NON NEOPLASTIC CYSTS

OF THE OVARY
Enlargement of the ovary presenting by an adnexal mass, is one of the common
gynaecological conditions encountered in clinical practice. The majority of such ovarian
swellings are non neoplastic in origin (functional cysts of the ovary), however others are
neoplastic representing either benign or malignant tumours of the ovary.

NON NEOPLASTIC CYSTS OF THE OVARY

Non neoplastic (functional) cysts of the ovary are by far more common than neoplastic cysts

Comparison between neoplastic and non neoplastic ovarian swellings

Non neoplastic cysts
1. Incidence
2. Nature

Commoner
Always benign

3. Aetiology

Functional hormone disorder

Excessive levels of hCG
Endometriosis
Inflammation

4. Examples

Follicular cysts
Corpus luteum cysts
Theca lutein cysts
Endometriotic cysts
Inflammatory cysts

Neoplastic cysts
Less common
May be benign or malignant
Unknown

Serous cysts Mucinous cysts

Endometrioid cysts Dermoid
cysts

5. Course

Usually regressive

Always progressive

6. Treatment

Usually conservative using;

Medical treatment
Hormonal treatment
Rarely surgical

Always surgical

TYPES OF NON-NEOPLASTIC CYSTS OF THE OVERY

I. FOLLICULAR CYSTS
Follicular cysts are 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. Spontaneous regression and resolution within a few weeks is almost always the rule,
unless they are complicated by haemorrhage, or rupture (see below).
Pathology:
Cysts are usually single, unilateral, small in size (<7 cm), unilocular, containing clear fluid. The
cyst wall is thin, lined by granulosa cells that may continue to produce oestrogen causing
menstrual disturbance. Follicular cysts of the ovary are commonly encountered with;

a) Metropathia Haemorrhagica (MH)

b) Polycystic ovarian syndrome (PCOS)
c) In association with fibroids and endometriosis.
Fate & Complications: Spontaneous resolution is the rule. Rarely haemorrhage may occur
(producing follicular haematoma), or the cyst may rupture spontaneously if large and rapidly
growing, producing pain with a picture simulating acute abdomen.
Clinical picture:

Asymptomatic; Follicular cysts are usually asymptomatic.

Menstrual disturbance; Delayed menstruation or irregular bleeding due to persistent
oestrogen production leading to endometrial hyperplasia (see abnormal uterine bleeding).
Pain (rarely acute abdomen): If the cyst is large, rapidly growing, or ruptures. It may cause pain
in one of the iliac fossae that may simulate that of appendicitis
Diagnosis:
Abdominal palpation may or may not reveal tenderness at the ovarian point (above the mid
inguinal point), or at one of the iliac fossae.
Bimanual examination may reveal fullness and tenderness on one of the adnexal. The cyst may
rupture during pelvic examination.
Ultrasonography: Pelvic TAS or TVS, is the gold standard in diagnosis, showing single, small,
unilocular, echolucent, thin walled cysts with no septations or internal echoes.
D.D.: From simple serous cystadenoma which is a benign ovarian neoplasm, lined by low
columnar or cuboidal epithelium (see later). Associated pain should be differentiated from
other causes of pain in either iliac fossa (appendicitis, ureteric stonesetc).
Treatment:
A) Conservative by follow up and repeat US: until complete resolution of the cyst. A decrease
in the size of a cyst on repeated US scan is an indication of its functional nature. During
follow up hormone therapy by Gestagens or combined oral contraceptive pills (OCPs) may
accelerate resolution of functional cysts.
B) Surgery (ovarian cystectomy): is rarely indicated except if the cyst ruptures causing acute
abdominal pain with intraperitoneal haemorrhage, or if the cyst is persistent (or increasing in
size), to exclude a neoplastic origin, particularly in the elderly patient. Ovarian cystectomy is
performed either by laparotomy or laparoscopy, with conservation of the ovary.
II. CORPUS LUTEUM CYSTS
They are less common than follicular cysts, arising from excessive haemorrhage inside the
corpus luteum during the stage of vascularisation. Spontaneous regression and complete
resolution is almost the rule. Rarely rupture with lower abdominal pain and intraperitoneal
haemorrhage may occur.
Pathology:
Cysts are usually unilateral, single, unilocular, small sized (3-7 cm), containing either
bloody fluid or clear content. The cyst wall is lined by leutinized granulosa cells that may
continue to secrete progesterone causing menstrual disturbance.
Fate & Complications:

Spontaneous resolution is the rule.

Haemorrhage may rarely occur (producing corpus luteum haematoma).

Spontaneous rupture in rapidly growing cyst may occur, resulting in pain simulating acute
abdomen.

Clinical picture:

Asymptomatic: the majority of corpus luteum cysts are usually asymptomatic.

Menstrual disturbance: may be present in the form of a short delay in the menstrual cycle,
due to persistent progesterone production, commonly followed by irregular vaginal bleeding
(D.D. from abortion and metropathia haemorrhagica).

Acute lower abdominal pain may be present in one of the iliac fossae if the cyst is
complicated with haemorrhage or rupture. (DD; from ectopic pregnancy, where a B-hCG will
be positive, and acute appendicitis if on the right side, where a CBC will be suggestive)

Diagnosis: is settled by detection of the cyst by pelvic TAS, or TVS.

Differential diagnosis: same as follicular cysts (see above)
Treatment:
A) Conservative: Follow up and repeat US is the rule as most cysts will regress then disappear
spontaneously. The possibility of early pregnancy should be always considered.
B) Surgery (Laparotomy, or laparoscopy); is rarely indicated if the cyst ruptures causing acute
pain with intraperitoneal haemorrhage. Cystectomy is performed with ovarian preservation.
III. THECA LUTEIN CYSTS
These are becoming more common in the last decade. They commonly arise due to ovarian
hyperstimulation by either:
a. Excessive amounts of hCG in the circulation; as in Hydatidiform or choriocarcinoma (rarely
in multifetal or singleton pregnancies), or during iatrogenic use of hCG injections for induction of
ovulation in anovulatory infertility.
b. Excessive amounts of Pituitary gonadotropins: as with induction of ovulation using HMG,
or Gn RH analogues or less commonly with clomiphene citrate (C.C.).
Pathology:
Cysts are usually multiple, commonly bilateral, bluish in colour, thin walled, containing clear
fluid. They may reach a large size > 20 cm. as in the serious complication of ovarian
hyperstimulation syndrome (OHSS). Cyst wall is lined by leutinized theca cells.
Fate & complications: The majority of cysts will undergo spontaneous regression whenever
hCG levels fall (after evacuation of a hydatidiform mole, or after discontinuing exogenous
HMG / Gn RH stimulation therapy). Less commonly cysts may undergo torsion or haemorrhage,
especially if moderate to large size.
Diagnosis: Pelvic Ultrasonography: Multilocular, bilateral, echolucent cysts in a patient with a
history suggestive of abnormally elevated hCG levels, or ovarian stimulation by HMG/CC..
Treatment:
Expectant treatment after removal of the source of gonadotropin stimulation (eg.; evacuation
of a molar pregnancy, or withholding ovarian stimulating drugs in OHSS).
Laparotomy should always be avoided if possible, unless cysts are complicated.

IV. ENDOMETRIOTIC CYSTS

Incidence & Origin: Not uncommon especially with infertility and pelvic endometriosis.
Pathology: These cysts represent haemorrhagic cysts of the ovary lined by endometrial tissue
(glands & stroma). Blood accumulates within the cyst due to the menstrual reaction of the
endometrium occurring every month. By time, absorption of the serous element of the retained
blood occurs leaving behind RBCs, which gives its contents their characteristic thick chocolate
appearance (chocolate cysts).
Endometriotic cysts have a relatively thick wall, their size is rarely large, and spontaneous
rupture is uncommon. They are surrounded by dense fibrous adhesions (due to repeated leakage
of the cyst as result of repeated haemorrhage), and therefore rarely undergo torsion.
Clinical picture and Treatment: (see chocolate cyst in endometriosis)
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. (specific or
non specific). Infection may reach the ovary either by lymphatics or a nearby- infected organ.
Clinically: Inflammatory cysts of the ovary are usually bilateral, and the patient usually presents
with a history of recent delivery or abortion, a recent surgical pelvic operation or IUD insertion.
Diagnosis and Treatment: (see chronic PID, tubo-ovarian cyst & abscess).
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.
Key points in functional cysts of the ovary

Non-neoplastic (functional) cysts of the ovary are the commonest ovarian swellings
encountered in clinical practice

Cysts are mostly unilocular, thin walled, with no internal echoes or solid areas

They are usually small in size and rarely exceed 7.0 cm in diameter

The majority are discovered incidentally during routine pelvic examination or US

They are sometimes associated with temporary menstrual disorders

Their fate is generally spontaneous resolution within few weeks of diagnosis

Surgical intervention is rarely needed, and only if complicated

OVARIAN NEOPLASMS
CLASSIFICATION OF OVARIAN NEOPLASMS
HISTOGENETIC CLASSIFICATION
CLINICAL 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

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
Epithelial ovarian tumours are 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, mucinous, or endometrioid tumours
resulting in tumours with cell lines similar to tubal, cervical or endometrial lining respectively.
Brenner tumour has epithelial component similar to transitional epithelium of the urinary tract.
2. GERM CELL TUMOURS
Germ cell tumours are among the commonest ovarian tumours seen in women <30 years of age.
They are 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
mesoderm). Germ cell tumours include:
a. Teratoma
b. Dysgerminoma
c.Endodermal sinus tumour
d. Choriocarcinoma
Germ cell tumour could be either:
Differentiated
Embryonic tissue (teratoma)
Extraembryonic tissue:
Yolk sac: Endodermal sinus tumour
Trophoblast: choriocarcinoma

Undifferentiated
No evidence of differentiation into embryonic or
extraembryonic tissue.
Dysgerminoma

3. SEX CORD STROMAL TUMOURS

These are the least commonly encountered tumours representing <4% of all ovarian
neoplasms. Tumours in this group 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.
Sex cord stromal tumours include:
Malignant
Ovarian Fibroma
Thecoma

Granulosa cell tumour

Androblastoma (Sertoli-leydig cell tumour)

BENIGN TUMOURS OF THE OVARY

Pathology and classification of benign ovarian tumours
Benign surface

Benign

Benign sex cord

Incidence

epithelial tumours
Commonest

germ cell tumours

Less common

stromal tumours
Least common

Origin

Surface epithelium

Germ cells

Sex-cord or Ovarian stroma

Types

Cystic

Cystic

Serous cystadenoma

Benign cystic

Mucinous cystadenoma

teratoma (BCT)

Endometrioid cystadenoma
Solid

Solid

Solid

Brenner tumour

Struma Ovarii

Fibroma

Gonadoblastoma

Theca cell tumour

PATHOLOGY OF BENIGN OVARIAN NEOPLASMS

I. BENIGN EPITHELIAL OVARIAN TUMOURS

A. Serous Cystadenoma
This is the commonest ovarian tumour representing nearly 10-15% of all ovarian neoplasms.
They are bilateral in up to 30% of cases, usually of moderate sizes (ranging 10-15 cm)
when first detected it may present in one of the following three types.

Simple serous cysts: The commonest type of serous cysts. They are unilocular, thin walled,
and filled with thin clear serous fluid.

Multilocular serous cyst: Less commonly serous cyst may be multilocular, with only few
locules.

Papillary serous cystadenoma: Characterized by the presence of papillary growths that may
be present either inside the cyst cavity (endophytic) or outside the external surface
(exophytic). The cyst is usually multilocular. They have the highest malignant potential in all
benign cysts.
Microscopically: cyst wall is lined by cuboidal cells which may be ciliated or non ciliated (tubal
like epithelium).
Psammoma bodies: These represent calcifications within the core of some of the papillae due to
obstruction at the neck and accumulation of secretions. They have no clinical
significance, but may appear as calcified radio-opaque shadows in pelvic X-ray.

B. Mucinous Cystadenoma
These are the second most common benign ovarian neoplasms. They are more commonly
unilateral, having a bluish or yellowish transparent colour, and characterized by being
multilocular with plenty of locules containing thick gelatinous like mucin material.
Mucinous cystadenoma may reach huge size almost 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 .
Mucinous cystadenomas have a possible but low malignant potential (<5%)

Pseudomyxoma peritonii:

This is a rare condition, in which huge amounts of gelatinous material are found free in the
peritoneal cavity. Most cases occur in association with rupture of a pre-existing
mucinous cyst. It may rarely occur secondary to peritoneal epithelial metaplasia, or
rupture of mucocele of the appendix, or in association with cancer of the colon.
Clinically; Progressive abdominal swelling, with emaciation. The diagnosis is seldom made
before laparotomy. Peritoneal adhesions may cause intestinal obstruction.
Prognosis: 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 1-2% of all ovarian neoplasms, and are bilateral
in 10-15% of cases. They probably arise from Wolffian metaplasia of the surface ovarian
epithelium. Microscopically: the tumour is characterized by epithelial cell nests with
characteristic coffee bean nuclei.
The tumour is solid in consistency, usually of small (<2.0cm) to moderate size, more
prevalent in women >40 years, and about half are incidental findings discovered only by
the pathologist.
The majority of tumours are benign, but border line or malignant tumours have been
reported. Some secrete oestrogen and may even present by vaginal bleeding.

II. BENIGN GERM CELL TUMOURS

A) Benign Cystic Teratoma (BCT)
BCT or Dermoid cyst is the only germ cell tumour which is common. It represents almost
40% of all ovarian neoplasms, and is the commonest tumour encountered below 20 years,
during pregnancy and during the child bearing period.
Cysts are bilateral in up to 12 % of cases. They are usually of moderate size (8-10 cm) when
first discovered, and rarely reach huge sizes. Most cysts have a long pedicle that makes them
more liable to complications as torsion.
Cysts are greyish in colour, mostly unilocular, but may contain few small locules.
Being derived from toti-potent germ cells they can differentiate to three elements;
Ectoderm: skin, hair, sweat and sebaceous glands.
Mesoderm: bone, cartilage and smooth muscle.
Endoderm: thyroid, bronchus, and intestinal tissue
N.B.: In BCT there is usually predominance of the ectodermal structures.

B) The cut section; usually shows a large locule, containing a mamilla (a small solid knob <
2cm), and variable tissue contents, representing the three elements, including; hair, teeth,
bone, and cartilage, mixed in a sebaceous material.
Microscopically: the cyst wall is lined by stratified squamous epithelium with sebaceous glands.
Malignancy: BCT have very low malignant potential (squamous cell carcinoma).
N.B.: Most tumours are asymptomatic, incidentally discovered, unless complicated by torsion,
rupture or infection.
B) Struma Ovarii
Rarely a single tissue may be present in a teratoma, in which the term monodermal teratoma
is used. Struma ovarii, is an example that is 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.
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,
particularly with a Y chromosome for fear of future development of malignant neoplasms
BENIGN SEX CORD STROMAL TUMOURS
A. Fibroma:
These rare tumours are mostly seen around age of 50 years. Most are derived from stromal
cells and are similar to thecomas. They are benign solid tumours, usually mobile with a
long pedicle and a lobulated glistening white surface. Less than 10% are bilateral.
Ascites may occur with many of the larger fibromas giving the picture of Meig's syndrome in only
1% of cases. (Meigs syndrome is the association of ovarian Fibroma with ascites and
pleural effusion that disappears on removal of the tumour).
B. Theca Cell Tumour: (Thecoma)
The majority of theca cell tumours (Thecoma or rather fibrothecoma) occur in post
menopausal women, but may occur at any age. Almost all are benign, solid, and
unilateral. Many are functioning tumours, producing oestrogen in sufficient amounts to
cause, precocious puberty, endometrial hyperplasia, postmenopausal bleeding and
endometrial carcinoma.
Microscopically; tumour is formed from cells resembling theca interna cells.
Gonadoblastoma is a benign 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 the 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,
particularly with a Y chromosome for fear of future development of malignant neoplasms
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,
incarceration, and malignant transformation.
1. TORSION:
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 torsion of the tumour leads to congestion, enlargement of the tumour and thrombosis.
Sudden complete torsion causes sudden occlusion of the arterial blood supply leading to
necrosis and gangrene of the cyst.
The clinical picture is that of acute abdomen, where the tumour is tense and tender on
palpation.
N.B.: BCT is the commonest cyst to undergoe torsion because of its long pedicle and huge fat
content.

Factors predisposing to torsion:

1. Moderate size and long pedicle of the cyst. (e.g.; Dermoid cyst, simple serous cystetc).
Large tumours cannot usually undergo rotation.
2. Absence of adhesions and free mobility favour torsion (fixed tumours do not undergo torsion).
3. Pregnancy and puerperium: Due to displacement of the tumour by pregnancy and laxity of
abdominal wall after delivery.
Treatment:
Ovariotomy via an emergency laparotomy is the treatment of choice in gangrenous cyst,
(clamping of the twisted infundibulopelvic ligament is performed to avoid dislodging of
venous thrombi during untwisting the pedicle).

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: Abdominal pain of varying intensity according to the amount of haemorrhage.
Treatment: Immediate laparotomy, where an ovariotomy is usually done.
3. RUPTURE:
Rupture of an ovarian cyst may occur as a result of torsion or haemorrhage, or may be
traumatic, during labour or due to rough vaginal examination.
Clinical picture: Bleeding in the peritoneal cavity gives the picture of internal haemorrhage
(abdominal wall rigidity, tenderness, rebound tenderness, dull flanks and shifting dullness if
haemorrhage is severe). Clinical picture depend also on contents of the cyst:
Rupture of dermoid cyst leads to severe chemical peritonitis.

Rupture of mucinous cystadenoma leads to pseudomyxoma peritonii.

Treatment: Ressuscitation of the patient (restore the B.P., IV fluids or blood transfusion, etc),
followed by Ovariotomy done via an immediate laparotomy and peritoneal lavage performed.
4. INFECTION:
Ovarian cyst may be infected either in the puerperium (following abortion or labour), or from
a nearby infected organ (as appendicitis or pyosalpinx), or following torsion (due to adhesions).
Clinical picture: General picture of infection as pyrexia. On bimanual examination, the tumour
becomes fixed, tender and rapidly increasing in size.
Treatment: Antibiotics then ovariotomy.

5. INCARCERATION:
Ovarian cyst may be impacted in Douglas pouch, particularly in large size tumours.
Clinically it may cause pressure symptoms on bladder and rectum or may cause obstructed
labour. Treatment is by surgical removal of the tumour by ovariotomy or cystectomy.
6. MALIGNANT TRANSFORMATION:
Potential of malignancy is higher in solid rather than cystic tumours.

Papillary serous cystadenoma has the highest potential to malignant change (up to 50%).
Mucinous cystadenoma has a 5% incidence of malignant transformation.
Benign cystic teratoma carries the least potential of malignancy in less than 1%.

CLINICAL PICTURE OF BENIGN OVARIAN NEOPLASMA

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;

Acute pain; if the tumour is complicated by torsion, rupture, haemorrhage, 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
disturbances, except in rare functioning tumours (theca cell tumour & functioning Brenner).
Physical Signs: These will depend largely on the size of the tumour.
a. Small tumours: are only detected on bimanual pelvic examination, felt on one side of the
uterus, as 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: can be detected by abdominal examination

Inspection: symmetrical abdominal enlargement.

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
associated with marked ascites, where flanks become dull with shifting dullness).

N.B.: in excessively large cyst ovarian cachexia may occur due to the rapidly growing tumour.
Diagnosis:
Ovarian swellings can be suspected by clinical examination, but always need confirmation
by other tools of investigations including;

Ultrasonography: TAS for larger tumours, and TVS for smaller ones, is the mainstay for
diagnosis of ovarian swellings. Both TAS & TVS can differentiate between unilateral and
bilateral tumours, cystic and solid ones, unilocular or multilocular cysts, presence of ascites,
and suspicions for malignancy (echogenicity of the tumour and Doppler flow studies).

C.T. scan and MRI: may help in differentiating adnexal from uterine or intestinal masses,
and may detect pelvic and abdominal lymph node affection.

I.V.P.: In larger tumours to delineate the course of ureter and pressure on urinary bladder.

TREATMENT OF BENIGN OVARIAN NEOPLASMS

1. Ovarian Cystectomy:
It consists of shelling out or enucleation of the cyst with preservation of the ovary. It is
indicated in young patients and particularly with bilateral cysts as in dermoid cyst. Ovarian
cystectomy may be done either by laparotomy or by laparoscopy.
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 are better
removed by laparotomy rather than laparoscopy as laparoscopic surgery may carry the risk of
dissemination of the contents.
2. Oophorectomy:
It 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 clamped
separately
Removal of larger cysts by laparoscopy remains controversial over the issue of
dissemination of the cyst contents including irritant fluid as in dermoid cyst, papillae,
mucinous material, and possibly malignant cells.
3. Panhysterectomy:
If the patient is premenopausal, and has completed her family, 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 in advancing age.
Key points in benign ovarian tumours
Benign epithelial ovarian tumours are the commonest tumours encountered.
Tumour may be silent or present with a complication (torsion, heemorrhage , rupture,

infection, incarceration, and malignant transformation

Diagnosis is best achieved by bimanual vaginal examination and Ultrasonography in most
cases
Treatment is usually conservative by ovarian cystectomy or oophorectomy

MALIGNANT OVARIAN TUMOURS

Malignant

Malignant

Malignant sex cord

epithelial tumours
Incidence Commonest
Origin
Surface epithelium

germ cell tumours

stromal tumours
Less common
Least common
Germ cells
Sex-cord or

Types

Serous adenocarcinoma

Dysgerminoma

Ovarian stroma
Granulosa cell tumour

Mucinous adenocarcinoma

Endodermal sinus

Sertoli-Leydig cell

Endometrioid adenocarcinoma
undifferentiated
adenocarcinoma

tumour

tumour

Choriocarcinoma
Solid teratoma

I. EPITHELIAL OVARIAN CANCER

Incidence:
Primary ovarian epithelial cancer forms 60-70% of all ovarian tumours, and 90% of all
ovarian malignancies. It is the third common malignancy of female genital organs, after cancer of
endometrium and cervix, however it is the most lethal.
Aetiology: The aetiology of epithelial ovarian cancer is unknown. Possible factors include:
1. Reproductive factor:
Nulliparous or infertile women are more liable to develop epithelial ovarian cancer, possibly
due to the continuous repeated minor trauma of the surface epithelium of the ovary caused by
uninterrupted ovulation. Evidence to this postulation include:
Suppression of ovulation by repeated pregnancy and lactation is associated with decreased
incidence of epithelial ovarian cancer.
Suppression of ovulation by prolonged use of OCP is associated with decreased risk of
ovarian cancer.
Prolonged use of ovulatory stimulating drugs in ovarian superovulation protocols has been
reported to slightly increase the risk of ovarian cancer after several years.
2. Hereditary 'Genetic' factor:
Five to 10% of epithelial ovarian cancer will occur in women with hereditary 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%).

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.
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 PRIMARY EPITHELIAL OVARIAN CANCER
Macroscopic appearance:
Primary ovarian carcinoma is usually solid but may be partially cystic partially solid. It may
be unilateral or bilateral. The size is extremely variable. At laparotomy, the capsule of the
tumour may be intact or ruptured and according to the stage of malignancy may be fixed to
surrounding structures. The substance of the tumour is the seat of extensive haemorrhage and
necrosis.
Microscopic picture: It is an Adenocarcinoma which might be either:
a. Well differentiated (Gr I); showing a preserved glandular pattern;
Serous cystadenocarcinoma
Mucinous cysadenocarcinoma.
Endometrioid cysadenocarcinoma.
b. Moderately differentiated (Gr II); showing glands and sheets of highly malignant cells
c. Undifferentiated (Gr III); showing sheets of highly malignant cells.
Border line epithelial tumours:
These are epithelial tumours with cellular features of malignancy, but no invasion of the
stroma. These are tumours of low malignant potential as it is confined to the ovary.
Tumours are mostly serous or mucinous, they occur in younger age, and usually
have a better prognosis.

MALIGNANT GERM CELL TUMOURS

Germ cell tumours are derived from primordial germ cells of the ovary. Their incidence is
only 20-30% of all ovarian tumours. Five per cent of germ cell tumours are malignant.
Classification of malignant germ cell tumours:
1. Dysgerminoma
2. Endodermal sinus tumour (yolk sac tumour)
3. Choriocarcinoma
4. 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:
1. Lower age incidence, more common in prepubertal girls, and younger women.
2. They are the commonest tumours of abnormal gonads and in sex chromatin negative
females.
3. They tend to grow rapidly resulting in pelvic pain and pressure symptoms occurring early
in the disease process.
4. Most tumours produce substances in the circulation that can be used as tumour markers;

Dysgerminoma secretes alkaline phosphatase and lactic acid dehydrogenase.

Endodermal sinus tumour elaborates alpha feto proteins.
Although benign Struma ovarii secretes thyroxine in 15% of cases.
Choriocarcinoma and other germ cell tumours elaborate hCG.
5. In contradistinction to epithelial tumours, germ cell tumours are radiosensitive,
chemotherapy in some of them gives excellent results in stage Ia.
6. Conservative surgery in the form of salpingoopherectomy is the first line of treatment in
these tumours as the patient is usually young, although the tumour is border line or
malignant.
A) Dysgerminoma:
Dysgerminoma is the commonest malignant germ cell tumour accounting for about 30-40%
of all malignant germ cell tumours. It represents 1-3% of all ovarian tumours. It tends to occur at
a younger age (10-20 years). In 5% of cases it occurs in patients with abnormal gonads. It may
be found in both sexes and may arise in gonadal and extra gonadal site (the mediastinum).
Some tumours may secrete alkaline phosphatase and lactic acid dehydrogenase, which may serve
as tumour markers.
Pathology: It is a solid ovarian tumour, usually of small or moderate size, bilateral in only 10%
of cases. Its colour is greyish with lobulated surface. On cut section there is 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: In early cases, unilateral salpingoophorectomy, is the line of choice particularly in

young patients. If fertility is not needed surgical management by TAH BSO, is the best
option (along the lines of treatment of epithelial ovarian cancer).

Radiotherapy: as adjuvant postoperative treatment since the tumour is very radiosensitive.

B) Endodermal Sinus Tumour EST
EST (yolk sac tumour) is 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 almost always unilateral. 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 : Early stage tumours are essentially treated by unilateral salpingoophorectomy with
surgical staging. More advanced malignancies are treated by TAH BSO as epithelial cancers.

Chemotherapy: All patients are treated with chemotherapy either as an adjuvant or

therapeutic treatment, since the tumour is chemosensitive.
MALIGNANT SEX-CORD STROMAL TUMOURS
Sex-cord stromal tumours may arise from non- functioning or functioning stroma of the ovary.
1. Functioning sexcord tumours may be:

Estrogenic: as granulosa cell tumour.

Androgenic: as Sertoli-leydig cell tumours

Both estrogenic and androgenic effect (very rare): as in Gynandroblastoma.

2. Non- functioning stroma may very rarely give rise to fibrosarcoma of the ovary.
A) Granulosa Cell Tumours:
These malignant tumours are usually unilateral, solid, yellow or yellow-grey in colour. They
are slowly growing and generally confined to the ovary when they first present, therefore they
usually carry a good prognosis. Some are functioning secreting oestrogen, while most appear to
secrete inhibin.
In 5% of cases, granulosa cell tumours are associated with endometrial carcinoma, and in
25%-50% with endometrial hyperplasia. They may occur at any age;

In prepubertal girls, they may cause irregular bleeding or precocious puberty, in the childbearing period, they may cause irregular uterine bleeding, and in post menopausal patients
they give rise to post menopausal bleeding.
Microscopically: The tumour is formed of granulosa cells arranged in different patterns. CallExner 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: is applicable in children, and during the child bearing period,
only in early cases (stage Ia),

TAH BSO: Is the best choice in older patients, and in more advanced disease. (surgical
treatment is along the lines of treatment of ovarian epithelial cancer).

There is no place for irradiation or chemotherapy as an adjuvant therapy in granulosa cell

tumour.

B) Sertoli-Leydig Cell Tumours:

They are usually small, unilateral, solid tumours, of low grade malignancy. They are very
rare representing < 0.2% of all ovarian tumours, and are more prevalent around the age
of 30 years.
Many are functioning producing androgens. In 75% of cases they will cause a state of
defeminisation at first, followed later by virilising effects in the form of acne, hirsutism,
clitoromegaly and deepening of voice. Rarely some may produce oestrogen.
Treatment: Either unilateral salpingoopherectmy if the patient is young or TAH BSO if
premenopausal or not desiring further fertility.
PATTERNS OF SPREAD OF OVARIAN CANCER
There are three primary methods of spread of ovarian cancer:
1. Direct extension to adjacent organs such as tube, uterus, colon and bladder.
2. Transcoelomic spread, by exfoliation of surface cells into the peritoneal cavity. Metastases
are typically seen in Douglas pouch, right paracolic gutter, right lobe of liver, right
hemidiaphragm and surface of intestine or omentum (pathway of peritoneal fluid).
3. Lymphatic spread mainly to paraortic lymph nodes.
4. Haematogenous spread is always late and uncommon. This would be to vital organs such as
liver, lung, brain and bones.

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. Krunkenberg 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 lymphatic spread.
Main characteristic microscopic feature is the signet ring cells in which the nucleus is pushed
aside by abundant cytoplasm.
Prognosis:
Is 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: 5565 years of age in the majority of cases. It is more
common in industrial countries. Risk factors have been mentioned before.
SYMPTOMS:
Unfortunately primary ovarian cancer has a very insidious onset, and symptoms are very
misleading;

A) Early stage disease: are mostly asymptomatic. It 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.
B) 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.
N.B; Because symptoms are mostly non specific and are common in this period of life in many
women, most tumours will be at least at stage II or III when first diagnosed. By the time the
patient notices an abdominal mass the condition is already late.
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 in ovarian 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 Meigs syndrome.
Associated breast mass, on breast examination
Unilateral leg & edema (unilateral pressure by tumour with venous and lymphatic obstruction).
C) Abdominal Examination:
Inspection: Abdominal enlargement, over lying skin showing peau dorange.
Palpation: Tumour which is solid (or partially solid), fixed especially if bilateral.
Percussion: Presence of ascites (except with ovarian fibroma in Meigs syndrome).
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 necrosis.
SPECIAL INVESTIGATIONS FOR OVARIAN CANCER
1. Pelvic ultrasound: This is the most useful and most important initial diagnostic tool.

It can accurately detect small pelvic masses and early ascites.

Sonographic features suggesting malignancy include; hyperechoeic and heterogenous
echopatterns, intracystic and extracystic papillae, bilaterality, and presence of ascites.
2. CT & MRI: useful in detection of spread to liver and or lymph nodes (not mandatory).
3. Chest X-Ray: for detection of pleural effusion and/or secondaries in the lungs.
4. Plain X-Ray abdomen: can detect calcification in dermoid cysts and psammoma bodies.
5. Barium meal and/or enema: to exclude primary cancer in the stomach or colon (or spread).
6. Upper and/or lower G.I. Endoscopy: to detect a primary in the stomach or colon (or spread)
7. I.V.P.; to evaluate the course of the ureters and to exclude back pressure on the kidneys.
8. Paracentesis: needle aspiration of ascitic fluid for cytologic examination.
9. Endometrial curettage: In cases of abnormal uterine bleeding to exclude a primary or spread
to the uterus.
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: (The aim is early diagnosis of ovarian cancer)
Routine yearly pelvic examination in premenopausal and postmenopausal women. A palpable

post menopausal ovary must always call for further investigation.

Periodic TVS coupled with a serum CA-125 in those with an enlarged ovary have been

proposed for screening of ovarian cancer. However CA 125 test is expensive and not specific
to ovarian cancer.

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, and 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 method.
Surgical staging of primary ovarian cancer: entails a mid line subumbilical suprapubic
exploratory laparotomy in which the following is performed:
1. 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 fluid in cul de sac (ascites), or perform peritoneal washings for Cytology to
detect malignant cells in the peritoneal cavity.
3. Performing an infracolic omentectomy (with or without appendectomy), to asses presence of
positive tumour deposits within the omentum
4. Pelvic and paraaortic lymph node sampling (whenever possible)
5. Resection of any visible enlarged nodules or masses in pelvic or abdominal cavities.
6. 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

Stage
Stage I

FIGO definition (simplified)

Growth limited to ovaries

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

Ic

Tumour either stage Ia or Ib but with

tumour on surface of one or both ovaries, or
capsule ruptured, or
ascites present containing malignant cells or +ve peritoneal washings

Stage II
IIa
IIb
IIc

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

Stage III

Growth involving one or both ovaries with peritoneal implants outside the pelvis or positive
retroperitoneal or inguinal nodes
tumour grossly limited to the true pelvis with ve nodes
tumour with implants < 2.0 cm on abdominal peritoneal surface. Nodes are -ve
tumour with implants > 2.0 cm or Nodes are +ve
N.B.; superficial liver metastases is included in stage III c.

IIIa
IIIb
IIIc

Stage IV

Growth involving one or both 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.

N.B.: Because primary epithelial ovarian cancer is by far the most common ovarian tumour
encountered, this surgical staging will then be applicable to all other ovarian malignancies.
SURGICAL TREATMENT OF OVARIAN CANCER
A) Early stage Ovarian Cancer:
1. 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 extent of the disease.
2. 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 Leydig cell tumours).
B) Advanced stage Ovarian Cancer:
1. Primary Cytoreductive surgery (initial Debulking):
Aim: To remove all primary cancer and if possible all metastatic disease within the pelvic
and abdominal peritoneal cavities (leaving residual small tumour deposits < 1.0 cm is
acceptable).
Structures removed: include; TAH BSO + omentectomy + peritoneal nodules and masses
>1-2.0 cm + segmental bowel resection if involved within the tumour mass.
Advantages of cytoreductive surgery:
a. Improves survival in patients with advanced disease
b. Improves response to subsequent chemotherapy where tumour residues left are < 1-2.0
cm
2. Interval Debulking: Chemotherapy prior to debulking surgery is sometimes applied to
minimize tumour bulk and control ascites to allow for later radical surgery.
3. Radical oophorectomy: describes a retroperitoneal approach where a TAH BSO is performed
with removal of pelvic peritoneum and colonic resection of fixed tumours.
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:
1. Early stage disease: It has a limited place only with poor prognostic factors as Poorly
differentiated tumours, ruptured capsule, or +ve peritoneal wash (even in stage I cases).
2. 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 (Taxol).
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
imbalance may occur.

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 forms are used:
1. Intraperitoneal radioactive colloids or
2. Whole external beam abdominal radiation.

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%
Key points in ovarian cancer
Epithelial ovarian cancer is commonest type of ovarian cancer encountered
Criteria of malignancy in an ovarian tumour includes; solid or mixed solid and cystic

consistency, bilaterality, fixation, presence of ascites and extracystic papillae.

 Most tumours will be stage II or III when first discovered due to the absence of specific

symptoms in early disease. The prognosis is generally poor if tumour is first discovered
beyond stage1 disease.
A staging laparotomy is indicated in every malignant ovarian tumour regardless its clinical

staging. During laparotomy removal of the main tumour bulk is performed together with
peritoneal fluid cytology, omenetectomy, and Lynph node sampling in order to assess the
extent of the disease, the prognosis and the need for adjuvant therapy.
Standard surgical approach entails performing a TAH BSO and Infracolic omentectomy.
Primary cytoreductive surgery in advanced disease aims at removal of maximum tumour

bulk leaving tumour residues less then 2,0 cm to facilitate postoperative chemotherapy
The vast majority of malignant ovarian tumours will require adjuvant post operative
chemotherapy. Some cases may benefit also from radiotherapy.

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 the fallopian tube.

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.