Transcript بسم الله الرحمن الرحيم

‫بسم هللا الرحمن الرحيم‬
Ovarian tumours
By Dr. Sallama kamel
Introduction:
• Ovarian cancer is the second most common
gynecological malignancy and the major cause
of death from a gynecological cancer.
• Unfortunately survival from ovarian cancer
remain poor (38%) , due in part to the late
presentation of the disease.
• Prompte identification and appropriate
treatment of cancer of the ovary are essential if
the survival rates are to be optimal.
-Although differentiating malignant from
benign disease is critical in optimizing
management for the individual case,
-Non invasive diagnosis continues to be elusive
Histopathology and classification of
ovarian tumors:
A cyst or amass in the ovary could be:
• Functional cysts
• Primary T.
• Secondary T.
-Follicular cyst.
-corpus Luteal cyst.
-Theca lutien cysts
-endometriosis cyst
-Epithelial cell T.
-Germ cell T.
-Sex cord T.
- Breast , colon, stomach
Epithelial tumours
Germ cell T.
Sex cord T.
-Serous tumours.
-Dysgerminoma
-Granulosa cell .
-Mucinous tumours.
-Teratoma(benign and malign)
-Endometroid tumours.
-Yolk sac tumor
-Clear cell tumours.
-Choriocarcinoma
-Brenner tumours.
-Mixed epithelial tumours.
-Undifferentiated tumours
-Embryonal carcinoma
-Thecoma
-Sertoli- leydig cell.
-Gynandroblastoma
-Fibroma
Physiological cyst
-They are simply large versions of the cysts that forms
in the ovary during the normal ovarian cycle.
-Most are asymptomatic and found incidentally on
pelvic examination or ultrasound.
-They are most common in young women.
-They may be a complication of induction of
ovulation.
-They also occur in women with trophoblastic disease.
Follicular cysts:
it result from the non-rupture of a dominant follicle or the
failure of atresia in a non-dominant follicle.
They are lined by Granulosa cells and contain clear fluid.
It can persist for several menstrual cycles and may achieve a
diameter of up to 10cm.
Small cysts are more likely to resolve spontaneously but may
require intervention if symptoms develop or if they do not
resolve after 8-16 weeks.
Occasionally they may continue to produce oestrogen,
causing menstrual disturbances and endometrial
hyperplasia.
Simple follicular cyst
Luteal cysts:
Less common than follicular cyst.
Are more likely to present with intra-peritoneal bleeding.
They may also rupture.
This is usually happens on day 20-26 of the cycle.
They should not called Luteal cyst unless they are more than 3cm.
In size.
Theca-lutein and granulosa lutein cysts.
-These occurs in association with hydatidiform moles or
Choriocarcinoma.
-They are caused by high output of gonadotrophin from the
chorion,and may reach a size of 10cm
-After treatment or removal of the abnormal chorion the cyst
resolves.
-Similar cysts may formed if excessive doses of gonadotrophins or of
clomiphines are given to induce ovulation causing hyperstimulation syndrome.
Epithelial tumours:
-These tumours arise from the ovarian surface epithelium.
-So they arise from the Coelomic epithelium overlying the
embryonic gonadal ridge.
Since the epithelial covering of the ovary and the mullerian
duct ( from which the tubal, endometrial and cervical
epithelium are derived ) are both from coelomic epithelium ,
comparable metaplastic transformation into different types of
epithelium is possible.
-So the cells may differentiate to endocervical cells giving rise
to mucinous cystadenoma.
-Differentiation into endometrial cells give rise to Endometrioid
tumour.
-Differentiation to tubal epithelium give rise to serous
cystadenoma.
-Differentiation along uro-epithelium give rise to Brenner
tumour.
They are most common in women over 40 years old.
1.Serous cystadenoma:
-These are the most common epithelial tumours with a range
from benign to the highly malignant .
-The benign form are called benign serous cyst.
-It is unilocular cyst with papilliferous processes on the inner
surface and occasionally on the outer surface.
-The lining epithelium is cuboidal or columnar and may be
ciliated.
-The cyst contain thin serous fluid.
-They are usually smaller than the mucinous tumour.
-They are often bilateral
-They occur most commonly in late reproductive and early
postmenopausal life.
The malignant form called Serous papilliferous
carcinoma:
-This is the commonest primary ovarian carcinoma.
-It is bilateral in 50%.
-The growth often penetrates the capsule and project on the
external surface with dissemination of the cells into the
peritoneal cavity giving multiple seedling metastases and
ascites.
-The cyst contains many papillary processes which have
proliferated so much that they almost fill the cavity and
there may be exophytic papillary growth on the surface.
-The lining cells are multilayer and may invade normal tissues.
Ovarian carcinoma
2.Mucinous cystadenoma:
-The 2nd most common epithelial tumour.
-They are large, unilateral , multilocular cysts with smooth
inner surface.
-The lining epithelium is columnar mucous-secreting cells.
-The cyst contain thick glutinous fluid.
-A rare complication is pseudomyxoma peritonei,
when there is shedding of cells on the surface of the
peritoneum and grow there and continue to secrete mucin
so the abdominal and pelvic cavities are slowly filled with a
gelatinous mass of mucin , causing matting together and
consequent obstruction of the bowel loops.
-A similar condition may occur after rupture of a mucocele of
the appendix and the two may co-exist, raising the
possibility of a metastasis from an ovarian primary.
Mucinous cystadenoma
Malignant mucinous cyst (Mucinous carcinoma):
-Constitute 10% of ovarian cancers.
-On histological examination, 5% of mucinous cysts found to be
malignant.
Epithelial tumours of borderline malignancy:
- mean that the tumour carry some of the features of
malignancy( e.g. multilayering of cells and nuclear atypia).
-But there is no stromal invasion.
-20% of epithelial tumours are of borderline malignancy.
-It is rare for such tumours to be more than stage1, i.e. beyond
one or two ovaries , and surgical removal of the pelvic
organs usually results in cure.
3.Endometrioid cystadenoma:
-These are very similar to ovarian endometriosis.
-They may be associated with pelvic pain and dyspareunia due
to adhesions.
-It may coexist with uterine endometrial adenocarcinoma.
4.Clear cell tumours( mesonephroid):
-They arise from serosal cells showing little differentiation, and
are only rarely benign.
-The typical histological appearance is of clear or hobnail cells(
which have scanty cytoplasm and large nuclei) arranged in
mixed patterns .
5.Brenner tumours:
-These account for only 1-2% of all ovarian tumours.
-They are bilateral in 10-15%.
-The vast majority is benign but can occasionally be borderline
or malignant
-Three quarter occurs in women over the age of 40.
-The majority is less than 2cm in diameter.
-Some secrete oestrogens and abnormal vaginal bleeding is a
common presentation.
Macroscopically: a Brenner tumour resembles a fibroma, being
a solid tumour with a white cut surface.
Histologically: -It consists of islands of round transitional-like
epithelium in a dense fibrotic stroma giving a solid
appearance.
Germ cell tumours:
•It is among the commonest ovarian tumours seen in women of less than
30years old.
●In women under 20 years ,up to 80% of ovarian malignancies are due to
germ cell tumours.
•Overall only 2-3 percent are malignant .
•These tumours arise from a totipotential germ cell
•Thus they contain element of all three germ layer( embryonic
differentiation).
Differentiation into embryonic tissues result in teratoma
(dermoid cyst).
•Differentiation into extra-embryonic tissues results in ovarian
Choriocarcinoma or endodermal sinus tumour.
•When neither embryonic nor extra-embryonic differentiation occurs,
dysgerminoma results.
Dermoid cyst (mature cystic teratoma)
-This is the commonest germ cell tumour and it is benign.
-It results from differentiation into embryonic tissues.
-It account for about 40% of all ovarian neoplasm.
-It is most common in young women and the median age of presentation is
30 years old.
-it contain a variety of tissues derived from the two or more of the primary
germ layers..
-The dermoid cyst is usually unilocular cyst.
-Less than 15cm in diameter
-It is often lined by epithelium like the epidermis and contain skin
appendages, teeth , sebaceous material , hair and nervous tissues,
cartilage bone and thyroid tissues.
-The cavity of the cyst contain yellow greasy material.
Dermoid cysts
-The majority of dermoid cysts (60%) are asymptomatic.
-However it may undergo torsion.
-Less commonly it may rupture spontaneously, either suddenly
causing an acute abdomen and chemical peritonitis, or
slowly causing chronic granulomatous peritonitis.
-During pregnancy, rupture is more common due to external
pressure from expanding gravid uterus or to trauma during
delivery.
-Some dermoid cysts contain single type of tissues like thyroid
tissue and called stroma ovarii and might present with
feature of hyperthyroidism.
Mature solid teratoma:
-These are tumours contain mature tissues just like the
dermoid cyst but are solid.
-They must be differentiated from immature teratomas which
are malignant.
Malignant germ cell tumours:
These are rare tumours accounting for only 3% of ovarian cancers.
1.Dysgerminoma:
-This
is the most common malignant germ cell tumours
accounting for about 50%.
-Nearly all occur in young women less than 30 years old.
-Spread mainly by lymphatics.
-They are solid tumours with a smooth or nodular external
surface.
-The mean diameter is 15cm.
-Approximately 10% are bilateral( the only malignant germ cell
tumour that can be bilateral ).
-Pure Dysgerminoma have a good prognosis as they are
normally stage 1 tumours in 75% of cases.
-It may occur in cases of gonadal dysgenesis,and it is
radiosensitive.
2.Yolk sac tumour ( endodermal sinus tumour).
-These are the second most common malignant germ cell
tumour of the ovary.
-Making 10-15% over all and reaching a higher proportion in
children
-The tumour is usually well – encapsulated and solid.
-It may present as acute abdomen due to rupture of the
tumour following necrosis.
-It secrete alfa-feto protein (AFP) which can be used as a
tumour marker.
3.Immature Solid Teratoma:
-These account for approximately 20% of malignant germ cell
tumours with a peak incidence in the second decade of life.
-They contain embryonic( immature) tissues and they are
highly malignant.
4.Non gestational Choriocarcinoma:
-These generally arise as a component of a solid teratoma.
-They consist of syncytiotrophoblast and cytotrophoblast and
secret gonadotrophin, which can be used as a diagnostic
marker.
sex cord stromal tumours:
-These account for only 4% of benign ovarian tumours.
-They occur at any age from prepubertal children to elderly,
postmenopausal women.
-They secrete hormones and present with the results of inappropriate
hormone effects.
1.Granulosa cell tumours:
-These are all malignant tumours but they are generally confined to the
ovary when they present and so have a good prognosis.
-They grow very slowly and recurrences are often seen 10-20 years later.
-They are solid in most cases.
-Some produce oestrogens causing postmenopausal bleeding in older
women or precocity in prepubertal girls and
-most appear to secrete inhibin which can be used to monitor treatment..
2.Theca cell tumours:
-Almost all are benign, solid and unilateral tumours.
-They present in the sixth decade of life.
-Many produce oestrogens in sufficient quantity to have
systemic effects such as precocious puberty,
postmenopausal bleeding , endometrial hyperplasia and
endometrial cancer.
3.Fibroma:
-These unusual tumours are most frequent around 50 years of
age.
-Most are derived from stromal cells and are similar to
thecomas.
-They are hard mobile and lobulated with glistening white
surface .
-Less than 10% are bilateral.
-Meig’s syndrome ( ascites , pleural effusion in association
with a fibroma of the ovary) is seen in only 1% of cases.
4.Sertoli- leydig cell tumours:
-These are usually of low grade malignancy.
-Most occur around 30 years of age.
-They are rare ( only 0.2% of ovarian tumours).
-Many produce androgens and signs of virilization are
seen in three-quarters of patients
Benign ovarian tumours:
presentation:
-Asymptomatic.
-Pain.
-Abdominal swelling.
-Pressure effects.
-Menstrual disturbances.
-Hormonal effects.
-Abnormal cervical smear.
1.Asymptomatic:
Many benign ovarian tumours are found incidentally in the
course of investigating another unrelated problem or during
a routine examination.
2.Pain:
-Acute pain from an ovarian tumour may result from
complication e.g. torsion, rupture, haemorrhage or infection.
-Torsion give rise to a sharp, constant pain caused by ischaemia
of the cyst and areas may become infarcted.
-Haemorrhage into the cyst may cause pain as the capsule is
stretched.
-Rupture of the cyst causes intraperitoneal bleeding mimicking
ectopic pregnancy (this happens mostly with a luteal cyst ).
-Chronic lower abdominal pain sometimes results from the
pressure of a benign ovarian tumour but is more common if
endometriosis or infection is present.
Twisted ovarian cyst
3.Abdominal swelling:
-Patients seldom note abdominal swelling until the tumour is
very large .
-A benign mucinous cyst may occasionally fill the entire
abdominal cavity.
4.Miscellaneous :
pressure effects. -Gastro-intestinal or urinary symptoms may result from
pressure of large tumour.
-In extreme cases, oedema of the legs, varicose veins and haemorrhoids
may result.
-menstrual disturbances:
- Occasionally the patient will complain of menstrual disturbances but this
may coincidence rather than due to the tumour.
-hormonal effects :
rarely Sex cord tumours may present with oestrogens effects such as
precocious puberty, menorrhagia and glandular hyperplasia, breast
enlargement and postmenopausal bleeding.
-Secretion of androgens may cause hirsutism and acne initially progressing
to frank virilism with deepening of the voice or clitoral hypertrophy.
Diagnosis:
1.Full history:
-Details of the presenting symptoms and a full gynaecological history should
be obtained with particular reference to the date of the last menstrual
period , the regularity of the cycle, any previous pregnancies ,
contraception, medication and family history ( particularly of ovarian,
breast and bowel cancer ).
2.Examination ( abdominal and pelvic examination):
-If the patient presented with acute abdomen look for evidence of
hypovolaemia.
-The neck , axilla and groins should be examined for lymphadenopathy.
A malignant ovarian tumour may cause a pleural effusion.
-This is much less commonly found with benign tumour.
-Also some patient may have ankle oedema.
-The abdomen should be inspected for distension by fluid or by the tumour
itself.
-A male distribution of hair may suggest a rare androgen-producing tumour.
Bimanual examination:
-This is an essential part of assessment.
-To palpate the mass , its mobility, consistency.
-Presence of nodules in the pouch of Douglas and the degree of
tenderness.
-A cystic mobile mass is mostly benign, while a hard, irregular
fixed mass is likely to be malignant.
Investigations:
. Ultrasound
-Trans-abdominal and trans-vaginal ultrasound can
demonstrate the presence of an ovarian mass with
reasonable sensitivity and specificity.
-However it can not distinguish reliably between benign and
malignant tumours but solid masses are more likely to be
malignant than the purely cystic mass.
-The use of colour- flow Doppler may increase the reliability of
ultrasound.
-MRI may have a role in differentiating benign and malignant
ovarian tumours.
Radiological investigations:
-A chest X- ray is essential to detect metastatic disease in the
lungs or a pleural effusion .
-Occasionally an abdominal X-ray may show calcification,
suggesting the possibility of a benign teratoma.
-A barium enema is indicated only if the mass is irregular or
fixed, or if there are bowel symptoms.
Blood test and serum markers:
-Elevated WBC count may indicate infection.
-Ca125
Raised serum Ca125 is strongly suggestive of ovarian carcinoma,
especially in postmenopausal women.
-Women with extensive endometriosis also have elevated
levels but the concentration is usually not as high as that
seen with malignant disease.
- B-HCG level is elevated in women with choriocarcinoma.
-Oestradiol levels may be elevated in some women with
physiological follicular cysts and sex cord stromal tumours.
-Androgens are increased with Sertoli-lydig tumours.
-Raised alpha-fetoprotein levels suggest a yolk sac tumour.
Management of benign ovarian tumours:
This will depend upon the
-Severity of the symptoms.
-Age of the patient .
-The risk of malignancy.
-Her desire for future pregnancy.
The asymptomatic women:
The older women:
Women over 50 years of age are more likely to have a
malignancy so surgery is usually indicated.
-but for a simple cyst less than 6cm in diameter with a normal
Ca 125 and normal vascular resistance pattern are likely to be
benign and may safely be managed conservatively.
-So a 2nd ultrasound should be made after 12 weeks if there is
no change in the cyst happened, follow up with sixMonthly ultrasound and Ca125 estimation is safe.
Most would resolve in 3 years but some do persist for up to 7
years.
In pre-menopausal women:
-Young women of less than 35 years are both more likely to
wish to have further children and are less likely to have
malignant epithelial tumour.
1-A normal follicular cyst up to 3 cm in diameter requires no
further investigation.
2-A clear unilocular cyst of 3-10 cm identified by ultrasound
should be re- examined after 12 weeks for evidence of
diminution in size .
- If the cysts persists, such women may be followed with a sixmonthly ultrasound and Ca125 estimations.
-The use of combined oral contraceptive pills is unlikely to
accelerate the resolution of a functional cyst.
-If the cyst does enlarge , laparoscopy or laparotomy may be
indicated.
3.A cyst of more than 10 cm is unlikely to be physiological or to
resolve spontaneously and operation indicated.
The patient with symptoms:
If the patient present with severe acute pain or signs of
intraperitoneal bleeding an emergency laparoscopy or
laparotomy will be required.
The pregnant patient:
-An ovarian cyst in pregnant women may undergo torsion or
may bleed.
-The pregnant women with an ovarian cyst is a special case
because of the risk of surgery to the fetus.
-Thus if the patient present with acute pain due to torsion or
haemorrhage into an ovarian cyst or if appendicitis is a
possibility, the correct course is to undertake a laparotomy
regardless the stage of the pregnancy.
-The operation should be covered with by tocolytic drugs and
performed in a center with intensive neonatal care.
-If asymptomatic cyst is discovered during the 1st trimester, it is
prudent to wait until after 14 weeks’ gestation before
removing it.
-This avoids the risk of removing a corpus luteal cyst upon
which the pregnancy might still be dependent.
-In the 2nd and 3rd trimesters , the management of an
asymptomatic ovarian cyst may be either conservative or
surgical.
-Cysts < 10cm , which have simple appearance on U/S , are
unlikely to be malignant or to result in cyst accident and may
therefore be followed by U/S.
-Many may resolve spontaneously .
If the cyst unresolved 6 weeks postpartum , surgery indicated.
-Malignancy is uncommon in pregnancy occurring in less than
3% of the cysts.
-However a cyst with a features suggestive of malignancy on
U/S , or one that is growing, should be removed surgically.
-The tumour marker C 125 is not useful in pregnancy since it
may be elevated in normal pregnancies.
Prepubertal girl:
-Ovarian cysts are uncommon and often benign.
-Teratoma and follicular cysts are the most common.
-Presentation may be abdominal pain, distension or precocious
puberty.
-Management depends on:
-relief of symptoms.
-exclusion of malignancy and
-conservation of maximum ovarian tissue without depressing
fertility.
Types of surgery for apparently benign ovarian
tumours:
For young women less than 35 years:
1.Cystectomy ( removal of the cyst only).
2.Oophorectomy( removal of the ovary).
For woman more than 45 years with ovarian cyst more than
6cm in diameter it is advisable to do total abdominal
hysterectomy and bilateral salpingo-oopgorectomy.
Malignant disease of the ovary:
-Most ovarian tumours are of epithelial origin.
-They are rare before the age of 35 years, but the incidence
increases with age to a peak in the 50-70 years.
-Most epithelial tumours are not discovered until they have
spread widely.
-Surgery and chemotherapy forms the main stay of treatment.
The results are poor.
-The 5 year survival is around 38%.
-Only 3 % of ovarian cancers are seen in women younger than
35 years and most are non-epithelial cancers such as germ
cell tumours.
1.-Epithelial tumours account for 60-65% of all ovarian
tumours and approximately 90% of those that are
malignant (it is the most common).
-It is a disease of late reproductive and postmenopausal
women (average presentation at 64 years).
2.Germ cell tumours, derived from the germ cells and
account for 30% of ovarian tumours.
Although they represent only 1-3% of all ovarian
malignancies, they are commonest tumours
encountered in children and adolescent (more than 60%
of ovarian cancers in this age group.
3.sex cord stromal tumours are derived from sex cord and
stroma of the ovary and account for approximately 8%
of all ovarian tumours (least common).
Incidence:
-The lifetime risk of developing ovarian cancer on the general
population is 1.4 % (one in 70).
-Ovarian cancers are more prevalent in developed nations.
-There are variations in incidence with ethnicity, Caucasian
women have the highest incidence (14 per 100 000) whereas
Asian women have a lower incidence (10 per 100 000).
-There is a significant genetic aspect to ovarian cancer with
earlier presentation at 54 years.
Aetiology and risk factors:
Epithelial ovarian cancer(EOC) is due to malignant
transformation of the ovarian epithelium.
There are two main theories regarding this malignant
transformation:
1.Incessant ovulation theory
Continuous ovulation causing repeated trauma to the ovarian
epithelium leading to genetic mutation and development of
cancer.
-This theory is supported by an increased incidence of EOC in
nulliparous women, women with early menarche or late
menopause .
-reduced incidence in multiparous women and women used
oral contraceptive pills
2.Excess gonadotrophin secretion:
This promotes higher levels of oestrogen which in turn leads to
epithelial proliferation and malignant transformation of the
ovarian epithelium.
Aetiology and risk factors (summery):
Increased risk:
1.Nulliparity.
2.Early menarche and Late menopause , both of these are associated
with long estimated numbers of years of ovulation.
3.increasing age at first birth.
4.The prolonged use of drugs for induction of ovulation.
A recent cohort study of over 50000 women attending fertility clinics in
Denmark found no evidence of a causal association between the use of
ovulatory stimulants and the subsequent development of epithelial ovarian
tumour and the association was due to the effect of nulliparity alone.
5.High fat diet and diet low in fibre and vitamine A
6- Perineal dusting with talcum powder. .
7. Obesity, endometriosis and the use of IUCD
Reduced risk of ovarian cancer:
1.Multiparity and early age at first pregnancy.
2.Breast feeding reduce the risk.
3.Oral contraceptive use reduces the risk by
20% after 5years of use.
4.Tubal ligation and hysterectomy with ovarian
preservation.
Genetic factors in ovarian cancer
-The life time risk for ovarian cancer is 1.4%
(one in 70).
-It is estimated that around 10% of ovarian cancer
have a genetic link.
-A woman with one affected close relative has risk of
3-4%, With two affected close relatives the risk
increase to 40-50%.
-Hereditary cancers usually occur around 10 years
before sporadic cancers and are associated with
other cancers.
-The most common hereditary cancer is the
breast ovarian cancer syndrome (BRCA)
account for 90% of hereditary tumors which
are two types:
BRCA1 (80%) and BRCA2 (15 %).
these are due to mutation of the tumor
suppression gene.
-lynch syndrome which is colorectal cancer,
endometrial cancer and 10% risk of ovarian
cancer.
Management of women with family history of ovarian
cancer:
-Till now there is no screening test which can be applied for low risk
population.
- Screening with TVUS and CA125 is not advisable and not reliable for low
risk population.
-However ,women with strong family history (risk more than 10% ) should
be referred to clinical genetics for assessment of the family tree.
-If this suggest a hereditary cancer , testing for BRCA1 and BRCA2 may be
offered.
-Screening with yearly TVUS and CA 125 is offered to women aged 35 and
over.
-Prophylactic bilateral salpingo-oophorectomy has a role in patient who are
found to be carrying a gene mutation and have completed her family.
Also the woman can be advised to use COCP to reduce their risk of ovarian
tumour.
Staging of ovarian cancer (FIGO staging ):
The staging of ovarian cancer is a clinical staging
Stage 1 growth limited to the ovaries.
Ia
growth limited to one ovary.
No ascites, no tumour on external surfaces ; capsule intact.
Ib
tumour limited to both ovaries.
No ascites, no tumour on external surfaces; capsule intact.
Ic
either stage 1a or 1b with ascites contain malignant cells or tumour on the
surface of one or both ovaries.
Stage II: growth involving one or both ovaries with pelvic extension.
Stage III: growth involving one or both ovaries with peritoneal implants outside the
pelvis or positive retroperitoneal or inguinal lymph nodes or superficial liver
metastasis
Stage IV :growth involving one or both ovaries with distant
metastasis, parenchymal liver metastasis equal stage 1V.
Stage III OVARIAN CANCER
Stage III a:
Tumours grossly limited to pelvis with negative nodes but
histologically confirmed peritoneal implants.
Stage III b:
Abdominal implants ˂ 2cm. In diameter.
Stage III c:
Abdominal implants ˃2cm. In diameter, or positive
retroperitoneal or inguinal lymph nodes
Technique for surgical staging
-A midline incision is essential to allow
adequate access for thorough surgical staging
and should be performed whenever ovarian
malignancy suspected.
-A systematic exploration of all peritoneal
surfaces and viscera is performed.
-The staging laparotomy involve the following steps:
• Sending ascites or peritoneal washing for
cytological assessment.
• Performing TAH and BSO.
• Omentectomy.
• Peritoneal biopsies of all suspecious areas or
multiple random sampling if all surfaces are
apparently normal.
• Diaphragmatic biopsies or scraping for cytological
assessment.
• Sampling of pelvic and para-aortic lymph nodes.
Spread of ovarian malignancies:
- direct spread: usually to the pelvic peritoneum and other
pelvic organs ( uterus and broad ligament ).
-Lymphatic spread commonly involves the pelvic and the paraaortic nodes.
Spread may also involves the nodes of the neck or inguinal
region.
-Haematogenous spread
-usually occurs late and involves mainly the liver, and lung.
-Bone and brain metastasis sometimes seen.
Presentation and diagnosis:
-Abdominal pain or discomfort is the commonest presenting complaint.
-Distension or feeling a lump is the next most frequent.
-The patient may complain of:
-Indigestion.
-Urinary frequency.
-Weight loss.
-Or rarely abnormal menses or postmenopausal bleeding.
-A hard abdominal mass arising from the pelvis is highly suggestive
especially with ascites.
-A fixed, hard, irregular pelvic mass is usually felt best by combined vaginal
and rectal examination.
-The neck and groin should also be examined for enlarged nodes.
Investigations:
1.full blood count.
2.Urea, electrolyte and liver function test.
3.Chest x-ray.
4.Sometimes, barium enema and colonoscopy is needed to
differentiate between an ovarian and a colonic tumour or to
assess bowel involvement.
5.IVP (intravenous urography).
6.Ultrasonography may help to confirm the presence of a pelvic
.mass and detect ascites.
7.Tumour markers e.g. Ca 125.
8.In most women the diagnosis is uncertain before laparotomy
is undertaken.
Surgery:
-Surgery is the mainstay of both the diagnosis and the treatment of ovarian
cancer.
-A vertical incision is required for an adequate exploration of the upper
abdomen.
-A sample of ascitic fluid or peritoneal washings with normal saline should
be taken for cytology.
-The pelvis and upper abdomen are explored carefully to identify metastatic
disease.
-The therapeutic objective of surgery for ovarian cancer is the removal of all
tumour tissues.
-This is usually possible in the majority of stage1 and stage 11, but
impossible in advanced cases.
-Because of the diffuse spread of the tumour throughout the peritoneal
cavity , microscopic deposits will persist in almost all cases even when all
macroscopic tumour have been excised.
-Thus additional therapy usually required in most cases beyond stage1.
to resect all visible tumour requires a total hysterectomy,
bilateral salpingo-oophorectomy and infra-colic omentectomy.
-However , in a young , nulliparous woman with unilateral
tumour and no ascites ( stage Ia ), unilateral salpingooophorectomy may be done after careful exploration to
exclude metastatic disease , and curettage of the uterine
cavity to exclude a synchronous endometrial tumour.
-If the is subsequently found to be poorly differentiated or if
the washings are positive, a second operation to clear the
pelvis will be necessary.
Borderline disease usually present as a stage 1a tumour confined to one
ovary , in young women this can be treated with unilateral oophorectomy.
-For older women who complete her family a total hysterectomy and
bilateral salpingo-oophorectomy is usually done.
-When tumour tissues remain after initial surgery, a second laparotomy may
be performed on those women who responded after two to four courses
of chemotherapy.( this is called interval de-bulking surgery)
-The chemotherapy is then resumed as soon as possible after the second
operation.
Chemotherapy:
-Women with stage Ia or Ib and well or moderately differentiated tumours
will not require further treatment.
-All other patient with invasive ovarian carcinoma require chemotherapy
(stage II-IV –possibly stage Ic ).
-There is no evidence that adjuvant therapy affects the outcome in women
with borderline tumour.
-Drugs used are Carboplatin, cisplatin and taxol.
Prognosis:
Borderline tumour:
Long term prognosis excellent in most cases.
Invasive tumours- 5 year survival rates.
-90% for Stage Ia and 1b ( well or moderately differentiated ).
-10 % for stage III.
-38% overall.