invasive cervical cancer.

Racial, ethnic, geographic and socioeconomic factors play important roles in the prevalence of
this disease. Sexual and hygienic habits are also important factors.
The slow progression of cervical cancers from precancerous lesions (ClN lll), to invasive cancer
provided the rationale for the preventive and early treatment strategies to control the disease.

Fig 24-1: Cervicsl concer

PREMATIGNANT TESIONS
Persistent infection with human papilloma virus (HPV) has been identified as the primary cause
in almost all cervical cancers.
There are 15 high risk HPV types of which types 15 & 18 are responsible for over 70% of cases.
Persistent high risk HPV infection will provide DNA material by which immature cells in the
transformation zone (TZ) may produce cervical intraepithelial neoplasia (ClN), via abnormal
squamous metaplasia.

zt)
216 lnvqsive Concer Of The Cervix

Natural History of CIN

- Low grade squamous intraepithelial lesions (LGSIL or CIN l) will undergo spontaneous regression
in the majority of cases.
Some LGSIL cases may progress to high grade lesions (HGSIL, CIN Il and CIN lll) within few years
- At least 35% of patients with HGSIL (ClNlll) develop invasive cervical cancer within 10 years.
(See chapter on premalignant epithelial lesions of female genitol tract CIN)

INVASIVE CARCINOMA OF THE CERVIX

INCIDENCE AND AETIOLOGY
Invasive cervical cancer has significantly declined in the last 3 decades, owing to the effective
screening programs using the Pap smear test.

The age incidence for cancer cervix is commonly between 45-55 years which is almost 10 years
younger than that for endometrial carcinoma, and 10 years older than that for CIN lesions.

RISK FACTORS: same as for CIN including;

- Early exposure to first intercourse, especially with multiple sexual partners

- Viral agents as HPV & HSV ll,
Untreated HSILs which may gradually progress to invasive cancer.
Cigarette smoking due to hypoxia of endocervical cells

PATHOLOGY
A. Squamous cell carcinoma of the Ectocervix (> 80%):
- Origin:
F Arise from squamous epithelium covering the ectocervix
D May rarely arise as metaplasia of glandular epithelium at the TZ.
- N.E. appearonce:
F Friable necrotic mass easily bleeding on touch, or -
) Deep ulcer with everted and indurated edges, or
) Indurated nodule that may break forming an ulcer.
- Microscopically:
) The tumor is formed of cell nests with or without keratin.
F The cells are commonly large with malignant criteria but may be small undifferentiated.

B. Adenocarcinoma of the Endocervix (15%l:

- Origin:
Arise from the columnor epithelium lining the endocervix. Being within the endocervix, it is more
difficult to be detected by naked eye.
- N.E. oppeoronce:
They may distend the cervix giving it a barrel-shaped appearance. By the time it appears at the
external os, the carcinoma has often spread extensively outside the cervix.
 Gynaecology 211

- Microscopically:
The cells are malignant columnar cells arranged in glandular pattern with malignant criteria. In
poorly differentiated tumors, the glandular pattern is replaced with unarranged cell nests.

HISTOLOGICAL GRADING:
a' Well dilferentioted (grode l); the majority of cells resemble the normal squamous epithelium
of the cervix. They grow slowly and are less likely for early spread.
b. Moderote and poorly difierentioted (grode 2 & 3); cervical carcinoma is predominantly of the
moderate or poorly differentiated type. Abnormal cells predominate; they are more likely for
rapid growth and early spread.

SPREAD: early direct and lymphatic spread.

1. Direct spread: To adjacent tissues including the body of the uterus, parametrium, upper ano
lower vagina, and uterosacral ligaments. Later spread may involve the bladder and rectum.
Spread to the parametrium may lead to ureteric obstruction with subsequent develooment of
renal failure (most common cause of death).
2. Lymphatic spread: Usually follows direct spread, but may coincide with it. lt involves;
a. Primory groups: include spread from the cervical lymphatics along to the paracervical LNs,
to the obturator and external iliac nodes, and occasionally backwards to the internal iliac
group.
b. Secondory groups: involve drainage into the common iliac and lateral sacral groups. Ulti-
mately the common iliac group drains into the para-aortic lymph nodes.
3. Blood stream spread: Least common, usually in late or advanced cases. Metastases may occur
to distant organs as to the liver, lungs, brain and bone.

Aortic 27%

. Comnon ihrc 3l t6
Soclsl ?|9[
Hypogrslric 3tg6
Pfr€qorvic,rl 3f %
Ertornrl ltirc 27t$

Obtunlor 27X Parrm0lrium 77tG

\rr- Ingurnar 616 nodea

Fig 24-2: Lymphatic droinoge ond spreod of concer cervix

218 lnvosive Concer Of The Cervix

CLINICAL PICTURE
A)SYMPTOMS:
- Contact bleeding; is the commonest presentation (postcoital bleeding or bleeding on touch).
- Metrorrhogia, or postmenopausal bleedingr, is the second most common presentation.
- Vaginol discharge which is excessive bloody or malodorous.
- Pain; deep pelvic pain and loin pain may be associated with advanced disease
B) SrGNS:
7. General exominotion:
- Early stages do not affect the patient's general condition.
- Advanced stages are associated with; chronic blood loss, urinary manifestations and ureteric
obstruction which may lead to severe anaemia, uraemia and cachexia.
2. Palpation by digitalvaginol examinotion (PV):
- Early stages: mass or ulcer that bleeds profusely when touched by the finger due to friability.
- Later stages: as the disease progresses, the cervix loses its mobility, becomes fixed, and the
surrounding parametrium becomes tender and indurated.
3. Bimonuol pelvic examinotion:
- The uterus is usually normal in size
- Symmetrical uterine enlargement may occur if pyometra develops.
4.lnspection vio o speculum vaginol exomination:
- Early stages: small friable warty mass, nodule, or an ulcer that bleeds on touch.
- Later stages: mass or ulcer extending to the vaginal walls obliterating the vaginal fornices.
5. Rectal examination (PR):
- For detecting parametrial extension and uterosacral involvement
DIAGNOSTIC PROCEDURES
Histopathologic examination of cervical tissue biopsies containing
the abnormal epithelium is the gold standard for diagnosis of cervical
cancer. Biopsies are obtained as follows;
1. Knife Biopsies; obtained from suspicious lesions seen by the naked eye
such as an ulcer, mass, polyp, or nodule. lt is done under general an-
aesthesia.
2. Colposcopic Directed Biopsies; Indicated when a Pap smear reveals
positive malignant cells in absence of a suspicious NE lesion on the cer-
vix. Biopsies are obtained from dcetowhite positive qreos or Schiller's
iodine negative areas, lt is an office procedure performed without an-
aesthesia.
3. Cone Biopsy: Removal of a cone shaped piece of the cervix with the Tlssue refiorred

apex including the TZ is done when a Pap smear is positive for malig-
nant cells while the extent of the lesion cannot be delineated colpo-
scopically. Cervical conization can be performed through cold knife,
laser conization, LLETZ, or LEEP procedures. The latter two are associ- Fig 23:3 cone biopsy
ated with less blood loss, but may be associated with charring at the
edge of specimen limiting reliability of its histopathologic evaluation
4. Fractional Curettage (FC): to obtain tissue from the endocervix thus diagnosing high endocervical
lesions together with obtaining separate endometrial biopsies to exclude the spread of cervical
cancer to the endometrium and body of uterus. (See of FC in gynaecologic operation).
 Gynaecology 219

CLINICAL STAGING AND PREOPERATIVE PREPARATION:

Before starting treatment, clinical staging of the disease should be complete. lt requires;
a. Examination under anaesthesia (EUA): done during performing cervical biopsies to test for
cervical mobility and to define the presence and extent of parametrial infiltration through
PV and PR examination.
b. Cystoscopy: to exclude bladder wall invasion which if present will shift staging from stages I
& ll, in which treatment is curable, to stage lV in which treatment is palliative.
c. Intravenous pyelography (lVP): to exclude ureteric compression if parametrial infiltration is
present.
d. Chest X-ray
& Abdominal U.S.: to exclude distant metastases in advanced cases.
Both, staging and grading, help to decide on the most appropriate treatment, and to predict
the possible prognosis of the case. The FlGo clinical staging classification is based on findings on
EUA, lvP, cystoscopy, and cervical biopsies. staging does not change after surgery.

F|GO STAGING OF CARCINOMA OF THE CERVIX UTERI 20L8. (simplified Clinical Staging)

:lGO Stage
Stage Description*

I The carcinoma is strictly confined to the cervix

Invasive carcinoma that can be diagnosed only by microscopy, with maximum depth
of invasion <5 mm

Invasive carcinoma with measured deepest invasion )5 mm

B
NB: involvement of the uterus is considered stage I

tl The carcinoma causes local spread, beyond the cervix and uterus

Involvement limited to the upper two-thirds of the vagina without the lower one
third and without parametrial involvement.
B With parametrial involvement but not reaching the lateral pelvic wall
ill The carcinoma causes more localspread and/or lymph node involvement
A Carcinoma involves the lower third of the vagina, with no extension to the pelvic wall
B Extension to the lateral pelvic wall and/or hydronephrosis or renal failure

lnvolvement of pelvic and/or paraaortic lymph nodes, irrespective of tumor size and
L
extent

The cancer is growing in the body of the uterus. lt has also spread to the para-aortic
|tc2
lymph nodes.

IV The carcinoma has extended beyond the true pelvis

IVA Spread of the growth to adjacent organs as mucosa of the bladder or rectum

VB Spread to distant organs

220 lnvasive Concer Of The Cervix

PREVENTION OF CANCER CERVIX:

Invasive cancer cervix is the most preventable female genital cancer. lt is achieved via;
A. SECONDARY PREVENTION: early detection and proper management of CIN lesions
Y Regular screening (Pap smears) for asymptomatic high risk patients, with colposcopy
and colposcopic directed biopsies performed to cases with abnormal Pap smears.
D Treqtment of CIN lesions by ablation or excision, and regular follow up after treatment.
N.B.; Regular screening resulted in a significant decrease in the incidence of invasive cancer
cervix, and a 10 fold decrease in mortality compared to unscreened population.
B. PRIMARY PREVENTION:
) An HPV vaccine has been approved for prevention of HPV infection especially types 6,
LL, t6 & 18 which account for 70% of all cervical cancers, and almost 90% of cases of
genital warts.
F The vaccine appears to be over 95% effective in preventing HPV L6, L8, related cervical
cancers.
F The vaccine is effective when given in age groups from 9-26 years, in non-previously in-
fected population. lt is not effective in treatment of already pre-existing infections.
TREATMENT OF INVASIVE CANCER CERVIX
r Stage lA1:
- Young patient/family not complete (needs to retain the uterus) = Therapeutic conization.
- Old patient/family completed = Simple extrafascial hysterectomy.
r Stage lA2,lB,llA = Radical/Wertheim hysterectomy + Concurrent chemoradiation
r Stage llB - lV = Concurrent chemoradiation.

It should be noted thot:

- Stage lA2,lB,llA are both radiosensitive and operable but operation is preferred due to:
) Preservation of the ovary and ovarian function.
) Preservation of the vagina for coitus.
F Psychologically better for the female.
- Cervical cancer almost never spread to the ovary, therefore ovarian removal is not a must.

SURGICAL TREATMENT OF CERVICAL CANCER:

I Wertheim's radical hysterectomy:
- This is the standard surgical procedure for invasive carcinoma of the cervix.
- lt involves a TAH-BSO + pelvic lymphadenectomy + removal of parametrial tissue and 2-3 cm
from the upper vaginal cuff.
- Pelvic lymphadenectomy: includes removal of the external, internal, and common iliac nodes,
together with obturator and presacral nodes.
- Patients in which surgery results in removal of the whole tumour, with a free safety margin of
healthy tissue, and negative LNs, do not need further postoperative radiotherapy.
- Patients with positive LN affection or non-free safety margin are best offered adjuvant radio-
therapy treatment.
- The ovaries may be preserved in younger women to benefit for their hormonal function.
r Schauta's vaginal hysterectomy and lymphadenectomy:
It is rarely resorted to owing to the limited access to pelvic nodes via such procedure ending in
incomplete lymphadenectomy.
 Gynaecology 221

Complications of Surgery:
Beside all known complications of general surgery, the principal complication of radical hyster-
ectomy is related to;
- Some degree of bladder dysfunction due to division of the parasympathetic nerve supply to
the bladder that runs within the uterosacral ligaments.
- Ureteric injury whether direct or indirect (i.e. necrotic due to devascularization or as a result
of extensive dissection).
I Five years survival rates after surgery alone ranges 75%-1.00% in stages from lA to llA.

RADIOTHERAPY IN CANCER CERVIX

- All stages of cervical cancer are radiosensitive.

- In early stages (l-llA) cure rates are comparable to those
for surgery.
- In more advanced stages (llB-lV) cancer will not be cura-
ble by surgery alone, and radiotherapy becomes the
preferred first line of treatment. lt may be given alone,
or in combination with surgery or chemotherapy.

Types of radiotherapy:
a. Primary therapy; usually involves external beam
radiotherapy (EBRT) to the pelvis followed by in-
tracavitary treatment or brachytherapy. Fig 24-4:
b. Adjuvonttheropy; administered after radical hys-
terectomy to high risk cases (positive safety margins, and or positive nodal involvement)

r Survival rates after radiotherapy

- The five years survival rates for radiotherapy alone are comparable for survival with surgery
alone for stages lA-llA disease.
- For advanced stages localized within the pelvis, 5- years survival ranges from5O%-8O%.
- For metastatic disease outside the pelvis, survival is less than 15%.

r Complications of radiotherapy include:

F Radiation induced menopause
F Variable degrees of vaginal narrowing and fibrosis, few weeks post treatment
F Rarely radiation vesico-vaginal fistulas may occur and are difficult to deal with.
CHEMOTHERAPY IN CANCER CERVIX
Chemotherapy has proved to play a role as a radiation sensitizer (chemoradiation) in cases of
cancer cervix (e.g.; weekly l.V. cisplatin), with a nearly l-0% increase in cure rates.

PROGNOSIS IN CANCER CERVIX

- Stage lA; cure rates may reach up to 95%

- Stage lB; 5 year survival rates may reach up to 85% whether with surgery or radiotherapy.
Stage ll; drops sharply to a 5 years survival of 50%.
- Sages lll and lV; 5 years survival may be as low as 25% and 5% respectively. The treat-
ment in these stages is therefore only palliative.
222 lnvosive Cancer Of The Cervix

CARCINOMA OF THE CERVICAL STUMP (after subtotal hysterectomy)

Cancer cervix may develop in the stump of the cervix left after subtotal hysterectomy per-
formed for benign indications as leiomyomata, and DUB.
Surgery (radical cervicectomy and lymphadenectomy) is complicated by presence of adhesions
and abnormal anatomic relations induced by the previous hysterectomy.
Radiotherapy: EBRT may be the best option as internal irradiation is compromised by the ab-
sence of the uterus as a container for intrauterine applicators, while vaginal irradiation may not de-
liver the sufficient dose without risk of damage to the bladder and rectum.

RECURRENT CERVICAL CANCER

'A. Recurrgnce after primary surgery (more than 6 months); is treated by palliative external
beam irradiation (EBRT). The aim is to control bleeding, pain, and infection. Prognosis is
ooor in all conditions.
B. Recurrence after radiotherapy; Palliative surgery through pelvic exenteration may be con-
sidered, in order to control pain, bleeding, and infection. Exenteration may be anterior
(involving the uterus, vagina and bladder, or posterior involving the rectum, or total involv-
ing both). The operation carries very high morbidity and mortality, and is rarely resorted to.

KEY POINTS
- Cervicol concer is highly correlqted with HPV infection and less commonly HSV type ll
- Regulor PAP smeqrs done onnuolly for young sexuolly active femoles ond those with previous +ve CIN
smeors will ollow prevention ond eorly detection of most lesions.
- A positive smear warrqnts repetition and Colposcopic guided biopsies if confirmed.
- Contoct bleeding is the most common presenting symptom for invqsive csncers
- Biopsy from o suspicious cervicsl lesion (ulcer, or o frioble moss) is the gold stondard for diagnosis.
- Stage lA1 in young patient/fomily not complete (needs to retoin the uterus) is treoted by theropeutic coni-
zation.
- Stoge l41 in old potient/fomily completed is treated by simple extrafasciol hysterectomy.
- Stage IA2, lB, llA are treoted by radical/Wertheim hysterectomy + Concurrent chemoradiotion
- Stage IIB - lV are treqted by concurrent chemorqdiotion.
- Although eorly stages are rqdiosensitive, surgery is preferable.
 Cancer of the vulva VAIN
- Squomous cell carcinomo Vaginol Cqncer
- Stoging - Secondory tumours
- Treqtment - Primary tumours
Voginal Adenosis

INVASIVE CANCER OF THE VULVA

Malignant tumours of the vulva are generally rare, although a gradual rise in its incidence has
been observed throughout the past two decades reaching up to 8% of malignancies of the female
genital tract.
This increase is both attributed to the continued rise in average age of female population, and
to the larger prevalence of VIN in the younger population. No race is spared and neither parity nor
gravidity is involved.
Aetiology and pathogenesis:
A, Carcinoma occurring in younger patients; this type is rare, it is related to HpV infection and
smoking, and is commonly associated with vulvar intraepithelial neoplasia (VlN). Carcinoma
in situ of the vulva (VlN-lll)appears to carry a significant risk of progression to invasive cancer
if left untreated.
B. Carcinoma occurring in elderly patients; this is the more common type, it is unrelated to
smoking or HPV infection, and concurrent VIN is uncommon.
Pathologic types
. Squamous cell corcinomos is the commonest type representing almostg2% of tumours
. Melanomas, adenocarcinomas, basal cell carcinomas, and sarcomas, are much less frequently
encountered.
Methods of spread:
- Direct extension to adjacent structures, such as the vagina, urethra, and anus.
- Lymphotic permeotion to regional lymph nodes (common).
- Hoematogenous spreod to distant sites, including the lungs, liver, and bones (rare).
SQUAMOUS CELL CARCINOMA OF THE VUTVA
Squamous cell carcinoma of the vulva occurs mainly in postmenopausal women, and the mean
age at diagnosis is 65 years. A history of chronic vulvar itching is common.
. Symptoms: Patients generally present with long standing pruritus, before a vulvar lump is de-
tected. other common symptoms include vulvar pain, bleeding, and discharge.
. Signs on examination:
- The lesion may be raised, ulcerated, pigmented, or warty in appearances. Most lesions occur
on the labia majora; the labia minora are the next most common sites. Less commonly, the
clitoris or perineum is involved. Approximately 5% of cases are multifocal.
- The groin lymph nodes should be evaluated carefully and a complete pelvic examination
should be performed.
- Colposcopic examination of the cervix and vagina should be considered to exclude the com-
mon association with other intraepithelial squamous neoplasia of the lower genital tract (ClN
& vArN).

zzJ
'r1 A
Malignoncies Of The Vulvq And Vogina

. Diagnosis: Definitive diagnosis requires biopsy from the lesion under local anaesthesia.
. Lymphatic spread pathways: Initial lymphatic spread reaches the superficial inguinal lymph
nodes, then to the lemoral nodes (located along the femoral vessels). From the inguino-femoral
nodes spread occurs to the deep pelvic nodes, particularly the external iliac group. (N.8.: Clo-
quet's node is situated beneath the inguinal ligoment, and is the most cephalad of the femoral
node group).
. The incidence of lymph node metastases in vulvar cancer is approximately 3O%. lt is related to
the size of the lesion and the stage of the disease.
o Haematogenous spread usually occurs late in the disease and rarely occurs in the absence of
lymphatic spread.
. Clinical Staging: Staging was based on a clinical evaluation of the primary tumour and regional
lymph nodes with a limited search for distant metastases.

FlcO STAGING OF CARCINOMA OF THE VUTVA 2009 (Simplified SURGICAL STAGING)

FIGO Stage Stage Description*

I Tumor confined to the vulva

Lesions <2 cm in size, confined to the vulva or perineum and with stromal invasion
<1.0 mma, no nodal metastasrs

Lesions >2 cm in size or with stromal invasion >1.0 mma, confined to the vulva or
B
perineum, with negative nodes

Tumor of any size with extension to adjacent perineal structures (lower third of
tl
urethra, lower third of vagina, anus) with negative nodes
Tumor of any size with or without extension to adjacent perineal structures (lower
ill third of urethra, lower third of vagina, anus) with positive inguinofemoral nodes
Tumor invades other regional (upper 2/3 urethra, upper 213 vaginal, or distant
IV
structures

Tumor invades any of the following:

IVA upper urethral and/or vaginal mucosa, bladder mucosa, rectal mucosa, or fixed to
pelvic bone, orfixed or ulcerated inguinofemoral lymph nodes

VB Any distant metastasis including pelvic lymph nodes

 Gynaecology 225

MANAGEMENT OF INVASIVE CANCER VULVA:

. Surgical treatment via a Radical vulvectomv and bilateral en bloc groin dissection. with or with-
out pefvic lvmphadencetomv has long been considered the stondord tredtment for oll operoble
potients. However such extensive surgery had a very high morbidity affecting the quality of life
after the procedure.
. Modifications to minimize morbidity of standard surgical treatment includes;
t. Seporate incisions are used for groin dissection; instead of the traditional large butterfly vulvo
inguinal incision, to decrease post operative wound breakdown (i.e. wide deep local vulvectomy +
separate incision for bilateral groin LN dissection).
2. Postoperotive pelvic ond groin external rodiation therapy; has eliminated the need for routine
pelvic lymphadenectomy unless metastases is documented in the inguinal node area.

3. Uuniloterollesions on one of the labia majora can be managed by unilateral inguino-femoral lym-
phadencetomy without contralateral groin node dissection. However in midline lesions invading
more than 1 mm bilateral groin dissection is necessary.

4. Very early tumours in which the depth of penetration is less than 1 mm, groin dissection moy be
eliminoted, where a wide and deep local excision (radical local excision) is as effective as radical
vulvectomy in preventing local recurrence.
5. ln odvanced vulvor cancer involving the proximal urethra, anus, or rectovaginal septum many
centres have been using preoperative radiation or chemo radiation'to shrinkthe primarytumour
followed by more conservative surgical excision.
6. Prognosis: The 5-year survival rates ranges from nearly 90% for stage 1 to !5% for stage lV.
Patients with nodal involvement have a 5 year survival rate50% whereas those with no nodal in-
volvement have a 5 year survival rate of about 9O%.

MALIGNANT NEOPLASMS OF THE VAGINA

7. Secondory Tumours; Malignant neoplasms of the vagina are usually secondary to a primary
growth elsewhere. Spread may occur as a) direct spread; from primary malignant tumour in the
vulva, cervix, urethra, bladder and rectum, or b) via blood and Lymph spread; as occurs second-
ary to a choriocarcinoma, or c) as seeding; from adencarcinoma of the body of the uterus.

2. Primory Tumours: Primary malignant tumours of the vagina are rare. They occur mainly in post
menopausal patients.
o Pathology: Squa mous cell ca rcinoma occurs in > 90% of cases. Other ra re types include; clear
cell carcinoma, melanomas, rhabdomyosarcomas and endodermal sinus tumours.
. Spread:

- Direct spread to local and near by organs is the main route.

- Lymphatic spread, is less common. When the growth in the upper vagina the lymphatic
spread is the same as cancer cervix; if it is situated in the lower vagina, the vulval lym-
phatics are involved.
. Clinical presentation:
- The main presentations are vaginal discharge.
- Vaginal bleeding and occasionally post coital bleeding.
226 Malignoncies Of The Vulvq And Vogino

- In more advanced cases a malignant ulcer or fungating growth are detected .

- A malignant fistula may develop either in the rectum or the bladder.

o Treatment: will depend on the site and stage of the tumour.

- A stage I in the upper vagina can usually be treated by radical hysterectomy with radical
vaginectomy and pelvic lymphadenectomy.

- Radiotherapy can be offered to more advanced cases.

Key Points

VIN is difficult to treot os disease is commonly multifocol

Vulval cqncer is very rore, ond mostly found in the elderly postmenopausal potients.
Surgicol treatment is effective especiolly in eorly disease with no nodol metostqses.
ln the recent yeors, extensive rodicol surgery has been reploced by more limited but complete surgery
with adjuvont radiotherapy ond sometimes chemotheropy.
Voginol cqncers ore omong the rorest in the female genital troct offecting the older femoles.
Early voginal concer may be treqted by surgery or internql brachytheropy, while more qdvqnced stoges
are better treoted with radiotheropy.
\-/

- Folliculor Cysts - Corpus Luteum cysts

- Endometriotic Cysts - Theca Lutein Cysts
- lnflammatory Cysts - Germinol inclusion cysts

Ovarian swellings usually present by an adnexal mass which may be either; neoplastic or non-
neoplastic, cystic or solid, benign or malignant, unilateral or bilateral.
Non neoplastic ovarian swellings, also described as functional cysts of the ovary, represent al-
most24% of all adnexal masses encountered in gynaecologic practice.

Fallopian tube

Fig 26-7: Normql ovory & Cystic ovarian swelling

CLASSIFICATION OF NON NEOPLASTIC OVARIAN SWELLINGS, according to their origin:

t. Follicular cysts
2. Corpus luteum cysts
3. Endometriotic cysts
4. Theca lutein cysts
5. Inflammatory cysts (ovarian and tubo-ovarian)

GENERAL FEATURES OF NON NEOPLASTIC OVARIAN SWELTINGS

a. Age incidence: They occur in the child bearing period mostly at extremes of age as in post
pubertal period, young childbearing age, and in the perimenopause,
b. Bilaterality: usually unilateral, except for theca lutein and some endometriotic cyst.
c. Size: small in size (3-6 cm in diameter, rarely exceed 7 cm)
d' Fate: spontaneous regression in few weeks is the rule, except for endometriomas which will
continue a slowly progressive course (see later).
e' Complications: functional ovarian cysts rarely undergo torsion, hameorrhage, or rupture
f. Management: functional cysts of the ovary are managed conservatively except if they reach
considerably large size, or become complicated where surgical treatment, usually via lapa-
roscopy, becomes mandatory

227
228 Non Neoplastic Ovqrion Swellings

1. FOLLICULAR CYSTS
Follicular cysts are the commonest non neoplastic cysts of the ovary. They usually arise from
cyctic over-distension of an atretic follicle, or due to unruptured dominant ovarian follicle. They
mostly occur in younger women in their early childbearing period, and in the perimenopause.
Most follicular cysts will undergo spontaneous regression without treatment unless complicated
by torsion, haemorrhage, or rupture.

PATHOLOGY
r Cysts are usually unilateral, unilocular, small in size (3-7cm), containing clear fluid.
r The cyst wall is thin, lined by granulosa cells that may continue to produce oestrogen caus-
ing menstrual disturbance.
r Follicular cysts of the ovary are commonly encountered with;

Fig 26-2: Folliculor cyst of the ovory Fig 26-3: Folliculor cyst by US

CLINICAL PICTURE AND DIAGNOSIS

A)Symptoms:
L. Asymptomatic: most follicular cysts are only accidentally discovered.
2. Menstruol disorders: in the form of deloyed cycles or intermenstruol spotting may occur due
to persistent oestrogen production by granulose cells
3. Pain: mild pelvic pain is not uncommon. Rarely pain may be severe and acute in cases when
the cyst is large, rapidly growing, or complicated by haemorrhage or rupture.
B) Signs on bimanual pelvic examination:

C) Special Investigation:
t. Pelvic TAS or TVS is the gold stonddrd in diognosis, showing a unilateral, unilocular, thin
walled cyst, < 7.0 cm size, filled with clear fluid, with no internal echoes.
2. Laparoscopy is diagnostic whenever diagnosis is in doubt, or cyst complicated
 Gynaecology 229

2. CORPUS LUTEUM CYSTS

Corpus luteum (CL) cysts are the second most common non neoplastic cysts of the ovary. They
arise from excessive haemorrhage inside the CL during the stage of vascularization. They mostly
occur during the child bearing period, and may occur in association with early pregnancy.
As with follicular cysts most CL will undergo spontaneous regression without treatment unless
complicated by torsion or rupture.

PATHOLOGY:

' Cysts are usually unilateral, unilocular, small in size (3-7 cm), containing haemorrhagic fluid.
I The cyst wall is lined by luteinized granuloza cells continue to secrete progesterone causing
menstrual disturbance.

Fig 26-4: Corpus luteum cyst Fig 26-5: Hoemorrhage in CL cyst by uS

CLINICAL PICTURE AND DIAGNOSIS

a)Symptoms:
1. Asymptomatic in most cases.
2. Menstrual disturbonce: in the form of short delay in cycles or intermenstrual spotting may
occur due to persistent progesterone (pRG) production.
3. Pain: acute lower abdominal pain may be present at one iliac fossa if the cyst is complicated
with haemorrhage or rupture, and may be misdiagnosed as appendicitis.
b)Signs on bimanual pelvic examination:
F Tenderness is commonly elicited at the mid-ovarian point at one iliac fossa
) Tenderness and fullness at one of the vaginal fornices
F A tender cystic adnexal mass may be felt in thin patients.
c) Special Investigations:
1. Pelvic TAS or TVS is the gold standard in diagnosis showing a unilateral, unilocular, cyst , < 7
cm, filled with blood that appears as fine particles within clear fluid.
2. laparoscopy is conclusive whenever diagnosis is in doubt or cyst complicated

DI FFERENTIAL DIAGNOSIS:

F From follicular cyst and simple serous cyst.

) Other causes of pain in right iliac fossa (as appendicitis, renal colic, & ectopic pregnancy)
230 Non Neoplastic Ovoriqn Swellings

3. THECA LUTEIN CYSTS

Theca lutein cysts of the ovary usually develop in response to abnormally high levels of pituitary
gonadotrophins (FSH & LH), or chorionic gonadotrophins (hCG). lt may be either;
a. Spontaneous: due to excessive amounts of natural hCG in circulation as in cases of hyda-
tidiform mole, choriocarcinoma, and multifetal pregnancy.
b. latrogenic: due to large doses of HMG/hCG in ovulation induction protocols

PATHOLOGV
r Cysts are multilocular, commonly bilateral, bluish in colour, thin wolled, containing c/eor
fluid.fhey may reach a large size > 10 cm as with ovarian hyperstimulation (OHSS).
r Cyst wall is lined by luteinized theca cells.

Fig 26-6: Theca lutein cysts Fig 26-7: Germinol inclusion cysts

CLINICAL PICTURE AND DIAGNOSIS

a. History: drugs for induction of ovulation, multifetal pregnancy, or hydatidiform mole
b. Symptoms: Pelvic pain which may be severe resembling acute abdomen
c. Signs on abdominal and bimanual examination:

restricted mobility.

d. Special investigations:
 Gynaecology z)l

4. ENDOMETRIOTIC CYSTS
Endometriotic cysts (also known as endometriomas), occur due to presence of functioning ec-
topic endometrium within ovarian stroma. In many cases they may occur in association with pelvic
endometriosis.

PATHOLOGY
I Endometriotic cysts represent haemorrhagic cysts lined by functioning endometrial tissue
(glands and stroma).
I Blood accumulates within the cyst wall concomitant with time of menstruation
I By time, absorption of the serous element of the retained blood occurs leaving behind RBCs
in a thick dark material giving it a liquid chocolate colour and appearance (chocolate cysts).
Cysts rarely undergo torsion as they are usually fixed to surrounding structures by dense
adhesions, secondary to inflammatory reactions associated with minor fluid leaks.
Cysts rarely rupture spontaneously due to its thicK wall due to a local inflammatory reaction

Fig 26-8: Endometriomo by loparoscopy Fig 26-9: Endometriomo by IJS

CLINICAL PICTURE AND DIAGNOSIS

o. History of infertility: is encountered in a significant group of patients.
o. Symptoms: Dull aching chronic pelvic pain usually associated with dysmenorrhoea.
c. Signs on bimanual pelvic examination:
F Adnexal mass which is markedly tender and almost fixed
) Nodules and tenderness over the uterosacral ligaments may be presenr
d. Specialinvestigations:
> TVS will reveal an adnexal mass with thick wall and turbid contents
> cA 125 may be elevated in most cases but not to very high levels
) Laparoscopy: is both diagnostic and therapeutic when surgical intervention is indicated.

5. INFLAMMATORY CYSTS
Inflammatory cysts may occur in the form of ovarian or Tubo-ovarian cysts or abscess, as a result
of specific or non specific infection.
Infection may reach the ovary either by lymphatic spread, or by direct spread from a nearbv in-
fected organ.
Inflammatory cysts of the ovary are usually bilateral.
232 Non Neoplqstic Ovoriqn Swellings

CLINICAL PICTURE AND DIAGNOSIS

a. History; of recent abortion, delivery, or IUD insertion
b. Symptoms:
F Fever, headache, malaise and generalized bony aches
F Dull aching pelvic pain stimulated by movement
Fig 26-10: Tubo-ovarion mqss
F Deep dyspareunia
Signs on bimanual pelvic examination:

d. Specia I investigations :

Fig 26-L1-: Tubo-ovarian com-

plex by US
shift to left, & toxic granules)

Treatment: (see chronic PlD, tubo-ovarian cyst & abscess).

5. GERMINAL INCLUSION CYSTS

They are microscopic cysts, that result from invagination of the germinal epithelium into the

substance of the ovary, near or after menopause. Previously they were considered of no clinical im-
portance, but now they are regarded as forerunners for ovarian epithelial cancers.

Fimbria
tn I
?.
,"tr1,...
f .' 't
a
tr*
Ovu al on I
, /,s le ? 5
#
Ovary +P

Fig 26-12: Epithetiol cells from the fimbria ore releosed ond implont on the denuded surfoce of the overy ot the
site of ovulation. B& C subsequenyly, an inclusion cyst is formed

MANAGEMENT OF NON NEOPTASTIC OVARIAN SWELLINGS

A) CONSERVATIVE MANAGEMENT
r Small non complicated functional cysts of the ovary are managed conservatively since
spontaneous regression is the rule in most of these cysts.
r During the few weeks of follow up US is used to monitor complete cyst resolution.
 Gynaecology ZJJ

B) MEDICAL TREATMENT
) Gestagens and OCP may accelerate regression of follicular, CL, ond theco lutein cysts
F GnRH agonists, Gestagens, and OCPs may help minimizing rate of growth of endometri-
otic cysts thus prolonging the period of conservative management and avoiding or delay-
ing the need for surgical intervention.
) Antibiotics with specific regimens according to CDC recommendations will allow shrink-
age in size of inflammatory cysts to control the symptoms and size, and avoid the need
for surgical intervention.

c) suRGrcAL TRAETMENT
Large cysts > 7.0 cm, complicated cysts (by haemorrhage or torsion), and persistently growing
ones (like endometriomas) are managed surgically from the start or after an adequate interval of
trying conservative approach and/or medical treatment.
I Laparoscopy is the preferable approach suitable for most cases. Operations include;
1'. Undoing torsion of a cyst before it becomes ischaemic and gangrenous
2' Ovarian cystectomy for cysts that reached large size or starting complication
3. Ova riotomy (remova I of the ova ry) is ra rely an option, only in cases with severe haem-
orrhage or gangrene in which ovarian preservation becomes impossible.

Key points in functional cysts of the ovary

Functionol cysts account for about 24% of all ovorian cysts.

They ore usuolly small in size ond rarely exceed 7.0 cm in diqmeter

The mojority qre discovered incidentqlly during routine pelvic examinotion or tJS

They are sometimes associoted with temporary menstruol disorders

Their fate is generolly spontqneous resolution within few weeks of diognosis

Surgicol intervention, usuolly vio loparoscopy is seldom resorted to in lorge ond complicated cysts
 Clossilication Complicotions
Pathology Clinicol picture
- Epitheliol ovqrian tumours Treatment
- Germ cell tumours
Sex card stromol tumours

CLASSIFICATIONS OF OVARIAN NEOPLASMS

The ovary is a common site for various types of neoplasms that are usually described according
to different classifications which include the following:
A) PATHOLOGfC CLASSIFICATION: Ovarian neoplasms are classified patholoeicallv into benign and
molignont tumours. Benign neoplasms are much more common than malignant ones.
B) Ctf N|CAL CLASSIFICATION: Ovarian neoplasms are clinicallv divided into cystr'c and solid tumours.
Cystic tumours are more common and are mostly benign, while solid tumours are much less
common and are mostly malignant.
C) HISTOGENETIC CLASSIFICATION: The most internationally accepted classification is the WHO his-
togenetic classification based on the cell of origin of the tumour, either from:
Y Surloce epithelium (epithelial tumours)
Y Ovarian germ cells (germ cell tumours)
Y Ovorian stomo (sex cord and stromal celltumours).

1. EPITHELIAT TUMOURS OF THE OVARY

These tumours originate from the surfoce epithelium which embryologically develops into Mul-
lerian and Wolffian epithelium, and can thus differentiate into different types of epithelia. Epithelial
tumours are by far the commonest tumours of the ovary, and are classified into;
a. Serous cystadenoma: lined by cells resembling tubal epithelium.
b. Mucinous cystadenoma: lined by cells resembling cervical epithelium
c. Endometrioid tumours: lines by cells resembling endometrial lining.
d. Brenner tumour has epithelial component similar to transitional epithelium of the urinary
t ra ct.

2. GERM CELL TUMOURS

These tumours originate form totipotent germ cells that may show either;
a. Difierentiation into Embryonic tissue: this will give various forms of teratoma, which con-
tains elements of the three germ layers (ectoderm, endoderm, and mesoderm). This is the most
common germ cell tumour.
b. Dilferentiotion into Extraembryonic tissue: this will give either;
.Trophob|astictissue;withdeve|opmentofg.h.@e,or
.
Yolk sac tissue: with development of volk sac tumour (Endodermal sinus tumour).
c. No diflerentiation of germ cells occur: this will result in the development of dvsserminoma.

ZJL+
 Gynaecology 235

3. SEX CORD STROMAL TUMOUR

These are the least commonly encountered tumours, originating from 2 gonadal elements;
The primitive sex cord; which developmentally gives origin to granulosa cells in the ovary, or
sertoli cells in the testicle. lt may give rise to malignant tumours either Granulosa cell tumour or
Androblastoma (also known as Sertoli-Leydig cell tumour).
The stromo of the gonod; which differentiates into theca cells in the ovary or Leydig cells in the
testicle. lt may give rise to either Fibroma or Thecoma

PATHOLOGY OF BENIGN OVARIAN NEOPLASMS

I. EPITHETIAL OVARIAN TUMOURS

Epithelial tumours are the commonest ovarian neoplasms constituting almost 60-70% of all
ovarian tumours. They are essentially benign but could be either border line or malignant.

A. SEROUS CYSTADENOMA

This is the commonest benign ovorian neoplosm representing nearly tO-:-5% of all tumours of the
ovary. They are bilateral in up to 3Oo/o of cases, usually of moderate sizes (ranging 10-15 cm) when
first detected it may present in one of the following three types.
1. Simple serous cysts: The commonest type of serous cysts. They are unilocular, thin walled, and
filled with thin clear serous fluid. Simple serous cysts have the lowest malignant potential in all epi-
thelialtumours.
2. Multilocular serous cyst: serous cysts may be multilocular, usually with only few locules.

3. Papillary serous cysts: Characterized by the presence of papillarv srowths that may be present
either inside the cyst cavity (endophytic) or outside the external surface (exophytic). The cyst is usu-
ally multilocular. They have the highest malignant potential in all benign cysts (up toSO%risk of ma-
ignant tra nsformation.
I

Microscopically:
Cyst wall is lined by cuboidal cells which may be ciliated or non ciliated (tubal like epithelium).
'
r Psammoma bodies: These represent calcifications within the core of some of the papillae due
to obstruction at the neck and accumulation of secretions. They occur occasionally in benign
serous cystadenoma, but more frequent in well differentiated serous cystadenocarcinoma.
They have no clinical significance, but may appear as calcified radio-opaque shadows in pelvic
X-ray.

Fig 27-1: Simple serous cyst Fig 27-2: Popillary serous cyst
236 Benign Ovqrion Neoplasms

B. MUCINOUS CYSTADENOMA

These are the second most common benign ovarian neo-

plasms. They are usually unilateral, having a bluish or yellowish
transparent colour. Although essentially benign mucinous
cystadenomas may have a very low malignant potential (<5%)
. Cut section: Mucinous cystadenomas are characterized by
being multilocular with plenty of locules containing thick ge-
Fig 27-3: Mucinous cyst
latinous like mucin material. They are known to reach huge
sizes sometimes filling the entire abdominal cavity.

. Microscopically: Cyst wall is lined by tall columnar epithelium with basally situated nuclei similar
to endocervical epithelium, rich in Goblet cells.
. Pseudomyxomaperitonii:
This is a rare condition, in which huge amounts of gelatinous mucin material are found free in
the peritoneal cavity. Most cases occur in association with rupture of a pre-existing mucinous cyst,
but may occur rarely secondary to; peritoneal epithelial metaplasia, rupture of mucocele of the ap-
pendix, or in association with cancer of the colon.

Diagnosis is seldom made before laparotomy, and prognosis is poor even after surgery, as re-
accumulation of gelatinous material after removal is the rule. The 5 years survival is around 50%.
Treatment: Chemotherapy (radioactive intraperitoneal colloid installation), after surgical removal of
the tumour and contents is evacuated.
C. BRENNER TUMOUR

These are rare tumours that account for only L-2% of all ovarian neoplasms. They probably arise
from Wolffian metaplasia of the surface ovarian epithelium, and are bilateral in only IO-15% of cas-
es, being more prevalent in women > 40 years. The majority of tumours are benign, but border line
or malignant tumours have been reported.
o Brenner tumours are solid in consistency, usually of small (< 2 cm) to moderate size, and about
half are incidental findings discovered only by the pathologist on examining specimens.
. Microscopically: the tumour is characterized by epithelial cell nests with characteristic coffee
bean nuclei.
. Hormonal function: occasionally some of Brenner tumours may secrete oestrogen and may even
present by vaginal bleeding (i.e.; functioning Brenner tumour).
si

Fig 27-4: Brenner tumour

Fig 27-5: Coffee beon appearance by microcopy
 Gynaecology zJt

II. GERM CELL TUMOURS

Germ cell tumours constitute almost 20-30% of all ovarian neoplasms, occurring mostly in the
younger women < 30 years age. They are generally benign tumours.

ftg 27-6:
Fig 2/-6: Biloteral cysts
tsiloterql dermoid cysts Fig 27-7: Cutsection in dermoid cystwith hairond cartiloge

A. BENIGN CYSTIC TERATOMA (BCT)

BCT, also known as dermoid cysts, is the only germ cell tumour which is common. They repre-
sent almost 50% of ovarian neoplasms occurring in young females below 20 years of age. BCT is
also the commonest ovarian neoplasm encountered during the childbearing period and especially
during pregnoncy.
BCT are bilateral in up to 12% of cases. They are usually of moderate size (5-10 cm) when first
discovered and rarely reach huge sizes. Most cysts have a long pedicle that makes them more liable
to complications as torsion.
o Cut section: Cysts are greyish in colour, mostly unilocular, but may contain few small locules,
with one larger locule containing a mamilla (a small solid knob <2cml, and variable tissue con-
tents including hair, teeth, bone, and cartilage, mixed in a sebaceous material.
. Teratomas are derived from toti-potent germ cells and can differentiate into all three embryonic
germ cell layers (ectoderm, mesoderm, and endoderm). lt is thought that this may occur via par-
thenogenesis; a form of asexual reproduction in which the ovum develops without fertilization.
- Ectoderm.' skin, hair, sweat and sebaceous glands (most predominant tissue).
- Mesoderm.'bone, cartilage and smooth muscle.
- Endoderm.'thyroid, bronchus, and intestinal tissue
. Microscopically: cyst wall is lined by strotified squomous epithelium with sebaceous glands.
o BCT have very low malignant potential <1% (squamous cell carcinoma).
N.B.: Most tumours are asymptomatic, incidentally discovered, unless complicated by torsion, rup-
ture or infection.
B. STRUMA OVARII
Rarely a teratoma may be composed of a single tissue, in which the term monodermal teratoma
is used. Struma ovarii is an example of a monodermal teratoma that is composed of hormonally
active thyroid tissue. They comprise only I-4% of cystic teratomas, with only 5% capable of produc-
ing sufficient thyroid hormone to produce symptoms. Some 5-10% of tumours develop into carcino-
ma.
238 Benign Ovarian Neoplasms

C. GONADOBLASTOMA
A benign solid tumour composed of germ cells mixed with other cells resembling granulosa and
sertoli cells. Although gonadoblastoma is initially benign, half of these tumours may predispose to
development of Dysgerminoma or other malignant germ cell tumours. Almost all patients with a
gonadoblastoma have an abnormal gonad, with a Y chromosome in 90% of cases.
N.B.: Prophylactic gonadectomy should be performed in patients with dysgenetic gonad, particular-
ly with a Y chromosome for fear of future development of malignant neoplasms.

III. BENIGN SEX CORD STROMAL TUMOURS

These tumours represent < 4% of all ovarian neoplasms. They are almost always benign.
A. FIBROMA:
Fibromas are rare tumours derived from stromal cells, seen mostly in women around age of 50
years. They are benign, solid, tumours, unilateral in >90% of cases, usually mobile with a long pedi-
cle and a lobulated glistening white surface.
Ascites may occur with many of the larger fibromas giving the picture of Meig's syndrome in on-
ly t% of cases. (Meig's syndrome is the association of ovarian Fibroma with ascites and right side
pleural effusion that disappears on removal of the tumour).

B. THECOMA (THECA CELL TUMOUR):

Theca cell tumours are rare, with the majority occurring in post menopausal women, Almost all
are benign, solid, and unilateral.
Many thecomas are functioning tumours, producing oestrogen in sufficient amounts to cause,
endometrial hyperplasia, postmenopausal bleeding and rarely endometrial carcinoma.
r Microscopically; tumour is formed from cells resembling theca interna cells.
COMPLICATIONS OF BENIGN OVARIAN NEOPLASMS
Benign ovarian tumours are liable to several complications that may form the main presenting
clinical picture in many cases. These include; torsion, haemorrhage, rupture, infection, incarcera-
tion, and malignant transformation.

1. TORSION:
Twisted pedicle
It is the commonest complication. Torsion may be gradual or
sudden, incomplete or complete and it may be initiated by a
sudden movement of the patient.
Gradual incomplete torsion; leads to congestion, enlarge-
ment of the tumour and thrombosis.
Sudden complete torsion; causes sudden occlusion of the
arterial blood supply leading to necrosis and gangrene of
the cyst. Fig 27-8: Torsion ovarian cyst
o Factors predisposing to torsion:
1,.Moderate size tumours with long pedicle of the cyst: BCT is the commonest tumour to undergo
torsion due to its long pedicle and fat content, another common example is simple serous cyst.
Large tumours cannot usually undergo rotation.
2. Free mobility with obsence of surrounding adhesions; facilitate torsion, whereas fixed tumours
do not undergo rotation.
3. Pregnoncy and puerperium: Due to displacement of the tumour by pregnancy and laxity of ab-
dominal wall after delivery.
 Gynaecology 239

. Clinical picture: is that of dcute obdomen, where the tumour is tense and tender on palpation.
o Treatment:
v a. Ovariotomy (removal of the entire ovary), usually via laparotomy, is the treatment of
choice in a gangrenous cvst, in absence of viable healthy ovarian tissue.
b' Ovarian cystectomy: untwisting of the pedicle and removal of the cyst with preservation
of the ovary has a place if there is still adequate healthy ovarian tissue present.
2. HAEMORRHAGE:
Haemorrhage in a cyst may occur as a result of torsion, trauma to the abdomen or may occur
spontaneously especially during pregnancy.
. Clinical picture: is that of ocute obdomen, where the tumour is tense and tender on palpation.
. Treatment: Ovariotomy usually via laparotomy.
3. RUPTURE:
v Rupture of an ovarian cyst may occur as a result of torsion or haemorrhage, or may be trau-
matic, during labour or due to rough vaginal examination.
v
. Clinical picture:
v a. Severe pain with picture of acute abdomen (abdominal wall rigidity, tenderness, and rebound
tenderness)
v b. Internal haemorrhage may occur with the picture of hypovolaemic shock (tachycardia, hypo-
tension, and oliguria). Palpation reveals dullness in the flanks with shifting dullness.
c. Rupture of a dermoid cyst may lead to severe chemical peritonitis, while rupture of a mucin-
ous cystadenoma may lead to pseudomyxoma peritonii.
o Treatment:
v a. Sedatives to alleviate pain
b, Resuscitation of the patient to restore the B.P., by lV fluids or blood transfusion, etc...
c. Ovariotomy done as an emergency procedure usually via laparotomy, and peritoneal lavage
v performed to remove contents of the cyst.

v 4. |NFECT|ON:
Ovarian cyst may be infected either;
the puerperium (following abortion or labour), or
In

- From a nearby infected organ (as appendicitis or pyosalpinx), or

- Following torsion (due to adhesions).
. Clinical picture:
- General picture of infection as general malaise, fever, tachycardia, tachypnea, etc...
Bimanual examination shows a fixed, tender tumour with rapid increase in size.
v o Treatment:
- Antibiotics to control infection (broad spectrum + anaerobic types)
- Ovariotomy, via laparotomy for removal of the whole ovary.
- 5. INCARCERATION:
Ovarian cyst may be impacted in Douglas pouch, particularly in large size tumours.
o Clinically: it may cause pressure symptoms on bladder and rectum. During pregnancy it may
cause obstructed labour,
r Treatment is by surgical removal of the tumour by ovariotomy or cystectomy, once incarcer-
ated.
240 Benign Ovqrian NeoPlasms

5. MALIGNANT TRANSFORMATION:
_ potential of malignancy is higher in solid rather than cystic tumours.
- Papillary serous cystadenoma has malignant potential up to 50%.
Mucinous cystadenoma has a 5% incidence of malignant transformation'
- Benign cystic teratoma carries less than t% risk of malignancy.

CLINICAL PICTURE OF BENIGN OVARIAN NEOPLASMS

A)SYMPTOMS:
1. Asymptomatic: many of the benign ovarian tumours are discovered only
incidentally during a routine clinical pelvic or gynaecologic examination, or
during ultrasonographY.
2. Abdominal swelling: may be felt by the patient only if the tumour is large'
3. Lower abdominal pain: and heaviness over the site of the tumour, may
be; Fig 27-9:
_ Acute pain; if the tumour is complicated by torsion, rupture, haemor-
rhage, or infection.
- Chronic dull aching pain; in large-sized swellings as in mucinous cystadenoma.
4. Pressure symptoms: if the tumour is huge or incarcerated.
- Abdominal pressure symptoms; Epigastric pain, dyspnoea and palpitation.
- Pelvic pressure symptoms: Frequency of micturition, retention of urine.
5. Menstrual disorders: ovarian neoplasms are usually not associated with menstrual disturb-
ances, except in rare functioning tumours (theca cell tumour & functioning Brenner).

B. PHYSICAL SIGNS: These will depend largely on the size of the tumour.
1. Smaf f tumours: are only detected on bimanual pelvic exomination, felt on one side of the uter-
us, as rounded, smooth, mobile, usually cystic ( rarely solid) mass, separate from the uterus (the
movement of the mass is not transmitted to the cervix).
2. Large tumours: can be detected by abdominal exomination
I nspection : sym metrica I a bdo m na I en a rgement'
i I

- palpation: abdominal mass that may be central or to one side of the midline, with a well
defined upper and lateral border, smooth or lobulated surface, usually tense, commonly
mobile from above downwards.
, Percussion; central dullness is elicited on the mass, with resonant flanks (except if associat-
ed with marked ascites, where flanks become dull with shifting dullness).
. in excessively large cyst ovarion cachexia may occur due to the rapidly growing tumour'

C. SPECIAL INVESTIGATIONS:
Ovarian swellings can be suspected clinically but always need further confirmation by:
1. Ultrasonography: This is the gold standard in diagnosis of ovarian swellings.
U.S. is important to diagnose the ovarian origin of the swelling and differentiate between
benign and malignant tumours.
Smaller tumour are best detected by TVS, while larger ones by TAS
- Both TAS and TVS can differentiate between unilateral and bilateral tumours, cystic and
solid ones, unilocular or multilocular cysts, and suspicions for malignancy (heterogeneous
echogenicity of the tumour, low resistance Doppler indices, presence of ascites, etc...').
 Gynaecology 241

2. Tumour markers: to exclude malignancy

- CA-125 is significantly elevated in epithelial ovarian cancer, however it may be also elevat-
ed in benign conditions as endometriosis and endometriomas
CEA and CA 19-19 are peculiarly elevated with mucinous carcinoma
3. Laparoscopy:
May be indicated if ultrasonography was inconclusive in evaluation of an adnexal swelling as in
differentiating between;
Ovarian cyst and tubal or tubo-ovarian cystic masses, or

Solid ovarian fibroma and pedunculated subserous myoma SSM.)

4. l.V.P.: may be beneficial in larger tumours to delineate the course of ureter.

TREATMENT OF BENIGN OVARIAN NEOPLASMS

The aim of treatment in benign ovarian neoplasms is surgical removal of the tumour, with or
without the affected ovary, for fear of complications as; torsion, rupture, and malignant transfor-
mation. The type of operation depends upon the age of the patient, her desire for future pregnan-
cies, together with the size and type of the tumour, and whether complicated or not.

1. OVARIAN CYSTECTOMY:

ft consists of shelling out or enucleation of the cyst with preseruotion of the ovory.lt is indi-
cated in young patients and particularly with bilateralcysts of smallsize as in dermoid cysts. Ovarian
cystectomy may be done either by loparotomy or by loporoscopy.
- Laparoscopic ovarian cystectomy is best reserved for the young women (< 35 years) with
small sized cyst. Cyst fluid may be sent for cytological examination.
- Dermoid cysts (BCT) are better removed by laparotomy rather than laparoscopy as lapa-
roscopic surgery may carry the risk of dissemination of its irritant contents.
- Larger cysts are better treated by oophorectomy (see later), because of difficulty in enu-
cleation of the cyst without rupture and dissemination of its contents, together with ab-
sence of adequate healthy residual ovarian tissue to be left. Fear of malignancy is also an
additional factor especially in larger, bilateral, and solid tumours.

nqr+dJtrus,

Fig 27-10: Ovorian cystectomy operation (enucleotion of the cyst and closure of the bed )
.,,
A.
Ben ig n Ova ria n Neoplasms

2. OOPHORECTOMY:
lt consists of removal of the whole tumour together with the ovary. The word ovariotomy is a
synonym still used by tradition to describe the same procedure however; oophorectomy is the
more correct term. Both the infundibulopelvic ligament, (lateral to the tumour and contains the
ovarian vessels, nerves & lymphatics), and the ovarian ligament (medial to the tumour and
attached to the uterus), are clamped and double ligated. The mesovarium can be clamoed
se pa rate ly

Oophorectomy can be performed via laparotomy in all kinds

of ovarian tumours. Laporoscopic oophorectomy can be safely
established only in smaller neoplasms. Removal of larger cysts by
laparoscopy remains controversial over the issue of dissemination
of the cyst contents including irritant fluid as in dermoid cyst, pa-
pillae, mucinous material, and possibly malignant cells. Any ascitic
fluid detected should be aspirated and sent for cytology.
3. PAN HYSTERECTOMY:
lf the patient is premenopausal, and has completed her fami-
ly, total abdominal hysterectomy with bilateral salpingo-
oophorectomy (TAH BSO) is usually indicated. This is considered
as a preventive step against the future development of ovarian cancer Fig 27-71: ovoriotomy

by advance of age.

PAROVARIAN CYSTS
Parovarian cysts are not ovarian in origin. They arise from cystic dilatation in the Wolffian
ducts remnants in a tubule of the Epoophoron between the layers of the broad ligament just be-
low the fallooian tube.

PATHOLOGY

Parovarian cysts are usually small to moderate in size rarely exceeding over ten centimetres in
diameter. Cysts are covered by peritoneum, with the fallopian tube being characteristically
stretched over their upper surface. They are thin-walled, unilocular, lined by flattened epithelium
(cubical) and contain clear fluid, They do not tend to be malignant.

CLINICAL PICTURE

They are usually asvmptomatic, incidentally discovered during regular pelvic examination, dur-
ing pelvic ultrasonography, or during laparotomy or laparoscopy for any other condition.

DIAGNOSIS
. Clinically: Parovarian cysts are always unilateral, usually fixed displacing the uterus to the oppo-
site side, free of any tenderness on bimanual examination.
. On ultrasonography: the cyst is thin walled, unilocular, echolucent, with no internal echoes or
solid areas. The ovary can be seen separate from the cystic mass especially on TVS.
. At operation: the nature of the cyst is recognised by finding the Fallopian tube stretched over it
and by the fact that the ovary is separate from the cyst, usually attached at a point on the pos-
terior surface of the cyst.
 Gynaecology z+J

TREATMENT

Surgical excision of the cyst by enucleation after incising the overlying peritoneum
is the only
treatment of parovarian cysts. The cavity left is obliterated by sutures and complete haemostasis
is
ensured to prevent haematoma formation.

The procedure can be performed both by laparotomy or laparoscopy according to

tumour size
and surgical facilities.

In the case of large cysts burrowing deeply in the pelvis care is required not
to injure the ureter
or uterine artery.

Key points in benign ovarian tumours

ovorian neoplosms are clossified according to their cett of origin into epitheliol, germ cell,
ond sex cord
stromal tumours
Benign epitheliol ovorian tumours (serous, mucinous, and popitlary cysts) are the
commonest tumours en-
countered, rega rd le ss wome n's age.
Germ cell tumours are generally rare except for BCT, which is the commonest germ
cell tumour, qnd is the
commonest ovorion neoplosm in young ond pregnant femoles.
Benign cystic tumours include; seroLts, mucinous, papiilary cystodenomos, ond BCT.
Benign solid tumours include; Brenner tumour, strumq ovorii, gonodoblostoma,
fibromo, ond thecomo.
They ore generolly rqre compared to cystic tumours

Clinicolly most ovarion neoplasms ore silent and asymptomatic except if torge size,
or if presenting with o
complicotion os; torsion, hoemorrhoge , rupture, infection, incorcerotion, and malignant
tronsformotion
Clinicolly lorge tumours can be polpated by abdominal exomination, intermediate
and smaller size tumours
con be felt through bimonuol vaginol exomination except in the obese patient,
Pelvic ultrosonography whether TAS or TVs is the gold standard in diognosis of
ovorian swellings. IJS can
also give accurate doto about the noture of the tumour, its biloterolity, its consistency,
unilocular or multi-
loculor, its malignant noture, qnd associated ascites, uterine, or odnexot masses.
Tumour markers, Loporoscopy, lvP, cT and MRI may be of hetp in certoin coses, especiaily if molignancy is
suspected.
Treatment of benign ovarion neoplosms is olways through surgical excision or enucleation
of the cyst olone
(ovorion cystectomy) or with the entire ovary (ovariotomy, ovoriectomy, or oophorectomy),
usually via lop-
arotomy or sometimes via laparoscopy in selected cases.
Abdominal hysterectomy, whether total or subtotol, is reserved only to the larger tLtmours,
in the older or
the menopausol patients, especially if the tumour was solid or bilateral, os prophylaxis ogoinst
future
threat of molignoncy.
 Clossificotion - Clinicol picture
t Epitheliql ovorion concer - Special investigations
t Molignont germ cell tumours , Surgicol treatment
t Malignqnt sex-cord stromal tumours Chemotheropy
- Potterns of spread Rodiotion theropy
Staging of ovorian cancer

INTRODUCTION AND OVERVIEW

Ovarian cancer is the third most common malignancy of female genital organs, after cancer of
endometrium and cervix, but is the most lethal of them all. More women die from ovarian cancer
than from carcinoma of the cervix and body of the uterus combined.
Most malignant ovarian tumours are epithelial in origin, non epithelial ovarian cancer (germ
cell and sex-cord tumours) are much less common. Ovarian cancer is generally rare before 35 years
of age but significantly increase by advancing age especially with a peak at 50-70 year old age
group.
Unfortunately the majority of cases with ovarian cancer are discovered after the disease has
already spread beyond the ovary giving generally poor prognosls.
Surgery is the mainstay in treatment both for staging and therapy. Adjuvant chemotherapy has
a major role following surgery in more advanced stages as the majority of tumours, especially epi-
thelial, show good response to chemotherapy. Some malignant germ cell tumours show good re-
sponse to treatment by radiotherapy.

H ISTOG EN ETIC CLASSI FICATION OF MALIGNANT OVARIAN TUMOURS

1. Epithelial ovarian cancer
o. Serou s ad e noco rci n om o
b. M ucino us ad e noco rci n omo
c. E nd ometrioid od e noca rci noma
d. U ndilfere ntiated o de nocorci no mo
2. Germ celltumours
o. Dysgerminomo OVAThN qRCNOM- SICONDARY
TO €AIOrcilA Of THE UIEIUS
b. Endodermol sinus tumour
c. Choriocarcinomo
d. Molignont terotoma
3. Sex cord stromaltumours
o. Gronuloso cell tumour
b. Androblostoma : Sertoli-Leydig cell tumour
c. Gynandroblostomo
4. Metastatic tumours
Fig 28-L: molignont ovorion tumour

244
 Gynaecology 245

EPITH ELIAL OVARIAN CANCER

Epithelial ovarian cancers are the commonest malignant neoplasms arising from the ovary
and constitute almost 60-70% of all ovarian cancers. They are either serous, mucinous, or endome-
tri oi d ade noca rci n om o s.
Epithelial ovarian cancers usually occur at older ages near to menopause. They grow rapidly,
usually without significant symptoms, leading to a delay in their diagnosis with almost 2/3 of cases
being first diagnosed at stage 3 (tumour has spread outside the capsule of the ovary with associat-
ed ascites and peritoneal implants), giving an over all poor prognosis.
Epithelial ovarian cancer is usually associated with markedly elevated levels of cA-125 which is
considered an important tumour marker that correlates with the stage of the disease. Most tu-
mours are chemosensitive, showing good response to adjuvant chemotherapy after primary sur-
gery.

AETIOLOGY
The aetiology of epithelial ovarian cancer is unknown. Possible aetiologic factors include:
1. Reproductive Factor:
Nulliparous women, and women with low parity, have a higher risk than parous women to de-
velop epithelial ovarian cancer. This may be related to the continuous, repeated, minor trauma of
the surface epithelium of the ovary caused by uninterrupted ovulation. Evidence to this postulation
includes:
a. Prolonged suppression of ovulotion.' as that occurring during pregnancy, lactation, and pro-
longed use of OCP is associated with decreased incidence of epithelial ovarian cancer.
b. Prolonged and repeated use of drugs for induction of ovulotion: as in treatment of anovula-
tory infertility or ovarian super-ovulation protocols in lCSl & IVF procedures, has been associ-
ated with a slightly increased risk of ovarian cancer after several years of cessation of treat-
ment.
2. Hereditary'Genetic' factor:
Five to
L0% of epithelial ovarian cancer will occur in women with hereditory predisposition i.e.
two or more relatives had ovarian or breast cancer. A woman with a single first-degree relative with
ovarian cancer has a relative risk of approximately 3.6 for developing ovarian cancer compared with
the general population. Three types of familial ovarian cancer are identified:
a. Site specific ovarian cancer syndrome (15%)
b. Hereditary breast / ovarian cancer syndrome (75%)
c. Hereditary non polyposis colorectal cancer syndrome with endometrial, breast, or ovarian
cancer (10%, Lynch type il).

' A particular feature of familial cancer is that it tends to occur at a younger age group.

' Genetic predisposition to epithelial ovarian cancer is due to gene mutations in the breast
-ovarian cancer tumour suppressor genes BRCA1 and BRCA2. These genes account for
most cases of familial breast and ovarian cancer
246 M o ligno nt Ovqriq n Neo plosms

RISK FACTORS FOR EPITHELIAL CANCER

1. Age: Increasing age is the strongest patient-related risk factor. The mean age at diagnosis
is 59 years and the risk of malignancy increases with advancing age.
2. Nulliparity & infertility; are associated with increased risk, compared to multipara.
3. White race: have more prevalence compared to black and African women.
4. Prior history of endometrial or breast cancer in the same patient.
5. Family history of ovarian cancer in first degree relatives.
N.B: Multiparity, prolonged lactation, and prolonged use of OCP seem to have a relatively protective
effect against epithelial ovarian cancer.

PATHOLOGY OF EPITHELIAL OVARIAN CANCER

A. Macroscopic appearance:
Most epithelial ovarian cancers have both cystic and solid elements, with marked variation in
the tumour size and consistency. The substance of the tumour is the seat of extensive haemorrhage
and necrosis.
At laparotomy, in early stage disease the tumour is usually unilateral with intact capsule. In
advanced stages, the tumour may be bilateral, the capsule may be ruptured, and the tumour may
be fixed to adjacent structures as the uterus, bladder, colon, etc...
B. Microscopic picture:
o Histofogicaltypes include adenocarcinomas of the Serous, Mucinous, or Endometioid,types.
. Tumour grading: each histologic type is graded according to cell differentiation into;
L.Well differentiated tumours (Grode f; showing malignant cells with a preserved glandular
oattern
2. Moderotely differentiated tumours (Grode lf; showing sheets of highly malignant cells
with presence of limited glandular pattern.
3.IJndilferentiated tumours (Grode llt) showing only sheets of highly malignant cells with
absence of a well defined glandular pattern.
. Serous cystadenocarcinoma: involve both ovaries in over 50% of cases and usually have both
cystic and solid components. Psammoma bodies, concentrically laminated concretions, are a
frequent histologic fi nding.
. Mucinous cystadenocarcinoma: are multilocular, bilateral in only 20%of cases, and contain mu-
cinous fluid with solid and cystic components. They may reach huge size, and in <5% of cases
concomitant pseudomyxoma peritonii may be present.
o Endometrioid tumours: are usually malignant, and closely mimic endometrial cancer in histo-
logic appearance. In around 30% of cases there is a coexistent second primary in the endome-
trium.

mours are mostly serous or mucinous, they occur in younger

age, and usually have a better prognosis.

Fig 28-2:
 Gynaecology 241

MALIGNANT GERM CELL TUMOURS

Germ cell tumours are derived from primordial germ cells of the ovary, and
compris e 20-25%
of all ovarian tumours. only 5% of germ cell tumours are malignant, they include
dysgerminomo,
endodermal sinus tumour, (yolk soc tumour), choriocarcinomo, and molignont
teratomd.
SPECIAT FEATURES OF MATIGNANT GERM CELL TUMOURS
Malignant germ cell tumours differ from epithelial ovarian cancer in the following;
a' Age incidence: Malignant germ cell tumours occur at a generally younger age group of wom-
en accounting for more than 2/3 of all malignant ovarian neoplasms in women <
30 years of
age' They should be suspected whenever a unilateral solid tumour is diagnosed
by US in a
young female.
b. Associated tumour markers: Most germ cell tumours produce
substances in the circulation that can be used as specific
markers, including lactic dehydrogenase (LDH), human chori_
onic gonadotrophins (hCG), and alpha feto protein (AFp).
c. Association with abnormal gonads: Germ cell tumours are
the commonest tumours occurring in patients with abnormar
gonads and in sex chromatin negative femares.
d. sensitivity to irradiation and chemotherapy: In contrast to
epithelial ovarian cancers, many of the malignant germ cell
tumours are radiosensitive giving a good response to postop_
i
erative radiotherapy, while others give better response to
chemotherapy.
a'
e. The place for conservative surgery: Unilateral salpingo_
oophorectomy is an appropriate treatment option in stage la
tumours when the patient is young and desirous for further Fig 28-3:
fertility preservation (Fig 2S-3).
A) pYSGERMTNOMA:
Dysgerminoma is the commonest malignant germ cell tumour although it
represents only 1-
3% of all ovarian cancers. lt occurs predominantly in young females aged
10-30 years. In 5% of cas-
es it occurs in patients with abnormal gonads, as in gonadal dysgenesis, or
testicular feminization
syndrome, In such cases dysgerminoma may arise in a gonadoblastoma. A
dysgerminoma may se-
crete LDH, which may serve as specific tumour marker.
PATHOLOGY:
o Macroscopically: lt is a solid ovarian tumour, usually of smoll or moderotesLe, bilateral in only
1'0%of cases. lts colour is greyish with lobulated surface. on cut section there is tendency
to
haemorrhage and necrosis. Dysgerminoma is more liable to early tymphotic
spreod to pelvic
and para aortic nodes
' Microscopically: lt consists of gem cells arranged in alveoli or nests separated
by fibrous tissue
septa' The cells are rounded, large, with abundant cytoplasm and large vesicular
nucleus. A
lymphocytic infiltrotion of the stroma is a characteristic feature.

B) ENDODERMAL SINUS TUMOUR "EST":

EST or yolk sac tumour is the second most common malignant germ
cell tumour of the ovary,
but comprises only L% of all ovarian cancers. The tumour is prevalent in young
women with a medi-
an age of 19 years, and rarely affects women over 40 years.
Most EST are associated with elevated serum levels of otpha-fetoproteins that
are used as a
tumour marker. Coexistent teratomas are found in 20% of patients.
248 Molignont Ovqrian Neoplasms

PATHOLOGY:
. Macroscopically: Small solid tumours which are almost always unilateral.
. Microscopically: characterized by Shiller-Duvol bodies, which are cystic spaces in which pro-
jects glomerulous-like structure with a central vascular core.

c) cHoRrocARClNoMA:
These tumours are very rore.
-
Macroscopically: it is usually a unilateral, solid, tumour'
Microscopically: it reveals sheets of malignant cytotrophoblasts and syncitiotrophoblasts
-
They secrete hCG and may present with precocious pseudo-puberty. They have poor progno
sis, and unlike gestational trophoblastic choriocarcinoma they do not respond well to chemothera-
pv.

D) MALIGNAT TERATOMA:
This rare malignant germ cell tumour may occur in one of two forms;
1. lmmature teratoma (malignant solid teratoma); is rare and accounts for 1% of all ovarian terato-
mas. lt characteristically occurs in children under 15 years of age.
- Macroscopically; it is usually a unilateral solid tumour. The cut section showing areas of
haemorrhage and necrosis.
- Microscopically; it reveals predominance of immature (i.e. embryonic type) of neural tissue
but epithelial and mesenchymal tissue may be also detected. lt does not produce AFP or
hcG.
2. Malignant transformation in a benign cystic teratoma (dermoid cyst); is very rare occurring in
<!% of BCT. lt predominantly changes into squamous cell carcinoma, and usually occurs in post-
menooausal women.

MALIGNANT SEX.CORD STROMAL TUMOURS

Malignant sex cord stromaltumours may arise from functioning or non functioning stroma
1. Functioning sex-cord tumours may give rise to:
- Granuloso cell tumour,' with oestrogenic activity.
- Sertoli-leydig cell tumour; with androgenic activity
- Gynandroblostoma; a rare tumour with both oestrogenic and androgenic effect.
2. Non- functioning stroma may very rarely give rise to fibrosorcomo of the ovary.

A) GRANULOSA CELL TUMOURSi -

These are functioning low grade cancers that account for around 5% of ovarian malignancies.
They are slowly growing and generally confined to the ovary when they first presenU therefore
they usually carry a good prognosis.T5% of granulosa cell tumours secrete hormones namely oes-
trogen, while others appear to secrete inhibin.
Oestrogen secreting tumours may lead to pseudo-precocious puberty in prepubertal girls. lt may
cause irregular menstrual bleeding, or postmenopausal bleeding depending on the age of the pa-
tient at presentation.|n25%-50% of cases, granulosa cell tumours are associated with endometrial
hyperplasia, and in 5% with endometrial carcinoma especially in postmenopausal patients.
. Macroscopically: Tumours are usually unilateral, solid, yellow or yellow-grey in colour.
. Microscopically: The tumour is formed of granulosa cells arranged in different patterns. ColI-
Exner bodies are pathognomonic, but are present in only 5O% of cases. These are cystic spac-
es surrounded by granulosa cells arranged in a rosette like shape.
 Gynaecology 249

B) SERTOLT-LEYp|G CELL TUMOURS:

These are among the rarest of all ovarian tumours comprising < 0.2% of such tumours, which
are of low grade malignancy occurring mostly in young women 20-30 years of age.
The majority of Sertoli-Leydig tumours are androgenic, and in
75% of cases they will cause a state of deleminisotion at first, fol-
lowed later by virilizing efiects in the form of acne, hirsutism, clit-
eromegaly, deepening of voice, and increased muscle bulk. Rarelv
some tumours may produce oestrogen.
o Macroscopically: tumours are almost always unilateral, solid,
small or moderate in size.
o Microscopically: they contain either Sertoli or Leydig cells, and ov4tlrN qRol\sA-stcoNoaRY
ro c4ct%Ot rtr uEt6
in the case of the latter may be accompanied by stroma oe-
rived fibroblasts.

M ETASTATIC OVARIAN CANCER

Metastatic ovarian cancer forms about 5-6 % of all ovarian tumours. The primary may arise
from genital tumours; from cancers of the endometrium, tube, contra lateral ovary, and very rarely
from the cervix, or extra genitaltumours; from cancers of the breast, GIT (as stomach, colon, & bili-
ary tract), or the thyroid gland.
Pathologically it is classified into 2 types;
A. Typical metastatic cancer; which resembles the primary cancer
B. Atypical metastatic cancer; e.g. Krrikenberg tumour (see below)

lt accounts of 3O-40% of metastatic cancer to the ovary. The primary is usually in the pylorus of
the stomach, less commonly in the colon, breast or biliary tract.
o Macroscopically: Krukenberg tumours are bilateral solid ovarian tumour retaining the shape of
the ovary. The main interest is in its histogenesis; the most acceptable theory is that malignant
cells reached both ovaries by retrograde lymphotic spreod.
. Microscopically: characteristic microscopic feature is the srgnet ring cells in which the nucleus
is pushed aside by abundant cytoplasm.
Prognosis is bad, where most patients die within one year because most of the lesions are not dis-
covered until the primary disease is advanced.
PATTERNS OF SPREAD OF OVARIAN CANCER
1. Direct extension to adjacent organs such as tube, uterus, colon and bladder.
2. Trans-coelomic spread, by exfoliation of surface cells into the peritoneal cavity, giving deposits
in the pouch of Douglas (felt as nodules on PV examination), right paracolic gutter, surface of
the right lobe of liver, right hemi-diaphragm and surface of intestine or omentum forming an
omental cake (pathway of peritoneal fluid).
3. Lymphatic spread mainly to para-aortic lymph nodes.
4. Haematogenous spread is always late and uncommon. This would be to vital organs such as
the liver parenchyma, lung, brain and bones.
250 M a li gno nt Ovoriq n Neoplosms

STAGING OF OVARIAN CANCER

Surgical staging for ovarian cancer via laparotomy is the only standard method for staging,
since attempts at staging the disease based on data obtained on clinical examination and special
investigations is of limited importance in affecting the prognosis and line of treatment,

SURGICAL STAGING OF PRIMARY OVARIAN CANCER:

This is performed through an exploratory laparotomy, via a mid line subumbilical suprapubic
abdominal wall incision in which the following is performed:
t. Exploration of the pelvic and peritoneal cavity to asses whether the tumour is confined to one
or both ovaries, or extending to other pelvic or abdominal organs.
2. Aspiration of any ascitic fluid present (or perform saline peritoneal washings if no ascites pre-
sent)for cytologic examination to detect malignant cells in the peritoneal cavity.
3. Performing a TAH-BSO, together with Infracolic omentectomy, and pelvic and para-aortic lymph
node sampling, whenever possible.
Resection of any visible enlarged nodules or masses in pelvic or abdominal cavities, or any pelvic or
extrapelvic tumour masses >2.0 cm (debulking or cytoreductive surgery).

FIGO STAGING OF OVARIAN CANCER 2018: (simplified SURGICAL STAGING)

FIGO Stage Stage Description*

I The cancer is only in the ovary (or ovaries)

The cancer is in one ovary, and the tumor is confined to the inside of the ovary. No
A cancer cells are found in the fluid (ascites) or washings from the abdomen and pel-
vis.
The cancer is in both ovaries. No cancer cells are found in the fluid (ascites) or wash-
B
ings from the abdomen and pelvis.
The cancer is in one or both ovaries. Cancer cells are found in the fluid (ascites) or
C
washings from the abdomen and pelvis.
The cancer is in one or both ovaries and has spread to other organs (such as the
tl
uterus, bladder, the sigmoid colon, or the rectum) within the pelvis.
The cancer has spread to or has invaded (grown into) the uterus or the fallopian
IA
tu bes,
The cancer is on the outer surface of or has grown into other nearby pelvic organs
IB such as the bladder, the sigmoid colon, or the rectum.
The cancer is in one or both ovaries. lt has spread to the retroperitoneal (pelvic
ill andlor para-aortic) lymph nodes only.
IV Distant spread to far organs
Cancer cells are found in the fluid around the lungs (called a malignant pleural effu-
IVA sion) with no other areas of cancer spread such as the liver, spleen, intestine, or
lymph nodes outside the abdomen.
The cancer has spread to the inside of the spleen or liver,to lymph nodes other than
VB the retroperitoneal lymph nodes, andf or to other organs or tissues outside the peri-
toneal cavity such as the lungs and bones.
 Gynaecology 251

DIAGNOSIS OF OVARIAN CANCER

This is a disease of late decade of life: 55-65 years of age in the majority of cases, with a very
insidious onset and misleading non specific symptoms in the majority of cases.

SYMPTOMS

A. Early stage disease: is usually asvmptomatic.

B. Later stages may be associated with;
- Non specific Glr symptoms; in the form of dyspepsia, indigestion, and anorexia
- Dull aching pelvic pain and heaviness
- Pressure symptoms; as urinary frequency and constipation may be present
Abdominal swelling, pain, and cachexia
- Abnormal uterine bleeding, especially postmenopausal bleeding in oestrogen producing
ovarian tumours.
N.B; Because symptoms are commonly non specific and mild, most tumours will be diagnosed late,
usually at stage ll or lll disease.

PHYSICAL SIGNS

The most important physical sign is the patpotion of a pelvic moss. In early stages of the disease
this may be accidentally discovered during routine gynaecologic examination for check up. In late
cases a large pelvic or pelviabdominal mass may be palpated with features suggestive of malignan-
cy as being bilateral, solid, fixed, associated with ascites, unilateral LL oedema, and rapid growth
(see later).

FEATURES SUGGESTING MALTGNANCy in ovarian tumours

1. History and symptoms:
- Tumours discovered at older age (postmenopause) are highly suspicious for malignancy.
- Tumours discovered in women with family history of breast, colonic, or ovarian cancer.
Tumours associated with rapid weight loss, rapid progressive abdominal enlargement, and
persistent GIT symptoms.
- Functioning tumours with feminizing or virilizing effects.
2. General examination:
Malignant cachexia (with marked and rapid weight loss and dehydration)
- Palpable supraclavicular lymph nodes especially on the left side, (Virchow's glands).
Pleural effusion, however it may be present in Meig,s synorome.
- Presence of an associated breast mass on breast examination
Unilateral lower limb oedema (unilateral pressure by tumour with venous and lymphatic ob-
struction ).
3. Abdominal Examination:
- lnspection; Abdominal enlargement, over lying skin showing peau d'orange.
- Polpotion.'Tumour which is solid (or partially solid), fixed especially if bilateral.
- Percussion.' Presence of ascites (except with ovarian fibroma in Meig's syndrome).
252 M a lig na nt Ovq rian Neoplosms

4. Pelvic examination:
1. Nodules in Douglas pouch in the presence of a non tender adnexal mass.
2. Bilateral, especially if solid adnexal masses are very presumptive.
3. Fixed pelvic masses especially if amulgamated with pelvic organs (frozen pelvis).
5. At Laparotomy:
Presence of ascites, especially if altered blood stained ascites.
- Bilaterality, fixation, and invasion of the capsule.
- Extracystic papillae and adhesions to surrounding structures.
- Peritoneal nodules or secondary deposits in omentum, intestine, liver, or lymph nodes
Variable consistency with a cut section of the tumour shows haemorrhage and necrosis.

SPECIAL INVESTIGATIONS in ovarian cancer

Aim: To diagnose presence of an ovarian swelling, to suspect malignancy within the tumour, to ex-
clude a hidden primary cancer elsewhere, and to determine spread of disease (stage).
1. Pelvic ultrasound:
TAS &TVS are the gold standard diagnostic tool that can accurately detect pelvic masses of
variable size and suggest their ovarian origin.
- Sonogrophic feotures suggesting malignancy include; heterogenous echopattern, intracystic
and extracystic papillae, bilaterality, presence of ascites, and low resistance Doppler flow of
the tumour vessels.
2. Chest X-Ray: for detection of pleural effusion and/or secondaries in the lungs.
3. Plain X-Ray abdomen: can detect calcification in dermoid cysts and Psammoma bodies.
4. CT & MRI: useful in detection of spread to liver and or lymph nodes (not mandatory).
5. Barium meal/enema: to exclude primary cancer in the stomach or colon (or spread).
5. Upper/lower G.l. Endoscopy: to detect a primary in the stomach or colon (or spread)
7.|.V.P.; to evaluatethe course of the ureters and to exclude back pressure on the kidneys.
8. Paracentesis: needle aspiration of ascetic fluid for cytologic examination.
9. Endometrial curettage: In cases of abnormal uterine bleeding to exclude a primary or spread to
the uterus.
10.Tumour markers:
- CAl25; commonly elevated in epithelialovarian cancers (Normal< 35 u/ml). lt may be slightly
elevated in benign conditions as endometriosis and chocolate cysts of the ovary. lt can be
used also to monitor response to chemotherapy (decreasing levels denote good response).
Other markers include; serum B-hCG (choriocarcinoma), serum alpha fetoprotein (EST), and
serum lactic acid dehydrogenase (dysgerminoma), CA 19-9 (mucinous cyst), and carcin-
embryonic antigen (CEA).

DIFFERENTIAL DIAGNOSIS of ovarian masses:

- Pelvic mosses: as adnexal masses, uterine enlargement (myomata & pregnancy), colonic
masses, retroperitoneal masses (pelvic kidney, retroperitoneal sarcoma, ...)
- Abdominal masses as liver or pancreatic tumour, and tense ascites.
 Gynaecology 253

SCREENING for ovarian cancer: (The aim is early diagnosis of ovarian cancer)
r Routine yearly pelvic examination in premenopausal and postmenopausal women. A palpable
post menopausal ovary must always call for further investigation.
o Periodic TVS coupled with a serum CA-125 in those with an enlarged ovary have been pro-
posed for screening of ovarian cancer (risk of malignancy scoring system).
o Genetic screening; testing for BRCAI- or BRCA2 mutation carriers in women with strong family
history of breast and ovarian cancer.
PREVENTION OF OVARIAN CANCER
1. Surgical removal of an benign ovarian tumour
2. Prophylactic gonadectomy in patients with dysgenetic gonad particularly with a y chromosome
3. In patients who are BRCA1 or BRCA2 mutation carriers, prophylactic oophorectomy is advisable
after completion of childbearing by the age of 35 years.
EXPLORATORY LAPAROTOMY in ovarian cancer
The final diagnosis of ovarian cancer can only be made at exploratory laparotomy, which will
serve not only for diagnosis but also for surgical staging and primary surgical treatment.

SURGICAT TREATMENT OF OVARIAN CANCER

A) EARLY STAGE OVARIAN CANCER:

In cases where there is no gross evidence for extension of the disease beyond the ovary;
1. TAH-BSO and Infracolic omentectomy is the standard treatment for patients with disease lim-
ited to the ovary (stages l-lla). Surgical staging is completed via peritoneal wash and lymph node
sampling for microscopic assessment of the extent of the disease.
2. Unilateral salpingo-oophorectomy may be occasionallv offered to selected cases of stage la
(tumour confined to one ovary, with capsule intact, and -ve peritoneal cytology), only when the
patient is voung and preservation of fertilitv is desired, Such conditions are mostly met with in;
a. Malignant germ cell tumours (dysgerminoma and EST)
b. Malignant sex cord stromaltumours (granulosa and Sertoli Leydig celltumours).
c. Borderline epithelial ovarian tumours

B)ADVANCED STAGE OVARIAN CANCER:

In cases with tumour extension beyond the ovaries:
1. nitiaf Debulking lPrimary Cytoreductive surgeryl:
f

The aim of initial surgery is

to remove all primory concer and if possible all metostotic disease
within the pelvic ond abdominal peritoneal cavities (leaving only residual small tumour depos-
its no more than 1.0 cm in diameter is acceptable).
. Debulking surgery includes a TAH-BSO + omentectomy + excision of pelvic masses and peri-
toneal deposits >t-2.0 cm + segmental bowel resection if involved within the tumour mass,
o Advantages of initial debulking surgery:
a. lt lmproves survivalin patients with advanced disease
b. lt lmproves response to chemotherapy,when residual tumour implants left are less than 1_2.0
cm in size
a<A Malignont Ovorian Neoplosms

2. Interval Debulking:
Chemotherapy prior to debulking surgery is sometimes applied to minimize tumour bulk and
control ascites to allow for subsequent more complete radical surgery,
Second-look Surgery in ovarian cancer:
Second look laparotomy or laparoscopy, have been advocated to asses residual tumour within
the abdominal cavity after primary surgery and chemotherapy, to decide on further adjuvant thera-
py needed.
Nowadays modern imaging technique, as spiral CT & MRl, together with serum CA125 tests
have largely nullified the need for second look surgery. At the present state its only place is when a
tumour marker is rising apart from negative imaging for tumour residues,

CHEMOTHERAPY IN OVARIAN CANCER

Chemotherapy whether single or multiple agents has a major role in the management of ovari- J
an cancer especially in advanced disease, and mostly with epithelial ovarian cancer:
1. Earfy stage disease: lt has a limited ploce only with poor prognostic factors as in poorly differen-
tiated tumours, ruptured capsule, or +ve peritoneal wash (even in stage I cases).
2. Advanced stage disease: Chemotherapy is indicated in oll ll-lV disease.
coses of stage
A. As adjuvant therapy in all cases after primary cytoreductive debulking surgery J
B, Palliative therapy in patients with irresectable tumours, or with recurrent disease.

Types of chemotherapy used:

Chemotherapy is usually recommended as soon as possible after surgery, and is given for five
or six cycles at 3-4 weekly intervals.
The most frequently used chemotherapeutic agents include: Cisplatin or Carboplatin alone or
in combination with Paclitaxel (Taxol).

Toxicity from chemotherapy:

Chemotherapeutic agents are highly toxic at therapeutic doses, and therefore need close mon-
itoring during treatment cycles, Toxicity includes; nausea, vomiting, myalgia and arthralgia. In se-
vere cases renal damage, peripheral neuropathy, hearing loss, dehydration and electrolyte imbal-
ance may occur.

RADIATION THERAPY IN OVARIAN CANCER

Radiation therapy has little place in epithelial ovarian cancer. lt may be used as an adjuvant
therapy following cytoreductive surgery in patients who refuse or are not good candidates for
chemotherapy, and in some radiosensitive germ cell tumours.
Even in cases of a dysgerminoma in a young age patient in which the tumour is radiosensitive,
radiotherapy has been replaced by chemotherapy as fertility is likely to be more preserved in the
latter.
o Forms of radiotherapy used:
1. Intraperitoneal radioactive colloids or
2. Whole external beam abdominal radiation.
 Gynaecology 255

PROGNOSIS IN OVARIAN CANCER

FACTORS AFFECTING PROGNOSIS:

- Histopathologic type of ovqrion cdncer; epithelial ovarian cancers generally carry poorer
prognosis than non epithelial ovarian cancer (germ cell and sex cord stromal tumours)
- Histologic grading of the tumour; Well differentiated tumours carry the best prognosis, while
poorly differentiated and clear cell carcinomas carry the worst prognosis.
- Stage of ovarian molignancy; the best prognosis is in stage la.
- Optimal versus suboptimol primary surgery; (TAH BSO + omentectomy, versus debulking).
- Response of the tumour to adjuvant theropy; epithelial tumours show good response to
chemotherapy, while germ celltumours are more radiosensitive).

The S-year survival rate in epithelial ovarian is estimated to reach; 8S-gO% in stage I and up to gO%
in stage ll. lt then sharply declines to only 15-20% in stage lll, and no more than 5% in stage lV dis-
ease.

Key points in ovarian cancer

- Epithelial ovarion cancer is the commonest type of ovorion cancer encountered

- Diagnosis is based on history, clinical exominotion, ultrosound findings, and tumour mqrker assessment.
Other investigotions os abdominol IJS, chest X-roy, C.T. scan, MRl, lVP, Borium fottow through, upper
and lower endoscopy, ore of help in defining the extent of the disease prior to surgery.

- lmportont criterio of molignoncy in on ovqrian tumour includes; solid or mixed solid qnd cvstic consisten-
cy, biloterolity, fixation, presence
of oscites ond extrocystic popiltae.
- Tumour morkers including; CA 125 in epithelial concers, LDH in dysgerminomo, hCG in malignont teroto-
' ma, qnd AFP in EST, ore of help both in diagnosis and in follow up after surgery.

- Tumours of stoge 1 corry the best prognosis, however unfortunately most ovqrion cancers wiil be diag-
nose ot stage ll or lll diseose, due to the qbsence of specific symptoms in eorly disease, leoding to a gen-
erolly poor prognosis.

- A staging laporotomy is indicated in every malignont ovorion tumour regordless its clinical stoging.

- During loporotomy removol of the moin tumour bulk is performed together with peritoneal
fluid cytolo-
gy, omentectomy, ond Lymph node sampling in order to ossess the extent of the disease, the prognosis
and the need for odjuvant theropy.

- Standord surgicol opproach entqils performing a TAH BSO ond lnfracolic omentectomy.

- Primory cytoreductive surgery in advonced disease aims ot removql of maximum tumour butk teoving
tumour residues less then 2.0 cm to focilitote postoperotive chemotherapy
- The vost moiority of molignont ovorian tumours will require odjuvont post operotive chemotherapy.
Some cqses moy benefit also from rodiotheropy.
- Molignont germ cell tumours con be monoged conservatively by unilaterol solpingo-oophorectomy in
cqses with stoge 1a diseose, to preserve fertility, as most tumours qre unilqterol, occurring in young
potients.
X-RAY RADIOGRAPHY:
1. Plain X-ray films of the pelvis to diagnose large tumours, calcifications in pelvic tumours, der-
moid cyst and renal stones.
2. X-ray chest for:
A. Preoperative assessment B. Diagnose of metastases C. Suspected T.B.
3. l.V.P. (intravenous pyelography) for:
A. Assessment of renal function. B. Diagnosis of urinary stones C. Diagnosis of geni-
to-urinary fistula
4. Hysterosalpingography (HSG)

HYSTEROSALPI NGOG RAPHY

This consists of the injection of radio-opaque substance into the uterine cavity & fallopian
tubes using a special cannula introduced into the cervical canal & an x-ray film is taken after the in-
jection & another film could be taken after 24 hrs (in case of infertility) to show spill of the dye from
the tubes to study tubal & peritoneal factors.
The dye used is either oil soluble e.g. Lipiodol (40% organic iodine in poppy seed oil) or water
soluble e.g. Urographin or renographin (in which situation
the second film is taken just 20 minutes after removal of the
cannula as they are rapidly absorbed)
Timing: during the first week after menstruation

Contraindications:
1. Pelvic infection 2. Suspicion of pregnancy
3. Allergy to iodine 4. During menstruation or
uterine bleeding
lndications:
l.lnfertility; to study uterine tubal and peritoneal factors.
2.To determine size, shape and anomalies of the uterus.
3.ln cases of uterine fibroids to detect a submucous fibroid
& to detect condition of the tubes before and after myo-
mectomy.
4.Before & after tubal surgery in cases of infertility
5.lrregular uterine bleeding to exclude organic lesions.
" 6.Recurrent abortions to determine shape of the isthmus Fig 29-1:
(isthmography) and to detect other possible uterine causes.
7. Study ofthe uterine scar after a previous C.S.

8. Missed IUCD.
9. Intrauterine adhesions
10. May diagnose pelvic T.B.

256
 Gynaecology 251

Fig 29-2:

Complications of H.S.G. :

1. Shock. 2. Oil embolism. 3. Disturbance of an undiagnosed pregnancy

4. Flaring up or introduction of infection. 5. lodine allergic reactions.
6. Intravasation (the oil passes into the uterine vessels during injection which is mainly lymphatic
& rarely venous)

NEW IMAGING TECHNIQUES:

The advances in cross-sectional imaging have dramatically changed the practice of gynaecolo-
gy. Ultrasound, computed tomography (CT) and magnetic resonance imaging (MRl) are tomographic
techniques that enable visualisation of organs and tissues previously unseen with standard plain
film radiography.

ULTRASOUND:
Normally, the human ear can pick up sounds with a frequency between 20 and 20 thousands
hertz (cycle/second). Sounds with a frequency higher than that are termed ultrasound. In medicine
we use sounds with high frequencies (more than million cycles/second i.e. Mhz). Ultrasound ma-
chines emit sound with high frequency from a part of the machine called the probe (or transducer),
which transforms electricity into sound. This emitted sound has 2 properties; penetration and re-
flection, both of them depends on tissue density, with increased tissue density e.g. bones, penetra-
tion will be less and reflection will be more. The reverse will occur with less dense tissues e.g. mus-
cles, fluids etc.

The returning echoes will be perceived by the probe which will transform it into electric im-
pulse which will be analysed by the machine & displayed on the monitor as grades of the grey col-
our so a view of the different organs studied will be seen (the bones will be seen white, the fluids
black while muscles and other tissues in between as different grades of grey). The examination can
be done either transabdominally or transvaginally.

Doppler ultrasound is a mode of ultrasound used to study blood flow in different blood vessels.
258 lmoging Techniques ln Gynaecology

ADVANTAGES OF ULTRASOUND:
1. Non-invasive procedure, which avoids the ionizing radiations of x-ray.
2. Can be done with little preparation of the patient
3. Can give rapid information which can be interpreted with no great difficulty
4. Can be explained to the patient with no much effort.
5. Ultrasound machines are relatively not so expensive in comparison to other diagnostic ma-
chines & needs no special preparations of the place of examination.

DIAGNOSTIC APPTICATIONS OF U.S IN GYNAECOIOGY:

1. Evaluation of genital anomalies.

2. Evaluation of pelvic masses

3. Evaluation of lower abdominal pain & inflammatory processes especially in patients with mus-
cular guarding or rigidity.

4. Monitoring of follicular growth as part of infertility workup.

5. Localisation of l.U.C.D. (either post insertion or in occasions of missed device)

5. Diagnosis of abnormal uterine bleeding

7. Diagnosis and evaluation of uterine fibroids (number, size, site, type, relation to the cavity)

8. Measuringendometrialthickness.
9. Diagnosis of ovarian cysts and neoplasms.

l0.Diagnosis of ectopic pregnancy

ll.Evaluation of urinary incontinence and residual urine volume.
l2.Sonohysterogra phy for tu ba I patency
L3.Can differentiate between benign and malignant conditions with a reasonable degree of effica-
cy.

Fig 29-3:
 Gynaecology 259

POSSIBTE THERAPEUTIC APPLICATIONS OF U/S IN GYNAECOLOGY:

1. U/S-guided follicular aspiration as a part of IVF programs.

2. U/S-euided aspiration of simple cysts 3. U/S- guided drainage of ascites

POSSTBTE USES OF U/S tN OBSTETRTCS:

1. During the first trimester:

a. Diagnosis of pregnancy.

b. Exclusion of extrauterine pregnancy

c. Diagnosis of unhealthy pregnancy

d. Determination of number of embryos

e. Determination of gestational age

f. Early diagnosis of some congenital anomalies and some chromosomal abnormalities e.g. Nu-
chalthickness in Down syndrome
g. Cervical measurements to exclude cervical incompetence

h. Guide for chorionic villous sampling

i. Helpful in conservative management of ectopic pregnancy.

Fig 29-4:
260 Imoging Techniques ln Gynaecology

2. Uses of U/S after the first trimester:

a. Diagnosis of multiple pregnancy
b. Diagnosis of lie, presentation & position.
c. To exclude IUFD.
d. Estimation of gestational age
e. Estimation of foetal weight
f. Diagnosis of congenital anomalies
g. Assessment of fetal well-being through biophysical profile (gross fetal movements, breathing
movements, tone, and amount of liquor amnii) & through Doppler study of placental, umbili-
cal and fetal BVs
h. Placental location and exclude placental separation (accidental haemorrhage)
i. Amount of liquor amnii
j. Assessment of fetal lung maturity -

U/S guided procedures during pregnancy:

1. Chorionic villous sampling
2. Amniocentesis: either diagnostic (chromosomal study - bilirubin level -immunoglobulins in in-
fections ..) Or therapeutic.
3. Cordocentesis.
4. lntrauterine blood transfusion in Rh isoimmunisation

CoMPUTED TOMOG RAPHY (CT)

CT depends on tissue differences in x-ray attenuation. Calcium, water, fat & air having different
coefficients are thus clearly separated. Soft tissues, however usually have only subtle density differ-
ences, hence intravenous contrast often is necessary to improve separation of normal and abnor-
mal by means of differences in vascularity.
CT is helpful in diagnosis of pelvic masses and its origin. However its main value is to demon-
strate metastases because of its capability to efficiently scan almost the entire body so it is useful in
staging cancer body, cervix and ovary (assessing spread to the pelvic side walls, lymph nodes and
distant metastases)
MAGNETTC RESONANCE IMAGING (MRl)

This technique relies on four tissue parameters; hydrogen content (in fat or water), T1 and T2
(tissue magnetic relaxation times) and blood flow.

Advantages:
1. A wide range of contrast differences are available to identify a certain tissue or disease
2. Because rapidly flowing blood does not generate a signal, vessels stand out from adjacent
structures obviating the need for lV contrast administration .
3. MRI is biologically safe because the energies involved are so small
 Gynaecology 261

Disadvantages of MRI:
\-/
1. The magnetic field used is many times that of the earth's gravity, patients with pacemakers,
\-/ implanted electronic devices & certain types of cerebral aneurysm clips cannot undergo MRI
. 2. Long scanning time
3. High cost,
\'/ Values of MRI in gynaecology:
\-1 L. Differentiating ovarian from uterine masses
2. Evaluation of uterine fibroids to depict the size, number, location, presence of degeneration
\-r
and large feeding vessels, especially in infertile patients before myomectomy & also to follow
\-/ response to treatment.
3. Distinguish between uterine myomata and adenomyosis
4. Diagnosis of different uterine developmental variants
\-/. 5. Diagnosis of uterine hypoplasia
'\- 6. Particularly useful in diagnosis of Dermoid cyst & endometriomas (since fat and blood have
characteristic appearance on MRl.
\-( 7. Used to follow the response of endomtriomas to treatment (after diagnosis & staging by lapa-
roscopy)
8. Pelvic floor assessment with dynamic evaluation
v 9. Assessment of different pelvic malignancies.
 LAPAROSCOPY
Laporoscopy is a procedure which ollows direct inspection of
the peritoneal cavity and pelvic orgdns by introduction of an
optic lens through the umbilicus alter properly insufilating
the peritoneum with CO2 gas. The procedure qlso qllows the
performing of variable types of pelvic surgery.

INDICATIONS:
A. Diagnostic laparoscopy:
1. Infertility whether primary or secondary.
2. Chronic pelvic pain.
3. Diagnosis of pelvic endometriosis.
4. Diagnosis of some undiagnosed pelvic masses.
5. Assessment of congenital anomalies of uterus &
tu bes.
Fig 30-L:
6. Follow up after radical surgery for malignancy.
B. Operative laparoscopy:
1. Tubal surgery:
a. Management of tubal obstruction and adhesion by adhesolysis, salpingostomy , fimbrial
dilatation and salpingectomy .
b. Management of ectopic pregnancy.
c. Removal of hydrosalpinx or pyosalpinx.
d. Tubal sterilization,
2. Ovarian surgery:
a. Selective removal of ovarian masses with no or minimal risk for malignancy by cystectomy,
ovariotomy or oophorectomy,
b, Drilling of polycystic ovarian disease in cases resistant to medical treatment.
3. Uterine surgery:
a. Myomectomy for myomas of small number <3 myomas and moderate size < 9 cm.
b. Hysterectomy whether total or subtotal is feasible in selective cases.
4. Endometriosis:
Variable procedures can be performed including laser ablation, fulguration and diathermy
cauterization of endometriotic foci, pelvic adhesiolysis, endometrioma excision and adnex-
al removal and hysterectomy.
5. Pelvic floor relaxation.
6. Some selective radical procedures for malignancy.
7. Omental and intestinal adhesiolysis to relieve variable degrees of pain resulting from adhesion
of previous surgery.

262
 Gynaecology zoJ

THE PROCEDURE:

Anaesthesia:
General anaesthesia is usually needed; however, diagnostic procedure may occasionally be
performed by local anaesthesia associated with adequate sedation and analgesics.

Patient positioning:
The patient is put in a steep; head-down (Trendelenberg) position with the legs semiflexed at
the knee level. This allows the abdominal viscera to slip to the upper abdomen giving clear view of
the oelvis.
Procedure:
After properly sterilizing the patient and proper drappings, the patient is catheterized using an
indwelling catheter and intrauterine manipulating cannula is put in place. The abdomen is inflated
using Co2 through the umbilicus using a thin needle (Verus' needle)to a pressure of l-5 mmHg using
3-5 liters of COz. An umbilical port is then passed through a 1 cm umbilical incision through which a
rigid fibroptic lens connected to a high power light source and a high resolution camera and moni-
tor is passed to the abdomen for proper inspection of the abdomen and pelvis. The abdomen and
pelvis are then inspected systemically and patency of the fallopian tubes is tested by injecting
suita-
ble amounts of colour dye through the transvaginally inserted intrauterine cannula.

To perform variable types of pelvic surgeries,2-3 other ports are being made along a line 3 cm
abovethe symphysis pubis, each of these ports are being 1./2-1,cm.A large scope of endoscopic
instruments e.g. scissors, graspers, diathermy coagulating instruments, needle holders and morcel-
lators exist for variable procedures.
At the end of procedure, haemostasis is checked, irrigation of the pelvis with lactated ringer
solution is done with suction and repeated rinsing. After final inspection the CO2 is evacuated from
the abdomen and allthe ports are removed and their entry sites are occluded.

Complications
Laparoscopic surgery is a variant of regular surgery with special features therefore a patient
undergoing laparoscopic surgery will be exposed to same complications with a variable desree
(more or less), in addition to special risks related to laparoscopy

1. Anaesthetic and cardiopulmonary complications, more especially Co2 embolism, arrhythmias,

gastric refl ux, hypotension.

2' Extraperitoneal insufflation due to malposition of insufflation needle will result in cutaneous
surgical emphysema.

3. Electrosurgical complication :

These can result in diathermy burns to important structures such as the bowel, nerves, uterus
and blood vessels and may end in fatalities if they are not recognized during surgery.

4. Haemorrhagic complications:

a' The most serious of these are injuries to the great vessels as the aorta and lVC. This can
happen during introduction of insufflation needle or the trocar.

b. Injury to the cutaneous abdominal wall vessels specially the inferior epigastric.

c. Injury to an intraperitoneal vessel by any type of surgery.

264 Endoscopy ln Gynoecology

5. Gastrointestinal complications:
a. Injury by an insufflations needle or a trocar especially in patients with previous ab-
dominal surgery.
b. Injury during dissection or by the diathermy current.
6. Urologic injury:
Injury to the bladder or ureter may happen secondary to mechanical dissection or thermal
trauma.
7. Neurological injury:
Peripheral nerve injury is usually related either to poor positioning of the patient. Nerve
injury may also occur as a result of surgical dissection or diathermy injury.
8. lncisional hernia and wound dehiscence
9. Infection: wound infection, crepitus, pelvic cellulites and pelvic abscess are rare happening.
Advantage of operative laparoscopy:
. Minimal hospital stay and early return to work.
. Minimal patient discomfort.
. Minimal patient adhesion and therefore minimal iatrogenic infertility.
. Better cosmetic results.
o Rare wound complications.
. Allow proper inspection and excludes the need for what is called exploratory laparotomy.

HYSTEROSCOPY
The procedure of hysteroscopy entails the introduction of lens inside the uterine cavity
through the cervix after distending the uterine cavity with suitable medium (COz-saline-glycine
L.5%) to visualize the endometrial cavity and perform variable intrauterine operative procedures.

INDICATIONS:
A. Diagnostic:
1. Infertility. Variable findings may be occasionally found such as polyps, synechiae, submucous
myoma, congenital anomalies e.g. septate uterus.
2. Habitual and recurrent abortions.
3. lrregular uterine bleeding.
B. Operative:
1-. Polypectomy.
2. Resection of uterine septae.
3. Resection of a submucous myoma.
4. Division of intrauterine synchiae.
5. Removal of a missed lUD.
6. Resection or coagulation of the endometri-
um.
7. lntrauterine tubal catheterization for cor- Fig j0-2:
neal obstruction.
8. Sterilization by injecting a sclerosing agent or a plug to the cervix.
 Gynaecology 265

THE PROCEDURE:

L. Place of the procedure

\-/ The procedure can be performed as office procedure unless operative intrauterine surgery
ay be needed.
\l- 2. Position of the patients: Modified dorsal lithotomy position.
\./ 3. Anaesthesia
No anaesthesia, local paracervical block or general anaesthesia may be needed.

4. Cervical dilatation
\.'' For diagnostic procedure; the cervix may be dilated to 4 mm where as for the operative pro-
cedure the cervix has to be dilated to L0 mm.

5. Uterine distension:
\/ For diagnostic procedure;
CO2, saline or glycine t.5% may be used. However, if electric current
istobeusedinoperativeprocedureanonconductivemediume.g.glycine !.5o/oisamust.
6. lmaging:
\-/ The endoscope is introduced, good illumination must be available together with a camera
head transmitting the picture to a suitable monitor.
\-'
- 7. operative procedures can be performed using cold scissors, electrosurgical equipment or laser
equlpment'
\-,
Complications:
1. Anaesthesia complications.
v 2. Perforation ofthe uterus.
\-/ 3. Bleeding due to myometrial vascular trauma.

\_' 4. Thermal trauma to adjacent structures.

, 5. Complications related to distending media:

a. CO2 can result in embolization.

b. Lowviscosityfluids (e.g, glycine 1,.5%)can result in fluid overload with serious electrolyte
\-,' imbalance that rarely may be fatal.

v
 Uterine polypi
Pelvi-abdominal Mass
Mass in the pouch or douglas
DD of Pelvic pain

UTERINE POLYPI
A) CORPOREAL POLYPS:
1. Adenomatous Endometrial PolyP:
Origin: from the endometrium, either as a single adenoma or multiple in association with
marked endometrial hyperplasia (EH).
Symptoms:

Signs: if it protrudes through the cervix, speculum examination will reveal the polyp as a

tongue like projection, soft in consistency, with a rather flat compressed tip.
Diagnosis: TAS, TVS, SlS, 3D US, and hysteroscopy are all efficient in diagnosis.

via;

2. SMF Polyp:
- Origin: from the myometriu m of the body of the uterus, as a SM M that attains a
pedicle and protrudes into the endometrial cavity
Symptoms.' AUB, menorrhagia, metrorrhagia, and foul discharge
Signs: if it protrudes through the cervix, speculum examination will reveal a
rounded mass, firm in consistency,with necrosed infected tip and long pedicle
Treotment:

my in young patients, or hysterectomy in the perimenopause.

3. Placental Polyp:
Origin:accumulated blood clots over the surface of a retained placentalfragment.
Symptoms: persistent bleeding after labour or abortion.
- Signs: subinvolution of the uterus, with softer consistency
Diagnosis:TVS, TAS, SlS, 3D US, and hysteroscopy are all efficient in diagnosis.
Treatment:
) Hysteroscopic guided polypectomy is the gold standard treatment
> D&C polypectomy can be performed if hysteroscopy is not available

266
 Gynaecology 267

N.B': Microscopic examination should be performed to exclude choriocarcinoma.

4. Malignant Polyp:
Carcinoma, sarcoma or chorionepithelioma.

B)CERV|CAL POLYPT:
1. Mucous Polyp:

origin: one or more reddish soft polyp seen within the endocervix.
Aetiology: hyperplasia of the endocervical epithelium due to chronic cervicitis.
Diognosis: speculum examination reveals the lesion by the naked eye, or hysteroscopy.

Treotment: polypectomy followed by treatment of chronic cervicitis.

N'B': Any polyp removed should be examined histologically to exclude malignancy.
2. Fibro-Adenomatous Polyp: lt is a mucous polyp in which the stroma is dense and fibrous.
3. Fibroid Polyp: Rare and appears as a firm polyp with necrosed tip attached to the cervix
by a short pedicle and treated by vaginal polypectomy.
4. Malignant Polyp: Either carcinoma, sarcoma or the rare highly malignant grape-like
sarcoma
of children which, is a mixed cell sarcoma characteri-sed by rapid invasion and formation of
grape- like mass of soft pinkish oedematous polyp which fill the upper vagina.
5. Bilharzia! Papilloma: Usually develop from the vaginal surface of the cervix. They may be sin-
gle or multiple, sessile or pedunculated, of variable sizes, firm in consistency, usually
rough
and covered by intact greyish pink mucous membrane.

D.D. OF PELVI-ABDOMINAL SWELLINGS

A) Uterine Causes
1. Normal pregnancy: (The commonest cause in the repro-
ductive period).
The patient is in the childbearing period with history of
amenorrhea, morning sickness and breast' signs. The uterus
is soft and intermittent contractions are felt. Detection of the
foetal parts or foetal heart sounds are sure signs. Ultrasonog-
raphy and pregnancy test are diagnostic.

N.B.:Abnormal pregnancy as vesicular mole or hydramnios

will alter the clinical picture and should be kept in mind. Ul-
trasonography helps in the diagnosis,

2. Fibroids:
The patient is usually over 35 years and commonly nul_ Fig 31-1.:
lipara. Menorrhagia is the com-monest symptom. The tumour is usually firm with knobby
surface,
mobile from side to side and not tender and during vaginal examination, movement of the tumour
is transmitted to the cervix,
268 Differentiol Diognosis ln Gynaecology

3. Large haematometra:
to congenital or acquired atresia at or below the cervix. There are amenorrhea,
This occurs due
and abdominal pain recurring every month; but if the condition is neglected, the abdominal pain
becomes persistent due to the irritation of the peritoneum by the blood passing through the; Fallo-
pian tubes. The symmetrical swelling felt represents the distended uterus due to the accumulated
menstrual blood inside it.

5. Large pyometra:
This occurs due to the presence of uterine infection accompanied by obstruction of the cervi-
cal canal. Lower abdominal pain and fever (that may be intermittent) are present. There is inter-
mittent purulent discharge, which stops after a period. There is symmetrical tender, cystic pelvi-
abdominal swelling, which represents the distended uterus. The passage of a uterine sound (if pos-
sible) will be followed by a discharge of pus.

B) Ovarian Causes:

1. Ovarian cysts and solid ovarian tumours:

Painless central enlargement of the abdomen without any menstrual irregularities. The swelling
with smooth or lobulated surface and is mobile. On percussion there
is cystic or solid in consistency,
is central dull-ness and resonant flanks.

On bimanual examination, the uterus is felt separate from the swelling. Menstrual irregularities
are encountered only in functioning tumours.

It may be impossible to differentiate a solid ovarian tumour from pedunculated subserous fi-
broid. Ultrasonography, CT, and MRI may help in the diagnosis.

2. Malignant ovarian tumour

See clinical picture suggesting molignoncy.

C) Tubal Causes:
Rarely, in some cases of hydrosalpinx or pyosalpinx, a
unilateral or bilateral cystic fixed mass with ill-defined margin
may be felt above the inguinal ligaments. On bimanual exami-
nation, the swellings are palpable in the region of the adnexa
and the uterus may be felt retroverted and fixed.

D)Vaginal Causes:
Haematocolpos: Cystic mass with a small firm nodule
(the uterus) on its top. Local inspection reveals imperforate
Fig 3L-2:
hymen or vaginal septum, and rectal examination will detect
the cystic mass formed by the distended vagina.
E) Other Extragenital Swellings:
1. The distended bladder: The swelling disappears after catheterisation of the bladder.
2. Large hydronephrosis: An oval swelling that extends into the loin. lt is dull with a band of reso-
nance over it corresponding to the colon. Intravenous pyelography settles the diagnosis.
3. Mesenteric and pancreatic cysts: Do not rise from the pelvis and cannot be pushed down into
it. There are areas of reso-nance over the mass due to superimposition of the intestine.
 Gynaecology 269

4. Retro-peritoneal tumours: A fixed swelling, which is resonant on percussion due to the overly-
ing intestine.
N.B.: All pelvi-abdominal swellings must be differentiated from ascites, pseudocyesis, obesity and
flatulence which cause abdominal enlargement.

SWELLINGS OF THE BROAD LIGAMENT

1. Broad ligament cyst:

Sometimes it is large enough to be felt'per abdomen. The cyst is of limited mobility and bimanuallv it is
lateral to the uterus, which is displaced to the opposite side.

2. Broad ligament haematoma:

This may occur due to rupture of tubal pregnancy in the broad ligament or due to rupture of a varicose
vein in the broad ligament or it may occur in cases of incomplete rupture of the uterus where a cervical lacer-
ation on either side extends upwards to the part of the lower seg-ment between the two layers of the broad
ligament. lt may be also due to improper haemostasis after abdominal operations on the pelvic organs espe-
cially operations done to remove a broad liga-ment cyst or tumour. There is a cystic swelling to one side of
the uterus displacing it to the opposite side, associated with the clinical picture of internal haemorrhage.

CAUSES OF CYSTIC ADNEXAL SWELLINGS

1. Tubal: hydrosalpinx, pyosalpinx and haematosalpinx.

2. ovarian: non-neoplastic and neo-plastic cysts and haemorrhage in the ovary.

3. Broad ligament: cyst, hematoma or abscess (suppuration of parametritis).

D.D. OF A MASS FELT IN THE POUCH OR DOUGLAS
A) Uterine Masses:
1. Retroverted uterus: The body of the uterus is felt through the posterior fornix continuous with
the cervix and moves with it. The external os is directed forwards and upwards.
2. Posterior wall fibroids: The tumour is rounded and firm and moves with the cervix.

B)Tubal Masses:
1. Hydrosalpinx and pyosalpinx: Bilateral, cystic, tender, fixed swellings postero-lateral to the uter-
us, and the uterus may be retroverted and fixed.

2. Tubal pregnancy: Amenorrhea, pain and bleeding. The uterus is slightly enlarged and soft and
pain is felt on one side on moving the cervix. Unilateral, firm, tender swelling is felt postero-lateral
to the uterus and pulsations may be felt at the swelling. Aspiration of the pouch of Douglas reveals
blood.

C) Ovarian Masses and Swellings:

Non-neoplastic cysts.

- Small cystic or solid ovarian tumours (benign or malignant).

- Very rarely ovarian ectopic pregnancy (see Obstet-rics).

N.B.: An Ovarian swelling is usually cystic (but may be solid), rounded, mobile (except if it is fixed by
adhesions or malignant infiltration), separate from the uterus, and its movement is not transmitted
to the cervix.
270 Dilfe re nti o I D i og n o sis I n Gy n o e colo gy

D) Extra Genital Masses In the Pouch of Douglas:

l.Pelvic haematocele and Pelvic abscess.

2. Encysted tuberculous peritonitis.

3.Nodules felt in the Douglas pouch: May be due to either T.B., endometriosis or secondaries
from malignant ovarian tumour.
4.Inflammatory mass as appendicular mass, or peridiverticulitis.
5.Rectal masses; as faecal mass (indentable), endometriosis of the rectovaginal septum, and
carcinoma of the rectum,
6. Retroperitoneal tumours; as ectopic kidney.
N.B.: In all cases with a mass felt in the pouch of Douglas do rectal examination to determine the
relation of the swelling to the rectal wall

CAUSES OF HAEMATOSALPINX

1.. Disturbed tubal pregnancy,

2. Haemorrhage in a hydrosalpinx or pyosalpinx.

3. Some cases of marked acute inflammation of the Fallopian tubes.

4. Endometriosis.
5. Malignant tumours of the Fallopian tube.
6. Congenital cervical atresia and rarely some cases of imperforate hymen or transverse vaginal
septum (accumulation of blood causes haematometra then haematosalpinx) .

7. In the very rare cases of torsion of a Fallopian tube.

CAUSES OF SYMMETRICAL ENLARGEMENT OF THE UTERUS

1. Pregnancy

2. Metropathia haemorrhagica
3. Single submucous or single interstitital fundal fibroid

4. Diffuse adenomyosis
5. Subinvolution of the uterus (in the puerperium)

6. Malignant tumours: as adenocarcinoma, sarcoma or choriocarcinoma:

7. Pyometra and haematometra: In pyometra, there is lower abdominal pain and fever. The uter-
us is, tender and cystic. In haematometra there is amenorrhea, recurrent lower abdominal pain
every month, atresia at or below the cervix.

CAUSES OF ENTARGEMENT OF THE CERVIX

1. Chronic cervicitis.

2. Congestion of the cervix (e.g. in pregnancy and prolapse).

3. Congenital elongation of the portio vaginall

 Gynaecology 211

5. Cervical tumours whether benign (e.g. fibroid) or malignant (e.g. carcinoma).

6. Distension of the cervix by an extruded uterine potyp.

v 7. Some specific inflammations e.g. tuberculosis, biliarziasis and syphilis.

8. Cervical abortion.
v 9. Cervical ectopic pregnancy.

10. Endometriosis of the cervix.

D.D. OF A MASS PROTRUDING FROM THE CERVIX

1. Any type of cervical polypi.
\-- 2. Uterine and endometrial polypi. The mass is not fixed to the cervix and is hanging by a long
pedicle.

3. Inevitable and incomplete abortion.

!- 4. Inversion of the uterus: The uterus is not felt in its normal position and the length of the uter-
! ine cavity is reduced when measured by a sound.

GYNAECOLOGTCAL CAUSES OF ACUTE ABDOMTNAL pAtN

v
1. Disturbed ectopic pregnancy.
2. Acute salpingitis.
v 3. Torsion, rupture or haemorrhage in an ovarian cyst.

v, 4. Red degeneration in a fibroid or torsion of a pedunculated subserous fibroid.

v 5. Haemorrhage in a corpus luteum or rupture of a corpus luteum cyst.
The above mentioned gynaecological causes should be differentiated from the non-
v gynaecological causes of acute lower abdominal pain e.g. acute appendicitis, acute pyelitis, divertic-
ulitis etc... Acute upper abdominal pain may be due to cholecystitis, pancreatitis etc...
v
- GyNAEcotoGtcAL cAUsEs oF cHRoNtc pELVtc pAtN
l-. Chronic pelvic inflammatory disease e.g. chronic salpingo-oophoritis

2. Pelvic adhesions
3. Pelvic endometriosis
v
4. Displacements e.g. prolapse and fixed retroversion
5. Pelvic con-gestion syndrome (vascular congestion of the uterus and varicosities in the veins of
the broad ligament. Careful clinical examination, and special investigations e.g. laparoscopy are
needed to reach the diagnosis.

CAUSES OF LOW BACKACHE

(A) Causes in the genitaltract:

L. Uterine prolapse (especially in the early stages). The low backache increases towards the end of
the day.
212 Differentiol Diognosis ln Gynaecology

2. Some cases of retroversion

3. Chronic cervicitis.

4. Endometriosis.
5. lmpacted tumours in the pelvis or malignant tumours of the genital organs.
6. Pelvic congestion.
Backache caused by gynaecological lesions is characterized by:

1. lt is diffuse (cannot be indicated with a finger point),

2. Situated in the mid-line or it is bilatera..

3. lts level is sacral or lumbosacral.

4, No localtenderness.
N.B.: After gynaecological operations with prolonged use of the lithotomy position or after pro-
longed lying on a flat table with relaxed muscles, the patient may complain of low backache.

(B) Extragenital causes --

N.B.: During pregnancy, the patient frequently complains of low backache due to increased lumbar
lordosis and relaxation of the ligaments.

CONTACT BLEEDING

It is bleeding following contact of the cervix, for example, after vaginal examination, sexual
intercourse or douching
Causes: lt may be due to:
1. Some cases of cervical erosion (especially papillary type as it is usually vascular).

2. Carcinoma of the cervix.

3. Ulcers of the cervix.

4. Polypi of the cervix.

Investigations:
L. Clinical examination including careful vaginal and speculum examination.

2. Special investigations to exclude early malignancy, as vaginal and cervical smears, Schiller's io-
dine test, colposcopy and cervical biopsy, which should be done in every case.

Treatment: According to the cause.

UTERINE CASTS

1. Decidual casts: Passed in cases of abortion or disturbed tubal pregnancy; but in the latter case,
no chorionic villi are detected.

2. Membranous casts: in cases of membranous dysmenorrhoea.

3. Blood casts: made up of red and white blood corpuscles in fibrinous network, may be passed dur-
ing severe general infections.
 SOUNDING OF THE UTERUS
The uterine sound is made of malleable metal and its tip is blunt. lt is graduated in inches or
centimetres. lt is slightly curved near the tip so that it can adapt to the angle of uterine flexion.
Before introducing the uterine sound, the uterus is palpated during the bimanual examination,
the cervix is exposed by a vaginal speculum and the anterior lip of the cervix is grasped by a
volsellum.
The sterile sound is introduced until resistance is felt at the internal os to measure the length
of the cervical canal and then it is pushed past the resistance until it reaches the fundus to measure
the length of the uterine cavity,

Fig 32-l:
Uses of the uterine sound:
1'. Degree of supravaginal elongation of the cervix in cases of prolapse.
2. Diagnosis of uterine hypoplasia (the uterine length is subnormal and there is alteration in the
ratio between length of the cervix and body).
3' Measurement of the length of the uterine cavity preliminary to dilatation.
4. Measurement of the uterine length before introduction of l.U.c.D.
5. Diagnosis of the direction of the uterus.
6. Diagnosis of cervical stenosis (inability to introduce the sound).
7. Abnormality inside the uterus as polyp or septum.
8. Differentiation between chronic inversion and fibroid polyp bulging through the cervix. In the
latter case, the uterine length is normal.
9. Detection of retained LU.C.D.
10. Diagnosis of endocervical carcinoma.

Dangers of using the uterine sound:

1,. Perforation.
2. Infection.
3. Abortion,

273
214 Operative Gynoecology

DILATATION OF THE CERVIX

Types of dilators:
1. Hegar: uniform thickness.
2. Fenton:tapers gradually towards the tip.
N.B.: The number of the dilator indicates the diameter in millimetres.

lndications:
A) Dilatation alone:
1. Spasmodic dysmenorrhoea.

2. Cervical stenosis.
Fig 32-2:
3. Drainage of pyometra or haematometra.
B) Dilatation preliminary to another operation:
1. Operations on the cervix: as trachelorrhaphy, amputation (including Fothergill's operation) and
cautery in nullipara.
2. Operations on the uterus: as curettage, evacuation, polypectomy and introduction of radium
into the uterus.
3. Operations on the tubes: as Rubin test if a large cannu-
la is used.

Steps of the operation:

1.. Anoesthesia: (usually general LV.or spinal /epidural).
2. Position: the patient lies in the lithotomy position.
3. Asepsis: the vulva, vagina, and surrounding skin are
painted with an antiseptic. Sterile towels are applied
leaving the operation area exposed. Fio 32-3:
4. The blodder is evocuated by a catheter.

5. Bimonuol exominotion under anesthesia to detect the size, position, shape and consistency of
the uterus and also to detect any other abnormality.
6. The cervix is exposed by a self-retaining posterior vaginal speculum and the anterior lip is
grasped by a volsellum. (N.B.: multiple teeth volsellum is less liable to cause cervical laceration
than single tooth volsellum).
7.The cervix is pointed with iodine solution and a sound is passed to determine the length and
direction of the uterus.
8.The cervicol canal is gradually diloted by introduction of the dilators starting with the smallest
size (Number 3). The chief resistance will be met at the internal os. The dilator is held like a
pencil with the index finger at the supposed length to enter the uterus and steady pressure is
applied until the resistance is overcome and the dilator enters the body of the uterus. The slight
curve in the dilator should confirm with the direction of the uterus.
9. Eoch dilotor is left in the uterus for 1. minute to allow the circular fibres to relax. lt is then re-
moved and the next larger size is introduced until the required dilatation is obtained (e.g. No. 8-
LO for curettage, and No. 1-4 in spasmodic dysmenorrhoea and No. 12 before doing amputation
of the cervix).
 Gynaecology 275

Complications:
L. Perforotion of the uterus (lt is detected when the sound or dilator can be introduced more
than the expected length of the uterine cavity. The patient is kept under observation and anti-
biotics are given, but if there are signs of internal haemorrhage or injury to abdominal organs,
laparotomy is necessary.
2. Lacerations of the cervix are more liable to occur if the cervix is dilated over number 12, espe-
cially if the dilatation is done very rapidly. Severe bleeding if the lacerations extend laterally to
involve the cervical branch of uterine artery. Lacerations may become infected leading to
chronic cervicitis. Incompetent isthmus and habitual abortion mav occur later on.
3. lnfection.
4. Shock is liable to occur if dilatation is carried out without anaesthesia or with improper anaes-
thesia.
5. Anoesthetic complicotions.

CURETTAGE
Types of curettes:
L. The loop curette: either sharp or blunt or combined. Blunt curette is used in cases of recent
pregnancy or suspected malignancy as the uterus is easily perforated.
2. Blunt flushing curette: used to curette the decidua when evacuation is done.
3. Fundal curette: has a tapering tip to curette the fundus and angles.
4. Biopsy curette: used without anaesthesia as its introduction through the cervix needs no dila-
tation due to its small diameter. lt is not used to diagnose diseases or malignancy of the endo-
metrium as it removes only a small strip of endometrium. lt is used-to detect the hormonal
effect on the endometrium os in detection of ovulation and in research purposes.
Indications of curettage:

Fig 32-4:

(A) Diagnostic (endometrial biopsy):

l-. Detection of ovulation.
2. Detection of the endometrial pattern in hormonal disorders e.g. amenorrhea
3' To determine the cause of uterine bleeding and to differentiate between dysfunctional bleed-
ing and bleeding due to organic cause.
4. Diagnosis of malignant diseases of the endometrium or endocervix.
5. Diagnosis of diseases of the endometrium as tuberculous endometritis.
(B) Therapeutic:
1. Post-abortive and puerperal bleeding due to retained products.
2. Endometrial and cervical polypi.
3. Dysfunctional uterine bleeding.
276 Operotive Gynoecology

Technique of dilatation and curettage:

Under anaesthesia, the cervix is dilated up to No. L0-L2
Hegar (see before). The curette is introduced and the whole
endometrium is scraped in long strokes from above down-
wards starting with the anterior than the posterior wall. The
fundus, angles and lateral walls are scraped using the fundal
curette. Curettage is continued until n grating sensation is
felt, and the material obtained is preserved in diluted forma-
line solution. The cervical canal and uterine cavity are then Fig 32-5:
painted with iodine solution.
Dangers and complications:
In addition to the dangers of dilatation (see before), a rare complication is overcurettage
(specially for a pregnant uterus) leading to permanent amenorrhea due to removal of the basal
pans of the endometrial glands or more commonly due to the formation of intrauterine synechiae
(adhesions) which is liable 10 occur with heavy curettage specially in the presence of infection
(Asherman's syndrome).

Perforation of the uterus during dilatation and curettage

Causes: The uterus may be perforated by the sound, the dilator or the curette. Perforation is more
liable to occur if the uterus is soft (pregnancy), friable (malignancy), in cases of pyometra (the uter-
ine wall is thin and the infection makes the uterine wall more liable to be perforated, if the uterine
wall is thin (due to postmenopausal atrophy or due to marked distension), or in cases of marked
retroversion flexion and acute anteflexia of the uterus (cochleate uterus which is C-shaped with the
concavity to the anterior side).

Dangers: Haemorrhage, infection, injury to the intestine or

omentum, and rupture of the scar in subsequent pregnancies.
Diagnosis:
1. Sudden release of the resistance
2. Vaginal bleeding
3. The sound or dilator can be introduced more than the ex-
pected length of .the uterine cavity
Fig j2-6: Perforation of the uterus
4. lf the perforation is very large, the intestine or omentum
may be protruded.
Prevention:
L. Pre-operative assessment of the size, direction and consistency of the uterus
2. Measurement of the length of the cervical canal and uterine cavity, before dilatation
th"uterus
3. In cases with marked retroversion-flexion or acute anteflexion, we try to straighten
by applying traction on the cervix with the volsellum
4. Proper holding of the dilator and proper technique of dilatation and avoid the use of great
force.
Management:
1. Observation: In the majority of cases the perforation is small and no interference is needed. The
operation should be stopped and the patient is observed forthe pulse, temperature, blood pressure
and evidence of internal haemorrhage. Antibiotics are given.
 Gynaecology 271

2. Laparotomy is indicated in the following conditions:

v a. lf the abdominal contents prolapse through the perforation.
!. b, In cases of septic abortion or pyometra.
c. In cases of malignancy.
d. lf the uterus still contains products of conception (in such cases we may do laparoscopy at first
and if the bleeding in the peritonealcavity is slight, we may continue evacuation of the uterus
under laparoscopic vision).
\- e. lf there is evidence of internal haemorrhage,
v f. In cases of excessive vaginal bleeding.

g' During laparotomy, the uterus is repaired or removed according to the circumstances. The
intestine, omentum and bladder should be inspected for any injury.

HYSTERECTOMY
v Hysterectomy may be done abdominally or vaginally. Vaginal hysterectomy is usually done for
some cases of uterine prolapse.
Indications of hysterectomy:
(A) Obstetrical:
1. Rupture of the uterus.
2. Uncontrollable postpartum haemorrhage.
\' 3. Couvelaire's uterus.
4. Placenta accreta.
(B) Gynaecological:
v L. Inflammatory as some cases of genital tuberculosis.
2. Neoplastic:
a. Benign: some cases of fibroids and benign ovarian tumours in old patients.
b. Malignant tumours of the cervix, body and ovaries.
v 3. Displacements: some cases of uterine prolapse or chronic inversion.
4. Some cases of endometriosis.
5. Some cases of dysfunctional uterine bleeding.
Abdominal hysterectomy (AH)
1. Subtotal AH: We remove the body and leave the cervix. lt is usually done in some cases of post-
partum haemorrhage and rupture of the uterus, or if there is extensive adhesions around the cervix.
2. Total AH: We remove the body and cervix and it is better than the subtotal.
3. Panhysterectomy: Total hysterectomy and bilateral salpingo-oophorectomy.
4. Radical hysterectomy: Wertheim's operation.
5. Ultraradical hysterectomy: pelvic excenteration.
In anterior pelvic excenteration, we remove the bladder in addition to the structures removed
in Wertheim's operation and we may implant the ureters at various sites e.g. the colon or skin. In
posterior excenteration, we remove the rectum and we do colostomy. In total excenteration, we
remove the bladder and rectum and we may implant the ureters in the colon before the opening of
colostomy.
- Advantages of subtotal hysterectomy:
1. lt is easier and quicker than total hysterectomy.
2. There is less danger of injuring the ureters and bladder.
3. There is less danger of pelvic infection, as the vagina is not opened.
218 Operative Gynaecology

4. The cervix left behind acts as a support for the vaginal vault.
5. The cervical discharge lubricates the vagina.

Advantages of total hysterectomy:

1. lf avoids the risk of carcinoma developing in the cervical stump left after subtotal hysterectomy.
The incidence of stump carcinoma is about 1%
2.|tprovidesbetterdrainageoftheoperationarea(throughtheopenedvagina)andtherefore
there is less risk of a pelvic haematoma developing after the operation.
3. lf the cervix is lacerated or infected, the source of irritant discharge is removed. For these rea-
sons total hysterectomy is the operation of choice.
Steps of total abdominal hysterectomy:
- Clamp and cut the round ligament, then the broad ligament on both sides.
- Clamp and cut the infundibulo-pelvic ligament.
- Dissect the bladder downwards.

- Clamp and cut the uterine arteries, then the parametrium on both sides.
- Open the upper vagina and remove the uterus.
N.B.: In subtotal hysterectomy, remove the body leaving the cervix after clamping and cutting the
uterine arteries.

Vaginal Hysterectomy
Indications of Vaginal Hysterectomy:
l-. Some cases of uterine prolapse or chronic inversion.
2. some cases of (DUB), some cases of small fibroids and occasionally in some cases of cancer
body. However, the uterus should be normal in size or only slightly enlarged and is not sur-
rounded by any adhesions.
3. Schauta operation is a radical vaginal hysterectomy, which may be done in cases of cancer cer-
vix, but it has the disadvantage that the lymph nodes cannot be removed

Advantages of vaginal hysterectomy:

1. Absence of an abdominal scar.
2. Lower incidence of intestinal complications and peritonitis.
3. An associated genital prolapse can be treated at the same time.

Disadvantages:
1. lt is unsafe and difficult in the presence of pelvic adhesions.
2. The ovaries cannot be removed in some cases.
3. lt cannot be done if the size of the uterus is larger than a L4 weeks pregnant uterus (unless the
uterus is bisected before removal).
4. Vault prolapse is more likely to occur than after abdominal hysterectomy.

Steps of vaginal hysterectomy:

Circular incision around the cervix. Dissect the bladder up-wards. Open the peritoneum of the
Douglas pouch, and the peritoneum of the vesico-uterine pouch, clamp and cut the Mackenrodt's
ligaments, then the Uterine arteries, then the broad ligaments, when the uterus will be removed.
 Gynaecology 279

MYOMECTOMY
Myomectomy is the surgical procedure in which myomas are enucleated from their bed in the
myometrium, while preserving the whole uterus for further menstruation and childbearing. The
procedure is more appropriate for young patients, with infertility or low parity.
Contraindications to Myomectomy:
L. During pregnoncy: increased uterine vascularity and poor contractility will predispose to ex-
cessive bleeding and increased risk for abortion (torsion in a pedunculated SSM is an excep-
tion that may call for emergency myomectomy).
2' After menopouse.'myomas that present by increase in size or PMB are highly suspicious for
malignancy, in such cases hysterectomy is the only choice whenever surgery is indicated.
3. suspicion of sarcomatous chonges (see complications of leiomyomas)
4. Multiparous perimenopousol women: No point for preserving the uterus with chances of re-
cu rrence
5. Multiple huge myomas regardless age and parity; where myomectomy is difficult and associat-
ed with marked blood loss that might endanger the life of the patient.

Types of Myomectomy:
Myomectomy could be performed via the following routes;
r Abdominal Myomectomy
r Vaginal Myomectomy
r Laparoscopic Myomectomy
r Hysteroscopic Myomectomy
A. Abdominal Myomectomy: (The commonest approach)
- Abdominal myomectomy is the operation of choice f or multiple and lorge leiomyomas.
- Loparotomy maY be performed via a transverse suprapubic or longitudinal midline skin incision
according to the size, site, and number of myomas to be removeo.
- The anterior rectus sheath is opened by sharp dissection, the rectii muscles separated laterally,
and the peritoneum is entered by blunt or sharp dissection, with care not to injure intestine.
- The myometrial incision is best planned at the midline of anterior uterine wall, according to
the site and number of myomas (to avoid injury to the tubes and ovaries, and to avoid postop-
erative adhesions posteriorly that may interfere with tubal function and oocyte pick up mech-
anism).
- Enucleation of myomas: is performed after cutting through its false capsule
(i ntraca psu la r).
- Obliteortion of the tumour bed: interrupted sutures to avoid haematoma formation.
- Opening the endometrial covity might be necessary for complete removal of a SMF. This
can be assessed preoperatively by saline infusion TVS, HSG, or office hysteroscopy.
- Reconstruction of the uterus is performed after removal of all myomas
- Closure of the abdominal woll;the abdominalwall is finally closed in layers

N.B.: Opening the uterine covity in tSM is considered a risk foctor for
future uterine rupture, and
therefore is on indication for cdesoreon section in subsequent pregnoncies.
280 Operative Gynoecology

Fig 32-7: Myomectomy

B. Vaginal Myomectomy:
For pedunculated SMF polyp in the endometrial cavity, or protruding through the cervix.
The pedicle of the tumour is ligated or coagulated by diathermy.
Cervical myomas arising from the portio-vaginalis can also be easily removed vaginally.
C. Hysteroscopic Myomectomy:
For removal of small SMM <5.0 c m diameter which protrude >50% in uterine cavity.
Diathermy, or laser resection, are better preceded by LH- RH agonist preparation to de-
crease vascularity and diminish the size of myomas.
The procedure is associated with minimal pain and bleeding with short recovery.

Resectoscope
Loop

/n'v
Resectoscope
" L
Fig 32-8: Hysteroscopic Myomectomy

D. Laparoscopic Myomectomy:
Myomectomy can be performed via laparoscopy when myomas are limited to <4 in number,
< 5 cm in size, mainly SSM (rarely ISM), provided the uterus is < 16 weeks size. lt has the ad-
vantage of less postoperative pain, shorter and better postoperative recovery period, and the
disadvantage of having limited indications, longer operative ti m e, need for advanced instru-
ments and well trained team. lt is not proven if it is associated with less postoperative adhe-
sions.
 Gynaecology 281

Complications of Myomectomy:
1. lmmediate Complications:

mostasis. This can be minimized through the use of intra-operative tourniquet (to com-
press the uterine and ovarian vessels), or injection of intra-myometrial vasopressin (to in-
duce vasoconstriction) or the use of GnRH agonists 3-6 months preoperatively (to induce
diminished size and vascularity of myomas).

2. Delayed Complications:

large myomas and associated adenomyosis.

More common after removal of multiple and large myomas in younger patients
- More common in high risk population (dark races, African women, +ve family history)
- More common with incomplete removal of leiomyomas at primary surgery leaving
seadling small myomas to grow by time especially in young patients.

ly intestina I obstruction.

POSTOPE RATIVE COM PLI CATIONS O F ABDOM I NAL OPERATIONS

(HYSTERECTOMY & MYOMECTOMY)

L. Shock.

2. Haemorrhage (primary (reactionary or secondary).

3. Infection, Intestinal complications as acme gastric dilatation, paralytic ileus or adhesions (those
lead to vomiting and distension) and Injuries to abdominal organs.

4' Pulmonarycomplications e.g.:(a) bronchitis, bronchopneumonia or lobar pneumonia. (b) pul-

monary collapse, (c) pulmonary embolism (resulting from phlebothrombosis of the deeo veins
in the calf muscles).

5. others (depending on the type of the operation) e.g. (a) Venous thrombosis: lt may be superfi-
cial (occurring in the superficial veins of the lower limbs) OR deep (occurring in the deep veins
of the lower limbs e,g. the femoral vein or in the pelvic veins). lt may be either phlebothrom-
bosis (without inflammation of the vessel wall) and the thrombus can "be detached easily lead-
ing to pulmonary embolism, or thrombophlebitis (associated with inflammation in the vessel
wall) and the thrombus is more firmly attached to the vessel wall and less liable to be detached,
(b) Wound infection and burst abdomen, (c) Urinary complications e.g. incontinence of urine
(which may be due to bladder or ureteric injury, or due to retention with overflow), cystitis,
retention of urine, suppression of urine (due to bilateral ligation of ureters or renal failure), (d)
Fecal and rectovaginal fistula.

5. Postoperative anaesthetic complications e.g, postoperative cyanosis, postoperative vomiting,

pulmonary complications (collapse or infection after inhalation of vomitus).
282 Operative Gynoecology

7. Remote complications e.g.

a. Comolications of the abdominal scar as keloid formation and incisional hernia,
b. Vaginal discharge due to infection at the vaginal vault.
c. Vaginal vault prolapse after hysterectomy
d. Dyspareunia. after hysterectomy (either due to a tender scar in the vaginal vault or an ad-
herent ovary to the vaginal vault.
e. Low backache either due to prolonged lying on a flat table during the operation or due to
persistent chronic pelvic cellulitis.
f. Menopausal symptoms following bilateral oophorectomy in a young patient.
CAUSES OF POST.OPERATIVE VOMITING
1. Effect of anaesthesia. 2. Acute gastric dilatation. 3. Paralytic ileus.

4. Peritonitis. 5. lntestinal obstruction.

Treatment of No. (2), (3), (4), (5) is by adequate fluid and electrolyte replacement, continuous suc-
tion by Ryle tube in No. (2) and Miller Abott tube in the rest, antibiotics if there is infection, and lap-
arotomy and dealing with the cause in No.(5).

CAUSES OF POST.OPERATIVE DISTENSION

1. Mild distension may occur on the 2nd post-operative day.
2. Acute gastric dilatation. 3. Paralytic ileus.

4. Peritonitis. 5. lntestinal obstruction.

POSTOPE RATIVE TH ROM BO.EM BOLISM

Femoropopliteal or calf deep venous thrombosis may occur after major gynaecological opera-
tions. The risk increases with age, presence of malignancy, use of oral contraceptives, prolonged
bed rest, obesity, varicose veins and it is higher with abdominal rather than vaginal operations. A
detached thrombus results in pulmonary embolism.

Diagnosis: Local pain, leg swelling, rise of temperature, local tenderness, use of local Doppler ultra-
sound, radioisotope labelled fibrinogen and ascending venogram.
Prophylaxis: Subcutaneous heparin 5000 units 2 hours before surgery and then repeated 12 -hourly
unit the patient is mobile.
Treatment: Heparin 1-0000 units l.V. every 6 hours for 48 hours, with 10 mg warfarin in the Lst day
and 5 mg in the 2nd day. Subsequently the daily dose of warfarin is adjusted according to the pro-
thrombin time. Patients who develop recurrent non-fatal pulmonary embolism are treated by place-
ment of inferior vena cava filter or by ligation of the inferior vena cava.

POSOPERATIVE HAEMORRHAGE AFTER VAGINAL SURGERY

l. Primary Haemorrhage
Occurs during the operation. Either due to bad surgical technique or bad choice of patient
(presence of local infection causing hyperaemia and con-gestion) or bad choice of timing of opera-
tion (presence of unsuspected pre-gnancy or operating in the premenstrual period). Treatment is
mainly pro-phylactic.
 Gynaecology 283

ll. Reactionary Haemorrahge

After operation, when the effect of the anaesthetic goes off, the blood pressure is raised and
returns to its original pre-operative level. lf a vessel is left unligatured or loosely ligatured, is going
to bleed. This type of haemorrhage occurs within the first 24 hours after the operation, that is why
routine vaginal packing for 24 h. (to cover the period of possi-ble reactionary haemorrhage) is highly
recommended. lf it occurs treat shock, if present, at first, then transfer the patient to the theatre,
suture any bleeding vessel then insert a tight vaginal pack.

lll. Secondary Haemorrhage

This occurs on the L0th post operative day due to sepsis. Sepsis might have been present pre-
operatively (trophic ulcer), induced during the opera-tion (septic instruments), or sepsis resulted
afterthe operation (septic dressings). lfoccurs, treat shock and then transferthe patient to theatre.
Do not take any sutures in the friable septic tissues as this will encourage further bleeding. Do im-
mediate tight vaginal pack and give parenteral broad spectrum anti-biotics.