‫بسم ال الرحمن الرحيم‬

NON NEOPLASTIC CYSTS

OF THE OVARY
NON NEOPLASTIC CYSTS
OF THE OVARY
 Enlargement of the ovary is one of
the common gynaecological
conditions encountered in clinical
practice.
 Ovarian cysts could be either non
neoplastic or neoplastic cysts.
 Non neoplastic cysts of the ovary
are by far more common than
neoplastic cysts
 Non neoplastic cysts of the
ovary include:
1. Follicular cysts
2. Corpus luteum cysts
3. Theca lutein cysts
4. Endometriotic cysts
5. Inflammatory cysts
6. Germinal inclusion cysts
7. Polycystic ovary
I. FOLLICULAR CYSTS
 the commonest non neoplastic
cysts of the ovary.
 They may arise either from cystic
over-distension of an atretic
follicle, or a dominant Graafian
follicle that failed to rupture.
 Pathology:

usually single
 unilateral

 small in size (<7 cm)

 unilocular, containing clear fluid.

 The cyst wall is thin, lined by

granulosa cells.
 Commonly encountered with:

a) Metropathia Haemorrhagica (MH)
 b) Polycystic ovarian syndrome

(PCOS)
 c) In association with fibroids and

endometriosis.
 Fate & Complications:
 rupture spontaneously
 haemorrhage

Spontaneous resolution
Clinical picture:
 Asymptomatic
 Menstrual disturbance

 Pain (rarely acute abdomen

Diagnosis:
 Abdominal palpation
 Bimanual examination

 Ultrasonography: Pelvic TAS or TVS,

it is the gold standard in diagnosis

 Pathology:
 lined by leutinized granulosa
cells
 usually unilateral, single,
unilocular, small sized (3-7 cm),
containing either bloody fluid or
clear content.
 D.D.: From simple serous
cystadenoma

 Treatment:
• Conservative by follow up
• Surgery (ovarian
cystectomy)
II. CORPUS LUTEUM
CYSTS
 They arise from excessive
haemorrhage inside the corpus
luteum during the stage of
vascularization.
 They are less common than
follicular cysts
 Pathology:usually

Unilateral
 Single

 Unilocular

 Small sized (3-7 cm)

 Containing either bloody fluid or

clear content.

Lined by leutinized granulosa
cells
 Fate & Complications:

Spontaneous resolution
 Spontaneous rupture

 Haemorrhage

 Clinical picture:
 Asymptomatic
 Menstrual disturbance

 Acute lower abdominal pain

 Diagnosis:
is settled by detection of the cyst by
pelvic TAS, or TVS.
 Treatment:
A) Conservative
B) Surgery
III. THECA LUTEIN
CYSTS
 They commonly arise due to
ovarian hyperstimulation by
either:
 a. Excessive amounts of hCG in
the circulation: or
 b. Excessive amounts of
Pituitary gonadotropins:
 Pathology:

usually multiple
 commonly bilateral

 bluish in colour

 thin walled, containing clear fluid

 they may reach a large size > 20

cm

lined by leutinized theca cells.
 Fate & complications:
 The majority undergo spontaneous
regression whenever hCG levels
fall.

Less commonly cysts may undergo
torsion or haemorrhage
 Diagnosis: Pelvic Ultrasonography:
Multilocular, bilateral, echolucent cysts
in a patient with a history suggestive of
abnormally elevated hCG levels, or
ovarian stimulation by HMG or CC
 Treatment:
 Expectant treatment after removal of
the source of gonadotropin
stimulation

 Laparotomy should always be

avoided, unless cysts are
complicated.
IV. ENDOMETRIOTIC
CYSTS
 Incidence & Origin:
Not uncommon especially with
infertility and pelvic endometriosis.
 Pathology:
 haemorrhagic cysts of the ovary lined
by endometrial tissue (glands &
stroma).
 They have a relatively thick wall.
 Their size is rarely large, and
spontaneous rupture is uncommon.
 The contents are characteristic
with thick chocolate appearance
(chocolate cysts):
 Blood accumulates within the cyst
 By time, absorption of the serous

element of the retained blood

occurs leaving behind RBCs
 Treatment:
 Superficial ovarian lesions can be
vaporized.
 Small endometriomas <3 cm can be
aspirated, irrigated, and the interior
wall vaporized.
 Large endometriomas >3 cm require
removal of the cyst wall to prevent
recurrence.
V. INFLAMMATORY CYSTS
OF THE OVARY

 Origin:

These may be in the form of Tubo-
ovarian cysts or Tubo-ovarian abscess.
 Infection may reach the ovary either by

lymphatics or a nearby- infected organ.

Tubo-ovarian cyst
Tubo-ovarian abscess
 Clinically:
 usually bilateral,

 the patient usually presents

with a history of recent

delivery or abortion, a recent
surgical pelvic operation or
IUD insertion.
VI. 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 importance, but now they are
regarded as forerunners for ovarian
epithelial cancers.
OVARIAN NEOPLASMS
CLASSIFICATION OF
OVARIAN NEOPLASMS
 HISTOGENETIC
CLASSIFICATION
Histologically, ovarian tumours can arise from
any of the three elements constituting the
ovary (surface epithelium, germ cell
apparatus, and ovarian stroma).
1. Epithelial Tumours
2. Germ cell tumours
3. Sex cord stromal tumours
 CLINICAL CLASSIFICATION
Clinically, ovarian tumours can be divided into:
1. Benign or malignant
tumours
2. Cystic or solid tumours
N.B.: Benign ovarian tumours are usually cystic while
malignant tumours are usually solid. N.B.: Malignant
ovarian tumours are usually primary, but may be rarely
metastatic.
 HISTOGENETIC CLASSIFICATION
1. EPITHELIAL TUMOURS OF THE OVARY
a. Serous Cystadenoma
b. Mucinous cystadenoma
c. Endometrioid tumours
d. Brenner tumour
2. GERM CELL TUMOURS
a. Teratoma
b. Dysgerminoma
c. Endodermal sinus tumour
d. Choriocarcinoma
3. SEX CORD STROMAL TUMOURS
a. Ovarian Fibroma
b. Thecoma
c Granulosa cell tumour
d. Androblastoma (Sertoli-leydig cell
1. EPITHELIAL TUMOURS
OF THE OVARY
 The commonest neoplasms arising
in the ovary.
 They are essentially benign, but
could be either border line, or
malignant tumours.
 Tumours originate from the surface
epithelium (derived
embryologically into Mullerian and
Wolffian epithelium), which can
differentiate into serous,
2. GERM CELL
TUMOURS
 Amongst the commonest ovarian
tumours seen in women <30 years
of age.
 Essentially benign, less than 2-3%
may be malignant.
 Tumours arise from totipotential
germ cells, and may therefore
contain elements of all three germ
layers (ectoderm, endoderm, and
 Germ cell tumour could be either:
 Differentiated
 Embryonic tissue (teratoma)
 Extra-embryonic tissue:
 Yolk sac: Endodermal sinus tumour

Trophoblast: choriocarcinoma
 Undifferentiated
 No evidence of differentiation into
embryonic or extra-embryonic tissue
(Dysgerminoma)
3. SEX CORD STROMAL
TUMOURS

 The least commonly encountered

tumours representing <4% of all
ovarian neoplasms.
Originate from two elements in
the gonad:
 The primitive sex cord; which
developmentally gives origin to
granulosa cells in the ovary, or
Sertoli cells in the testicle.
 The stroma of the gonad; which
differentiate into theca cells in
the ovary or Leydig cells in the
testicle.
BENIGN TUMOURS OF
THE OVARY
Classification of benign
ovarian tumours
 Benign surface epithelial
tumours:
Cystic
Serous cystadenoma
Mucinous cystadenoma
Endometrioid cystadenoma
Solid
Brenner tumour
Classification of benign
ovarian tumours (ctd.)
 Benign germ cell tumours:
Cystic
Benign cystic teratoma
(BCT)
  
Solid
Struma Ovarii
Gonadoblastoma
Classification of benign
ovarian tumours (ctd.)
 Benign sex cord stromal
tumours:
(Solid)

 Fibroma

 Theca cell tumour

Pathology of benign
ovarian tumours

I. BENIGN EPITHELIAL OVARIAN

TUMOURS
  Serous Cystadenoma:
This is the commonest ovarian
tumour representing nearly
10-15% of all ovarian
neoplasms.
 Bilateral in up to 30% of cases

 Of moderate sizes (ranging 10-

15 cm)
 it may present in one of the
following three types:
 Simple serous cysts
 Multilocular serous cyst


Papillary serous cystadenoma
 Microscopically: cyst wall is lined
by cuboidal cells which may be
ciliated or non ciliated (tubal like
epithelium).
 
Mucinous Cystadenoma
 These are the second most common
benign ovarian neoplasms.
 commonly unilateral
 bluish or yellowish transparent colour
 multilocular
 containing thick gelatinous like
mucin material
 may reach huge size
 Microscopically: Cyst wall is lined
by tall columnar epithelium
with basally situated nuclei similar
to endocervical epithelium, rich in
Goblet cells .

 N.B. Pseudomyxoma peritonii

  Brenner tumour
 Rare tumours accounting for
only 1-2% of all ovarian
neoplasms.
 Solid in consistency.
 Usually of small (<2.0cm) to
moderate size.
 More prevalent in women >40
years.
 Microscopically: the tumour is
characterized by epithelial cell
nests with characteristic coffee
bean nuclei.
 They probably arise from Wolffian
metaplasia of the surface ovarian
epithelium.
II. BENIGN GERM CELL TUMOURS
 Benign Cystic Teratoma (BCT)
 It is the only germ cell tumour
which is common, representing
almost 40% of all ovarian
neoplasms.
 It is the commonest tumour
encountered below 20 years,
during pregnancy and during the
child bearing period.
 Bilateral in up to 12 % of cases.
 Usually of moderate size (8-10
cm).
 Most have a long pedicle.
 Greyish in colour
 Mostly unilocular, but may contain
few small locules.
 The cut section; usually shows
 Being derived from toti-potent
germ cells, they can differentiate
to three elements:
 Ectoderm
 Mesoderm

 Endoderm

 Microscopically: the cyst wall is

lined by stratified squamous
epithelium with sebaceous glands.
 Struma Ovarii
 It is an example of monodermal
teratoma, composed of hormonally
active thyroid tissue.
 They comprise only 1-4% of cystic
teratomas.
 Only 5% produce sufficient thyroid
hormone to produce symptoms.
 Some 5-10% of tumours develop into
carcinoma.
 Gonadoblastoma
 A benign solid tumour composed of
germ cells mixed with other cells
resembling granulosa and sertoli
cells.
 Patients have an abnormal gonad,
with a Y chromosome in 90% of
cases.
 Predispose to development of
Dysgerminoma or other malignant
germ cell tumours.
III. BENIGN SEX CORD STROMAL
TUMOURS
 Fibroma
 rare tumours are mostly seen
around age of 50 years.
 Usually mobile with a long
pedicle
 They have lobulated glistening
white surface.
 N.B. Meig's syndrome
 Theca Cell Tumour: (Thecoma)
 The majority occurs in post

menopausal women.
 Many are functioning tumours,

producing oestrogen.
 Microscopically: tumour is

formed from cells resembling

theca interna cells.
COMPLICATIONS OF BENIGN
OVARIAN NEOPLASMS

1. TORSION
2. HAEMORRHAGE
3. RUPTURE
4. INFECTION
5. INCARCERATION
6. MALIGNANT
TRANSFORMATION
Torsion
Traumatic rupture
Malignant transformation
CLINICAL PICTURE OF
BENIGN OVARIAN
NEOPLASMA
 Symptoms:

Asymptomatic
 Abdominal swelling

 Menstrual disorders

 Pressure symptoms

 Lower abdominal pain

Detected only by bimanual
examination or
ultrasonography
 Physical Signs: These will depend
largely on the size of the tumour.
 a. Small tumours:
 Felt only by bimanual pelvic
examination

on one side of the uterus,
 rounded, smooth, mobile,

 usually cystic ( rarely solid) mass,


separate from the uterus (the
movement of the mass is not
transmitted to the cervix)
 b. Large tumours:
 Inspection: symmetrical abdominal
enlargement
 Palpation: - Abdominal mass that may be
central or to one side
- Well defined upper and lateral
border
- Smooth or lobulated surface
- Commonly mobile from above
downwards.
 Percussion: central dullness with resonant
flanks
N.B. Ovarian cachexia
 Diagnosis:

clinical examination
 Ultrasonography

 I.V.P


C.T. scan and MRI
TREATMENT OF BENIGN
OVARIAN NEOPLASMS

2. Ovarian Cystectomy:

2. Oophorectomy:

3. Panhysterectomy:
Ovarian cystectomy
Ovariotomy
MALIGNANT OVARIAN
TUMOURS
 Malignant epithelial tumours:

Serous adenocarcinoma
 Mucinous adenocarcinoma
 Endometrioid adenocarcinoma
 undifferentiated adenocarcinoma
 Malignant germ cell tumours:

Dysgerminoma
 Endodermal sinus tumour
 Choriocarcinoma
 Solid teratoma
 Malignant sex cord stromal tumours:

Granulosa cell tumour
 Sertoli-Leydig cell tumour  
I. EPITHELIAL OVARIAN
CANCER
Incidence:
 Primary ovarian epithelial cancer

forms 60-70% of all ovarian

tumours.
 90% of all ovarian malignancies.

 It is the third common malignancy

of female genital organs.

Aetiology:
Possible factors include:
3. Reproductive factor:
Nulliparous or infertile women are more
liable to develop it.
2. Hereditary 'Genetic' factor:
 5- 10% of epithelial ovarian cancer occur in
women with hereditary predisposition.
 A particular feature of familial cancer is that it
tends to occur at a younger age.
 Hereditary predisposition is due to a defective
gene in their families, which is tumour
suppression gene BRCA, BRCA2 .i.e. gene
mutation.
Three types of familial ovarian
cancer are identified:
 Site specific ovarian cancer syndrome
(15%)
 Hereditary breast / ovarian cancer
syndrome (75%)
 Hereditary non polyposis colorectal
cancer syndrome with endometrial,
breast, or ovarian cancer (10%).
Risk factors for epithelial
cancer:
 Age
 Nulliparity & infertility
 White race
 Prior history of endometrial or
breast cancer
 Family history of ovarian cancer
 PATHOLOGY OF PRIMARY
EPITHELIAL OVARIAN CANCER

Macroscopic appearance:
 Usually solid but may be partially

cystic partially solid.

 Unilateral or bilateral

 The size is extremely variable

 The substance of the tumour is the

seat of extensive haemorrhage and

necrosis.
Microscopic picture: It is an
Adenocarcinoma
Which might be either :
 Serous cystadenocarcinoma
 Mucinous cystadenocarcinoma.
 Endometrioid cystadenocarcinoma.
Which could be either :
a. Well differentiated (Gr I)
b. Moderately differentiated (Gr II)
c. Undifferentiated (Gr III)
N.B. Border line epithelial tumours
MALIGNANT GERM CELL
TUMOURS
 The incidence of germ cell
tumours is only 20-30% of all
ovarian tumours.

 Five per cent of germ cell

tumours are malignant.
Classification of malignant germ
cell tumours:
• Dysgerminoma
• Endodermal sinus tumour (yolk sac
tumour)
• Choriocarcinoma
• Malignant teratoma
 Benign cystic teratoma with
malignant transformation
 Malignant solid teratoma
Special Features of Germ Cell
Tumours:
They differ from epithelial ovarian cancer by
the following points:
• Lower age incidence
• The commonest tumours of
abnormal gonads and in sex
chromatin negative females.
• tend to grow rapidly resulting in
pelvic pain and pressure symptoms
occurring early tend to grow rapidly
resulting in pelvic pain and pressure
symptoms occurring early.
1. Most tumours produce substances
in the circulation that can be used
as tumour markers;
 Dysgerminoma: alkaline phosphatase
& lactic acid dehydrogenase.
 Endodermal sinus tumour : alpha
feto proteins.
 Choriocarcinoma :hCG
2. Radiosensitive, chemotherapy in
some of them gives excellent
results in stage Ia.
3. Conservative surgery in the form of
salpingoopherectomy is the first
line of treatment.
• Dysgerminoma:
 The commonest malignant germ
cell tumour accounting for about
30-40% of all malignant germ cell
tumours.
 Represents 1-3% of all ovarian
tumours.
 Tends to occur at a younger age
(10-20 years).
 May secrete alkaline phosphatase
Pathology:
 Solid ovarian tumour, usually of

small or moderate size

 Bilateral in only 10% of cases.

 Greyish with lobulated surface with

tendency to haemorrhage and

necrosis.
Microscopically:
 Consists of gem cells arranged in

alveoli or nests separated by fibrous

tissue septa heavily infiltrated with
lymphocytes.
 Cells are round, large, with abundant

cytoplasm and a large irregular

nucleus.
Treatment:
 Surgery:

 Unilateral salpingoophorectomy,
 TAH&BSO
B) Endodermal Sinus Tumour
“EST”
 Prevalent in a young age (median

age of 16-18 years).

 Most EST secrete alpha-

fetoproteins that are used as a

tumour marker.
Pathology:
 Small solid tumours which are
Microscopically:
 EST have a characteristic microscopic
picture; Shiller-Duval bodies. These are
cystic spaces in which projects a
glomerulous-like structure with a central
vascular core.
Treatment:
 Surgery :

 unilateral salpingoophorectomy
 TAH&BSO
 Chemotherapy: the tumour is
chemosensitive
MALIGNANT SEX-CORD
STROMAL TUMOURS
Sex-cord stromal tumours may arise
from non- functioning or functioning
stroma of the ovary.
 Functioning sex–cord tumours

may be:
 Estrogenic: as granulosa cell tumour.
 Androgenic: as Sertoli-leydig cell
tumours
 Both estrogenic and androgenic effect
(very rare): as in Gynandroblastoma.
 Non- functioning stroma may very
rarely give rise to fibrosarcoma of
A) Granulosa Cell Tumours:
 Usually unilateral, solid, yellow or yellow-

grey in colour.
 Some are functioning secreting oestrogen,

while most appear to secrete inhibin.

 Associated with endometrial carcinoma in

5-10% of cases, and with endometrial

hyperplasia in 25-50% of cases.
 They may cause irregular bleeding or

precocious puberty (before puberty),

menstrual irregularities or post
menopausal bleeding.
 Microscopically:
 The tumour is formed of granulosa

cells arranged in different patterns.

Call-Exner bodies are
pathognomonic, but are present in
only 50% of cases. These are cystic
spaces surrounded by granulosa cells
arranged in a rosette-like shape.
Treatment:
 Unilateral salpingoophorectmy:
 TAH BSO:
 No place for irradiation or
B) Sertoli-Leydig Cell Tumours:
 They are very rare representing <

0.2% of all ovarian tumours.

 They are usually small, unilateral,

solid tumours, of low grade

malignancy.
 Many are functioning producing

androgens.
 Treatment: Either unilateral

salpingoopherectmy if the patient is

young or TAH&BSO.
PATTERNS OF SPREAD OF
OVARIAN CANCER
Primary methods of spread of
ovarian cancer are:
 Direct extension

 Lymphatic spread

 Transcoelomic spread

 Haematogenous spread
 Metastatic Ovarian
Cancer
Metastatic ovarian cancer forms about
5-6% of all ovarian tumours. The
primary may be:
 Genital tumours: From the
endometrium, cervix, tube, and
contralateral ovary.
 Extragenital tumours: From the
stomach, colon, breast, biliary tract, and
thyroid gland.
 Krukenberg Tumour:
 It accounts of 30-40% of metastatic
cancer to the ovary.
 The primary is usually in the pylorus,
less commonly in colon, breast or
biliary tract.
 They 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
Bilat. Krukenberg tumours
Prognosis:

Bad, most patients die within one

year because most of the lesions
are not discovered until the
primary disease is advanced.
 CLINICAL PICTURE OF
PRIMARY MALIGNANT
OVARIAN TUMOURS
 This is a disease of late decade of life:
55–65 years of age in the majority of
cases.
 It is more common in industrial countries.
SYMPTOMS:
• Early stage disease: are mostly
asymptomatic.
 may be associated with non specific GIT
symptoms in the form of dyspepsia,
indigestion, and anorexia. Pressure
symptoms as urinary frequency, and
constipation may be present, with or
without pelvic pain.
• Late stage disease: may
present with:
 Abdominal pain and cachexia,
abdominal swelling.
 Abnormal uterine bleeding, and
especially postmemnopausal
bleeding.
 Rarely ascites may be the first
clinical presentation.
PHYSICAL SIGNS:
 The most important physical sign is the

palpation of a pelvic mass.

 If the patient is lucky this pelvic mass is

discovered during routine pelvic

examination.
 In late cases a pelviabdominal fixed

solid mass is felt.

 Bilateral solid fixed masses are always

suspicious of malignant ovarian tumour.

CLINICAL FEATURES
SUGGESTING MALIGNANCY
INOVARIAN TUMOURS

A) History:
 Age, especially extremes of age

(before puberty, or > 40-60 years).

 Rapid growth of the tumour.

 Pain and loss of weight are always

late symptoms.
 Post menopausal bleeding and

symptoms of virilisation, are

suspicious.
B) General examination:
 Malignant Cachexia (with marked and

rapid weight loss and dehydration)

 Palpable supraclavicular lymph nodes

especially on the left side, (Virchows

glands).
 Pleural effusion, however it may be

present in Meig’s syndrome.

 Associated breast mass, on breast

examination
 Unilateral leg & edema (unilateral
C) Abdominal Examination:
 Inspection: Abdominal

enlargement, over lying skin

showing peau d’orange.
 Palpation: Tumour which is solid

(or partially solid), fixed especially

if bilateral.
 Percussion: Presence of ascites

(except with ovarian fibroma in

D) Pelvic examination:
 Nodules in Douglas pouch in the

presence of a non tender adnexal

mass.
 Bilateral, especially if solid adnexal

masses are very presumptive.

 Fixed pelvic masses especially if

amalgamated with pelvic organs

(frozen pelvis).
At Laparotomy:
 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 or liver

 Variable consistency with a cut section of

the tumour shows haemorrhage and

SPECIAL INVESTIGATIONS
FOR OVARIAN CANCER
 Pelvic ultrasound
 Endometrial curettage
 Chest X-Ray
 Plain X-Ray abdomen
 Barium meal and/or enema
 Upper and/or lower G.I. Endoscopy
 I.V.P.
 Paracentesis.
 CT & MRI.
Tumour markers:
 CA 125 (n < 35 u/ml):
 This the most important marker used.
 However it may be elevated in some benign
conditions; as endometriosis and chocolate
cysts.
 It can be used also to monitor response to
chemotherapy (decreasing levels denote good
response).
 Other markers include; serum B-hCG
(choriocarcinoma), alpha fetoprotein (EST),
serum alkaline phosphatase, and lactic acid
dehydrogenase (dysgerminoma).
SCREENING for Ovarian Cancer:
 Routine yearly pelvic examination

in premenopausal and
postmenopausal women.
 Periodic TVS coupled with a serum

CA-125 in those with an enlarged

ovary
DIFFERENTIAL DIAGNOSIS of
ovarian masses
 Pelvic masses: as
 adnexal masses.
 uterine enlargement (myomata &
pregnancy).
 colonic masses.
 retroperitoneal masses (pelvic kidney,
retroperitoneal sarcoma, ...)
 Abdominal masses as
 liver or pancreatic tumour.
 tense ascites.
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.
STAGING OF OVARIAN
CANCER
Clinical staging
For a malignant ovarian tumour
will always
be short of important items that will
affect
the prognosis and line of treatment,
surgical
staging is therefore the only
standard
Surgical staging of primary
ovarian cancer:
entails a mid line subumbilical suprapubic
exploratory laparotomy in which the
following is
performed:
 Exploration of the pelvic and peritoneal
cavity
 Aspiration of any fluid in cul de sac
(ascites), or perform peritoneal
washings for Cytology.
 Performing an infracolic omentectomy.

 Pelvic and paraaortic lymph node

sampling
 The complete procedure will then
be a TAH BSO (or debulking of the
malignant tumour),
omentectomy, lymph node
sampling or resection, removal
of any pelvic or extrapelvic tumour
masses >2.0 cm, and cytology
to peritoneal fluid.
 FIGO surgical staging for
primary epithelial ovarian
carcinoma
Stag FIGO definition (simplified)
e
Stag Growth limited to ovaries
eI
Ia Growth limited to one ovary
No ascites; No tumour on external
surfaces; capsule intact
Ib Growth limited to both ovaries
No ascites; no tumour on external
surfaces; capsule intact
FIGO surgical staging for
primary epithelial ovarian
carcinoma (ctd)
Ic  Growth involving one or both
ovaries with pelvic extension
to
Uterus and tubes
Other pelvic tissues
Stages IIa, or IIb with tumour on
surface of one or both ovaries,
capsule ruptured, or presence of
ascites containing malignant cells
or +ve peritoneal washings
FIGO surgical staging for
primary epithelial ovarian
carcinoma (ctd)
Stage Growth involving one or both
II ovaries with pelvic extension
to
IIa uterus and tubes
IIb other pelvic tissues
IIc stages IIa, or IIb with tumour on
surface of one or both ovaries,
capsule ruptured, or presence of
ascites containing malignant cells
or +ve peritoneal washings
 FIGO surgical staging for
primary epithelial ovarian
carcinoma (ctd)
Stage  Growth involving one or both
III ovaries with peritoneal implants
outside the pelvis or positive
IIIa retroperitoneal or inguinal
tumour grossly limited nodes
to the true pelvis
with –ve nodes
IIIb tumour with implants < 2.0 cm on
abdominal peritoneal surface. Nodes are
-ve
IIIc tumour with implants > 2.0 cm or Nodes
are +ve
N.B.; superficial liver metastases is
included in stage III c.
FIGO surgical staging for
primary epithelial ovarian
carcinoma (ctd)
Stage Growth involving one or both
IV ovaries with distant
metastases.
If pleural effusion is present

there must be +ve cytology to

allot a case to stage IV.
Parenchymal liver metastasis

equals stage IV.

SURGICAL TREATMENT OF
OVARIAN CANCER
A) Early stage Ovarian Cancer:
 TAH BSO and infracolic

omentectomy is the standard

treatment for patients with disease
limited to the ovary (no gross
evidence for extension beyond the
ovaries Stage I-IIa). Surgical
staging is completed via peritoneal
wash, and lymph node sampling,
for microscopic assessment of the
 Occasionally, unilateral salpingo-
oophorectomy may be done in
selected cases of stage Ia disease
(tumour confined to one ovary, with
capsule intact, and –ve peritoneal
cytology), only when the patient is
young and fertility is desired. Such
conditions are mostly met with in
some early epithelial tumours
(border line tumours), but more
commonly with malignant germ cell
tumours (dysgerminoma and EST),
and malignant sex cord stromal
tumours (granulosa and Sertoli
B) Advanced stage Ovarian
Cancer:
 Primary Cytoreductive surgery

(initial Debulking)
 Interval Debulking

 Radical oophorectomy
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 therapy needed.
 Nowadays modern imaging technique,
as spiral CT & MRI, 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
ovarian
cancer especially in advanced disease,
and mostly
with epithelial ovarian cancer:
• Early stage disease: It has a limited
place only with poor prognostic factors
as Poorly differentiated tumours,
• Advanced stage disease:
Chemotherapy is indicated in all
cases of stage II-IV disease.
a) All cases after primary cytoreductive
debulking surgery
b) Palliative therapy in patients with
irresectable tumours, or patients
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
Toxicity from chemotherapy:
 Chemotherapeutic agents are
highly toxic at therapeutic doses,
and therefore need close
monitoring during treatment
cycles. Toxicity includes; nausea,
vomiting, myalgia and arthralgia.
In severe cases renal damage,
peripheral neuropathy, hearing
loss, dehydration and electrolyte
RADIATION THERAPY IN
OVARIAN CANCER

Radiation therapy has little place in

epithelial
ovarian cancer. It may be used as an
adjuvant therapy following
cytoreductive
surgery in patients who refuse or are
not
good candidate for chemotherapy.
Two main
PROGNOSIS IN OVARIAN CANCER

The prognosis depends upon:

 Histopathological type of ovarian cancer

(epithelial or non epithelial ovarian cancer)

 Stage of ovarian malignancy: the best

prognosis is in stage Ia
 Optimal versus Suboptimal surgery (TAH BSO

+ omentectomy, versus debulking)

 Histology and grading of the tumour. Well

differentiated tumours carry best prognosis,

while poorly differentiated and clear cell
carcinomas carry the worst prognosis.
 Response of the tumour to adjuvant therapy

(chemotherapy – irradiation).
 The 5-year survival rate in
epithelial ovarian cancer is as
follows:
 In stage I 85-90%
 In stage II 80%
 In stage III 15-20%
 In stage IV 5%
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 below
Pathology:
 Parovarian cysts are rarely over

ten centimeters. They are covered

by peritoneum, and the fallopian
tube is characteristically stretched
over their upper surface. They are
thin-walled, unilocular, and lined
by flattened epithelium (cubical)
and contain clear fluid. They do not
tend to be malignant.
Clinical Picture:
 They are usually asymptomalic,

incidentally discovered during

regular pelvic examination, during
pelvic ultrasonography, or during
laparotomy or laparoscopy for any
other condition.
Diagnosis:
 Clinically: Parovarian cysts are differentiated

from ovarian cysts by their fixity and the

displacement of the uterus to the opposite side.
They differ from hydrosalpinx by being free of any
tenderness and by being uni­lateral.
 On ultrasonography: the cyst is unilocular,
thin walled, 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 posterior surface of the cyst.
Treatment:
 Treatment of parovarian cysts
consists of removal of the cyst by
enulceation after incising the
overlying peritoneum. 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.
Thank you