(27) ovarian swellings

الرحمن الله بسمالرحيم

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 cysts2. Corpus luteum cysts 3. Theca lutein cysts 4. Endometriotic cysts5. Inflammatory cysts 6. Germinal inclusion cysts7. 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:1. Conservative by follow up2. 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) ConservativeB) 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 CLASSIFICATIONHistologically, ovarian tumours can arise from any of the three elements constituting the ovary (surface epithelium, germ cell apparatus, and ovarian stroma).

1. Epithelial Tumours2. Germ cell tumours3. Sex cord stromal tumours

CLINICAL CLASSIFICATIONClinically, 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 CLASSIFICATION1. EPITHELIAL TUMOURS OF THE OVARY

a. Serous Cystadenomab. Mucinous cystadenomac. Endometrioid tumoursd. Brenner tumour

2. GERM CELL TUMOURSa. Teratomab. Dysgerminomac. Endodermal sinus tumourd. Choriocarcinoma

3. SEX CORD STROMAL TUMOURSa. Ovarian Fibroma

b. Thecoma c Granulosa cell tumourd. 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, mucinous, or endometrioid tumours.

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 mesoderm).

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:

CysticSerous cystadenomaMucinous cystadenomaEndometrioid cystadenoma

SolidBrenner tumour

Classification of benign ovarian tumours (ctd.)

Benign germ cell tumours: Cystic

Benign cystic teratoma (BCT)  

SolidStruma OvariiGonadoblastoma

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

mamilla

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. TORSION2. HAEMORRHAGE3. RUPTURE4. INFECTION5. INCARCERATION6. MALIGNANT

TRANSFORMATION

Torsion

Traumatic rupture

Malignant transformation

CLINICAL PICTURE OF BENIGN OVARIAN NEOPLASMA

Symptoms: Asymptomatic Abdominal swelling Menstrual disorders Pressure symptoms Lower abdominal pain

Asymptomatic ov. SwellingDetected 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

1. 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:1. 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:

1. Dysgerminoma2. Endodermal sinus tumour (yolk sac

tumour)3. Choriocarcinoma4. 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 incidence2. The commonest tumours of abnormal

gonads and in sex chromatin negative females.

3. 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.

4. 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

5. 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.

A) 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 and lactic acid dehydrogenase.

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

Radiotherapy

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 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 :

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 the ovary.

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

chemotherapy

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 reached both ovaries by retrograde lymphatic spread.

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:A. 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.

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.

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 pressure by

tumour with venous and lymphatic obstruction).

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 Meig’s syndrome).

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 necrosis.

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 CANCERThe 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 affectthe prognosis and line of treatment,

surgicalstaging is therefore the only standardmethod.

Surgical staging of primary ovarian cancer:

entails a mid line subumbilical suprapubicexploratory 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 Resection of any visible enlarged nodules or

masses.

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

FIGO definition (simplified)

Stage I

Growth limited to ovaries

Ia Growth limited to one ovaryNo ascites; No tumour on external surfaces; capsule intact

Ib Growth limited to both ovariesNo ascites; no tumour on externalsurfaces; 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 II

Growth involving one or both 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 III

 Growth involving one or both ovaries with peritoneal implants outside the pelvis or positive retroperitoneal or inguinal nodes

IIIa tumour grossly limited 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 +veN.B.; superficial liver metastases is included in stage III c.

FIGO surgical staging for primary epithelial ovarian carcinoma (ctd)

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.

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 extent of the disease.

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:

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 agentshas 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: Intraperitoneal radioactive colloids 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%

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 uni lateral.

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.

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