This document provides an overview of malignant ovarian tumors. It discusses the epidemiology, risk factors, pathology, diagnosis, screening, staging, prognosis, and management of ovarian cancer. Some key points include:
- Ovarian cancer has a high mortality rate and is often diagnosed at an advanced stage. The most common type is epithelial ovarian cancer.
- Risk factors include age, nulliparity, family history, and hereditary conditions like BRCA mutations. Protective factors include pregnancy and oral contraceptive use.
- Theories on pathogenesis involve repeated ovulation and inflammation damaging the ovarian surface.
- Staging involves determining if the cancer is confined to ovaries or has spread within the pelvis or abdomen.
3. 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
4. • 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
5. 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
6. 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
7. • 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
8. 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
9. ~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
10. 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
11. 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
16. 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
17. 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.
18. 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
21. 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
22. • 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
23. 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
25. Low grade: papillary and
glandular structures
predominate
High grade: solid sheets of
cells , high mitotic activity ,
nuclear pleomophism
26. • 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
27. • 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
28. 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
29. • 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
30. 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
32. 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
33. 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 .
34. 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
35. 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 .
36. 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
37. 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
38. 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
39. 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
40. 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
41. 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 %
42. 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.
43. 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.
44. 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.
45. 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)
46. 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)
47.
48. ̴̴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
49. 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
50. 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
52. 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
53. 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.
54. 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
55. 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)
56. 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
57. 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
.
58. • 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
59. • 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
60. 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
61. 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
64. STAGE II: TUMOR INVOLVE 1 OR BOTH OVRIES WITH PELVIC EXTENSION OR
PRIMARY PERITONEAL CANCER
65. 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
68. 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
71. 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
72. • 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
73. 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.
75. • 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.
76. 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.
77. SURGICAL THERAPY
BORDERLINE TUMOUR
Primary resection- Unilateraloophorectomy
no subsequentchemoor RT required.
Stage I epithelial ovarian cancer:
TAH + BSO with omentectomyand lymph nodesampling
78. STAGE II
TAH + BSO with careful surgicalstaging
Followed by chemotherapy usually platinum based.
80. 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.
81. 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
83. 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
84. PRINCIPLES:
Close observation & treatment ofany
complications duringchemotherapy
Assessment for response & monitoring forany
long term complications.
Chemosensitivity/ resistanceassay.
85. NUMBER OF CYCLES OF TREATMENT
6-8 cycles: advanced-stagedisease
3 to 6 cycles: earlier-stagedisease
86. 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
87. • 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
88. 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
89. 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
90. 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
91. 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
92. 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%
93. DYSGERMINOMA
TREATMENT:
SURGERY:TAH &BSO, if fertility not required.
Unilateral oophorectomy- minimum surgery
CHEMOTHERAPY
Advantage : fertility preservation
RADIOTHERAPY VeryRadiosensitive
problem :Loss of fertility
94. 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