diagnosis and treatment of ovarian tumours

1. Malignant ovarian tumor

2. Dr Aisha Nazeer
Assistant professor
Dept of OB-GYN
QAMC/Civil hospital,Bahawalpur

3. Learning objectives
• Learn how malignant disease of ovary,fallopian tube and
peritoneum presents
• Learn how ovarian cancer is investigated and staged.
• Learn how ovarian cancer is managed

4. • Ovarian cancer is second most common gynaecological
malignancy and major cause of death from gynaecological
cancer.
• There are approximately 7000 new cases and 4000 deaths
from ovarian cancer per year.
• Ovarian cancers -6% of all cancers among women
• lifetime risk of developing ovarian cancer in general
population is 1.4%(1 in 70)
• Mean age at presentation is 64 years.
• 54 years of age in hereditary type.
• Only 3% of ovarian cancer occur under 35 years of age
• More prevelant in higher income nations.
• Incidence varies with ethnicity,
• White women ; 14/100,000
• Asian women ; 10/100,000
EPIDEMIOLOGY

5. The “silent killer”: asymptomatic in early stages
 75% diagnosed with advanced stage disease; 5-year
survival only 10-20%.

6.  Age
 Rare before 40yrs,
increases steadily
thereafter, peaks at65-
75yrs.
 Reproductive history
 early menarche,
nulliparityorage >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

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
• 1.4 % (1 in 70)without family
history.
• 5%(1 in 20)if one relative is affected
.
• 40-50% if two first degree 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.(RR reduced by upto
50%)
• Tubal ligation.
• Salpingectomy
• Hysterectomy .
• Bilateral oopherectomy -↓ risk by 80% to 95% .does
not eliminate the risk of peritoneal cancer.
• 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

12.  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

13.  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.

14.  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
DuttaGynae

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

16. 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

17. • 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

18. 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 .
Novak's
PSAMMOMABODIES

19.  Theseareextracellularround laminardark
eosinophilic collections ofcalcium.

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

21. • 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

22. • 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

23. 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

24. • 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

25. 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

26. 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 immatureNOVAKS

27.  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

28. 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 .

29.  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

30. 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 .

31. 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

32. 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

33.  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

34. 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

35. 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

36. 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 %

37. 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.

38. 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.
WILLIAMS GYNAE

39. 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.
NOVAK'S GYNAE

40. 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)

41. 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)

43. Primary peritoneal carcinoma
PPC is a high grade pelvic serous carcinoma. It is histologically
indistinct from tumours arising from fallopian tube or ovary.
Criteria for diagnosis include:
1- Normal sized or slightly bulky ovaries
2- More extraovarian disease than ovarian disease
3- Low volume peritoneal disease
The clinical behaviour prognosis and treatment is same as for
other high grade pelvic serous carcinoma

44.  ̴̴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

45. Symptoms are Non specific amd vague.
-Bloating ,abdominal distension
-Pelvic or abdominal pain
-Difficulty eating or feeling full quickly
-Change in urinary and bowel habits.
Backache,irregular bleeding.
Symptoms present for less than one year and occur on
more than 12 days per month
SYMPTOMS IN OVARIAN CANCER

46. 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

47. TRANSVAGINAL SONOGRAM
SERIAL CA125 Testing
OVARIAN CANCER SCREENING

48.  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

49. 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.

50.  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
DUTTA GYNAE

51. Serum CA125 has been widely used as marker for possible
epithelial ovarian ca in assessment of pelvic mass.
 Poor sensitivity (elevated in only 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)

52. Tumor markers
Tumor marker Tumor type usesTumor marker Tumou type uses
Ca 125 Epithelial ovarian
cancer(serous),BOT
Preoperative,follow
up
Ca 19-9 Epithelial ovarian
cancer(mucinous)
,BOT.
Preoperative,follow
up
inhibin Granulosa cell
tumors
Follow up
hcG Dysgerminoma,
choriocarcinoma
Preoperative,follow
up
AFP Endodermal yolk
sac,Teratoma
Preoperative,follow
up

53. Ca 125 is also raised in benign conditions
• Pregnancy
• Endometriosis
• Uterine fibroids
• Pancreatitis
• Normal menstrution
• PID
• Cirrhosis of liver

54. 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

55. 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

56. FIGO staging of Ca Ovary

57. FIGO STAGING
Stage 1; Tumor confined to ovaries
1a : limited to one ovary,no external tumor,capsule
intact,no ascites
1b: limited to both ovaries,no external tumor,capsule
intact,no ascites
: 1c: either 1a or 1b but tumor on surfce of ovary or with
capsule ruptured or with ascites positive for tumor cells
Stage 2; Tumor confined to pelvis
2a: extension and /or metastasis to uterus or tubes
2b; extension to other pelvic organs
2c:as 2a or 2b but tumor on surface of ovary or with
Capsule ruptured or or with ascites positive for tumor cells

58. FIGO STAGING
Stage 3; tumor confined to abdominal peritoneum or
+ve retroperitoneal or inguinal lymph nodes
3a : tumor grossly limited to pelvis with negative nodes,
But histopathology confirmed microscopic peritoneal
implants.
3b : abdominal implants less than 2 cm in diameter.
3c : abdominal implants greater than 2 cm or +ve
retroperitoneal or inguinal lymph nodes.
Stage 4; distant metastasis.
must have +ve cytology or pleural effusion,liver
parenchyma.

59. MANAGEMENT OF OVARIAN
TUMORS

60. 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

61. Ovarian cancer survival by stage at diagnosis
FIGO stage 5 year survival(%)
1 80-90%
2 66-70%
3 30-50%
4 15%

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

63. 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

64. ROLE OF FNAC
Diagnosticcytology has poorsensitivity todetect malignancy
 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

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

66. 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.
71
 Abdominal inspection and palpation in a systematic fashion.
TE LIINDE’S

67.  What is thesequenceof systemic explorationof
abdominal organs???

68.  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.

69.  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 becarefully
documented.
74TE LINDE’S

70. SURGICAL THERAPY
BORDERLINE TUMOUR
Primary resection- Unilateraloophorectomy
no subsequentchemoor RT required.
 Stage I epithelial ovarian cancer:
 TAH + BSO with omentectomyand lymph nodesampling
ovariancancer 75

71. STAGE II
 TAH + BSO with careful surgicalstaging
 Followed by chemotherapy usually platinum based.
76ovariancancer

72.  Indications for fertility sparing surgery?

73. 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 thecompletion of
childbearing.

74. 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

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

76. 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 cm ingreatest
dia.
 SUBOPTIMAL DEBULKING- Bulky residual disease > 2 cm
Complications:
Infection,
hemorrhage
prolonged ileus
cardiopulmonaryproblems
81TE LINDE'S

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

78.  Number of cycles of treatment??

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

80. 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.
Bevacizumab is also effective in improving recurrence
when combined with carboplatin and paclitaxel.
85

81.  Regime followed-----
 Before starting chemotherapy, Hydrate thepatient.
 Inj. Palonosetron, Inj avil, inj dexameethasone, inj
rantac given ½ hr before startingchemotherapy.
 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

82. 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

83. • FOLLOW UP
1 .. Clinical examination.
2 .. Ca125 measurements
levels of ca125
start to rise prior to clinical evidence of
disease recurrence. When disease recurs
treatment is largely palliative.If duration of
remission is more than 6 months,carboplatin
may be used again,otherwise taxol or
topotecan can be given.
• 8

84. U
ROLE OF NEOADJUVANT
Chemotherapy
 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

85. SECOND LOOK SURGERY
 performed on a patient with no clinical evidence of
persistent tumor forthe 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 90

86. 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%
91ovariancancer

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

88. 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

89. CASE SCENERIO
Mrs tariq,, 62 years,para 1 presents with non specific abdominal
pain,change in bowel habit and bloating.On usg bilateral
complex solid/cystic masses ,large volume ascites and omental
caking. What is the most likely diagnosis? What are key
points in examination and investigation? How would you
manage her?

90. ANY QUESTIONS?

91. THANK YOU