Ovarian Malignant PPT.pptx

 Epidemiology
 Risk factors
 Pathology and pathogenesis
 Diagnosis
 Screening
 Staging
 Prognosis
 Management
OVERVIEW

 Ovarian malignancies represent the greatest challenge of all the
malignancies because of its high mortality.
 Ovarian cancers -6% of all cancers among women
 Approximately 27% of gynecologic cancers are of ovarian origin
 75% diagnosed with advanced stage disease; 5-year survival only 10-28%
 About 53% of all the deaths of gynecological cancers are of ovarian origin
(highest fatality to case ratio)
American cancer society incidence
INTRODUCTION
The “silent killer”: asymptomatic in early stages

• Incidence of ovarian cancers are highest in Sweden (19.6/100000)
united states (15.4/100,000) and lowest in Japan (10.1/100,000)
• Incidence in India 0.9 to 8.4 per 100,000
• Ovarian cancer is the second most common gynecologic
malignancy, endometrial cancer being the most common,
but is the most common cause of death among women who
develop agynecologic malignancy.
• In general, ovarian cancer is a disease of the postmenopausal
woman, with the highest incidence among patients ages 65–74
year .
EPIDEMIOLOGY

 Age
 Rare before 40yrs, increases
steadily thereafter, peaks at65-
75yrs.
 Reproductive history
 early menarche, nulliparityor
age >30 at first child-bearing,
and late menopause
 Nulliparity is the most
important non genetic factor.
 Fertilitydrugs
 prolonged use especially
without achieving pregnancy
 Personal history of breast
Cancer
 Hormonereplacement
therapy > 10years
 May be associatedwith
30% increased risk
 Talcumpowder
 Some studies have shown
slightlyincreased risk in
women who use talc powder
on genital area
American Cancer Society2001

Symptoms
Early symptoms of ovarian cancer:
•Pain in the pelvis
•Pain on the lower side of the body
•Back pain
•Indigestion or heartburn
•More frequent and urgent urination
•Pain during sexual intercourse
As ovarian cancer progresses these symptoms are also possible:
•Nausea, Weight loss, Breathlessness, Fatigue (tiredness)
•Loss of appetite

• Hereditary breast-ovarian cancer syndrome (HBOC)
• Hereditary site – specific ovarian cancer
syndrome(HSSOC)
Hereditary nonpolyposis colon cancer syndrome (HNPCC)
• Inherited -10% of ovarian cancers while 90% sporadic
• Mode of inheritance is autosomal dominant
• Occurs 10 years younger than sporadic
FAMILIAL OVARIAN CANCERS

Lifetime risk of ovarian cancer is estimated
• 39 % of BRCA 1 mutations
• 11% with BRCA2 mutations
Life time probability of ovarian cancer
• 1.6 % without family history
• 5% if one relative is affected
• 7% if two relatives affected

 ~7% of hereditary ovarian cancer cases
 Responsible genes: mutation in mismatch repair genes
(MMR) including MLH1, MSH2, and MSH6
 Predominance of early onset proximal colon cancer, ca
ovary and endometrium.
 Estimated lifetime risk of ovarian cancer 10-12%.
HNPCC OR LYNCH SYNDROME

 Multiparity: First pregnancy before age 30
• Oral contraceptives: decreases approx 11% peryearof use.
Max of 46% after 5 years of use.
• Tubal ligation
• Hysterectomy (Salpingectomy/ Fimbriectomy)
• Bilateral oopherectomy -↓ risk by 80% to 95%
• Lactation
PROTECTIVE FACTOR

 Role of ovulation in the pathogenesis of the malignancy.
 Risk is related directly to the number of uninterrupted
ovulatory cycles.
 As repair follows multiple ovulations, the surface
epithelium of the ovary often extends into the ovarian
stroma to form inclusion glands and cysts.
PATHOGENESIS

 Incessant ovulation
 Retrograde menstruation hypothesis.
 Retrograde transportation of carcinogens from lower
genital tract.
 Exposure of ovarian epithelium to persistently high levels
of pituitary gonadotropins.
THEORIES ……..
TeLinde's

 Very recently, Lee et al. have proposed
 many high-grade serous carcinomas actually arise in the
mucosa of the fimbriated end of the fallopian tube.

Types of ovarian cancer
The ovaries contain 3 main kinds of cells:
1. Epithelial
2. Germ cells
3. Stromal cells
Each of these cells can develop into different
type of tumors.
Subsequently there are 3 main types of
ovarian tumours:
1. Epithelial tumours
2. Germ cell tumours
3. Stromal tumours

 PRIMARY(80%)
1)Surface epithelial – 80-90%
2)Non-epithelial
Germ cell tumors – 15-20%
Sex cord stromal– 5-8%
 SECONDARY(20%)
1) Typical
2) Atypical (Krukenberg)
PATHOLOGIC CLASSIFICATION

 Serous (tubal) ----75-80%
 Mucinous (endocx & intestinal)-----8-10%
 Endometrioid-----10%
 Transitional cell – Brenner-------<1%
 Clear cell-----<1%
SURFACE EPITHELIAL TUMORS

All types can be benign, borderline , or malignant,
depending upon;
 Benign
 Gross: mostly cystic
 Microscopic; fine papillae, single layer covering (no
stratification), no nuclear atypia, no stromal
invasion)
 Borderline
 Gross; cystic / solid foci
 Microscopic; papillary complexity, stratification,
nuclear atypia, no stromal invasion
 Malignant
 Gross; mostly solid & hemorrhage / necrosis
 Microscopic; papillary complexity, stratification,
nuclear atypia, stromal invasion
SURFACE EPITHELIAL TUMORS

• Formed by cells that resemble
internal lining of fallopian tube.
o Most common. 75% of
epithelial ovarian tumor.
o Most common in 4th & 5th
decades of life
o Bilateral in 50% of cases.
SEROUS TUMORS

Malignant (low grade serous and high grade serous
carcinomas)
Stromal invasion . Abundant
delicate to coarse papillae
Psammoma bodies in 80%
per-se do not denote
malignancy .
PSAMMOMABODIES

 Theseareextracellularround laminardark
eosinophilic collections ofcalcium.

Low grade: papillary and
glandular structures
predominate
High grade: solid sheets of
cells , high mitotic activity ,
nuclear pleomophism

• 8-10% of epithelial ovarian tumors.
• Largest ovarian tumors; may fill entire abdominal cavity.
• 5% are malignant.
• Bilateral in 8-10% cases.
•Cystic tumor; have loculi lined with mucin secreting
epithelium. Cut surface shows honey-comb appearance. If it
ruptures, may lead to formation of pseudomyxoma
peritonei & adhesion formation
MUCINOUS TUMOURS

• Resemble either those of
the endocervical
epithelium (endocervical
or mullerian type) or,
more frequently, those of
the intestinal epithelium
(intestinal type)
• Histologically, distinction
may be impossible
without clinical
correlation.
Irregularglandularspaces lined with a
layer of tall columnarcells

ENDOMETRIOID TUMORS
 6-8% of epithelial tumors.
 Most are unilateral (40% are
bilateral)
 Almost all are malignant
 Associated with endometrial
cancer (15-20%)
Patient may have concurrent
endometriosis (10-20%)
 May be cystic or solid
Content tends to be hemorrhagic
rather than serous or mucinous
Resembling proliferative
endometrial glands

• Clear, peglike or hobnail-like cells.
• Most clear cell ovarian tumors are
malignant.
• 50–70% have endometriosis
• One-fourth of all clear cell tumors
arise in the lining of benign
endometrioid cyst.
• These tumours are almost
invariably high grade (grade 3) ,
hence not graded.
CLEAR CELL TUMORS

Resemble those of the internal lining of the urinary bladder .
Borderline brenner tumors – surgical removal results in
complete cure .
• Malignant Brenner – benign or borderline when coexisting
with invasive transitional cell carcinoma
• Transitional cell carcinoma- when primary resembles
transitional cell ca of Bladder without a recognisable
brenner tumor -- sensitive to chemotherapy , more
favourable prognosis .
BRENNER TUMORS

Germ Cell Tumors
Embryonic, ectoderm,
mesoderm,
endoderm
Teratoma
(hcg- AFP-)
Extra embryonic
structures
(Vitelline)
Endodermal
Sinus tumour
(AFP+ HCG-)
(Yolk Sac Tumour)
Totipotent
cells
Embryonal
Carcinoma
AFP (+)
hCG (+)
Embryonic
differentation
Seminoma,
Dysgerminoma
(primitive germ
cells)
AFP (-)
hCG (-)
GERM CELLTUMORS
(Trophoblastic)
Choriocarcinoma
(AFP- HCG+)
mature immature
NOVAKS

 Germ cell tumors -20-25% of all ovarian cancers
 Benign 97% ,malignant 3%
 M.C age – young women. In 1st two decades of life, 70%
are of Germ cell origin.
 Rapidly growing; Palpable abdominal mass and pelvic
pain.
 FIGO staging same as epithelial ovarian tumor

DYSGERMINOMA
• Commonest malignant germ cell tumors (30 to 40% )
• 75 % occur between 10 to 30 years of age. Rare after 50yrs.
• Consists of germ cells that have not differentiated to form
embryonic or extraembryonic structures .
• Tumor marker - Elevated LDH , HCG or AFP
• As they present relatively at early stage - surgery followed
by radiation has excellent cure rate . Loss of fertility is a
problem.
• 85% of all patients with dysgerminoma are younger than 30
yrs , CONSERVATIVE THERAPY & PRESERVATION OF
FERTILITY of major consideration .

 3rd most frequent malignant GCT of
ovary.
 Median age 16 – 18 yrs
 Unilateral in 100 % hence biopsy from
opposite ovary is not needed
 Highly malignant with rapid growth
 Abdomen or pelvic pain (75 %) ,
Asymptomatic pelvic mass (10%)
 Gross appearance soft grayish brown
with cystic areas
 Histology – SCHILLER DUVAL bodies
 Tumor maker- AFP correlates extent of
disease
& monitoring response to treatment
YOLK SAC TUMOR/ ENDODERMAL SINUS TUMOR
Schillar Duval bodywith
its central capillary and
mantle of endoderm

TERATOMA
MATURE CYSTIC TERATOMA
Tissues usually derived from 2 or 3 germ cell layers.
Accounting 95% of all ovarian teratomas
Age < 20 years
Clinical manifestation related to size ; TORSION most common
complication – 16%
Ovarian cystectomy appears to be adequate .

Has age specific incidence – Mc in first 2 decade
According to Norris et al the quantity of immature neural tissue
alone determines the grade .
Grade I – mature teratoma containing only rare immature foci
Grade III- large portion embryonal tissue with atypia and
mitotic activity
Rarely bilateral. So present method of therapy unilateral
SALPINGOOPHERECTOMY with wide sampling of
peritoneal implants .
IMMATURE TERATOMA

Most malignant but rare (4%).
Very young (4-28yrs) Median age
is 14yrs.
Manifests as abdominal mass
pelvic mass. Associated with
hormonal abnormalities (may
secrete estrogen).
Tumor makers - AFP, HCG
EMBRYONAL CARCINOMA

 Extremely rare
 Composed of numerous
embryoid bodies that resemble
morphological normal embryo.
 Occur in very young,
premenarcheal girls.
 Highly malignant .least sensitive
to chemo & radiotherapy
POLYEMBRYOMA

Atleast 2 or more malignant germ cell elements, one of
which is primitive.
Components –dysgerminoma(commonest)
yolk sac tumor, immature teratoma, embryonal ca ,
choriocarcinoma, and polyembryoma.
Most significant component of the MIXED GC tumor
determines therapy and follow-up .
MIXED GERM CELL TUMORS

Classification the sex cord-stromal tumors are divided into :
• Granulosa cell tumor
• Thecoma –fibroma group
 Sertoli-Ledyig cell tumors(Androblastoma)
• Gynandroblastoma
• Sex cord tumor with annular tubules
• Unclassified
• Steroid cell tumors
SEX CORD-STROMAL TUMORS

10% of all solid tumor,
Bilateral in 2%
• Two SUBTYPES : Adult
and Juvenile
• Adult GC – (95%) MC in
postmenopausal . Avg age
is 50years.Associated with
ESTROGEN production.
Endometrial HYPERPLASIA
( 25-50%) and Ca
endometrium (5-10%)
GRANULOSA CELL TUMORS
 Juvenile GC – In children and
young adults ; 90% before
puberty. Mean age at
diagnosis is 13 years.
Menstrual irregularities ,
amenorrhea, precocious
puberty.
True GC tumors are low grade;
confined to one ovary with
EXCELLENT PROGNOSIS :
long term survival 75-90 %

M/E- classic adult granulosa cell is round/ovoid with scant
cytoplasm. “COFFEE BEAN” grooved nuclei are characteristic
CALL- EXNER BODIES- adult granulosa cells show a tendency to arrange
themselves in small clusters or rosettes around a central cavity, resembling
primordial follicles.

THECOMA-FIBROMA GROUP
THECOMA
 Rarely malignant.
 In postmenopausalwomen;
typically in 60’s.
 Most hormonallyactive.
Usually produce excess
estrogen.
 Abnormal bleeding , pelvic
mass.
 Cells resemble thecacells
 B/L involvment rare. Surgical
resection iscurative.
FIBROMA
 Generally benign.
 Perimenopusal and menopausal
women.
 Hormonally inactive.
 1% women present with MEIG’S
SYNDROME( TRIAD of solid
ovarian mass, ascites andpleural
effusion).
 Arise from spindled stromalcells
that form collagen.
 Malignant transformation in1%
cases.

SERTOLI-LEYDIG CELL TUMOUR (ARRHENOBLASTOMA)
 Extremely rare(0.2% of ovariancancers)
 Occur most frequently in 3rd or 4th decade
 75% seen in women <40yrs
Produce androgens  clinical virilisationin
70-85%
 Signs of virilisation  oligomenorhoea f/b
amenorrhoea, breast atrophy, acne, hirsuitism,
clitoromegaly, deepening of voice, receding hair
line
 Rarely estrogenisation (iso-sexual precocity,
irregular or postmenopausal bleeding)seen.

Metastatic tumours
 About 5-6% of ovarian tumoursare metastatic most frequently from
the female genital tract,breast & GIT (pylorus, colon, rarely small
bowel, pancreas, gall bladder)
 Twoforms of secondary ovariancarcinoma
1. Growthcorresponds in its histologywith its primary
growth
 Dissemination by implantation from metastasiswithin
peritoneal cavity
 Retrograde lymphaticspread
 Ovarian tumoursare much largerthanothersecondary
deposits
 Solid, irregularsurface, nearly always bilateral, ascitis is
common, peritoneal metastasis(omentum)

Krukenberg tumour
1. Usually bilateral
2. Mostoftenarise from primarycarcinomaof stomach(70%),
large bowel (15%), breast(6%)
3. Smooth surface, slightly bossed, freely movable in pelvis
4. No infiltration through thecapsule, no tendency to form
adhesions
5. Tumourretains theshape of normal ovary, solid waxy
consistency
6. Histologically, cellularor myxomatous stroma, scattered signet
ring cells (ovoid cell with granular cytoplasm, nucleus
compressed againstone poleof thecell)

 ̴̴75% to 85% of patients with epithelial ovarian cancer
are diagnosed at the time when their disease has spread
throughout the peritoneal cavity.
 Our main aim is to identify women at high risk ,offer
management option .. Suspect and establish diagnosis
and treat cancer aggressively
DIAGNOSIS AND CLINICAL EVALUATION

Symptoms are Non specific amd vague.
-Bloating ,abdominal distension
-Pelvic or abdominal pain
-Difficulty eating or feeling full quickly
-Urinary symptoms ( frequency and urgency)
Symptoms present for less than one year and occur on
more than 12 days per month .
SYMPTOMS IN OVARIAN CANCER

Signs
 Anaemia
 Left Supraclavicular (Virchow’s) & inguinal
lymphadenopathy
 Unilateral non-pitting oedema of legs
 Tumours are often bilateral &fixed
 Ascitis, abdominal lump, enlarged liver
 Vaginal examination: fixed nodules in POD,adnexal
massess felt separate fromuterus
 Pleural effusion

• TRANSVAGINAL SONOGRAM
• SERIAL CA125 Testing
OVARIAN CANCER SCREENING

 Initial imaging modality of choice for benign vs malignant
 Results of screening trials have consistently demonstrated
that US detects more stage I ovarian carcinomas than
CA125 levels and physical examination
 TVS showed very high sensitivity (>95%) for detection of
early stage carcinoma.
 Each ovary is measured in threedimensions.
 Ovarian volume is calculated using the prolate
ellipsoid formula (L x H x W x 0.523).
Premenopausal women vol>20cm3
postmenopausal womenvol>10cm3
Anysolid orpapillary projection from tumorwall
ULTRASOUND
ABNORMAL

RISK OF MALIGNANCY INDEX (RMI)
 Most valuable clinical tool by combining serum CA125
values with ultrasound findings and menopausal status to
calculate a Risk of Malignancy Index (RMI).
 RMI = U x M x CA125
 U is ultrasound score. 1 point each for :
multilocular cysts, solid areas, metastasis, ascites
and bilateral lesions.
 M is menopausal status ; scored as 1 = pre-
menopausal and 3 = post-menopausal
 Serum CA125 in IU/ml and can vary between 0 and
hundreds or even thousands of units.

 It yielded a sensitivity of 85% and a specificity of 97%.
 LOW RISK: RMI <25
 MODERATE RISK: RMI 25-250
 HIGH RISK: RMI >250
 Risk of cancer is 75% when RMI value is >250

Serum CA125 has been widely used as marker for possible
epithelial ovarian ca in assessment of pelvic mass.
 Poor sensitivity (elevated in only 25-50% of women with Stage
I disease)
 Poor specificity (elevated in many gynecologic and non-
gynecologic malignancies and benign conditions).False positive
results common.
- Postmenopausal women = > 35 U/ml
- Premenopausal women = > 200 U/ml
- CA125 is important tumor marker for diagnosis , treatment
and follow up care of patients with epithelial ovarian ca , can
be used to determine response to t/t , relapse and survival.
TUMOR MARKERS( CA-125)

Benign conditions
• Endometriosis
• Uterine fibroids
• PID
• Pregnancy
• Menstruation
• Diverticulitis
• Pancreatitis,liver disease
• Renal failure
• Appendicitis, IBD
Malignantconditions
• Cervical CA
• Fallopian tube CA
• Endometrial CA
• Pancreatic CA
• Colon CA
• Breast CA
• Lymphoma
• Mesothelioma

Several other markers studied
• Human epididymis protein 4
• Mesothelin
• B7-H4
• Decoy receptor 3
• Spondin 2
OVA1 is an FDA-cleared blood test that uses results of 5
biomarkers (transthyretin, apolipoprotien A1, transferrin, beta-2
microglobin and CA-125), with an algorithm to indicate the
probability of malignancy of an ovarian mass. Sensitivity
: 93%, specificity: 43%
OvaSure screening test- 6 biomarkers
Leptin, prolactin, osteopontin, IGFII, MIF and CA-125. Not
recommended
.

• Several publications have demonstratedHE4 ‘s superiority
over CA125. Specifically , HE4 ‘s ability to distinguish benign
diseases with malignancies(ie its sensitivity )
• As a single marker, HE4 had the highest sensitivity at 72.9%
(specificity 95%)
• Combined, CA125™ and HE4 yielded the highest
sensitivity at 76.4% (specificity 95%)
• The combination of CA125 and HE4 added 33.1% to the
sensitivity of CA125 alone and 4.5% to the sensitivity of HE4
alone.
HE-4 A NOVEL TUMOR MARKER

• Recently, a more sensitive risk of ovarian cancer
algorithm (ROCA) has been developed. Thisalgorithm
is based on the slope of serial CA125 measurements
drawn at regularintervals.
• It has been proposed to increase the performance of
single-threshold measurements of CA-125 concentrations.
• ROCA method is being evaluated in conjunction with TVS
as a two-stage screening process, and results from trials
are pending.
ROCA

Patterns Of Spread
1. Transcoelomic
Most common & earliest mode byexfoliationof cells which
implant along surfaces of peritonealcavity
Follows circulatory path of peritonealfluid
Metastasis typically seen on POD, paracolic gutters, right
hemidiaphragm, liver capsule, peritoneal surface of intestine
& mesenteries, omentum
It seldom invades intestinal lumen, butprogressively
agglutinates loops of bowel  functional intestinal
obstruction  carcinomatous ileus

2.Lymphatic
First involves pelvic lymph nodes through broadligament
Advanced stagedisease  retrograde disseminationvia
lymphatics to round ligament to inguinal lymph nodes follows
ovarian vein to precaval & paraaortic lymph nodes
3.Hematogenous
Hematogenous dissemination at the timeof diagnosis is
Uncommon
Spread to vital organs parenchyma (lungs & liver)occur only in
2-3% patients

STAGE I: TUMOR CONFINED TO OVARIES

STAGE II: TUMOR INVOLVE 1 OR BOTH OVRIES WITH PELVIC EXTENSION OR
PRIMARY PERITONEAL CANCER

STAGE III: TUMOR INVOLVE 1 OR BOTH OVRIES WITH CYTOLOGICALLY
OR HISTOLOGICALLY CONFIRMED SPREAD TO PERITONEUM OUTSIDE
THE PELVIS AND /OR METASTASIS TO THE REPTROPERITONEAL NODES

STAGE IV: DISTANT METASTASIS EXCLUDING PERITONEAL
METASTASIS

a) PATHOLOGICAL FACTORS:
a)Histologictype: Clearcell & Mucinous histologies – poorersurvival
low malignant potential – bettersurvival
b) Grade of tumor: poorly differentiated – poorersurvival
c)Stage of disease: According toFIGO
b) BIOLOGICAL FACTORS:
a) Aneuploidy poorerprognosiscompared todiploidy
c) CLINICAL FACTORS:
a) Extent of residual disease post primarysurgery,
b) Volumeof disease: small volume disease have betterprognosisdespite the
stage
c) Age: Older age poorerprognosis
Prognostic factors affecting the Outcomes

Management:
 Preoperativeevaluation
 Surgical management
 Chemotherapy
 NACT
 Follow up
 Management of commonly encounteredtumors
67

PREOPERATIVE EVALUATION
 CBC, Coagulogram, LFT, RFT
 ECG/ CXR
 Urine R/E & C/S
 F/PP Sugars
 IMAGING:TAS/ TVS
CECT abdomen & pelvis / MRI/ PETScan
 Paracentesis
Ruleoutotherprimarysites :
 Mammography
 GI Endoscopies
Tumormarkers 68

ROLE OF FNAC
Diagnosticcytology has poorsensitivity todetectmalignancy
 Aspiration of a malignant mass may induce spillage and seeding of
cancer cells into the peritoneal cavity, thereby changing the stage and
prognosis.
INDICATION :
Advanced ovarian cancer patients who are medically unfit
to undergo surgery permitting initiationof neoadjuvant
chemotherapy(NACT)
69

• PRIMARY SURGERY
1. EARLY STAGE OVARIAN CA( stage 1 and stage2)
•
• COMPREHENSIVE SURGICAL STAGING
FERTILITY SPARING SURGERY
2. ADVANCED STAGE OVARIAN CA
• PRIMARY CYTOREDUCTIVE SURGERY
• NEOADJUVANT CHEMOTHERAPY AND INTERVAL
CYTOREDUCTIVE SURGERY
• LAPAROSCOPY SURGERY
• SECONDARY SURGERY
• SECOND LOOK LAPAROTOMY
MANAGEMENT SPECTRUM

COMPREHENSIVE SURGICAL STAGING
 Vertical midline abdominal incision
 Peritoneal cytology. Minimum of 25cc should be sent.
 In the absence of ascites, separate saline washings should be
obtained from
(a) pelvic cul-de-sac,
(b) right paracolic space,
(c) left paracolic space, and
(d) undersurface of each hemidiaphragm.
 The ovarian tumor should be inspected for presence of papillary
excrescences or rupture of the capsule.
 Abdominal inspection and palpation in a systematic fashion.

What is thesequenceof systemic
explorationof abdominal organs???

• Beginning with– peritoneumof cul-de-sac and small
bowel mesentry.
• Ascending colon
• Liver
• Omentum
• Undersurface of right and lefthemidiaphragm
• Stomach
• And Finally----
• Tranverse colon, spleen, descending colon andbladder
peritoneum.

 TAH + BSO
 Infracolic omentectomy in patients with epithelial ovarian cancer
and an omental wedge biopsy taken in patients with germ-cell or
stromal tumors.
 Suspicious areas to bebiopsied
 Retroperitoneal lymph nodesampling
 Appendectomyshould be performed in all patientswith mucinous
epithelial cancers involving theovary.
 Operative findings presentat staging laparotomy must be carefully
documented.

SURGICAL THERAPY
BORDERLINE TUMOUR
Primary resection- Unilateraloophorectomy
no subsequentchemoor RT required.
 Stage I epithelial ovarian cancer:
 TAH + BSO with omentectomyand lymph nodesampling

STAGE II
 TAH + BSO with careful surgicalstaging
 Followed by chemotherapy usually platinum based.

Indications for fertility sparing surgery?

Fertility sparing surgery:
 Desirous of preserving fertility
 Pt & familyagrees forclosefollowup
 No e/o dysgeneticgonads
 Unilateral GCT, Sex cord stromal tumor, borderlinetumor.
 Early stage ovarian carcinoma(IA)
Follow up :
 Routine periodic pelvic examinations and determinations of serum CA125
levels.
 Endometrial biopsy / curettage as 5% to 15% of patients with granulosa cell
tumordevelop endometrial canceror hyperplasia.
 Generally, theotherovaryand the uterus areremoved at thecompletionof
childbearing.

ADJUVANT THERAPY ??----- RISK
ASSESSMENT
 Benefit of post-oporadjuvant therapydepends
on risk of relapse.
 EARLY STAGE OVARIAN CANCER classified
into
LOW RISK HIGH RISK
Stage IA or IB, grade 1 and2
Standard treatment is SURGERY
ALONE. 5year survival is atleast
95%.
[ No role of adjuvanttherapy]
Stage IA or IB,grade 3 Stage IC
ALL Stage 2
Platinum based chemotherapy.
Optimal regimen & duration of therapy
ELUSIVE

ADVANCED OVARIAN CA
Stage III/ STAGE IV
MAXIMUM CYTOREDUCTIVE SURGERY F/B
COMBINATION CHEMOTHERAPY

Stage III/ IV:
 PRIMARY CYTOREDUCTIVE SURGERY :
 Goal is toreduce theamountof tumoras much as possible in a patient
with metastatic ovariancancer.
 It is considered in contextof responsivenessof residual tumortopost-
operative therapies.
 Lesser the residual tumorvolume, better is thesurvival.
 OPTIMAL DEBULKING- Minimal residual disease ≤ 1-2 cm ingreatest
dia.
 SUBOPTIMAL DEBULKING- Bulky residual disease > 1-2 cm india.
Complications:
Infection,
hemorrhage
prolonged ileus
cardiopulmonaryproblems

PRINCIPLES:
 Close observation & treatment ofany
complications duringchemotherapy
 Assessment for response & monitoring forany
long term complications.
 Chemosensitivity/ resistanceassay.

 NUMBER OF CYCLES OF TREATMENT
 6-8 cycles: advanced-stagedisease
 3 to 6 cycles: earlier-stagedisease

CHEMOTHERAPY
 Platinum-based combination chemotherapy is generally
recommended. They can be used singly or in combination
with Paclitaxel.
Currently, Paclitaxel and Carboplatin combination found to
have better survival rate.
85

• Regime followed-----
• Before starting chemotherapy, Hydrate thepatient.
• Inj. Palonosetron, Inj avil, inj dexameethasone,
inj rantac given ½ hr before starting
chemotherapy.
• Inj PACLITAXEL 175mg/m2 IV infusion in D5%
glass bottle through CODON SET.
• Inj. CARBOPLATIN 450mg(5-6 AUC) IV infusion
Every 3 weekly with Monitoring of CHG, RFT,LFT&
Serum electrolytes.
D
A
Y
1

INTRAPERITONEAL CHEMOTHERAPY
 Patients with low volume residual disease after
surgical cytoreduction are potential candidatesfor
intraperitoneal (IP) therapy.
 Not been accepted universally as a result of issues
with catheter placement and therapy associated
toxicities
87

FOLLOW UP
Complete clinical remission is defined as no objective evidence of
disease
Recommendations : After the completion of primary surgery and
chemotherapy ; Visits : every 2-4 mo for 2 y, then twice yearly for 3 y,
then annually after 5 y
• CA-125/ other tumor markers every visit if initially elevated
• CBC / LFT/RFT as indicated
• Complete physical & Pelvic examination
• Chest/ abdominal/ pelvic USG/ CT/ MRI
• PET-CT, or PET as clinically indicated

ROLE OF NACT
 INDICATIONS: Poor surgicalcandidates
Possibility of suboptimalresection
Stage IIIC/IV
 Giving 3-6 cycles of CT upfront will reduce tumor burden, makes
subsequent surgery more feasible ( Allow maximal cytoreduction of
residual tumor)
 surgery post NACT c/as: INTERVAL DEBULKING SURGERY
 Priortogiving NACT, the pathologicdiagnosisshould beconfirmed by
eitherfine needleaspiration, CT-guided biopsyor paracentesis.
89

SECOND LOOK SURGERY
 performed on a patient with no clinical evidence of
persistent tumor for the purposeof determining disease
status after a planned interval of treatment with
chemotherapy
 Primary purpose not debulking 0r treating complication
Classification of findings
 Negative - 30% to 50%( seen with Early-stage disease )
 Microscopically positive-20%
 Macroscopically positive- 30% to50%
NOT RECOMMENDED due to increased surgicalmorbidity

ROLE OF LAPAROSCOPY
 Primary surgery forearly-stageovarian cancer
 Restaging of unstaged ovariancancer
 Assessment of resectability
 Intraperitoneal catheterplacement
 Second-look surgery
 Secondary cytoreductivesurgery.
Port site metastasis 1% to2%

DYSGERMINOMA
TREATMENT:
SURGERY:TAH &BSO, if fertility not required.
Unilateral oophorectomy- minimum surgery
CHEMOTHERAPY
Advantage : fertility preservation
RADIOTHERAPY VeryRadiosensitive
problem :Loss of fertility

GRANULOSA CELL TUMOR
 Unilateral salpingo-oophorectomy
 Ovarian biopsy if enlarged
 Endometrial biopsy if uterus left
 Palliative RT for pelvic recurrences (otherwise not
useful).
EMBRYONAL CARCINOMA
Rx-: Unilateral oophorectomy followed by
CT with BEP

Ovarian Malignant PPT.pptx

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