OVARIAN TUMORS

ADNEXAL MASS
• Adnexal mass – one of the most common
gynecologic conditions
• It is estimated that women have a 5-10%
lifetime risk of undergoing surgery for a
suspected adnexal mass
• Adnexal masses – suspected in both –
symptomatic and asymptomatic women
 ADNEXAL MASS
• In premenopausal women the most common
adnexal masses include:
- Physiologic follicular cysts and corpus luteum
- Ectopic pregnancy
- Policystic ovaries
- Endometrioma
- Ovarian Neoplasms
- Tubo-ovarian abscess
 ADNEXAL MASS
• In postmenopausal women the most common
adnexal masses include:
- Fibroids
- Ovarian neoplasms
 ADNEXAL MASS
• Once the suspicion of adnexal mass is established, the
clinician should exclude acute pathology such as:
- Ectopic pregnancy
- Adnexal torsion
- Tubal abscess

And then to determine whether the adnexal mass is:

- Benign
- Borderline (indeterminate)
- Malign
 Differential diagnostic of an adnexal mass –
gynecologic benign pathology
Gynecologic benign ovarian pathology Corpus luteum
Follicular/functional cysts
Mature cystic teratoma (dermoid cysts)
Ovarian Torsion
Serous/mucinous cystadenoma,
cystadenofibroma
Theca-lutein cyst/luteoma of pregnancy
Tubo-ovarian abscess
Endometroid cysts/endometrioma
Gynecologic benign non-ovarian Ectopic pregnancy
pathology Uterine leiomyomas
Hydrosalpinx
Endosalpingiosis
Morgagni cysts(embryonic remnant)
 Differential diagnostic of an adnexal mass –gynecologic
malignant pathology
Gynecologic malignant ovarian/tubal pathology Tubal malignant tumors
Borderline tumors of the ovary
Epithelial ovarian malignancies
Ovarian sarcomas
Ovarian germ cell tumors
Sex cord/stromal tumors
Gynecologic malignant non-ovarian/tubal pathology Endometrial cancer
 Differential diagnostic of an adnexal mass –
nongynecologic pathology
Nongynecological benign pathology Appendicular abscess/ appendicitis
Diverticular abscess
Pelvic kydney
Bladder diverticulum
Peritoneal inclusion cysts
Nerve sheath tumor
Nongynecological malignant pathology Krukenberg tumors (gastrointestinal
metastases)
Other metastatic lesions (breast)
Retroperitoneal malignant tumors
Primitive malignant tumors of the peritoneum
 ADNEXAL MASS – SYMPTOMS
• The spectrum of symptoms in a patient presenting an
adnexal mass can widely vary:
- Clinic asymptomatic
- Diffuse pelvic pain
- Acute pelvic pain
- Vaginal bleeding
- Asthenia
- Weight loss
- Increasing the abdominal volume
DEPENDING ON THE NATURE OF THE ADNEXAL MASS!!!
ADNEXAL MASS – SIGNS AND SYMPTOMS
ECTOPIC PREGNANCY ADNEXAL TORSION FUNCTIONAL CYSTS
- Vaginal bleeding - syncopal pain influenced - Midcycle pain (at
- Unilateral pelvic pain by movement ovulation)
- Positive pregnancy - Vomiting
test

ENDOMETRIOMA/ENDOMETRIOSIS TUBO-OVARIAN ABSCESS

- Infertility - Fever
- Long standing dysmenorrhea - Purulent vaginal discharge
- Dyspareunia - Cervical motion tenderness

OVARIAN CANCER
- Family history of breast/colon/ovarian cancer
- Nulliparous postmenopausal women
- Increased abdominal size/ bloating/ back pain
- Urinary urgency
- Weight loss/ anorexia
- Diffuse pelvic pain
ADNEXAL MASS – PHYSICAL EXAMINATION
• PHYSICAL EXAMINATION SHOULD INCLUDE:
- Vital signs (pulse rate, arterial tension, respiratory
frequency)
- abdominal examination (tenderness, distension, pain,
bloating, bowel sounds, ascites, muscular contracture)
- General clinical examination (cervical, axillary, inguinal
lymph nodes)
- Pelvic examination (vaginal discharge/bleeding, bimanual
uterine palpation, vaginal touch – adnexal, cul de sac,
parametrial examination)
- Rectovaginal examination (uterosacral ligaments, tumoral
masses)
 ADNEXAL MASS – PARACLINICAL EVALUATION

LABORATORY TESTS:
REPRODUCTIVE AGE WOMEN:
 Pregnancy urinary test
 Beta HCG (pregnancy is
suspected)
 CBC (ectopic pregnancy,
abscess is suspected)
 Clotting studies (heavy
vaginal bleeding)
 Tumor markers (CA125, CA
15-3, AFP, CEA) (malignant
lesion is suspected)
POSTMENOPAUSAL WOMEN:
 Tumor markers (CA125, CA 15-3,
AFP, CEA) (malignant lesion is
suspected)
 Inhibins A/B (granulosa cell tumor
is suspected)
 Beta HCG (germ cell tumor is
suspected)
 CBC (heavy vaginal bleeding)
 Clotting studies (heavy vaginal
bleeding)
 ROMA score (combination
between CA 125 and HE4 values –
malignant ovarian tumors)
ADNEXAL MASS – PARACLINICAL ASSESMENT
IMAGISTIC STUDIES:

- Abdominal ultrasound (A.U)

- Vaginal ultrasound (V.U)
- Computed tomography (CT)
- Magnetic resonance (MR)
- Positron emission computed tomography (PET CT)
 ADNEXAL MASS – PARACLINICAL ASSESMENT

• ULTRASOUND should assess:

The size of the lesion
The shape of the lesion
Mass characteristics:
- solid/cystic lesions
- Septation
- Excrescences
The presence/absence of Doppler flow
ADNEXAL MASS – PARACLINICAL ASSESMENT
ULTRASONOGRAPHIC ASPECT– BENIGN GYNECOLOGIC
PATHOLOGY
LESION SONOGRAPHIC ASPECT
BENIGN CYST - unilocular/multilocular smooth lesion, no solid component
- Acoustic shadowing, no blood flow
ENDOMETRIOMA - Ground glass appearance, might contain clots, might have color
Doppler flow (if blood flow is present in interior)
CORPUS LUTEUM - Thickened wall, circumferential color Doppler flow
HEMORRHAGIC CYST - Fishnet or reticular pattern
TERATOMA - Hyperechoic nodules, calcifications, floating globules,
- Absence of Doppler flow
HYDROSALPINX - Tubular structure with indentations along opposite walls (waist
sign)
PEDUNCULATED - Solid hyperechoic mass with heterogeneous aspect
LEIOMYOMA - Presence of Doppler flow
PERITONEAL INCLUSION - Septated cystic mass surrounded by bowel/ovary
CYST - Perilesional adhesions
 ADNEXAL MASS – PARACLINICAL ASSESMENT
ULTRASONOGRAPHIC ASPECT – MALIGNANT GYNECOLOGIC
PATHOLOGY
LESION SONOGRAPHIC ASPECT
MALIGNANT OVARIAN PATHOLOGY - Irregular multilocular lesions
- Intralesional papillary structures
- Thick (>2-3mm) septations
- Association with free peritoneal fluid (ascites)
- Other peritoneal lesions
- Pelvic/inguinal/para-aortic adenopathies
 The simple rules for ovarian cysts sonographic diagnostic
• The simple rules were described by IOTA (International Ovarian
Tumor Anaysis group)
• They consist in dividing 10 ultrasonographic features in 2 groups:
benign (B) and malignant (M)
B features M features Features Type of lesion
B1 – unilocular cyst M1 – irregular solid tumor At least 1B and no M BENIGN

B2 – solid M2 - ascites At least 1M and no B MALIGNANT

component<7mm
Both B and M are present INDETERMINATE
B3 – acoustic shadow M3 - at least 4 papillary
structures None B or M are present INDETERMINATE

B4 – smooth multilocular M4 – irregular multilocular

tumor <10 cm solid tumor>10 cm
B5 – no blood flow M5 – very strong color
Doppler Additional imagistic
studies are needed
ADNEXAL MASS - PARACLINICAL ASSESMENT
MAGNETIC RESONANCE IMAGING (MRI)
- For a long period of time clinicians have performed
laparoscopic surgery for adnexal mass exploration
just based on the ultrasonographic features (more
than 70% of adnexal masses being accurately
diagnosed using AU and VU)
- Recent data on the impact of ovarian surgery on
fertility have modified the protocol and therefore
recommend performing pelvic MRI studies
- Another utility of MRI is to better plan the surgical
procedure (by orientating the histopathological
features of the lesion)
ADNEXAL MASS - PARACLINICAL ASSESMENT
MAGNETIC RESONANCE IMAGING (MRI)
WHICH LESIONS SHOULD BE ASSESSED WITH MRI?
1. Bi/multilocular cysts
2. Cystic ovarian lesions with papillary projections
3. Mixed heterogeneous mass
4. Enlarged ovaries (including purely solid masses that means more
than 80% of solid component in the lesion)
ADNEXAL MASS - PARACLINICAL ASSESMENT

CT and PET-CT
CT- is used especially in malignant lesions in
order to assess the extension of the disease (the
presence of distant metastases)
PET-CT – is used in lesions with high suspicion of
malignancy if the other imagistic studies failed
to demonstrate the benign/malignant character
of the lesion as well as for the identification of
distant metastases
 OVARIAN TUMORS - CLASSIFICATION
• BENIGN OVARIAN TUMORS
• BORDERLINE OVARIAN TUMORS
• KRUKENBERG TUMORS
• MALIGNANT OVARIAN TUMORS
BENIGN OVARIAN TUMORS
 BENIGN OVARIAN TUMORS
• Account for 80% of all ovarian tumors
• The most common histopathological subtypes
include:
1. Cystadenomas
2. Cystadenofibromas
3. Mature teratomas
4. Benign sex cord stromal tumors
5. Brenner tumors
 BENIGN OVARIAN TUMORS
1. CYSTADENOMAS
• Account for 37-50% of benign ovarian tumors in the
reproductive age
• Their frequency increases with age, after menopause
cystadenomas account for up to 80% of all benign
ovarian tumors
• Thin walled unilocular or multilocular cystic lesions
filled with serous, mucinous or hemorrhagic content
• Papillary projections can be rarely seen
• Histopathological types include:
a. Serous cystadenomas
b. Mucinous cystadenomas
 BENIGN OVARIAN TUMORS
1.a. SEROUS CYSTADENOMAS
• Prevalence: 11% among patients with adnexal
masses
• Accounts for 40% of all benign ovarian tumors
• Peak incidence in the fourth and fifth decades
of age
• Bilateral in up to 20% of cases
• Precursor of ovarian cancer and may slowly
transform to borderline tumors
 BENIGN OVARIAN TUMORS
1.b. MUCINOUS CYSTADENOMAS
• Prevalence of 7% among patients with adnexal
masses
• Account for 20% of all benign ovarian tumors
• Commonly large tumors usually found in young
women
• Might present intramural calcifications
• May be associated with pregnancy
• Rarely bilateral lesions (<5% of cases)
• Precursor of ovarian cancer and may slowly
transform to borderline tumors
 BENIGN OVARIAN TUMORS
1.CYSTADENOMAS – IMAGISTIC STUDIES
• Serous cystadenomas usually present as
unilocular lesions while mucinous cystadenomas
are usually multilocular lesions
• Both subtypes present as:
- well-circumscribed cystic lesions
- thin walls
- thin septa (if present septa measure<3mm)
- Small papillary projections (if present papillary
projections measure<3-5mm)
 BENIGN OVARIAN TUMORS
2.CYSTADENOFIBROMAS
• Account for <2% of al ovarian tumors
• Benign cystic lesions composed of epithelial
and solid stromal elements
• Well defined and smooth lesions
• Unilateral/bilateral lesions
• Unilocular/multilocular lesions
 BENIGN OVARIAN TUMORS
3.MATURE TERATOMAS
• The most common ovarian neoplasms in
women<45 years old and account for 70% of
tumors in females<20 years
• Originate from germ cell tumors
• Histopathological subtypes:
- Mature cystic teratomas – most common lesions
- Monodermal teratomas (struma ovarii)
- Carcinoid tumors
 BENIGN OVARIAN TUMORS
MATURE CYSTIC TERATOMAS=DERMOID CYSTS
• Typically contain: sebaceous fluid, adipose tissue, teeth,
hair, bones -> at imaging studies calcifications are seen
• Are typically unilateral lesions (less than 15% of cases
present bilateral lesions)
• Usually unilocular lesions
• Usually asymptomatic and tend to grow slowly
• Complications include:
- Torsion (in up to 16% of cases)
- Rupture -> granulomatous peritonitis secondary to the
leakage of fatty content in the peritoneal area
- Malignant degeneration (especially in larger than 10 cm
lesions)
 BENIGN OVARIAN TUMORS
4.BENIGN SEX CORD STROMAL TUMORS
• Include tumors originating from:
- Granulosa cells
- Theca cells
- Luteinized derivates: Sertoli cells, Leydig cells and
fibroblasts of gonadal stromal origin
• The most common histopathological subtypes
include:
- Fibromas and thecomas
- Sclerosing stromal tumors
 BENIGN OVARIAN TUMORS
4.BRENNER TUMORS
• Rare ovarian tumors (1-3% of all ovarian
tumors) usually incidentally diagnosed in the
fifth decade of age
• Less than 2% might suffer malignant
transformation
• Typically small, solid, unilateral lesions (60% of
cases being smaller than 2 cm)
• Might produce estrogen -> endometrial
thickening
 BENIGN OVARIAN TUMORS
ENDOMETRIOMAS
• Usually found in patients with endometriosis
• Consist of large cystic lesions containing blood
products
• Unilocular/multilocular lesions
• Fibrous perilesional adhesions might be also
present
 ADNEXAL MASS IN PREGNANCY
• Adnexal masses have been reported in 1-2% of all
pregnancies
• Most of them – functional cysts which will
disappear during the first 16 weeks of gestation
• Other types of lesions include:
- Mature cystic teratomas
- Cystadenomas
- Ovarian malignant tumors
 BENIGN OVARIAN LESIONS
THERAPEUTIC STRATEGIES
• Conservative treatment should be attempted
to preserve endocrine function unless there is
a history of cancer risk
• Systematic bilateral adnexectomy:
 is not recommended in pre-menopausal
women
Reduces the risk of ovarian cancer in
postmenopausal women but increases the
cardiovascular risk
 BENIGN OVARIAN LESIONS
INDICATIONS FOR SURGERY
• Indications for surgery:
- Ovarian cysts > 5cm followed for 6-8 weeks
- Solid lesions
- Presence of papillary vegetation, intracystic
septa, calcifications
- Mass larger than 10 cm at diagnostic
- Palpable mass
- Suspicion of complication: torsion/rupture/
intracystic hemorrhage
 BENIGN OVARIAN LESIONS
INDICATIONS FOR SURGERY
Unilocular anechoic cyst
- Hormone treatment is not effective
- Symptomatic patients, or asymptomatic patients with
lesions >10 cm – laparoscopic cystectomy
- Asymptomatic patients, lesions<10 cm – the risk of
cancer is comparable to that of women without cysts –
conservative management is recommended
- Asymptomatic cysts in patients with family history of
breast/ovarian cancer – laparoscopic cystectomy
should be performed irrespective of dimension
 BENIGN OVARIAN LESIONS
INDICATIONS FOR SURGERY
Dermoid cyst:
- Surgery is indicated in:
 symptomatic lesions - laparoscopic cystectomy
 Larger than 10 cm lesions - laparoscopic cystectomy

Endometrioma:
- Surgery is indicated:
 in symptomatic lesions
 In cases in which the medical treatment has failed
BORDERLINE OVARIAN TUMORS
 BORDERLINE OVARIAN TUMORS
Are represented by the tumors considered to
have a low malignant potential:
- Serous ovarian tumors (2/3 of cases)
- Mucinous ovarian tumors (1/3 of cases)
 SEROUS BORDERLINE TUMORS
Patients with serous borderline tumors are on
average younger than patients with malignant
lesions
Might present histopathological features of
micropapillary pattern
Prognosis is far better than in patients with
serous/mucinous carcinomas
MUCINOUS BORDERLINE TUMORS
• Usually present as large lesions (>15 cm in diameter)
• Since 2014 – only the intestinal type is included in this
class. The other histopathological subtypes are
included in a specific class –seromucinous borderline
tumors
• Multicystic and bilateral lesions in 5% of cases
• Differential diagnostic with:
- Metastatic neoplasia (especially with colorectal origin)
• Excellent prognosis
 BORDERLINE TUMORS
MANAGEMENT STRATEGIES
• Standard therapeutic approach:
- Staging laparotomy/laparoscopy
- Removal of all suspect lesions
- Appendectomy
- Biopsies from several sites if no suspected
peritoneal lesion is present
 SEROUS BORDERLINE TUMORS
MANAGEMENT STRATEGIES
Young age, benign appearance of the ovarian tumor

Laparoscopic cystectomy

SEROUS BORDERLINE TUMOR SEROUS BORDERLINE TUMOR WITH

MICROPAPILLARY PATTERN

UNILATERAL SALPINGO-
OOPHORECTOMY, PARTIAL UNILATERAL SALPINGO-OOPHORECTOMY,
OMENTECTOMY, CYTOLOGY PARTIAL OMENTECTOMY, CYTOLOGY FROM THE
FROM THE PERITONEAL FLUID PERITONEAL FLUID, LYMPH NODE BIOPSY
IF INVASIVE IMPANTS ARE FOUND – TOTAL
HYSTERECTOMY WITH BILATERAL ADNEXECTOMY
ROUTINE FOLLOW UP

CLOSE FOLLOW UP FOR LONG TERM

 MUCINOUS BORDERLINE TUMORS
MANAGEMENT STRATEGIES
Young age, benign appearance of the ovarian tumor

Laparoscopic cystectomy

MUCINOUS BORDERLINE TUMOR – SEROMUCINOUS BORDERLINE TUMOR

intestinal type

UNILATERAL SALPINGO-OOPHORECTOMY,
Recheck pathology
PARTIAL OMENTECTOMY, CYTOLOGY FROM
THE PERITONEAL FLUID, APPENDECTOMY
UNILATERAL SALPINGO- IF INVASIVE IMPANTS ARE FOUND – TOTAL
OOPHORECTOMY, HYSTERECTOMY WITH BILATERAL
Malignant
APPENDECTOMY, CYTOLOGY ADNEXECTOMY
lesion
FROM THE PERITONEAL FLUID

CLOSE FOLLOW UP FOR LONG TERM

ROUTINE FOLLOW UP
KRUKENBERG TUMORS
 KRUKENBERG TUMORS
• Krukenberg tumors are ovarian metastases secondary to
specific malignancies, most of which derive from the
gastrointestinal tract (gastric cancer and colon cancer being
the most frequently reported origin)
• Uncommon metastatic tumors in the ovary initially described
by Friedrich Krukenberg in 1896
• The metastatic nature of these lesions was demonstrated in
1902
• The estimated incidence ranges from 0,7% to 6,7%
• The most common primary sites include the gastrointestinal
tract (in Asia is estimated that up to 10% women with gastric
cancer will develop Krukenberg tumors)
• Extremely poor prognosis compared to primary ovarian
cancer although surgery might play a role
 KRUKENBERG TUMORS
CLINICAL PRESENTATION
• Krukenberg tumors (KT) are diagnosed before the primary
neoplasms in up to 65% of cases
• KT – can be also detected:
- During staging – synchronous lesions
- After resection of the primary tumors – metachronous
lesions
• KT – might be asymptomatic a long period of time; when
symptomatic, the most common symptoms include:
- Abdominal/pelvic pain, weight loss, bloating, abdominal
distension (ascites)
- Hormonal imbalance (hirsutism/virilization, vaginal
bleeding)
 KRUKENBERG TUMORS
DIAGNOSIS
• Ultrasonographic features include:
- Bilateral solid lesions sometimes with
intramural cystic lesions
- The “lead vessel sign” – large lead vessel
penetrating the tumor from periphery and
then branching in a tree pattern
• CT features include:
- Lobulated solid lesions with homogenous
aspect
 KRUKENBERG TUMORS
MANAGEMENT STRATEGIES
• Poor response to chemotherapy, therefore attention was focused on surgery
• Management strategies vary depending on the time of diagnosis
1. When the ovarian tumor is diagnosed first
- Paraclinical tests to differentiate it from a primary ovarian cancer
- oophorectomy
- histopathological studies in order to clarify the origin
2. Synchronous presentation
- Radical surgery for both primary tumor and KT if possible
- If KT originates from peritoneal seeding – HIPEC might be associated
- If KT originates from lymphatic seeding – pelvic and para-aortic lymph node
dissection might be associated
3. Metachronous presentation
- Radical surgery (Oophorectomy in association with other visceral resections if other
metastatic lesions are present)

Palliative surgery – palliative oophorectomy in strongly symptomatic patients – rarely

recommended
 KRUKENBERG TUMORS
PROGNOSTIC FACTORS
• Prognostic factors include:
- Resection to no residual disease
- Absence of extraovarian disease
- The origin of the primary tumor (patients with
Krukenberg tumors in the context of gastric
cancer have a poorer outcome than those
with colon cancer)
PRIMARY MALIGNANT TUMORS OF
THE OVARY
 PRIMARY MALIGNANT OVARIAN
TUMORS
• Primary ovarian malignancies account for 3% of cancer
in females but ranks fifth in cancer mortality (and the
leading cause of death among gynecological cancers)
• Ovarian cancer is often asymptomatic – due to this
aspect 75% of women present in advanced stages of
the disease
• Primary ovarian cancer includes:
- Surface epithelial cancer
- Germ cell tumors
- Sex cord stromal tumors
 PRIMARY MALIGNANT OVARIAN
TUMORS
• The strongest patient related risk factors for
ovarian cancer include family history and age (the
vast majority of epithelial carcinomas being
diagnosed in the postmenopausal period)
• In patients with genetic predisposition ovarian
cancer occur approximately 10 years earlier
• In younger than 20 years of age patients germ
cell tumors account for more than 2/3 of
malignant ovarian tumors
 PRIMARY MALIGNANT OVARIAN
TUMORS
• Risk factors:
 Genetic factors
- Lynch syndrome (association of colon/breast/ovarian/endometrial cancer) –
estimated ovarian cancer risk =10%
- BRCA 1/2 mutation: BRCA 1 - estimated ovarian cancer risk =36-60%, BRCA2 -
estimated ovarian cancer risk = 12-25%
- Other genetic factors include the presence of high risk genes such as PTEN, TP53,
CDH1, STK11
 Reproductive factors
- Prolonged times of uninterrupted ovulation
- Infertility, nuliparity
- Late menopause, early menarche onset
- Polycystic ovary syndrome
- Endometriosis
 Environmental factors
- Cigarette smoking
PRIMARY MALIGNANT OVARIAN TUMORS
OVARIAN CANCER SCREENING
• Various tests such as association between CA125
determination and transvaginal sonography have
been proposed with poor results
• Therefore screening for ovarian cancer is
currently not recommended in general
population (high prevalence of false positive
results)
• However patients with high risk (relatives with
BRCA1/2 mutation, Lynch syndrome) should be
referred to genetic counseling
PRIMARY MALIGNANT OVARIAN TUMORS
CLINICAL PRESENTATION
• Silent killer
• Nonspecific symptoms – may mimic
gastrointestinal or urinary disorders
• Abdominal bloating/abdominal swelling
(ascites)
• Vaginal discharge/bleeding – rarely seen
• Paraneoplastic syndromes: hipercalcemia,
thromboses, neurologic disorders, Cushing
syndrome, collagen vascular disease
PRIMARY MALIGNANT OVARIAN TUMORS
TUMOR MARKERS

• CA125 – values higher than 35 U/ml might be

suggestive for ovarian cancer but in nonspecific
• However other malignant tumors (pancreatic,
lung, breast, colon cancer) or benign pathologies
(endometriosis, ovarian cysts, pelvic
inflammatory disease) might induce CA125 serum
levels elevation
• Other proposed tumor markers include: AFP,
HCG, LDH, CEA, CA 15-3
PRIMARY MALIGNANT OVARIAN TUMORS
IMAGING CHARACTERISTICS
• Local findings:
- Lesion size>4cm
- Wall/septal thickness >3 mm
- Papillary projections
- Lobulated mass
- Necrosis
- Solid and cystic architecture
• Distant findings:
- lymph node enlargement
- Peritoneal lesions
- ascites
PRIMARY MALIGNANT OVARIAN TUMORS
FIGO classification - 2014
SURFACE EPITHELIAL OVARIAN CANCER
• HIGH GRADE SEROUS OVARIAN CANCER
• LOW GRADE SEROUS OVARIAN CANCER
• MUCINOUS EPITHELIAL OVARIAN CANCER
• ENDOEMTROID OVARIAN CANCER
• CLEAR CELL CARCINOMAS
SURFACE EPITHELIAL OVARIAN CANCER
HIGH GRADE SEROUS CARCINOMA (HGSC)
Clinical:
- Aggressive tumors which typically present at
advanced stages with ascites
- Only 1% of HGSC are confined to the ovary at
diagnostic
- Declining incidence (probably due to the
protective effect of oral contraceptives)
SURFACE EPITHELIAL OVARIAN CANCER
LOW GRADE SEROUS CARCINOMA (LGSC)
• Are usually unilateral and may be confined to
the ovary at diagnosis
• Usually arise in serous cystadenomatous
tumors of low malignant potential (serous
borderline tumors)
• Good long term prognosis (10 year survival
rate – 50%)
SURFACE EPITHELIAL OVARIAN CANCER
MUCINOUS CARCINOMA
• Represent up to 3% of all ovarian carcinomas
• Good prognostic if diagnosed in early stages of
disease
• Poor prognostic (worse than in serous
carcinomas) if diagnosed in advanced stages
SURFACE EPITHELIAL OVARIAN CANCER
ENDOMETROID CARCINOMAS
• 10-15% of all ovarian carcinomas
• Associated with endometriosis in 40% of cases
• Bilateral in 25% of cases
• Associated with synchronous endometrial carcinoma in
20% of cases
• Usually diagnosed at younger age, lower stage and
higher likelihood of coexisting endometrial carcinoma
(when compared to serous carcinomas)
• Prognosis is similar with the one reported in serous
carcinomas
SURFACE EPITHELIAL OVARIAN CANCER
CLEAR CELL OVARIAN CARCINOMAS
• 10-15% of all ovarian carcinomas
• Diagnosed in younger women (average age of 55
years old) compared to HGSC
• 50-70% of patients will associate endometriosis
• Usually associated with paraneoplastic syndromes
such as hypercalcemia or thromboembolism
• In early stage these ovarian tumors have better
prognosis than HGSC
• However in advanced stages of the disease the
prognosis is poorer than in HGSC
 MALIGNANT OVARIAN TUMORS
SEX CORD STROMAL TUMORS
1. Granulosa cell tumor, adult type – the most common
subtype
2. Granulosa cell tumor, juvenile type
3. Sertoli- Leydig cell tumors
4. Thecomas
5. Fibromas
6. Fibrosarcomas
7. Sclerosing stromal tumors
8. Steroid cell tumors
9. Leydig cell tumors
10. Gynandroblastomas
 MALIGNANT OVARIAN TUMORS
GRANULOSA CELL TUMORS – adult type
• Granulosa cell tumors – up to 90% of sex cord stromal
tumors (which represent 7% of all malignant tumors)
• Usually occur in postmenopausal women
• Might be hormonally active (capacity of hormones
synthesis) and therefore might induce vaginal bleeding
and even endometrial carcinoma development
• Might suffer ruptures and induce the apparition of
hemoperitoneum (in up to 15% of cases)
• Up to 50% of cases develop recurrences (which may be
late – up to more than 20 years after primary
diagnostic)
 MALIGNANT OVARIAN TUMORS
MALIGNANT GERM CELL TUMORS
• Represent up to 30% of ovarian tumors
• The most common type of malignant ovarian
tumors in the first two decades of life
• The most frequent subtypes include:
1. Dysgerminomas
2. Yolk sac tumors
3. Embryonal carcinomas
4. Choriocarcinomas
 MANAGEMENT OF OVARIAN CARCINOMA
PRIMARY THERAPEUTIC STRATEGIES
• Primary treatment for presumed ovarian cancer –
SURGICAL STAGING and CYTOREDUCTION:
• Early stage ovarian cancer:
- Total hysterectomy with bilateral adnexectomy, partial
omentectomy, surgical staging of the lymph nodes
- Selected premenopausal women in stage I with low grade
tumors who desire fertility preservation – salpingo-
oophorectomy
- Adjuvant systemic chemotherapy: in patients with stage IC
lesions (patients with stage IA-IB usually not necessitate
further chemotherapy)
MANAGEMENT OF OVARIAN CARCINOMA
PRIMARY THERAPEUTIC STRATEGIES
• Advanced stage ovarian cancer:
- The gold standard of surgery is to resect all
macroscopic visible lesions
- Therefore, multiple resections might be
needed in order to achieve complete
cytoreduction
MANAGEMENT OF OVARIAN CARCINOMA
PRIMARY THERAPEUTIC STRATEGIES

- Once the cytoreductive phase is ended, the patient will be submitted to adjuvant
chemotherapy
INTRAOPERATIVE ASPECTS
MANAGEMENT OF OVARIAN CARCINOMA
PRIMARY THERAPEUTIC STRATEGIES

-if cytoreduction to no residual

disease is not achievable, patients
will submitted to chemotherapy
- however, in certain cases
palliative surgical procedures
might be needed
MANAGEMENT OF OVARIAN CARCINOMA
RECURRENT DISEASE
• Even in cases in which surgery is performed with
curative intent, relapse can occur
• In these cases surgery might be performed in
order to achieve cytoreduction to no residual
disease
• Adjuvant chemotherapy is usually recommended
• If cytoreduction to no residual disease is not
feasible, palliative chemotherapy might be taken
in consideration
Secondary cytoreduction
TOTAL PELVIC EXENTERATION FOR PELVIC RECURRENCE
SFTER SURGICALLY TREATED OVARIAN CANCER
DEBULKING CYTOREDUCTION FOR RECURRENT OVARIA
CANCER INVADING THE ILIAC VESSELS
 CHEMOTHERAPY IN OVARIAN CANCER

Chemotherapy whether single or multiple agents

has a major role in the management of ovarian
cancer especially in advanced disease, and mostly
with epithelial ovarian cancer:
1. Early stage disease: It has a limited place only
with poor prognostic factors as Poorly
differentiated tumours, ruptured capsule, or +ve
peritoneal wash (even in stage I cases).
2. Advanced stage disease: Chemotherapy is
indicated in all cases of stage II-IV disease.
a) All cases after primary cytoreductive debulking
surgery
b) Palliative therapy in patients with irresectable
tumours, or patients with recurrent disease.
Types of chemotherapy used:
• Chemotherapy is usually recommended as
soon as possible after surgery, and is given for
five or six cycles at 3-4 weekly intervals.
• The most frequently used chemotherapeutic
agents include: Cisplatin or Carboplatin alone
or in combination with Paclitaxel (Taxol).
Toxicity from chemotherapy:
• Chemotherapeutic agents are highly toxic
at therapeutic doses, and therefore need close
monitoring during treatment cycles. Toxicity
includes; nausea, vomiting, myalgia and
arthralgia. In severe cases renal damage,
peripheral neuropathy, hearing loss,
dehydration and electrolyte imbalance may
occur.
 RADIATION THERAPY IN OVARIAN CANCER
Radiation therapy has little place in epithelial
ovarian cancer. It may be used as an
adjuvant therapy following cytoreductive
surgery in patients who refuse or are not
good candidate for chemotherapy. Two main
forms are used:
• Intraperitoneal radioactive colloids
• Whole external beam abdominal radiation.
 PROGNOSIS IN OVARIAN CANCER

The prognosis depends upon:

• Histopathological type of ovarian cancer (epithelial or non
epithelial ovarian cancer)
• Stage of ovarian malignancy: the best prognosis is in stage Ia
• Optimal versus Suboptimal surgery (TAH BSO + omentectomy,
versus debulking)
• Histology and grading of the tumour. Well differentiated
tumours carry best prognosis, while poorly differentiated and
clear cell carcinomas carry the worst prognosis.
• Response of the tumour to adjuvant therapy (chemotherapy –
irradiation).